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In memoriam

Jonathan H. Musgrave

crypt, n.

Pronunciation: kript

Origin: A borrowing from Latin. Etymons: Latin crypta, crupta.

Etymology: < classical Latin crypta (also crupta) covered passage, arcade, (perhaps) underground room for religious rites, vault, crypt < Hellenistic Greek κρύπτη vault, used as noun of feminine of ancient Greek κρυπτός hidden, concealed < κρύπτειν to hide…

- 1. A cave, cavern, or grotto. Now rare.

- 2.

a. An underground cell, chamber, or vault; esp. one used as a burial place and typically lying beneath a church. Also: such a space used as a chapel or oratory.

b. figurative. Something likened to a crypt, esp. in being dark, deep, or hidden.

OED Third Edition, June 2011; most recently modified version published online March 2022

OSTEOBIOGRAPHY Literally: written in bone.

It is through written language that we transcend the communication barriers of distance and time. Ideas and images, reconstructed in words, flow from one human brain to another. It’s the most extraordinary technology, allowing us to read something that has been in someone’s mind, far away, perhaps even on the other side of the world. We may never have met that person; maybe we never will. We can also read the thoughts of someone who is no longer here, who passed away last year, or a few decades ago, or hundreds, thousands of years ago.

(I think about this when I’m writing. How extraordinary and yet how ordinary it has become, that I can write these words and that you, somewhere, sometime, are reading them. Well, you’re only two pages in, so I hope you like the rest!)

In the depths of prehistory, we don’t have any written record of the world, of the lives of our ancestors. That is, after all, the definition of that time: it is pre-history. But we have archaeology, which is both a branch of anthropology and a historical science. We can look at the physical remains of our ancestors’ culture and technology, the things they made and built, and even at the physical remains of them, and draw inferences about a world, about lives, long forgotten. Advances in our technology, the scientific techniques we use to interrogate the past, mean that we can now unlock more of those secrets than ever before. We can collect information from satellite data, drone footage and from geophysical surveys. We can date objects very precisely using radiometric dating techniques, such as radiocarbon dating. We can analyse the chemical composition of rocks and minerals to find out where they came from before humans moved them around. And when it comes to human remains, we now have an impressive toolkit of techniques that can help us to find out where someone grew up as a child (by analysing the chemical composition of their teeth) and – perhaps most excitingly – we can extract and sequence ancient DNA; not just fragments of it, but entire genomes. Those genomes can tell us an enormous amount: about individuals, about kinship between people buried in the same tomb or cemetery, about how much people were moving around and migrating from one place to another.

All that archaeology is a precious resource for our understanding of prehistory, but those same sources of information exist in the historical era, too. There, archaeology can show us a very different picture from history. It’s not just there to illustrate the written sources, either; it’s an independent source of data that enables us to look at wider questions, to track changes through time and – sometimes – to test what the historical documents seem to be saying. It also lets us glimpse the lives of ordinary people – people missing from the historical record.

Archaeology is not ancillary to history; it is not its slightly scruffier, grubbier handmaiden. It’s unashamedly earthy, grounded and physical, but out of the dirt come gems of understanding. Bringing together these two disciplines – history and archaeology, with all these new scientific techniques – we now have an extremely powerful way of interrogating and understanding the past.

This is the third book of a series in which I have explored the stories of the past that archaeology can now reconstruct, focusing on burials and the analysis of human remains. But don’t worry if you haven’t read the other two. There’s a chronology running through them: in the first book, Ancestors, I looked at what prehistoric burials tell us about ancient lives; in the second book, Buried, I moved into the first millennium of the Common Era (Anno Domini in old money), with stories of Romans, Vikings and Anglo-Saxons. This book is located in the High and Late Middle Ages – roughly 1000 CE to 1500 CE – with a brief but useful foray into the sixteenth century. And it’s a bit different from the others in that there’s a focus on pathology: on disease and injury; the experience of human suffering in the past; and on the evolution of the diseases themselves. The study of diseases and injuries in the past has its own name: palaeopathology. That investigation starts with looking for marks on bones, the stigmata of inflammation, infection or injury, and continues with radiological and genetic analyses.

I’m particularly fascinated and excited by the revolutionary new technology of archaeogenomics, where geneticists are extracting and analysing entire ancient genomes – barely a week goes by without another revelation from this fast-moving field of enquiry. In Ancestors, I wrote about the inception of the most ambitious ancient-DNA study in Britain to date: the Thousand Ancient Genomes project, headed up by Pontus Skoglund in his lab at the Francis Crick Institute in London. That project is still going, and I have been able to share some of the emerging data, as they come to light, in these books. We’ve seen evidence of close kin being buried in Neolithic long barrows, confirming the suggestion put forward by some archaeologists that these monumental, stone-lined tombs were used – at least in some cases – as family ‘vaults’. We’ve learned that the early Bronze Age in Britain, which saw the arrival of metal-working for the first time as well as new styles of pottery and burial, was mediated by a large migration, perhaps over several centuries, replacing much of the previous population. We’ve realised that the scourge of the Justinianic Plague of the sixth century, which ravaged the Byzantine Empire, reached as far as Britain – something the historical documents were simply silent on.

In Pontus’s lab, postgraduate student Pooja Swali has been focusing on palaeopathology from a genetic perspective. The data she’s interested in is not the human DNA but the non-human – the metagenome. The ability to track down ancient pathogen DNA and sequence it has given us a new way of looking at infectious diseases in the past.

Pooja looks for the genetic traces of diseases that entered bodies and were then carried to the grave. We’re not just looking at the lesions that a disease may create in the skeleton, but at the genome of an agent of disease. And Pooja has found evidence of systemic infection in bones that appear entirely unmarked by disease. Thanks to the work of archaeogeneticists, we can now pin diagnoses on ancient afflictions in a way that seemed unthinkable just a couple of decades ago. It means we can now track diseases over time, sometimes finding them in unexpected times and places. I explore how genetic research is uncovering cryptic clues and shedding light on the identity and evolution of diseases – including leprosy, syphilis and the plague – in a way that can even inform our understanding of contemporary diseases.

In the Middle Ages, there’s barely a written note for most people’s lives. The rich and powerful take up most of the oxygen of publicity (just as they do today), and the evidence of more ordinary lives may be reduced to an inscription on a tombstone, a mention in a legal case or in a financial transaction – or, nothing at all. Even when it comes to very well-known people, like Shakespeare and Chaucer, we know very little about their lives, really; most of the documentary evidence we have relates to business matters. Contemporary images, portraits, are the same – they are few and far between, except when it comes to nobility.

The information we can extract from archaeological human remains represents another biographical source (as well as providing useful data on a population level). It’s another way of looking at an individual, even if we don’t know their name. That life-story (and sometimes death-story) written in bone has been called an osteobiography. Given that we simply don’t have textual biographies for the vast majority of medieval people (or indeed, for most people in almost any period), the osteobiography is an essential tool for understanding past lives.

The stories in this book are not comforting tales. We learn of an episode of terrible brutality, when hate speech unleashed a tide of violence against an ethnic minority in multicultural England; of life-changing disease as incurable epidemics swept through medieval Europe; of a protracted battle between Church and State for the heart of England – a battle that saw the most famous tomb in England created and destroyed, and a tumultuous story, forged in the heat of warfare, that takes us out of the Middle Ages into the sixteenth century and the reign of Henry VIII.

We see, in macrocosm, society struggling to make sense of disease, disability and death, where those struck down by disfiguring afflictions could be seen as cursed or blessed, or both. In microcosm, the minute cells that build and destroy our skeletons on a daily basis strive to keep bones alive and strong – or are led astray by their own genetic programme and the insults hurled at them by the environment. And between those macro and micro scales, there are real people. We come face to face with individuals who lived and died between ten and five centuries ago: the victims of the St Brice’s Day Massacre; the patients at one of the earliest hospitals in England; the archers who went down with the Mary Rose.

Most of these dead remain anonymous. It is very rare that we can connect a name with an individual skeleton. But, in the final chapter, we meet someone where osteobiography and historical biography coincide: an individual whose life and bones were marked by chronic debilitating disease – and whose name might just be found in history.

1. COCKLE AMONGST THE WHEAT

It seems to be all too easy for human societies to divide themselves up, to fracture, along any lines that might be discernible, especially when there is competition for resources, but sometimes, even when there isn’t. One of the worst things that any leader can do is to stoke division, to encourage one group to look suspiciously at another, and dehumanise them. Religion, language, dress, skin colour – any or all of these can be used to mark out a group of people as ‘other’. Once that othering has happened, the more powerful group may rationalise restricting access to certain resources, denying those others access to certain spaces and certain rights. It can go further, even leading to physical attack.

In 2011, I made my way to Reading to look at a group of skeletons that had been exhumed three years before, from a pit in Oxford where the bodies of at least thirty-five people had once been slung into a mass grave. The grave hadn’t been dug out – it was simply a section of an existing ditch. And this ditch was part of a large, previously unknown Neolithic earthwork, possibly a henge monument, which ran right under Oxford University’s St John’s College and Keble College. Three thousand years after its construction, in the Middle Ages, it had still been an obvious feature in the landscape, forming a convenient, ready-made grave for the disposal of these corpses.

I met up with osteologist Ceri Falys from Thames Valley Archaeological Services, who had been examining the remains. In a lab, Ceri had laid out the skeletons on tables covered with bubble-wrap; one skeleton per table. There were obvious and undeniable signs of violent injury on the bones.

The very first skull that had been discovered had been found and recovered as a heap of fragments – and had been carefully reconstructed in the lab. As soon as it was put back together, it was clear that at least some of the breaks had been created by violent blows. I picked up the partially reconstructed calvarium, or skull-cap, and across the frontal and left parietal bone there were three long, chopping blade wounds. I could see where the sword – for this is surely what must have caused these injuries – had sliced into the bone, breaking off a flake behind the blade. There were shallower, glancing wounds as well, and Ceri pointed out two triangular puncture wounds that could have been caused by the point of a spear. There were at least ten separate injuries on this one skull. It was horrific. Holding the skull in my hands, I was suddenly confronted and connected with that moment of violence, that moment of death. The same skeleton also had puncture wounds in two vertebral laminae – the broad pieces of bone forming the back of each vertebra. Ceri thought these looked like wounds from a thrusting spear, rather than a thrown one. From the rest of the bones, and the teeth, we could conclude that we were looking at the remains of a young man. From the position of the puncture wounds to his spine, the injuries were most likely to have been inflicted when he was already lying face down.

Another skeleton bore even more chilling signs of violence. Once again, there were numerous blade wounds to the skull, one of which had cut across the left ear. The mastoid process – the chunky bony protuberance that you can feel just behind and below your ear – was sliced right through, revealing the honeycomb spaces inside the bone. There were also two blade wounds on the left side of the mandible or lower jaw, and Ceri showed me four blade wounds to the upper cervical – or neck – vertebrae. Amongst these multiple injuries, it looked as though one blade strike had cut across the angle of the mandible on the left, slicing through the mastoid, then continuing to cut into the vertebrae under the skull. An attempted beheading.

Moving down the skeleton, there were more puncture wounds on the side of the left pelvic bone, the force of the attack driving the point of the weapon right through the bone; another puncture wound entered the front of the pelvis on the right – the weapon causing that injury would have been thrust through the belly, through the guts, into the bone. This man had been assaulted from all angles.

Drawing my attention to the skull again, Ceri showed me how the frontal bone was damaged and charred. The right hand bones were also burned. And some of the other skeletons showed similar signs of burning.

What was missing amongst these injuries was the type of wounds you might expect when someone is defending themselves – often on forearms, being held up as protection. Had these men been running away when they were mown down? And who were they? Ceri had determined that most of the individuals had been young men, aged between sixteen and twenty-five years old on the day they met their deaths. And there was no doubt that their ends had been exceptionally vicious and violent: they had been hacked to death. A thousand years on, with the blood long since soaked away and just their dry bones left, that brutality is still utterly shocking.

It’s rare to find archaeological evidence of a specific historical event, and always very difficult, if not impossible, to prove. But when the archaeologists had originally excavated these remains, they had wondered whether they represented some of the victims of a particularly horrific event, mentioned in the Anglo-Saxon Chronicle and later annals, that took place in 1002 CE.

The Anglo-Saxon Chronicle is a record of events, year by year, begun in the late ninth century during the rule of Alfred the Great, King of Wessex, and continuing into the twelfth century. It includes various events taking place in the year 1002 CE.

At this time, Æthelred II (known as ‘Æthelred the Unready’, which means something like ‘The Nobly-Advised Poorly-Advised’ or ‘Wise Unwise’) was on the throne of England. This relatively new kingdom was experiencing fairly constant attacks from neighbours across the North Sea. The previous couple of years had seen numerous attacks by the ‘Danes’ (a term which could be used quite generally to refer to Scandinavians broadly), in Kent, Hampshire and as far west as Devon and Somerset, from their base on the Isle of Wight.

Æthelred’s forces had met and fought with the Danish invaders, with losses on both sides. But in 1002, Æthelred and his council decided to broker a peace settlement, agreeing to send provisions and a tribute of £24,000 to the fleet alderman, Leofsy. But, still, Leofsy then slew one of the king’s representatives.

In the same spring, the Anglo-Saxon Chronicle tells us, Emma of Normandy arrived in Britain to marry Æthelred. She was the daughter of the Norman ruler, Richard I (aka Richard the Fearless), and his wife Gunnor (who came from a noble Danish family). Richard and Æthelred had been enemies for a long while, and the Vikings often sailed from Normandy to mount their attacks on England. This marriage had a clear diplomatic aim: to create a virtual alliance between England and Normandy. But the Danes – and presumably the huge sum he’d had to pay them to ‘desist from their mischief’ that year – were still very much on Æthelred’s mind. The Chronicle records that: ‘in the same year the king gave an order to slay all the Danes that were in England. This was accordingly done on the mass-day of St. Brice.’

This lashing-out at the Danes came after what had been centuries of strife between groups who we may loosely and broadly define as Vikings and Anglo-Saxons, tussling for power and territory in England. Scandinavian raiders had repeatedly attacked the east coast of Britain (and, indeed, all around the north of Britain) from the eighth century onwards. In the ninth century they banded together, and the Great Heathen Army (‘magna paganorum classis’) pitched up, sailing their longboats right up the Humber into the heart of York. The Vikings eventually seized a huge swathe of what is now northern and eastern England, forming the territory of what later became known as the Danelaw – the region under Danish rule. The Danelaw was recognised in the peace treaty drawn up by Alfred the Great and Guthrum in 886, after the Vikings had tried to push further west and were defeated. A diagonal line, from the Mersey estuary in the northwest to the Thames estuary in the southeast, marked the border between the Anglo-Saxon kingdom of Wessex, and its dependencies, to the south and west, and the Danelaw, to the east and north. But the power struggles continued, with the tenth century seeing the Danes repeatedly making incursions into Anglo-Saxon territory – sometimes victoriously, though at huge cost; sometimes being beaten back.

In 927, King Alfred’s grandson, Æthelstan, took control of Northumbria to become the first ‘Rex Anglorum’ – King of the English. But the new, united kingdom of England would be short-lived. Just twelve years later, Northumbria and much of what is now the English Midlands would be seized by the Irish Vikings. The Anglo-Saxons wrested back control in the 940s, but there were still periods when the elite ruling families of the north preferred Viking kings to southern rule. After a brief reign as king of Northumbria, the famous Viking Eric Bloodaxe was expelled in 954, and with his deposition the Danelaw came to an end. Then, after a few decades of relative peace in England, Danish raids started up again.

In 991, Æthelred II was on the English throne when a Danish fleet sailed up the Blackwater River in Essex and attacked the East Saxons, defeating them at the Battle of Maldon. Rather than continue fighting, Æthelred settled on paying them tribute instead – £10,000, according to the Anglo-Saxon Chronicle. He must have hoped that this would solve the problem. But the raids continued. In 994, Æthelred was forced to pay the Vikings off again, when they’d taken to besieging London. This time they were given £16,000 pounds. But just a couple of years later, the raids were back on, and in 1002, Æthelred offered the Scandinavians that enormous payment of £24,000. These tributes would later be called Danegeld, or ‘Dane-yield’ (reminding us that all taxes essentially start off as a protection racket). But it clearly rankled, and it was later that same year that Æthelred turned against his own subjects with his order to slay the Danes. He seems to have been reacting to the external threat of Viking raids – which were very real and very frequent – by stoking up hatred and inciting violence against ethnic Danes settled in England.

The earliest account of the St Brice’s Day Massacre comes not from the Anglo-Saxon Chronicle, but from a royal charter issued by Æthelred just two years after the event, in 1004, relating to the rebuilding of the church of St Frideswide in Oxford. And this is what it says:

To all dwelling in this country it will be well known that… a decree was sent out by me with the councel of my leading men and magnates, to the effect that all the Danes who had sprung up in this island, sprouting like cockle amongst the wheat, were to be destroyed by a most just extermination, and this decree was to be put into effect even as far as death…

It’s so chilling. ‘Cockle amongst the wheat’ is such an invidious phrase. Cockle, darnel or darnel ryegrass is sometimes known as ‘false wheat’; it looks almost identical to wheat until the ear appears, and it turns black rather than golden when it ripens. The Danes were being compared with weeds. It’s a familiar trope in hate speech, through the centuries to the present – the comparison of a certain group to weeds, vermin or parasites: Rohingya in Myanmar, Jews in Nazi Germany, Tutsis in Rwanda; Danes in eleventh-century England. The purpose of such language is quite clear: it is designed to dehumanise, to ‘other’, to elicit disgust. Contemporary studies have demonstrated how this disgust, directed towards immigrants, can be further accentuated if felt in the context of a strong national identity.

Æthelred, being a good Christian Anglo-Saxon king, would have been well aware of the religious connotations of the phrase he chose to describe the Danes in England. In the Gospel of St Matthew, the Parable of the Tares describes a man sowing good seed in his field, but an enemy creeps in under cover of night to sow the ‘tares’. Later, servants spot the weeds sprouting amongst the wheat; the landowner tells the servants to wait until harvest time and then gather the wheat into the barn, but bundle up the tares separately and set fire to them. The original Greek word used in the Bible, later translated as ‘tares’, is zizania – also occasionally translated as ‘darnel’ – or ‘cockles’.

Some early theologians interpreted the Parable of the Tares as a message of religious tolerance. St Augustine said the angels, who could not make mistakes, would perform the separation at the moment of harvest, implying that mere mortals shouldn’t pre-empt that divine reckoning and take it upon themselves to weed out the ‘tares’. Similarly, St John Chrysostom, the ‘golden-mouthed’, preached that it was wrong to put heretics to death as mistakes could be made, and ‘tares’ should not be deprived of the opportunity to turn into ‘wheat’. But parables can be read in many ways, and Æthelred seems to have missed the memo about this tolerant interpretation of the fable as he issued his decree for the extermination of the Danes.

The St Frideswide charter continues:

… those Danes who dwelt in [Oxford], striving to escape death, entered this sanctuary of Christ, having broken by force the doors and bolts, and resolved to make a refuge and defence for themselves therin against the people of the town and the suburbs; but when all the people in pursuit strove, forced by necessity, to drive them out, and could not, they set fire to the planks and burnt, as it seems, this church with its ornaments and its books.

The burning-down of a church containing refugees seems to violate the sacred principle of sanctuary, even if it wasn’t completely illegal. This charter is the only mention we have of a specific instance of violence against the Danes, apparently carried out in response to Æthelred’s decree. While the order was intended for ‘all the Danes who had sprung up in this island’, Oxford is the only place where we can be sure that people – ‘of the town and the suburbs’ – seemingly responded to this incitement to violence. On the other hand, the fact that the execution of this order is referenced, however briefly, in the Anglo-Saxon Chronicle (where Oxford is not specifically mentioned) suggests it was a more widespread phenomenon. Questions remain as to the nature of the victims and the perpetrators. What’s impossible to know from the royal charter, for instance, is whether the attack on the Danes in Oxford was carried out by a general mob, or by a more official band of law enforcers. And who were the ‘Danes’ that were attacked, anyway? There must have been people with Danish roots settled amongst the peasant classes; after at least two centuries of raiding, some of the raiders would have stayed and settled. There may have been groups of Danish soldiers still over in England. And there were certainly Danish mercenaries around – whom Æthelred himself paid to fight against their compatriots. Given that we don’t know exactly who the victims or who the pursuers were, the connection between Æthelred’s decree and this violent attack in Oxford could possibly be even more tenuous. Perhaps Æthelred was keen to make an explicit link between what seems to have been an ethnically motivated attack and his own rhetoric. Whether or not it really was instigated by his decree, the connection suited his political aims. Æthelred had suffered a series of embarrassing and costly defeats at the hands of the Danes and had also handed over more than a small fortune to them in tribute. But was his motivation simply about being seen to do something about the Danish problem? Or was there more to it?

The St Frideswide charter doesn’t mention a specific reason for Æthelred’s savage decree – but the Anglo-Saxon Chronicle does. The order to slay the Danes came about, it says, ‘because it was told the king, that they would beshrew him of his life, and afterwards all his council, and then have his kingdom without any resistance’. Whether or not these Danes were settlers or soldiers who should have been bound by the terms of the treaty signed and settled in the spring of 1002, or indeed mercenaries, this version of events suggests that Æthelred had been warned to suspect treachery from them. Perhaps, as one historian has suggested, it’s most likely that the Danes in question were those mercenary soldiers whose services Æthelred had bought, but now he was worried that they would betray him and switch to supporting the Danish king, Sweyn Forkbeard, who clearly had designs on England that went beyond raiding. Just the previous year, a key ally called Pallig, believed to have been a Danish mercenary, had defected, ‘for he had shaken off his allegiance to King Ethelred’, reports the Anglo-Saxon Chronicle, ‘against all the vows of truth and fidelity which he had given him, as well as the presents which the king had bestowed on him in houses and gold and silver’.

It’s important to note the fairly perfunctory mention of the St Brice’s Day Massacre in the royal charter of 1004 and the Anglo-Saxon Chronicle, because later historical records contain much more, fairly gory, detail. As so often, this was a story that grew with the telling. One chronicle, that of William of Jumièges, written around 1070, contains particularly horrific details that didn’t appear anywhere in the contemporary accounts:

… Æthelred, king of the English, defiled a kingdom that had long flourished under the great glory of most powerful kings with such a dreadful crime that in his own reign even the heathens judged it as a detestable, shocking deed. For in a single day he had murdered, in a sudden fury and without charging them with any crime, the Danes who lived peacefully and quite harmoniously throughout the kingdom and who did not at all fear for their lives. He ordered women to be buried up to their waists and the nipples to be torn from their breasts by ferocious mastiffs set upon them. He also gave orders to crush little children against door-posts.

Vicious. Another chronicle, penned by the monk Florence of Worcester even later, around 1124, was less bloody. But, like the account by William of Jumièges, it also suggested that civilians were targeted in the attack:

The same year, King Ethelred gave orders for the massacre of all the Danes of every age and both sexes, in consequence of their having conspired to deprive him and his nobles of their life and kingdom and reduce the whole of England under their dominion.

This was the first time that anyone described the event as a ‘massacre’, though Florence does provide Æthelred with a similar rationale for such an assault: the suspicion of treachery. When William of Malmesbury mentioned the event, in 1140, he was unequivocally critical of Æthelred, writing about the event as an example of the king’s ‘insolence’ and claiming that the decree to murder Danes was ordered ‘on the strength of flimsy suspicions’, compelling ‘every man… to betray his beloved guest-friends, whom he had made even more dear by close ties of relationship, and to disrupt those embraces with the sword’.

In the accounts of William of Jumièges, Florence of Worcester and William of Malmesbury, there is a clarity about the victims that doesn’t exist in the near-contemporary accounts. They see these Danes not as soldiers or mercenaries but as settled and integrated families; the attackers are their friends and even relatives, and Æthelred’s decree tears apart those communities. But how much was their point of view influenced by the political landscape of the eleventh and twelfth centuries? After all, something seismic had happened in the middle of the eleventh century, in 1066 to be precise. These later chroniclers were writing from an Anglo-Norman perspective – it would have fitted their contemporary agenda to paint late Anglo-Saxon kings as weak, treacherous and despotic – ripe for being supplanted, just as Harold Godwinson had been, by William I.

And in fact, the earliest of these Anglo-Norman accounts, from William of Jumièges, written just four years after the Norman Conquest, goes on to explain how it was Æthelred’s decree, and the massacre that followed, that led to his undoing:

When thus on the appointed day this outburst of violence, death and murder accumulated beyond measure, some quick and active young men took hold of a ship and fled, speedily rowing down the Thames out into the open sea. They crossed the wide sea and finally reached the harbour they sought in Denmark, and there they reported the bloody fate of their people to King Swein…

This is the aforementioned Sweyn Forkbeard, or Haraldsson, who’d deposed his father Harald to become king of Denmark in 986, later adding Norway to his domain. Hearing about the massacre in England, Sweyn called his nobles together and asked for their advice: ‘They were all much distressed and bewailed the calamity of their friends and kinsmen and with one voice decreed that every effort should be made to seek vengeance for their blood.’ According to the later account of William of Malmesbury, Sweyn himself lost close relatives in the massacre, with his sister, Gunhild, and her husband, Pallig Tokesen, the Danish Jarl (or Earl) of Devon, amongst the casualties. William of Jumièges wrote that Sweyn responded to the atrocity by announcing conscription in Denmark to raise an army, but that he also advertised the opportunity to mercenaries elsewhere: ‘He sent couriers in all directions to invite soldiers greedy for wealth from other countries to take part in this expedition and to assemble on the appointed day.’

Sweyn mustered a large army and sailed across the North Sea to Yorkshire – but then he made a detour. Taking a few ships, he sailed to Rouen to meet King Richard I of Normandy, and there he signed a treaty of ‘continuous peace’ between ‘the kings of the Danes and the dukes of the Normans as well as their heirs in the future’. The treaty also included a clause permitting the Danes to sell any of their spoils of war in Normandy. With this alliance sealed, Sweyn returned to England to subject ‘the realm of the English to the flames of revenge’. Yorkshire capitulated immediately (presumably being quite used to flip-flopping between Danish and Anglo-Saxon rulers by now), and Sweyn headed south, where Kent also surrendered. Sweyn headed up the Thames to lay siege to London, which soon yielded. Æthelred was in Winchester, ‘completely deserted by the English’. He dug up his treasure, gathered his wife and sons and fled to Normandy, where his somewhat duplicitous father-in-law, Richard, welcomed him with open arms. This is, however, not the last we shall see of Æthelred or his family – nor of Sweyn.

Ultimately, all these battles and power struggles were about one thing: control of the seas – command over the arteries that kept wealth flowing through raiding and trading. We tend to view history through the lens of high politics, focusing on shifting borders and territories, as though these abstract entities are somehow more real than family histories. The experience on the ground, amongst ordinary folk, would have been very different. Languages and customs may have distinguished people living in Scandinavia, northern France and England to some extent – but the seas were not the barrier to movement, language and ideas that we might assume. Going right back into prehistory, we see cultural links across the North Sea and the Channel. There would have been kinship ties too, as we see so clearly in those royal families, with their interconnected bloodlines, but ordinary people would also have had family connections across the sea.

The ‘Vikings’ themselves are hard to pin down. The term refers to Danes and Norsemen on the move, striking west from Scandinavia to raid the coast of Britain in the eighth century, arriving in the form of the Great Heathen Army to invade and settle in the ninth. (There were Swedish Vikings too; the traditional narrative has always had it that they went east, though the latest archaeological and scientific investigations cast doubt on this simple differentiation between Vikings from different geographic areas, as Cat Jarman brilliantly articulated in her book River Kings.)

We tie ourselves up in knots with language too. The old texts don’t actually mention ‘Vikings’; they more often refer to ‘Danes’ or ‘Norwegians’ and sometimes mix them up completely, as in this entry for the year 787 in the Anglo-Saxon Chronicle (my emphasis):

In this year… came first three ships of Norwegians from Hørthaland: and then the reeve rode thither and tried to compel them to go to the royal manor, for he did not know what they were: and then they slew him. These were the first ships of the Danes to come to England.

In fact, it wasn’t until the nineteenth century that the word ‘Viking’ became widely used for those Scandinavians raiding England in the late first millennium. The word comes from Old Norse; although its original meaning is contested, by the end of the eighth century víkingr was being used in skaldic poetry simply to mean ‘someone who went off on expeditions’, which may or may not have included raiding. So it meant something like ‘adventurer’ or ‘explorer’; it wasn’t an ethnic term. But a few centuries later, it was being used in a much more negative way: in the medieval Icelandic sagas víkingar were most definitely pirates.

The way we use the word now is more expansive, including traders as well as raiders, but also settlers. And just as Vikings settled in Britain, they settled in northern France as well. Normandy itself was named after the Norsemen who settled there in the tenth century. A Viking army, led by Hrólfr – or Rollo, as he became known – had laid siege to Chartres in 911. Like Æthelred the Unready, Charles the Simple of West Francia had decided to buy off the Vikings, not in silver, but in land. Rollo became the ruler of a swathe of northern Francia, stretching between the Seine and Rouen. And his descendants would continue to play significant political roles: a grandson of Rollo would become Richard I of Normandy. And a great-great-great-grandson was none other than William the Conqueror.

And let’s not forget that Æthelred also had an intimate connection with this Viking lineage. He was married to Emma, daughter of Richard I and Gunnor – the Norman king and queen, both of Viking descent. (And, of course, the origin myth of the Anglo-Saxon kings had them, too, tracing their heritage back to Scandinavian roots.) It makes his decree of 1002 seem even more extraordinary. The Danes he was prepared to incite hatred against, those ‘cockles in the wheat’, must have seemed somehow different, to him, from the Danes in his own family. Did he have a concept of the ‘Danes with us’ and the ‘Danes against us’? I’m left wondering what Emma thought of it all. (The Encomium Emmae Reginae – ‘Praise of Queen Emma’ – thought to have been written in the 1040s, focuses on her reign with Cnut, and completely misses out her earlier marriage to Æthelred.)

The later Anglo-Normans, like William of Jumières, clearly saw the decree and the Massacre of St Brice’s Day as an abhorrent act. It happened in an era blighted by conflict as rulers in Scandinavia, Britain and France battled for supremacy and seafaring pirates attacked along coasts and up rivers, but in his decree, Æthelred seems to have been doing something different: turning on a minority group amongst his own subjects. In politically tense times, differences – rather than similarities – can easily be brought into sharp focus. And such differences can be exploited by any politician who ultimately cares more about their own power, or indeed some abstract idea of nationhood, than about the lives of ordinary people and the ordinary communities that they govern.

Could it be that the skeletons from the ditch in Oxford, blade-scarred and burned, represent some of those ordinary people slain in the St Brice’s Day Massacre – a chilling physical record of that brutal assault?

At the time of excavation, the team from Thames Valley Archaeological Services suspected it was possible that the mass grave could be connected with this early-eleventh-century massacre. The blade wounds on the bones spoke of violence. So did the burning, which didn’t look like an attempt at cremation and instead seemed to fit well with the story of the people of Oxford burning down the church of St Frideswide, where the Danes had sought refuge. There was no other burned material discovered in the ditch, so it appears the bodies had been burned elsewhere, before being disposed of in the ditch. Just a single iron belt buckle was found, next to one skeleton that was buried a little apart from the others. There were no other grave goods at all, which suggests the bodies had been stripped of clothes and possessions before burial. The evidence fitted with a mass execution.

More clues would emerge from the post-excavation analysis. Of the thirty-five individuals recovered from the ditch, all were determined to be male, apart from two – and that pair were too young for sex determination (as skeletal differences between the sexes develop during puberty). Every single one of them bore evidence of violent injury inflicted around the time of death. There were only two old, healed wounds on the bones, leading Ceri Falys to think it unlikely that these young men had been professional fighters. Twenty of them were between sixteen and twenty-five years of age; nine were in their late twenties to mid-thirties; four were around the age of forty.

There were very few archaeological clues to help date the skeletons. They were buried in the top of a silted-up Late Neolithic ditch, on top of layers that had accumulated in the Bronze Age, Iron Age and Roman period. But how much later could they be? Samples of bone from three individuals were sent off for radiocarbon dating. The combined, calibrated date came back at 893–978 CE – too early, then, for the St Brice’s Day Massacre.

But there’s something that can throw a spanner in the works with radiocarbon dating – something that Cat Jarman realised she had to take into account when she re-analysed skeletal remains from Repton in Derbyshire, which she originally thought might be associated with the Great Heathen Army. There, the original radiocarbon dates had also looked too early – until she realised that diets heavy in marine protein could be influencing the result, potentially making the dates look earlier by several centuries. Could this also be the reason that the date for the Oxford bones looked too early? The team investigating the St John’s College mass grave sent further samples off, this time for analysis of stable (as opposed to radioactive) isotopes of carbon and nitrogen, which can reveal aspects of diet – including, crucially, how much marine protein was being consumed.

Vikings, it seems, liked their fish. And although this can skew radiocarbon dating, it’s a dietary phenomenon that may prove useful in other ways. Could it, for instance, help us to distinguish between populations that were following a more ‘Viking’ way of life, with sea fish forming a significant part of the diet, compared with ‘Anglo-Saxon’ communities? While this sounds like a neat idea, unfortunately it’s just too neat, too simplistic. The reality is that, over time, Anglo-Saxon populations also show increased consumption of marine protein. Some researchers place this Anglo-Saxon ‘fish event-horizon’ around the year 800, which would make contemporary Anglo-Saxon and Viking communities indistinguishable by this measure after this point in time; while some place it later, around the turn of the millennium, in which case it could potentially prove useful for differentiating communities in the eighth and ninth centuries.

Either way, the increase in fish consumption itself is a phenomenon that deserves closer inspection. The story of the Vikings in the late first millennium is one of mobility, with víkingr heading off on expeditions, engaging in recurrent raiding and long-distance trading as well as widespread settlement and the creation of new polities governed directly from Scandinavia, or by Scandinavian lineages. The Viking diaspora reached the Faroes, Iceland and Greenland, and as far afield as North America, as well as Orkney and Shetland, the Hebrides and the Isle of Man, parts of Ireland, the Danelaw and, of course, Normandy. Some of these places were uninhabited when the Vikings arrived, and so the settlers must have included both sexes. But what was the pattern elsewhere? Just how much migration took place, and how were populations connected after the first settlements were established? These are questions that have been extremely difficult to answer. The historical sources are important and provide clues, but it’s impossible to quantify the scale of population movement and change just by studying ancient texts. Archaeology gives us a different sort of evidence, in the form of material culture, and we can see certain styles and technologies appearing, spreading, evolving, disappearing through time. We get a wider perspective across a landscape and across the different echelons of society from archaeology, too. But we can’t tell how much migration contributed to these culture changes just by looking at pots, brooches or indeed fish consumption, because people can adopt new styles, new ways of behaving and new diets just as the Anglo-Saxons did after that fish event-horizon.

Since the early 2000s, another branch of science has joined the fray to reveal how populations themselves have changed over time: genetics. It got off to a slow start. At first we got some insights from modern populations, focusing on discrete parts of the genome, particularly the Y chromosome and mitochondrial DNA. The Y chromosome, carried only by men, can be used to track paternal lineages. Mitochondria are present in all of us, but we only inherit them from our mothers, so mitochondrial DNA (mtDNA) can reveal maternal lineages. Early studies showed, for instance, that two thirds of Icelandic men bore Norwegian ancestry, with the other third coming from Britain and Ireland; the pattern was the opposite in Icelandic women. The pattern was similar, with that same disparity between the sexes, in the Outer Hebrides. We’re glimpsing something about the nature of the diaspora here – who was travelling, and from where, within the expanding Viking world. Another study of modern DNA revealed a connection between certain surnames in Britain and a particular Y-chromosome-type common in Norway. But these studies were limited because they were only looking at modern, living people and trying to pick out those ancient threads buried in their DNA. Now we’re in the era of archaeogenomics, where ancient DNA (aDNA) is extracted from archaeological bones and entire genomes are sequenced. Ancient DNA is crucial to mapping the Viking diaspora and understanding its implications for societies, culture and identity.

The largest study of Viking Age genomes to date was published in 2020: 442 genomes from individuals from archaeological sites across Europe and Greenland. These genomes were compared with DNA sequences from almost 4,000 modern people, and with other ancient genomes from more than 1,000 prehistoric individuals. The results are incredibly detailed. They show gene flow over time from south to north in Scandinavia, though there were also two individuals from northern Norway who had genetic links with modern Sámi populations, showing that these Arctic communities were in contact with their southern neighbours during the Viking Age or earlier. Genetic diversity was higher along the coasts of Scandinavia, and lower inland, emphasising the importance of maritime connections. Although we’re using ancient DNA to try to understand population movements in the past, it’s incredibly important to realise that the DNA is not a badge of identity. Two individuals from Orkney demonstrated this very clearly; theirs were the first Pictish genomes to be published, and while their DNA was similar to modern Scottish and Irish DNA, they were buried in a characteristically Scandinavian fashion. And the flow of culture and genes wasn’t all one-way: five individuals with Pictish-like genomes were found in Scandinavia too. In fact, the study more broadly found plenty of evidence for inward migration into Scandinavia, with Baltic ancestry flowing west into what is now Sweden, and ancestry from the British Isles arriving in Denmark and Norway. At a finer level, genome analysis can also reveal family connections, and at the early-Viking site of Salme in Estonia, where forty-one men who died violent deaths were interred in boat burials, there were four brothers, buried side by side.

The ancient genomes reflected what archaeologists and historians have long believed about the pattern of migrations, based largely on geography. Eastward migrations largely involved people with Swedish-like ancestry, whereas the westward migrations carried the signatures of Norwegian- and Danish-like ancestry (although there were some exceptions to this rule). Norwegian ancestry flowed around the north of Britain and beyond – to Ireland, Iceland and Greenland. Danish ancestry flowed to more southerly parts of Britain – though it’s impossible to tease apart this contribution from that of earlier migrations of Angles and Saxons (even though it must be said that we’re still not entirely sure of the scale of that influx). But as well as uncovering evidence of migration from Scandinavia, this seminal study uncovered traces of inward migration, too. What’s really striking is that, when we look at modern populations, immigration has left a stronger genetic signal in Scandinavia than in the areas traditionally associated with the Viking diaspora. The Viking contribution to ancestry in the British Isles is less than 6 per cent, the study found (with that caveat about existing Anglo-Saxon ancestry); but present-day Norwegians possess between 12 and 25 per cent North Atlantic-like ancestry (which includes genetic signatures which seem to originate in the British Isles).

Judith Jesch, Professor of Viking Studies at the University of Nottingham, is trying to encourage a synthesising approach – bringing together history, literature, genomics and linguistics – in order to understand the Viking diaspora. The links are fascinating, though it’s sometimes easy for experts in one area to jump to conclusions that researchers in other fields might raise their eyebrows at. But it’s interesting to find resonances between genetics and language, for instance, such as the evidence for sustained south-to-north gene-flow in Scandinavia, which seems to reflect the northward spread of the donsk tunga – ‘Danish tongue’. While language doesn’t map neatly onto ancestry, it is of course important in communication – and in relationships. Rather than being anything to do with an original Danish identity as such, Jesch has argued that the donsk tunga may have created a sense of unity across the whole Viking diaspora – one that was more loosely ‘Scandinavian’. (We’ve already noted that the Anglo-Saxon Chronicle could confuse and conflate Danes and Norwegians, and genetics and linguistics are revealing a very fluid and dynamic picture – the blurred distinction was real. Another way of saying this, of course, is that those ‘ethnic groups’ are constructs.)

Over time, we’ll be able to build up an even more detailed picture, showing how the connections worked between all the different parts of the Viking world. With genome studies revealing family connections too, it may be possible to understand more about who was on the move. Elites? Families? Slaves? Mercenaries? Pirates?

The origin of the Viking diaspora is linked to developments in seafaring – particularly advances in deep-sea navigation – by people setting off from the coasts of Scandinavia and around the Baltic. We often focus on raiding and trading when discussing these voyages, but there’s something else that could have been, if not driving these expeditions, at the very least supporting or facilitating them. And there have been some extraordinary recent revelations about this potentially crucial factor. Once again, the clues have emerged from aDNA analysis of ancient bones. But this time the bones were not those of humans, but fish.

Fish bones are light and porous. They don’t sound like good candidates for preservation of ancient DNA. And yet a team of archaeologists and geneticists from Norway, Sweden, Germany and England were not deterred. They set about trying to extract and sequence DNA from fish bones from five archaeological sites, sampling nineteen specimens in total. Using a new technique to maximise their chances, they successfully extracted DNA from fourteen of these fish. The fish were cod and their genomes bore the signatures of their source populations – in the North Sea and, further north, in the Arctic seas around Norway. Up in the far north of Norway, especially around the Lofoten archipelago, people were catching and drying cod to preserve it, before salting was introduced in the seventeenth century. Today, Lofoten is the focus of the world’s largest cod harvest. It takes place from January to March, when migrating cod from the Arctic Barents Sea arrive to spawn in the Vestfjord, between the islands and the mainland. Some of this harvest is still naturally air-dried, to produce stockfish. The climate from February to June is just right for drying: neither too warm nor too cold, with a light breeze. This low-tech method of preservation may go right back to the Stone Age. But in the Middle Ages, it seems long-distance trade in this valuable source of preserved protein really took off, with the dried fish making its way to cities around the southern Baltic and North Sea. So, what drove the emergence and development of that trade?

This is where this new fish aDNA study comes in. Firstly, the data showed that the fish populations had remained quite genetically stable through the centuries; cod are incredibly faithful to their spawning grounds, returning to spawn around the same coasts where they started life, and it seems that this fidelity persists through time. This means that the bones of fish dug up in one place could be traced back to where the cod was originally caught.

One of the Viking Age sites investigated in the study was Haithabu (which means ‘Marsh Town’), the predecessor of modern Hedeby on the Jutland Peninsula, in what’s now the most northerly part of Germany. The aDNA from the fish bones from Haithabu matched cod from northern Norway – around Lofoten. Those two points are about 1,500 kilometres apart, as the crow flies; further if you’re travelling by sea from Lofoten to Jutland. This is only one small study, but it’s very exciting because it shows the potential for aDNA from fish bones – which everyone had previously thought would be dead in the water – and because it shows there was long-distance trade in (what must have been) dried cod during the Viking Age.

Look at the modern geographic range of Atlantic cod, and what you see could be a map of the Viking diaspora, with the seas lighting up around Scandinavia, northwest Europe, Britain and Ireland, then in an arc around the North Atlantic, from the Faroes to Iceland and Greenland, and the northeast coast of North America. Isotope analyses of the bones of humans living in northern Norway show a shift to a more heavily marine-based diet after 800 CE, which has been linked to an increase in the production of stockfish. In the Northern and Western Isles, isotope analysis of human bones shows a shift to eating much more seafood around this time, coinciding with Norse contact. The Scandinavians were experts in deep-sea marine fishing, and experts in preserving fish. Whatever else they were trading, it seems that cod – and the maritime technology to bring in that harvest going hand in hand with deep-sea navigation – was fundamental to the spread of these seafaring people from Scandinavia. The stockfish would sustain them on their voyages as well as being a marketable commodity, offering a dependable source of protein to the urban centres growing up around the coasts of Scandinavia – and beyond.

But what of the Oxford skeletons, and the diets of those people? Had they been eating lots of fish? And if so, what might that tell us?

Stable isotope analyses carried out on the Oxford bones revealed that the nitrogen-15 values for the three individuals who’d been radiocarbon-dated were indeed very high; they were similar to values from Viking sites in Sweden and Orkney. So it looked like these people had indeed been eating a diet rich in seafood, arguably in keeping with a Viking way of life. Add to this the fact that Ceri and her colleagues had pored over the archaeological data from late-Saxon Oxford and found no evidence of any fish bones in this period, and the Viking link seems even stronger. The fishy diet of these individuals is also likely to have skewed the radiocarbon dating on the bones, making them appear older than they actually are. If that date range of 893–978 is too early, these unfortunate individuals could have been victims of the St Brice’s Day Massacre in 1002 after all.

The archaeological team had sent off other samples – this time, of tooth enamel – for stable isotope analysis, focusing on the elements oxygen and strontium. This technique can reveal where an individual lived in childhood, as teeth preserve the local geological signature. The balance of oxygen and strontium isotopes in the rocks, groundwater and food of the place you grew up in becomes trapped in the enamel of your teeth. You don’t remake enamel, so that childhood signal is always there. The results from the Oxford bones were largely inconclusive – most of the individuals could have grown up either in Scandinavia or in northern Britain. But a couple were unusual, and looked to have come from elsewhere in Europe – which might be expected amongst a group of Vikings.

These incredible scientific techniques provide us with so much detail, but what can we conclude about this group of young men? They certainly died violent deaths – we can be sure of that – and their bodies were buried in a mass grave. Many of them could have been immigrants from Scandinavia, from the isotopic signature etched into their tooth enamel – but they could also have come from northern Britain.

The nature of the mass burial is extremely important. If these men had been Anglo-Saxons, killed in a battle or a skirmish, you’d expect them to be buried in the standard Anglo-Saxon way, with individual burials. Instead, the mass grave suggests that they were buried by people who saw them as strangers and not worthy of the usual burial rites.

So we’re left with various possibilities. If we accept that these young men are likely to have been Scandinavian in origin, then they could have been members of a raiding party who were executed and buried in a mass grave, but perhaps unconnected with the St Brice’s Day Massacre. Some of the experts who have been involved in the analysis of these bones favour this interpretation.

Another possibility is that the young men were mercenaries killed in the massacre in 1002. Some scholars have suggested the St Brice’s Day Massacre could have been specifically targeted at Danish soldiers taken on by Æthelred to help him repel Viking incursions and whom he suspected might be about to turn against him. But that interpretation seems at odds with what the historical documents are telling us. The later Anglo-Norman chronicles explicitly tell a story of Danes in settled communities – men, women and children – being attacked in the massacre. Crucially, the document written closest to the date of the event, within two years, is the St Frideswide charter – containing Æthelred’s chilling decree calling for the extermination of the Danes who had sprung up ‘like cockle amongst the wheat’. This doesn’t sound as though Æthelred was targeting soldiers, but rather immigrant communities, growing like weeds. Another reason to perhaps doubt that the victims were mercenaries is that Æthelred continued to recruit Danish swords-for-hire in later conflicts. And, just a few years after the St Brice’s Day Massacre, he also granted land in Oxfordshire to a Dane called Toti. His approach to the Danes in England was complicated, even psychopathically inconsistent.

For a resolution, we must go back to the bones. Ceri doubts that the young men buried in the mass grave were soldiers, either professional or mercenaries. She would have expected to see much more evidence of old, healed wounds in their skeletons if that were the case. She even found one individual with signs of active TB infection in his bones – he’s very unlikely to have been a serving soldier. Instead, the combination of violent injuries sustained around the time of death, with patterns suggesting people who were running away from aggressors, as well as the burning of the skeletons, fits with that chilling story set out in the St Frideswide charter. Taking all the archaeological evidence into account, Ceri believes that these young men really were victims of the St Brice’s Day Massacre – people who had been living in Oxford alongside their Saxon neighbours when Æthelred unleashed his fateful decree.

This investigation has shown how scientific techniques applied to archaeological human remains can help us to open another window on the past, providing a different perspective to set alongside, or against, the written history. The testimonies etched, cut and burned into bone have one important advantage in that they are not skewed by politics, not managed as propaganda, not favouring one version of events over another. They are simply oxygen and strontium, carbon and nitrogen, the shape of a male pelvis, the mark of a blade cutting into bone. They do not obfuscate, deceive or embellish. They are just there. And we try to contextualise them – to understand how they fit into the historical pattern of power grabs, population shifts, trading and raiding, battles and skirmishes, clashes and alliances.

But when I looked at the skeletons, laid out on the tables in the lab, they were more than clues to the bigger picture, characters in a story, abstractions. Here were the human remains of fathers, husbands, brothers, sons – they were the story. The bones told me of terror and violence, pain, grief and loss. That’s what stayed with Ceri, too. ‘I never want to see this level of violence again,’ she told me.

And there is one final piece to this puzzle that emerged with that large Viking Age genome study, which included individuals from the Oxford mass grave. The ancestries of the people buried in that grave were diverse: some Scandinavian-like, including both Danish- and Norwegian-like signatures, and some with North Atlantic ancestry – connected with the British Isles or beyond. There was diversity amongst them, but there was also an astonishingly close connection with someone buried far away from Oxford. One of the individuals from the St John’s College mass burial was closely related to another man, buried in the cemetery of Galgedil on the Danish island of Funen. That man – who was probably around the age of fifty when he died – also seems to have suffered a violent death, with a stab wound to his pelvis. The closely related individual from Oxford was none other than that first skeleton Ceri Falys had shown me in her lab: the man with ten injuries on his skull and the puncture wounds to his vertebrae. Buried more than 500 miles apart, these two men were second-degree relatives: grandfather and grandson, nephew and uncle, or half-brothers.

Two travellers, then, from the Age of Vikings – the voyages, the shifting alliances, the violence of the era written into their bones.

2. ST MARY MAGDALEN AND THE SCALLOP SHELL

Peel off the napkin

O my enemy.

Do I terrify?—

The nose, the eye pits, the full set of teeth?

The sour breath

Will vanish in a day.

Soon, soon the flesh

The grave cave ate will be

At home on me

from Lady Lazarus by Sylvia Plath

Just a handful of generations after the St Brice’s Day Massacre, the Norsemen were back in England, this time via their territory in northern France, and invading under a papal banner.

A neatly ordered view of history lays it all out as a succession of Ages, which are first designated by technological changes – stone, bronze, iron – and then by geopolitics and royal dynasties – Roman, Anglo-Saxon, Norman, Plantagenet, Tudor. This partitioning gives us a way of talking about history, but it also emphasises the boundaries between one era and the next, as though these are fault lines that run all the way down, between kingdoms and empires to the level of farms and families, descending and hitting the ground with a huge shudder. The dust settles – and people open their eyes on a new period of history.

Parcelling up history in this way obscures the continuity that exists at so many levels. Delving just a little into the connections between European monarchs opens up a view of the past where ruling elites are busily forging alliances, arranging marriages for overtly political and diplomatic reasons (with women treated as commodities to be exchanged), squabbling with relatives over inheritance rights and trying to keep inherited assets in the family. (Perhaps it’s not surprising that incest, a universal taboo in human societies, seems to occur more often as an exception to this rule in powerful elites, going all the way back to the Neolithic: aDNA analysis of one individual buried in Newgrange in Ireland revealed that he was the son of an incestuous union.)

In school history books, 1066 marks the fault line between Anglo-Saxon England and the Norman period. But it’s really not that simple. We must dig down into the tangled relationships of the ruling classes in ninth-to-eleventh-century northwest Europe and take a wider geopolitical perspective, to understand how territories were being carved up, marked out and distributed between the ruling elites of Europe. Let me pick out three individuals we’ve already met in passing: the Viking Rollo or Hrólfr, Emma of Normandy and King Cnut.

In the tenth century, Rollo, of Danish or Norwegian descent, invaded the north coast of West Francia and took over the territory that would become Normandy; he married a local, Frankish woman, Poppa of Bayeux. Historians studying individuals’ names have suggested that Rollo may have been related to the Norseman Ketill Flatnose, who was King of the Isles (comprising the Isle of Man and the Outer Hebrides).

Rollo’s great-granddaughter, Emma of Normandy, would marry two English kings and bear two more. In 1002, she married Æthelred, forging an alliance between England and Normandy. Following the St Brice’s Day Massacre, Sweyn Forkbeard, king of Denmark and Norway, raided and then eventually invaded England, seizing the throne in December 1013. Sweyn died just five weeks later, but he’d already managed to arrange a marriage between a member of the Mercian elite, Ælfgifu of Northampton, and his son Cnut.

On Sweyn’s death, Cnut was accepted as king in the old territory of the Danelaw, but other English nobles invited Æthelred back from his brief exile in Normandy. Æthelred ousted Cnut, but in 1015, Cnut was back – with an army. Æthelred and his heir, Edmund Ironside (whose mother was Æthelred’s first wife, Ælfgifu of York), both died in 1016, leaving Cnut to become king of all England. The following year, Cnut took steps to secure his legacy by marrying Æthelred’s widow, Emma of Normandy.

When Cnut’s older brother, Harald, died in 1018, Cnut became king of Denmark too. And in 1028, he added Norway, to form the vast but short-lived North Sea Empire. This made Cnut the most powerful man in Europe after the Holy Roman Emperor, Conrad II, whose coronation Cnut had attended, in Rome, in 1027. Emma of Normandy was the only woman ever to be crowned queen of England, Denmark and Norway. For a time, Cnut also held sway in Dublin and Scotland. He died in 1035, at which point the North Sea Empire was briefly split, with England ruled by Harold Harefoot (Cnut’s son with his first wife, Ælfgifu of Northampton) and Harthacnut (Cnut’s son with Emma of Normandy) on the throne of Denmark. Then, when Harold Harefoot died, in 1040, the empire was briefly reunited under his half-brother, Harthacnut. It was rent asunder again only two years later, when Harthacnut died, aged twenty-four – unmarried, with no heirs. The throne of Denmark passed to a Norwegian prince, Magnus, while England was inherited by Edward the Confessor, Emma of Normandy’s firstborn child, her son with Æthelred.

Edward the Confessor died in 1066, a year that is less remembered for his exit, more for the arrival of the Normans. This might seem like a great watershed event, when the reins of England passed from Anglo-Saxon to Norman hands. But just take a closer look at the tangled connections of the rulers on either side of that apparent divide.

Like Harthacnut, Edward died leaving no heirs, creating a power vacuum. Political stability falters at such moments. Of three leading earls in England during Edward’s reign, one in particular had risen to prominence: the Earl of Wessex, Godwin. One of Godwin’s daughters, Edith, had married Edward the Confessor. Godwin himself was succeeded in his earldom by his son, usefully named Harold Godwinson, in case he forgot who his father was. As the most powerful earl in England, and brother to the widowed Queen of England, Harold must have seemed like an obvious candidate to be the new king. And yet there was another contender: a cousin of Edward’s, over in Normandy. William, Duke of Normandy, was a descendant of Rollo (of course) and his great-aunt was none other than Emma of Normandy. With her body, her marriages and her progeny bridging the geopolitical divides of the eleventh century, Emma of Normandy emerges as a fascinating political figure: a node and mother-lode of power. Unfortunately, it seems Edward may have unhelpfully promised the succession to both Harold and William, setting the stage for the later events of 1066. When Edward died, the king’s council, the Witan, swiftly settled on Harold as heir – rushing to get him crowned the very next day, before the old king’s body was even cold. William was none too pleased. And the rest, as they say, is history.

Rather than ‘the Normans’ invading ‘Anglo-Saxon’ England, following the threads of the family trees reveals a densely woven tapestry of lineages, studded with power grabs and adorned with inherited status. ‘Danes’ and ‘Vikings’, ‘Anglo-Saxons’ and ‘Norsemen’ intermarry, emigrate, go into and come out of exile, with endless quarrels and squabbles over who’s going to govern where amongst the fluctuating kingdoms facing the North Sea, the Channel and the Irish Sea.

The lives and fortunes of those rulers are intimately tied to the formation, splitting and fusing of states. They’re also reasonably well documented, in a time when literacy was not at all widespread through all levels of society. One of the important philosophical contributions of archaeology to our view of the past is its completely separate and strikingly different perspective compared with written history. Archaeology explores the past from the ground up, not the top down. It is more concerned with ordinary lives – with the wider social impacts of evolving technologies, migration, trade and conflict; with climate and changing use of the landscape – than with individual elite personages (even when they are as alluring as Emma of Normandy). Archaeology also gives us a different way of investigating health and disease in past populations. We don’t need to rely solely on incomplete reports and obscure historical diagnoses when we can detect the signs of disease for ourselves in ancient skeletons. Archaeology also allows us to test what we think we know about how past societies reacted to and treated disease and the diseased. The spread of diseases through historical populations also reveals contact and connections.

While Emma of Normandy’s great-nephew, William of Normandy, was claiming the land that he saw as his birthright, there was one particular disease that was also gaining new territory in Britain, arguably affecting ordinary people much more than whichever relative of Emma’s was on the throne at any point in time.

In 2007, archaeologists from the University of Winchester began investigating Magdalen Hill, to the east of Winchester. They were searching for hidden traces of a medieval hospital – specialising in the treatment of patients with leprosy.

Today, the area is a grassy down, full of butterflies and moths in the summer. These include the rare striped lychnis moth, a gorgeous, velvety beast with wings the muted colour of lichen and tree bark; its caterpillar is a mint-green number with large yellow-and-black ‘eyes’ painted along its back.

During the First World War, Magdalen Hill was home to an army camp. Thousands of years ago, it was a cemetery, with five flattened barrows, which, though flattened, are still visible today. There’s a modern cemetery at its eastern end, including Commonwealth war graves from the First World War. But in between, in the Middle Ages, it was the site of the Hospital of St Mary Magdalen – a leprosarium or leprosy hospital. In the nineteenth century, a fair was still being held on the hill each year, on the second of August, the feast day of Mary Magdalene, even though the hospital itself was long gone.

St Mary Magdalene’s name crops up again and again in association with leprosy hospitals – in fact, it’s the most popular dedication for these establishments. And it’s a mistake. Or at least, it seems to be based on mistaken identity. It all begins with the New Testament, which features two men called Lazarus. One is a character in a parable: he’s a beggar, covered in sores (suggesting a connection with leprosy), at a rich man’s gate. When this Lazarus dies, he goes to heaven, while the rich man descends into the fiery pit of hell. More famous is Lazarus of Bethany: he’s the one who famously dies and is then improbably reanimated by Jesus a whole four days later. That Lazarus had a sister called Mary (of Bethany), and in the sixth century Pope Gregory decided that she was probably the same person as the follower of Jesus described in the Gospels as Mary of Magdala. And so Mary Magdalene became, in a very convoluted way, the patron saint of people with leprosy.

This particular hospital was built, like many others, outside the city. But although it lay only around a mile beyond the margins of the medieval town, the site escaped urban development in subsequent centuries. It was investigated in the year 2000 for the Channel 4 archaeology series Time Team. Bad weather played havoc with the three-day dig and the small excavation uncovered four graves but left more questions than answers. Several years later, Simon Roffey and Phil Marter from the University of Winchester resolved to look further into the mystery of the disappearing hospital. Forming a research group, they dug out all the historical documents they could lay their hands on, walked over the fields looking for archaeological clues on the surface, and used geophysical techniques to scan the ground, looking for cryptic archaeology. They began to piece together the evidence, finding links between buried walls and ditches that they’d picked up in their geophysical survey and drawings of the chapel, almshouses and gatehouse that had been made in the eighteenth century, when parts of these buildings were still standing.

Exploring the historical documents, Roffey and Marter traced the hospital back to the twelfth century, finding a reference to it in the Winton Domesday book, which recorded landholdings in and around Winchester in 1148. This made sense as hospitals are thought to be a Norman introduction to England. The Winton Domesday record means the hospital could have been founded around that time – by Henry of Blois, Bishop of Winchester (a grandson of William the Conqueror and the younger brother of King Stephen) – or perhaps even some time earlier.

The hospital was still caring for people suffering with leprosy in the fourteenth century, according to the 1325 Bishop’s Register. Some institutions disappeared around this time, while others morphed into chantries or schools. In the fourteenth-century records, St Mary Magdalen is described as a chantry, a place where the residents would pray for the souls of the founders and benefactors. Many hospitals were plagued by the Black Death, by inflation in the fourteenth and fifteenth centuries, and by bad management. St Mary Magdalen didn’t escape: records from the time show that the hospital, originally designed for eighteen – nine men and nine women – had shrunk to accommodate just fourteen. The hospital’s administration must have looked questionable as, in 1400, William of Wykeham, the bishop of Winchester (who had for a period of time also been Chancellor of England), sent a delegation to investigate. The result was that many ‘delinquencies, crimes, and excesses, [were]… brought to light’. History is silent on the punishments that were dealt out, but the hospital itself survived, with Wykeham leaving a bequest to the institution in his will.

In the later medieval period, many hospitals passed from religious to secular administration, sometimes being run by guilds. The Reformation saw a further shift, where support of the poor became the business of the parish, funded through taxation rather than almsgiving. Gone were the prayers of intercession, though later almshouses still often included chapels. In the sixteenth century, Henry VIII seized many of the Church’s assets in Britain; hundreds of hospitals were shut down – especially those that looked a bit too much like monasteries. Chantries tended to fare poorly, but even though St Mary Magdalen had been described as a chantry, it survived.

In the Civil War, it was occupied by Royalist troops, who reputedly burned every scrap of wood, slaughtered all the sheep and stole wheat. After the war, the almshouses were renovated, but then seized by the Crown in 1665 to be repurposed as a jail for prisoners of war captured in the Anglo-Dutch Wars. The prisoners once again burned all the woodwork, and reduced the hospital to a near-ruin. In the late eighteenth century, the remaining buildings, including the chapel, were pulled down. The antiquarian and draughtsman Jacob Schnebbelie visited in 1789 and drew what was left. He was only just in time – soon after he sketched them, the ruins were demolished.

Armed with this documentary and graphic evidence, and their new geophysical surveys, Roffey and Marter planned a campaign of excavation, which would also provide training for their students. They started, in 2008, by excavating the later medieval almshouses. Underneath them, they discovered the stone foundations of a large hall that they believed to be the original infirmary. They also found the flint-faced walls of the chapel. And crucially, they could see signs that the chapel had been rebuilt. Schnebbelie’s drawing showed a characteristic Norman chapel – so if this was the re-build, how old was the original chapel?

In fact, there was a tantalising historical suggestion hinting at the possibility of a very early hospital here. The Life of St Oswald, written by the English monk Byrhtferth, includes a brief mention of Bishop Æthelwold founding a monastery in Winchester – in the tenth century. Could that ‘monastery’ actually have been the leprosy hospital? It was an intriguing possibility, and one that would suggest not only that St Mary Magdalen Hospital could have been founded much earlier than previously thought, but that the idea of hospitals was not invented by the Normans; instead they could have been building on Anglo-Saxon foundations – quite literally, in this case.

Pinning down the precise date of the foundation of the Hospital of St Mary Magdalen became a major focus for continuing excavations on the site. In 2009 and 2010, the excavations were extended into the cemeteries around the chapel. Bones from graves inside the chapel had been radiocarbon-dated to the fourteenth century. But north of the chapel, and south of the infirmary, there was a collection of at least fifteen burials. They didn’t line up neatly with the orientation of the chapel, indicating that these burials could predate the building. When they were radiocarbon-dated, the result was very early: 970–1030 CE. Other clues included what appeared to be a sunken-floored building under the infirmary. At this point in the archaeological investigation it seemed possible that the origin of the hospital could indeed have been pre-Norman.

The archaeological investigation helped to reveal how the hospital had grown up – and then disappeared. The very first hospital on the site at Winchester seemed to have consisted of a small stone chapel with timber buildings to the north (appearing as postholes in the excavation) and a cemetery. This appears very similar to a description of the earliest-recorded leprosy hospital in England, founded in Canterbury in the 1080s. A second phase of construction saw the chapel at St Mary Magdalen being rebuilt, probably in the twelfth century, with a large stone hall replacing the earlier timber structures. At the same time, a second, southern cemetery was also added to the complex. There was also evidence of heavy renovation in the later Middle Ages, when the brick-built almshouses were constructed, leaving the chapel as the only surviving stone building from the earlier medieval period.

But it wasn’t really the history and archaeology of the buildings that drew me to St Mary Magdalen. It was the graves, the bones – and the promise of learning something about the individuals who lived and died in a medieval leprosarium. The northern cemetery of St Mary Magdalen was extensively excavated, with thirty-eight graves uncovered in total. Thirty-three of these bore the tell-tale signs of leprosy – and some were children. Roffey and Marter’s team went on to perform the twenty-first century’s most thorough scientific investigation into medieval leprosy. Using cutting-edge techniques to uncover clues about identity and disease, they have been able to examine the social context of leprosy in a way that’s never been possible before. What could we hope to learn about the people who had lived here? Could they come and go? I wondered: once admitted to a leprosarium, did any of them ever leave? And what of the children in that cemetery?

In 2014, I visited the University of Winchester to meet Simon Roffey and look at the human remains from the cemetery of St Mary Magdalen. The skeletons were laid on long tables in the bone lab, where they had already been analysed by osteoarchaeologist Katie Tucker. Leprosy directly attacks the facial bones and produces secondary effects in the hands and feet: damage to sensory nerves means that injuries and infections go unnoticed, developing into destructive septic arthritis and osteomyelitis. Looking at these bones, I could see plenty of evidence of lesions in hands, feet and faces. But one skull, that of Skeleton 19, really stood out. Where the maxillae, the bones that form the upper jaw, should have been – framing the triangular opening of the nasal cavities and housing the upper teeth – there was a huge, gaping, figure-of-eight-shaped hole. The upper part of the hole was the enlarged nasal opening; the lower part was where the upper front teeth once were, but they and the bone that supported them had disappeared. This wasn’t something that had happened post mortem, when the bones were buried in the ground. It had occurred when this individual was still alive. I was looking at the skull of someone who had suffered extreme facial disfigurement. In fact, the upper jaw and palate were missing all the way back to the first molars. The remaining back teeth hanging on in the maxillae, and those in the mandible (lower jaw), were swathed in calculus, the hardened substance that forms when dental plaque builds up and eventually becomes mineralised. Heavy calculus build-up is often seen in leprosy: inflammation of the nasal cavities makes breathing through the nose difficult, and mouth-breathing predisposes to an accumulation of plaque. That can have a knock-on effect: as well as producing bad breath, hard calculus irritates the gums, which become inflamed – swollen, red and tender. The underlying bone reacts too, resorbing, or shrinking back, until the teeth are left unsupported and wobble out of their increasingly shallow sockets.

The hands of Skeleton 19 had also been wracked by the disease. The smooth articular surfaces of some of the phalanges, or finger bones, had completely disappeared, replaced with ragged bone that left the fingers permanently flexed; the hand would have been stuck in a claw-like position. Other phalanges had shrunk down so much so that the shafts had completely disappeared, leaving stubs at the ends of the bones. New bone tissue had formed on the surfaces of the tibiae, fibulae and left femur. Down in the right foot, the bones of the tarsus, just below the ankle joint, were fused together, and the adjacent bases of the metatarsals were also fused. But the distal parts of the metatarsals and the phalanges of the toes were completely missing. This wasn’t an oversight on the part of the archaeologists, who had excavated the graves extremely carefully and even sieved the earth around the burial, the ‘grave-fill’, to catch any stray bones. Those toe bones had clearly been missing in life. In fact, the extensive remodelling of the remaining foot bones suggested that the right toes had been lost many months, if not years, before death. Over on the left side, there was even less to see: the entire left foot was missing: the tibia and fibula ended abruptly, the surfaces healed and smoothed over. That foot had been amputated.

This person would have been severely disabled by the destructive changes that leprosy had wrought on their body. With one foot completely missing and the other reduced to a stump, mobility would have been extremely difficult. With hands blighted by destructive changes and some fingers stuck in a clawed position, they would have struggled to use a crutch, and must have needed help to dress, to keep clean and to feed themselves. The loss of teeth and destruction of the palate would have made chewing and swallowing difficult, too. Two pottery bowls, almost intact, were found in the grave alongside the skeleton of this individual. It’s highly unusual to find grave goods in burials from this period; perhaps these were personal food bowls, a clue to the palliative care this person received at the hospital. (A recent research project has revealed evidence that animal bones excavated from the site were boiled, perhaps to make soups for the patients.)

It’s rare to find evidence of leprosy in juvenile skeletons, but here amongst the graves at St Mary Magdalen were several where the signs of the disease were clear to see. One was the skeleton of a child who was only about ten years old when they died, showing unequivocal evidence of the characteristic bony changes to the face, hands and legs; they must have first contracted the disease when very young indeed to have developed these signs. Webs of new bone had formed on the surface of their tibiae and fibulae. There was thickened, porous bone just inside the opening of the nasal aperture. The roots of the upper incisor teeth were short and underdeveloped. One root was strangely nipped in, with a narrowing just above the crown of the tooth. Malformed teeth like this are rare, and have been reported in only a handful of other archaeological cases of leprosy: four from Denmark and one from Sweden. It’s a subtle sign, and one that can be observed only if the maxillary bone supporting the teeth is broken so that the roots are exposed, if the teeth have fallen out post mortem, or if X-rays are carried out on an intact jaw. In this case, the teeth had come loose and had fallen out of the upper jaw, and their abnormal roots had not escaped Katie Tucker’s osteological eagle eye. This was a sign of active leprosy during the time when the teeth had been forming, in early childhood. Fascinated by the social context of the disease, and this rare evidence of leprosy in children, Tucker would later return to investigate these skeletons in more depth.

Leprosy is caused by a mycobacterium. This type of bacteria are all rod-like in shape, most grow slowly and when cultured they form a film, rather like mould. That’s why they have that prefix, myco-, which comes from the Greek for ‘fungus’. Individual bacilli have a thick, waxy cell wall, making them very good at surviving in adverse conditions, outside and inside the human body. They can survive immersion in detergents, in acid and in alkali. Many live freely in water (even if it’s chlorinated) while others are pathogens, with a special predilection for infecting mammals. Some are obligate parasites and can only survive with the help of a host – including two species in particular that are responsible for an enormous burden of disease in humans: Mycobacterium tuberculosis, which causes TB, and Mycobacterium leprae, the pathogen responsible for leprosy.

M. leprae has settled into its role as a parasite, becoming very lazy indeed, completely losing the ability to survive on its own. It is actually impossible to grow a culture of this particular mycobacterium in the lab. It will only grow inside a body. And even when it’s inside its host, it reproduces extremely slowly compared with other bacteria; an M. leprae generation lasts twelve-and-a-half days, whereas other common pathogens will double in number inside a body within hours. This mycobacterium is also very picky about its hosts – or perhaps it’s the other way round: most animals kick out this mycobacterium quite quickly. The only mammals that fail to do this, that become chronically infected with it, are humans and, somewhat weirdly, the nine-banded armadillo. (The Centers for Disease Control in the US advises steering well clear of armadillos for just this reason.) Once M. leprae bacilli have entered the body, they invade certain cells and live inside them. They have a distinct preference for cooler parts of the body, and target keratin-producing cells and certain immune cells in the skin, but they also have a distinct predilection for the cells that wrap around and insulate peripheral nerve fibres, called Schwann cells.

The way that leprosy manifests itself varies from patient to patient. As with any disease, the way it affects the body is down to an interplay between the pathogen and its host. In some people, there may be just a few skin lesions and limited nerve damage, and the disease may never progress further than that. This milder version is called tuberculoid leprosy. In other people, the effects develop to become much more pronounced, with widespread skin lesions affecting both sides of the body, extensive nerve involvement and deformation of the facial bones. This more severe type is known as lepromatous leprosy. But really, it’s not a binary; there are not two discrete, separate forms of leprosy – instead, there’s a continuous spectrum of severity.

It can take years for any indication of the disease to emerge. The very first signs may be lumps and bumps on the skin, as affected immune cells clump together to form a tight ball known as a granuloma, a common feature of chronic infections. The word ‘granuloma’ is formed from the Latin granulum, meaning ‘small grain’, together with the Greek ending ‘-oma’, which is used to denote a tumour or swelling of some kind. Granulomas in leprosy, or ‘lepromas’, may be small and discrete or they may be very large and obvious lumps. But it’s the way that leprosy attacks nerves that leads to the most destructive and disabling features of the disease. When nerve-cell fibres lose the protection of their enveloping Schwann cells, they are vulnerable to injury and may be destroyed in ‘friendly fire’ by the body’s own inflammatory response to the presence of the pathogen.

When motor nerves – the nerves supplying muscles – are affected, this leads to weakness and even paralysis. This loss of muscle function can lead to foot drop, where someone drags their feet as they walk, and claw hand, where the fingers are permanently flexed. It can also cause lagophthalmos, where the eyelids can’t completely close. This can be disastrous, as it means that the eyes dry out and that any foreign bodies that enter can’t be blinked out effectively. The transparent cornea on the front of the eye is all too easily damaged and turns cloudy, eventually causing blindness.

Damage to sensory nerves leads to a loss of touch and pain sensation, and impairs the ability to differentiate between hot and cold. There tends to be a gradual loss of sensation over the hands and forearms and the feet and lower legs. This means that minor injuries to hands go unnoticed and untreated, and get progressively worse, leading to the development of pressure ulcers and nasty, chronic infections as other bacteria move in to colonise the open wounds. The lesions are painless – that’s why they happened in the first place – so patients will just go on walking on an ulcer on the sole of the foot, for instance, making it even worse.

It’s not M. leprae itself causing these infections – it’s other, pus-forming bacteria picked up from the environment – but the leprosy pathogen generously creates the ideal conditions for those others to invade the body. Starting off on the surface, infection tracks deeper and deeper until it reaches bones and joints. First, the periosteum, the lining around the outside of bones, becomes infected and inflamed. Looking at archaeological human bones, the signs that a person had reached this stage of the disease include pitting and plaques of new bone on the bone surface. Then the sepsis can move right inside the bone. In the hand, the pus-forming infection tends to stay in the fingers, but infections in the feet can affect the entire extremity and sometimes creep up the leg as well, causing bony changes in the lower tibia and fibula.

The signs of such deep infection are clear to see in skeletons. When bone is infected, it reacts in two ways simultaneously: bone tissue is destroyed but also created. The result can be a dramatic change in osseous architecture: individual bones may shrink down or balloon out; bones that started off as separate entities, such as those in the tarsus of the foot or the carpus of the hand, can fuse into a single block. The surface of these new, coalesced clumps of bone appears ragged. Inside, the infection forms an abscess – a pus-filled cavity – and there’s often at least one large hole through which pus would have escaped. The channel is called a cloaca – the Latin word for ‘sewer’. All of these features are generic signs of bacterial infection, of osteomyelitis. But crucially, what’s different in leprosy is the way that the hands and feet have been rendered insensitive by the disease. If you see evidence of bone or joint infection in just a single hand or foot, this could be a straightforward infection; you wouldn’t suspect leprosy. But if both hands and feet are affected, that strongly suggests there’s an underlying cause.

As well as facilitating infection caused by other bacteria, M. leprae can directly impact bones itself. A leproma within the periosteum, the membrane lining the outside of bones, can lead to a cavity forming in the bone itself. Clusters of erosions like this can eat into the foot and hand bones. Lepromata may form inside bones, particularly under joint surfaces, causing the joint to collapse, sometimes creating a pit or cup-shape. But the absolutely unequivocal sign of leprosy results from the direct effect of M. leprae on the facial bones, where local inflammation causes the bone to resorb and shrink back.

The facial changes in lepromatous leprosy mainly involve the upper jaw bones or maxillae, which also frame the nasal aperture, creating a characteristic widening of that aperture. This is such a striking feature of the disease that it has a name – ‘facies leprosa’ or ‘rhinomaxillary syndrome’ – and it is pathognomonic of lepromatous leprosy. In other words, if you observe those characteristic changes – exactly what I saw in Skeleton 19 from the St Mary Magdalen cemetery – a diagnosis of leprosy is virtually guaranteed. But even in the absence of such characteristic changes to the skull, a probable diagnosis of leprosy may be made on the basis of symmetrical bony changes in the extremities. What will be missing from traditional palaeopathological diagnoses, based on observation and X-rays of skeletal remains, are earlier or less severe cases, including tuberculoid leprosy.

Leprosy, or Hansen’s disease, is actually quite hard to catch. And most people seem to be naturally resistant to it, with only one in twenty people appearing to be susceptible. It was thought to spread primarily by droplet infection, when an individual infected with leprosy coughs or sneezes and someone else breathes in those pathogen-laden droplets. It doesn’t seem to waft around in minute, aerosolising particles – as is the case with SARS-CoV-2, the virus causing Covid-19, for instance. And unlike SARS-CoV-2, which can be caught from a fleeting contact with an infected person, leprosy transmission appears to require prolonged contact with a patient, over a period of months.

But advances in genetics are changing our understanding of this disease, as of so many others. In 2001, the genome of M. leprae was sequenced and published, opening the door to PCR-testing for the presence of the disease. And new genetic studies present a challenge to the idea that leprosy is caught only via droplet infection from nasal secretions. In one study, PCR-testing of various tissues of untreated leprosy patients revealed the presence of the pathogen not only in the nasal mucosa – in 60 per cent of patients – but also in the epidermis or uppermost layer of the skin – in 80 per cent. Amongst the contacts of those cases, PCR tests were more often positive for skin samples (17 per cent) compared with nasal swabs (just 4 per cent). This suggests that a skin-to-skin route of transmission could be at least as important as one involving nasal secretions. It’s also become clear through genetic tests that a large number of household contacts of patients with leprosy are actually infected but asymptomatic. One recent study found that a quarter of asymptomatic close contacts tested positive. Perhaps this isn’t surprising – we have known for many years that leprosy has a long incubation period and is difficult to spot in the early stages of the disease; some of those asymptomatically infected people may eventually go on to experience signs and symptoms.

Leprosy remains a significant problem today, though with modern medicine and, particularly, multi-drug therapy, cases have been steadily decreasing over recent decades. In 2019, around 200,000 new cases of leprosy were detected around the globe, representing an amazing 40 per cent reduction since 2014. The current global target, spearheaded by the World Health Organization (WHO), is to virtually eradicate leprosy – or at least to achieve a 90 per cent reduction in new cases per million people – by 2030. The impact of leprosy worldwide is hugely variable, within and between countries. It’s classed as a ‘neglected tropical disease’ by the WHO, but its prevalence is linked to socioeconomic deprivation just as much as latitude. In 2020, just over half of the world’s new leprosy cases occurred in India, and around 30 per cent occurred in just four other countries: Brazil, Indonesia, the Democratic Republic of the Congo and Bangladesh.

It’s estimated that, around the world, 3 to 4 million people are living with leprosy-related deformities, but the number is likely to be higher, because people with leprosy still tend to be socially excluded in many communities. Social stigma and exclusion remain a huge problem for people suffering with the disease. Part of the WHO’s current strategy focuses on combating stigma and discrimination against people with leprosy. In 2011, the United Nations issued guidelines for eliminating discrimination, including making sure that people affected by leprosy remain in their communities, are not excluded from schools and hospitals, and are supported if living with disabilities. Early detection is extremely important, and the potential for identifying the presence of M. leprae in asymptomatic contacts of patients using PCR tests could now be transformative. Picking up infection early means that patients can be promptly treated with multi-drug therapy (using a cocktail of antibiotics – dapsone, clofazimine and rifampicin), practically eliminating the risk of further transmission, and curing the disease. There’s also ongoing research into a vaccine for leprosy.

No such treatments were available in the Middle Ages, of course. Management of the disease was purely palliative. And it was surging through Europe in the eleventh to fourteenth centuries. It wasn’t a new disease – it had been in human populations for many centuries – but something about the pathogen itself, or the environment it found itself in, stimulated a great wave of infection.

In around 150 CE, the Greek physician Aretaeus wrote a detailed and accurate description of an affliction he called Elephantos. He suggested that it was possible to catch this disease from the corrupted breath of those affected, and that it caused nodules and ulceration of the extremities as well as affecting the face:

… the lichen sometimes embraces the chin all round; it reddens the cheeks… eyebrows prominent, thick, bald… eyelid therefore much retracted… as in enraged lions; on this account it is named leontium… Nose, with black protuberances, rugged; prominence of the lips thickened, but lower part livid; nose elongated; teeth not white indeed, but appearing to be so under a dark body; ears red, black, contracted, resembling the elephant… deep fissures, like black furrows on the skin; and for this reason the disease has got the name of elephas.

Aretaeus also wrote about how the disease was transmitted:

… there is a danger in living or associating with it no less than with the plague, for the infection is thereby communicated by the respiration…

He also suggested that early cases might be curable (though we know that was not possible with the treatments available at the time):

Wherefore what sufficient remedy for it shall we find in medicine? But yet it is proper to apply every medicine and method of diet, even iron and fire… if you apply these to a recent disease there is hope of a cure. But if fully developed, and if it has firmly established itself in the inward parts and has also attacked the face, the patient is in a hopeless condition.

Another Greek physician, Galen – physician to the Roman emperor Marcus Aurelius – suggested some specific treatments for what he called elephantiasē, including eating viper meat and applying plasters loaded with lead oxide and olive oil to the sores.

The literature of the Roman and post-Roman period, including the Bible, suggests that leprosy was widespread but diffuse in Europe at this time, before it became more problematic in the early centuries of the second millennium. But it’s possible to trace it back even further. There are descriptions of a disease that may be leprosy in ancient Egyptian and Indian texts from the first millennium BCE – though it often seems to be lumped together with other skin diseases. Archaeology has confirmed the deep antiquity of this specific infection, with an osteological diagnosis of 4,000-year-old leprosy in India.

Genetic studies have contributed to our understanding of the history of this disease, as well as its modern manifestations. The genome of Mycobacterium leprae contains 3.3 million base pairs (the matched-up ‘letters’ of DNA in the double helix). This is a bit smaller than the average genome of ‘free living’ terrestrial bacteria, at around 3.8 million base pairs. (Just for comparison, the human genome is around a thousand times larger, at around 3 billion base pairs.) But M. leprae’s genome also contains a lot of obsolete DNA – sequences that were once genes but that have mutated into undecipherable strings of base pairs that can no longer be ‘read’ and translated into proteins. Half of its genes have decayed in this way, leaving around 1,300 defunct ‘pseudogenes’ kicking around in its genome. It’s not surprising that it’s impossible to culture it in the lab, or that it reproduces so slowly inside its hosts.

Genotyping of modern strains of M. leprae show how these variants are all related, on a family tree with five main branches, which map onto different geographic areas. Branch 0 strains are found in China and North America (New Caledonia); branch 1 strains are found in India and Southeast Asia; branch 2 in Iran and Turkey; branch 3 in North America; and branch 4 in Mali and Brazil.

Around ten years ago, geneticists began to prospect for M. leprae DNA from archaeological skeletons, scraping samples from bones with signs of the disease into test tubes, under sterile conditions, to prevent contamination with other, more modern DNA. They often took their samples from the keel-like vomer, which forms part of the septum separating the nasal cavities, as this seemed to be a favoured site for M. leprae invasion in lepromatous leprosy.

When they extracted the DNA and began sequencing it, they were astonished to see how relatively intact the mycobacterial DNA was in those archaeological remains. It had survived much better – it was less fragmented – than the human DNA in the same bones. Presumably the thick cell wall that protects living mycobacterial cells also helped to preserve their DNA when they were dead – like a minute, waxy coffin. (The presence of mycolic acid, from the cell wall, is also used as a marker for leprosy in archaeological human remains, though it’s not as informative as DNA.) The geneticists were also surprised to find that thousand-year-old leprosy didn’t look all that different – in terms of its genetic sequence – from modern leprosy. There weren’t any large insertions or deletions, which are usually quite common as genomes evolve.

When medieval and modern M. leprae genomes are compared, the differences between them can be counted. Quantifying that difference means that it’s possible to estimate how fast M. leprae has evolved: how quickly it has accumulated changes in its DNA. And then it’s possible to project that rate back in time, to predict how long all the strains have been evolving away from each other. Pushing back into the past, the different strains converge on a common ancestor somewhere between 2,000 and 5,000 years ago. With the very oldest osteological evidence for leprosy dating to 4,000 years ago, in India, the bones and the genetic projections are matching up nicely.

One study, published in 2013, involved sequencing five ancient M. leprae genomes: one from Sweden, two from Denmark and two from the UK – from the St Mary Magdalen Hospital cemetery in Winchester, in fact. Those ancient genomes could be fitted onto the family tree of modern strains. One of the Winchester M. leprae genomes, together with one Danish genome, belonged on branch 3 of the leprosy family tree, bearing very close affinity to a strain found in the US today; it must have been exported at some point from Europe to the Americas. The other three genomes in the study, including one of the Winchester samples, clustered on branch 2. Two other Winchester skeletons were later sampled, with strains that also fitted on branch 2. This is one of the rarest types in existence today, only found in Iran and Turkey, but it may have been the predominant strain in medieval Europe.

The spread of leprosy across Europe in the Middle Ages has traditionally been associated with increased contact with the Middle East (and with the Crusades in particular, although some leprosy hospitals, including St Mary Magdalen, were founded before the first Crusade, in 1095). The genetic picture seems to be consistent with that interpretation. Travel for whatever reason – trade, tourism or war – is an effective way of spreading diseases around the globe. But after a few centuries when leprosy was rife in Europe, it went into decline, between the fourteenth and sixteenth centuries. What happened? Did it evolve into a milder or less transmissible form? The genetic analysis of those five ancient genomes suggests not. Looking at the Danish and Winchester genomes that are closely related to the modern strain isolated in the US, there were very few genetic differences. So it seems that it must have been an external factor – not something intrinsic to M. leprae itself – that caused the drop in infections. This could either have been something that reduced the opportunities for transmission, such as better social conditions, or something that made humans more resistant. It may be that other infections that were on the rise – perhaps TB or even the plague – could have produced some cross-immunity. (Today, the BCG vaccination, given primarily as prophylaxis against TB, also helps to reduce the risk of infection with leprosy.) By the sixteenth century, leprosy had largely disappeared from Europe. But for five centuries, it had been a scourge that demanded a social response.

The graves at St Mary Magdalen Hospital were those of women, men and children. The graves contained an astonishingly high proportion of individuals with convincing evidence for leprosy. Simon Roffey and his colleagues have now excavated just over a hundred burials from the site, and 85 per cent bear signs of the disease.

Other hospital cemeteries that have been excavated have contained much lower rates of osteologically identifiable leprosy. For comparison, in the cemetery of the St James and St Mary Magdalene Hospital in Chichester, only around a fifth of individuals were obviously leprous (75 out of 384 burials), with a similar rate found at the leprosarium cemetery of St John Timberhill in Norwich (35 out of 180 burials). It could be of course that some genuine leprosy cases have been missed in those osteological analyses; leprosy only affects the skeleton in around 5 per cent of cases. But historical texts also suggest that, over time, leprosy hospitals tended to broaden their remit and take in a wider range of patients. And it’s been suggested that the diagnosis of ‘leprosy’ could have been much wider in medieval times, embracing various other diseases, particularly skin diseases such as psoriasis, eczema and erysipelas, as well as joint diseases such as rheumatoid arthritis.

A US Navy doctor, Richmond Cranston Holcomb, who took a keen interest in the history of diseases, put forward a theory in 1941 that much of what was described as leprosy in Latin texts from the eleventh century to the fifteenth was in fact venereal syphilis. During this period there was a shift in who was making those diagnoses – originally, it would have been priests, but by the thirteenth century medical professionals had assumed the role. Holcomb pointed to a seminal French text from the thirteenth century, the Lilium Medicinae, a handbook of medical treatments, written by the French doctor and professor of medicine at the University of Montpellier, Bernard de Gordon. The Lilium described the aetiology of leprosy:

Leprosy is either introduced from within the uterus, or after birth. If from within the uterus, it is because of conception at the time of menstruation, or because it is the child of a leper, or because a leper has had intercourse with a pregnant woman and thus the baby will be leprous, for leprosy is generated out of these great corruptions that befall the conception.

So there seems to be some concept of transmission or contagion here, in the idea that the child of a person with leprosy might also suffer from the disease, or that an unborn baby could be affected if its mother had sex with someone who had leprosy. The idea that leprosy could affect a child if it was conceived while the mother was menstruating, though, reminds us that we are peering back to a time way before germ theory had emerged. The theories about what could cause leprosy after birth were no less muddled:

… this could be because the air is bad, corrupted and pestilential, or because of prolonged use of melancholic foods, such as lentils and other legumes, and from such melancholic meats as that of foxes, bears, wild boars, hares and other quadrupeds such as asses and the like, since in some regions all wild animals are eaten.

Just to be clear, there is no way that breathing foul air, eating lentils or wild boar could cause leprosy. But Bernard de Gordon goes on to suggest some other causes:

Leprosy also arises from too much company with lepers, and from coitus with a leprous woman. And also in him who lies with a woman who has lain with a leper whose seed still remains in her womb… Everyone ought to guard against lying with a leprous woman… Fortunate is he who is made cautious by the dangers of others.

It’s clear that Bernard de Gordon sees leprosy as partly a venereal disease (even if you could also get it, in his view, from eating ‘melancholic’ foods) as well as something that could affect a fetus in the womb. In fact, congenital leprosy is very rare, and leprosy is not sexually transmitted. The focus on venereal causes of leprosy in the Lilium Medicinae prompted Holcomb to conclude that Bernard de Gordon and others were lumping together leprosy and syphilis. However, other physicians writing in the thirteenth and fourteenth centuries make no mention of leprosy having a sexual cause, so it seems unlikely that syphilis was regularly being misdiagnosed as leprosy.

However confused medieval doctors were about the aetiology of leprosy, they were fairly clear about its signs on the body. Bernard de Gordon, for instance, was very cautious about making a diagnosis of leprosy in the absence of facial lesions. Medieval physicians drew up great lists of signs and symptoms, and though some of these were spurious, they were trying to be methodical and systematic diagnosticians.

There are a couple of medieval Danish leprosy hospitals, in Næstved and Odense, which present a similar picture to Winchester, containing a large proportion of individuals with osteologically confirmed leprosy. These hospitals with high levels of leprosy suggest that a fairly precise diagnosis of leprosy was certainly possible in the Middle Ages, as Simon Roffey has argued. But, to muddy the waters, while some leprosaria seem to have been intended exclusively for patients with leprosy, others were more general hospitals. For instance, a twelfth-century record from another leprosy hospital dedicated to St Mary Magdalene, in King’s Lynn in Norfolk, refers to just three individuals with leprosy amongst thirteen residential patients. St Mary Magdalen in Winchester, on the other hand, appears to have been more specifically dedicated to caring for people with leprosy.

The creation of these institutions reveals one way in which societies were reacting to the practical challenge represented by rising numbers of people with leprosy. But how did people ‘learn to live with’ this disease? There’s been a traditional perception that the disease carried enormous stigma, and that people with leprosy were feared, shunned and shut away from society. New readings of history, as well as new insights from archaeology, are now challenging that view.

The nature of the graves at St Mary Magdalen, Winchester, may tell us something important about the way that these individuals were treated. The early graves in the cemetery were cut down into hard bedrock, with niches for the heads in a typically monastic style, and would have been covered with a wooden board. They were lined up regularly and didn’t cut into each other, suggesting that they may have had grave-markers above ground. These individuals appear to have been treated with respect and dignity in death. This archaeological evidence seems surprising. Were people with leprosy stigmatised and treated as outcasts as much as later historians have led us to believe?

The traditional view of society’s response to people with leprosy in the Middle Ages is that they were shunned and ostracised, and that their disease was viewed as a sign of inner sinfulness. Many scholars have espoused this view, drawing on contemporary texts as evidence. But as medical historian Luke Demaitre has pointed out, this perspective may have emerged through translation, introducing a more moralising tone than the original authors, writing in Latin, intended.

Medieval doctors described leprosy as a ‘malus morbus’, which can be translated as a ‘bad disease’, or more pejoratively, as an ‘evil disease’. Similarly, an imbalance in the humours, a ‘peccatum humoris’, could be translated as a ‘sin of the humours’. And ‘corruptio formae’, causing ‘corruptio virtutis’ – a deformity leading to a disability, in other words – sounds much more value-laden if literally translated as ‘corrupted form’ and ‘corrupted virtue’. But there are clues that physicians weren’t being quite as moralising as this literal translation suggests. Doctors at the time were certainly aware of the stigma associated with leprosy; Bernard de Gordon, for instance, was very cautious about making the diagnosis unless he was absolutely sure, because, he said, ‘lepers are judged very badly in our day’. Demaitre argues that the medieval physicians’ relatively objective approach to leprosy could even have encouraged a more objective and less prejudiced view of the disease and those suffering with it. But still, there’s a difference between how doctors may have reacted to the disease and the response of wider society.

There’s good evidence for a longstanding tradition in which people with leprosy were separated from their original communities. A biblical law in Leviticus stated that people with leprosy should live ‘outside the camp’, and this was reflected in later medieval laws. In the twelfth century, the Lateran Council in Rome mentioned that ‘lepers… cannot dwell with the healthy or come to church with others’, but also stipulated that people with leprosy should be able to have their own churches, priests and cemeteries. There is no suggestion there that leprosy was seen as innately sinful – just something for the rest of society to steer clear of. But given the social stigma that is still attached to leprosy today, it would be extraordinary if something similar hadn’t operated in the Middle Ages. And as we see so graphically in those skeletons from St Mary Magdalen, lepromatous leprosy is a disease that attacks the face, cruelly disfiguring its victims. People with facial disfigurement still suffer ostracisation today; they tend to be pushed to the margins of society, and always have been.

Even while twenty-first-century surgeons do wonders reconstructing damaged faces, and charities such as Changing Faces try to encourage kinder, more thoughtful responses, facial disfigurement is difficult to see and difficult to live with. A violent attack with the aim of causing damage to the face is seen as an appalling act today, because the implications for the victim’s quality of life are profound.

In the Middle Ages, violent attacks that resulted in damage to the face or teeth of victims were treated extremely seriously in law, while accidental facial injuries were sometimes described as the work of the devil. Facial disfigurement could also be carried out as a punishment, and it was imbued with heavy religious, biblical resonance. In Byzantium, political crimes could be punished with facial mutilation, with noses or lips being cut off, eyes being put out. Pimps, sex-workers and adulteresses could have their noses cut off, following the example of the punishment meted out to the prostitute Oholibah, in Ezekiel. And so it’s easy to see how a disease which seemed to recreate such horrific, biblically sanctioned punishments might be interpreted as divine retribution, and how such disfigurement could be linked to ideas that the crime itself may have been sexual.

But some people, it seems, could turn facial disfigurement into an advantage – if it wasn’t too severe. Thietmar, Bishop of Merseburg in Germany, was beaten up by pirates on the east coast of England in 994, but he claimed to have been more concerned with the sins of his soul than with his broken nose; physical suffering providing an opportunity for spiritual growth. The single survivor of a disastrous mission by St Bruno to the Rus in 1009 was a priest named Wipert. This priest is said to have claimed that he led a more fulfilling spiritual life after that episode, where he escaped with his life, but not with his eyes. A priest called Walchelin, whose story appears in the twelfth-century Historia Ecclesiastica penned by the chronicler Orderic Vitalis, apparently bore a scar on his face that he claimed was proof of an attack by a burning zombie-knight fifteen years before. (Orderic appears not to have doubted this explanation.) These pious men managed to give their facial injuries and deformities a positive, spiritual spin. This seems to have been unusual, though, even amongst those in the higher echelons of society. For most – or at least, for most of those that appear in historical texts, and that’s overwhelmingly elite men – it seems that facial disfigurement was a socially damaging stigma, bringing shame and inviting ridicule. For some, it really could be a fate worse than death. A minstrel at the court of King Henry, having been sentenced to being blinded, took his own life.

Still, the stories about Thietmar, Wipert and Walchelin show how very visible affliction could, in certain contexts, be seen as a blessing rather than – or, perhaps, as well as – a curse. There are hints, too, that leprosy could also be viewed as a mark of divine favour, rather than punishment of sinfulness. Some clerics and theologians saw it as offering the sufferer something in common with Christ; an opportunity to experience purgatory while still alive and therefore get fast-tracked to heaven; a sacred malady, a gift from God. (Christianity has always been great at this salesmanship, promising life after death and reframing suffering as some kind of bonus.) But perhaps some people with leprosy really did see their disease as almost akin to a religious calling.

What of the role of religious communities in accepting, accommodating and caring for those with facial deformities? Thietmar, Wipert and Walchelin were all clerics before they suffered their facial injuries (though the origin of Walchelin’s scar is debatable), and apparently continued in these roles despite the fact that, according to Leviticus, anyone with a deformed face could not be a priest. Historical accounts also suggest that people with deformities could enter monasteries. One thirteenth-century monk, Aldevrandus, is described as having had a large, misshapen head and hair growing on his forehead.

Like monasteries, hospitals provided spaces where those with facial disfigurement could perhaps lead fulfilling lives, in a community that accepted them and where many others were living with similar challenges. Today, surgical treatment of disfigurement often removes or reduces the deformity itself, thus lessening the stigma. But does that mean we have in fact become less tolerant of difference as a society? Has modern reconstructive surgery, as historian Patricia Skinner has asked, ‘heightened expectations that everyone can – even should – look more “normal” ’? Once again, we’re reminded how the past – a different country, where people do things differently – can prompt us to look at our own society with new eyes.

The solution to the large numbers of people developing deformities through leprosy in the Middle Ages was to create a new type of institution. (Hospitals had existed before, of course. They didn’t appear out of nowhere. But there were more leprosy hospitals founded in the 150 years from 1100 to 1250 in England than over eight centuries, across the entire Byzantine Empire, before that.) Phil Marter and Simon Roffey argue that archaeology supports the idea of leprosaria representing a solution to a social need. Rather than being driven by purely exclusionary principles, they were founded much like monasteries – as a religious community where the residents also happened to be patients. Although hospitals were clearly seen as separate from religious houses – they were identified separately on maps and treated differently in law – they were still religious at their heart. They were run and staffed by monks. Daily worship was part of the deal, and the main building of the hospital was essentially a large church, where inmates could see the altar from their beds. No doubt, for some this really would have been a source of comfort, but on the other hand, there was no getting away from it. The inmates were expected to follow a monk-like lifestyle, to be involved in worship and prayer, and to help look after each other. They would also be expected to pray for the soul of wealthy benefactors; the good PR for these individuals extended to the afterlife. In the hospital, spiritual care was seen as even more important than medical care (which is fortunate as medical treatments were largely ineffective). That spiritual care would also extend to being given a proper burial. This was one of the Seven Comfortable Acts, or Christian corporal Acts of Mercy – corresponding with the Jewish commandment, or mitzvah, of burial. It was fundamental to the charitable mission of medieval hospitals: the living joined a community, and the dead remained part of that community.

As a result, hospitals, as an essentially medieval invention, have been viewed as offshoots of the monastic tradition across Europe. And there’s no doubt that they share features with monasteries. But it’s too trite to see hospitals as simply an expression of piety and religious charity. The Church was an engine of the State, and it was responsible not just for the spiritual needs of the population, but for physical and social needs, as well as fulfilling the role of state media and mass communication (forgive the pun) in a largely non-literate society. It was there to preserve the social order – and to support wars in foreign countries. It was a department of social care, a state broadcaster, a Ministry of Defence and much more, all rolled into one.

And so we start off on the wrong foot, perhaps, if we look at ‘religious’ institutions as principally spiritual in their remit. Religion was incredibly important in medieval European society, as the enduring legacy of the Roman Empire. It infused everything; it was politically and economically important. And so, if you look for religious causes of any medieval phenomena, you’ll find them – whether that’s wars, massacres, dubious scars or hospitals. But if you focus exclusively on religious causes of social changes, you miss the bigger picture, and you may even fail to understand broader economic and political imperatives underlying those changes. You may also miss the complexity of different religious reasons underlying a certain development.

Hospitals are a good example; they fulfilled various spiritual needs, as archaeologist Martin Huggon pointed out in his epic 2018 study of these institutions. Those imperatives included charitable ones, certainly, but also the need to solve the problem of a spiritually corrosive presence: idle, infirm and economically unviable members of society. The hospital whisked them away, giving the diseased a chance at a life of piety, while removing unsightly disfigurement and literally crippling poverty from public gaze. As a bonus, it gave rich benefactors a chance to publicly demonstrate their wealth and generosity.

Some monks – especially Benedictines – may have been famously hospitable, but sometimes that hospitality didn’t extend beyond the gate of the abbey. Early hospitals sprang up outside abbeys, meaning the main abbey guesthouse could be reserved for more wealthy guests. Hospital numbers boomed in the later medieval period, frequently sited at town gates, at ports and near bridges. On the one hand, as with monasticism, there’s a sense of separation from the rest of society. On the other, being sited on well-used roads meant that hospitals were very visible to passers-by – and very obvious symbols of the piety and generosity of local clerics and elites. St Mary Magdalen is a case in point, on the busy road east out of Winchester. It’s the medieval equivalent of a massive billboard advertising just how pious, generous (and, by extension, how wealthy) its benefactors were.

While there are links with monasteries, those connections are perhaps not what they seem at first sight. Although undoubtedly charitable and worthy in some ways, medieval hospitals also served to preserve the status quo. Huggon writes that, ‘in a sense, the hospital acted as a weapon of social order… simultaneously protecting the marginal social strata from destitution and sin and also protecting society from the marginal social strata’. Hospitals formed a link between the outlying ends of a highly stratified society, with the urban poor at one extreme, and at the other the moneyed rich, whose charity could literally make those disenfranchised by the structure of society… disappear from sight.

In some sense, the existence of an impoverished sector of society can be seen as necessary, and perhaps even desirable. As Huggon writes, ‘poverty and illness were problems that were acknowledged and mediated but never resolved, and in fact the existence of these groups was necessary for the social order’. And if this feels somewhat distasteful, reflect that this is still how philanthropy operates today: social and financial inequality is what creates the opportunity for philanthropy. And philanthropists are rarely shy about emblazoning their name on institutions, even if they don’t all think they are buying themselves a fast-track ticket through purgatory any more.

This is the bigger picture, a wide perspective. But what of the people inside those hospitals? The root of the word ‘hospital’, from the Latin hospitale, helps us to understand their original inception – not as medical institutions, but as places that accommodated guests or hospites. Those guests, or perhaps inmates, were not necessarily sick (though many were); they were simply, for one reason or another, unable to look after themselves, and required support. Theoretically, hospitals would provide ‘succour for the needy’ free of charge, or at least at the point of delivery. In actuality, many inmates paid a fee, and those who became too infirm to live independently would hand over their house when they entered the hospital. (This is a version of social care that doesn’t sound a million miles away from what we have in England today.) Hospitals for travellers and pilgrims could also be part-funded by offerings at shrines, the medieval equivalent of the organisation JustGiving.

But it’s also important to recognise that, while medieval hospitals performed an important social welfare function, care for most of those who fell ill or into poverty came from family and friends, not institutions. (How far has our social care system come, some may ask.) Not all people with leprosy were cared for in leprosaria, by a long chalk. In 2002, a survey of forty-one British archaeological sites containing individuals with signs of leprosy revealed that only five of these sites appeared to be dedicated leprosy hospitals. In the thirty-six other sites, people with leprosy were being buried in the same cemeteries as the rest of the community. Again, this seems different from the traditional story, or at least the stereotype we’re used to. The leprosy hospitals have drawn our eye, perhaps, but the bigger picture across wider society looks more like integration, not exclusion or even segregation.

So it seems the people who entered the leprosaria represented the tip of the iceberg of the medieval leprosy epidemic. And for them, this would have been a huge change. Those who entered a hospital, long-term, would have been leaving behind their previous lives; some may have entered with quiet resignation, having no other choice. But that prospect of a new communal life must surely have been attractive for others, who found themselves alone and struggling.

We have looked at the common features of medieval hospitals, but in reality they were incredibly diverse, in terms of their size, structure and the nature of the people they housed – from the elderly and infirm, the sick and the deserving poor, to pilgrims and other travellers. Some tiny hospitals cared for just a couple of people while others served hundreds, but the majority were modestly sized, with between twelve and twenty inmates at any time. St Mary Magdalen, Winchester, fits into the middle range of these hospitals. In modern terms, the medieval hospital might be more like a hospice, a hostel or social housing, or a combination of all of these. There were often strict rules about who could and who could not be admitted, and these varied enormously. The hospitals of St John in Cambridge and another St John’s in Bridgwater, Somerset, explicitly denied entry to anyone chronically ill, permanently disabled, wounded, insane, pregnant or leprous. Whereas others, like St Mary Magdalen, specialised in leprosy.

Although hospitals as institutions existed elsewhere in Europe from the sixth century onwards, it seems that they only took off in England under the Normans. There are no definite records of Anglo-Saxon hospitals, but the Domesday Book does contain references to parcels of land being given to tenants with disabilities, by a lord, as a form of alms. As the Domesday Book was compiled in the first couple of decades of Norman rule, to record taxable property and estates, this suggests that there was already a tradition of charitable almsgiving in place before the arrival of William the Conqueror. And as Simon Roffey has argued, it’s possible that leprosy hospitals, in particular, may have evolved out of existing communities of sufferers.

We know from historical records that there were around 300 leprosy hospitals in early Norman England – more than a quarter of the total number of hospitals in the country. This speaks volumes about the prevalence of the disease in medieval Britain, although we still have to be a little careful as it’s clear that even some of these designated leprosy hospitals had a wider remit than others. But the spread of leprosy certainly seems to have driven the development of hospitals. In the late eleventh century, when we have the first definitive records of hospitals being founded, they are leprosy hospitals. And the rapid rise in the number of leprosy hospitals through the eleventh to fourteenth centuries seems to reflect a real increase in cases of leprosy, even while some were also home to those suffering from a range of other diseases.

We can see how the hospital site on Winchester’s Magdalen Hill fits into the wider landscape of medieval Britain, as part of the response to increasing cases of leprosy, but it does seem to have been established very early. The initial set of radiocarbon dates on bones from the cemetery came back suggesting a range from 970 to 1030 CE. This suggested that there was a possibility that it could have been established before the Norman Conquest – perhaps as a hospital attached to the monastery founded by Bishop Æthelwold. If so, this would make St Mary Magdalen unique: the earliest hospital in England, and the first evidence of such an institution in pre-Norman times. In order to test this idea, the archaeologists needed to be very sure of their data.

In 2018, I caught up with Simon Roffey again, while filming another history and archaeology series, Britain’s Most Historic Towns, for Channel 4. Having obtained that very early, pre-Norman date from one of the skeletons in St Mary Magdalen’s northern cemetery with clear signs of leprosy, Simon had sent off another sample for dating. I was really hoping that this might confirm an unusual, pre-Conquest inception of the hospital – it would have been a scoop. But the new radiocarbon date came back as 1010–1160 CE, straddling the crucial 1066. And in fact, this makes more sense; the rest of the archaeology supports an early Norman, mid-eleventh-century date.

But the revised date still meant that the archaeological investigation had pushed back the date of the hospital well beyond the first historical record of its existence. The hospital had clearly been in operation for decades before its first mention in the 1148 Winton Domesday book, with the earliest phase pinned down to 1070–1100 CE. It fits with the general picture in England, with hospitals appearing after the Norman Conquest. It’s tempting to see this phenomenon as cultural – the Normans bringing hospitals to England in the same way that the Romans brought baths, villas and apple trees. But in fact it may be more of a coincidence: the creation of leprosaria was a Europe-wide phenomenon in the late eleventh, early twelfth centuries: a social response to the dramatic increase in leprosy in the eleventh century. In England, this just happened to correspond with the arrival of the Normans.

Archaeology provides the opportunity to examine aspects of material culture, such as hospitals, on their own terms. Whereas the historical documents tell us perhaps what hospitals were meant to be about, archaeology can help to reveal how they worked in practice. And while history tells us more about the founders and benefactors of hospitals, archaeology can reveal astonishing details about the people who actually lived and died in them.

While hospitals were a reaction to a wave of disease, they weren’t focused – as we might expect today – on curative treatment. Medieval hospital accounts tacitly acknowledge that there was no known cure for leprosy; it is very rare that medicines or doctors are mentioned. Instead, medieval texts emphasise other aspects of palliative care: there was a general recognition of the importance of good nutrition, even if the details were somewhat sketchy and unscientific. Clean clothing and bedding, and bathing – sometimes in healing waters, just to boost the effect – were also considered important. But it seems that medical interventions, even those aimed at relieving symptoms, were rare in England.

Medical or surgical instruments are vanishingly rare in archaeological investigations of medieval hospital sites, although admittedly it can be hard to distinguish specifically ‘medical’ objects from household items at this time. The clearest evidence of what limited medical intervention existed comes from burials. A few graves from medieval hospitals have been found to contain metal plates that may have been parts of padded splints, for instance. Well-aligned healed fractures in skeletons also indicate medical care in the form of splinting. And there is some evidence of surgical intervention at St Mary Magdalen, Winchester: the healed foot amputation seen in Skeleton 19.

It seems many people simply had to learn to live with the disease – some of them from a very young age. The St Mary Magdalen cemetery contained a large number of children and adolescents. Twenty-three burials – more than half of the graves – in the earlier, northern cemetery were those of young people. What had led to these youngsters being admitted to the hospital? Had they been expelled from society or abandoned, or had their parents sent them to the hospital as the best place for care (if not medical treatment)? One review of early medieval literature, before 1100 CE, uncovered sixty-four records of children, of all classes, being taken to monastic institutions for medical care, sometimes at great expense. Some wealthy parents even founded leprosaria specifically for their own children. This speaks perhaps of a concern with care, rather than abandonment.

So who were the young people buried at St Mary Magdalen? How many males and females were amongst them? And were they suffering from leprosy or other diseases, and were they local children or had they come from further afield? These are precisely the sort of questions that history is silent on, but to which archaeological science can now provide answers. A recent study focused on nineteen individuals from the cemetery who were less than twenty-five years old, judging by tooth development, and who exhibited signs of leprosy.

All of these juvenile individuals showed signs of physiological stress: in other words, lesions in bone or teeth that show that someone has suffered poor health as a child – long enough to leave such a mark on the body. Physiological stress can be caused by malnutrition or disease, or both, and includes furrows on the incisors where enamel has failed to form properly and pitting in the roof of the orbits, or eye sockets, thought to be associated with anaemia. There was also some evidence of rickets, TB and healed fractures amongst these juvenile skeletons in the St Mary Magdalen cemetery.

Four children from the cemetery had teeth with very short roots, likely to be caused by leprosy bacilli invading developing teeth. Others had classic signs of leprosy, including bone loss around the nasal opening and in the hands, grooves on the finger bones from flexion deformities, plaques of new bone laid down on the surfaces of tibia and fibula, fused tarsal bones in the upper foot, and the harrowingly descriptive ‘knife-edge’ narrowing of the long metatarsals within the foot.

The archaeologists also wanted to determine the biological sex of these individuals. Skeletons of boys and girls begin to develop differently during puberty – before that, it’s impossible to tell them apart on the basis of bony morphology. So osteological assessment could reliably sort the older individuals in the sample into males and females, but not the younger ones. Some aDNA analysis had already been carried out on the Winchester burials, and that included one of the youngsters, aged around nine, whose sex could then be established; geneticists can determine biological sex where osteologists cannot, as long as the DNA is preserved. But there were still five individuals with no determination of sex. In order to rectify that, the team decided to use amelogenin analysis.

Amelogenin is the main protein in tooth enamel. Together with other proteins, like the ingeniously named enamelin, it forms a tangled mass that helps crystals of the mineral hydroxyapatite to grow. And it’s slightly different in men and women. Due to a quirk of biology, the amelogenin gene appears on both the X and Y chromosomes, in slightly different forms on each. DNA analysis focusing on the amelogenin gene has become a standard method for determining sex in forensic cases. DNA samples are extracted from the pulp cavities of teeth, and amplified in the presence of a ‘primer’, which sticks to the particular sequence of DNA that you want to copy. When you have enough DNA, you can perform agarose gel electrophoresis to separate and visualise the fragments. This is a tried and tested technique that has been around for about fifty years.

It works a bit like paper chromatography. When you place a dot of ink onto filter paper and dip the edge of the paper in solvent, the fluid will carry the various components in the ink different distances up the paper. Instead of paper, though, geneticists use agarose gel as a substrate. This is a gift from the sea, made out of purified sugars from kelp. Legend has it that a seventeenth-century Japanese innkeeper noticed that some leftover seaweed soup had coagulated into a gel. After that happy accident, agar gel became a staple in Asian cuisine and, by the end of the nineteenth century, microbiologists had realised it would be a very useful medium for growing bacteria on. And it’s also turned out to be very useful for sorting out smaller from larger fragments of DNA, when a mixture of these is introduced to an agar gel with an electric current passed through it. DNA is negatively charged and gets dragged towards the positive anode: small molecules surge ahead, while larger ones get trapped in the gel. But – unlike the pretty colours of a separated ink splodge in paper chromatography – DNA doesn’t show up on agarose gel, which sounds like a bit of a problem. Geneticists (and indeed chemists) do not give up that easily. They stain the DNA with a dye which shines under UV light.

The Y-chromosome version of the amelogenin gene (which is called AMELY) is smaller than the X-chromosome version (called AMELX): 1.3 kilobases compared with 1.5 kilobases. (Kilobase, abbreviated to kb, is the standard unit for measuring DNA length – related to the individual nucleotide bases, which are the building blocks of the stringy molecule: a kilobase is a thousand bases.) So, getting back to our forensic DNA sample: if it’s from a female individual, with two X chromosomes, there will be a single line on the gel at a distance along it corresponding with a DNA molecule that’s 1.5kb in size. If it’s from someone who had both an X and a Y chromosome, there will be two bands on the gel, one at 1.3kb and another at 1.5kb.

So, sex estimation using aDNA often targets the amelogenin gene, because of its presence on the sex chromosomes (X and Y) and the differences between the genes in those two loci. But it’s not just the amelogenin that differs between sexes – the protein does too (unsurprisingly, because genes encode proteins). And this creates an opportunity for archaeologists to use a less destructive technique for sex determination. Accessing the pulp cavity to extract a DNA sample requires cutting a tooth in half. But the amelogenin protein can be harvested from teeth using an acid etching technique, effectively just scratching the surface of the crown. The sample can then be analysed using mass spectrometry, which can differentiate between the X and Y forms of the amelogenin protein. If any trace of the Y form is present, this is considered to be an unambiguous indicator of male sex. It’s difficult to be so definite about female sex, though, as the lack of any Y signal could be either because there really was no such protein originally or because there’s too little to detect. But if there’s a strong signal associated with the X form of amelogenin, and no trace of the Y form, it’s probable that the sample really is from a female. The presence of these proteins has now been demonstrated in archaeological samples dating to more than 5,000 years ago, so this is looking like a very promising technique for determining the sex of archaeological skeletons when osteologists like me are stumped – either because the individual was a juvenile or, indeed, when remains are simply too fragmentary for traditional analysis.

Amongst the five mystery juvenile skeletons from Winchester, amelogenin analysis revealed the presence of three males and two females. In fact, these were the only two females in the whole sample of nineteen under-25-year-olds with signs of leprosy. At the time of writing, they’re also the youngest known females with signs of lepromatous leprosy in the archaeological record, anywhere. That is undoubtedly partly down to this study using cutting-edge techniques to determine sex in juveniles, but it’s really important for understanding the make-up of the community in the hospital. Amongst the older individuals in the St Mary Magdalen cemeteries, there are only two other females. It’s been suggested that some leprosaria were single-sex, and that the presence of women in cemeteries full of boys and men relates to a caregiving role. But the statutes of St Mary Magdalen indicate that it was open to residents of both sexes, and the presence of two young females with definite signs of leprosy is physical evidence that this was the case, even if females were a small minority.

The next stage of the investigation into the adolescents at St Mary Magdalen involved analysis aimed at determining where these individuals had lived as very young children – were they locals or incomers? The archaeologists knew that isotopes of oxygen and strontium in tooth enamel could indicate where these young people grew up – as we saw in the case of the St Brice’s Day Massacre. These elements exist naturally in slightly different forms, or isotopes, and the ratios of different isotopes in tooth enamel can be linked to geography. Crudely, strontium isotope ratios link to different types of bedrock, and oxygen isotope ratios link to local climatic factors. Winchester is located on the South Downs, so the crucial question was: did the isotope values for the teeth match up with that Cretaceous chalk geology and local climate?

Twelve of the individuals turned out to have strontium and oxygen isotope values that were compatible with growing up somewhere with a lot of chalk geology and a relatively high level of rainfall – somewhere like Winchester, indeed. Six individuals had strontium isotope values that suggest a childhood home somewhere else, though that ‘somewhere else’ could still have been in England. The oxygen isotope values for two of these six suggest that they grew up either in the extreme west of Britain or perhaps even further afield, somewhere around the Mediterranean. One individual had strontium isotope values suggesting that they hadn’t grown up on chalk downland; their oxygen isotope values indicated that they’d come from somewhere significantly cooler and further north, perhaps Denmark or Norway.

Putting these results into context, we see that the majority of young people with leprosy in the cemetery had most likely grown up in the Winchester area. They had not caught leprosy somewhere further afield and brought it into Britain. And this suggests that the branch 2 strain of M. leprae, which other studies suggest to have originated in western Asia, had already spread to become endemic in Britain. On the other hand, seven of these younger individuals came from further afield, so we have learned that the hospital wasn’t limited to caring for locals only.

In the grave of one of the younger people with leprosy in this cemetery, Skeleton 27, was something that seems to relate to long-distance travel. It’s a small but wonderful clue, and it comes not from the bones themselves, but from an object buried in the grave.

Just like others in the cemetery, this particular individual was buried in an anthropomorphic grave dug down into the chalk, with a cut-out for the head. He was in his late teens or early twenties when he died, and around 1.7 metres or 5ft 7in tall – average for the time. His face and hands were unaffected by leprous changes, but his toe-bones were porous and there was new bone growth on his tibiae and fibulae, too. He had horrendous calculus: great slabs and nodules of hardened plaque had accumulated on the outer surfaces of his teeth like barnacles on a ship’s hull. This could be evidence of inflammation of the soft tissues of the face and mouth, consistent with leprosy, even without the classic bony changes around the nasal opening and maxillae. There were also degenerative bony changes in the spine, shoulder and elbow, as well as bony growths at points of muscle attachment – unusual in one so young. The bony changes are suggestive of leprosy, but not definitive. But a PCR test for M. leprae DNA provided the unequivocal evidence of leprosy. It may not have been leprosy that killed him – he died relatively young; the cause of death, as so often in osteology, remains elusive. But even with the relatively subtle evidence of the disease in his bones, in life he probably bore the obvious signs of leprosy in the soft tissues of his face.

The fact that leprosy had started to make its mark on his bones suggests that he must have contracted the disease when he was very young. And it may be that this young man was someone of relatively high social status. Analysis of other isotopes – carbon and nitrogen – in his bones suggests he ate a rich diet with plenty of animal protein, different from most other people in the hospital cemetery. And he was buried very close to the early chapel on the site.

At the left hip of this young man in his grave was a shell from the species Pecten maximus – an Atlantic scallop. It was pierced with two holes – suggesting it had originally been sewn onto something organic, that hadn’t survived. The scallop shell was the traditional souvenir of pilgrimage to the shrine of St James at Santiago de Compostela, in Spain. Compostela was one of the most popular pilgrim destinations in the eleventh and twelfth centuries, along with Rome and Jerusalem. It’s estimated that up to 2 million pilgrims visited the shrine at Compostela each year. The name Santiago comes from the Latin, Sancti Iacobi – St James. Although St James was thought to have been beheaded in Jerusalem, a legend arose that his body was miraculously conveyed in a crewless boat to Spain, and Compostela is where his remains were traditionally said to have been buried. At least, this is where his relics were apparently discovered – somewhat later, in the ninth century – and the shrine was then set up. If you wanted to create a tourist destination in the Middle Ages, there really was nothing better than having a dead saint as a draw. And this particular one would eventually reach the heady heights of becoming the patron saint of Spain.

With the scallop shell in his grave, it is surely likely that this young man had completed the pilgrimage to Compostela. That was the only place officially licensed to give out scallop shells – though, of course, fakes were available, and you could get one yourself off a beach. But this seems too sceptical. Simon Roffey showed me this pierced shell back in 2018, and he believed it was most likely to have been attached to a very characteristic pilgrim’s bag, or scrip. If we take the shell at face value, it seems more than reasonable to conclude that this young man was a pilgrim and had visited Compostela. As for where he came from originally, it seems that this young pilgrim didn’t grow up in Winchester. He’s one of those individuals who, according to the isotope analysis, was not local but may have still come from elsewhere in England.

Winchester itself was also an important site for pilgrimage, taking its place in the wider network of European medieval religious tourism. Within southern England it lay centrally, with other pilgrimage hotspots around it: Glastonbury to the west, Reading Abbey to the north and Canterbury to the east. It was also handily close to the port of Southampton, just 12 miles to the south. (In the twelfth century, Reading apparently got hold of the hand of St James, creating a gruesomely visceral link with Compostela.) Having grown from an Iron Age oppidum, or fortified settlement, to a Roman town, to a proto-capital under Alfred the Great, where William the Conqueror would build one of his palaces, and with a huge, new Norman cathedral, Winchester was still an important city in the twelfth century. It couldn’t claim to house an apostle’s relics, but it did have the mortal remains of a few other saints: Birinus, Judoc, Grimbald and Swithin. St Swithin was a ninth-century bishop of Winchester who seems to have led an almost entirely unremarkable life but really came into his own when he died: his body was dug up (against his wishes) and transferred to a shrine in the cathedral, where he proceeded to cause a slew of miracles to happen, on an almost daily basis. The urban historian Derek Keene suggested that the re-foundation of the St Mary Magdalen leprosy hospital itself in the twelfth century – with that idea of leprosy as a holy disease – may have served to reinforce Winchester’s association with the Resurrection, Jerusalem and pilgrimage. Rather than places of exclusion, then, this perspective sees these hospitals as integrated components of a wider sacred landscape, almost as shrines in their own right.

Perhaps, as far as a medieval pilgrim was concerned, the leprosy hospital of St Mary Magdalen at Winchester would not have been a bad place to end up.

3. TOMB OF A MARTYR

The Church’s Restoration

In eighteen-eighty-three

Has left for contemplation

Not what there used to be…

… Sing on, with hymns uproarious,

Ye humble and aloof,

Look up! and oh how glorious

He has restored the roof!

from The Church’s Restoration by John Betjeman

It was a windy day; the sky was overcast and brooding, threatening rain. I was more than a little nervous ascending in a rickety lift, travelling up through scaffolding, clanking its way up to a roof 70 metres above the ground. When we shuddered to a halt, I carefully climbed out to stand right on the top of the cathedral tower. Two stonemasons had prepared a brand-new finial for me to set in place. I trowelled on the mortar and we winched the tall finial over and gradually lowered it into position on its pedestal. It looks like a tiny spike from the ground, but it was a full metre tall: a heavy, tapering obelisk.

I was lucky enough to be visiting the cathedral while it was undergoing some major restoration work in 2019, giving me the opportunity to add this finishing touch to the northwest tower of this iconic building. I’m not religious, but I loved, for that moment, being part of history in that lofty place.

It is, of course, a turbulent history. Canterbury Cathedral once contained the most magnificent tomb in England, a shrine that held the remains of the most powerful saint in English history, a martyr whose power was indestructible. The story of that tomb – its creation and destruction – encapsulates in microcosm the tension between Church and State that existed in the Middle Ages and beyond. And the search for the lost, holy relics that this tomb once contained continued right into the twentieth century.

Canterbury was established by the Romans soon after the Claudian invasion of 43 CE, as Durovernum Cantiacorum – or, perhaps more accurately, the Romans continued to use a town that was already established in the Iron Age but were the first to record its name in the historical record. ‘Cantiacorum’ means ‘of the Cantiaci’ – the tribe or people of Kent. Cant… Kent. It’s one of those wonderful echoes where the name we use today for a region harks back at least 2,000 years. And not only that – as I discussed in my earlier book, Ancestors, the modern county town of Canterbury is the ancient capital of what we can reasonably assume was a pre-Roman Iron Age kingdom. (The same goes for Dorchester in Dorset, Exeter in Devon, and many others.)

When Britain exited from the Roman Empire in the early fifth century, elites seem to realign – culturally, religiously and politically – with northwest Europe. In fact, those connections may always have been there, just somewhat obscured by the Mediterranean influence of the Roman Empire. And so, when the pope sent St Augustine to Kent in the sixth century, this wasn’t just a religious mission; it was a diplomatic effort to bring England back into the political sphere of influence centred on Rome. The most obvious symbol of allegiance to what had become of the old Roman Empire was to adopt its religion. St Augustine wasn’t sent just to ‘convert’ the pagan king of Kent, Æthelberht – he was there to secure his political and economic allegiance. This was probably helped along by the fact that Æthelberht had already married Bertha, the daughter of the Christian king, Charibert I, of the Franks, connecting him to that kingdom by marriage. Having extracted themselves from the sway of Rome in the fifth century, English kingdoms were being inexorably drawn back into its compass. And it would always be a tense alliance. The Church would support monarchs, conferring divine authority on their right to rule, working as a press agency in every community, with preachers delivering messages of personal salvation wrapped up with political propaganda and garnering support for military action where the ambitions of monarchs and the Church coincided. With a largely illiterate population, the Church had the edge when it came to mass communication. But Rome demanded fealty: politically manipulative, fiscally demanding, its support for a monarch didn’t come cheap.

Æthelberht was ready for the deal. He gave Augustine land to found a monastery, and very soon the emissary from Rome became the very first archbishop of Canterbury. A new cathedral was built in Canterbury itself. Six centuries later, the arrival of the Normans in England signalled the establishment of an even stronger link with Rome. When William the Conqueror invaded in 1066, he was flying a papal banner that had been personally blessed by Pope Alexander II himself. This was a holy war: William had promised the pope a strengthened allegiance if he prevailed in England. And he did. Following his victory, the Normans set about rebuilding Anglo-Saxon cathedrals, writing themselves – and that renewed link with Rome – in stone.

Historians have argued that papal influence reached its peak in England under the Normans. They practically obliterated earlier buildings – and started from the ground up. Out with the old, in with the new. But to be fair to them, their ecclesiastical architecture was magnificent, and when we encounter it today, even with layers of later additions and renovation, it never fails to impress. Church architecture is all about evoking the sublime – creating an expansive feeling of something huge and magnificent. Even if the stonemasons didn’t buy into the spiritual message – indeed, even if the church leaders didn’t – they knew the effect it would have on churchgoers. It’s undeniably effective. I’m an atheist through and through, but I love a good cathedral. And Canterbury is right up there. It is sublime.

For medieval pilgrims, though, it wasn’t just the architecture that proved a draw and inspired them. It was the presence of a saint in the building. And not just any old saint – one that had been martyred. The most famous martyr in England.

We know a lot about Thomas Becket’s life, in particular through the writings of a man who’d grown up in Salisbury, went on to study in France and became thoroughly embedded in the Anglo-Norman Church. Eventually, at the end of his career, he would become bishop of Chartres – but he’d got to know Thomas Becket much earlier in his career.

John of Salisbury – or ‘Johannes Parvus’, Little John, as he called himself – was secretary to the man who was archbishop of Canterbury before Thomas, Theobald of Bec. Theobald had been the abbot at the prestigious Abbey of Bec in Normandy before King Stephen appointed him to the top position in the English Church. And lest you should think of John’s role of ‘secretary’ as menial – a mere pen-pusher – it was much more senior and politically powerful than that; think more of a Secretary of State. John was incredibly well connected, politically. Despite the fact that Theobald had been granted his archbishopric by King Stephen, John had openly supported the opposing Duke of Normandy in the twelfth-century civil war known as the Anarchy. This would prove a judicious position: when Stephen died, in 1154, that Duke of Normandy (the great-grandson of William I) became the first Plantagenet king of England: Henry II. John had also been friends with a man called Nicholas Breakspear, who would change his name to Hadrian IV in the same year, when he became the only Englishman ever to be anointed Pope.

But it was earlier, while he was secretary to Archbishop Theobald and while Stephen was on the throne, that John of Salisbury first worked closely with Thomas Becket. It is said that they first met at this time, but it seems perfectly possible – likely, indeed – that their paths crossed earlier, when they both attended the proto-university cathedral schools of Paris. They were around the same age, and some historians have assumed that the two men were good friends, but if they were, that didn’t stop John of Salisbury being quite critical of Becket at times (that is, up until the point that his contemporary was murdered).

Thomas Becket was also a servant of Theobald’s; it’s been suggested that he may have been related to him, through his father – who came from Normandy – and that’s how he landed the job. Like John of Salisbury, Becket studied in Paris and then went on to be a clerk, finding a position in Theobald’s household. Unlike John, who is regarded as having been very widely read and a consummate classical scholar, Thomas never qualified as a magister, or ‘master’, and seemed more interested in hunting and fowling than study. And yet he was educated enough – and presumably showed prowess in other ways – to impress Theobald. His biographers describe the young Thomas as tall, lean and handsome, gregarious and charming. In 1154, Theobald made Becket archdeacon of Canterbury – and then recommended him to Henry II, who appointed him to the highest position in the royal household, making him Chancellor in 1155.

Henry was keen to rebuild the power of the monarchy after the decades of political turmoil during the Anarchy. He sought to curb the power of rebellious barons and to extend the power of the royal courts over local feudal jurisdiction. He also wanted to extend his royal power over ecclesiastical courts and to ensure that crimes committed by clergy could be tried in secular courts. (This tussling between ecclesiastical and secular authority wasn’t restricted to Britain – it was rife across Europe in the eleventh and twelfth centuries.) Perhaps Theobald imagined that Thomas would support the Church in such altercations, but Thomas clearly saw it his duty to uphold royal authority once he was in post. And so Henry seemed to have gained the upper hand, exerting his own influence over the Church by appointing this archdeacon and acolyte of Theobald as his Chancellor. And indeed, there’s a documented instance of Thomas supporting Henry, against papal authority, in the Chronicle of Battle Abbey.

Then, in 1161, Theobald died, and Becket was elected as the new archbishop of Canterbury. It was an unusual appointment: Thomas had worked for the old archbishop and he’d held a high administrative position in the Church as archdeacon, but he wasn’t a man of the cloth. Even Theobald, who reputedly behaved like more of a secular clerk, had originally been a monk. But the old archbishop had wanted Thomas to succeed him; he must have believed that his protégé would be able to manage the difficult relations amongst monks and bishops and between Church and Crown. In a matter of days after being elected to his new (and final) role, Thomas resigned from the chancellorship (which Henry seems not to have expected), was ordained as a priest, and then consecrated as archbishop in 1162. John of Salisbury stayed in post as his secretary. As for Becket, having been such a staunch ally of Henry as his Chancellor, he now found God. He pivoted to defend the Church against what he saw as Henry’s overreaching ambitions, and John supported him. Becket’s shifting loyalties are invariably described in pious terms, but it’s hard to imagine that his motives didn’t include his own career ambitions. After all, he’d already notched up the highest position in the land under the king, as Chancellor. But as Archbishop of Canterbury, there were suddenly even higher roles to aspire to, in a powerful, supranational organisation – the Church.

Becket’s resignation from the chancellorship was the first sign that he perceived a fundamental conflict of interest between Crown and Church, and the first sign for Henry II that things were going to go less smoothly than he’d perhaps hoped. Once archbishop, Becket immediately reclaimed land and revenue that had once belonged to Canterbury, and he clashed with the king over appointments and payments from clergy to the Crown. He also resisted attempts to refer charges of corruption and crime within the Church to the royal courts. Meanwhile, murders committed by clergy were going unpunished. Eventually, news of the dispute reached the pope, who seems to have been faintly embarrassed by Becket’s overzealous demands and actually suggested that the archbishop should acquiesce to the king’s demands. In 1164, Becket and his bishops met Henry and his barons in a hunting lodge at Clarendon, and there, Henry presented a new set of constitutions – which included the right to try churchmen facing criminal charges in the royal courts.

At the time, the Church represented not only another system of political power, but a completely separate system of jurisdiction. With Henry’s new Constitutions of Clarendon, appeals arising in ecclesiastical courts would be referred upwards to bishops then to the archbishop as before – but then, to the king, not to the pope. The increased legal power of the English royal courts would of course also boost revenue to the Crown. In this way, Henry took control, effectively making the ecclesiastical legal system subordinate to the English monarchy, reinforcing his sovereignty and limiting the power of foreign courts. This wasn’t an entirely new arrangement; despite arriving under a papal banner, William I had been very clear that as the English monarch, he – and not the pope – would be head of the Church in England. During Stephen’s rule and the chaos of the Anarchy, ecclesiastical courts had gained power at the expense of royal authority and jurisdiction. Henry was seeking to reverse those changes and regain the power held by his ancestors.

Becket seemed to agree to the new constitutions, but then apparently regretted this decision fairly swiftly. In October 1164, he faced various charges including contempt of royal authority – and fled to France. While in exile, he threatened Henry with excommunication. The disagreement rumbled on. Meanwhile, Henry arranged to have his son, Henry Junior, crowned in preparation, so that he could immediately step into his father’s clogs when he popped them.

In July 1170, Becket and Henry met in a meadow near the village of Fréteval, near Orléans. They reached some sort of rapprochement, and in December of that year, after six years of exile, Becket returned to Canterbury. He didn’t come back quietly. He immediately excommunicated a few bishops who’d helped Henry with the pre-coronation of his son. Becket seemed to know he was playing a dangerous game. Just as he was about to leave France, he embraced the bishop of Paris, saying, ‘I am going to England to die.’ And another ominous comment emerged in Becket’s sermon on Christmas Day 1170. In it, he referred to one of his predecessors, St Alphege, an eleventh-century archbishop who’d been killed by Vikings. Becket said to the congregation, ‘you have one martyr archbishop… before long you’ll have another’.

Henry was away in Normandy over Christmas, and when he heard that Becket, reinstalled in Canterbury, was already creating ructions and excommunicating bishops, he is said to have exploded in rage: ‘Will nobody rid me of this turbulent priest?’ As so often with famous quotes, this one seems to be apocryphal, an eighteenth-century invention. But while the words may not be accurate, it seems that Henry did voice disquiet. Another contemporary biographer of Becket, Edward Grim, recorded a different version: ‘What miserable drones and traitors have I nourished and brought up in my household, who let their lord be treated with such shameful contempt by a low-born cleric?’ Regardless of what exactly Henry II said that Christmas in 1170, four knights interpreted it as an instruction, and set off across the Channel – with murder in their hearts. Before the year was out, Becket would be lying, dead, on the cold stone floor of Canterbury Cathedral.

In the aftermath of Becket’s assassination, Henry II had little choice but to back down. He swore allegiance to Pope Alexander III, restored the possessions of Canterbury and provided military support to the crusader states in the eastern Mediterranean. Although some historians have portrayed this as a significant blow to Henry’s authority, it seems the implications were perhaps less profound. Following Becket’s murder, Henry promised to reverse legal customs that he’d introduced, but it was really only one point that was revoked, permitting the ecclesiastical courts to refer cases to Rome, and even then, a few crimes could still be prosecuted through the secular courts. In reality, Henry could still intervene in cases when he wanted to, and he was present at several settlements presided over by papal judges. Gerald of Wales, Archdeacon of Brecon and historian, reported on a complaint from a bishop that Becket’s martyrdom had achieved nothing for the Church. But there’s no doubt that Henry lost some political power: the divide between secular and ecclesiastical law shifted a little, and the Church was able to wrest back some control over ecclesiastical appointments, too. In the years following Becket’s murder, supporters of the ultimate authority of the pope found themselves promoted to senior positions in the English Church. As for Henry himself, although he could exercise his own power, he would never resist or obstruct papal authority as openly as he’d done before Becket was murdered. And the martyrdom of the archbishop would echo down through the centuries.

The death of the archbishop was such a hot topic that when Geoffrey of Vigeois was writing his chronicle in Limoges, in the late twelfth century, he excused himself from covering it. Others had already done it to death. By 1180, at least ten authors had written accounts of the life (and death) of Becket. John of Salisbury was one of the chroniclers of the incident and he was actually present in the cathedral – though hiding behind an altar. One of the archbishop’s clerks, William FitzStephen, was a direct eyewitness, however – and what follows is the sequence of events that he described.

Four knights – Hugh de Morville, William de Tracy, Reginald FitzUrse and Richard le Breton – arrived to confront Thomas in his archbishop’s palace. There, they told him that they’d been sent with orders from the king: Becket was to reinstate the excommunicated bishops and recognise the coronation of the young Henry. Becket replied that it was the pope who had excommunicated the bishops and that ruling would stay in place, but he did say that he recognised the new king. After an increasingly tense exchange, the four knights asked the members of the archbishop’s household to leave them alone; when everyone stayed put, the knights told them instead to guard Becket. Then they left. William FitzStephen and the others debated how to handle the situation, but it wasn’t long before the knights returned with a larger, armed force. Some monks who were with the archbishop urged him to take refuge in the cathedral, and eventually he agreed. Becket walked slowly through the cloisters into the Chapel of St Benedict in the northwest transept. Some of the monks who had been saying Vespers came down to meet him.

Becket was ascending the stairs to the main body of the cathedral when the knights – led by FitzUrse – caught up with him, their swords drawn, with a crowd of other soldiers. The archbishop turned around and walked back down into the transept. At this point, most of the people with Becket, including John of Salisbury, ran away to hide. Canon Robert, the clerk Edward Grim and William FitzStephen stayed with the archbishop.

‘Where is the traitor?’ called out one assailant. ‘Where is the archbishop?’ cried another.

‘Here I am. No traitor, but a priest of God,’ said Becket. ‘What do you want?’

‘That you die. It’s impossible for you to live any longer,’ came the reply.

One of the knights struck Becket between the shoulders with the flat of his sword, crying, ‘Flee – you’re a dead man.’

Becket stayed put, while some of the knights attempted to drag him out of the cathedral, but the archbishop resisted. ‘I’m going nowhere,’ he said. ‘Do here what you will to me – what you have been ordered to do.’

According to FitzStephen, William de Tracy was the first to raise his sword (though other chroniclers say it was FitzUrse), and Edward Grim held up his arm to try to protect Becket. De Tracy’s sword came down, slicing through Grim’s arm – and striking Becket’s head. The archbishop wiped the blood from his head and commended his soul to God. At a second strike (from Reginald FitzUrse, Grim recounted in his biography), the archbishop fell onto his face in front of the altar of St Benedict. Richard le Breton landed another blow, with such force that the blade cut through Becket’s skull and broke on the stone floor. There was a fourth blow, also to the archbishop’s head. The top of his skull was cut off.

A priest who had entered with the knights, Hugh of Horsea, trod down on Becket’s neck and used his sword to draw out blood and brains from the fragment of Becket’s skull. The moment of the archbishop’s death was, FitzStephen wrote, accompanied by a sudden crashing thunderstorm and violent rain.

The aggressors rushed away – but not before they’d looted the house of the murdered archbishop, taking gold and silver treasures, papal bulls, signet rings and precious fabrics, and the horses from the stables.

For a long time, the bloodied body was left alone in the transept. Once the monks, servants and clerks were sure that the assailants had gone, they returned. They carried Becket’s body up to the main body of the church and laid it before the altar, having tied a cloth over the wound to his head. Canon Robert showed the monks that, under his robes, the archbishop had worn a hair shirt. This was important, as FitzStephen noted, because it demonstrated that since his days dressed in finery as Chancellor, Becket had truly become a pious man.

Fearing that his assailants might return and seize his body, the monks made haste to bury Thomas Becket in the crypt of the cathedral, dressed in his archiepiscopal robes over his blood-stained hair shirt. Immediately, FitzStephen related, miracles started to occur. One man dipped his shirt into Becket’s blood, washed the shirt and gave the water to his wife to drink, and she was instantly cured of paralysis. The miracles continued – even the dead could be brought back to life when water containing the blood of Thomas was poured onto their faces.

FitzStephen and other writers were quick to make unsubtle analogies between the death of this martyr and the passion of Christ himself. Language crystallises around polarised positions in our modern-day culture wars, creating an illusion of simplicity in complex social arguments and honing words into emotive whistles and weapons. It was the same story in the Middle Ages; medieval churchmen didn’t shy away from a ready ‘language of persecution’, drawing on a rich vein of the stuff in scripture. Becket himself had tried this tack. He’d written a series of letters to Pope Alexander III in which he was keen to portray the dispute between himself and Henry II as much more than a personal contretemps; the king wasn’t just attacking Becket, he was attacking the Church itself.

John of Salisbury would write about Becket’s martyrdom in a similar way, though he hadn’t always been the archbishop’s biggest fan. He’d continued as secretary to Becket after the death of Archbishop Theobald, but from around 1165 he sought to distance himself from the archbishop, perhaps sensing that the quarrel with the king had become too personal. By 1166, when Becket had embroiled himself in the business of excommunicating some of Henry’s officials – and had even threatened to excommunicate the king himself – John couldn’t sit on the fence any longer; he had to pick a side, and he picked Becket’s. In that year he wrote many a letter not only making it clear that any enemies of Becket’s were also enemies of the Church, but also drawing that same analogy between the suffering of Becket in exile and the Passion of Christ. His support of Becket, and the language of persecution that he used, grew even keener after the archbishop’s murder.

John of Salisbury penned a letter to the bishop of Poitiers in 1171, describing the death of Becket in some detail. The assassins, he wrote, had defiled a holy day and desecrated a church with their violence, and had even looted the bishop’s palace for treasure. He added the detail that the assailants were intent on returning to claim the body in order to throw it in a marsh or hang it on a cross. But the Canterbury monks hurried to bury Becket in a curiously convenient marble tomb in the crypt, in front of altars to John the Baptist and St Augustine. Again, John of Salisbury mentions that they buried him in his hair shirt and the monk’s habit he’d been wearing the day he was killed – and on top of that, the vestments, mitre and staff of an archbishop. John ended his letter describing the miracles that were taking place at the tomb:

For in the place of his suffering, as well as where he was finally buried, paralytics are cured, the blind see, the deaf hear, the dumb speak, the lame walk, those with fevers are cured, the possessed are freed from the devil, the ailing are cured of various diseases, the blasphemers who are possessed by the devil are confuted, and He performs all these and many other miracles which it would take too long to recount… now under no condition would I dare write these statements did not an enlightened faith make me absolutely certain of the facts. And so it remains for one of your learning to instruct our humble selves as to whether it would be safe to invoke him as a guardian of salvation among the lists of the martyrs… without the authority of the Roman pontiff…

John was desperate for Thomas to be recognised as a saint, and indeed in the closing paragraph of this letter he goes further, saying that they’ve actually all decided to venerate Becket as a martyr anyway, without bothering to wait for papal sign-off, as he’s fairly sure that would be God’s will. John wrote similar letters to other friends in France, and included the details in his later hagiography, the Vita S. Thomae Becket, as well. Abbot Peter of Celle wrote back to John to say he thought it right to venerate Thomas Becket. By 1173, with reports of miracles occurring in Canterbury burgeoning, Pope Alexander III made Becket a saint. Three years after the event, the anniversary of his murder became a feast day, with the gruesome details of the murder of Saint Thomas – based on John of Salisbury’s Vita – read out in church. And the miracles spread further, first throughout England, and then to France and Germany. Thanks to his gruesomely heroic demise, Becket was becoming far more famous in death than he’d ever been in life. And he would be an enduring problem for Henry II.

When Becket was murdered, the news spread fast. Henry was still in Normandy when he first heard of the assassination, and he is said to have shut himself in his apartments for forty days. Word quickly reached the French archbishop, William of Sens, and Henry was immediately cut off from his continental lands. A report was sent onwards to the papal court in Tusculum, near Rome, arriving with the pope before Henry’s own envoy turned up to tell his side of the story. Pope Alexander promptly excommunicated the homicidal knights and banned Henry himself from entering any church. In March, Henry wrote to the pope to present his case, claiming he had not incited the murder, and even implied that Becket had brought his fate upon himself. But he couldn’t continue with that tack for long.

Henry II was facing both internal and external threats to his power. His wife, Queen Eleanor, had abandoned him and, in 1173, joined forces with his three eldest sons in an attempt to overthrow him. King William of Scotland and a couple of French counts joined in. It was easy for Henry’s detractors to interpret this as divine retribution for his involvement in the assassination of St Thomas. Whether in reality he had incited the murder or not, everyone in western Europe seemed to lay the blame firmly at his door. He had to do something to counter this disastrous stain on his reputation. And not only that, he had to somehow take control of the expanding cult of St Thomas.

Henry had attempted to lay the ghost of Becket to rest with a public repentance in 1172, but by 1174, with his family rising up against him, it was clear he needed to do more. That summer, while trying to suppress the rebellion, Henry made a special detour to Canterbury. Two miles outside the city, he dismounted his horse and walked to a chapel just outside the walls. There, he took off his cloak and his shoes, and then he walked, barefoot, into the city, all the way to Becket’s tomb in the crypt of the cathedral. He prayed at the tomb all through the night, promised substantial funds to the church and committed to building a new monastery.

Henry’s very public act of penitence seemed to work. In less than two weeks, the Scottish king, William I, had been captured; bad weather had disrupted the invasion fleet of Henry’s oldest son; and his enemies in Normandy had been appeased. St Thomas – his friend-turned-nemesis – had seemingly become his saviour. Henry had neutralised the potential of the cult to damage him, and had instead spun it round so that, now, St Thomas became the protector of Henry, his kingdom and his lineage. A verse written in celebration of the victory over the rebels summed it up:

‘Seint Thomas’, dist li reis, ‘guardez-mei mu reaume.

A vus me rent cupable dunt li autre unt le blasme’.

‘St Thomas,’ said the king, ‘guard for me my realm.

To you I declare myself culpable, for which others have the blame.’

Henry had adroitly turned a PR nightmare to his own advantage, embracing the booming cult of this ‘people’s saint’ who was rapidly becoming one of the most popular saints of the entire Middle Ages.

Canterbury would become the top pilgrim destination in England, and the cathedral invested heavily in this tourism opportunity. In 1174, the east end of the cathedral was destroyed in a fire, and it was rebuilt over the next twelve years to create an extension ending in a round apse – very much like a Roman basilica. This addition was the Trinity Chapel: a martyrium dedicated to the new saint, decorated with twelve stained-glass windows showing scenes from the life of St Thomas, as well as various post mortem miracles that had been recorded amongst the visitors to his tomb.

The investment in St Thomas’s image was just extraordinary: these twelve windows represent, as historian Marie-Pierre Gelin puts it, the ‘most extensive iconographic programme dedicated to a single saint in the Middle Ages’. Just like the written accounts of Becket’s life, where authors clearly struggled to portray him as particularly pious in his youth, instead casting him in the role of a ‘new man’ when he became archbishop, the pictures were essential to his brand, especially when some doubted that he deserved a sainthood.

The Trinity Chapel had its own mini-extension at its eastern apex – a small, round chapel called the Corona (as in ‘crown’ of the head), intended to hold a separate shrine containing the piece of skull that had been detached from Becket’s head on that fateful night in 1170. The focus was undoubtedly St Thomas, but his light didn’t eclipse the fame of other saintly ex-archbishops of Canterbury, like St Alphege and the tenth-century St Duncan (who’d also locked horns with a king and been exiled). If anything, their lights burned a little brighter in the glow of St Thomas; the Canterbury monks added new material to the liturgies read on these archbishop-saints’ feast days, and new stained-glass windows depicting scenes from their lives were installed in the choir, near their tombs, either side of the cathedral’s main altar.

In the stained-glass windows in the Trinity Chapel, St Thomas is portrayed in exactly the same way as his predecessors, St Alphege and St Duncan. Each of them is shown with a short beard, wearing a mitre and sporting a red chasuble (a poncho-like cape), over a green surplice (a shorter robe), over an alb (a full-length white robe). It’s a uniform that clearly says ‘archbishop’, but it also helps to create a clear visual link between the three saints, almost fusing them into a single, eternal, archetypal figure – someone who’s always been there, while kings, Anglo-Saxon or Norman, come and go – defending the rights of the Church.

Whoever commissioned those windows (presumably Becket’s successor, the monk-turned-archbishop Richard of Dover), they didn’t waste a chance to include a not-so-subtle message for kings. There’s a panel showing a vision that St Dunstan is meant to have experienced about his contemporary, King Eadwig: the king dies and his soul is dragged off by devils, but then Dunstan intervenes, drawing the dead monarch up out of the fiery, sharp-toothed jaws of hell. It was a stark warning to any kings who dared to defy clerics, as so many of them did. And it was a clear message to all who saw it that the power of the Church superseded the temporal power of kings. I wonder what Henry II thought of it. Whatever he thought privately, in public he kept visiting the tomb in the cathedral and paying devotion to the sainted remains of his one-time Chancellor. He simply couldn’t afford to distance himself from this populist cult.

Henry II would return at least nine times to visit the tomb of Becket in Canterbury, and his successors, Richard and John, would continue this tradition of royal veneration of the saint. Meanwhile, Henry II’s three daughters, marrying kings in Castile, Sicily and Saxony, helped to spread the Cult of St Thomas across Europe. (It seems odd, perhaps, that Henry’s rebellious sons and daughters would embrace the cult their father had championed, but perhaps it was more about legitimising the wider Angevin royal dynasty.) The cult of St Thomas would always be something of a double-edged sword for this royal family. While the Angevin kings aligned themselves with it, seeking St Thomas’s protection, the saint would also – thanks to his biographers – always stand for the rights of the Church and the papacy above that of any monarch. Richard and John would persist in electing men from their courts as bishops, and many bishops – unlike Becket – held on to secular roles as well. The tussle between secular and religious power extended across Europe. Popes were endlessly either threatening or actually imposing interdicts and excommunication on kings, and they didn’t shy away from calling on saints to back them up when it came to negotiating the balance of power between Church and Crown. In 1207, Pope Innocent III wrote to King John to let him know that ‘to fight against God and the Church in this cause for which St Thomas, that glorious martyr and archbishop, recently shed his blood, would be dangerous for you’. If it sounds like a threat, that’s because it was.

St Thomas was proving useful to the Church for keeping unruly kings in order, and he continued to be spectacularly popular with ordinary people. Pilgrims flooded to Canterbury, and the miracles just kept coming. In 1179, King Louis VII of France joined the pilgrims, travelling to Canterbury to pray for the recovery of his son, who’d fallen ill after a hunting trip. The son pulled through (though Louis VII had a stroke on his way home) and St Thomas netted a further PR boost, helping to make Canterbury the premier pilgrimage destination in northwest Europe.

The saint had quickly gained a posthumous reputation for healing various afflictions, including – somewhat implausibly – leprosy. His identity as a martyr played into the view of people with leprosy as having been divinely chosen for suffering in life. Becket came from Normandy originally, his mother from Caen and his father from Rouen, and his cult became quickly established there too. One way in which his celebrity status was memorialised and magnified was through the founding or re-dedication of at least a dozen leprosy hospitals, including Mont-aux-Malades near Rouen, La Chapelle Saint-Thomas at Aizier and Saint-Thomas at Caen. Reminding us once again of that link between pilgrims, shrines and leprosy hospitals, the leproserie at Mont-aux-Malades possessed relics: fragments of Becket’s robes, hair shirt and even a bone. Those relics would form a magnet for worship – and donations.

St Thomas was also celebrated in pictorial form in various cathedrals in Normandy, with new stained-glass windows depicting scenes from his life appearing in Sens, Chartres, Coutances and Angers. These windows seem to have been installed around the time that, back in Canterbury Cathedral, Becket’s body was being transferred from its original tomb in the crypt, up into a tailor-made shine in the Trinity Chapel. This happened in 1220, fifty years after Becket’s murder, and during the reign of Henry III. This king, too, clearly wanted to visibly and publicly identify himself with the cult of St Thomas. The ‘translation’ of the mortal remains of the saint to their new resting place, on 7 July 1220, was accompanied by a massive public festival; free wine was dished out at the gates of the city and a recurrent jubilee celebration was set to be held every fifty years on the anniversary of the translation.

The removal of Becket’s body from his tomb in the crypt provided a chance to see his physical remains and for pieces of him to be separated out. If the leproserie at Mont-aux-Malades really did have a genuine bone from St Thomas’s body, this is the point when it would have been taken.

The sepulchre was opened either the evening immediately before the translation took place or a few days previously – depending which account you read – in the presence of the then archbishop, Stephen Langton. The fourteenth-century Icelandic Thómas saga Erkibyskups (‘Saga of Archbishop Thomas’) adds a detail, saying that the body of Thomas crumbled to dust as it was extracted from its original tomb, and that his bones were transferred to a new coffin. The saga and other accounts describe a few bones being taken as relics to be distributed to other churches, suggesting that the soft tissue had all but disintegrated over that half-century, and all that was left at this point were skeletal remains.

On the morning of 7 July, the monks carried the coffin containing Becket’s bones up into the church, placing it into another casket covered in gold and encrusted with pearls and precious stones. And that casket was placed in a highly ornate shrine in the specially constructed Trinity Chapel, beyond the high altar. This shrine consisted of a platform, with steps up to it, an altar and a suspended wooden canopy which could be lowered with a pulley system over the casket. The magnificent shrine was designed to attract pilgrims, and it did its job, becoming the star attraction in Canterbury Cathedral, although pilgrims would also descend to the transept to see the exact spot where St Thomas’s blood and brains had been spilt. Pilgrims could also visit the Corona shrine, containing the fragment of the saint’s skull that had been detached during the murderous assault.

Almost three centuries later, the Dutch humanist philosopher and theologian, Erasmus, wrote about Canterbury Cathedral and the shrine of St Thomas in one of his Colloquies, entitled ‘A Pilgrimage for Religion’s Sake’. The Colloquies, or ‘conversations’, were designed as Latin primers but they also lightly satirised contemporary religious attitudes, practices and superstition. One colloquy takes place between two fictional characters, Ogygius and Menedemus. Ogygius, whose name carries connotations of gullibility but also travel, has been on a long pilgrimage to Compostela, Basle and Walsingham. He has returned home ‘full of superstition’ and festooned with scallop shells, lead and tin trinkets, straw necklaces, and a bracelet of snakes’ eggs to top it off. Menedemus, a more down-to-earth character, whose name means ‘stay at home’, has only gone as far as Canterbury – and that visit was clearly enough for him. The details appear to be based on Erasmus’s own visit, in around 1512, accompanied by John Colet, the dean of St Paul’s Cathedral. In the colloquy, Menedemus describes going on a tour of the cathedral, with a companion, during which they were exposed to an unsettling combination of glitzy wealth, macabre body parts and other relics that formed the centrepiece of Canterbury’s ‘St Thomas Experience’.

The guided tour started in the crypt:

‘There was first exhibited the perforated skull of the martyr; the forehead is left bare to be kissed, while the other parts are covered in silver… There also hang in the dark the hair shirts, the girdles and bandages… striking horror with their very appearance…’

Returning to the choir, up in the main church, Menedemus describes a display of more relics and impressively opulent treasures:

‘… the armaries were unlocked: it is wonderful to tell what a quantity of bones was there brought out, –sculls, jaw-bones, teeth, hands, fingers, entire arms; on all which we devoutly bestowed our kisses; and the exhibition seemed likely to last forever… We next viewed the altar and its ornaments, and then the articles which are kept under the altar, all most sumptuous; you would say that Midas and Croesus were beggars, if you saw that vast assemblage of gold and silver.’

Next on the tour was the Trinity Chapel:

‘… behind the high altar you ascend again, as into a new church. There, in a little chapel, is shown the whole figure of the excellent man, gilt, and adorned with many jewels.’

The rhetorical conversation then turns to a discussion about whether St Thomas might have preferred that such riches were used to ‘relieve… the wants of the poor’. Menedemus says that this suggestion, when voiced by his companion, seems to have angered the priest giving the tour. He dwells on the question: ‘But to what purpose are so many holy-water vessels, so many candlesticks, so many golden statues?’

Ogygius, though, tends to excuse such ‘extravagant piety’ and says that rulers who seize wealth from churches only lose it ‘in gaming or in war’. Menedemus goes back to describing his tour: ‘At this moment the [prior] came forward… He opened to us the shrine, in which what is left of the body of the holy man is said to rest.’

‘Did you see the bones?’ asks Ogygius.

Menedemus replies:

‘That is not permitted… [but] a wooden canopy covers the golden shrine; and when that is drawn up with ropes, inestimable treasures are opened to view… The least valuable portion was gold; every part glistened, shone, and sparkled with rare and very large jewels, some of them exceeding the size of a goose’s egg… The Prior with a white rod pointed out each jewel, telling its name in French, its value, and the name of its donor; for the principal of them were offerings sent by sovereign princes.’

Then they return to the crypt, where a shrine to the Virgin Mary is protected by an iron screen, prompting the question from Ogygius: ‘What was she afraid of?’

‘… Nothing, I imagine,’ says Menedemus, ‘except thieves. For I have never seen anything more burdened with riches.’

Finally, the tour ends with a visit to the sacristy, or vestry, where a black leather box is brought out; inside it were fragments of St Thomas’s clothing:

‘… torn fragments of linen; and most of them retain marks of dirt. With these, as they told us, the holy man used to wipe the perspiration from his face or neck, the runnings from his nose, or such other superfluities, from which the human frame is not free…’

The prior offers one of these fragments to Menedemus’s companion as a souvenir, but he refuses it in disgust. After a cup of wine, the tour of the cathedral is over. But then Menedemus describes what happens when you leave Canterbury, as the road narrows: ‘On the left hand of this road is a hospital of a few old men, one of whom runs out as soon as they perceive any horsemen approaching; he sprinkles his holy water, and presently offers the upper part of a shoe… [saying] it was the shoe of St Thomas.’

The travellers are meant to kiss the shoe, and pay for the privilege. Ogygius steps up to defend the cult of St Thomas here, saying that in death the saint has perhaps been even more useful than in life; that he’s helped to fund the magnificent cathedral, increase deference to priests, and even support, with this fragment of his shoe, ‘this little community of poor men’.

The Colloquies of Erasmus are entertaining to read, and poke fun at religious myths and superstitions while raising some serious concerns about the wealth being amassed by the Church and serving as an argument for reform. Erasmus was right on the money here, in every sense. The Colloquies also preserve a precious record of riches, shrines and relics that just a few decades later would be dispersed and destroyed. There are many other accounts that, while they may not concur on precise details, are all in agreement on one thing: the tomb was incredibly opulent. A Venetian ambassador visiting in 1500 made this report:

… the magnificence of the tomb of St Thomas the martyr, Archbishop of Canterbury… surpasses all belief. This, notwithstanding its great size, is entirely covered over with plates of pure gold; but the gold is scarcely visible from the variety of precious stones with which it is studded, such as sapphires, diamonds, rubies, balas-rubies and emeralds; and on every side that the eye turns, something more beautiful appears. And these natural beauties are enhanced by human skill, for the gold is carved and engraved in beautiful designs, both large and small, and agates, jaspers, and cornelians set in relief, some of the cameos being of such a size, that I do not dare to mention it: but every thing is left far behind by a ruby, not larger than a man’s thumb-nail, which is set to the right of the altar. The church is rather dark, and particularly so where the shrine is placed, and when we went to see it the sun was nearly gone down, and the weather was cloudy; yet I saw the ruby as well as if I had it in my hand; they say it was the gift of a king of France.

Two of the stained-glass windows in the Trinity Chapel depict the shrine, both of them showing a golden (or at least, yellow) gable-roofed feretory, or reliquary, standing up high on slender columns joined by arches. But these panels are thought to date from around 1212–16, before the translation happened, and so may be imaginings of what the shrine might look like, rather than faithful representations. A painted altarpiece in Germany depicts a more elaborate shrine at Canterbury, with a tiny angel pointing out the large ruby that was bequeathed by Louis VII. But the details of the tracery supporting the shrine look more German than English in style, so perhaps, again, this is just an idea of the shrine.

Art historian Sarah Blick tracked down another – very tiny and overlooked – visual record of the splendid shrine, in the form of images on pilgrim badges. Although around just 7cm tall, moulded, and clearly symbolic rather than realistic depictions of subjects, these souvenirs contain a surprising level of detail – and agreement. While other details vary, they all show the gabled feretory, spotted with jewels, and, in the centre, the great ruby gifted by the French king, being pointed out by an angel with a wand (rather like the prior with his white rod in Erasmus’s description). They also show the shrine held metres aloft on an ornate base with columns and pointed arches, looking like a miniature church, helpfully removing the priceless jewels from the easy reach of would-be thieves. The style of the shrine shown on pilgrim badges also suggests that the original shrine was refurbished around the turn of the fourteenth century, making it even more ornate and resplendent.

Nothing at all of that extraordinary, glittering shrine exists today. The only trace of it is the scuffed tiles on the floor where it once stood.

And that’s because Henry VIII tried very hard to wipe out the cult of St Thomas, destroying the shrine, and – perhaps – the remains of Thomas Becket himself.

The historian Anne Duggan has described Thomas Becket’s influence on religious attitudes through the Middle Ages as persisting like a ghost. And by the time the sixteenth century rolled around, Henry VIII was determined to lay that spectre to rest.

Henry’s attack on the cult of Becket was part of the wider English Reformation, which saw the Church in England distancing itself from the Roman Catholic Church. Henry VIII was aided politically by the Protestant movement sweeping across Europe, and he would eventually seize the opportunity to declare himself supreme head of the Church of England, taking legal and fiscal control over church affairs in the country. As the Reformation took hold, certain religious superstitions and rituals, such as praying to saints, were rooted out and many religious holidays were annulled. The veneration of saints’ bodies, bones and images became anathema. And the most famous relics, the most famous shrine, the most famous saint in England, would now become a target.

This was an extraordinarily iconoclastic reaction to the memory of a man whose shrine Henry VIII himself had visited in 1520 with the Holy Roman Emperor, Charles V. And Henry had continued the royal tradition of granting gifts to the shrine of St Thomas after that. But the Reformation movement was gathering momentum, and Becket’s shrine symbolised not only the alternative power-system in England, but the flow of English money out of the country: the Church had been demanding half of the profit from Becket’s shrine to fund the re-build of St Peter’s in Rome.

Initial moves to create some distance from the Church in Rome were subtle. In 1532, a somewhat troublesome archbishop of Canterbury died (naturally, this time) and Henry VIII installed theologian and ambassador Thomas Cranmer in the post. Cranmer began to abolish holy days, and seemed to snub the cult of Becket by refusing to fast on the eve of a feast day associated with St Thomas. But by 1534, Henry VIII had had it with the papacy and declared himself the supreme head of the Church of England. Two years later, he began the dissolution of the monasteries, seizing those estates for the Crown. St Thomas, for the second time, was a marked man. In 1536, the feast of the translation of his remains was abolished, and in 1537, the scene showing his martyrdom was removed from the seal of Canterbury. Meanwhile, Royal Commissioners for the Destruction of Shrines had begun a state-sponsored pillaging spree. Many figurines of saints were brought to Chelsea to be publicly burned.

Becket had become a potent symbol of the power of the Church, of the pope, of Rome itself, and Henry VIII wanted to stamp all of that out. In 1538, a set of royal injunctions called for the avoidance of ‘works devised by men’s phantasies… as in wandering to pilgrimages, offering of money, candles, or tapers to images or relics, or kissing or licking the same, saying over a number of beads… as things tending to idolatry and superstition, which of all other offences God Almighty doth most detest and abhor’. And Becket got a special mention in these injunctions: the ‘Commemoration of Thomas Becket, sometime Archbishop of Canterbury… shall be omitted’.

In early September 1538, the elaborate shrine was pulled down, the treasures broken up and carried off in twenty-six carts to London, and whatever remained of Becket’s body in the inner casket… disappeared.

In early 1888, an archaeological investigation in Canterbury Cathedral, aimed at exploring whether there were any traces of architecture associated with Becket’s original tomb, uncovered two graves. They lay in the gaps between the three central marble pillars in the crypt. The eastern grave was empty of a coffin or bones, and full of rubble. The western grave contained a stone coffin. The lid was levered off, exposing a heap of bones, mixed with earth, lying at one end of the coffin. There was a carved stone ‘pillow’ for the head, and no other objects with the bones.

The skeleton was removed from the coffin, placed in a box, and taken to the house of the cathedral architect George Austin. A couple of days later a surgeon, William Pugin Thornton, arrived to examine the bones. He laid out the skeleton and noted that there were quite a few bones missing: four vertebrae, parts of ribs, the right patella and part of the upper jaw. There were several teeth missing too – their sockets were present so they had fallen out post mortem. Thornton reckoned the skeleton had belonged to an adult man, around 6ft 2in in stature, who had been around fifty when he died. He published a booklet about the bones in 1901, containing photographs of the skeleton laid out on a board, as well as separate images of the skull. This had been in a very fragmentary state, and looked as though it had been smashed rather than fallen apart. Thornton had reconstructed it in a slightly strange way, around a clay mould. He was a fan of the (now discredited) ‘science’ of phrenology, and starts his assessment of the skull by saying: ‘That its bones had formed the head of a man of large intellect there can be no doubt. The circumference of the skull, when the bones were fitted on the mould… was 22 ¾ inches… [showing] that the head of the man was much above ordinary size.’

It should be said at this point that skull size varies with body size: you’d expect a large man to have a large skull. And human intelligence does not correlate with skull size.

Although fragmented, the skull looks complete. And that’s a problem – as Thornton put it, it ‘militates against the statement that the crown of Becket’s head was cut off’ (and, we may add, had its own chapel and shrine). But then Thornton rows back, remarking that the chronicles disagree with each other on the attack and the precise nature of the wounds inflicted. He points to a six-inch-long injury on the left side of the skull from the crypt, which he says ‘looks as if it could only have been made by a heavy sharp cutting instrument, such as a two-handed sword’. And he then links this injury to the third strike to Becket’s head, by which time the archbishop had fallen to the floor – the strike carried out by Richard le Breton, breaking his sword on the stone floor of the transept.

So, could this skull, this skeleton, possibly have been those of Becket? What if the monks – who had been given three months’ notice about the imminent demolition of the shrine – had removed the saint’s bones and reburied them, down in the crypt? They could have substituted some other bones to throw Henry VIII’s Commissioners off the scent, Thornton suggests.

Thornton concluded there were good reasons to believe that these bones from the crypt were those of Becket himself: eight good reasons, indeed. First, he thought the position of the burial – close to the original interment of Becket’s body (before the translation) – suggested a connection. Second, the arrangement of the bones in the coffin pointed to re-burial of skeletal remains, rather than a primary interment of a corpse. Third, the part of the crypt where the grave had been discovered had been walled off, and used as cellars, from 1546 to 1830: no burial would have taken place there during that time, at least. Fourth, the bones were of a ‘great age’, Thornton claimed, giving as proof of this the slightly unscientific fact that ‘after rinsing them in water for about a minute, to remove the dust… they sucked up so much that the water continued draining away for three days’. Fifth, the bones had belonged to a tall man, and ‘Becket was said to have stood above his fellow men’. Sixth, the pronounced muscle attachments on the bones meant that this man had been ‘unusually powerful’ and Becket, while Chancellor, had been ‘a warrior and a sportsman, noted for his strength’. Seventh, the bones and (five) teeth indicated an age of around fifty years at death; Becket was fifty-two when he was murdered; other potential saints suggested to have been buried in the crypt were in their sixties and seventies when they died. Eighth, and finally, the phrenologist–surgeon mentioned once again the skull’s ‘great size’, indicating it had contained the brain of a man ‘of more than ordinary intelligence’.

I agree with the logic behind most of these assertions, while the fourth and seventh statements are a little flaky and the eighth is sheer nonsense. But what the other ones add up to is, unfortunately, a whole lot of circumstantial evidence – and nothing definite. We’re left thinking: ‘Well, these could be Becket’s bones, but on the other hand, they could be those of some other tall, fiftyish-year-old man who died centuries ago.’

The completeness of the skull is a real problem for Thornton’s hypothesis. The weapon injuries he identifies are not convincing in the photographs, and the uppermost part of the skull is present, if fragmented. The chronicles, while disagreeing on some details, consistently describe the top of Becket’s skull, the corona, being chopped right off. But Thornton finds some documentary support for his counterclaim – that Becket’s skull was not cleaved in this way – from a document written by a court clerk in 1539, the year after the shrine was destroyed. This document is entitled ‘A Declaration of Faith, and a Justification of the Proceedings of King Henry VIII, in Matters of Religion’. It refers specifically to Becket, exonerating Henry II and squarely blaming the archbishop for making himself unpopular, by falling out with the bishop of York. The Declaration claims that Becket, ‘by the strife thereof procured forwardly his own death, which they untruly call martyrdome’ and that he was not assassinated but killed in a scuffle: ‘in the throng, Beckett was slayne’. There follows a character assassination of Becket, who ‘never did act in his life sufficient to prove any holliness, but came to the king’s chancellorship by mony, was a great warriour, a brenner [burner] of townes, a croacher [thief] of benefices, a hunter and a hawker, proud and seditious’. It also says that Becket became archbishop ‘by corruption and unlawful means’. The Declaration records that shrines, revered corpses and reliquaries are to be generally destroyed or taken away, and it then refers specifically to the shrine of St Thomas – and what was found inside it: ‘his head almost [w]hole was found with the rest of the bones’. This doesn’t sound like the description of a skull that has had its top cut off.

The Declaration also mentions that there was ‘a great skull of an other head’ in the cathedral, but that this skull was much larger than the piece that was missing from the cranium inside the shrine. And, indeed, it was presumably much more of a cranium than just part of the cranial vault; otherwise, why would it be described as ‘a great skull’? Perhaps this was the ‘perforated skull’ that Erasmus had described, which was presented in the crypt as the skull of the martyr, covered in silver but with the frontal bone bare? Whether this ‘great skull’ described in the Declaration was that silver-embellished relic or not, it seems very unlikely that it was actually Becket’s skull, as there was another cranium with the rest of his bones, inside the shrine. And the one in the shrine was described as ‘almost [w]hole’. There was clearly part of it missing, though which part we’re not told. It’s all very frustrating.

After three days, Thornton completed his examination of the skeleton. But it would be sixteen days in total before the bones were returned to the crypt. In the meantime, news had got out, and a man from Margate brought his son, who was losing his eyesight, to seek help from the relics. The boy knelt down and brought his face close to the eye sockets of the reconstructed skull. Whether or not he regained his eyesight is not recorded, but the medieval superstition that Henry VIII had sought to eradicate was evidently still alive and well.

On 10 February 1888, the skeleton, including the skull on its clay mould, was replaced in the crypt, in a new oak coffin designed to fit inside the stone casket. A glass bottle containing a newspaper and a report of the investigation was placed beside the skull. Then an oak lid was screwed onto the coffin, a new stone lid was placed on the outer casket, earth shovelled in, and finally the stone slab was cemented into the floor.

Thornton thought it most likely that he had indeed been examining the bones of Becket himself. The Reverend Charles Francis Routledge, an honorary canon at Canterbury, who was also present at the discovery and opening of the stone coffin in 1888, concurred. When the story got into the newspapers, there was even less room for doubt. The Morning Post reported that ‘the remains… have practically proved to be those of Thomas à Becket’. The Times announced that ‘the remains of Thomas à Becket have been discovered’.

And yet there was no conclusive proof. Plenty of people raised doubts about the identity of the skeleton, pointing to the inconsistency of the cranial injuries and to documentary evidence suggesting that Becket’s bones had either been moved away from the cathedral or completely destroyed in the sixteenth century. Routledge published a report in 1895, attempting to tackle these doubts. The Declaration certainly suggested that the intent was to move Becket’s bones, not destroy them. This seems to have been the standard practice in other cathedrals, where shrines were destroyed but relics were reinterred close to their original position.

On the other hand, there are other sources that suggest Becket’s bones were burned at the time of the Reformation. In 1538, Pope Paul III lamented the ‘new cruelty and impiety of the English King, who had ordered the body of the Blessed Thomas of Canterbury to be burned, and the ashes to be scattered and given to the wind’. And a chronicle of the same year, written by Secretary of State Thomas Wriothesley, recorded that, ‘the bones of S Thomas of Canterbury were brent [burned] in the same church by my Lord Cromwell’. A later document, written in the mid-sixteenth century by an archdeacon of Canterbury, also recorded that the bones had been burned.

So some contemporary sources say the bones were burned; others that they were buried. Amongst the texts that refer to burial is that 1539 Declaration of Faith – which adds some more detail on what happened to Becket’s remains: ‘… it was arrested that his shrynes and bones should be taken away, and bestowed in suche place as the same shuld cause no superstition afterwards’, suggesting that the bones were moved but not destroyed. In the original manuscript, as Routledge mentioned, there followed this crossed-out phrase: ‘… as [the bones are] indede amongst others of that sorte conveyed and buried in a noble toure [tower]’. Was the phrase redacted because it was an error, or because – as Routledge supposed – it was thought imprudent to announce the new resting place of Becket’s bones? If it wasn’t an error, where was this mysterious ‘noble tower’? There are no clues. Routledge suggests it could have been the Corona, though this seems like an odd description of that chapel, and anyway, no bones had been found in that part of the cathedral. He goes on to write, ‘I do not think it is any great straining of the words to suppose that the site indicated is… the Crypt… immediately beneath the Trinity Chapel.’ He’s desperate to believe the bones he studied are those of Becket. But the description of the crypt as a ‘noble tower’ seems just a little too, well, cryptic.

The 1888 investigation of the grave in the crypt left a lot of questions hanging. The ghost of Becket was still haunting Canterbury. Could the bones in the crypt have been Becket’s? Yes, if they were moved there by monks attempting to save them from Henry VIII’s Commissioners – but no record of such a reverse translation existed. Yes, if they were removed from the shrine and placed in the crypt by the Commissioners themselves – but again, no specific record of such a reburial existed. No, if the bones were burned as Pope Paul III and Thomas Wriothesley claimed. And no, if the bones were not burned but were buried in another place, away from Canterbury, as the redacted phrase in the Declaration suggested. There’s so much inconsistency and vagueness in these reports from the time of the Reformation that it was possible to pull out evidence in favour of each of these hypotheses, but it was impossible to reject any of them.

After that investigation, there was a genuine historical possibility that the reburied human remains in the crypt could have been those of Becket. But what about the bones themselves? We have to accept Thornton’s determination of the bones as male – there’s not enough detail in the photographs to make an assessment now. Thornton excluded the possibility of the skull belonging to an elderly man, but it’s very difficult to age older individuals with any degree of accuracy. However, it’s Thornton’s description of the cranial injuries that was most problematic. The fact that the skull from the crypt didn’t have a missing crown, and that the eyewitness accounts of Becket’s murder seemed very clear on this injury, seems like a final nail in the coffin. One contemporary account provided this gory detail: by the third sword-strike, ‘corona capitis amputata est’ – ‘the crown of the head was amputated’; and by the fourth, ‘the crown was thrown forward, hanging on the forehead, adhering by the skin’.

Routledge examined these sources, and expressed doubt that a skull could have been sliced through by a sword. I have no such doubt. But Routledge also suggested that the correct interpretation of ‘corona’ was in fact the shaven scalp, or tonsure, of a medieval monk or cleric: it was this soft tissue that had been cut away, he posited, not the top of the skull. But then, what about those graphic descriptions of Hugh of Horsea scraping out the brains from the skull? That wouldn’t have been possible if it was only the scalp that had been cut off. Routledge had an answer for that: he suggested that the terrified monks, writing their accounts of the murder, may have been guilty of exaggeration. And he concluded: ‘The bones discovered in 1888 are almost certainly the remains of some distinguished saint, and it appears to me quite a probable conjecture that they are the veritable relics of St Thomas of Canterbury.’ He ended his report with the hope that the dean of Canterbury would soon erect a suitable memorial over the grave – a new shrine for St Thomas. The dean and chapter were much more reserved, and the cathedral’s Investigating Committee recorded an uncertain verdict: ‘there is no distinct evidence to shew to whom they belong’.

There were so many questions – questions that cannot be answered by looking at the photographs of the bones. Why was the skull smashed into fragments? Skulls can break into pieces when bodies are buried in the ground, with the weight of earth on them. But if Becket’s body and then his bones had always been contained in a stone coffin, why wasn’t the skull more intact? Was there really evidence of sharp force trauma on the left side of the skull? What was the nature of the ‘earth’ that was found in the stone coffin – and might its presence suggest a burial somewhere outside the cathedral before the bones were reburied in the crypt?

The identity of the bones in the crypt continued to be debated, with public opinion veering towards acceptance that the bones were Becket’s. In 1949, records show, the dean and chapter of Canterbury Cathedral were planning to create some sort of memorial or shrine, just as Routledge had hoped might happen. And so they’d reached the point where they really needed to be sure about the identity of the bones; the slightly flaky reports from 1888 simply weren’t good enough.

There was only one way to lay the matter to rest, and that was to re-open the coffin.

On the evening of 18 July 1949, two workmen began attacking the cement around the huge slab that formed the lid of the stone coffin. They removed the slab and could then see that the lid of the inner, wooden coffin had split and collapsed in. The bones were there inside, the skull still on its plaster mould. The glass bottle with the record from 1888 was smashed, its contents illegible. Everything was damp.

The skeleton was examined again by Alexander Cave – not just a surgeon, but also professor of anatomy at St Bartholomew’s Hospital in London. He kept hold of the bones for two years and submitted his report to the dean and chapter in 1951. It was quoted in a short article published around the time, but when researchers tried to track down the full report in the 1990s, it had mysteriously disappeared from the cathedral archives. They turned to Cave himself, then ninety-three years old – and fortunately, he’d kept a copy of it.

The bones, when examined in 1949–51, had decayed considerably since 1888, being exposed to moisture and fungal spores. The nasal bones, base of the skull, and parts of the pelvis and spine, had virtually disintegrated. What was left was washed and carefully reconstructed. The cranium, Cave concluded, was definitely male. The cranial sutures had largely closed, and this was interpreted as indicating an age of at least sixty years at death. (We no longer use cranial suture for establishing age at death as it varies so much between individuals.) Cave saw that the upper part of the vault had been separated from the rest of the skull on the nineteenth-century clay mould, forming the impression of a breach. The clay showing in the gap beneath this piece of skull seemed to have been painted red, to emphasise the ‘wound’. But just as I’d suspected when looking at the photographs from 1888, the separation between the fragments on the left side of the skull was artificially created. There was no real gap. And the edges of the fragments were broken in a rough, jagged way, showing that these breaks had happened post mortem. There was no sign of a blade wound; in fact, there were no signs of sharp force trauma anywhere on the skull. Cave wrote: ‘All the cracks, breaks, fractures and erosions are most emphatically of a post-mortem nature.’

Whether or not the vault of Becket’s skull had been sliced right through when he was attacked, all sources attest to the violent injuries on his head – and there were no traces of sharp trauma on what remained of this skull from the crypt. Cave also remarked on the presence of several animal bones – the tooth and foot bone from a pig, vertebral fragments from a sheep or goat, foot bones from a small ox – found alongside the human bones in the coffin. These extraneous bones, and the earth in the coffin, suggest that the human skeleton was exhumed – fairly carelessly – from an earthen grave before ending up in that stone coffin in the crypt. There’s no record of Becket’s body ever being buried anywhere outside the cathedral.

In 1951, the remains were all reburied in the floor of the crypt. All, that is, except for one tooth – which had been sent away to Sweden for dating and was then returned, seemingly undated – which probably still lies in an envelope in the cathedral archives. That tooth could be subjected to further analysis – to radiocarbon dating, for instance, which could exclude the possibility of these being Becket’s bones if they turn out to be from another century. But if the date range (and it is always a range, with radiocarbon dating) accommodated 1170, this still wouldn’t be positive proof of identity. Ancient DNA could provide a robust answer, as was performed so elegantly by Turi King in the analysis of Richard III’s skeleton, found under a car park in Leicester. But this would depend on DNA having survived in reasonable condition in that tooth, and on matching the ancient DNA from the bones with that of living relatives of Becket, if any could be reliably traced.

But in the end, such further analyses are not really needed. There’s no evidence of the wounds to the head that are so well attested in the chronicles. And then there’s also the evidence suggesting these remains spent some time in an earthen grave – something that was never described for Becket’s body – before being relocated to the crypt.

Whoever those bones once belonged to, it seems extremely unlikely that it was Thomas Becket.

Becket’s bones may have been carried off and buried in an unmarked grave; they may have been burned. It’s likely we’ll never know; they have been effectively erased from the archaeological record. The ornate and ostentatious shrine, with all its gold and prodigiously sized jewels, was also erased – dismantled and broken up. And in 1546, eight years after the destruction of the shrine in the Trinity Chapel, the part of the crypt below, where Becket had originally been buried, was walled off. But one thing’s for sure: Henry VIII’s attempt to obliterate the relics and shrine of the sainted Thomas from view and memory – to end the superstition, pilgrimage and popishness – did not work.

Becket’s body had already been partly broken up, with bones and, apparently, drops of his blood ending up in various reliquaries in Europe, but the destruction or relocation of the majority of his bones was carried out with a clear intent to squash the cult of Becket out of existence. Henry VIII followed up with a proclamation in November 1538, when he declared that Becket ‘shall no longer be named a saint’, that he was ‘really a rebel who fled the realm to France’, and that, ‘His pictures throughout the realm are to be plucked down and his festivals shall no longer be kept, and the services in his name shall be razed out of all books.’ This was a kindness, Henry VIII insisted, to ensure his ‘subjects shall no longer be blindly led and abused to commit idolatry’. His subjects responded, painting over murals of the martyrdom of Becket, erasing names, and deftly switching dedications from St Thomas Becket to St Thomas the Apostle. On what had been the feast day of St Thomas, religious primers would be amended to simply note ‘Becket traitor’. The playwright John Bale lamented the corruption wrought by Rome on the pure, English Church. And he made a distinction between legitimate martyrs, who had died in the name of Christ, and illegitimate ones, like Becket, who had died for the pope.

Some, particularly Protestants, approved of the shrine’s destruction, but others wrote of the ungodliness of Henry, and the sacrilege and barbarity of the act. In December 1538, Henry VIII was excommunicated by the pope, who specifically mentioned the destruction of Becket’s shrine as one of the many reasons for booting the king out of Catholic Christendom.

When Henry’s daughter, Mary, came to the throne, bringing with her the return of Roman Catholicism to England, Becket’s liturgy was resurrected – but his shrine couldn’t be restored. The subsequent reign of her sister Elizabeth I saw another religious swing away from Catholicism and another attempt at the final erasure of the cult of Becket – though he would remain a saint for Catholics. His light faded but was not entirely extinguished. Towards the end of the twentieth century, the Anglican Church seemed to become more accepting of the sainted archbishop. In 1970, a Catholic mass was held in Canterbury Cathedral to mark the eighth centenary of Becket’s death. And then, in 1982, something really astonishing happened, something that would have set Henry VIII spinning in his grave: Robert Runcie, Archbishop of Canterbury, and Pope John Paul II knelt and prayed together in the transept where Becket had been murdered. Becket’s sainthood and piety were reaffirmed. His argumentative and rebellious nature – and any questions of personal ambition or treachery – were forgotten. By the turn of the twenty-first century, theologians of various stripes seemed to be embracing Thomas Becket as a saint – uncritically, unreservedly. But what more should we expect from hagiographers? The political complexity, the true character, and most significantly the flaws of heroes, are deliberately shed in such myth-making. There’s one thing we can be sure of, though: Becket may have been destined for sainthood from the moment he was ordained as archbishop – this being the standard post mortem career path for those in that lofty post – but it was that brutal murder, the blood and brains spilt on the stones of the cathedral, that raised him to the apogee of sainthood, drawing thousands of pilgrims to Canterbury, driving and sustaining the myth, and eventually bringing an Anglican archbishop to kneel at the site of his martyrdom.

When I visited Canterbury in search of this story, I met someone who had just uncovered an incredible trace of the very earliest pilgrims to Becket’s shrine. Rachel Koopmans was a visiting researcher from Canada and had been studying the Trinity Chapel windows for years, carefully reconstructing the narratives told in coloured glass. Amongst the miracles depicted were the curing of ‘mad Henry’ from Fordwich, the recovery of Etheldreda of Canterbury from fever and sight returning to a blind woman from Rochester. Rachel’s work was somewhat complicated by the fact that the Victorians had done a very thorough job of renovating the windows, patching and tidying them up. The round panels had been removed and re-leaded, with irreparably broken pieces of glass replaced. Some of the original coloured-glass panels had been lost before this round of renovation and replaced with plain glass. In the Victorian renovations, these plain panels were swapped for brand-new copies of other medieval panels, cobbled together using fragments of old and new glass. While the restored windows look great from a distance, closer inspection reveals an abstract assemblage of painted details, blank faces and nonsense lettering. But in many cases it was hard to tell old and new panels apart – some of the faux-medieval panels looked so good, they’d even fooled the experts – but Rachel knew what she was looking for. The focus of the Victorian restorers seems to have been the overall artistic impression, overlooking the serialised stories told by sequences of panels. When repaired original panels were returned to the windows, they weren’t necessarily in the right order, playing havoc with the miracle narratives. Luckily, there were written descriptions of the stories that Rachel could draw on to work out the original placement of the panels.

In 2018, Rachel grasped a precious opportunity when some of the windows were once again being removed for restoration. The work was being carried out by the cathedral’s team of expert conservators, led by Leonie Seliger.

Rachel had been poring through old documents describing the Trinity Chapel glass, including the first guidebook describing the windows, Emily Williams’s Notes on the Painted Glass of Canterbury Cathedral, published in 1897. Amongst Williams’s notes, a sketch of one particular window caught Rachel’s eye. The drawing included one of the panels that were thought to be entirely nineteenth-century fabrications: that trick of old glass cobbled together with new. But in the circle representing this specific roundel in Williams’s sketch, she had clearly written ‘old’. Rachel dug out the earliest photograph she could find of that window – one of the earliest photographs of the cathedral, taken in 1861, decades before the glass restoration was carried out. She could see the stained-glass panel in place, and the photograph was clear enough to make out the figure of a man on horseback. It looked like the same panel that was currently in that window. Rachel showed the evidence to Leonie, who agreed that they should take a closer look.

The panel was removed from the window and brought down to the conservation studio, where it could be studied more closely. When I visited, Leonie had brought the panel out, and there it was, glowing with gem-like colours on the lightbox. I looked carefully at the beautiful picture in stained and painted glass. There was a pale horse in the centre, and three more horses almost hidden behind it, their heads and legs peeking out, in green, yellow and brown. One man in front of the horses, on the right side of the image, seemed to be leading them. There were four figures mounted on the horses, and three or four more following behind on foot. But was I looking at clever Victorian fakery or something genuinely medieval? Fortunately, Leonie and Rachel knew what to look for. The image was broken up like crazy paving by the leading, with single blocks of colour broken into many sections. I must admit I’d always thought that this was just the style of medieval stained glass, but in fact this effect was a product of broken medieval glass being mended. So this suggested the glass really was old – but then it turns out you can’t entirely rely on this clue, as the Victorians often copied that appearance of antiquity, creating faux-medieval panels by adding unnecessary bars of leading across blocks of colour. The glass itself contained the vital clue: viewed through a magnifying glass, and scrutinised even more closely under a microscope, minute imperfections spoke of its antiquity, confirming what the 1861 photograph and Emily Williams’s sketch had suggested. This panel was not a Victorian replacement; it was original medieval glass, dating to between 1182 and 1186, when the finishing touches were being put to the Trinity Chapel.

Leonie told me to look carefully at the broken-up strip of yellow glass beneath the green, grassy hummocks that the human figures and horses were walking over. She shone a torch across the glass, the raking light allowing me to pick out shapes: faint letters. They spelled out ‘PEREGRINI:ST’ – ‘Peregrini Sancti’, the Pilgrims of the Saint. This was astonishing. The glass was installed around fifteen years after Becket’s death, when Henry II was still on the throne. With the shrine destroyed and the relics lost, this was one of the last surviving physical links to the early cult of Becket: the earliest depiction anywhere of pilgrims coming to Canterbury, to the tomb of St Thomas.

Almost 500 years since Henry VIII destroyed the shrine of St Thomas, people still embark on pilgrimages to Canterbury. The twenty-first century even saw the launch of a newly invented pilgrim route, the ‘Old Way’, purporting to resurrect a well-trodden medieval path, cobbled together like the Victorian stained glass, creating an impression of antiquity. In an article, one modern pilgrim described – in very New-Age-sounding terms – how singing songs along the route, and especially in the cathedral itself, served to ‘activate spaces’, with ‘music, like the Becket water collected by pilgrims… perceived as having the capacity to heal’. The creators of the Old Way route map encourage ‘ritual praxis’ along the way, which could include drinking holy water from wells, dunking yourself in rivers, and the laying of hands and foreheads on the stones of ruined abbeys. It all sounds like just the sort of superstition that would have appalled Henry VIII. A phrase from that modern pilgrim’s article drives home just how impossible it was for Henry VIII to exorcise the saint’s influence, describing ‘the centrality of Becket [at Canterbury] even in the absence of his remains’.

As for earlier generations of pilgrims, Chaucer gave us the most famous glimpse of their varied nature in his Canterbury Tales, penned some two centuries after the glaziers created that image of the first Peregrini Sancti, and it seems not much has changed: one modern group of pilgrims comprised ‘a man who wanted to re-frame negative experiences he had at sites that would be visited, a woman who was there as part of her shamanic training, a raver who had been up clubbing the previous night and had stumbled upon the group, a banker who wanted to reconnect with nature, and an American cyclist and university administrator with a penchant for history’. And of course, many modern ‘pilgrims’ are not seeking to connect spiritually with a place or a saint, but more simply with history and heritage.

And amongst them, there was I, a confirmed atheist and humanist, placing that finial on the lofty tower of Canterbury, descending to the transept to look at the spot where the martyr’s head was cleft, contemplating the creation and destruction of the magnificent shrine, gazing at that rediscovered medieval stained glass, and leaving the cathedral with a small pewter badge, of Becket himself.

I was just another pilgrim, in search of an ancient story.

4. MYSTERY AT A PRIORY

When Henry VIII swept away the holdings of the Roman Church in England, abbeys, priories and friaries were ransacked, monks and nuns turned out, buildings were pulled down and treasures seized by the Crown. Cathedrals like Canterbury survived, and there the monks could even stay on as clergy under the new regime. But in most places, the Dissolution of the Monasteries was much more destructive.

The remains of many once-magnificent ecclesiastical buildings have effectively disappeared from our modern landscape, reduced to foundations and built over, and over again, in our towns and cities. But some still stand tall, as romantic ruins, often with adjuvant museums drawing in modern pilgrims – tourists seeking a heritage-based day out, or artists in search of the sublime. From Strata Florida in West Wales, to Tintern in the Wye Valley and Fountains Abbey in Yorkshire, these relics of medieval Christianity and the power of Rome litter our countryside. Some were virtually forgotten for centuries, or just formed a convenient source of dressed stone for local communities. Others became transformed into secular stately homes, and archaeologists would later turn their attention to uncovering their medieval origins.

The abbey of St Mary at Norton, near Runcorn in northern Cheshire, is one of these almost-lost-and-found abbeys. Today, you can see the ground floor of the medieval abbot’s lodgings, topped with another, barn-like, modern storey in cedar and glass. And the foundations of the abbey church itself and the cloisters are laid out alongside – only the much-reduced skeletons of the buildings are visible, as a series of low walls interrupting the immaculate turf.

The foundations go on into the woods to the east of the green lawns, and archaeologists have been uncovering more traces of them in the last few years. I visited in the summer of 2022 and saw the new trenches where the remains of the infirmary hall were laid bare. But it wasn’t really the new excavations that intrigued me the most – it was the new scientific investigation into the human remains from the site. Amongst the ruins of the abbey church, like rocky outcrops in the grass, there are numerous head-niche stone coffins. They stand exposed and empty, the skeletal remains of their occupants having been long since removed.

Some of those skeletons are on display in the Norton Priory Museum, and their bones are extraordinary: thickened, overgrown, heavy. I’d come across an earlier strand of this story, at least a decade ago, when scientists were seeking to explore the reason for a preponderance of a particular bone disease amongst these medieval skeletons. But once again, it was new DNA analysis that had moved the story on and uncovered threads connecting this disease in the Middle Ages with its modern-day manifestations. The priory contained secrets: echoes of its medieval magnificence, its destruction in the Dissolution, and the traces of this mysterious bone disease in its tombs.

The twelfth century saw an extraordinary land-grab by the Church in England, entirely sponsored by the Norman ruling class. Sometimes old Anglo-Saxon religious estates were refounded; sometimes entirely new institutions were created. These had to be economically viable, while also providing local preachers – inbuilt PR for the new religious estate and its overarching brand, the Church. The new institution would depend on the local economy and would have to be seen as enhancing that, as well as providing cultural and spiritual sustenance to locals. (Like the National Trust, with religious strings attached.)

Local nobles could secure themselves a bevy of monks to pray for their souls in the afterlife – a post mortem pension arrangement – by granting land to these new endowments. And don’t forget, these lands had only recently come into the possession of their Norman landowners. Now, these ‘new men’, granted swathes of England after the Norman Conquest, could hope to more firmly establish themselves using the power of the Church. (By this time, it was a centuries-old trick: the rulers and landowners derived and displayed their power and legitimacy by allying themselves with the Church in Rome and its ministries.)

It’s thought that there was already an Anglo-Saxon church in the old fort, or burh, at Runcorn, on the south bank of the Mersey, and that this church formed the ecclesiastical centre of an endowment granted to Augustinian canons by the local Norman baron of Halton, William Fitz Nigel, in 1115. At least, this is what the name of the Augustinian priory at Runcorn suggests: it was called St Bertelin, a French-sounding corruption of the Anglo-Saxon name Beorhthelm. This Beorhthelm (or Bertram) was an eighth-century Mercian prince and popular Christian evangelist, who’s still the patron saint of Stafford, which he is said to have founded.

The Augustinians, an order that had only recently arrived in England, were proving themselves very effective at taking over old Anglo-Saxon churches and estates, and bringing them under the control of bishops. Less than twenty years later, the canons from Runcorn relocated to a new site, just over 2 miles to the east, at Norton. The reason for the move is somewhat obscure, but the new foundation gave the canons an opportunity to ditch the appellation of the lesser-known Anglo-Saxon prince-turned-saint. Instead, they went very mainstream with their new priory at Norton, plumping for the ever-popular St Mary as their patron (or matron).

The relocation seems to have paid dividends, although the Black Death, floods and chronic mismanagement would then take their toll. But by the end of the fourteenth century, things were looking up again, and with the help of the local Dutton family, the foundation had acquired abbey status – an unusual upgrade for an Augustinian priory. (Despite its elevated status, the name ‘Norton Priory’ has stubbornly stuck.) But then its fortunes turned again: the abbey shrank over the fifteenth century – sixteen canons were recorded in 1401, but only nine by 1496. Just seven were left in 1524, and at this time the abbey seems to have descended into physical and spiritual chaos. The chapter house badly needed repairs, part of the abbey had burned down, and meanwhile the abbot and prior were being accused of profligacy and debauchery. Come the first wave of the Dissolution, in 1536, and the canons were kicked out. The proceedings were led by the local Royal Commissioner, Sir Piers Dutton – from the very family that had bankrolled the priory for centuries. The financial irregularities at the monastery had developed into a very personal battle; Piers Dutton must have been delighted to finally expel the abbot, Thomas Birkenhead, and seize his empire – he’d already tried to hang the man for illicit coining. (The ex-abbot didn’t go far. Despite his financial meanderings in the past, he successfully reinvented himself as a secular, or diocesan, priest and, seven years after the dissolution of the monastery, he found himself the recipient of a few parcels of what had been the priory’s land, gifted to him in a will. History doesn’t record what Piers Dutton thought of this turn of events.)

Nine years after the expulsion of the canons, the whole estate was put up for sale, and it was bought by the Brooke family, who would own it for the next four centuries. They moved in, adopting the abbot’s lodging as their main house. They didn’t rush into altering the buildings; for a while, there was always a slim possibility that the Dissolution could be reversed and land returned to ecclesiastical orders, and the Brookes had already mortgaged themselves to the hilt to buy the place. A hundred years later, the priory church had been demolished. In the eighteenth century, the Brookes knocked down most of the remaining medieval buildings and replaced them with a modish neoclassical mansion. By the 1920s, though, the family had abandoned their formerly magnificent seat, which itself fell into ruin and became used as yet another convenient, ready-made quarry of dressed stone.

In 1966, the site was earmarked for development as a public amenity, and its heritage potential was recognised. Archaeologists were commissioned to excavate and lay bare the remains of the medieval priory: the priory church, the cloister and chapter house, and associated buildings. In 1975, the site became Norton Priory Museum, and within the decade a new building had risen from the ruins, to accommodate all the finds from the excavations: pottery, glass, medieval floor tiles, carved pieces of stone – and the human remains.

As you walk into the modern museum, your attention cannot fail to be grabbed by the huge fourteenth-century stone statue of St Christopher. Spend a moment examining it, because it’s worth it. St Christopher strides through the river, carrying the Christ-child. His hair and beard are immaculately coiffured, curling in stone spirals, like Michelangelo’s Moses. The folds of his robe and cloak are beautifully chiselled out; around his ankles and feet, serpentine currents swirl and fish weave. It’s an astonishingly beautiful piece of medieval sculpture, rhythmic and monumental. And yet, while St Christopher, with his open, honest features, is such a calm presence, the Christ-child sits like an entitled brat on his shoulder, staring off into the distance, slightly disgruntled at the time it’s taking to carry him over the river. It’s been suggested that this statue of St Christopher may hark back to the original site of the priory, at Runcorn, which controlled an important crossing point on the Mersey, while also emphasising the role of the priory in providing lodging for travellers.

Inside the atrium of the modern museum, you can walk into the old abbot’s lodging, the building that became the core of the later neoclassical mansion and has now been stripped away to reveal its medieval nucleus. From that cool and vaulted stone space, you emerge out into the open, where low walls trace the outlines of the cloisters and the abbey church on the ground.

It seems the priory was an entirely new build when the canons arrived in this place to create it, in 1134. At least, the archaeologists found no traces of any earlier buildings in their excavations, and pollen analysis of samples of subsoils buried under the foundations revealed a historic landscape of scrubby woodland, with oak and birch, alder, hazel and bracken. There would have been plenty of work to do to prepare the area for the priory: clearing woodland and digging ditches to drain the marshy land in the north of the estate, along the bank of the Mersey, to create new fields as well as to lay the foundations of the buildings.

The main business of the priory, the way it generated its funds, was agriculture – just as it was for any estate at the time, ecclesiastical or secular. Farming would provide food for the canons and visiting pilgrims, but also an income for building and maintaining the priory. Combining archaeological evidence with historical records from Norton Priory itself, but also from other neighbouring manors, it’s likely that this farmland was used for growing a range of crops including barley, wheat, peas and beans, as well as flax for linen, with cattle grazing on the northern marshes. The priory also had some sheep and pigs, geese and chickens, and orchards. The canons also owned several fisheries in the River Mersey, as well as the mill pond, which doubled up as a fish pond. Fuel came from coppiced woodland and from turf. As far as building supplies were concerned, there was plenty of local sand, gravel and clay to be had, and a source of red sandstone on the ridge to the southeast – now known as Windmill Hill. The native woods would have provided some timber, but larger oaks may have been gifted from managed forests.

It seems the construction work dragged on somewhat. At one point, at least a decade after the foundation of the priory, a certain Hugh de Cathewic, probably the master mason, was given a hundred sheep on the condition that the church was finally finished. And, of course, it never really would be, being renovated and extended over time, right up to the point when Sir Piers Dutton arrived to give the monks their marching orders. What nobody could have anticipated, around the time of the Dissolution, is that nearly 500 years later, Norton Priory would be far from forgotten.

The archaeological investigation of the priory began in 1970. Runcorn was being developed as a ‘New Town’ to alleviate overcrowding in nearby Liverpool, and it seems that the authorities felt that, alongside all this brash novelty, the growing community needed a sense of itself rooted in the past. To that end, the Runcorn Development Corporation funded almost two decades of excavations at the priory, uncovering the foundations of the priory church and monastic buildings. Just as you might expect from an excavation of this nature, many burials were also uncovered, within the church, the cloisters and the adjacent cemeteries. The reports of the digs in the 1970s and 1980s record the discovery of 144 graves in total. A few were left undisturbed, but 130 were excavated, with the generally very well-preserved skeletal remains of at least 156 people (some graves contained bones from more than one individual) now residing in the archive of Norton Priory Museum.

Some of the burials were in earth-cut graves, which may have contained coffins or simple shroud-burials. Others, particularly those under the floor of the church, were in monumental stone coffins with niches carved out for the heads. Some of these had very beautiful carved stone lids featuring elaborate crosses, floral and foliate patterns, and even a ‘green man’ image. There were no grave goods inside the coffins, but the graves could be roughly dated by context and style, and are thought to span the lifetime of the priory, from the twelfth to sixteenth centuries. The burials inside the church are clustered at the east end – in the chancel, close to the altar – and in the chapels added to the west of the transepts. The eastern cluster is likely to include high-ranking priors and abbots, while the chapels are more likely to contain lay burials, probably for generations of rich benefactors and their families, including the barons of Halton and the well-heeled Dutton family. More lowly members of both the religious and secular communities associated with the priory would have been buried in their respective cemeteries, outside the church. These cemeteries were not a focus for the excavations, though; all but ten of the excavated burials came from inside the medieval buildings. This inevitably means that the sample is focused on the more elite sections of society at and around Norton Priory. And it’s also heavily male-dominated – osteological determination of sex in the skeletons showed that there were three times as many men as women. It’s what you might expect at a monastery, and is similar to other sites in this respect. Just nine burials were those of children younger than eleven years old, and three were adolescents. Most of the burials were those of middle-aged or older men. Calculation of stature produced an average height for these medieval men of 1.7 metres or 5ft 7in, very similar to that found at other sites. What was extraordinary about these skeletons, though, was the evidence in many for a metabolic disruption – an increased rate of osseous breakdown and replacement, producing heavy, thick bones. But in order to understand this pathology, we must take a detour into the biology of bone.

All of the bone in your body renews and replaces itself on a fairly regular basis. This may come as a surprise – there is perhaps a tendency to view bones as inert lumps of mineral inside your body. But bone is a living tissue. As well as mineral and protein components, which exist together in a hard matrix, it also contains various different types of cells. Some of these bone cells create the mineral-and-protein matrix, others eat it away. Some are not so productive or destructive, but are essential nonetheless to the upkeep of bone. These cells, osteocytes, sit in hollows, or lacunae, within the hard matrix, but they are not completely isolated from each other. Each osteocyte possesses long, slender, filament-like processes which reach out through narrow tunnels in the matrix, called canaliculi, and make contact with the processes of other osteocytes. In this way, they are able to communicate with each other – and with cells on the surface of the hard matrix. They send messages both via direct contact with the cell membrane of other cells – at the ends of these long processes – and by secreting certain hormone-like substances that can be picked up by other osteocytes.

Osteocytes start out as bone-forming cells, and at this earlier stage of their life they are called osteoblasts. These are plump, cuboidal cells that are dedicated to pumping out collagen, forming sheets of this structural protein as well as calcium phosphate, which crystallises as a form of the mineral hydroxyapatite around the collagen. ‘Apatite’ is a strange name – it comes from Greek and means ‘the deceiver’, as it’s often mistaken for other minerals; hydroxyapatite is a version of calcium phosphate that includes a hydroxy group – containing hydrogen and oxygen. The deposition of apatite around collagen in bone is similar to the way that molluscs and sea urchins create their shells, with calcium carbonate crystallising around chitin. Osteoblasts are packed full of layered membranes (endoplasmic reticulum) that are used for protein synthesis, and also contain tiny bubbles, or vesicles, containing calcium phosphate, ready to be released outside the cell. The two-phase nature of bone matrix – with the stringy protein collagen and the hard apatite crystal – makes it extremely strong and tough. Without the mineral, the protein would be flexible; this is seen in bones that have become demineralised, like those in bog bodies. And without the protein, the mineral would be hard but brittle, and liable to shatter. The balance of protein and mineral in the matrix is clearly extremely important and tightly regulated, with various enzymes, proteins, hormones and vitamin D all playing a role.

Once an osteoblast has completely surrounded itself with matrix, it changes into an osteocyte (meanwhile, new osteoblasts are recruited from stem cells). This involves a change in shape; the osteocyte is spider-like, with a small cell body and plenty of those long, spindly processes – very similar to the dendrites of nerve cells – for communicating with the neighbours. The osteocyte will live out the rest of its life inside its lacuna, in the hard matrix. (For some osteocytes, that life could be as long as your own life. The tiny ossicles in the middle ear – the incus, malleus and stapes – are highly unusual in that they don’t undergo any remodelling. A microscopic study of these ossicles from the ear of one 95-year-old found that half of the lacunae stood empty – their osteocyte inhabitants had long since withered away; but half of them were still occupied, and those osteocytes must each have been around ninety-five years old, as ossicles are fully formed at birth.)

So, just what kind of conversations are these osteocytes having with each other, deep inside your bones? It seems to be that they’re mostly sharing their worries about just how much stress and strain they are under, like good friends sharing their concerns. Osteocytes act as sensors within bone. They’re doing something that almost all cells are capable of, in that they’re sensitive to mechanical stresses, which might include deformation of the substrate around them, but they’re particularly sensitive to these changes. It seems that precisely what the osteocytes detect are changes in the flow of the fluid that exists in the narrow gap between the surface of the mineral matrix and the cell membrane, in the lacunae around the cell bodies and in the canaliculi, where the long processes of the cell lie. (The osteocyte doesn’t completely fill the lacunae and canaliculi, in the same way that a monk’s body doesn’t completely fill the space within a head-niche stone coffin; there’s air around the body – and later fluid, as the body decomposes; similarly, there’s fluid around all the parts of the bone cell.)

The flow of fluid creates a sliding or shear stress on the cell membrane of the osteocyte. But there’s another possible way that the fluid movement may be affecting the processes in the canaliculi, in particular. Using an electron microscope, which can visualise minute structures down to the level of molecules, scientists have seen tiny tethers connecting processes to the walls of canaliculi, like miniature guy ropes. And these guy ropes are linked to proteins that span the cell membrane and that are, in turn, connected to densely packed protein filaments that form the internal ‘skeleton’ of the cell process. Fluid moving along canaliculi as bone deforms under loading will tug on those guy ropes and, by extension, on intracellular protein filaments. In some places, the cell membrane of the process may also be directly attached to canalicular walls. Again, fluid moving around the process will tug on these attachments. These strains on the membrane open up gateways within it, allowing calcium ions to flow into the cell. Laboratory experiments have shown that the slender processes of osteocytes are much more sensitive to such mechanical strain than the body of the cell is. But the further details of how these physical effects on the osteocyte are detected, and then integrated and acted upon, are still under investigation. What’s become clear, though, is that the spindly tentacles of the osteocyte are extremely important for both sensing physical changes and communicating that information through bone.

The communication network is created by the tip of one osteocyte process making contact with the tip of a process extending from another osteocyte. Where the two tips meet, there are actually tiny pores, so that the insides of the processes – their cytoplasm – is connected. Molecules and ions can pass from one cell to the other through these pores, allowing chemical and electrical communication. The pores are called ‘gap junctions’ and, on each side, they’re made of a six part protein. They lock together, a bit like rivets, with a hole through the middle. Another way in which osteocytes can communicate with each other is by releasing hormone-like chemical messengers into the fluid around them; these chemicals diffuse through the system of interconnected canaliculi and lacunae, carrying messages to other osteocytes.

The fascinating conversations that osteocytes are having amongst themselves (‘I’m really under stress over here…’, ‘It’s not so bad over this way…’) are all very well, but there’s not much point in moaning about something if you can’t do anything about it. Osteocytes themselves are physically unable to respond, having backed themselves into a corner, sealing themselves up inside their cave-like lacunae. (They remind me of ascetic monks, anchorites, whose hermit-like habits are often exaggerated; many were not entirely sealed off from the outside world – their pious behaviour was performative, designed to be seen and commented on, not to slip by unnoticed.) Osteocytes also need to get their message out – in this case, to other cells, on the surfaces of bone tissue. A recent research paper describes the role of the osteocyte as a ‘major regulator of skeletal activity’; together, these networked bone cells monitor the physical and chemical environment and then stimulate activity in other cells.

Osteocytes communicate with osteoblasts in the same way they talk to each other, sometimes directly, via those gap junctions, sometimes via chemical signals that pass into the extracellular fluid. The messages from osteocytes may stimulate osteoblasts to be more active, to produce more bone matrix, or they may be inhibitory, telling the osteoblasts to down tools for a while.

Communication with the large cells that resorb bone, called osteoclasts, is quite complex. It seems the main signal from osteocytes to osteoclasts is inhibitory. Experiments have shown that osteolysis, or osteoclast-mediated bone resorption, increases in areas where osteocytes are disappearing – committing suicide, undergoing programmed cell death, and removing themselves from the conversation in a very final way. At first it seemed as though the osteoclasts were somehow responding to the death of osteocytes. But in fact it’s not simply that osteoclasts become more active, there are actually more of them in areas where osteocytes are dying off. There isn’t a great army of osteoclasts waiting to jump into action – instead, bone resorption relies on new osteoclasts appearing. They develop from blood-cell precursors – so, somehow, the osteocytes must be sending out signals that draw these precursor cells out of the bloodstream and tell them to turn into bone-eating osteoclasts. In fact, it turns out that it’s not the dying cells, but their neighbours, that are calling in the osteoclasts. It seems to be that microscopically tiny cracks in bone cause local osteocytes to die – and then the osteocytes immediately around that area of damage start pumping out signals to recruit the osteoclast precursor cells.

It’s been known for a couple of centuries that bone remodels itself throughout life, and that it’s sensitive to mechanical loading, responding by strengthening itself (or indeed weakening itself) accordingly. But it’s really only within the last two decades that the crucial role of osteocytes as both sensors and orchestrators of a response has been elucidated. There are still plenty of details to be worked out, including exactly how dying osteocytes signal to their surviving neighbours to kickstart osteolysis, for instance, but we know far more about how bone functions as a living tissue than we did when I was first learning about this fascinating part of our bodies at medical school. We all know that we can build muscle by doing strength-training, but our skeletons also respond to such activity. And, like muscle, our bones will weaken if they’re not challenged. As the old (and truthful) adage puts it: use it or lose it. (What have you done today, and how will your skeleton be remodelling itself right now, as you read this?)

Most of the time, these cellular conversations and responses, monitoring and rebuilding our skeletons, do a fine job. But unsurprisingly, any broken links in these complicated chains of cause-and-effect, any breakdown in communication between these different populations of cells that live in and around bone, can lead to pathology. The vast majority of bone diseases can be understood – at least in terms of their ultimate manifestation, if not their primary causes – as problems with this system that balances bone formation against bone resorption. Some diseases, such as osteoporosis, will happen if too much bone resorption occurs. Others may happen if too much bone formation happens. Many will see bone being lost in some areas and added in others. Osteoarthritis is a good example of this: altered mechanics at a joint will lead to extra bone being laid down around the margins of the joint surface, while bone directly under the joint surface may be eaten away, producing cystic lesions. In this case, the bone is really responding in a normal way – to an abnormal situation. But other diseases may result from a problem that arises with bone metabolism itself, with those systems of making and breaking bone, and one of these is Paget’s disease.

The disease was first recognised as an entity by the nineteenth-century English surgeon and pathologist Sir James Paget. (He gave his name to a suite of other pathologies too, including a specific type of breast cancer, blood clots in veins draining blood from the arm, and recurrent abscesses – but it’s the bone disease that we’ll stick with here.) Paget was a pioneer of microscopy in pathology, focusing in on the fine detail of diseases and the way that they manifested in the tissues of the body. He recognised, in the bone disease that would hold his name, signs of an increased rate of bone turnover: excessive breakdown, and replacement with disorganised new bone. But he believed the disease to be the result of chronic inflammation, calling it ‘osteitis deformans’ – in other words, deformity-inducing bone-inflammation. He published the first description of the disease, a case study involving a coachman, in 1876. Paget had first seen this patient in 1854, at St Bartholomew’s Hospital. The man was then forty-six years old and, up until this point in his life, had exhibited no sign of disease. He was, as Paget reported, ‘a tall, thin, well-formed man, father of healthy children, very active in mind and body. He lived very temperately, could digest, as he said, almost anything, and slept always soundly.’ But then the patient suddenly developed aching pains in his legs, usually after exercise. After a year of these aches, he noticed that his left shin had become deformed.

When Paget examined him, he could feel that the man’s left tibia, or shin bone, was very broad, with an uneven and nodular surface. He prescribed potassium salts, but these had no effect. Three years later, he saw the man again. The patient was still generally healthy, but his left tibia was even larger and had developed a marked curve; his femur was also affected. The patient had also noticed that his hats no longer fitted him – his skull had enlarged. Paget noted that the man had tried ‘various medicines, but none had done any good’. Over the following seventeen years, the patient’s right leg bones and his spine had also become deformed. The man was a reservist, a member of the voluntary Yeomanry Corps, and every year, he’d had to have his military cap enlarged. In 1844, the diameter of his head was 22 ½ inches; by 1876, it had grown to 27 ¼ inches. In January of that year the patient also noticed a painful swelling in his left forearm, which Paget was sure was a cancerous growth. The tumour grew very rapidly, and the patient himself became weak and emaciated. He died on 24 March.

A post mortem examination of the patient’s body revealed an enlarged heart with a calcified mitral valve, numerous small masses of cancer in the pleural membranes around the lungs, and a large, soft, grey-white oval tumour on the radius, just as Paget had anticipated. And there were many signs of pathology in the man’s skeleton. The vault of the skull was enlarged, with the bones four times thicker than normal. The bone also appeared porous, peppered with holes for small blood vessels, but was very dense and compact on the inner surface, ‘like limestone or white brick’. The facial bones were unaffected. But the bones of the leg were profoundly abnormal. Both femora and tibiae were thickened and irregular on the surface, with, like the skull, many extra channels for blood vessels. The marrow cavity of these long bones was preserved, but it was full of ‘bright crimson’ tissue, whereas this is normally yellowish, fatty marrow in adults. Some of the inner bone, around the marrow cavity, looked almost normal, while the outer layers had become porous and overblown. But in most places, all the bone had transformed ‘into a hard, porous or finely reticulate substance, like very fine coral’. Paget obtained the histology report on the bones from a Mr Butlin, who noted that the canals containing blood vessels were widened, while the blood vessels themselves were of a normal size. Osteoblasts were found lining the walls of the canals, just as when bone is forming in a fetus.

Paget thought that other doctors would undoubtedly have seen this disease, but lumped it together with other bone conditions, such as osteoporosis and hyperostosis. But he recognised it as a distinct entity and something he had detected in more than one patient. As well as that very detailed case study of the coachman, Paget described four other patients, all men, with similarly affected legs and bone pain; one case also involved a tumour on the humerus (upper arm bone) while another included cancer within the skull. Paget had also scoured the wider literature and pulled out three other potential cases from elsewhere in Europe. From these reports and his own observations, he was able to define, for the first time, a disease with a distinct pattern:

It begins in middle age or later, is very slow in progress… The disease affects most frequently the long bones of the lower extremities and the skull, and is usually symmetrical. The bones enlarge and soften, and those bearing weight yield and become unnaturally curved and misshapen… In its earlier periods, and sometimes through all its course, the disease is attended with pains in the affected bones…

He also noted that ‘in three out of the five well-marked cases that I have seen or read of, cancer appeared late in life’.

He interpreted the histological appearance of the affected bone as showing inflammation because of the signs of increased blood supply. The histologist, Mr Butlin, suggested this basis for the disease, arguing that only three things could cause such a rapid growth in bone: tumour, hypertrophy or chronic inflammation. Having ruled out the first two – the altered bone didn’t have the abnormal appearance of cancer or the normal architecture that accompanies hypertrophy – the third seemed like the only option.

And yet, we now know there was a fourth option, not anticipated by Butlin or Paget.

Paget’s disease is not an osteitis but a fundamental disorder of bone metabolism: a problem with the way that bone tissue functions. In fact it’s the second most common metabolic bone disease after osteoporosis, although its prevalence varies widely in different parts of the world. It’s almost unheard of in Africa, Asia and Scandinavia, while it is most common in the North West of England. (Indeed the coachman in whom Paget first recognised the disease came from the North of England.) It’s also relatively common in places where British migrants settled in the nineteenth and twentieth centuries, such as Australia and New Zealand. It tends to affect older people – over the age of forty. But today, it’s much less pervasive than it was in Paget’s day. In the UK, where large surveys of X-rays have captured the prevalence of Paget’s disease over time, incidence has been found to have been steadily dropping. In the 1970s, amongst women and men over fifty-five years of age the rate of Paget’s disease was 3.9 per cent and 6.2 per cent respectively, and 5 per cent overall. (The sex ratio was inverted in the city with the highest rate, Lancaster, where 10 per cent of women and 6.5 per cent of men over fifty-five had signs of the disease on radiographs.) In the early 1990s, that had dropped to 1.6 per cent and 2.5 per cent for the same groups, in a sample drawn from ten towns. Amongst them, Lancaster was once again found to have the highest prevalence, but it had more than halved since the ’70s and the sexes were almost affected equally: in over-55-year-olds, 3.8 per cent of women and 3.7 per cent of men had radiographic signs of the disease. In 2018, more data emerged from Lancaster, now based on CT scans, which are even more sensitive, and this time, the rate had dropped to 1.2 per cent in older men and 0.4 per cent in older women, with an overall prevalence of 0.8 per cent. As well as the rate of the disease declining in recent decades, the severity, as experienced by patients, has also reduced. And in more than 50 per cent of modern cases of Paget’s disease, only one bone in the whole skeleton is affected.

So the disease is declining and becoming less severe, even in northwest England, where it has been historically most prevalent. But nobody knows why, largely because the underlying cause of the disease itself is still quite mysterious, with both genetic and environmental factors at play. Taking a long view of Paget’s disease – including examining archaeological, or palaeopathological, cases of the disease – may help us to better understand it.

When genetic and environmental factors align to produce Paget’s disease, the carefully coordinated balance of bone metabolism breaks down. Affected bones become expanded and, when you’re handling dry bones in the osteology lab, strangely heavy. Sometimes just one bone is affected; sometimes many, throughout the skeleton. On an X-ray, those bones almost look woolly and the architecture is disrupted. Towards the ends of long bones such as the femur or humerus, the normal internal structure of the bone is trabecular or ‘spongy’ – comprising a scaffold of fine, interconnected struts, following patterns of stress. In Paget’s disease, this trabecular bone is replaced with a fluffy and somewhat moth-eaten-looking tissue. At a microscopic level, the osteoblasts look quite normal, whereas the osteoclasts are very strange indeed. These bone-eating cells are usually large and contain several nuclei, but in Paget’s disease, they go crazy: they become enormous and can contain up to a hundred nuclei. They’ve also been shown to be oversensitive to signals promoting bone resorption – they are cells with an itchy trigger finger. The bone marrow looks odd too: it has switched into a state where it will produce many more osteoclasts from blood-cell precursors than normal.

Paget’s disease follows a particular trajectory, starting with an osteolytic, or bone-resorbing, phase. There’s a characteristic appearance of this phase on a radiograph, where you see a narrow, pointed wedge of darkness – a ‘blade of grass’ lesion – representing bone loss, pushing down into a long bone such as the femur or tibia. After that, it’s almost as though the bone panics and tries to make up for the loss. In this bone-forming phase, new bone is laid down around seven times more quickly than normal. And it’s untidy: rather than regular sheets of collagen that then become mineralised, which is the way that mature bones typically grow and repair themselves, the osteoblasts pump out a messy tangle of collagen fibres. The ‘woven’ bone that results looks more like the type of tissue that’s created when bones start forming in the fetus, or when fractures are healing. The bone gets denser and denser, until cells start to die off and blood vessels also disappear. After the frenzied activity of the osteolytic and bone-forming phases, this final stage sees bone metabolism grinding to a halt – it’s called the ‘burned out’, or sclerotic, phase. (The word ‘sclerosis’ comes from ancient Greek, meaning ‘to harden’.) In the skeleton of someone with Paget’s disease, each affected bone will pass through these three phases – osteolytic, bone-forming and sclerotic – but different bones in the skeleton, and indeed different regions of one bone, may be at different stages of progression.

As far as the person with the disease is concerned, they may or may not be aware that something is awry with their bones. Paget’s disease can be completely asymptomatic, especially early on. The condition may be picked up incidentally, when a patient has an X-ray taken for something else and Paget’s disease is spotted by the radiologist. Or it could be that a blood test turns up high levels of the enzyme alkaline phosphatase, which is often associated with active bone formation. Alternatively, it may be that the patient themselves has noticed a change in their bones, such as growth in the skull or a curve developing in the tibia or shin bone. And some people with Paget’s disease may experience pain – in fact, this is how the condition is most commonly found. There are several reasons why a bone with this metabolic problem might become painful: because of increased blood flow; because the very sensitive membrane around bones, the periosteum, is becoming stretched by new bone forming; because the bone is experiencing unusual mechanical stress – and, related to this, because that shifting stress creates tiny fractures. Paget’s disease can also have the knock-on effect of producing osteoarthritis, when the ends of bones, which form joints, are affected. Around half of cases are picked up because a patient is complaining about painful joints, often the hip, knee or spine.

Another effect of Paget’s disease, and sometimes the feature that initially prompts investigation and diagnosis, is pain from nerves that are being constrained and compressed by the abnormal bone growth. That might be lower nerves emerging from the spine, causing sciatica and numbness around the pelvis, or higher up – all the way up to cranial nerves emerging from the skull, affecting vision and hearing, and causing headaches.

As well as the change in the internal bony architecture, Paget’s disease can cause an alteration in the overall shape of bones. The skull can grow larger, with bossing of the frontal bones underlying the forehead and an expansion of the bones under the cheeks. Although pagetic bone is dense, it is not as strong as normal bone, and skeletal deformities can develop. Weight-bearing long bones, such as the femur and tibia, can become bowed, with stress fractures occurring on the outside of the curve. Sometimes the bone completely breaks in two. In modern populations, it’s often these changes – painful and deformed bones – that lead to a diagnosis of Paget’s disease. In X-rays, the bones look moth-eaten and fluffy, but also often wider. In archaeological human remains, it’s often that increased thickness of bones and their heaviness that makes the osteologist pause and think, This is different.

There can be other knock-on effects as well. The high metabolic turnover in pagetic bones draws increased blood flow, and the demand can eventually lead to heart failure. Paget’s disease also comes with an increased risk of bone cancers, especially osteosarcoma. Only 1 in 100 people with Paget’s disease develop osteosarcoma, but this is a rate that is thousands of times higher than that seen in the general population. To put it the other way round, a fifth of patients with osteosarcoma have Paget’s disease. These tumours are osteolytic, bone-eating and spread quickly – within the bone, but also breaking away and producing tumour colonies, or metastases, in the lungs. Even with modern cancer treatment, the prognosis is not good: a few more years at most.

It might seem that we know a lot about Paget’s disease. But we still don’t really know why it happens, in each case. James Paget was certainly at a loss when it came to the cause of the disease: referring to the bone pains that the coachman developed at the age of forty-six, he wrote that they emerged ‘from no assigned cause, unless it were that he lived in a rather cold and damp place in the North of England’.

It seems clear that there’s a genetic basis to the disease as well; there is with almost every disease, but the fact that Paget’s disease seems to have travelled with British-born people to Australia and New Zealand and has then been passed on to their descendants suggests that genetic predisposition is important. The observation that Paget’s disease seemed to run in families goes back to the late nineteenth century. It’s not clear-cut, though; in large epidemiological studies only 10–40 per cent of patients appear to have relatives with the disease (though there may have been others, as yet undiagnosed).

With the ability to sequence DNA, it has become possible to identify locations in the genome where mutations can lead to an increased risk of Paget’s disease. One gene is found in a mutated form in around half of patients with familial Paget’s disease. It encodes a protein called p62 or sequestome 1. This protein is named after one of its effects on cells: leading them to group, or sequester, together. And somehow – the precise mechanism is still being worked out – an altered sequestome 1 leads to overstimulation of osteoclasts. Some mutations in the gene lead to only slightly abnormal versions of sequestome 1; others produce a drastically truncated version of the protein, rendering it functionally useless – and these more radical changes are linked to a more severe form of Paget’s disease.

But in fact there are many genetic variants that can lead to an increased risk of the disease. Large studies carried out in 2010 and 2011 uncovered seven novel regions across the genome that were implicated, including genes that were already known to encode proteins that have an effect on osteoclast activity. One of them is DC-STAMP, which sounds like a mark of approval for a comic-book character but actually stands for dendritic cell-specific transmembrane protein (even though that should be DC-STMP, but the discoverers stuck in the ‘A’ to make it easier to say). DC-STAMP is a molecular switch that drives individual precursor cells to fuse together, creating the oversized, multinucleate osteoclast. An altered DC-STAMP protein clearly has the potential to create monster osteoclasts. Other culpable genes in Paget’s disease encode other proteins that act as chemical signals regulating the activity of bone cells.

But it’s not as though any of these genetic variants throw a simple on–off switch in Paget’s disease. It’s possible to possess the variants and not develop the disease. So there must also be a significant role for environmental factors: something that someone is exposed to during their life that activates the hair-trigger that the genetic variants have set up. The decline in prevalence over time also supports the existence of environmental factors, as does the fact that the disease affects certain bones and not others.

It’s been proposed that the main environmental factor is viral infection; viral-like particles have been spotted, under the microscope, inside the nuclei and cytoplasm of osteoclasts from patients. A rural focus for the disease perhaps suggests that the guilty virus might be one that is contracted from animals – a zoonotic infection. It’s also been suggested that Paget’s disease could be a long-term effect associated with various other viral infections, including measles and respiratory syncytial virus (RSV). But attempts to prove links with past infection by specific viruses have foundered, and it could be that the osteoclast inclusions might be protein detritus from disorganised cellular machinery. On the other hand, lab experiments have shown that introducing certain viral genes into osteoclasts can turn them into hypernucleated monsters just like those seen in Paget’s disease. Other environmental factors could also be implicated, such as smoking, exposure to wood smoke and other toxins, calcium deficiency, and unusual stress on bones. (Coldness and dampness do not seem to be factors, though.)

So it’s a complicated picture: many different genetic mutations may coincide to create a level of susceptibility, and it’s likely that several environmental factors may also play a role.

In terms of treatment, understanding the origin of the disease and the way it progresses has been crucial. It starts with disrupted, overactive osteoclasts, so the target for current treatment is to dampen down their activity. The later bone-forming phase of Paget’s disease is a response to the manic osteolysis – if you sort out the bone-eating osteoclasts, the bone-forming osteoblasts will also behave themselves. Treatment with anti-resorptive drugs tackles the metabolic basis of the disease, but also helps with bone pain, though some patients need painkillers on top. Treatment can stop the disease progressing, and some case reports have also shown a reversal of some of the effects of the disease, with bony architecture becoming more organised, a reduction of deformities and even a return of hearing in patients whose auditory ossicles have been affected. A reduction in osteosarcoma rates amongst patients with Paget’s disease is likely to be partly due to treatments that have been available since the mid-1970s. Sometimes, surgery is needed to mend broken bones, replace failing joints and relieve pressure on nerves. None of these treatments were available, of course, for the medieval sufferers of Paget’s disease.

The characteristics of Paget’s disease in archaeological human remains are just as Paget himself described in the post mortem examination of his patient: bones are thick and heavy, and yet porous. Paget likened the texture to limestone, white brick and coral; others have compared the bony texture to pumice. X-rays show up the expansion of bones, thickening of the outer cortex, patchy increases in density – including a ‘cotton wool’ appearance of skull bones and that characteristic ‘blade of grass’ lesion, or osteolytic wedge.

The archaeological evidence appears, at first sight, to point to a hotspot of Paget’s disease around London: this is where the highest number of cases have been reported. But you always have to be careful with archaeological data, as it can be drastically skewed by the uneven nature of the sample. London is a huge city with endless construction work taking place, and as a result it is the most heavily excavated area in the UK. The large number of cases of Paget’s disease must be set against the vast number of graves that have been excavated in the capital to make way for new buildings, railways and roads. A better way of assessing the prevalence of a disease from archaeological data is to look at its rate within a region, or even within a single cemetery. However, this can also be problematic, especially if only part of a cemetery has been excavated, or if only certain sections of the community are buried in a particular cemetery, which can again skew the data.

But right from the outset, it looked like Norton Priory had a particularly high rate of the disease. In 2005, an analysis of the skeletons from the priory was published, with six adult individuals identified as having Paget’s disease – one in twenty. For comparison, the rate of Paget’s disease in the well-studied medieval cemetery at Barton-on-Humber, on the other side of the country, was around one in fifty.

Those six affected skeletons from Norton Priory have recently been re-examined, and – with the help of radiography to aid diagnosis this time – even more extensive evidence of Paget’s disease was identified. In two individuals, pagetic changes were found to affect more than 75 per cent of the skeleton. One of these also had signs of osteosarcoma affecting both hip bones. But in addition to the original six individuals bearing signs of Paget’s disease, the latest analysis identified a further twelve skeletons with pagetic lesions, tripling the total number of affected individuals and pushing the crude rate up from around 5 per cent to around 16 per cent of the population. This goes to show just how important it is to hold on to physical archives from archaeological excavations, as well as how useful radiography can be in extending the potential for palaeopathological diagnosis. The twelve newly diagnosed skeletons were also examined in great detail, from head to toe, and fully X-rayed as well.

Of the eighteen individuals identified as having Paget’s disease, fifteen were male and just three were female. It’s important to note that the entire sample was biased, as may be expected of a monastery: there were eighty-five males and twenty-nine females; even so, the rate of disease was higher amongst men (18 per cent) than amongst women (10 per cent).

We obviously use our modern understanding of Paget’s disease in order to identify it in ancient human remains; the lesions are familiar and recognisable on the surface and in X-rays. There’s a particular focus on the skull, spine and lower limbs, including the pelvis. But at the same time, there is a difference with the archaeological cases: the lesions appear more severe and are more widespread across the skeleton than we see in patients today. And here’s the thing: if we can find out why Paget’s disease has decreased over time, not only in prevalence but also in severity, that might give us useful information to help with managing the disease today.

Despite the severe nature of the disease in those skeletons from Norton Priory, few complications were seen: there was no deformity; no fractures; just that evidence of osteosarcoma – a very rare finding in archaeological human remains – in a single individual. The individuals with Paget’s disease were also young compared with modern patients. Estimated age at death ranged from thirty-five to fifty-nine years, and thirteen of the eighteen were under fifty.

The recent reanalysis of the remains went beyond the palaeopathological reassessment of the bones. The researchers also took the opportunity to radiocarbon-date the skeletons, showing that the eighteen affected individuals lived across the centuries spanning the entire lifetime of the priory, from its foundation to its dissolution. Isotope analysis added further details, with high levels of nitrogen indicating a diet that must have included plenty of fish – fairly typical for monastic communities. Radiocarbon dating and stable isotope analysis are now fairly common techniques, but the team also employed cutting-edge scientific techniques to explore the characteristics of the disease at a molecular level. Given that we now know so much about the genetic basis of the disease, and the proteins that are involved, the researchers thought that probing such details in ancient human remains might provide some insights into aetiology and perhaps show how much Paget’s disease had changed over time, at a fundamental level.

The researchers chose one of the skeletons, SK101, that showed extensive evidence of Paget’s disease, and took a sample of bone from the petrous temporal bone, in the base of the skull. They extracted proteins from this sample, finding evidence of nineteen different ones, including various types of the structural protein collagen, as well as other proteins that form the supporting skeleton inside cells. But they also found p62, aka sequestome 1. Next, they compared that p62 protein from SK101 with p62 from lab-grown human cells – and found that the medieval molecule was larger. They wondered if this was just a one-off. They decided to do more tests, on other skeletons. Samples from nine other individuals with clear evidence of Paget’s disease were added to the mix. The researchers tried out a mixture of different sites, taking small samples from petrous temporal bones, teeth and femurs. They tracked down p62 in three other individuals. It was the first time that this protein had ever been detected in archaeological human remains. The researchers also extracted and sequenced aDNA from several skeletons, examining the p62 gene in detail to see if it contained any of the mutations associated with Paget’s disease in modern patients – but it didn’t. They then considered the possibility that the larger-than-normal versions of the p62 protein they’d found were due to some sort of chemical changes after death – but they thought this unlikely. It seemed more plausible that the large proteins really were pathological.

This led to a potentially interesting insight. Modern studies have revealed the presence of ‘inclusions’ in pagetic osteoclasts, which some have interpreted as evidence of previous viral infections, and others have suggested could be full of accumulated protein detritus. Those inclusions are known to contain p62 protein. It’s possible that these old, pagetic bones contained detectable levels of p62 because they’d once been populated by osteoclasts stuffed full of p62-rich inclusions. And even though no familiar mutations were seen in the p62 gene, perhaps there was something else about those genes (or in related genes) that meant that p62 grew into chains and accumulated inside cells. Perhaps it was even possible that the underlying mechanism of the disease involved not just an altered chemical signal, but a physical build-up of this particular protein – analogous to the way that other proteins accumulated inside cells in some neurodegenerative disorders. Crucially, no viral proteins were detected in the aDNA analysis, strengthening the case against an infective trigger for Paget’s disease.

This careful reanalysis of the Norton Priory skeletons – finding so many more individuals with the disease than had been previously picked up – raised the distinct possibility that lots of cases may have been missed in other archaeological settings. Nevertheless, the high frequency of disease in this population seems to reinforce the traditional geographic picture of Paget’s disease, with the hotspot in northwest England having existed for centuries. But did all those individuals come from the surrounding area, or from further afield? Perhaps, the researchers suggested, the priory could have been seen as a ‘referral centre’ for musculoskeletal problems. Isotope analyses have been carried out on some skeletons that reveal at least five were local to the area, but really, a wider study would be needed to assess whether some patients might have travelled to the priory from further afield. The fact that most of the burials that have been investigated came from within the church, many from stone coffins, perhaps suggests that these people were more likely to have been locals, well known in the community and of some social standing. The close association between Norton Priory and the local Dutton family meant that many Duttons ended up buried there. The placement of burials reflects status and it’s likely that many of the tombs inside the church itself, and in the cloisters, are those of Dutton family members. Some of those with Paget’s disease may well have been Duttons.

The medieval Paget’s disease looks much more severe than its modern counterpart, so what environmental factors might have changed to account for this? Given that these individuals appear to be high-status and ate a diet rich in marine protein, it’s unlikely that they were suffering from any dietary deficiency that could act as an environmental trigger for the disease. Inhalation of wood smoke from smoky, open fires in draughty lodgings could be an option. There’s still a mystery to be solved here, and if the triggers for that more severe form of medieval Paget’s disease can be tracked down, that might even help to provide some answers for modern patients. But even without these answers for now, we may take some comfort from the fact that cases of Paget’s disease are still declining, the age at onset is rising, the skeleton tends to be less widely affected and the bony lesions are less severe than those seen in the graves at Norton Priory. But what we learn about Paget’s disease, ancient and modern, has wider implications. By examining what happens when control of bone-remodelling goes awry, we may better understand the fundamental process – those chemical conversations between osteocytes, osteoblasts and osteoclasts. And we may also get closer to unravelling the detailed disease process of other conditions, such as rheumatoid arthritis, where bone is also lost from the skeleton.

In the end, it’s likely that there are various environmental triggers that interact with a person’s genetic predisposition to produce Paget’s disease. That may sound vague, but while we understand much more now about this disease than Paget himself did, we’re still some way from solving the mystery. There’s plenty of ongoing research involving people who are currently living with the disease, but the analysis of the people with Paget’s disease buried at Norton Priory reveals how archaeological approaches can also be illuminating, not only in understanding the range of pathologies that affected people in the past and how societies reacted to that burden of disease, but also, sometimes, adding to our understanding of modern illness.

Palaeopathology – the study of ancient diseases, ancient bones – isn’t just about the past.

5. THE BLACK DEATH

Some diseases kill so quickly, there are no traces left on bones.

This biological fact underlies what is known as the ‘Osteological Paradox’, because individuals who possess evidence of disease in their skeletons may in fact have been healthier than those with none. Less healthy individuals may have died before a disease had a chance to wreak any bony changes. It makes it very difficult to assess the general health of past populations from skeletal remains. It also means that there will be some diseases that are practically invisible in the archaeological record. Or at least they were, until very recently.

In the middle of the fourteenth century, a terrible pandemic swept through Africa and Europe. In the eighteenth century, a German description of this medieval plague appeared in the literature, calling it ‘der schwarze Tod’: the Black Death. The name may have referred to dark marks on the skin of the infected, but it was probably symbolic as well. And it stuck. But the cause of the Black Death remained a mystery for many centuries.

We have masses of historical evidence for the Black Death, from contemporary reports. And we have archaeological evidence in the form of mass graves. But the skeletons in those graves epitomise the Osteological Paradox: they are, on the face of it, from healthy individuals. But they are of course dead – and many of them died young. Nevertheless, the skeletons of those who died in the Black Death are informative: we can look at the range of ages, the ratio of men and women, and the evidence for physiological stress amongst the individuals in those graves.

But, for a long time, we’ve only been operating on an assumption that these medieval mass graves do indeed represent victims of the Black Death. It seemed a reasonable assumption; however, it’s only recently that we’ve actually been able test it – using aDNA to identify pathogens. But in fact the first contribution of aDNA in this case was to define which pathogen was actually responsible for the Black Death in the first place.

The year 2000 was an important one for advances in genetics. It was the year that the first working draft of the human genome was published. And it was also the year that the pathogen that caused the medieval Black Death would finally be identified. But making that link would depend on a microbiological breakthrough that had happened more than a century earlier, in a different outbreak – in nineteenth-century Hong Kong.

In 1894, a Swiss–French physician called Alexandre Yersin arrived in Hong Kong. Yersin had come from Paris, where he’d worked in the laboratory of pioneering microbiologist Louis Pasteur before going on to join the newly established Pasteur Institute.

These were heady days for microbiology. Medicine had a formidable new tool in its arsenal against disease. In 1891, Pasteur himself had written – in an article on leprosy – ‘with the process of science… I have not the slightest doubt that in time the microbes of all diseases which attack the human body will be discovered and cultivated’.

Just three years later, Yersin was in Hong Kong on a mission to identify the cause of a major outbreak of bubonic plague. The signs of the disease were unmistakable, as described here by Staff Surgeon Wilm of the Imperial German Navy:

After the onset of the disease signs of a constitutional disorder followed, severe dull headache, great weakness, and overpowering sensation of fatigue… Around the eyes, on the forehead, and on the cheeks, the skin usually assumed a blue-black colour; the eyes were sunken; and expression was fixed and vacant…

Wilm treated 300 patients: 189 adult males, 51 adult females and 60 children. ‘No age,’ he wrote, ‘was exempt from the disease.’ He described how many patients became delirious, throwing themselves around on their beds, and that fever was also present. Most of his patients, around 70 per cent, died in the first six days of the disease; 3 per cent would die in later days and weeks. (But that mortality rate of 73 per cent did not account for patients dying before they reached hospital; Wilm thought the true mortality rate for the epidemic was closer to 85 per cent.) If a patient survived the initial phase, the fever could continue for weeks. A few patients developed rashes and some had carbuncles on the skin, which turned into ulcers. But by far the most common signs of the disease, as Wilm reported, were visible swellings of lymph nodes: the buboes that give bubonic plague its name:

In 73% of the cases, in one or more parts of the body, buboes appeared, from the size of the pigeon’s egg to that of the fist… [most commonly in] the groin… the axilla… and the neck… The skin over the buboes [would then become] red and oedematous; and an indurated, elastic, painful swelling was formed, extending often in the case of inguinal buboes to the middle of the abdomen and to the middle of the thigh, and in the case of axillary buboes to the shoulder-blade and to the sternum… the skin covering such buboes became gangrenous.

Wilm went on to describe how, in the later course of the disease, the buboes would become more widespread and turn into pus-filled abscesses. And there were other symptoms: uncontrollable vomiting and diarrhoea.

When he arrived in the stricken city of Hong Kong in 1894, Yersin went about taking fluid from the buboes of infected patients and culturing the bacteria they contained on agar plates. A reporter for the Hong Kong Daily Press visited Yersin in his makeshift lab and was amongst the first to see the plague pathogen with his own eyes – growing on an agar plate, spreading ‘in numerous small blotchy looking branches’. He peered down Yersin’s microscope and saw, ‘ “colonies” of bacillus… differentiated into tiny dots of uniform size and appearance’. Those dots were individual microbes. Yersin’s findings were published in the Annales de l’Institut Pasteur later that year, including drawings of the plague bacterium, seen under a microscope.

The report described how the microbe was to be found ‘in prodigious quantities in the buboes’, as well as in the spleen – and, in a terminally ill patient, in the blood. Yersin had also found that inoculating rodents with pulp from buboes led to infection and death, within days. And he suggested a reservoir and route of infection: ‘The dead rats that are found in abundance in the streets and houses of Hong Kong almost always have large quantities of the microbe in their organs. Many of them present buboes… It is likely that rats are the main vehicle.’

Yersin would name the pathogen Pasteurella pestis, in honour of his mentor. But in 1944, the pathogen was renamed as Yersinia pestis, enshrining the memory of Yersin instead. (Naming organisms after their discoverers can be fraught; it turns out that a Japanese doctor, Kitasato Shibasaburo, had actually isolated the pathogen several days before Yersin did, but Kitasato’s descriptions weren’t as accurate.)

Despite Yersin’s discoveries, other reports about the Hong Kong plague were vague about its origin. The plague-germ, it was conjectured, had arrived in Hong Kong in bales of opium, travelling along Chinese rivers. The spread of the plague was understood to have followed the flow of commerce. And it seems true, at least, that the outbreak had spread from Guangdong, to the north, into Hong Kong. European reports of the outbreak are laced with anti-Chinese sentiment. Robert Peckham, a historian of medicine with a special interest in epidemics in Asia, has drawn attention to the way that descriptions of the Hong Kong plague played into colonial discourse, in the way that it ‘linked the Chinese to a disfiguring disease, [and] helped to construct an image of China itself as a pathological body’. As the plague spread westwards, India and goods emanating from southern Asia were similarly pathologised. These reactions had been rehearsed earlier in the century, with the spread of ‘Asiatic’ cholera. And of course similar sentiments would emerge once again, in the twenty-first century, as a novel pandemic pathogen spread across the globe.

Even when the plague pathogen was identified and, several years later, its transmission securely linked to rats and fleas, there was still a prevailing suspicion that it might be possible to catch the disease from any manner of object – especially objects coming from East Asia. An 1897 article in The Lancet lamented the persisting conviction that merchandise could be a source of infection, emphasising that there were no epidemiological or scientific reasons to back up this claim. (Again, this recalls the entrenched idea that Covid could be caught from infected objects and surfaces, and that these should be the focus of disinfection efforts, despite the rapidly accumulating evidence in the early months of this recent pandemic that it was primarily an airborne disease. Perhaps that’s because it’s easier to wipe a surface than it is to clean the air in a room.)

With the late-nineteenth-century plague in Hong Kong, there was a general idea – and not an entirely unfounded one – that it was linked to poor sanitation. A longstanding theory for the spread of infection involved miasma, which could float around in the air and infuse objects with infectious potential too. Even when germs had been identified as causative agents, the miasma theory still hung around. The soil was also suspected to be a source of disease, and indeed both Yersin and Kitasato had reported finding evidence of Y. pestis in soil samples around the houses of plague victims. In fact, more recent studies have demonstrated that virulent Y. pestis can survive in soil for nine months – and only three days on hard surfaces. Contaminated soil can be a source of infection for animals, though not for humans.

In Hong Kong, British troops emptied out Chinese homes, burning some to the ground and disinfecting others. Kitasato supported the measures. ‘Whoever has looked into a Chinese dwelling,’ he wrote, ‘is at once persuaded that here is a suitable hunting-ground for the plague bacillus.’ But as the crowded tenements of Hong Kong were cleared, disinfected, sealed or burned to the ground, there seems to have been very little recognition that it wasn’t Chinese culture that was to blame for creating the conditions for the plague to run rife, but poverty and overcrowding in these communities. The plague was characterised, at that point, as a Chinese disease. There was a similar discourse around opium use at the time, which was seen as another scourge spreading out of China. (Somewhat ironically, as the British had taken control of Hong Kong, in 1842, specifically to ease their import of opium into China.) As attempts to quell the plague continued, it’s estimated that 350 houses were sealed and 7,000 people dispossessed in Hong Kong.

The attempt at disinfecting Hong Kong may have been successful in some ways, though it’s also likely that the displacement of people would have contributed to the spread of the disease. But the 1894 outbreak in Hong Kong, which had begun in May, was fading by September, with just a few sporadic cases towards the end of the year. In 1895, the pestilence largely stayed away, but in 1896, there was another surge, gathering momentum in February and March.

Yersin had sent a specimen from a bubo, sealed in a glass tube, to the Pasteur Institute in 1894. In 1895, he returned to Paris to catch up with his colleagues, who had been using the sample to develop an antiserum – a potential treatment. The following year, as the plague broke out again in Hong Kong, Yersin went back, this time to try to treat patients. The antiserum seemed successful at first: Yersin gave it to twenty-three infected Chinese patients in 1896, and only two of them succumbed to the disease. Later trials suggested that the antiserum was less effective than this suggested, though it was still estimated to significantly reduce mortality, from around 82 per cent in untreated patients to 35 per cent in those receiving the treatment. There’s no doubt that Yersin and his colleagues’ work saved lives at the turn of the twentieth century.

And yet, year after year, the plague would return as a regular summer visitor to Hong Kong. Meanwhile, the route of transmission had finally been elucidated. In 1898, another doctor working for the Pasteur Institute, Paul-Louis Simond, was carrying out experiments on plague transmission in Karachi. He was sure that rats were a reservoir for the bacteria: an outbreak of plague in humans always seemed to be preceded by an outbreak in rats, with the appearance of many dead rats in the streets – but how was the infection travelling from one rat to another, and then on to humans? He carried out experiments on dead rats, showing that neither the faeces nor sputum of infected rats were capable of inducing the disease in other animals, and he also observed that infected animals rarely showed any signs of injury. And so Simond began to suspect that a parasite could be the key. He found that if he kept a healthy rat in a cage, separated from a flea-infested, plague-ridden rat, it wasn’t long before the initially healthy rat contracted plague and died.

Simond opened the intestines of fleas to look at their contents under the microscope, and found them to be teeming with plague bacilli. In fact, Yersin had made the same observation in his report four years earlier: ‘It appears almost certain that the fleas could transmit the disease because those found dead around the bodies of infected animals in the laboratory have countless quantities of bacilli in their bodies.’ Simond followed up with an experiment: when he injected the flea extract into healthy animals, they contracted plague. Based on this, he advised disinfecting clothes and destroying vermin to counter plague outbreaks.

In 1902, William Simpson, Professor of Hygiene at King’s College and lecturer at the new London School of Tropical Medicine, was clear that prevention of plague must focus on controlling rats in the city. He wrote:

It does not serve any very useful purpose to remove the sick and cleanse everything in the infected houses and above the ground if the infection is being carried by plague-stricken rats from house to house or district to district by the subterranean movements of rats, whether this be effected by rat burrows or by sewers and drains.

Simpson was right that Yersinia pestis was essentially a zoonotic disease – one that jumps from other animal species into humans (just as it’s thought Covid did at the start of the recent pandemic). But he seems not to have bought Simond’s (and Yersin’s) theory that fleas were the vectors, and neither did other medical officials – at least not until 1905, when more experiments finally confirmed that route of transmission beyond a shadow of a doubt. But even with transmission better understood, and effective preventive measures brought in, plague continued to wrack Hong Kong for decades, with particularly severe outbreaks happening in 1912, 1914 and 1922. Despite all these attempts at prevention and treatment, the period 1894 to 1929 saw around 22,000 people dying from plague in Hong Kong.

This pandemic continued into the middle of the twentieth century and spread far beyond Hong Kong. In total, it’s estimated to have claimed 15 million lives, most of these in South and East Asia. Senegal and Madagascar were also hit hard. Between 1899 and 1950, there were also 30,000 plague deaths in Central and South America – but only 7,000 in Europe and just 500 in the US. It’s thought that the differences in mortality around the world were heavily influenced by differences in both wealth and public health – differences that have persisted into the twenty-first century. The victims of plague in late-nineteenth and early-twentieth centuries were the urban poor, living in dense, rat-infested, unsanitary conditions.

Great strides would be made in the medical treatment of plague in the twentieth century – and yet the inequalities endure.

Antiserum treatment would soon be overtaken by the development of perhaps the most significant therapeutic intervention in medical history, second only to the sanitation revolution in its impact on human health: antibiotics.

The discovery of penicillin famously falls into the category of discoveries made by accident. In September 1928, some agar plates left out by an open window had gone mouldy – the fungal spores having blown in on the breeze. A particular bacteriologist returned from his holiday and looked at the plates. ‘That’s funny,’ he mused, noticing that the bacteria he’d been trying to grow on the agar plates clearly didn’t get on well with the fungus: around each spot of mould, there was a clear ring where the bacteria had been wiped out.

The bacteria were Staphylococcus aureus, tiny round microbes that happily live all over the surface of our skin but will gleefully get underneath it, given half a chance, multiplying into boils, carbuncles and abscesses, or causing cellulitis. The accidental fungus on the plates was a Penicillium, and the bacteriologist recognised that it was making something that could kill the microbes. He called that ‘something’ penicillin, publishing his findings in 1929. It may have all started with an accident, but the discovery depended on the bacteriologist’s prepared mind and his keen attention and observation.

Alexander Fleming was recognised with a Nobel prize for this work, in 1945, but the bigger prize is the millions of lives saved by penicillin, around the globe. And, of course, this was just the start: the discovery of penicillin spurred on generations of scientists to embark on a quest to find other antibiotics.

Penicillin wasn’t effective against plague, but by the mid-1930s, German chemists had developed a synthetic antibiotic based on coal-tar dyes. It was called Prontosil and it was a sulphonamide – a molecule containing a branch with a sulphur dioxide group (SO2) together with an amino group (NH2). It may have had a relatively simple chemical structure, but it had a devastating effect on a very wide range of bacteria. It was first used on plague patients in East Africa and India in 1938, to good effect – reducing mortality rates to around 30 per cent. Later trials found that combining Prontosil with antiserum brought mortality down to less than 20 per cent. By 1947, another antibiotic had been developed and was proving useful in treating plague: streptomycin, bringing fatalities in patients down to just 7 per cent. Other antibiotics came along, and now gentamicin and doxycycline are the drugs of choice, with worldwide mortality from plague in the twenty-first century standing at around 7 per cent, with the vast majority of cases in Africa. Plague is endemic in the Democratic Republic of the Congo, Madagascar and Peru. In Madagascar, there are cases of plague almost every summer.

Mortality is now down to between 1 and 200 people a year, worldwide. But although, in the majority of cases, the disease can be successfully treated with antibiotics, it still has the capacity to be dangerous and deadly. Between 2010 and 2015, there were 3,248 reported cases and 584 deaths attributed to plague. In 2017, more than 2,000 people became infected and more than 200 died. Three quarters of the cases were found to be a very severe form of the disease, spread by airborne transmission.

There are two main forms of the plague: bubonic and pneumonic. They are both caused by Yersinia pestis, but with the bacterium entering the body via different routes. Bubonic plague – historically the most common, and characterised by those painful swellings of lymph nodes – is usually contracted through flea-bites. Pneumonic plague, which is even more severe, is much rarer. It is usually breathed in – spread by droplets from one person to another. It’s often fatal if not caught and treated very early, within twenty-four hours of symptoms appearing. Bubonic plague can also become pneumonic if the infection spreads to the lungs. Both types can become septicaemic if the pathogen enters the bloodstream, but sometimes septicaemic plague can develop first, and plague can also be contracted through direct contact with infected bodily fluids. In a 1997 outbreak in Madagascar, a traditional healer sucked blood from the first patient to go down with the disease, developing pneumonic plague that he then passed on to his family. More people were infected by airborne spread at the healer’s funeral. Even more rarely, a pharyngeal and gastrointestinal version of the disease can be caused by ingesting contaminated raw meat.

Plague prevention centres on avoiding contact with potentially infected animals, and this includes a wide range of species, not just rats: squirrels, rabbits, prairie dogs, marmots and various other rodents; cats, camels and even birds. Also important is using appropriate personal protective equipment (PPE) and antibiotic prophylaxis (or vaccination) when attending patients, and avoiding unprotected contact with body tissues and fluids. In outbreaks, it’s advised that fleas should be eradicated first, before rodents; if rodents are killed first, infected fleas will jump away to find new hosts. And doctors should immediately start treating patients suspected of plague, rather than waiting for the results of lab tests. Those tests include microscopic examination of body fluids: sputum, blood or lymph node aspirates. But modern diagnosis can also employ molecular techniques – amplifying and analysing the DNA contained in samples.

Archaeogenetics applies the same techniques to long-dead patients, enabling us to specifically diagnose diseases from the distant past.

The Black Death tore through Asia, Europe and Africa in the fourteenth century. Raging across the continent between 1347 and 1353, the Black Death is estimated to have felled between 30 and 60 per cent of the population of Europe – around 50 million people. The estimates are based on historical data – very often, records of taxation. In England, these include records of heriots, or death duties: historians compare the number of people recorded as liable for that tax with the number of death duties that were actually paid during the time of the Black Death. It’s also possible to track the number of workers on manorial estates through time. Any male labourers over the age of twelve were liable to pay a ‘head tax’ or ‘tithing penny’, and those numbers were recorded. These sources are not without their problems. Tax evasion and people moving from the countryside to cities would certainly sway the data. Even so, the available evidence points to mortality being around 50 per cent – and that can be adjusted upwards to account for the women, children and poor people who don’t feature in the tax records.

First reported in Central Asia in 1339, the Black Death spread westwards, with a particularly gruesome story emanating from Caffa on the coast of the Black Sea (modern-day Feodosia, in Ukraine). Caffa was an important port, which had been bought by Genoese traders from the Mongols, who ruled much of western Asia at the time. But in the fourteenth century, it seems the Khan of the Golden Horde, Janibeg, wanted Caffa back, and he laid siege to the city. After an outbreak of disease amongst his troops, infected cadavers were catapulted over the city walls – a very early example of biological warfare.

From Caffa, it was believed that merchant ships carried the pestilence to Messina, Marseille and Genoa by November 1347 – and then the Black Death spread rapidly across Europe. The Byzantine historian Nicephoros Gregoras was one amongst many who recorded the outbreak of this disease:

The calamity did not destroy men only, but many animals living with and domesticated by men… even the rats that happened to live within the walls of the houses. The prominent signs of this disease, signs indicating early death, were tumorous outgrowths at the roots of thighs and arms and simultaneously bleeding ulcerations, which, sometimes the same day, carried the infected rapidly out of this present life.

The Byzantine emperor, John VI Kantakouzenos, wrote his own account of the plague of 1347, in which his youngest son died:

[Some] died the same day, a few even within the hour. Those who could resist for two or three days had a very violent fever at first, the disease in such cases attacking the head; they suffered from speechlessness and insensibility… In others, the evil attacked not the head, but the lung, and forthwith there was inflammation inside which produced very sharp pains in the chest… Sputum suffused with blood was brought up and disgusting and stinking breath from within… Black blisters appeared. Some people broke out with black spots all over their bodies… Great abscesses were formed on the legs or the arms, from which, when cut, a large quantity of foul-smelling pus flowed… Some, by treating others, became infected with the disease. It caused great destruction and many homes were deserted by their inhabitants… No words could express the nature of the disease. All that can be pointed out is that it had nothing in common with the everyday evils to which the nature of man is subject, but was something else sent by God to restore chastity…

The terror of this dreadful disease infuses those words. It was a disease that caused death and destruction on a scale that was unimaginable, and there was no cure. The detailed descriptions of the effects of this pandemic, from these authors and many others, led many modern experts to believe that the fourteenth-century Black Death was the same as the bubonic plague seen in the nineteenth and twentieth centuries, caused by Yersinia pestis. But other possibilities had been suggested at various times, based on contemporary accounts of the nature of the disease; these potential alternative diagnoses included anthrax, typhus, TB and haemorrhagic fever.

The controversy could not be resolved until advances in archaeogenetics provided a means for direct, precise diagnosis. In 1998, a team of French scientists from the French National Centre for Scientific Research and the University of the Mediterranean in Marseille published the first attempt at molecular detection of the plague pathogen in archaeological human remains. They were looking at skeletons from two mass graves in Provence, southern France, historically recorded as burial grounds for bubonic plague victims from quarantine hospitals. One grave in Lambesc contained the remains of individuals buried in the summer of 1590, and the other, in Marseille, contained victims from an outbreak of plague in 1722.

The team chose to take samples from the dental pulp of unerupted teeth – from juvenile remains in each grave – reasoning that this would be the most likely tissue to preserve DNA from any systemic pathogen, and the least likely to be contaminated with DNA from any external sources. They extracted four teeth from two skeletons from the Lambesc mass grave, and eight teeth from three skeletons in the Marseille grave. They cracked each tooth open along its length, in order to access the pulp cavity inside, which in a living tooth contains connective tissue, blood vessels and nerves. They scraped the remnant of these tissues into sterile tubes, then set about extracting DNA and amplifying it using a standard PCR technique. Then they sequenced the DNA and looked for matches with published sequences of DNA from modern Yersinia pestis. They applied the same procedure to seven ‘control’ teeth from a medieval cemetery in Toulon, where there was no known historical link to any plague outbreaks.

The results for the control teeth were negative. But in two of the four teeth from Lambesc, and four of the eight teeth from Marseille, the researchers found a sequence matching a specific gene in Yersinia pestis. It was the first time that a molecular diagnosis of plague had been made using archaeological remains, confirming that the epidemics hitting France in the sixteenth and eighteenth centuries were indeed caused by Yersinia pestis.

But what about the fourteenth-century Black Death? Two years later, the same French lab published its results on DNA from dental pulp of a child and two adults from a cemetery in Montpellier in southern France. This cemetery had been in use from the ninth to the seventeenth centuries, and 800 graves had been excavated across the site. Amongst those graves were four that had been dug into an embankment, beneath a wall dating to the second half of the fourteenth century. Fourteenth-century Montpellier was hit hard by the Black Death, with the initial surge in 1348 followed by several more waves in the 1360s through to the 1390s. The population was decimated, falling from around 9,500 households in 1348 to just 1,000 by 1379. The four graves in the bank contained multiple burials, with no evidence for shrouds – it seemed likely that they represented catastrophic deaths. In one grave, the skeletons of an adult man, an adult woman and a child aged between eight and ten years old were found. The archaeogeneticists took ten teeth from the man’s skull, nine from the woman’s and four from the child’s. Once again, they used other teeth from medieval graves in Toulon as controls. They used the same technique they’d employed in their previous project, employing DNA primers to lock onto a specific Yersinia pestis sequence, and then amplifying any DNA binding to the primers using PCR. They also used primers for two other pathogens: typhus (Rickettsia prowazekii) and anthrax (Bacillus anthracis).

The results were clear: there was no DNA from R. prowazekii or B. anthracis in any of the samples, and the control teeth contained no Y. pestis DNA. But one of the child’s teeth and all nineteen teeth from the adults from the Montpellier grave yielded a positive signal. The DNA sequence that the researchers had looked for was very specific – it was only found in Y. pestis, and not in any of the other closely related species of Yersinia that had been discovered in the twentieth century. The DNA sequence from the child’s tooth was identical to that of the modern Y. pestis; in the adult teeth, there was a slight difference, a single mutation.

Finally, DNA analysis had proven that the Black Death was caused by the plague pathogen, Yersinia pestis. And yet, not everyone believed it. A team of English researchers sought to replicate the results reported by the French team. They sampled teeth from five different mass graves associated with plague outbreaks, and found no evidence of Yersinia pestis at all. They concluded the French researchers’ samples must have been contaminated, and so the question remained unsettled for a few more years. Meanwhile, ancient DNA technology advanced, with new techniques being developed for extraction and sequencing, and more labs started to tackle the conundrum. In 2011, an international team including researchers based in Canada, the US and Germany published an entire reconstructed genome of Yersinia pestis, sequenced from samples obtained from the East Smithfield burial ground in London – a specific cemetery for plague victims, opened in late 1348 or 1349. The debate was finally settled, and more genomic data began to pile up. As aDNA was recovered from more and more mass burial sites across Europe, it showed that most of these were the graves of plague victims. And it wasn’t just the fourteenth-century and nineteenth-century pandemics that were demonstrated to be caused by Yersinia pestis. After the peak of infections and mortality represented by the Black Death, Europe suffered regular outbreaks – caused by the same pathogen – for four centuries.

Once Yersinia pestis was identified as the causative pathogen of the Black Death, it quickly became clear that the same bacterium had been responsible for even earlier ‘plagues’. Evidence emerged that the first historically attested pandemic – starting with the Justinianic Plague, which swept through the Byzantine Empire in the sixth century, with outbreaks continuing into the eighth – was also caused by Yersinia pestis.

Having reliably associated Yersinia pestis with the plague, by taking samples from mass graves matching the time and place of historically attested outbreaks, geneticists could spread the net wider and show how plague reached places that were not even documented at the time. A large study of sixth-century burial grounds across Europe included one from England, Edix Hill in Cambridgeshire, and revealed that individuals interred in multiple graves there carried the unmistakable genetic trace of Yersinia pestis. So we now know – from genetics, not history – that the Justinianic Plague reached Britain.

When I came across this evidence of Y. pestis at Edix Hill, I wondered if there might be traces of the pathogen to be found at a cemetery I worked on in the early 2000s: Breamore, in Hampshire – a site I wrote about in Buried. Just like Edix Hill, Breamore had contained many double burials. I contacted Pooja Swali in Pontus Skoglund’s Ancient Genomics Lab at the Crick Institute to see if she might be interested in investigating – and she was. In 2021, her colleague Tom Booth managed to track down the skeletons in a Hampshire museum and took samples of bones and teeth. Pooja then attempted to extract DNA – but it was a very difficult process. The remains were extremely fragmentary and crumbly; Pooja warned me right from the start that the DNA preservation may be too poor to permit analysis. She kept me updated through 2022, but it seemed very unpromising. The DNA was in as bad a shape as the bones themselves. But Pooja had one final trick up her sleeve: DNA ‘capture’ – using a probe to look specifically for traces of Y. pestis DNA; to ‘go fishing’ as she put it. I kept my fingers crossed and, in April 2023, Pooja emailed me with exciting news. Despite the samples being so poorly preserved, her capture technique had worked, and she had, remarkably, managed to pull out something – from the skeletons in trench seven. There were fewer than 3,000 sequence reads, but these could be the last remaining fragments of pathogen DNA. Being very cautious, it’s possible – if not definite – that Yersinia pestis is present in these remains after all.

The large Europe-wide study of the First Pandemic – the Justinianic Plague – had suggested that ‘otherwise broadly typical cemeteries where multiple burials are relatively frequent are indeed a good indicator for epidemic events’. I’d suspected that Breamore could be another plague cemetery – and Pooja seemed close to providing genetic confirmation. There will undoubtedly be other cemeteries containing victims of that sixth-century pandemic right across Britain.

We’re now at a point where the three major pandemics recorded in history have been shown to have been caused by the same pathogen: the First Pandemic, starting with the Justinianic Plague in the sixth century; the Second Pandemic, beginning with the scourge of the Black Death, with recurring waves following through the centuries, including the Great Plague of London in 1665; and the Third Pandemic, starting in China in the mid-nineteenth century and spreading around the world. All of them have now been genetically proven to have been caused by Yersinia pestis. And the genetic data allows us to track the extent of those outbreaks further than the historical documents reach. We can also see how the bacterium evolved over time.

Before the genomic breakthrough, some researchers who had favoured Yersinia pestis as the most likely causative agent for the Black Death – and for the sixth- and nineteenth-century pandemics as well – had suggested that each of these may have been caused by a different variant of the pathogen. They’d even given those strains putative names: Antiqua, Medievalis and Orientalis, connecting them with modern variants. The genomic data added much more detail, superseding the simple story of ‘three variants: three pandemics’, as geneticists began to be able to track evolving lineages over time. The similarity between Y. pestis genomes across Europe in the fourteenth century suggested that the Black Death had entered Europe as a single wave. Smaller waves in subsequent centuries showed some diversification, with two main sister lineages forming. One of these lineages persisted in Europe up until the eighteenth century, when it then went extinct. The other spread back to Asia after the Black Death, and eventually formed the source of the Third Pandemic, emerging in the Yunnan province of China as early as the eighteenth century, following a huge expansion of urban populations as rural workers moved to cities. An important and evocative record of the outbreak of plague comes in the form of a poem written in the 1790s by the poet Shi Daonan, The Death of Rats:

Rats die in the east,

Rats die in the west.

People look upon the dying rats

As if they were tigers.

A few days following the death of the rats,

People die like city walls.

Do not ask how many people die,

The dim sun is covered by gloomy clouds…

The dead litter the ground,

Traces of human habitation diminish.

More epidemics broke out in Yunnan in the second half of the nineteenth century, following the upheaval from a civil war between Qing troops and Muslim separatists. Chinese officials seemed to believe that the outbreak had originated in Burma or Tibet. From Yunnan, the plague would spread to Guangdong and on to Hong Kong, where Yersin first identified the plague pathogen. From there, it spread around the world, helped on its way by steamships and railways. This Third Pandemic would seed new foci in Africa and the Americas, which are the sources of continuing outbreaks to the present day.

This most recent plague pandemic is certainly not remembered in Europe in the way that the fourteenth-century outbreak of the Black Death still is: as an unmitigated disaster. Unlike the cholera pandemics of the nineteenth century and the great flu pandemic of 1918, Europe escaped relatively lightly in the Third Pandemic. That’s prompted some to suggest that the pathogen itself had evolved to become significantly less virulent by the nineteenth century, but as reports from Hong Kong revealed, the disease was estimated as killing more than 80 per cent of those infected – before the introduction of treatment.

Going back to the First Pandemic, the original source of the Justinianic Plague remains somewhat elusive. But it seems unlikely – looking at the relationship between genomes of Y. pestis in different places – that it started in Africa (as the contemporary Syrian scholar Evagrius Scholasticus suggested). A potential overland route from Central Asia, where a basal strain of this outbreak has been identified, has also been put forward. But the current data makes it somewhat more probable that the infection turned up in the Byzantine Empire on ships arriving from India. The picture should become clearer as more data comes in. After the Justinianic Plague of 541–544, waves of the disease continued to roll across Europe and the Mediterranean region for another two centuries.

The ability to genetically diagnose this disease means that we can spot it in places where we have no historical data, such as sixth-century Britain. But it also means that we can go further back, before any historical records. One of the astonishing revelations that has emerged in just the last few years is that Yersinia pestis was infecting humans thousands of years before the ‘First Pandemic’, going right back into the Late Neolithic and Bronze Age.

Genetic analyses have also solved the puzzle of where Yersinia pestis itself came from – and when. There were suggestions in the past that Y. pestis evolved in rodents – potentially millions of years ago – before making the jump to humans. But then geneticists came along and looked at the degree of difference between the genome of Y. pestis and the closely related Yersinia pseudotuberculosis, which lives in certain worms and can persist in contaminated soil for months. In animals, Y. pseudotuberculosis causes a tuberculosis-type disease (hence its name), with inflammatory nodules appearing in the spleen, liver and lymph nodes. In humans, it causes fever and inflammation of lymphoid tissue in the mesenteries – the membranes supporting the intestines – with accompanying abdominal pain. After a few weeks, it usually clears up on its own, without treatment. But at some point, an ancient strain of Y. pseudotuberculosis evolved to become much more virulent, transforming from an enteric (gut) pathogen into a blood-borne pathogen: Y. pestis. In 1999, based on the differences between the two pathogens’ genomes, geneticists suggested that they could have diverged some time between 1,500 and 20,000 years ago. That’s a very big window. But once Bronze Age Y. pestis was identified and sequenced, it became possible to date the divergence more narrowly – to around 6,000 years ago. We know that there were large population movements during the Bronze Age, with, in particular, a large expansion, both eastwards and westwards, of hunter-herders from the Pontic–Caspian steppe. It’s very possible that these migrations helped to spread the plague across Eurasia.

When the first Bronze Age Y. pestis genomes were sequenced, they were found to be lacking a key gene called ymt. This gene seems to be linked to a propensity for the bacteria to clump together and block a flea’s gut. This makes the flea hungry on the one hand, and also means that it is more likely to vomit Yersinia bacteria into the bloodstream of a host they are trying to bite. It’s thought likely that this key change in the Y. pestis genome facilitated easy transmission between rats and humans, via fleas. Those early genomes were also missing another important variant called pla (plasminogen activator), which seems to switch Y. pestis from being a pathogen that primarily affects the lungs – causing pneumonic plague – to being a disease that becomes more systemic, attacking the lymphatic system and turning lymph nodes into pus-filled swellings – the hallmark of bubonic plague.

Studies found the ymt gene to be missing from Bronze Age genomes but present in later Iron Age samples, suggesting that this crucial genetic change could have happened around 3,000 years ago, making Y. pestis more virulent and transmissible. Nevertheless, it was postulated that the ymt-free version of Y. pestis would still have been able to cause pneumonic and septicaemic, if not bubonic, plague, and could still have contributed to a population decline in Europe in the late fourth millennium BCE. Further research, however, uncovered evidence of Y. pestis genomes containing the crucial ymt variant in the Bronze Age, and the earliest evidence of ymt currently comes from a burial dated to 3,800 years ago, in Samara in Russia. The researchers who identified it concluded that the genetic change itself originated as early as 5,000 years ago. So, it now looks as though there were different variants of the plague pathogen circulating in Europe and Asia in the Bronze Age, with the more virulent, flea-adapted version representing a source for the lineage that would go on to produce the three historical pandemics.

An even more recent study led to the identification of Y. pestis in a 5,000-year-old skeleton. In 1875, an amateur archaeologist called Carl George Count Sievers had excavated a shell midden – a great pile of mussel shells and fish bones – at Rinnukalns, on the banks of the River Salaca in Latvia. The midden contained two burials: that of a man in his twenties, and an adolescent. Sievers thought the burials to be prehistoric, but few believed him at the time. The crania from the burials were sent to Berlin, to be analysed by the famous physician and pathologist Rudolf Virchow, who produced a report on them in 1877. But then the skulls disappeared – until 2011, when they were rediscovered in Virchow’s anthropological collection. This sparked renewed interest in the original site at Rinnukalns, and new excavations revealed two more burials: this time, an adult male and a neonate. And it looked like Sievers had been right all along: the stratigraphic layers containing the graves appeared to be prehistoric. Then came confirmation through radiocarbon dating: the four skeletons dated to between 5,300 and 5,050 years ago. They came from a relatively settled community of hunter-fisher-gatherers, and had been buried in the remains of their diets.

The new research on the Rinnukalns burials included aDNA analysis – and that incorporated screening for pathogens. This is when it was discovered that one of the male individuals had been carrying Y. pestis. It was an unusual strain, not directly related to later Neolithic and Bronze Age variants. Like most of the other early prehistoric examples, this lineage lacked the ymt variant. It was calculated to have diverged from all those other strains around 7,100 years before the present day – and from Y. pseudotuberculosis 7,400 years ago. So, this pushed the origin of plague back even further into prehistory.

This is a story that has only emerged since the dawn of archaeogenomics, and it’s completely changed the way we understand plague. We still talk about the ‘three pandemics’ of the last 2,000 years, but we’re seeing evidence of many other, earlier outbreaks, some of which may also have been geographically widespread. Plague is an ancient pestilence that has been with us for thousands of years.

The earlier date for the emergence and spread of the plague pathogen, between 7,000 and 5,000 years ago, also changes how we interpret its impact. Previously, the prehistoric emergence of plague was postulated to be linked to a population decline in the later stages of the Neolithic. But these earlier dates mean that plague was taking hold at just the time when the Neolithic revolution – including a fundamental shift in subsistence from hunting and gathering to farming – was unfurling across Eurasia. We know from studies of human genomes that this involved large migrations as farming populations expanded into what had previously been hunter-gatherer territory. Early farmers across Europe contain traces of Anatolian ancestry, linking them back to the first farmers of the Fertile Crescent, although this is actually not the case in Latvia, where Neolithic farmers seem to be descended from local Mesolithic hunter-gatherer populations. Nevertheless, the spread of these ideas was mediated by people moving around, perhaps linked to increased trade between populations. And with the exchange of goods and ideas came the exchange of pathogens as well. This early plague, not yet adapted to being spread by fleas, was spreading with the Neolithic itself – possibly transmitting via other parasites, including human lice.

The spread of the Neolithic across Europe was followed, from around 5,000 years ago, by an expansion of a population from the Eurasian steppe. These people were mobile pastoralists: they had domesticated horses, for the first time, and moved around the landscape with wagons. The Eurasian steppe became a corridor connecting human populations to the west and east, and provided new opportunities for pathogens to spread, between wild animals, humans and livestock.

What we don’t yet know is just how virulent or lethal those ancient strains of Y. pestis were. We now have at least twenty examples of prehistoric individuals with Y. pestis on board, from across Eurasia and spanning several millennia. This evidence could represent sporadic zoonotic events: occasional instances of humans dying from septicaemic plague, perhaps after being bitten by infected animals. But others have suggested that we’re seeing just the tip of the iceberg of a profound, ancient pandemic of pneumonic plague. As more cases come to light, this may be emerging as the more likely scenario.

In 2022, Pooja Swali and colleagues published the earliest evidence of plague in Britain. It took the form of Y. pestis genomes sequenced from teeth of two children interred in a 4,000-year-old mass burial at Charterhouse, on the Mendip Hills in Somerset. The particular strain of the pathogen was close to that identified in Bronze Age burials in Germany; like most of the variants from this period of prehistory, it lacked the ymt gene. It’s also a strain that is found later in Asia. It’s perhaps unlikely to have been transmitted with the help of fleas, but this doesn’t seem to have hampered its spread. ‘While the severity of disease is currently unclear,’ Pooja and her colleagues concluded, ‘the wide geographic distribution within a few centuries suggests substantial transmissibility.’

I caught up with Pooja to talk about this new evidence of prehistoric plague. ‘It’s the first time we’ve seen evidence of Bronze Age plague in Britain,’ she said, ‘and it’s really important because this is the first time we’ve seen plague away from mainland Eurasia. People must have been travelling by boat. We don’t know how sick they would have been, but they’re bringing plague with them. It reminds us that being an island isn’t a protection against the spread of these diseases.’

Pooja also told me that, as well as the Somerset examples, they’d found plague elsewhere in Bronze Age Britain. ‘There’s a double burial from Levens in Cumbria, and we found plague in one of the individuals.’

Finding traces of Y. pestis from two widely separated sites in Britain suggests that the disease was widespread.

‘How virulent do you think it was?’ I asked her.

‘We’re not sure,’ she replied. ‘It’s missing key virulence genes. It’s losing parts of its genome. But on the other hand, we’re using modern-day reference genomes to do our capture. There could be an ancient virulence gene in this genome that we’re not finding. But we do know that this particular clade [group of strains], which is potentially becoming less virulent, is spreading from Germany all the way to Britain, and all the way to central Russia, in the space of just a hundred-or-so years. It’s managed to travel a huge distance. So it could be highly transmissible but causing less severe disease in humans. We don’t yet know how long it sticks around.’

‘Do we know where it came from originally? Where it started?’

‘We don’t know – researchers are finding earlier and earlier strains in Neolithic Europe. From the data so far, the modern-day strains descend from the clade where we first see the ymt gene – which was better adapted to our changing lifestyles.’

Whenever I speak to Pooja, I’ve always been amazed by the revelations coming from archaeogenetics, helping us to understand disease in the past – right back into prehistory – in a way that has simply not been possible before. It’s completely revolutionised our ideas about the plague – from showing that the three historical pandemics, including the Black Death, were all caused by Yersinia pestis, to revealing the prehistoric origins and extent of early plague. And genetics continues to challenge what we thought we knew about this disease. The presence of widespread plague before the emergence of that strain with the ymt gene, and the continuing circulation of non-flea-adapted Y. pestis after that point, has prompted some scientists to question something about our understanding of plague that seemed almost set in stone.

It’s widely accepted that the main route of transmission for historical plague outbreaks was from rats to fleas to humans, with the rodents acting as a natural reservoir for the disease, and the insects facilitating (and performing) the jump to humans. Paul-Louis Simond, working on the Third Pandemic, proved the concept in his lab when he showed that healthy rats could contract plague after being bitten by fleas from infected rodents. The discovery of the ymt gene, which allows plague bacteria to proliferate in flea intestines, fitted perfectly with this idea. But we now have ancient DNA evidence revealing the presence of plague in a whole range of different environments – warm and cold, wet and arid – which strongly suggests it might not all be down to rats and their fleas, after all.

Some scientists have pointed out that we simply don’t have robust historical evidence of rat infestation – or unusual numbers of rats and their fleas – to go along with plague outbreaks. In particular, in Scandinavia, where the Black Death spread extremely quickly and effectively, the implicated black rat, Rattus rattus, was virtually unknown in the Middle Ages. Also missing is evidence of the rat fleas themselves. And another important finding has come from experiments showing that these fleas become incapable of transmitting Y. pestis at low temperatures. While we can be reasonably sure that rats, together with Oriental rat fleas, Xenopsylla cheopis, may have been responsible for the outbreak of the Third Pandemic and its spread to southern Europe, these rodents and their minute minions are in fact unlikely suspects when it comes to the spread of the Black Death across Europe.

Could there have been other routes of transmission in pandemics? The Black Death in particular seems to have spread so fast that it can’t have been propagated by rats and their fleas alone. The speed suggests there must have been human-to-human transmission happening as well. But infection through droplets, causing primary pneumonic plague, is not that common and is relatively ineffective – it doesn’t explain how the medieval bubonic plague could have spread so quickly.

So how about human fleas, jumping from human to human: could they be responsible for some outbreaks? Probably not, it turns out, as they’re just not very good at transmitting plague. The finger of suspicion is now pointing towards, perhaps scratching at, another diminutive arthropod and sucker of human blood: Pediculus humanus – the human louse.

Since the dawn of our species and even before that, humans have had lice. Lice carry several notable infections that they can pass on to their hosts, including trench fever (caused by Bartonella quintana) and epidemic typhus (caused by Rickettsia prowazekii). Studies of historical outbreaks of these two diseases show that they often occur together during the same epidemic, such as the one that wiped out a third of Napoleon’s troops during the failed invasion of Russia in 1812. But there also seems to be an association with plague. The trench fever pathogen, B. quintana, has been found alongside Y. pestis in medieval skeletons from Venice in Italy and Bondy in France, suggesting that the same vector, a human louse, could have been responsible for the transmission of both pathogens. The common sites for buboes, in the groin and armpit, are also favourite hiding places for body lice.

We also have direct evidence of an association between Y. pestis and human lice. Plague-infected body lice were found amongst the clothes of a plague victim in 1914 and on the bodies of patients with septicaemic plague in a 1941 outbreak in Morocco. More recent experiments have demonstrated the potential for lice to carry and transmit Y. pestis to rabbits. But it’s not a completely new idea: in the eighteenth century, a Dutch physicist and microscopist, Nicolaas Hartsoeker, suggested that plague was transmitted by ‘invisible insects’.

The contemporary advice for prevention of plague focuses on avoiding potentially infected animals and flea-bites. Some precautions taken against fleas would also be effective against lice, although fleas tend to bite bare legs, while lice like to hide under cover. The current foci of plague outbreaks may perhaps suggest a role for lice: while plague is extremely rare in high-income countries, even those with plenty of rats, it remains a risk in several low-income countries. Hygiene undoubtedly plays a role – but that goes for both fleas and lice; the same is true of the synergy between war, relocation of refugees and plague.

Based on current evidence, it seems likely that, as well as zoonotic transmission (usually involving fleas), human-to-human transmission (involving lice) is important. We can imagine how rat fleas might kick off an outbreak, which can then spread from person to person via body lice. A study involving computer modelling of the Second Pandemic, which began with the Black Death, suggested that human-to-human transmission was in fact the predominant mode of spread, and that the disease was most likely carried via human ectoparasites – such as fleas – rather than droplet infection. This explains how, despite the lack of animal reservoirs in Europe, the Black Death could still tear through the continent, though it’s possible that it was reintroduced time and time again from persistent rodent reservoirs in Asia, during the Second Pandemic, over some five centuries.

We emerge with a picture much more complex than the simple model of rat-and-flea-mediated plague. We are also starting to understand how the pandemics of the past may have involved outbreaks of multiple pathogens, transmitted in many ways – but with plague, Yersinia pestis, the deadliest of them all.

As well as changing the big picture and the long view of plague, archaeogenetics is also enabling us to look at this pathogen and its impact in a fine-grained way. We can look at the vast sweep of time, over centuries and millennia, and track how pathogens have evolved over time and travelled with humans around the globe, but we can also focus in on how societies responded to those terrifying outbreaks of disease, and look at the impact on communities.

One recent study – once again combining archaeology and genetics – has helped to shed light on how a rural community in England faced up to the dreadful, catastrophic mortality of the Black Death.

We hear about the devastating effects of the Black Death from historical sources, but as we’ve seen, the archaeological evidence has been fairly scarce. (This may prompt us to wonder, perhaps, if we would even have interpreted what little we have as evidence of pandemic, in the absence of the written testimonies.) Documentary sources tell of two large emergency cemeteries in London, for plague victims; one of these, at East Smithfield, has been extensively archaeologically investigated, while small excavations at the West Smithfield site have also uncovered graves of individuals confirmed to be carrying traces of Y. pestis.

The dreadful impact on rural communities is also well documented, but it’s been suggested that mass graves never became necessary in the more sparsely populated countryside. Archaeologically, there hasn’t been any sign of mass graves in rural settings – until one was discovered at Thornton Abbey in Lincolnshire. Hugh Willmott, at the University of Sheffield, led the excavations. It all started with a mysterious mound in the Outer Court of the ruined priory. A geophysical survey revealed a strange, almost rectangular feature buried under the grass of the mound. Was it a later garden feature, the archaeologists wondered? They opened a trench across the geophysical anomaly to investigate it – and immediately began to uncover human remains. What they found was a great mass of skeletons, representing bodies that had clearly all been buried in one event, in a huge communal grave. It took two seasons for the university archaeologists to fully excavate the grave, in the summers of 2013 and 2014.

The bodies had been laid in the grave carefully, individually wrapped in shrouds. A single belt buckle was found; other than that, there were no personal ornaments or fittings from clothes. Part of the mound had been disturbed by later quarrying, which may have damaged a portion of the grave, but the archaeologists still recovered the remains of forty-eight individuals laid out neatly in eight rows. They ranged from children to older adults, and included both males and females, and must have represented a large proportion of the local community.

When a mass grave like this is found, it’s clear that a community has suffered a catastrophic event – and radiocarbon dating of the bones placed that event to the fourteenth century. There are no specific records of the Black Death at Thornton Abbey, but chronicles from the nearby Louth Park Abbey and Meaux Abbey document the scale of mortality. At Louth Park Abbey, ‘obierunt multi Monachi’ – many monks died. At Meaux, only ten of the fifty monks and lay brothers survived, while the majority of the abbey’s tenants also died. Willmott and his colleagues thought it most likely that the initial 1349 outbreak of the Black Death had carried off the individuals buried in the Thornton Abbey mass grave, although they could have succumbed in a later wave in 1361–1362. The archaeologists sent samples from the skeletons to an archaeogenetics lab in Canada to be screened for Y. pestis. They didn’t hold out much hope, as the skeletons were fairly poorly preserved, but the geneticists were able to find definite traces of DNA from the plague pathogen.

The identification of a rural mass grave, in the fourteenth century, with confirmed Y. pestis present is important as it shows that the experience of Black Death in the countryside could – just as in the cities – demand a change in burial practice to deal with a huge spike in mortality over a short time. The site of the grave – near the priory church but separate from the main burial ground – seems unusual. Most of the general community in the area would have been buried in the parish churchyard at the nearby village of Thornton Curtis. Was this churchyard overwhelmed, and so the priory stepped in? Perhaps, but there was another possibility, which is that Thornton Abbey could have included a hospital. There’s just one single reference to a hospital of St James, next to the monastery, in 1322. Further archaeological investigations to the south of the mass grave revealed an unknown building: a stone-built chapel with a brick-built annexe. So, the archaeological work carried out at Thornton Abbey has uncovered not only the first rural Black Death mass grave in Britain, but also the existence of a lost hospital, where those victims of the plague may have spent their last hours. And although they were buried in a communal grave, they were wrapped in shrouds and laid carefully in the ground. In the face of that extraordinary, overwhelming, unimaginable tragedy, there was still some dignity in death.

There’s dignity in the archaeological work carried out on those human remains, too. Investigations such as that at Thornton Abbey add to our understanding of the past, of the impact of pandemics on communities, and the social response to catastrophe. In the next chapter, we leap ahead two centuries to dive into a story emerging from the study of another mass grave – not on land this time, but under the sea.

6. THE ARCHERS OF THE MARY ROSE

The Mary Rose is the stuff of real history and legend: the ship that was lost and found. There are historical truths, hard facts, and then there are the myths that have wreathed themselves around her. She sank in the Solent, in 1545; that is true. She was sailing out on her maiden voyage; that is far from the truth. She was Henry VIII’s favourite ship; as far as we can tell, this seems to have been true. He must have been devastated when she went down. But so must all the families of the sailors and soldiers on board – hundreds of them. Because the Mary Rose was not just a shipwreck, but a mass grave.

I visited the Mary Rose archive back in 2010, when it was housed in temporary stores, before the beautiful new museum opened. Archaeologist Alex Hildred, who had started working on the ship when she was still resting on the sea bed of the Solent, showed me around the stores. There, I saw stacks of beautiful and deadly yew longbows, wooden bowls and spoons, tankards and gaming dice. And laid out on long tables were some of the skeletons recovered from that watery grave.

The bones of the men who went down with Henry VIII’s warship are very well preserved, having been entombed for centuries in the anaerobic silt of the Solent. Most are pale-cream-coloured, some even purer white. A few are remarkably different, stained russet-brown, like mahogany. These are the bones that came to lie close to cannons in the wreck, becoming infused with iron oxide, turning rust-red. Most of the bones are complete, not fragmented, and every detail is sharp and clear. They’re a gift to an osteoarchaeologist, and over the years, more and more clues have emerged from these bones – about these men who went down with the ship, allowing us to see them more clearly as individuals, and to learn about their way of life. And when I saw some of those bones in 2010, I knew that there were still more secrets to be unlocked.

The Mary Rose is such an iconic archaeological entity: a Tudor time-capsule, lying beneath the waves for 437 years, then saved, miraculously, from the sea bed. I avidly followed the rescue operation on television in 1982, tuning in to the tea-time children’s magazine programme Blue Peter to see the drama unfold. I’d seen archaeologist Alex Hildred surfacing from a dive to talk to the cameras about the wreck. I’d heard Project Director Margaret Rule describing her ambitious plan to raise the remains of the ship. I was entranced by the whole thing: the engineering challenge, the archaeological narrative, the formidable women at the helm. For the nine-year-old me, the raising of the Mary Rose wasn’t just about ancient history, it was about what was possible. Because, eventually, on 11 October 1982, the seemingly impossible was achieved and the Mary Rose rose: dripping, in a great yellow steel cradle, from her watery tomb, as all around ships’ sirens sounded to herald her return.

To get to this point, the steel lifting-frame had been lowered over the wrecked hull of the Mary Rose as she lay on the sea bed. The frame was supported on four legs that were inserted into holes prepared, by the army’s Royal Engineer divers, around the wreck. The frame had eleven cross-beams, corresponding with the eleven strongest points on the hull. Level with these beams, tunnels were dug under the wreck to place back-plates on the bolts to which cables would be attached – and these cables were attached to the cross-beams of the frame above. The first stage of the raising of the ship then began: the legs were jacked up, very slowly, to tension the cables, and then, inch by inch, the Mary Rose was lifted up from the sea bed. Now the wreck was hanging from the lifting-frame, and the job of raising the wreck to the surface of the sea passed to a crane mounted on a barge, the Tog Mor. This floating crane – more usually employed in laying pipes on the sea bed – was perfect for the underwater engineering challenge. The crane had already been busy, lowering a steel cradle onto the sea bed close to the Mary Rose. And now it was used to lift the wreck up and transfer it across onto the cradle. The four legs of the lifting-frame – each guided by a diver – were lowered into sockets on the cradle. Once the lifting-frame was locked onto the cradle, the Tog Mor crane could start to winch up the whole contraption, with the Tudor ship enclosed inside it.

But once the hull had surfaced, there was a terrible heart-stopping moment: with a huge, rending crash, the cradle half-collapsed. A crucial pin had sheared through. The onlookers were aghast: was the Mary Rose about to sink for a second time? Was the hull now fatally damaged? Anxious moments passed as checks were carried out. The lift was paused completely and more water was pumped out from inside the hull. There was a huge collective sigh of relief as it was announced that the Mary Rose was still safe. Slowly and cautiously, the winch started to turn again, and the ship, in its cradle, was lifted out of the water.

The skeletal hull of the Mary Rose was transferred across to a barge, which brought her to the dockyard at Portsmouth. Thousands of people had congregated, pressed up against the harbour walls to catch a glimpse of the ship as she came in. Margaret Rule turned to the cameras documenting the event and announced, ‘She was ours when she was down there, but now she belongs to everybody.’

Hundreds of sailors and soldiers died when the Mary Rose went down in the Solent on 19 July 1545.

The warship had set sail from Portsmouth that afternoon, as part of the fleet dispatched to defend the English coast from an attack by the French. Despite a strangely persistent myth that the Mary Rose sank on her maiden voyage, she was in fact a venerable veteran by this time. Her story began thirty-five years earlier, when she, together with her sister ship, the Peter Pomegranate, was built in Portsmouth, as Henry VIII began to create his brand-new navy.

The two ships were launched in the summer of 1511, christened with names that wove together religious and royal allusions. The rose symbolised the Virgin Mary; the recitation of prayers to Mary being known as a ‘rose garden’ – a rosarium or rosary – with the string of beads used as a handy mnemonic for those prayers taking the same name. But the rose was also a symbol of the Tudors, so it neatly stood for the king as well. In the same way, paired up with St Peter, the pomegranate was a recognised Christian cipher and an emblem of the papacy, but the fruit was also the symbol of Henry VIII’s first wife, Katherine of Aragon. (When Henry divorced Katherine, the ship would become known as simply Peter; the link with an ex-wife and the papacy would have stuck in the throat.)

Both ships were carracks: four-masted ships following a state-of-the-art Portuguese design. They represented a shift in form and function: where earlier warships were mainly for transporting troops, these new carracks were designed to take the battle out onto the high seas – they were weapons of attack. Carracks were built to ride low in the water, with a deep draught, but they had high castles built up at the front and back (fore and aft if you’re a sailing type). Those castles were useful for jumping off onto other ships. But – and this is very pertinent to the story of the Mary Rose – they meant carracks could be cumbersome in high winds.

Mary was much larger than her sister ship, Peter; she weighed in at 600 tons compared with Peter’s 450. And unlike the Peter Pomegranate, the Mary Rose was designed to carry heavy guns. A lot of heavy guns.

Over the course of his reign, Henry VIII threw money at shipbuilding and also invested in a permanent, standing navy – England’s first. Previous monarchs had relied on requisitioning merchant ships as and when they needed them; various ports held charters that came with a feudal obligation to provide ships for a king when he asked for them. But requisitioning merchant ships was not a sustainable strategy in politically-volatile sixteenth-century western Europe – especially for a particularly belligerent king – and neither was it overly popular with merchants.

When Henry ascended to the throne in 1509, there were just five ships in his fleet. Over the next four decades, he built another forty-seven, acquiring thirty-five more on top of that during various naval exploits. Portsmouth became the base for the expanding new English navy, and the burgeoning fleet wasn’t just for show. The navy was to see plenty of action, and the Mary Rose and Peter Pomegranate would be right in the heart of it.

Back in the fourteenth and fifteenth centuries, Edward III and then Henry V had captured swathes of southwest and northern France, but these territories had later been lost. In the early sixteenth century, the dominant political powers in western Europe were the Holy Roman Empire – extending across Germany, Italy and the Low Countries – and France. Just two years into his reign, the nineteen-year-old Henry VIII decided, against the advice of his councillors, and perhaps inspired by his forebears, to go to war with the neighbours across the Channel. Like his predecessors, Henry had taken the title of ‘King of England and France’, and he was extremely keen to recapture the parts of that land across the Channel that had once been English property.

Meanwhile, the War of the League of Cambrai was rumbling on. This was a conflict that lasted from 1508 to 1516, with various western European powers coming together, in shifting alliances, to fight over territory in northern Italy. In 1512, England joined the fight, siding with Spain, the pope and the Holy Roman Empire – against France. It would be the first test of Henry VIII’s new navy; the Mary and the Peter were amongst seventeen ships assembled as a fleet to attack the French. The admiral of the fleet, Sir Edward Howard, chose the Mary Rose as his flagship. She may not have been the largest ship – that was the thousand-ton Regent – but she was one of the newest. Howard had spent the summer of 1512 profitably, menacing fishing boats and merchant ships in the Channel, and attacking towns along the coast of Brittany, taking French ships where he could. Gradually, the French were getting their act together and assembling their own fleet to fight back. By 6 August, Howard had heard that the French fleet was gathered at Brest – and he set sail to meet them.

The French were clearly not expecting an imminent attack. On 10 August, they were busy celebrating the Feast of St Lawrence, having invited local luminaries and their families on board the ships for the party. When the English fleet arrived, most of the French ships rushed to escape, leaving two large vessels, the Grand Louise and the Cordelière, to face the enemy.

The Mary Rose led the attack, firing her guns at the Grand Louise, toppling the mainmast and killing 300 men. This was the dawn of a new era for battles at sea: rather than ships fighting at close quarters, these massive guns could critically impact an enemy ship at a distance. The battle went on, with the Regent attacking the Cordelière. It was looking as though the English would take the French ship – troops had started to board her – when a fire on the Cordelière spread to the powder magazine. A massive explosion engulfed both ships, killing over a thousand men.

Over the next few days, the English gained the upper hand, burning twenty-seven French ships, capturing five and taking hundreds of prisoners. On his return to England, Edward Howard would be warmly congratulated for his efforts, handsomely rewarded and promoted to Admiral of England.

It was the following spring that the Mary Rose would prove her prowess. In a brief interlude between naval battles with the French, Howard tested his fleet, lining them up and ordering them to race along the Kent coast. The Mary Rose finished half a mile in front of the next fastest ship, the Sovereign; the rest lagged more than 3 miles behind. Howard, on board the Mary Rose, wrote to the king on 22 March 1513 with this slightly garbled praise for the ship: ‘Sir, she is the noblest ship of sail [and] great ship at this hour that I trow be in Christendom.’ It’s clear from this letter that Henry VIII was taking a keen interest in the performance of his ships. Howard writes, ‘I beseech your g[race not to be] miscontent that I make so long a matter in writing to you… but that you commanded me to send your grace word how every ship did sail.’

The fleet would be kept busy for the rest of that year and into the next, battling it out with the French in the Channel and chasing them back to Brest. In fact, Edward Howard himself would be killed during one of these attacks, and he was succeeded as admiral by his brother, Thomas Howard. The last attack on the French during this war took place on 14 June 1514, and the newly appointed Admiral Howard wrote from the Mary Rose to describe the action, including landings on the Normandy coast to burn the land and houses for several miles around Cherbourg.

Diplomatic efforts were also taking place and, later that summer, Cardinal Wolsey managed to successfully negotiate a peace treaty with France. Part of the deal involved Mary, Henry VIII’s younger sister, marrying Louis XII of France – thirty years her senior.

Following the ceasefire, large warships suddenly became unnecessary – and expensive to keep. Most of the fleet – including the Mary Rose – was decommissioned. She was stripped of her masts, rigging, anchor and munitions. In 1520, she was briefly back in service, leading the fleet to take Henry VIII to Calais for a regal tournament and summit meeting with Louis XII’s successor, Francis I, to celebrate the new peace treaty signed two years earlier. The ostentatious meeting was an opportunity for the two kings to publicly declare their commitment to peace, while demonstrating their military capabilities. And it was also a demonstration of wealth so glitteringly magnificent that it became known as the Field of the Cloth of Gold. The pageantry, power and riches on display at this meeting awed everyone present. But the rapprochement between England and France was to be short-lived, as Wolsey soon fixed up an alliance with the Holy Roman Emperor, Charles V – pitting England against France once again. Charles V visited England in 1522 and Henry VIII gave him a personal tour of what had become his favourite ship, the Mary Rose. Skirmishes with the French, and their Scottish allies, continued for a few years until peace broke out once more in 1525 and the Mary Rose was mothballed again. She was kept at Deptford and then Portsmouth, undergoing maintenance and repairs.

But once again, peace would be temporary. Finding himself without a male heir, Henry VIII had begun to explore other options, and another potential wife. He’d asked the pope to annul his first marriage to Katherine of Aragon, but there was a complication: the pope was being detained at the pleasure of the Holy Roman Emperor, Charles V. And Charles V was Katherine’s nephew. Henry VIII eventually came up with a radical solution to this problem: if the Church would not annul his marriage and release him, he would leave the Church. It was a politically and economically attractive proposition too: cutting off the flow of funds from English dioceses to the centre in Rome, and denying Rome political power in England.

In 1534 – a year after he’d gone ahead and married Anne Boleyn – Henry passed the Act of Supremacy, declaring himself head of the Church in England. He was still a Catholic, but a Catholic who no longer recognised the ultimate authority (on earth) of the pope. Splitting with the rest of Catholic Europe in this way was bound to cause ructions. Henry VIII needed his navy back, and fast. And it would need to be bigger and better than ever.

The Mary Rose and the Peter Pomegranate were amongst several ships that underwent significant renovations between 1536 and 1538. The historical accounts of the work carried out on the Mary Rose are incomplete, but once the ship was lifted, the archaeologists could see the evidence of the modifications. The hull was strengthened and extra gunports created. Before the refit, she would have carried seventy-seven guns, including six large, anti-ship cannon. Afterwards, she’s recorded as carrying ninety-one guns, including twenty-six large, anti-ship cannon. The heavy cannon were emblazoned with both the Tudor rose and fleur-de-lis – the royal insignia of the king of England and France. The Mary Rose was now packing impressive firepower – historians have called her the ‘Dreadnought of her day’. But it’s likely that these alterations made her less seaworthy. A letter from the Vice Admiral, John Dudley, to the king in April 1537 noted that some of the ships in the fleet were ‘unweatherly’. He mentioned in particular ‘the ship that Mr Carew is in’. Unfortunately, the ship itself is not named, but we know that eight years later, when the Mary Rose sank, the captain was George Carew. It seems reasonable to assume that the Vice Admiral may have been referring to the Mary Rose in his 1537 report, even if we can’t be absolutely sure.

In 1539, the Mary Rose was anchored in the loop of the Thames that embraces the Isle of Dogs, ready to defend London against any maritime invasion from Catholic Europe. But the anticipated invasion never came. Meanwhile, Charles V and Francis I had fallen out again, and now Charles V seemed willing to overlook Henry VIII’s break with Rome – if the English king would join him to attack France once again. An alliance was formally agreed in early 1543. Some historians have suggested that the 51-year-old king may have been keen on the opportunity to prove his warrior status, and perhaps distract people from the unfaithfulness of his fifth wife. But his motive for joining the war was probably less personal and more political: he was being presented with the opportunity to team up with an old ally and mend some of the rift with Europe. Henry was also in the unusual position (for him) of having plenty of funds to fight a war, thanks to the recent Dissolution of the Monasteries bringing in a rich harvest of cash.

Henry VIII turned first to attacking the allies of the French in the north: the Scots. He was late joining the war on the continent, but in 1544, the English fleet – with Henry VIII on board – sailed across the Channel to lay siege to Boulogne. By September, English forces had taken Boulogne – just as Charles V turned around and signed a peace treaty with the French. Henry had been abandoned by his ally on the continent. And now Francis I began to prepare for retaliation by gathering together a huge armada of over 200 ships. The English Lord Admiral, Viscount Lisle, sent a small fleet over to Le Havre to burn the French ships, but this did not stop the French armada crossing the Channel. On 12 July 1545, led by Admiral Claude d’Annebault, the French set sail for Portsmouth, where the English fleet, some eighty ships – including the Mary Rose – were gathered. And this time, the English were caught out. Henry VIII was actually having dinner on one of the ships when the French were spotted. A letter written just days later by François van der Delft, ambassador to the Holy Roman Emperor, Charles V, records the moment:

… On the following day, Sunday [19 July], whilst the King was at dinner on the flagship [the Henry Grace à Dieu, also known as the Great Harry, not the Mary Rose this time], news came that the French were only five short leagues away. This turned out to be true, for within two hours their fleet in great force was seen… and the King hurriedly left the flagship. The English fleet at once set sail to encounter the French, and on approaching them kept up a cannonade against the galleys, of which five had entered the harbour…

Henry VIII, safely back on dry land, watched from Southsea Castle as the French galleys advanced under oar in the Solent, firing their heavy bronze cannons at the English, while the English returned fire – though little damage was caused to either side. It seems the wind dropped and the English ships were stuck. In the afternoon, though, the wind picked up, filling the sails of the English warships – with the Mary Rose in the lead. And now they advanced to attack the French.

The Mary Rose fired at the French – probably from her starboard side – then went to turn around to take aim with her other guns. But she turned too tightly, too fast, heeling over. And suddenly, it was all over. With her starboard gunports still open, water rushed in – and in moments, the Mary Rose, just a mile offshore, was sinking.

This is the version of events described by the imperial ambassador, van der Delft, as well as by the herald and chronicler Charles Wriothesley (the son of Thomas Wriothesley, who wrote about the burning of Becket’s bones). Van der Delft picks up the story:

Towards evening, through misfortune and carelessness, the ship of Vice-Admiral George Carew foundered, and all hands on board, to the number of about 500, were drowned, with the exception of about five and twenty or thirty servants, sailors and the like, who escaped.

Carew went down with the ship, as Wriothesley reported: ‘Sir George Carew, knight, captain… was drowned.’ Like van der Delft, Wriothesley mentions misfortune, but leaves out the bit about carelessness.

A later French account, by Martin du Bellay, would report that the ‘Marirose’ had been sunk by cannon fire, but nothing of the sort is mentioned in the contemporary reports, and the archaeological investigation of the recovered hull hasn’t revealed any signs of such damage, so this seems to be French propaganda.

Perhaps Carew ordered her to turn too sharply. Perhaps a squally gust of wind accelerated her into the turn. Perhaps it was both – a combination of ‘misfortune and carelessness’, as van der Delft had written. The carrack design, the modifications that had added so much weight, and the heavy ordnance she was carrying can’t have helped.

It was certainly a terrible disaster. But the Mary Rose was the only ship lost in this battle. After she sank, the wind dropped again, and the two fleets remained in deadlock in the Solent. The English ships were able to manoeuvre a little, using currents, and they assumed a defensive position that prevented the French from attacking with their larger gunships. The French landed on the Isle of Wight and attempted to seize it, but met fierce resistance. After just three days, with their supplies running low, the French fleet turned tail and sailed back to France. Although the Mary Rose and her crew had been lost, the Battle of the Solent, as it became known, was a victory for the English.

But it wasn’t the last battle that summer. In August 1545, there was another clash between the French and English fleets, just off Beachy Head. Admiral Lisle had beefed up his fleet to a hundred ships and was ready for a fight, but the wind dropped again and the French seemed to lose heart. When the morning of 11 August dawned, the French ships had gone – they had sailed off in the night. And then, the following spring, Henry VIII would sign yet another peace deal with Francis I.

Meanwhile, starting just weeks after she sank, a serious rescue operation was underway to recover the precious wreck of the Mary Rose, and her ordnance, from the bottom of the Solent. It was anticipated that the task would be easy – or, at least, the missives sent to the king were full of positivity and promises. Charles Brandon, Duke of Suffolk, whose duties included protecting Portsmouth, wrote to the Secretary of State, Sir William Paget, on 31 July 1545, to say that the salvage operation would be carried out as soon as possible. He followed this up on 1 August, having consulted with Venetian experts, including free-divers, listing the equipment that would be needed:

First, 2 of the greatest hulks that may be gotten.

More, the hulk that rideth within the haven.

Item, 4 of the greatest hoys within the haven.

Item, 5 of the greatest cables that may be had.

Item, 10 great hawsers.

Item, 10 new capstans with 20ty pulleys.

Item, 50 pulleys bound with iron.

Item, 5 dozen ballast baskets.

Item, 40lb of tallow.

Item, 30 Venetians, mariners, and one Venetian carpenter.

Item, 60 English mariners to attend upon them.

Item, a great quantity of cordage of all sorts.

Item, Symond, patron and master in the foist doth agree that all things must be had for the purpose aforesaid.

So, it seems the plan was to loop huge cables around the hull of the Mary Rose where she lay, on the sea bed, and use two large merchant ships – the ‘greatest hulks’ – to winch up and rescue the wreck. The project was to be overseen by the last item on the list, a man named Symond. Suffolk writes to Paget again on 2 August, keeping him up to date with the plans and saying that the preparations are all in place to attempt the lift the following day.

But it doesn’t go to plan. Suffolk and others write to Paget again on 5 August, starting with some good news: the sails and spars from the Mary Rose have been recovered, and the salvage team have managed to tie three cables to her masts. But that’s as far as they’ve got. On 7 August, Suffolk reports that the lift will be attempted either that afternoon or the following day. Two days later, reports come in that the Italians have broken the ship’s foremast and are changing tack: they’re now planning to drag the wreck into shallower water before they attempt to set it upright and lift it. But then it all goes very quiet – or, at least, no letters survive to record the progress of the salvage operation over the next weeks and months.

On 8 December 1545, the register of the Privy Council mentions a payment to two Venetians ‘for their pains taken about the weighing of the Mary Rose’. But it seems that the attempts to recover the ship itself are then abandoned. After that, we have a scatter of accounts from 1547 to 1549 recording payments to an Italian diver called Peter Pawlo, or Peter Paule, for recovering anchors and ordnance from the Mary Rose. But then in October 1549, Peter Pawle appears again – and this time, he’s a prisoner in the Tower of London. It seems he had been caught trying to make off with some of the guns he’d rescued from the wreck.

And then the memory of the Mary Rose receded. The site of the wreck was forgotten – until almost 300 years later. In 1836, a pair of pioneering divers, John and Charles Deane, were exploring an area of the sea bed where nets of local fishermen were often caught. They found old timbers – and a bronze cannon, which bore a date, 1542, and a name, Henry VIII. The Mary Rose had been rediscovered. Several more guns were lifted – as well as bows and glass bottles and a few human skulls – but then the site was abandoned and forgotten once again, for over a hundred years.

In 1965, the historian and diver Alexander McKee teamed up with the Southsea branch of the British Sub-Aqua Club, embarking on a survey of the Solent specifically designed to locate wrecks, including the iconic Mary Rose. There was a professional archaeologist on the team: Margaret Rule. Their first season was frustratingly devoid of results. Hampered by poor visibility in the swirling, turgid waters of the Solent, the divers came up empty-handed. But the following year, a sonar scan revealed some subtle features in one particular area. Now the divers could focus their attention on this region of the sea bed – and their persistence paid off. In 1970, a Tudor gun was recovered from the site: the Mary Rose had, once again, been rediscovered.

More and more artefacts were uncovered and brought up to the surface, but the ship itself was elusive. Then, late in the 1971 season, the divers found large timbers. Gradually, over the next seven years, they worked to reveal what was left of the hull, and then they could see why the wreck had been so difficult to spot on the sea bed. The uppermost, port side of the hull had completely collapsed, leaving the intact starboard side to be covered over in clayey silt, disappearing from sight, leaving just a few obscure lumps and bumps on the surface – which is what had been picked up by the sonar. But while the enveloping clay may have made the job of finding the wreck difficult, it had preserved almost 40 per cent of the hull, beautifully.

In 1979, the Mary Rose Trust was created, with Margaret Rule as Archaeological Director. And plans began to be laid not just to fully excavate the wreck, but to lift it. Three years later, modern engineers succeeded where the sixteenth-century Venetian salvage team had failed: lifting the hull of the Mary Rose out of the water.

Excavation on the sea bed would continue, recovering everything possible from the site of the wreck, including wooden bowls, bows and even an intact medicine chest. The hull would enter a lengthy programme of conservation work to preserve the waterlogged timbers, and a bespoke museum would be created to contain, preserve and display the precious remains: the great hull together with some 19,000 objects and the thousands of bones from the watery, concealed grave of the Mary Rose – a shrine for the ship and all those who lost their lives when she sank.

The sea-bed-bound grave of the Mary Rose is unusual in so many ways. It is a mass grave, containing the human remains of many different individuals, all killed in the same tragic event. In death, their bones mingled together. Around 9,000 separate bones were recovered from the site of the wreck: a cemetery’s worth. But with the remains settling into the silt of the Solent, it has proven exceptionally difficult to determine just how many men these skeletal remains represent.

The historical documents record varying numbers of crew on board the ship. One source – the Anthony Roll naval inventory of 1546 – states that there were ‘200 sailors, 185 soldiers and 30 gunners’, so a total of 415 men on board the Mary Rose. This is the closest contemporary record that we have, but it was compiled the year after she sank and the number sounds more like a generic idea of the size of the crew that would be expected for a ship of her size and class.

In 1577, the chronicler Raphael Holinshed wrote that, ‘In hir was Sir George Carew, knight, and four hundredth souldioures under his guidyng. There escaped not paste fortie persons of all the number.’ If that 400 includes soldiers, sailors and gunners, then these two sources are in broad agreement – and, indeed, the Anthony Roll inventory may have been Holinshed’s source.

The imperial ambassador at the time of the sinking, van der Delft, put the number somewhat higher, at 500. But in a biography of Peter Carew, the captain’s brother, written around 1575, the number was stated to be 700. This is so much higher than the other accounts, it’s thought to be an exaggeration. But what all the sources agree on is that the vast majority of this crew went down with the ship. It seems extraordinary that so many men drowned, but the upper deck of the ship was covered with netting to prevent boarding by enemies. Tragically, that netting seems to have sealed the fates of many of the sailors and soldiers on board, who simply couldn’t leap overboard as the ship sank.

How many men really went down with the ship? The bones contained within the wreck of the Mary Rose should give us a minimum number, even if some remains ended up scattered across the sea bed. The bones were dispersed through the sediment within the wreck, mingled together. But they were excavated methodically, with their precise location plotted on a grid of the wreck, across four levels – hold, orlop, main and upper decks – and eleven segments through each deck. The bone was remarkably well preserved, and there was very little breakage.

The original report on the Mary Rose skeletons was compiled by osteologist Ann Stirland in 1985. It seems that there was at the time some threat to the completion of the work; in her acknowledgements, Stirland thanked Margaret Rule for ‘having enough strength of character and confidence in my work to fight for the skeletal material to be kept so that my researches could continue’. Stirland pored through the assemblage, attempting to fit bones together into individual skeletons, and counting the numbers of single bones – how many left humeri, how many right femora, how many skulls were in the collection? Her analysis produced a minimum number of 179 people, most of whom were young men. She also documented the injuries and diseases exhibited on the bones. As well as the bone report, Stirland wrote up her results and gave them context in a wonderfully accessible book, The Men of the Mary Rose: Raising the Dead.

The bones have remained above water, above ground, as an important part of the physical archive associated with the Mary Rose. Various other researchers have visited to analyse this important collection over the decades, with one of the latest being Hannah Matthews, who examined the assemblage in the summer of 2020. ‘As soon as I applied to do my master’s in osteoarchaeology, I knew that I wanted to do my placement at the Mary Rose,’ she told me. ‘I’ve always loved the Mary Rose. I love history and the early sixteenth century period in particular. And this skeletal assemblage is unique – we know the exact day that all these individuals died, and the cause of death.’

It might seem that, more than thirty-five years on, there wouldn’t be much left to find out from the Mary Rose bones, but when Hannah started to explore the collection, she realised there were some bones that had been largely overlooked. ‘Ann Stirland was the first person to look at the assemblage in its entirety. All the research that’s been done since then has focused on specific bones or skeletons – particularly what had been defined as the “fairly complete skeletons”. No one had looked at all the “odd bones” in boxes since they were recovered and first analysed. So, I set myself the challenge: I wanted to go through the entire assemblage. It was quite intense – it took eight weeks.’

Hannah had indeed embarked on a gargantuan task, which involved poring over 8,847 bones, many of them in those ‘odd bones’ boxes. ‘As a result, we now have a complete database. I’ve recorded every single element; I’ve sided it; I’ve included the catalogue number.’

This was an incredibly useful exercise in itself, but Hannah had also carried out new analyses on the bones. First, she’d wanted to reassess the minimum number of individuals in the collection, and to do this, she used a technique borrowed from assessment of animal-bone assemblages. Animal bones are rarely discovered in discrete graves, but often co-mingled, with bones from different animals mixed together, in pits. So, you need a systematic way of looking at a collection of jumbled bones.

The technique involved dividing each bone up, conceptually, into individual zones. So, an upper arm bone, or humerus, for example, would be divided into eleven zones – count ’em: one for the head, which articulates with the scapula to form the shoulder joint; one for the tubercles at the neck, where the short scapular, or ‘rotator cuff’, muscles attach; five defined zones of the long shaft of the bone; two for the articular surfaces at the bottom, or distal, end of the bone, which form joints with the radius and ulna bones in the forearm; and two for the prominent epicondyles sticking out of each side of the lower end of the bone – the attachment sites of forearm muscles.

This method of counting fragments representing different zones reduces the potential for counting the same bone twice. At the same time, the method accounts for matched pairs of bones, and this increases the estimate of the minimum number of individuals in the sample. This is hard to appreciate without an example, which Hannah provided in her report. Imagine you have identified 32 left femora and 19 right femora. Using the traditional method, you’d simply end up with a minimum number of 32 individuals. But now imagine you’ve also been able to match up 13 bones from each side as pairs. That means there are 6 right femora that can’t be matched up with their left-sided counterparts, and conversely, 19 left femora that are also unmatched. So, the grand total is: 13 + 6 + 19 = 38. Or more simply – if left-sided bones are L, right-sided bones are R and pairs are P:

Pair-matching can also be carried out with skulls and mandibles. Using the zonation method to ensure she wasn’t double-counting fragments of crania, Hannah’s revised estimate based on skulls alone was 129. But then the pair-matching comes into play – and while 74 mandibles could be matched up with their skulls, 32 could not. So, the grand minimum total comes out at 161. But in the end, it was not skulls but forearm bones – specifically, ulnae – that produced the highest total, taking matched pairs into consideration: there were 110 left ulnae, 107 right ulnae, and – among those – 38 matched pairs. And so, after all that painstaking work, Hannah arrived at a robust grand minimum total of 179, concurring with Ann Stirland’s original estimate.

It’s not too surprising that ulnae were the most commonly represented bones: they are relatively long and fairly robust bones. In contrast, just as you might expect, the least well-represented bones of the body were the smallest: the diminutive carpal bones from the wrist, the phalanges from fingers and toes, then the slightly larger tarsal bones of the foot and the patella, or kneecap. These small bones are the most likely to be scattered and lost as the body decays, and the most likely to be missed at excavation, especially underwater. Having said that, foot bones were more common than hand bones – perhaps, Hannah suggested, because shoes had helped to keep them together.

But Hannah wanted to go further: could she use numbers of bones to ascertain the original number of people on board? It seems like an impossibility – a number lost to the centuries and to the shifting sand and silt of the sea bed. But Hannah knew she could turn to an established anthropological and forensic technique for assessing mixed-up and incomplete skeletal remains. This technique is based on estimating the probability of recovering bones from a site. And that number is not plucked out of the air; it’s calculated by looking at the number of paired bones in the sample.

Taking those ulnae as an example, there were 110 left ulnae, 107 right ulnae, but only 38 matched pairs. This means that there were 72 unmatched left ulnae and 69 unmatched right ulnae. Or, to put it another way, at least 72 right ulnae and 69 left ulnae were missing. These numbers enable us to estimate the probability, ‘r’, of recovering these particular bones. Thirty-eight pairs of ulnae represent 76 matched bones in total. But the sum of the right and left ulnae, at 217, is much higher than this.

In other words, the probability of recovering an ulna is 0.35, or 35 per cent. Then you can turn this around: if there’s a 35 per cent probability of recovering an ulna, and we have 217, this means it’s likely the original number was 217/35x100 = 620. And those 620 ulnae would have belonged to 310 people. A slightly different methodology enables a calculation of the Most Likely Number of Individuals (MLNI) and this comes out at 306, based on the numbers of ulnae. Including multiple elements – different bones – in this calculation brings the MLNI down to 249.

These numbers are significantly lower than the contemporary reports, which suggested that at least 400 men should have been on board. Those same sources tell us that a small number, perhaps around 40 men, escaped drowning. But there’s still a huge discrepancy between 360 and Hannah’s new estimate of MLNI at 249.

Of course, it’s possible that there were more survivors than reported at the time. It’s also possible that some sailors managed to jump clear of the ship – but then drowned. Some bodies may have been scattered from the ship as it sank, and others may have been washed away as the Mary Rose settled and shifted on the sea bed.

A detailed analysis of precisely where the recovered bones were found within the wreck presents a harrowing picture. Even with the movement of bodies and bones that must have occurred in the water, there are clear collections of bones near to ladders and access hatches between the decks – we can imagine the crush as people desperately tried to escape. In her thesis, Hannah suggested that a very large number of bones – more than 1,600 – in one of the segments inside the ship’s sterncastle may represent sailors who were seeking an escape route through this built-up part of the ship – which would have brought them out above the netting spread across the deck, which is believed to have proved fatal for so many. That netting also makes it less likely that bodies were swept away as the ship sank. Perhaps that new MLNI is telling us something important. Because, if there were fewer than 300 men on board the Mary Rose on 19 July 1545, she would have been significantly undermanned. Could this even explain why gunports were left open, as she heeled around? It’s possible that we’re now closer to understanding why this iconic warship sank in the Battle of the Solent.

As well as giving us a clearer measure of the numbers who went down with the ship, and where the bones were distributed in the wreck, this new study reminds us of the importance of holding onto skeletal remains for research, while treating those remains with utmost respect. Methods evolve, new techniques come on line, and there may be information locked away in bones that is not accessible at the time of an excavation but which may emerge decades later.

In 2022, another new study was published, looking at evidence for injuries amongst the skeletons from the Mary Rose. This investigation was carried out by postgraduate researcher Emily Mitchell, and her osteological report formed part of her thesis. She noted that, amongst the objects excavated from the ship, there was a medical chest – discovered in what was presumed to have been the surgeon’s cabin. Amazingly, this chest had survived the sinking intact and still contained nine wooden canisters. One contained peppercorns and another, frankincense, both of which may have been used for medicinal purposes. While wooden objects were almost miraculously well preserved, any metal tended to have rusted away. Eight small wooden handles in the chest may once have held metal scalpel blades or cauterising tools, while a larger handle may have been that of an amputation knife, saw or chisel. There was also a metal syringe and a mallet, both of which may have had surgical uses. Alongside those were other objects: a few razors, five stoneware jars and a whetstone. On their own, those could be interpreted as more ordinary, everyday items, but here they were grouped together in the same chest and were probably all part of the ship surgeon’s kit.

By examining the bones for signs of pathology, Mitchell hoped to identify some of the diseases and injuries that the Mary Rose’s surgeon may have had to deal with. Mitchell reviewed the bones belonging to previously identified ‘fairly complete skeletons’, relating to ninety-two individuals. Wherever it was possible to determine the sex of these relatively complete skeletons, these individuals were deemed to be male or ‘probable male’. That determination of sex was largely based on pelvic and cranial features, as usual. She looked at the ages of those fairly complete skeletons, too, agreeing with previous reports that the majority had been young men, in their twenties or thirties. There were a few ‘middle adults’, aged from mid-thirties to mid-forties, and no one older than that. There were also a few youngsters, under eighteen years of age, including a twelve-to-thirteen-year-old identified in the original assessment. But in her investigation, Mitchell also found evidence of another child on board: amongst the portion of the sample considered to be mixed-up remains from many individuals, she found pieces of two matching immature femora, a humerus and a scapula. When bones are actively growing, the very ends of the bone, the epiphyses, are separated from the shaft by a cartilage plate, which is where most of the growth happens. In these immature bones, the epiphyses were completely separate from the shaft – because the cartilage, being a soft tissue, decays away. Based on the stage of development of these bones, this child could have been as young as ten on that fateful day.

Looking through the bones for signs of pathology, Mitchell found three individuals with bony pathology around the hip joint, which she interpreted to be evidence of traumatic dislocations. Ann Stirland noted two other cases. It’s possible that these signs of dislocation – with extra bone growing around the upper margin of the socket – may have been caused by hip dysplasia. This is a condition where the acetabulum, the socket of the hip joint, develops in such a way that it’s too shallow. This means the head of the femur is loose, in mild cases, or dislocates out of the socket, in more severe cases. Hip dysplasia is something that is checked for in infants today and treated, but Tudor paediatrics still had a long way to go. All three of the individuals with evidence for instability in the hip were young – in their late teens when they died. In all of them, the bony changes around the hip socket were active, suggesting that hip instability was not just something they’d had in younger childhood, but that it was an ongoing problem at the time of death.

Another pathology that Mitchell found amongst the skeletons involved a lesion on joint surfaces, where a small piece of bone – which would originally have been covered in cartilage too – breaks away. It’s called osteochondritis dissecans. Like most conditions, there can be a genetic predisposition to developing it; it tends to run in families. But it’s also more common in people who play a lot of sport. It can develop in young people, and may lead to osteoarthritis in the affected joint, but some people have it without ever knowing about it. In an archaeological skeleton, the condition looks like a discrete divot in the joint surface, as though someone has attacked it with a tiny ice-cream scoop. It’s usually found in a joint on only one side, though it can be bilateral. Mitchell spotted two examples in the Mary Rose skeletons; in both cases, these lesions affected the lower joint surface – specifically, the medial (inner) condyle – of a femur, a common site for osteochondritis dissecans. It was difficult to come up with a precise age for these two individuals, but they looked to be younger adults.

Other pathology detected amongst the bones included enthesophytes – bony spurs where ligaments and tendons attach to bones – and osteoarthritis, the most common degenerative disease to affect joints, ancient and modern. Mitchell spotted bony spurs on calcanei, or heel bones, and on patellae, or kneecaps. One skeleton showed particularly advanced osteoarthritis at the elbow – so severe that the bone was polished and pitted in an area where all the cartilage would have been worn away. There were also a few examples of mild spina bifida, affecting the sacrum. There was plenty of evidence of poor dental hygiene, with build-up of hard calculus on teeth and lots of tooth-loss, too. There were also a few cases of scurvy and rickets. Surprisingly, perhaps, there was very little evidence of traumatic injury on the skeletons: one healed, fractured femur; a fracture to a fibula; and just three possible examples in skulls – a nasal fracture, a healed, depressed fracture to the side of a head, and a healed sharp force injury to the side of another skull.

Ann Stirland had recorded a few other fractures in her original report, including three broken ankles, where the fibula had fractured, probably in an inversion injury. She also spotted spiral fractures in a tibia and fibula, which would have been caused by a traumatic, twisting injury such as falling off a horse or, she suggests, falling from rigging. There were two breastbones with evidence of old fractures that had healed, and just seven ribs with old breaks. She also recorded a few more instances of head injuries, all of them in the process of healing – so these had not been sustained around the time of death. There were old depressed fractures and a few penetrating injuries, which could have been caused by arrows.

Overall, the skeletons reveal a crew of mainly younger men, who were fit and healthy at the time they died. The collection is very unusual: we so rarely know the cause of death for any archaeological human remains. This time, though it has left no mark on their bones, we know it: drowning. And what we must remember about the various pathologies seen in their skeletons is that these represent conditions they were living with, or had experienced in the past, such as vitamin deficiencies in childhood and adulthood, and old fractures. Those injuries and diseases weren’t stopping them from being active, from being part of the crew of the Mary Rose. But some of the lesions may have been intrinsically linked to their work.

In the spines, Mitchell found – just as Ann Stirland had done – plenty of evidence of Schmorl’s nodes. These are small pits or cavities in the endplates – the upper or lower surfaces of the vertebral bodies, the part which sits next to the intervertebral discs in life. The centre of the disc is made of a gel-like fibrocartilaginous substance that helps to resist compression and to distribute load evenly across the vertebral body. But sometimes the pressure in one particular place is too high and the gel can rupture through the surrounding annular ligament to push out at the back (commonly known as a ‘slipped disc’) or into the bone itself – and this is what’s known as a Schmorl’s node (named after a German pathologist, Christian Georg Schmorl, who first identified the condition). Although the intervertebral discs themselves decay away, the depressions in the bone are still obvious in archaeological skeletons. The rate of Schmorl’s nodes varies hugely between different populations – with reported prevalence ranging from around 4 to 76 per cent – but it is thought to very generally reflect an individual’s level of tough, physical activity. In this sample of the Mary Rose crew, 73 of the relatively complete skeletons had at least one vertebra present, and 33 had at least one Schmorl’s node – some of them very large. Schmorl’s nodes are fairly common findings in archaeological skeletons, and are also common in living people today; they tend to predominate in the lower thoracic and lumbar portions of the spine. They often accompany other degenerative changes in the spines of older people, but young people can have them too, especially if they have engaged in strenuous physical activity. Schmorl’s nodes are usually asymptomatic – people don’t even know they have them – but they can also be associated with lower back pain.

The causes of Schmorl’s nodes are complex and not entirely understood. The shape of vertebrae seems to predispose some people to developing them; age is certainly a factor; low bone density, as in osteoporosis, can contribute. The nodes represent a mechanical failure in the spine, and this can be precipitated by all those other factors, but it also depends on what you do with your spine and how much load you place on it. Weight-gain is thought to play a part in failure of the endplate, and so is lifting heavy objects. In her osteological analysis, Ann Stirland had compared the Mary Rose skeletons to a broader assemblage from a medieval churchyard in Norwich. There, she’d seen similar spinal pathologies, but tending to affect older adults. Something, she suggested, was accelerating the changes amongst the spines of the Mary Rose crew. Amongst a population of Tudor soldiers and sailors, perhaps it’s not so surprising that Schmorl’s nodes were common, despite the relative youth of those men. No doubt they had all engaged in strenuous activity over the course of their military careers, and Mitchell drew attention in her thesis to one particular area on board the ship that seemed to be an occupational health nightmare. There was a stack of 155 metre-long logs in the galley – an area where the men would not even have been able to stand upright when hefting these logs. She also suggested another possibility: the stresses and strains on the backs of the gun crew on board.

There were other vertebral pathologies amongst the crew. Eighteen of the relatively complete skeletons showed evidence of ossification of the ligamentum flavum (OLF). I know – sounds painful, doesn’t it? It means the ligament that stretches between vertebrae at the back had turned to bone. The causes of this condition are even more opaque than those of Schmorl’s nodes. It’s thought to be caused by excessive flexion of the spine, stretching the ligament – and then chemical signals turn fibroblasts, the type of cells that usually reside in ligaments, into chondroblasts, which make cartilage, and then into osteoblasts, which make bone. In severe cases, the ossified ligament can press on the spinal cord and eventually cause paralysis of the legs; such extreme cases can be treated today with spinal surgery. As with so many of these pathologies, we know more about how they develop than why. In the modern world, OLF was thought to almost exclusively affect East Asian, and particularly Japanese, people, but it has been found in other populations around the globe.

This geographical focus suggests that it has a strong genetic component, and indeed, several genetic variants have been identified that seem to increase the risk of the condition. But once again, there are physical, mechanical factors at play, too. One report from Japan covered the cases of two young professional baseball pitchers, aged just twenty-seven and twenty-two. One had complained of numbness in the chest, the other of pain. In both, the ossification of the ligamentum flavum was clear to see on CT scans. One pitcher had to change jobs, while the other recovered after a period of rest. This report, published in 2021, was important as it flagged up the potential for OLF to develop in young people, apparently in response to repetitive mechanical stress. In order to throw a ball at high speed, a pitcher twists their body rapidly, transferring that energy to the ball as it leaves their hand. And as the report stated, ‘Both patients were highly active pitchers engaged in intensive training, including pitching almost every day.’ The researchers spread their net a little wider and found eight newspaper reports of Japanese professional baseball pitchers who had had to have surgery for OLF. It seems that while Japanese people may be particularly predisposed to developing this spinal condition, baseball pitching creates just the type of mechanical stress on the thoracic spine that can push those fibroblasts over the edge.

However, it could be possible that the high frequency of OLF in Japan compared with the rest of the world, or at least the rest of the world beyond East Asia, may not reflect the real pattern of the condition. Perhaps Japanese doctors have learned to be good at identifying OLF, as well as having ready access to MRI scans. The low prevalence elsewhere could just be an artefact: it’s not being found where it’s not being looked for. A group of Indian anatomists decided to test out this hypothesis by looking for evidence of OLF in the skeletons in their anatomical teaching collections. They examined 1,786 thoracic vertebrae and found OLF in 261 – crudely, 15 per cent. Most heavily affected were the lower thoracic vertebrae – T9 to T12 – with 50 per cent of these showing signs of OLF. So, it seems the condition may be much more prevalent and widespread around the world than previously recognised.

But what about those eighteen on the Mary Rose with OLF in their spines? Most were adults in their mid-twenties to mid-thirties; three were definitely younger – in their teens or early twenties at the time of death. They’re reminiscent of those young baseball pitchers in Japan, prompting the question: what could these crew members have been doing to cause similar repetitive mechanical stress?

The shoulders of the Mary Rose crew hold further clues. There, Ann Stirland and Emily Mitchell both recorded evidence of a particular anatomical variant that’s once again subject to both genetic and mechanical influences. The outermost and uppermost prominence of the shoulder blade, or scapula, is called the acromion. Its name comes from the Greek akros, meaning ‘high’, and ōmos, meaning ‘shoulder’. Just as the Acropolis is the ‘upper city’ towering over the rest of Athens, the acromion is the highest point of the shoulder blade. It’s the outward continuation of the spine of the scapula – which you can easily feel if you place one hand up and over the opposite shoulder. A sharp bar of bone runs diagonally, and as you trace it laterally, or outwards, it ends in a broader wedge – the acromion. You should also be able to feel the joint where the front of the acromion articulates with the lateral end of your clavicle, or collar bone.

When it’s developing and growing, the acromion is a separate epiphysis all of its own, with plates of cartilage dividing it from the scapular spine. In most of us, these cartilage plates ossify when we’ve finished with growing, leaving the acromion completely fused to the spine of the scapula, usually by the mid-twenties. But in some people, it never fuses, and remains as effectively a separate bone, an ‘os acromiale’, into adulthood.

This anatomical variant was first recognised in 1849, by a French anatomist, Jean Cruveilhier, who was writing a treatise on anatomy and pathologies. He described a clear line separating the acromion from the rest of the scapular spine. In 1863, an anatomist called Wenzel Gruber, from the region of Pernarec – now in the Czech Republic, then part of the Austrian Empire – was working in St Petersburg. He’d carried out a survey of a hundred cadavers and found os acromiale present in three of them – and not just as a cartilaginous feature, but as a synovial, or fluid-filled, joint. Later researchers identified different forms of the variant, depending on the pattern of fusion of three separate ossification centres in the acromion.

When you find this in an archaeological skeleton, where all the other usual growth plates have disappeared, and the epiphyses fused, you then know you’re looking at an adult with os acromiale. Again, it can be something that is completely unknown to the person who has it, but it can predispose to other problems around the shoulder joint in time, including impingement.

In her investigation into the Mary Rose skeletons, Ann Stirland had looked at the 52 matched pairs of scapulae amongst the collection and found evidence of os acromiale in ten pairs, six of which were affected bilaterally, and four unilaterally – with three of these exhibiting it on the left side, and one on the right. There are different ways of expressing that frequency: you can either say that 10 out of 52 individuals (19 per cent) had os acromiale, or you can say that 16 out of 104 scapulae (15 per cent) were affected. If all the scapulae from the Mary Rose are included, that brings the number of scapulae up to 207 – with os acromiale in 26, bringing the rate down to 13 per cent.

That still seems high, but what we need are comparisons, to make sense of this data. A recent large study, in 2017, looked for os acromiale in the shoulders of living people, in Italy. Radiologists assessed 726 sets of MRI scans and found os acromiale in only 3 per cent of individuals. An even larger study, published in 2022, included MRI scans of the shoulders of 3,050 participants in Germany, revealing the presence of os acromiale in 58 – just 2 per cent. Of those 58 people, 14 had it in both shoulders, 21 had it only on the left and 23 only on the right.

Those large modern studies, then, have produced rates that are very similar to Gruber’s original frequency. But more recent investigations of large anatomical skeletal collections – mainly comprising individuals who died in the early twentieth century – have produced higher rates, of around 8 per cent, while the average for archaeological populations comes out at around 6 per cent. These results seem to suggest that os acromiale has become less common in twenty-first-century populations (in Europe, at least), perhaps because mechanical stresses on shoulders are not as high as they’ve been in the past – even as recently as the early twentieth century.

That’s interesting, but these varying rates through time mean that we need to be quite careful about which populations we use as a comparison for the Mary Rose. We want to know what the frequency of os acromiale was around the same time, around the same area (because it may be that different populations around the world also have different frequencies). And there are a couple of reports of os acromiale in archaeological populations that fit the bill. Amongst scapulae from a fifteenth-century mass grave in Yorkshire, linked to the Battle of Towton, the rate of os acromiale was 9 per cent. And in a cemetery on the Isle of Ensay in the Outer Hebrides, spanning the sixteenth to twentieth centuries, the rate of the condition was 8 per cent. Compared with these, then, the Mary Rose results really do stand out as being particularly high – 50 per cent higher than the rate found in those comparable archaeological samples, and in the anatomical collections.

Ann Stirland wrote that she ‘thought at first that some kind of traumatic accident might be responsible for this increase [in the rate of os acromiale]’. But she couldn’t think of an injury that might affect so many people in the same way. ‘This led me to speculate,’ she went on, ‘… about a possible occupation or specialised pattern of activity that might have a similar effect.’

A Tudor warship, we know from historical records, would have had a large number of longbow archers on board. And in fact, the inventory of the Mary Rose included 250 longbows, 864 bowstrings and 9,600 arrows. We have a fantastic physical record too: amongst the numerous objects found in the wreck of the Mary Rose were 137 yew bows. Archers would have trained from a young age, producing high extension and torsion forces on bones. The suggestion is that these high forces would cause inflammation of the cartilage growth plate in the acromion, ultimately inhibiting its fusion.

It seems every man in England was expected to be able to use a bow. Going back to the mid-thirteenth century, Henry III had issued a proclamation called the Assize of Arms, or to give it its full name, the ‘Writ for Enforcing Watch and Ward and the Assize of Arms’. (It’s often described as the 1252 Assize of Arms, but this seems to be a clerical error – it was first recorded in 1242.) It was a legal writ that re-emphasised an earlier Assize of Arms issued by Henry II, in 1181, laying out the legal duty of male citizens to bear arms for their king when required. And that earlier Assize effectively reinvigorated an obligation that had existed in England before the Norman Conquest, when all freemen were expected to help with military defence if necessary. The importance of this obligation being reinstated was that it meant the English population owed this duty directly to the king, and not to their local baron. It was designed to stop barons rallying forces against each other – as had happened in the mid-twelfth century, when an argument over succession led to that period of civil war known as the ‘Anarchy’. Anyway, the 1242 Assize of Arms laid out the duty of men in England to hold arms and be ready to fight if needed. Different ranks of citizens were expected to arm themselves in different ways, providing the king not only with a large number of potential fighters, but with a variety of specialisations.

The 1242 Assize of Arms starts off with a stipulation about the number of armed men expected to form the regular watch in towns and cities, and then sets out what types of arms should be kept ready by every male citizen – ‘citizens, burghers, freeholders, villeins and others of 15 to 60 years of age’. There were different ranks, depending on the amount of land held by each man. Someone with more than fifteen pounds’ worth of land was expected to have at the ready a hauberk (a long coat of mail), an iron helmet, a sword, a dagger and a horse. Bows and arrows are only mentioned as part of the weapons kit in a couple of classes – for those with 40 to 100 shillings’ worth of land and for those with just 9 marks’ worth of chattels. But then there’s a note that, ‘Everyone that is able shall keep bow and arrows outside the forest, however those who live in forests, shall keep bow and javelins.’

This has been taken to suggest that all able-bodied men between fifteen and sixty years of age were expected to keep and be able to use bows – but it’s not clear how widely this law was enforced. If everyone was using longbows regularly, perhaps we might expect an even higher rate of os acromiale from the Battle of Towton skeletons and those from Ensay. Regardless of the wider picture, the crew of the Mary Rose – which we know included many trained archers – had a lot of separated acromia between them. Ann Stirland concluded: ‘the high frequency of os acromiale in the skeletons from the Mary Rose may be associated with the long-term use of the heavy war bow by some of the men’.

It seems a very reasonable conclusion, and I hesitate to sound a note of caution. It’s very tempting to link the high rate of os acromiale to archery. The Mary Rose skeletal assemblage is extraordinary in so many ways, not least because we know who these men were, collectively – and we know there were many archers amongst them. But we also know that this crew was relatively young. Ageing skeletons is tricky, and large age-ranges are used. Given that most of the Mary Rose skeletons were determined to be ‘young adults’ – aged between eighteen and twenty-five at death – and the acromion usually fuses in the early twenties, it could be that the high rate of os acromiale is down to youth more than archery.

And so we must be wary about jumping to conclusions. Still, Ann Stirland found some other bony evidence that could reinforce the archer hypothesis. She found that the areas for muscle attachment around the head of the humerus, particularly the greater tuberosity, tended to be larger on the left side. She also found that the humeri from the Mary Rose were remarkably symmetrical, with little difference between bones from the right and left arms. Archery is an activity that involves both arms. The non-dominant arm (so, usually the left) holds the bow out, as the ‘bow arm’, while the dominant arm (usually the right) is used to pull the bowstring back: the ‘draw arm’. It’s been argued that a decrease in humeral asymmetry seen in skeletons from the Mesolithic (from around 10,500 years ago) might be linked to a switch from unimanual weapons, such as spears, to bimanual weapons, like a bow. In the same way, Stirland argued, the lack of asymmetry in the Mary Rose humeri – together with larger dimensions of areas of muscle attachment around the humeral head on the left – could be related to archery.

The argument from form to function – linking pathology and size differences to specific uses of the shoulder, for instance – seems compelling. But it’s good to have some experimental data to back up such connections. In 2022, anthropologists at the University of Massachusetts, frustrated by claims for evidence of archery derived from the shape of old bones, provided just such data.

The researchers started by recruiting participants for their trial, putting up flyers on campus and in gyms. Nine men were included in the experiment, with varying levels of experience of archery. Four were beginners, with less than a year of shooting arrows under their belts (if that’s not too much of a mixed metaphor). Five were more seasoned archers, with more than five years’ experience apiece.

The researchers used wireless surface electromyography to collect data on the electrical activity in eight muscle areas on each arm, at the same time. The muscles were latissimus dorsi, pectoralis major, biceps brachii, the anterior, lateral and posterior parts of deltoid, and the long and lateral heads of triceps brachii. The participants used a standard recurve bow, with a draw-weight of 0.45kg. The bow itself was labelled with reflective markers, and the movements of the archers were picked up using an eleven-camera motion-capture system. After warming up, each archer shot arrows at a target placed 6 metres away.

The results were fascinating. All eight muscles were activated in both arms throughout the draw phase, as the archer pulled his arrow back into position. Different muscles were variably recruited at different phases of the draw, in both arms. The level of muscle activation was similar in both arms – until the archer reached around 40 per cent of the draw distance, when activation peaked in the bow arm, particularly in the lateral fibres of deltoid and in the lateral head of triceps. This makes perfect sense: the bow arm needs to hold the bow out straight. This requires abducting the shoulder – and that’s achieved by the lateral fibres of deltoid, which run over the top of the shoulder joint – and holding the elbow straight, in extension – which is achieved by triceps.

The researchers concluded that the results supported claims that archers may have more symmetrical arm bones than non-archers, because of the high mechanical demands placed on the non-dominant arm. But then again, they sounded a note of caution, because even with these measurements of muscle activation during archery, the pattern of loading on the humerus itself is still unknown. And of course, it’s that loading that’s the essential part of the puzzle, because the forces experienced by the bone trigger changes in bony architecture, through the action of those tiny osteoblasts and osteoclasts. ‘The complicated relationship between muscles and bones,’ wrote the researchers in their conclusion, ‘complicates inference of specific activities based on skeletal morphology.’ That complicated relationship is at the heart of both the joy and the frustration of working in osteoarchaeology and palaeopathology. Like so many scientists before them, this team concluded: ‘more research is clearly required’. It’s a phrase that’s practically banned now by many journals because it’s ubiquitously true. It’s the nature of science, after all: it never ends – and that is also what makes it so exciting.

Almost 4,000 miles away from the University of Massachusetts, another team of scientists were carrying out a similar research project, at Charles University in Prague (founded by Charles, King of Bohemia, in 1348). This time, they were particularly interested in the potential link between skeletal changes and an increased use of archery at the end of the Ice Age.

They started out by acknowledging that the problem with linking any particular feature or lesion in bones to a specific activity during life is that humans are complex creatures. We don’t just do one thing. Some researchers have questioned that appealingly simple link between decrease in asymmetry in right and left humeri and use of bows. They’ve pointed out that lots of things were changing at the end of the Ice Age, around 12,000 years ago: people were not only using bows more (which is well attested in the archaeological record) but probably using spears less and doing many other things like paddling canoes, swimming and setting traps for prey. Archery was just one activity amongst many. Taken en masse, what was happening was a reduction in the frequency of unilateral activities – such as throwing and thrusting spears – and an increase in bilateral activities, using both arms. Archery is in the mix, but it’s not the only change.

It’s also been suggested that there should be a massive difference when comparing Palaeolithic and Mesolithic archers with medieval archers. The latter were using powerful longbows, packing a much higher punch than the lightweight bows used in prehistory. However, pathological changes around the shoulder in Neolithic individuals, as well as more robust clavicles and ulnae, suggest that the bows used by this period may well have been producing high enough loads to impact the skeleton. That seems to be backed up by studies of modern archers using sporting bows, who often develop pathology in shoulder and elbow joints. The Czech scientists argued that the power of simple bows has been underestimated. Even relatively light bows produce significant loads: the draw-weight of modern sporting bows ranges from 24 to 42lbs, while that of contemporary hunter-gatherer Hadza bows has been measured at around 50–90lb. The draw-weight of Mesolithic bows has been estimated to have lain in the upper end of that range, at 70–90lb. And in terms of the effects of the activity on bone remodelling, it’s not just the magnitude of the load that’s important, but its frequency.

The Czech group designed their experiment to examine the effects on the body of archers using replica prehistoric bows. They worked with twenty men who were not professional sportsmen but who enjoyed using wooden bows, recreationally or in historical re-enactment. They had a special bow made for the experiment, carved from a single branch of Osage orange wood. This type of wood is, in itself, historically interesting. Originating in the Americas, these trees were used by the Osage people of the Great Plains to make their bows. When French settlers saw this, they named the trees bois d’arc, and this has become corrupted to ‘bodark’ and ‘bodock’, other names for the Osage orange. The wood is strong, reliable and robust – perfect for an experimental bow.

Like the Massachusetts team, the Prague scientists used electromyography to pick up the activity of muscles around the shoulder. They asked their archers to draw the bow to its full extent but not to fire it, as the vibrations played havoc with the EMG trace. Their results suggested little activation of the anterior deltoid, in either arm, throughout the draw. But all the other muscles increased in activation, peaking in the final third of the draw. They found very high activation in triceps, and in the lateral and, this time, posterior parts of deltoid. In triceps, the activation was higher in the bow arm compared with the draw arm. They went on to develop a force model that showed, perhaps counterintuitively, that the loading on the arm holding the bow is significantly higher – 15–28 per cent higher – than that on the draw arm. While other activities would have still tended to affect the dominant arm more, this increased loading on the non-dominant arm may explain some of the reduction in asymmetry in humeri at the end of the Ice Age.

As an anatomist, I find myself wanting to delve into the detail of muscles and attachments to see if there’s anything to help us there. In 2006, forensic anthropologist Petra Molnar published a study of Neolithic skeletons from the island of Gotland in the Baltic Sea, in which she’d carefully scrutinised areas of muscle attachment, particularly around the shoulder. She was interested to look for any skeletal correlations with activities indicated by the archaeology, including archery. She looked at the surface of bones, where muscles attached, and scored them for markers of ‘stress’ – including furrowing and pitting, ridges and crests. And she found bony changes at the attachment sites of deltoid and triceps, predominating on the left side. That’s a pattern that echoes the more recent EMG studies, which demonstrated a higher activation of deltoid and triceps in the bow arm compared with the draw arm. Interestingly, Molnar found the opposite to be true for the attachment points of the short scapular, or ‘rotator cuff’, muscles around the shoulder – these were more often subject to markers of stress on the right side. This correlates with patterns of injuries in modern archers – most commonly affecting the shoulder, on the draw arm side, and involving the rotator cuff muscles.

Going back to the Mary Rose, Ann Stirland had looked carefully at sites of muscle and ligament attachment amongst the fairly complete skeletons in the collection. She was looking for ridges and spurs that could be signs of stress, and found these to be present in 39 skeletons – 42 per cent of the sample. They were most common around the upper humerus, and she found a signal of stress at the site of attachment of infraspinatus, which seems to agree with the recent Czech EMG study, if not the Neolithic archers of Gotland.

And it’s not just the shoulders that provide clues. Of course, the forces being produced as a bow is drawn are going to affect the upper limbs right along their length. There are those well-documented asymmetries around the shoulder, but when a team from Swansea University – including biomechanists Nick Owen and Simon Annan – investigated variation in the Mary Rose skeletons, they found that the bones that showed the highest degree of asymmetry were radii, from the forearm. This makes a lot of sense, as, while both the bow arm and draw arm are loaded when a bow is drawn, the forces they experience are different. The forearms, in particular, experience different patterns of loading: the forearm of the bow arm will be loaded in compression, whereas the forearm of the draw arm will be under tension, with the bowstring pulling away from it.

Simon Annan analysed motion-capture data of an archer drawing a bow, to estimate the forces generated. For a modern longbow with a draw-weight of 445 Newtons (100lb), the draw arm is subjected to a tensile load of 430N while the bow arm is under 375N of compressive load. Of the two forearm bones, it is the radius that transmits most of any compressive load in the forearm – around 85 per cent – because the radius articulates directly with the bones of the wrist, whereas the ulna does not. This means the bow-arm radius would be transmitting a force of 319N.

Annan and Owen used laser scanning to capture the external shape of twenty pairs of radii from the Mary Rose assemblage. From this data, they then calculated the areas of the joints at either end, and the cross-sectional area in the middle of the radial shaft. It’s known that the cross-sectional area of bones increases in response to compressive loading.

They found considerable variation in many pairs of radii, but the joint surfaces and cross-sectional areas weren’t consistently larger on the left compared with the right. In fact, for around half the sample, joints were larger on the right, and for the other half, on the left. But some of the most extreme differences seemed to favour the left. Annan found one left radius, from Skeleton 82, where the size of the distal (lower) joint surface was 25 per cent larger than that on the right, suggesting the left side had experienced significantly higher mechanical loading over time. It’s possible that this method has identified an archer amongst the crew – someone whose left arm would regularly have been placed under even greater load than a modern Olympic archer.

The draw-weight of longbows has been a subject of considerable debate, with wide-ranging estimates being fired out. Even the length of longbows has been contested – along with an argument about whether the longbow used by English archers from the fourteenth to sixteenth centuries was simply the product of a gradual lengthening of bows during the Middle Ages or a distinctly new class of weapon. One thing seems clear, though: the longbow in its longest form did seem to be a peculiarly English type of weapon. Sir John Smythe, a nobleman and soldier in the sixteenth century, wrote a whole treatise about the superiority of longbows compared with newfangled firearms. He described ‘the Long-bowes of England’ as ‘the most excellent weapons for the field… used by anie Nation in Christendome’, and wrote that ‘our English Bowes, arrowes and Archers do exceed and excell al other Bowes used by all forren Nations not only in substance & strength, but also in the length & bignes of the arrowes’.

In the fourteenth century, a renowned hunter, Gaston III of Foix, wrote a Livre de Chasse, or ‘Book of the Hunt’. In it, he admitted to knowing little about archery himself, and said, ‘if you want to know more, you best go to England where it is a way of life’. But he did, at least, describe a longbow as being best made out of yew or boxwood, and 70 inches long between the points where the string was attached – that’s around 1.8 metres in new money. But actual bows from the period are few and far between – or at least they were, until the Mary Rose was excavated and recovered, along with the 137 longbows still on board. And they were very long longbows, ranging from 1.9 to 2.1 metres in length. They were also exceptionally thick, about 3.5cm thick in the middle, and that’s also related to the power of the bow. They’d been underwater for so long, though, that the Mary Rose bows couldn’t be used to provide reliable experimental data (and it might be argued that they’re too precious to try). But there are plenty of clues from their dimensions – and those of the arrows too, which varied in length from 61cm to 81cm – to give a measure of the maximum draw distance: computer modelling predicts that the draw-weights of the bows would have ranged between 100lb and 172lb.

Whether or not they represent one end of a spectrum, or a new class of weapon, the bows on the Mary Rose certainly represent the extreme of what is possible: these fully developed longbows would have propelled arrows further, faster and with greater accuracy than any shorter bow. They stood taller than the men shooting them, and only a well-trained archer would have been capable of using them. It’s likely that the men on the Mary Rose, Henry VIII’s favourite ship, would have been the elite of the elite – the finest archers in England. Their prowess in archery is written into their bones. And we haven’t finished uncovering their story yet.

When I saw some of the skeletons from the Mary Rose back in 2010, it was the shoulders that leapt out at me. I was familiar with patterns of pathology around the shoulder – in fact, this had formed the backbone of my PhD. Peering at those bones, I could see tell-tale ragged crests of bone and pitting on the tuberosities at the neck of the humerus.

Some of the analyses of the Mary Rose bones had touched on changes at the insertion points of the rotator cuff muscles, but I couldn’t help wondering if there was more work to be done. Rotator cuff disease is the most common pathology affecting our shoulders today, and I knew that it had been historically under-diagnosed in ancient skeletons. Like many degenerative joint diseases, it’s something that becomes much more prevalent in later life, but it can also develop in younger people when their shoulders are subject to specific stress and trauma; rotator cuff pathology is an occupational hazard for archers today. Just how prevalent was this condition amongst the crew of the Mary Rose, regularly pulling those powerful longbows? I knew that one day, I’d have to find out.

And so, in February 2023, I returned to Portsmouth to visit the award-winning Mary Rose museum for the first time – together with Nick Owen, who was also convinced there was more to find amongst those bones. Hannah Matthews and Alex Hildred showed us into the dark cavern of the ship hall where the timbers of the hull are displayed. The hull is immense; it took my breath away. I walked very close to it but resisted touching the ancient timbers. They’re dried out now and impregnated with waxy polyethylene glycol to preserve them. Opposite the hull, objects from the ship are displayed on mezzanine floors that mirror the decks in the ship. More artefacts, along with some of the skeletons, are in galleries at either end of the ship hall.

After we’d explored the public galleries, we retreated to the lab and the bone store where the skeletons from the Mary Rose are curated, in boxes labelled with the precise location where they were discovered in the wreck. We laid out some of the bones on tables in the lab. Even just looking at a small sample, I could see plenty of evidence of rotator cuff disease. We talked about the biomechanics of archery, about shoulders, about those elite archers. And Alex, Hannah, Nick and I started to put together the skeleton of a new research project.

The analysis of skeletons, unearthing clues about lives, and sometimes deaths, seems to me to be a fitting way of honouring the dead. We’ll never know the names of all those men – and boys – who perished on that fateful day. But we see them in the lab, as individuals once again, as their osteobiographies emerge.

7. THE ANCHORESS AND THE SPIRAL BACTER

In the summer of 2007, archaeologists in York began excavating what remained of a medieval church: All Saints, Fishergate. They had some idea of what to expect on site, having looked at maps and carried out a smaller investigation some years before. There was a large cemetery associated with All Saints Church, and the archaeologists would end up excavating 653 skeletons from it. With the thirty-one that had been lifted in the earlier dig, that brought the total up to 684 skeletons. The task of analysing all of these human remains fell to osteoarchaeologist Lauren McIntyre.

Poring over those bones – laying each skeleton out in the lab, looking for clues to age, sex, pathology – there was one that caught her eye. Lauren couldn’t stop thinking about it – about her. Just who was this woman? Her bones bore the stigma of disease, but she’d also been interred in an unusual way, in a crouched position in a pit-like grave – in a prominent position within the apse of the church. Why was she buried where she was, and what did that have to do with the pathology that was so evident in her bones?

As archaeological scientists, osteoarchaeologists must be objective in their analyses and search for answers amongst the bones of the long-dead. We record the events of lives and deaths, written into bones. We give those findings to our archaeological colleagues for interpretation. But, as I know only too well, there are times when those bones demand more of our attention; when there’s a long-forgotten story to be found – and told.

This particular medieval skeleton, SK3870 from All Saints Church, Fishergate, was 75 per cent complete, but key parts of it were missing, including the skull and upper cervical vertebrae. The right hand was also missing. The mandible, with the lower teeth in situ, was present. Based on the amount of wear on those teeth, and on the appearance of joint surfaces on the pelvic bones, Lauren estimated that this individual had died when they were somewhere between thirty and fifty years old. The pelvis and mandible were not only useful for ageing the skeleton, but for establishing sex. The bony pelvis – comprising two pelvic bones and the sacrum, held together in life by strong joints – tends to be broader in females, as it must accommodate the birth canal. Any notches and angles that you can observe on separated pelvic bones in an archaeological skeleton also tend to be wider. The pelvic bones of this individual each had a wide sciatic notch, and they framed a wide, concave angle under the pubic bone at the front. These features are indicative of female sex. The mandible of Skeleton 3870 was gracile, relatively slender, with no heavily marked areas of muscle attachment; the chin was gently rounded, rather than squared. Again, these features suggest that this individual was female. And then the joints were relatively small: the diameter of each femoral head (the ball in the ball-and-socket joint of the hip) was only just over 4cm. From measurements of long bones, Lauren estimated the height of this individual to have been 160cm, or 5ft 3in.

A woman, then, who had died when she was middle-aged. If that had been all there was to learn from her skeleton, her bones – treated respectfully and analysed appropriately – would have been put back in a box. Perhaps they would have been kept in a museum archive, perhaps they would have been reburied – which usually leads to fairly rapid destruction. But there was more to see in these skeletal remains.

This is what Lauren found:

The woman’s teeth were generally in good condition, although she had concretions of calculus on them. She may have been eating a lot of starchy foods. She was certainly not brushing her teeth well or regularly.

She had arthritis in many joints: in her right jaw joint; in the joints where her clavicles met the breastbone; in her shoulders and in her right foot. She also had some signs of osteoarthritis in her spine, and a Schmorl’s node in a thoracic vertebra, where the intervertebral disc had punched into the bone.

The bones of this woman felt light in the hand. Where bones were broken so that their inner architecture could be observed, it looked thinned-out. That kind of bone loss can be down to so many things: calcium deficiency, post-menopausal changes – and lack of physical activity.

None of this is particularly unusual. For a middle-aged woman from the Middle Ages, you might expect some bone loss or even osteoporosis, a bit of osteoarthritis and some evidence of poor dental hygiene. But there was much more to see in these bones: signs that the whole body had been reacting to a disease at the time of death.

As we’ve seen, bones can react to challenges by either producing new bone tissue – or destroying it. In SK3870, there was evidence of bone responding to infection by pumping out new bone tissue in a widespread variety of locations: in the chest, arms, hand, pelvis, legs and feet. Almost everywhere. It looked like this person had been suffering from a chronic or longstanding infection when they died. An infection that had spread throughout the body, with systemic effects.

Most of these signs of disease in the skeleton were ‘non-specific’. They speak of infection, but they are reticent about telling us what the pathogen was. There were just a few lesions that seemed more specific: crater-like holes in the sternum or breastbone, in the left scapula and humerus, the left femur and both shin bones, or tibiae. There was new bone around the edges of these holes. They had a very characteristic appearance – and Lauren knew exactly what she was looking at: the bony traces left by gummata.

A gumma is a specific type of granuloma – a ball of immune cells that can sometimes form in chronic inflammation. Its name means ‘gum’ in Latin, and in a living patient, the gumma would appear as a nodule with a rubbery texture. In archaeological human remains, what’s left is the impression that this inflammatory nodule leaves on bone – the characteristic crater-like gummatous lesion, with ragged edges. And it’s typical of advanced syphilis.

Syphilis is caused by a bacterium called Treponema pallidum. It’s a type of bacterium known as a spirochaete, which means ‘spiral hair’ in Greek – the cells are long and coiled. In fact, Treponema means practically the same thing: ‘twisted thread’, while pallidum means ‘pale’ or ‘pallid’. It’s usually a sexually transmitted infection, but it can also be transmitted from a mother to a fetus, causing congenital syphilis. The first sign of infection is a pustule that develops into an ulcer, at the place where the bacterium first enters the body – often in the vagina, on the penis or around the anus. These ulcers go by the old-fashioned term chancre, a French word that comes from the Latin cancer. But they’re not cancerous – they’re infective in origin. (The terminology dates from a time when diagnoses were much more vague than they are today.) The chancre forms between nine and ninety days after exposure and it’s usually painless – and so it can go unnoticed. And at a microscopic level, too, the spirochaetes do their best to be invisible.

T. pallidum is a dastardly foe. It’s not instantly recognisable to the immune system in a way that many similar bacteria are. The surface of each spirochaete is covered in a mucus-like layer made up of proteins with sugars attached. But the bacterium doesn’t make this layer itself – it seems to secrete enzymes that break down substances made by host cells in order to create its disguise. And it’s very effective – it makes the T. pallidum almost invisible to the host’s immune system. Many bacteria have characteristic biochemical markers on their surfaces that the immune system can recognise as alien even before specific antibodies kick in, but T. pallidum has very few of these markers – another way in which it evades early detection. On top of this, it seems that T. pallidum also releases some proteins that cause the death of certain immune cells in the host, effectively suppressing the immune system.

Eventually, immune cells called phagocytes will successfully detect the alien invaders, and then make a move to engulf them and destroy them. These cells gobble up the bacteria and then spit out bits of them, sharing information about what the enemy looks like, at which point lymphocytes start to produce antibodies in response. Antibodies then latch on to the outside of the bacteria, tagging them and making them more attractive to phagocytes. But unfortunately – due to all of T. pallidum’s clever wiles – this response is just too slow, and plenty of bacteria escape. Just as the primary ulcer begins to heal, the bacteria are multiplying and heading off elsewhere in the body – and they have an extraordinary way of getting around.

T. pallidum is a motile bacterium: it can move on its own. Bacteria have two main ways of moving themselves around, both relying on filaments that protrude from the surface of the cell. Some bacteria have pili (from the Latin for ‘hair’) that stick out in all directions and act like tiny grappling hooks, allowing the cell to drag itself over surfaces. Others can swim in fluids using a long, helical filament called a flagellum (from the Latin for ‘whip’), which rotates very quickly to power the bacterium along. T. pallidum has flagella, but they are internal, lying between an inner and an outer cell membrane; two or three are anchored at each end. Rather than propelling the cell along like a spinning tail, when these flagella rotate they cause the entire bacterium to spin along its length, driving it along like a corkscrew. It’s able to wriggle and screw itself into tissues, penetrating blood vessels and quickly spreading itself around the body. In fact, syphilis gets into the blood within minutes of infection.

It’s not surprising that spirochaetes – like T. pallidum and Borrelia burgdorferi, which causes Lyme disease – are some of the most invasive pathogens out there. They’re good at getting into the body and, once in, they’re able to pierce through barriers that would keep lesser bacteria out, eventually getting deep into the brain and even burrowing through the placenta to infect a fetus in the womb. It’s the perfect bacterial all-terrain vehicle. And T. pallidum has another trick up its sleeve. It secretes some proteins that encourage immune cells to deliberately damage the lining of blood vessels, making it even easier for T. pallidum to get into the bloodstream.

Together, these features of the spirochaete represent an extraordinary suite of adaptations: the syphilis pathogen is highly successful at manoeuvring through the human body, avoiding detection and even turning the host’s defences against itself.

Even during the primary phase of infection, when the localised chancre forms at the point of entry, syphilis is already spreading more widely through the body, hitching a lift in the bloodstream and entering lymph nodes. The lymph nodes then become enlarged and the patient also develops a rash on the palms and the soles of the feet, as well as more ulcers or wart-like lesions around the genitals. This widespread or systemic stage of infection, emerging four to ten weeks after the primary phase, is known as secondary syphilis. It usually clears up, on its own, in three to twelve weeks, but that doesn’t mean that syphilis itself has gone away. Despite the immune system’s best efforts, it’s able to persist in the body.

Deep inside the body’s tissues, syphilis endures and festers. Around a third of patients eventually go on to develop tertiary syphilis. It’s in this advanced phase of the disease that gummata form. These inflammatory masses can grow in any organ. They erupt into ulcers on the surface of the skin and burrow into bone. Sometimes they destroy the nasal septum and palate, a bit like leprosy. Tertiary syphilis can affect the heart, causing angina, and the aorta, causing an aneurysm; in the brain, it can lead to stroke-like syndromes, personality and mood changes; in the spinal cord, it can disrupt both motor and sensory pathways, causing muscle weakness and loss of sensation.

Although syphilis has been recognised as a disease entity for centuries, its slow and complex development meant that diagnosis was confused. In the nineteenth century, doctors recognised a horrific terminal illness that they called ‘General Paresis/Paralysis of the Insane’. It was thought to be related in some vague way to stress, smoking, alcohol – and sex. Around a fifth of men admitted to Victorian asylums were diagnosed as suffering with this disease that was emblematic of degeneration. Sufferers often had grandiose delusions, their speech would be slurred and eventually they’d be unable to speak at all, or to walk. Confined to bed, the end would often come in a fit of convulsions. Syphilitic insanity was recognised as a disease but thought to be a completely separate entity to General Paresis of the Insane, right up until the 1930s.

In 1905, Treponema pallidum was identified as the causative agent of syphilis, paving the way for laboratory diagnosis of the disease and the eventual realisation that General Paresis of the Insane was one and the same thing. The first effective treatment soon followed, with German chemist Paul Ehrlich developing a drug called arsphenamine, marketed as Salvarsan, in 1909. By the following year, it had become the most popular drug in the world, with thousands of patients being treated. But it had major drawbacks: based on arsenic, it had serious toxic side effects and it didn’t work at all in the later stage of the disease. Like plague, the real breakthrough would come in the form of antibiotics, with penicillin proving to be effective against syphilis. Today, the mainstay of syphilis treatment is still intramuscular injection of penicillin, together with public health measures to notify sexual partners and offer them treatment.

Syphilis is preventable and curable, but still very much with us. Around 8,000 people are diagnosed with syphilis in the UK each year, with around two fifths of those being gay or bisexual men. The rates are highest in the most deprived areas. It’s a pattern that is reflected globally: the disease is more prevalent in low- and middle-income countries, and men who have sex with men bear a high burden of the disease. Around 7 million new cases are diagnosed globally each year, making syphilis one of the most common sexually transmitted diseases in the world. But given that this is a disease that, untreated, tends to stick around, this is only the peak of the iceberg. The latest estimated global prevalence of syphilis is surprisingly high: on average, it’s 0.5 per cent, meaning that 1 in every 200 people in the world has syphilis. (For comparison, the global prevalence of gonorrhoea is around 0.8 per cent, or 1 in 125 people.) There’s a lot of variation embraced by this average; in some regions, the prevalence is as low as 1 in 1,000; in others, it’s as high as 1 in 60.

Amongst men who have sex with men, the rate is even higher: 1 in 12. The World Health Organization recognises a need to improve testing, treatment and prevention, particularly in this group. But syphilis also affects heterosexual men and women. Untreated syphilis in a pregnant woman presents a huge risk to the fetus. Some babies survive, with their bodies already devastated by the disease; many die in utero or soon after birth. Syphilis is a leading cause of stillbirth worldwide, second only to infant deaths during birth. But if a woman is tested and treated early enough, the baby can be saved. The rate of syphilis in pregnant women is higher than that quoted for the general population, ranging from less than 0.1 per cent to over 2 per cent in different countries. These rates, picked up by antenatal screening tests, may be a better reflection of the real prevalence of the disease than case reports, because some patients are asymptomatic and access to healthcare also varies hugely around the world.

Data from antenatal screening for syphilis, as well as case reports, reveal the huge impact that penicillin has had in combating this disease globally, but has also laid bare health inequalities. In the pre-antibiotic era, some countries, such as Canada, Denmark and Norway, already had low rates of positivity amongst pregnant women – around 1 per cent – perhaps in part because of Salvarsan. In contrast, the rate in South Africa, in the Black population, was around 15 per cent. Between 1945 and 1958, when antibiotics became widely available, syphilis rates rapidly declined everywhere – except Africa. Economic inequality can’t explain all of this disparity, because low- and middle-income countries in Asia did experience a fast reduction in cases. In the second half of the twentieth century, the prevalence of syphilis in sub-Saharan Africa more than halved, but it still remained an order of magnitude higher than the rate in Europe. One suggestion is that sexual networks are more connected in Africa, but the data seems equivocal. Other factors could include difficulties accessing healthcare, the effect of conflicts and social disruption, and lower use of barrier contraception. It’s surely pertinent that the parts of the world with higher rates of syphilis in the 1980s were precisely the same places where HIV became most prevalent. In 2017, there were 37 million people living with HIV globally, two thirds of whom were in Africa. In the nineteenth century, Christian missionaries set out to convert the continent, and were very successful. But with some branches of the Church defining condom-use as a sin, Christianity has proven itself to be a great ally of sexually transmitted infections. Nevertheless, as society globally responded to the threat of HIV, changes in sexual practice and antibiotic prophylaxis meant that syphilis incidence declined in the last decade of the twentieth century. But since 2010, it’s been on the rise again. Some strains have developed resistance to certain classes of antibiotics – but not, thankfully, to the type of penicillin that is the main treatment.

Genetic studies of modern syphilis have enabled the ‘family tree’, or phylogeny, of the pathogen to be constructed. The research has been challenging as Treponema pallidum proved very difficult to culture in the lab – it just would not grow outside of a warm, living host. And the first genome analyses focused only on samples from the US, Europe and East Asia. In 2021, the results of a wider study, taking in Africa, Asia, Australia, South America and the Caribbean, were published, looking at variation both between and within countries. What the researchers uncovered was a remarkable degree of homogeneity: syphilis all around the world was genetically very similar.

All modern T. pallidum genomes clustered into two lineages, both of which were found, circulating together, all around the world. Looking at the variation between and within these strains, and knowing something about the rate of mutation in syphilis genomes – with around one substitution (or nucleotide change) per genome every seven years – the geneticists were able to date the timing of particular branches. Most of the circulating sublineages of the two main strains were quite young – they’d emerged between 1980 and 2000. The researchers wondered what had given these particular sublineages ‘the edge’, allowing them to spread around the world and outcompete older strains of syphilis. Could it have been antibiotic resistance, they wondered? They checked the genomes for particular variants involving changes in a single nucleotide in the string of DNA and did indeed find some known to be associated with antibiotic resistance (but not to penicillin). They could also see clearly that there had been a ‘genetic bottleneck’ in the late twentieth century, followed by a rapid global expansion and proliferation of sublineages in both major strains of the disease. It’s likely the bottleneck – which represents a crash in the global population of syphilis, effectively pruning the phylogenetic tree and producing a reduction in genetic diversity – was caused by the safe-sex messaging in the HIV pandemic, as well as widespread antibiotic therapy, which would have wiped out some vulnerable strains of syphilis. And then, once effective retroviral therapy became available for HIV, sexual behaviour changed again, and the heavily pruned family tree of syphilis began to sprout once more, sending out all those new sublineages.

The insights from genomics into how this sexually transmitted infection operates are important as they can help us to design better public health measures to combat the disease. But the decoding of the DNA of current strains also hints at the deeper history of the disease, because when the geneticists looked at the differences between the two main lineages, and dated their convergence in the phylogeny, they found that this branch-point went back some 500 years, to around 1534 – just as a syphilis epidemic was raging across Europe. What’s curious about that date and that epidemic is that syphilis was either unnoticed or unrecognised in Europe before the late fifteenth century.

So what happened in the late fifteenth century that unleashed this new scourge? Did syphilis jump from another host into humans? Did a new virulent strain emerge? Or was it something about human society that changed?

For a long time, it’s been thought that the driver for this epidemic was a social change – and a momentous one. It was one driven by expanding trade networks, but it marked a real sea-change for humanity, and for many other species as well, because in the late fifteenth century, Europeans discovered two continents that they had been previously unaware of. And the world would never be the same again. In the decades and centuries that followed, people – some of them free, some enslaved – would cross between the Old and New Worlds. Other species would do the same. From a broad ecological perspective, it’s been cited as the most significant event affecting ecosystems since the asteroid that slammed into the Yucatan Peninsula in Mexico 66 million years ago and wiped out the dinosaurs. In this ‘Great Exchange’, wheat, oats, rye, coffee, cotton, sugar, bananas, sheep, pigs, cattle, horses and chickens travelled from the Old World to the New. Potatoes, cocoa, maize, pineapples, chilli peppers, tomatoes, tobacco, turkeys, llamas and grey squirrels travelled in the opposite direction. (I wrote about some of these species, and the consequences of the Great Exchange, in my book Tamed.) But along with all those humans, animals and plants switching continents, so did pathogens. Europeans took smallpox and influenza to the Americas, with disastrous effects for the population of those continents. They also introduced measles, chicken pox, cholera, typhus, malaria and plague. It’s thought that around 90 per cent of the American population was wiped out in the first 100–150 years after Christopher Columbus’s fateful trip in 1492.

A longstanding theory, the ‘Columbian hypothesis’, suggests that one disease in particular travelled back the other way: none other than syphilis. This hypothesis suggests that Columbus and his crew contracted syphilis from the inhabitants of the island where they first built a fort in December 1492. The island was called Haiti by the people who lived there, but Columbus, with colonising zeal, named it Insula Hispana, claiming it for Spain. We still know it as Hispaniola. On returning to Spain, some of the crew joined the army of Charles VIII of France. In 1495, that army laid siege to Naples – and a disease broke out in the troops. Historians believe this to be the first record of syphilis. When the army broke up, the mercenaries went off to spread the disease around Europe. By the end of the century, the disease had also reached Russia, Africa, the Middle East and India. And it kept spreading, reaching China by 1505 and Australia by 1515. By the early sixteenth century, the idea that Columbus and his crew had brought syphilis back to Europe was entrenched in the literature of the time. More recently, the virulence of the outbreak in the late fifteenth century into the sixteenth, and the rapidity of its spread, have been taken to indicate a novel pathogen surging through an immunologically naive population.

But this was only ever a hypothesis, and standing in opposition to it was another explanation: the ‘pre-Columbian hypothesis’. Proponents of this theory suggest that the lack of documentation of the disease before the late fifteenth century was simply down to medical ignorance, and to syphilis being lumped in with other diseases that caused similar signs and symptoms. There was also a possibility that syphilis had existed in a milder form up to the fifteenth century, and then a new, more virulent and sexually transmitted strain emerged, perhaps even driven by increasing urbanisation and crowded cities.

This is an argument that has been going on for centuries, and it was clearly never a debate that was going to be resolved by poring over historical documents. What was needed was hard evidence. Verifiable evidence of syphilis in human skeletons from Europe dating to before 1492 would destroy the Columbian hypothesis.

The trouble is, the same problem that plagued the fifteenth-century doctor also stalks the palaeopathologists’ lab: there are some other diseases that produce a similar pattern of lesions to syphilis. Although the gummatous lesions of syphilis look very different from most other bony pathologies, there are two very closely related, but non-venereal, diseases that can cause similar changes. These are yaws and bejel (also known as endemic syphilis). In fact, they’re so closely related to syphilis, they’re even caused by different subspecies of Treponema pallidum – T. pallidum pertenue producing yaws and T. pallidum endemicum causing bejel, while the strain causing syphilis is T. pallidum pallidum. There’s now plenty of evidence of treponemal disease in the Americas before European contact – and in fact, going right back to 7000 BCE, but in the 1980s, nobody had found any evidence of pre-Columbian treponemal disease in Europe. This seemed to tacitly point to syphilis, and the other less virulent forms of treponemal disease, being imports from the Americas. Absence of evidence is always tricky, though – it’s brave to claim that it is evidence of absence. And indeed, in the last few decades, discoveries of cases of pre-Columbian treponemal disease in skeletons from the Old World began to mount up. But was it syphilis?

The origin hypotheses are very difficult to test by looking at the bony evidence. Some researchers have suggested that it is possible to discern between yaws, bejel and syphilis based on the pattern and frequency of lesions, but others have remained sceptical. It’s been suggested that lesions in young adults are indicative of endemic disease rather than syphilis, but again this is not definitive. As evolutionary biologist Kristin Harper and colleagues wrote in a 2011 review of the palaeopathological evidence, ‘While one can state there is evidence of pre-Columbian treponemal disease in a sample, one cannot state that there is evidence of syphilis.’ And in fact, when looking at single bones, or when faced with what could be early signs of treponemal disease in the skeleton, it’s difficult to be sure about even this broad diagnosis. It’s only when tertiary syphilis is advanced, in a relatively complete skeleton, that the palaeopathologist can be sure about the diagnosis; in such cases, you see gummatous lesions affecting many bones, on both sides of the body, as well as damaged joints, destruction of facial bones, and a cratered, worm-eaten appearance of the cranial vault, called caries sicca.

One particular manifestation of syphilis may lead to a more robust diagnosis, though, and that’s congenital syphilis. Yaws and bejel are very rarely transmitted from mother to fetus, through the placenta, so if it’s possible to detect treponemal disease in a fetus or child skeleton, this should be indicative of syphilis itself. Some of the skeletal signs, such as fractures, osteomyelitis and loss of bone in the tibia, are not specific to congenital syphilis, but there are several features in teeth that have been considered to be more strictly associated with congenital syphilis. All involve problems with enamel formation.

One dental defect is ‘Hutchinson’s incisors’, named after Sir Jonathan Hutchinson, a surgeon at the London Hospital – in 1861 he described the affected incisors as barrel-shaped with a notch in the cutting edge. Another is ‘Moon’s molars’, also known as ‘bud molars’. The defect was first described by a dental surgeon at Guy’s Hospital, Henry Moon, in 1877. It affects the crown of the first permanent molars, which narrows to unusually small, bud-like cusps. A third dental defect associated with congenital syphilis is ‘Fournier’s molars’, where the cusps of permanent molars are cinched-in or waisted, due to thin enamel, giving the tooth a characteristic appearance that is well described by its other name: ‘mulberry molars’. Unfortunately, it turns out that even these apparently dependable signs of syphilis can occasionally occur in other conditions. Palaeopathologists are better off using a whole suite of features to diagnose the disease, but even then, the diagnosis is not absolutely certain.

When Kristin Harper and her colleagues set out to scour the literature for mentions of diagnosed syphilis in skeletons from the Old and New Worlds, before and after the time of Columbus, they looked carefully at diagnostic methods – and at dating, as not all the reported cases were directly dated using modern radiocarbon techniques. They found eleven well-dated Old World examples that were highly likely to be syphilis, all of which dated to after 1493, when Columbus returned to Europe. Nine potential Old World cases dating to earlier than this crucial date were considered to be uncertain diagnoses, while three pre-Columbian cases from the New World were considered to be certain. The authors concluded: ‘we find that despite intense research interest, credible evidence disproving the Columbian Hypothesis is lacking’.

And yet, there could be other reasons for the lack of convincing evidence in the pre-Columbian Old World. Perhaps it’s just the sparseness of the archaeological record – bone isn’t always affected in syphilis, and skeletons don’t always survive the ravages of time, and even if they do, archaeologists may not have found them. But then again, tens of thousands of archaeological skeletons have been analysed from Africa and Eurasia (although with a definite concentration around Europe and the Mediterranean) and there’s no certain case of pre-1493 syphilis amongst them. And it can’t come down to a lack of training amongst palaeopathologists, as they’re spotting plenty of cases in remains dating from after 1493. Some researchers have suggested that life expectancy may be important: if people were generally living shorter lives before the fifteenth century, they wouldn’t have had the time to develop syphilitic bony changes. Perhaps an increased lifespan after the fifteenth century could then account for what appears to be a sudden emergence of cases. And yet there is no evidence that life expectancy changed much around this time; it wasn’t until the nineteenth century that we start to see a demographic shift towards increased longevity. Another possibility has been suggested, which is that syphilis could have been confused with leprosy during the Middle Ages, meaning that anyone with advanced syphilis is likely to have been cared for in a leprosarium. Relatively few medieval hospital cemeteries have been investigated, and perhaps even in those that have, syphilis hasn’t been recognised for what it is. But that seems somewhat unlikely – the very careful analyses of the cemeteries that have been investigated would surely have thrown up examples of syphilis, had it been there.

Somewhat frustratingly, when the palaeopathological evidence is looked at en masse, it’s difficult to draw a definite conclusion. We may still wonder if there could be some as-yet undiscovered cases of pre-1493 syphilis, perhaps in relatively under-investigated regions of the Old World, such as sub-Saharan Africa. But Harper and her colleagues concluded that – given the apparently sudden appearance of robust cases of the disease after Columbus returned from the Americas – it was probable that this really does represent the introduction of a novel disease to Eurasia and Africa. But in the absence of definitive evidence, the whole Columbian-versus-pre-Columbian debate rumbled on.

And then genomics arrived on the scene. Surely some much-longed-for clarity would now emerge out of the murk. Just one example of a T. pallidum pallidum genome from a pre-Columbian skeleton could bring the Columbian hypothesis crashing down. Except – as so often happens when new forms of data emerge – the picture of treponemal diseases got even more complicated. The genetic data revealed even more overlap between the diseases caused by the three subspecies of T. pallidum than we thought existed. There have been clinical cases which look like syphilis, but the DNA isolated from lesions has turned out to be that of the endemicum subspecies. Conversely, T. pallidum pallidum has been found in cases of yaws. It’s starting to look like these diseases are very flexible. And in fact, these genetic insights seem to support another hypothesis about the origins of syphilis, the ‘Unitarian hypothesis’, which suggests that the treponemal diseases are so closely related that they really are the same thing: a single, flexible disease. The idea is that this shape-shifting disease would tend to exist in its milder, endemic form where it would enter the body through tiny skin abrasions, but would emerge as an altogether nastier, sexually transmitted infection with improvements in bodily hygiene, when sex would remain its only chance of penetrating another host. The genetic identification of different and overlapping patterns of disease produced by different subspecies of T. pallidum seems to fit that picture, meaning that it’s not possible to map particular subspecies onto specific, individual diseases. It could be – rather like plague – that the way treponemal disease manifests in a particular human body may be influenced by the route of transmission, as well as by the immune system of the host.

In 2018, the first genomic evidence of treponemal infection in archaeological skeletons was published. The samples came from a convent site in Mexico City and dated to the seventeenth century. The skeletal remains were those of tiny babies, with evidence in their bones of treponemal disease – expansion of limb bones and plaques of periosteal bone – potentially representing congenital syphilis. Samples were taken from the bones of five individuals, and three were found to contain treponemal DNA. Comparing the DNA with that of modern T. pallidum strains, it became clear that two of the samples were T. pallidum pallidum, while one was closest to the modern yaw-causing T. pallidum pertenue. These seventeenth-century samples can’t shed light on the Columbian question, but the detection of treponemal DNA in historic samples was an important step forward. And once again, the results emphasised the flexible nature of treponemal disease, with the strain associated with the modern clinical disease of yaws being proven to be capable of vertical transmission – from mother to fetus.

More genomic evidence began to accumulate. Genomes of T. pallidum pallidum were recovered from historical samples from Europe dating to the end of the fifteenth century. But one sample, positive for T. pallidum pallidum, was radiocarbon-dated to the early to mid-fifteenth century. Could this be the early, pre-Columbian evidence that would finally fell the Columbian hypothesis? Unfortunately, the date is frustratingly too close. Even though two independent radiocarbon dates were obtained, there’s a possibility that contamination could skew the date by a few decades. So it’s not the unequivocal smoking gun that it first appears to be. But other genome data is now seriously challenging our preconceptions about treponemal diseases, with genetic evidence of T. pallidum pertenue – the strain associated with yaws, only seen in tropical regions today – being found in bones dating to the fifteenth-to-sixteenth centuries, from Finland. What’s also become clear from the archaeogenomic evidence is that the three strains of T. pallidum were not completely independent: they had clearly swapped bits of DNA with each other. It’s also been possible to identify some genes associated with virulence – just as with Yersinia pestis – and it’s likely that DNA-swapping or recombination is one way in which T. pallidum has evolved into modified strains.

Where does this leave us? Craving more data, certainly, but with a certainty that the ‘Columbian hypothesis’ is a massive oversimplification. With other strains of treponemal disease existing in Europe from the fifteenth century, we may have been too quick to assume that T. pallidum pallidum was the culprit of the historically attested outbreak. And as we learn more about how this disease operates and manifests – and the historical data is part of that wider investigation – we’ll get better at combating it in the present, too.

We don’t yet have any metagenome evidence from the remains of the woman buried in the apse of All Saints, Fishergate, but radiocarbon dating of her skeleton indicates that she died sometime between the mid-fifteenth and mid-sixteenth centuries – straddling that crucial date of 1493. So it seems her bones could not disprove the Columbian hypothesis even if they were to contain T. pallidum pallidum DNA. And if the bones were ever shown to have harboured another strain, that would no longer be so surprising, as we’re seeing that the other strains could, in some cases, cause similar lesions. If pathogen DNA were detected and sequenced, this burial could contribute to the bigger picture of syphilis evolution and the appearance of the disease in Europe. But there’s also a more personal story to be told, an osteobiography. Whatever bacterium it was that invaded her body and colonised it so extensively, this woman had clearly suffered.

It’s tempting to look at those ravaged bones and presume that this woman must have been in agony for many years. From what we know of patients’ experience of untreated syphilis, she may have been in pain from very early in the course of the disease, within the first three years. Some patients experience severe pains in their limbs, feeling as though someone is drilling or boring into the bone. Headaches are also common. Gummata of bone may occur several years or even a couple of decades later. Sometimes the lesions are associated with severe, intractable pain, but in some people, they can actually be painless.

In the pre-antibiotic era, the neurological effects of syphilis were much more common and profound than they are today. The spiral treponemes screw themselves through body tissues to enter the bloodstream minutes after initial infection, and, within the first hours or days, get to the brain and spinal cord. If the disease is left untreated, some patients can go on to develop meningitis – with headaches, nausea and vomiting, photophobia and seizures – and blood clots in the brain or spinal cord, causing stroke-like symptoms. Late neurosyphilis is a feature of the tertiary stage of the disease. It’s caused by chronic inflammation of the meninges and the brain itself, and it starts with mood and personality changes. Even later symptoms include labile mood, impairment of memory and judgement, confusion and delusions, and seizures. Depression, mania and psychosis may also occur. These are the progressive features of the syndrome that was once known as General Paresis of the Insane. Meanwhile, degeneration in the spinal cord can cause ‘lightning’ pains, bladder dysfunction and muscle weakness. Untreated neurosyphilis can cause paralysis, dementia and death.

It’s impossible to know if the woman buried at Fishergate would have suffered from neurosyphilis, but we can look at the recorded prevalence amongst untreated patients with syphilis in the early twentieth century. Some 3–15 per cent of those patients would go on to develop meningitis or stroke in early neurosyphilis, while around 10 per cent would eventually develop the progressive and devastating features of late neurosyphilis. We will never know precisely what this woman’s lived experience of advanced syphilis was, but she may well have suffered extreme pain, seizures, physical disability and serious psychiatric illness. This is something that is important to bear in mind when we think about who she might have been, and how she may have been treated by her community in life – and in death.

Lauren McIntyre was so fascinated by this grave, by this individual, buried in an unusual way, in a pit inside the apse of All Saints Church, that her investigation went beyond her osteological, palaeopathological analysis of the bones. She turned to historical documents to see if there was any mention of someone who might potentially have been laid in such an irregular grave, in such a prestigious position, inside the church. The site of the grave suggests that this was a high-status individual – someone who was either a very wealthy benefactor to the church or who played a significant religious role.

And astonishingly, there was someone who seemed to fit the bill.

Lauren tracked down a name in a fifteenth-century record of probate held at the University of York. It read:

Probacio testamenti Domine Isabelle Germann nuper de Eboraco Recluse

[Probate of the testament of Lady Isabella Germann recently recluse of York]

Probatum fuit testamentum Domine Isabelle Germann’ nuper Anacorite in ecclesia parochiali Omnium Sanctorum in Fysshergate defuncte terciodecimo die mensis Augusti Anno Domini Millesimo ccccmo quadragesimo octauo et administracio commissa Roberto Smeton executori in eodem testamento nominato iurato in forma iuris.

[The testament of Lady Isabella Germann’, recently anchorite in the parish church of All Saints in Fishergate, deceased, was proved on the thirteenth day of the month of August in the year of our Lord 1448 and administration granted to Robert Smeton the named executor of the same testament sworn in the legal form.]

The testament itself is missing from the historical record – it may even have been verbal. But the existence of this document indicates that she had possessions that needed to be dealt with after she died. There are seven other mentions of Isabella Germann, and they all come from the wills of other people – people who had made bequests to her in return for her prayers. One of these wills dates to 1455, suggesting that Isabella Germann was still alive at that point, and that the probate of 1448 had been granted – somewhat strangely – before she died.

And the dates fit – at least, there is overlap between the dates of the bequests to Lady Isabella Germann, ranging from 1428 to 1455, and the radiocarbon date of 1443–1536 CE.

As the probate makes clear, Isabella Germann was a female anchorite – or anchoress. This was a religious role that went beyond the usual vows of monks and nuns in its asceticism. An anchorite or anchoress was someone who would be enclosed in a cell in a church – literally ‘anchored’ to it – for the rest of their life. If you wanted to be an anchoress, you’d have to apply to the local bishop and also prove that you were financially independent, even though it was likely that you’d receive donations once you were installed.

The walling-up of an anchoress in the church would have been a ceremonial occasion. The earliest rite of enclosure – Servicium Recludendi or Service of a Recluse – comes from a twelfth-century compendium of bishops’ services, and it’s essentially an adapted burial rite. During the service, the intended anchoress or anchorite would lie on the floor while the clergy chanted the Litany of the Saints. Then the bishop (or another priest if the bishop wasn’t available) would sprinkle the person with holy water and wave a censer over them. After that, the clergy would help the individual to her feet and place two burning candles in her hands. While the choir sang a hymn, she’d approach the altar and kneel three times, saying:

‘Suscipe me Domine secundum eloquium tuum et vivam, et non confundas me ab expectatione mea.’

‘Receive me, Lord, according to your word and I will live, and let me not be ashamed by my hope.’

Then she would be led to the anchorhold, the cell in which she would be living the rest of her life, where she would say: ‘Ingrediar’ – ‘I will go in.’

A priest would then sprinkle the cell with holy water and wave incense around it, and then commend the soul of the anchoress, just as would be done in a burial service. Then she would enter the cell and the priest would throw some earth over her – a symbolic burial. Then everyone else would depart, leaving the priest alone with the recluse for some final words of advice, before the door of the cell would be sealed up. This symbolic social death transformed the woman into an anchoress, placing her closer to God. There, she could act as a prophet and intercessor.

There was no obvious archaeological evidence of a cell amongst the remains of All Saints, Fishergate, but it’s possible that the apse itself was used as an anchorhold in this small church. The high altar would have been close by, viewable through a small window or squint, perhaps.

There was a handy guidebook for anchorites and anchoresses, called the Ancrene Wisse. It contained practical advice for daily life as well as hints and tips on how to be more pious, pure and penitent, and how to avoid temptation. Plain, warm clothing should be worn; a frugal diet was to be eaten, consisting of two meals a day and only involving meat on special occasions; the anchoress was permitted to keep a cat. Speaking directly to any visitors was discouraged; it was recommended that communication happened via a mediating maidservant. And the windows of the cell were to be kept covered with black curtains to stop the anchoress from looking out, and voyeurs from looking in. As idleness could lead to temptation and sin, it was suggested that the anchoress should keep herself busy by mending clothes and by digging a pit with her hands – a pit that would, one day, form her grave.

The crouched position of the body in the grave at Fishergate is highly unusual; in most inhumations at the time, bodies were laid out straight, lying on their backs. Perhaps Isabella herself had dug this unusual, pit-like grave.

This life of extreme privation proved strangely popular in the later medieval period. There are historical records of 96 anchorites or anchoresses in twelfth-century England, 198 in the thirteenth century, 214 in the fourteenth century and 204 in the fifteenth century, with a drop to 68 in the sixteenth century. These numbers could be underestimates, but they give us an indication of the trend. York was a bit of a hotspot, with eight recorded religious recluses in the fifteenth century, including Lady Isabella at All Saints, Fishergate.

The boom in these religious hermits is often framed as driven solely by spiritual factors – a ‘growth in lay piety’. Anchoritism has been described as ‘an especially important (and perhaps empowering) mode of religious expression for women’. But it does make me wonder about other factors that must surely have influenced the trend. As Lauren and her colleagues noted in an article on the Fishergate burial, anchoritism can be seen as a development of the asceticism that characterised the monastic way of life. And both need to be seen in the wider social context. For women in particular, with few legal rights in medieval England, joining a convent could be a way to achieve autonomy and to avoid forced marriage and a lifetime of domestic drudgery. Choosing to become an anchoress might seem an extreme decision, but it could have been seen as a rational alternative to worse fates. And there is something else that’s quite curious about these recluses. They’re not choosing to secrete themselves away in a truly secluded way, disappearing from society. They’re actually doing it in a very public way. From the highly conspicuous enclosure ceremony to the ongoing visits that people would make, and the bequests that would be granted, the anchoress was a celebrity. With seclusion came fame. And, just as possessing relics of a saint could be good for business, a church could certainly benefit from having a local recluse living in the walls.

But there’s yet another dimension in this case – if the skeleton in the apse is indeed that of Lady Isabella Germann – and that is the evidence of advanced syphilis. Like leprosy, the disease was considered to be linked with sinful behaviours: with lust, promiscuity and immorality. As Lauren McIntyre and colleagues suggested, even if her disease was not specifically diagnosed, the link between a disfiguring condition and sinfulness would still have existed. There was also that strange duality that we considered in the chapter on leprosy, where a disease could be perceived as a sign of sin but at the same time made the sufferer into a martyr, bringing them closer to God. It’s possible that this woman was already facing social stigma and exclusion. Alternatively, it’s possible that the visible signs of advanced disease appeared only after she became an anchoress. Perhaps, at the ceremony of enclosure, she knew her fate, but no one else did.

There is a further possibility that hasn’t been suggested before, to my knowledge, but that may be relevant in this case. It is entirely speculative, but it’s based on the clinical features of syphilis – in particular, the neurological and psychiatric features of the disease. These could have played a role, both subjectively and objectively. A person suffering with seizures may have interpreted these attacks in a spiritual way, and people around them could have done the same. Similarly, the labile mood, personality changes and psychoses of late neurosyphilis could have been seen as religiously inspired. (There is a tenuous link between anchoritism and mental illness, in Simeon Salus, or Simeon ‘the Fool’, who was a sixth-century anchorite famous for erratic behaviour in public.) It’s recognised today that delusions often involve religious themes. There’s a very blurred line between religious belief and religious delusion; interestingly, hearing the voice of Jesus may not be considered delusional in a Christian society today, while more idiosyncratic and culturally anomalous delusions would be. Could delusions have driven a personal decision to become a celebrity recluse? Or could other people have chosen this path for someone whose behaviour was becoming increasingly erratic? At least, walled up in the church, they would be fed and clothed, if frugally.

It’s easy to see the practice of anchoritism as cruel, from a twenty-first-century perspective, though we do have to be very careful about viewing the past through our own cultural, moral lens (it’s also impossible to be completely objective). If the anchoritic life was in some cases imposed, rather than chosen, it may have been essentially cruel: locking someone away. But it could have been a kindness – and it perhaps could even have helped. Today, people with schizophrenia may find solace in culturally acceptable religious beliefs, which can provide a coping mechanism.

There’s been a tendency to poeticise the cultural practice of medieval anchoritism; it’s acquired quite a thick veneer of Victorian religious romanticism. As attendance at Anglican services declined in the nineteenth century, there was a desire in some quarters for ‘re-enchantment’; a return to a mythical Golden Age; a revival of the faith of the Middle Ages. This was seen in a very visible way with the renovation of churches in mock-medieval style, as Victorian Gothic elbowed neoclassical architecture out of the way.

In 1827 or 1828, William Wordsworth penned a sonnet about a fourteenth-century anchoress called St Catherine of Ledbury. He describes how she was drawn to Ledbury by church bells:

Warned in a dream, the Wanderer long had sought

A home that by such miracle of sound

Must be revealed: she heard it now, or felt

The deep, deep joy of a confiding thought;

And there, a saintly Anchoress, she dwelt

Till she exchanged for heaven that happy ground.

It’s a poem soaked in mystical romanticism and pious religiosity, which, as medievalist Liz McAvoy has pointed out, also suggests the Welsh borders, where the poem is situated, to have been a much more serene and tranquil place than it actually was at the time. Amidst violence and conflict, women held positions of power, managing their husbands’ estates when they were away fighting, or in perpetuity when they died. Upon the death of her husband, a noblewoman in the medieval Welsh Marches would have become a sought-after commodity. Religious seclusion may have offered another route to those widows: a safe space in a politically volatile and dangerous climate. It may be that an anchoress could have freely chosen that lifestyle – but the reality is that the choices such women could make were very limited.

Wordsworth’s ‘St Catherine of Ledbury’ was in fact the aristocrat Katharine de Audley, who was enclosed in the church of St Martin and All Saints, very close to the chapel and hospital dedicated to St Katherine of Alexandria, in Ledbury (so the poet’s confusion is understandable). And in fact, many anchoresses seem to have been noble laywomen, unlike their male counterparts, anchorites, who were often monks or priests before they became pious hermits. We know a little more about Katharine de Audley than we do about Isabella Germann, but her story has become transmuted into myth. A wealthy widow, legend has it that she was courted by various aristocratic men throughout her life, and that – as was traditional for anchoresses – her religious calling began with a prophetic vision: fleeing to the countryside, Katharine hears church bells (ringing on their own) and these lead her to the church in Ledbury. Different versions of the legend then tell of her living the rest of her life either in that Ledbury anchorhold or in another hermitage in the nearby village of Much Marcle.

Inspired by the legend, Wordsworth’s poem transforms Katharine de Audley into an archetype, an alluring poetic figure. Philosophers have mused on the strange draw of that idea of the religious recluse. The figure of the anchoress, in particular, has been seen variously as a feminist symbol of liberation from patriarchal control, an embodiment of that idea of a lost Golden Age of faith, and a cultural scapegoat, laden with communal guilt.

But Katharine de Audley was a real woman. She was the daughter of a powerful Marcher lord, John Giffard, whose landholdings swelled into Wales after he helped to quell the Welsh rebellion of 1264–65, and a high-born noblewoman, Maud de Longspee. And in fact, the matter of her parents’ marriage perfectly illustrates how noblewomen were commodified at this time. Aged thirty-seven, Maud, the widow of the third earl of Salisbury, William de Longspee, was captured from her own castle and carried off to Giffard’s home at Brimsfield. Despite appealing to Henry III, Maud was forced to marry Giffard, who paid 300 marks to the king for the privilege. That same year, 1271, Maud gave birth to Katharine. She had two more daughters before she died, less than twelve years later.

Katharine married Nicholas de Audley in 1288 and had three children; when Nicholas died in 1299, Katharine was probably left managing a very large estate. And she appears to have resisted remarriage – something that, as Liz McAvoy puts it, ‘would have sent out shock-waves within this powerfully patriarchal Anglo-Norman environment’. This noblewoman wasn’t about to become a commodity. And then tragedy struck the family: in 1307, her seventeen-year-old daughter, Ela, was widowed, and her eldest son and the heir to the family fortune, Thomas, died. The following year, Katharine had arranged a licence passing most of the family’s land to her second son, Nicholas, leaving herself with an annual stipend. She clearly had her eye on an escape route – something that would remove her from the ‘market’ and save her from being just a ‘valuable receptacle’, an object to be exchanged by powerful men. In 1313, she handed over the land in Wales, inherited from her father, along with Llandovery Castle, to Ela. The grant of these lands, which would also have provided her with a pension, was witnessed by the bishop of Hereford and the vicar of Ledbury, amongst other notable clerics. And then Katharine, in her early forties by this time, disappears from history; it’s thought that this is the point she became an anchoress.

But the best-laid schemes often go awry. Having divested herself of land and wealth – to protect herself from being carried off as her mother had been – Katharine must have felt safe in her anchorhold. Her family, however, may have been left more vulnerable. Three years later, her son Nicholas died, and his wife followed him in 1322. Two small orphans were now set to inherit the family’s estate, with a half-brother of Katharine’s, John Giffard, holding that land in trust. Then John was executed for treason and his inheritance passed back to – you’ve guessed it – Katharine. At the same time, it seems the stipend she’d been living on had evaporated, through financial mismanagement or outright fraud. Liz McAvoy tracked down a final reference to Katharine, in a petition lodged to the king in 1326–27; although the details are lost, it seems likely that she had been left impoverished. She would have been about fifty-six.

This biography, painstakingly extracted from contemporary records, lets us see one woman who became an anchoress more clearly, in the social and political context of the time. She is so much more than just that cipher of piety in a romantic poem. Liz McAvoy has analysed and then stripped away that myth to find a real life, and the story of one woman rejecting social norms and trying to create a different destiny for herself.

There’s a striking similarity in the meticulous, forensic approach to historical documents that Liz McAvoy has employed, to reconstruct the biography of Katharine de Audley, and the work of Lauren McIntyre, extracting every detail from a skeleton to create the osteobiography of a woman who may well have been Isabella Germann. And both these biographies lead us to dig down into the myths that cling so tenaciously to the Middle Ages. They help us to extract ourselves from generic and romanticised ideas about the ‘saintly anchoress’ and to encourage a more nuanced perspective, where we try to look at personal, political, social, psychological and perhaps psychiatric aspects. This is not to strip away the religious and spiritual dimensions of the phenomenon and experience of anchoritism, but to explore it more widely, in the round. To see those people as clearly as possible. History and archaeology bring the past, and – most importantly – the people who lived in it, into focus.

EPILOGUE

The new synthesis of history, archaeology and genetics offers us a much more detailed picture of the past than we’ve ever been able to see before. Not just at a grand scale – though it certainly does that too – but at an individual level. Piecing together different sources of information, we can paint detailed portraits of people, some of whose names we know; many we don’t.

Osteoarchaeology, palaeopathology and now archaeogenomics are transforming our understanding of the past, making us look again at the broad sweep of history, now that we see more clearly how epidemics were ignited and spread, and now that we can so precisely diagnose the diseases that people were suffering from. We can unlock secrets from bones preserved for centuries in tombs, graves and crypts. We see how disease is an enduring part of the human condition; how pathogens we thought had come along recently have been with us for millennia; how changes in microbes and changes in society can alter the human experience of disease; how easily words spoken by those in power can be translated into violence; and what Japanese baseball pitchers and medieval archers have in common.

Archaeology is not the handmaiden of history. It provides us with an alternative version of history, one where some biographies – including those that were never written – become clearer, in bone and in the biomolecules still hiding away in them; cryptic, hidden – until our newest technology brings them to light.

Putting the history and archaeology together, we can make more sense of the past, and perhaps feel a greater connection with all those generations of people who have gone before. To be human is to feel pain, to experience loss. We are not ethereal creatures, made of pure thought, but physical beings – biological entities. We experience the world through our bodies, and our lives are written into those bodies and into our bones.

And this is what the skeletons of the dead say to us when we find them: Listen to us. We have stories to tell.

Skeletons found in a mass burial site underneath St John’s College in 2008 by Thames Valley Archaeological Services. © Thames Valley Archeological Services

A skeleton from the St John’s College, Oxford site laid out in the lab. An injury is clearly visible on the skull.

Dr Ceri Falys in the osteology lab.

Skull from the St John’s College, Oxford site with chopping blade wounds to the parietal and frontal bones.

Burned, charred bones were also found at the site.

The left pelvis with a puncture wound entering the anterior (deep) surface of the bone.

Part of a left temporal bone with a clean slice through the mastoid process, just behind and below the ear.

A skeleton from the St Mary Magdalen, Winchester site laid out on a table in the lab.

Destructive changes to finger bones, St Mary Magdalen, Winchester.

The skull from Skeleton 19, showing the dramatic resorption of the bones around the nasal aperture and upper jaw known as ‘facies leprosa’.

With Dr Simon Roffey and Dr David Ashby in the osteology lab at the University of Winchester.

Excavations at St Mary Magdalen, Winchester. © Simon Roffey

Mycobacterium leprae under the microscope: the small red rods are the bacteria, among human skin cells with their nuclei stained blue; taken from a leprosy skin lesion (CDC, US Government public domain, 1979).

The pierced scallop shell from the grave of Skeleton 27 – a pilgrim’s badge? © Simon Roffey

The burial of Skeleton 27 – with the scallop shell resting over the left pelvic bone. © Simon Roffey

Trinity Chapel, Canterbury Cathedral.

Photographs of the skull from Thornton’s 1912 report.

Newly discovered panel, dating to the mid-1180s, in lightbox. Photo courtesy of Rachel Koopmans.

Panel being examined under a microscope by Leonie Seliger. Photo courtesy of Rachel Koopmans.

Excavation of the graves at Norton Priory in the 1970s. © Norton Priory Museum

Photos courtesy of Norton Priory Museum. © Norton Priory Museum

© Norton Priory Museum

The head-niche coffins at Norton Priory Museum today. © Norton Priory Museum

The hull of the Mary Rose on display in the ship hall in the Mary Rose Museum.

Visiting the Mary Rose Museum – with curator Dr Hannah Matthews.

The upper ends of two humeri (arm bones) from the Mary Rose, both showing evidence of pitting and osteophyte on a tuberosity – where the subscapularis, one of the rotator cuff muscles, is attached.

Longbows on display in the Mary Rose Museum.

Images of Yersinia pestis under the microscope – from Georges-Félix Treille and Alexandre Yersin (1894) La peste bubonique à Hong Kong.

Treponema pallidum, the spirochaete bacterium which is the agent of syphilis – imaged using a Scanning Electron Microscope. © Phanie / Alamy Stock Photo

The syphilis lesions on the bones from the grave of the possible anchoress. Image courtesy of Lauren MycIntyre.

APPENDIX

The Bubonic Plague in Hong Kong

By Dr G.-F. Treille [Director of the French Colonial Health Service] (Paris, 1894)

First translation into English by Charlotte Wright (2023)

At the start of last May, an epidemic of the bubonic plague broke out in Hong Kong that proved highly fatal for the Chinese population in this town. The disease had raged as an endemic infection for a long time in the Yunnan Plateau and occasionally appeared close to the French Indochina border at Mong-Tzé, Lang-Tchéou and Pakhoi. In March this year, it appeared in Canton and, within several weeks, caused more than 60,000 deaths in this town.

The extensive trade routes between Canton and Hong Kong, and between Hong Kong and Tonkin, and the difficulty in establishing a truly effective quarantine along the coastline of these centres, caused the French government to fear that the epidemic would reach French Indochina.

Consequently, I suggested to the Minister of Colonies to send Dr Yersin, a doctor from the colonial health service in Hong Kong, to study the plague, the conditions under which it spreads and to research the most effective measures to prevent it from reaching our colonies.

I have the honour of providing Congress with a succinct statement about the work of Dr Yersin, who has succeeded in isolating the microbe responsible for the plague and has experimentally reproduced this disease in animals using cultures.

This microbe is found in prodigious quantities in the buboes; it is abundant in the spleen and much rarer in the blood, where it is mainly found at the end of life.

It is present in the lymph nodes in the form of a short, stocky bacillus with rounded ends and stains well with aniline dye, which mainly fixes to the extremities, leaving a clear space in the middle. It does not stain with the Gram method. Sometimes it appears to be surrounded by a capsule. It has a longer shape in the blood.

It can be cultured on peptone agar, producing white, transparent colonies with iridescent edges when examined against the light. The first cultures are always scarce. In culture medium, the cultures have a very characteristic appearance; they do not cloud the liquid but produce lumps that build up on the walls and the base of the vessels. Under the microscope, these lumps are formed from small chains of bacilli.

In the old cultures, the microbes swell up into a ball and only take up stain at their periphery. They are also arranged in chains made up of bacilli joined laterally.

If we inoculate mice, rats and guinea pigs with pulp from a bubo, these animals die and at post mortem present characteristic lesions with abundant bacilli in the blood, spleen and lymph nodes. The guinea pigs die within two to five days on average, and the mice within one to three days. Pigeons appear resistant.

It can spread from guinea pig to guinea pig. Death occurs more rapidly after several transmissions.

When animals are given either cultures, fragments of infected spleen or liver to eat, the mice often die, and rats almost always die. At post mortem, bacilli are found in the organs.

The dead rats that are found in abundance in the streets and houses in Hong Kong almost always have large quantities of the microbe in their organs. Many of them present buboes.

If we place healthy mice and infected mice in the same cage, the infected mice die first. However, over the following days all the healthy mice succumb, one after the other, and present plague-related lesions.

The plague is therefore a contagious disease that can be inoculated. It is likely that rats are the main vehicle. It appears almost certain that flies could transmit the disease because those found dead around the bodies of infected animals in the laboratory have countless quantities of bacilli in their bodies. Crushing one of these flies in culture medium and inoculating a guinea pig with it will very effectively infect the animal with the disease. The plague bacillus has been found in the floor of an infected house; it produced characteristic colonies but they were devoid of virulence.

In those recovering from the plague and in several relatively mild cases, it has been possible to isolate bacillus colonies that have almost no virulence or are completely devoid of virulence, even for mice.

There is therefore reason to assume that inoculation with certain attenuated types or varieties of the specific bacillus could produce immunity to the plague. Dr Yersin continues his research into this.

ACKNOWLEDGEMENTS

Science doesn’t just happen. Fascinating facts and astonishing revelations don’t just present themselves to the world. Science is a human-made thing – a vast collection of findings which have been produced by sustained collective endeavour. Even in just this one corner of one branch of science – focusing on certain stories within burial archaeology and archaeogenomics – innumerable people have contributed countless hours of research to uncovering the details of these tales. I couldn’t have written this book without them, and I hope this book serves to bring their hard work, and their research, to the attention of a wider readership.

I am particularly indebted to a number of colleagues whose research features heavily within these pages, and who have not only let me pick their brains on numerous occasions, but have been kind enough to read and critique chapters of this book as I wrote it. It is traditional, and quite right, to stress at this point that any errors which remain are mine, and mine alone.

This trilogy of books – Ancestors, Buried and Crypt – was inspired not just by new discoveries emerging from burial archaeology, but from the revelations being yielded up by genetic research on archaeological human remains. Throughout these books I have documented research taking place in the Ancient Genomics Laboratory at the Francis Crick Institute in London, carried out by Dr Pontus Skoglund and his colleagues, including Dr Tom Booth and Dr Pooja Swali, working on their ambitious Thousand Ancient Genomes project. That project was put on hold in 2020, when the Crick Institute focused its energies on the coronavirus pandemic and became a major testing facility. But now the project is back on track – in fact, the team have now reached their target of sequencing a thousand ancient genomes, and are deep into analysing the hundreds of terabytes of data that they have collected.

There are already some incredible insights emerging: research by PhD student Kyriaki Anastasiadou has revealed the first prehistoric cases of diverse biological sex, including one individual with a single X chromosome (X0 – Turner syndrome) and several with XXY (Jacob’s Syndrome). Postdoctoral researcher Marina Silva has uncovered interesting family relationships among individuals from the Roman site of Childrey Warren, as well as evidence of long distance travel across the Roman Empire in a Sarmatian individual. Pooja Swali, focusing on infectious diseases, has found the first prehistoric Borrelia recurrentis, a pathogen causing relapsing fever, as well as the earliest evidence for plague in Britain, going back to the Bronze Age. Pooja Swali joined the Skoglund Lab as a postgraduate researcher, and in the summer of 2023 gained her doctorate. It’s been a great joy and a privilege to be involved with the Thousand Ancient Genomes project and to see the early results emerging. I will always be indebted to Pooja (now Dr Swali) for her dogged persistence in looking for traces of Yersinia pestis DNA in skeletons from the Breamore Anglo Saxon cemetery. The Thousand Ancient Genomes project will continue to generate results over the coming months and years – watch this space! At this point in time, we know that many of the skeletons I wrote about in Ancestors, from Pitt Rivers’ Cranborne Chase estate, contain well-preserved ancient DNA. I can’t wait to see what their genomes reveal once they are sequenced. I might have to write another book about that!

I must also extend my thanks to Sir Paul Nurse, Director of the Crick – whose belief in the power of science to transform society for the better, the need for scientists to engage with the wider public, as well as his generosity of spirit, infuses that Institute.

Enormous thanks to all the other researchers and archaeologists who have helped me with this book: Dr Ceri Falys, Lecturer in Bioarchaeology at the University of Reading; Dr Simon Roffey, Reader in Medieval Archaeology at the University of Winchester; Rachel Koopmans, Leonie Seligman and the producers of Britain’s Most Historic Towns; Lynn Smith, Senior Keeper at the Norton Priory Museum Trust; Dr Hannah Matthews and Dr Alex Hildred, Curators at the Mary Rose Museum; Dr Nick Owen of Swansea University, and Dr. Lauren McIntyre at Heritage Burial Services, Oxford Archaeology.

Thanks to my wonderful literary agent, Luigi Bonomi, and to the whole fantastic team at Simon & Schuster – my brilliant editorial team: Holly Harris, Kat Ailes, Sophia Akhtar and Kris Doyle; project editor Kaiya Shang, and Jo Edgecombe in production. I’m very grateful to copyeditor Alex Newby and proofreader Loz Jerram for ironing out the text. I’m lucky enough to have the brilliant designer Craig Fraser producing a great cover design for me – once again! Special thanks to Becky McCarthy and Hannah Paget at Simon & Schuster for their amazing work promoting the book. I’d also like to thank the team at Jo Sarsby Management for all the work they do organising live events, from book festivals to talks and theatre tours. And a special thank you to all the bookshops, and of course, all the readers!

Last but not least, I must thank my family. My children seem happy to listen to endless stories of death and disease, pestilence and plague (at least, they rarely grumble when I wax lyrical about the latest chapter I’m writing, on a dog walk); my wonderful husband, on whom my wellbeing depends in so many ways; and my cousin – who is more like a sister to me – Charlotte Wright. As a French-English medical translator, she produced the first English translation of the report on Yersin’s work, identifying the causative agent of the plague. Merci beaucoup, Charlotte!

More from the Author

Anatomical Oddities

Buried

Ancestors

Wolf Road

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3. Tomb of a Martyr

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2. Barush, K. R. (2020) The afterlife of Becket in the modern imagination. Journal of the British Archaeological Association 173: 204–17.

3. Bollerman, K., Nederman, C. (2016) John of Salisbury. Stanford Encyclopedia of Philosophy. Available at https://plato.stanford.edu/entries/john-salisbury/ (accessed 11 May 2023).

4. Brenner, E. (2016) Thomas Becket and leprosy in Normandy. In Webster, P., Gelin, M.-P. (eds) The Cult of St Thomas Becket in the Plantagenet World, c.1170–c.1220. Boydell Press, Woodbridge, 81–93.

5. Brown, A. (1959) John of Salisbury. Franciscan Studies 19: 241–297.

6. Duggan, A. J. (2016) Becket is dead! Long live St Thomas. In Webster, P., Gelin, M.-P. (eds) The Cult of St Thomas Becket in the Plantagenet World, c.1170–c.1220. Boydell Press, Woodbridge, 25–52.

7. Duggan, A. J. (2020) Becket’s cap and the broken sword. Jacques de Vitry’s English mitre in context. Journal of the British Archaeological Association 173: 3–25.

8. Desiderius Erasmus (1524) Pilgrimage for religion’s sake. In Pilgrimages to Saint Mary of Walsingham and Saint Thomas of Canterbury. Translated by J. G. Nichols (1849). John Bowyer Nichols and Son, Westminster.

9. Gelin, M.-P. (2016) The Cult of St Thomas in the liturgy and iconography of Christ Church, Canterbury. In Webster, P., Gelin, M.-P. (eds) The Cult of St Thomas Becket in the Plantagenet World, c.1170–c.1220. Boydell Press, Woodbridge, 53–79.

10. Henry VIII: November 1538 16–20. In Letters and Papers, Foreign and Domestic, Henry VIII, Volume 13 Part 2, August–December 1538. Edited by James Gairdner (London, 1893), 353–69. Available at British History Online, http://www.british-history.ac.uk/letters-papers-hen8/vol13/no2/pp353-369 (accessed 11 May 2023).

11. Hume, D. (1754–61) History of England.

12. Koopmans, R. (2017) Kentish pilgrims in Canterbury Cathedral’s miracle windows. Journal of the Warburg and Courtauld Institutes 80: 1–27.

13. Mayr-Harting, H. (1965) Henry II and the papacy. The Journal of Ecclesiastical History 16: 39–53.

14. McLoughlin, J. (1984) The language of persecution: John of Salisbury and the early phase of the Becket dispute (1163–66). Studies in Church History 21: 73–87.

15. O’Connor, J. F. (1947) An Annotated Translation of the Letters of John of Salisbury. Master’s Theses, Loyola University Chicago, 672.

16. Routledge, C. F. (1895) The bones of Archbishop Becket. Archaeologia Cantiana 21: 73–80.

17. Scully, R. E. (2000) The unmaking of a saint: Thomas Becket and the English Reformation. Catholic Historical Review 86: 579–602.

18. Sinclair, M. A. (1944) An annotated translation of the life of St Thomas Becket by William Fitzstephen: (Part Two). Master’s Theses, Loyola University Chicago, 369.

19. Thornton, W. P. (1912) Becket’s Bones. Cross & Jackman, Canterbury.

20. Webster, P. (2016) Crown versus Church after Becket: King John, St Thomas and the Interdict. In Webster, P., Gelin, M.-P. (eds) The Cult of St Thomas Becket in the Plantagenet World, c.1170–c.1220, Boydell Press, Woodbridge, 147–69.

21. Wesseling, A. (2010) Erasmus: peculiar words in the ‘Colloquies’ and his concept of proper Latin diction. Journal of the Warburg and Courtauld Institutes 73: 355–65.

4. Mystery at a Priory

1. Abdullah, O. et al. (2018) Prevalence of Paget’s disease of bone in Lancaster: time for an update. Rheumatology 57: 931.

2. Boonrungsiman, S. et al. (2012) The role of intracellular calcium phosphate in osteoblast-mediated bone apatite formation. PNAS 109: 14170–5.

3. Bourne, L. E. et al. (2021) Regulation of mineralisation in bone and vascular tissue: a comparative review. Journal of Endocrinology 248: R51–65.

4. Brown, F., Howard-Davies, C. (2008) Norton Priory: Monastery to Museum – Excavations 1970–87. Oxford Archaeology, Oxford.

5. Gennari, L. et al. (2019) Paget’s disease of bone. Calcified Tissue International 104: 483–500.

6. Paget, J. (1877) On a form of chronic inflammation of bones (osteitis deformans). Medico-Chirurgical Transactions 60: 37–64.9.

7. Schaffler, M. B. et al. (2014) Osteocytes: Master orchestrators of bone. Calcified Tissue International 94: 5–24.

8. Shaw, B. et al. (2019) Molecular insights into an ancient form of Paget’s disease of bone. PNAS 116: 10463–10472.

5. The Black Death

1. Barbieri, R. et al. (2021) The role of louse-transmitted diseases in historical plague pandemics. Lancet Infectious Diseases 21: e17–25.

2. Barbieri, R. et al. (2021) Yersinia pestis: the Natural History of Plague. Clinical Microbiology Reviews 34: e00044–19.

3. Bartsocas, C. S. (1966) Two fourteenth century Greek descriptions of the ‘Black Death’. Journal of the History of Medicine and Allied Sciences 21: 394–400.

4. Benedict, C. (1988) Bubonic plague in nineteenth-century China. Modern China 14: 107–55.

5. Butler, T. (2009) Plague into the 21st Century. Clinical Infectious Diseases 49: 736–42.

6. Butler, T. (2014) Plague history: Yersin’s discovery of the causative bacterium in 1894 enabled, in the subsequent century, scientific progress in understanding the disease and the development of treatments and vaccines. Clinical Microbiology and Infection 20: 202–09.

7. Dean, K. R. et al. (2018) Human ectoparasites and the spread of plague in Europe during the Second Pandemic. PNAS 115: 1304–09.

8. De Witte, S. N., Stojanowski, C. M. (2015) The Osteological Paradox 20 years later: Past perspectives, future directions. Journal of Archaeological Research 23: 397–450.

9. Drancourt, M. et al. (1998) Detection of 400-year-old Yersinia pestis DNA in human dental pulp: an approach to the diagnosis of ancient septicemia. Proceedings of the National Academy of Sciences of the United States of America 95: 12637–40.

10. Drancourt, M., Raoult, D. (2016) Molecular history of plague. Clinical Microbiology and Infection 22: 911–15.

11. Echenberg, M. (2002) The initial years of the Third Bubonic Plague Pandemic, 1894–1901. Journal of World History 13: 429–49.

12. Gilbert, M. T. P. et al. (2004) Absence of Yersinia pestis-specific DNA in human teeth from five European excavations of putative plague victims. Microbiology 150: 341–54.

13. Haensch, S. et al. (2010) Distinct clones of Yersinia pestis caused the Black Death. PLOS Pathogens 6: e1001134.

14. Hufthammer, A. K., Walløe, L. (2013) Rats cannot have been intermediate hosts for Yersinia pestis during medieval plague epidemics in Northern Europe. Journal of Archaeological Science 40: 1752e1759.

15. Keller, M. et al. (2019) Ancient Yersinia pestis genomes from across Western Europe reveal early diversification during the First Pandemic (541–750). PNAS 116: 12363–72.

16. Peckham, R. (2016) Hong Kong junk: Plague and the economy of Chinese things. Bulletin of the History of Medicine 90: 32–60.

17. Pryor, E. G. (1975) The Great Plague of Hong Kong. Journal of the Hong Kong Branch of the Royal Asiatic Society 15: 61–70.

18. Raoult, D. et al. (2000) Molecular identification by ‘suicide PCR’ of Yersinia pestis as the agent of medieval Black Death. PNAS 97: 12800–03.

19. Rasmussen, S. et al. (2015) Early divergent strains of Yersinia pestis in Eurasia 5,000 years ago. Cell 163: 571–82.

20. Rogers, L. (1899) La propagation de la peste. Indian Medical Gazette 34: 182–3.

21. Spyrou, M. A. et al. (2016) Historical Y. pestis genomes reveal the European Black Death as the source of ancient and modern plague pandemics. Cell Host & Microbe 19: 874–81.

22. Spyrou, M. A. et al. (2018) Analysis of 3800-year-old Yersinia pestis genomes suggests Bronze Age origin for bubonic plague. Nature Communications 9: 2234.

23. Spyrou, M. A. et al. (2019) Phylogeography of the Second Plague Pandemic revealed through analysis of historical Yersinia pestis genomes. Nature Communications 10: 4470, doi.org/10.1038/s41467-019-12154-0

24. Stenseth, N. C. et al. (2022) No evidence for persistent natural plague reservoirs in historical and modern Europe. PNAS 119: e2209816119.

25. Susat, J. et al. (2021) A 5,000-year-old hunter-gatherer already plagued by Yersinia pestis. Cell Reports 35: 109278.

26. Swali, P. et al. (2022) Yersinia pestis genomes reveal plague in Britain 4,000 years ago. bioRxiv preprint, doi.org/10.1101/2022.01.26.477195

27. Treille, G.-F., Yersin, A. (1894) La peste bubonique à Hong Kong. VIIIe Congrès international d’hygiène et de démographie 2: 310–11.

28. Valtuena, A. A. et al. (2022) Stone Age Yersinia pestis genomes shed light on the early evolution, diversity, and ecology of plague. PNAS 119: e2116722119.

29. Wilm (1897) A report on the epidemic of bubonic plague at Hongkong in the year 1896 (translated for the Government of Hongkong by Maurice Eden Paul, M. D.). Indian Medical Gazette 32: 167–71.

30. Wilmott, H. et al. (2020) A Black Death mass grave at Thornton Abbey: the discovery and examination of a fourteenth-century rural catastrophe. Antiquity 94: 179–96.

31. Wood, J. W. et al. (1992) The Osteological Paradox: Problems of inferring prehistoric health from skeletal samples. Current Anthropology 33: 343–70.

32. World Health Organization, Plague, https://www.who.int/news-room/fact-sheets/detail/plague (accessed 11 May 2023).

6. The Archers of the Mary Rose

1. Adams, B. J., Konigsberg, L. W. (2004) Estimation of the most likely number of individuals from commingled human skeletal remains. American Journal of Physical Anthropology 125: 138–51.

2. Alberola-Zorrilla, P. et al. (2022) Where do archers hurt? Physiotherapy Theory and Practice, doi.org/10.1080/09593985.2022.2136507

3. Annan, S. A. (2014) Bilateral asymmetry as a measure of occupational activity in human remains from the Mary Rose. MSc thesis, College of Engineering, Swansea University.

4. Biswal, R. et al. (2018) Ossification of ligamentum flavum: A morphological study in dried vertebrae. Journal of Dental and Medical Sciences 17: 22–6.

5. Dorshorst, T. et al. (2022) Archery’s signature: an electromyographic analysis of the upper limb. Evolutionary Human Sciences 4: e25, 1–13.

6. Fischer, C. S. et al (2022) Os acromiale: prevalence and associated patient-related factors – a population-based study of three thousand and fifty participants. International Orthopaedics 46: 1583–90.

7. Guo, C. et al. (2022) Analysis of rotator cuff muscle injury on the drawing side of the recurve bow: A finite element method. Computational and Mathematical Methods in Medicine, doi.org/10.1155/2022/8572311

8. Hegg, V. (2021) English and Norwegian military legislation in the 13th century: The Assize of Arms and Norwegian military law. Master’s thesis, Department of Archaeology, History, Cultural Studies and Religion, University of Bergen.

9. Hunt, D. R., Bullen, L. (2007) The frequency of os acromiale in the Robert J. Terry Collection. International Journal of Osteoarchaeology 17: 309–17.

10. Kato, K. et al (2021) Progressive enlargement of thoracic ossification of the ligamentum flavum in professional baseball pitchers: a report of two cases. Journal of International Medical Research 49.

11. Mahmoodi, P. et al. (2015) A computational method of obtaining reliable measurement of periosteal cross-sectional area of human radii from laser scans. Proceedings of the 23rd UK Conference of the Association for Computational Mechanics in Engineering 2015, Swansea, 73–6. In Owen, N. J. (2018) A biomechanical investigation into force, power and bone morphology. PhD thesis, Faculty of Science and of Engineering, Swansea University.

12. Mann, D. L., Littke, N. (1989) Shoulder injuries in archery. Canadian Journal of Sport Science 14: 85–92.

13. Matthews, H. (2021) ‘How many men were onboard?’: An osteological quantitative evaluation of the Mary Rose human skeletal assemblage. MSc Osteoarchaeology thesis, Department of Archaeology, University of Sheffield.

14. McElvogue, D. (2021) Tudor Warship Mary Rose. Osprey Publishing, New York.

15. Mitchell, E. (2022) War, wounds, and medicine: A re-examination of the crew of the Mary Rose. PhD thesis, Department of Archaeology, University of Southampton.

16. Molnar, P. (2005) Tracing prehistoric activities: Musculoskeletal stress marker analysis of a Stone-Age population on the Island of Gotland in the Baltic Sea. American Journal of Physical Anthropology 129: 12–23.

17. Owen, N. J. (2018) A biomechanical investigation into force, power and bone morphology. PhD thesis, Faculty of Science and of Engineering, Swansea University.

18. Pontzer, H. et al. (2017) Mechanics of archery among Hadza hunter-gatherers. Journal of Archaeological Science 16: 57–64.

19. Roberts, A. M., Peters, T. J., Robson Brown, K. (2007) New light on old shoulders: palaeopathological patterns of arthropathy and enthesopathy in the shoulder complex. Journal of Anatomy 211: 485–92.

20. Rogers, C. J. (2011) The development of the longbow in late medieval England and ‘technological determinism’. Journal of Medieval History 37: 321–41.

21. Rovesta C. et al. (2017) Os acromiale: frequency and a review of 726 shoulder MRI. Musculoskeletal Surgery 101: 201–05.

22. Samartzis, D. et al. (2016) Classification of Schmorl’s nodes of the lumbar spine and association with disc degeneration: a large-scale population-based MRI study. Osteoarthritis and Cartilage 24: 1753–60.

23. Stirland, A. J. (1993) Asymmetry and activity-related change in the male humerus. International Journal of Osteoarchaeology 3: 105–113.

24. Stirland, A. J. (2013) The Men of the Mary Rose: Raising the Dead. The History Press, Stroud.

25. Yammine, K. (2014) The prevalence of os acromiale: a systematic review and meta-analysis. Clinical Anatomy 27: 610–21.

7. The Anchoress and the Spiral Bacter

1. Ayers L., Bahr, V. (2019) A twelfth-century service for enclosing an anchorite or anchoress: Introduction, Latin text, and translation. The Expositor: A Journal of Undergraduate Research in the Humanities 14: 1–12.

2. Beale, M. A., Lukehart, S. A. (2020) Archaeogenetics: What can ancient genomes tell us about the origin of syphilis? Current Biology 30: R1071–95.

3. Beale, M. A. et al. (2021) Global phylogeny of Treponema pallidum lineages reveals recent expansion and spread of contemporary syphilis. Nature Microbiology 6: 1549–60.

4. Cagé, J., Rueda, V. (2019) Sex and the mission: the conflicting effects of early Christian missions on HIV in sub-Saharan Africa. Journal of Demographic Economics 86: 213–57.

5. Curran, T. M. (2018) The Medievalizing Process: Religious Medievalism in Romantic and Victorian Literature. PhD thesis, College of Arts and Sciences, University of South Florida.

6. Espí Forcén, F., Espí Forcén, C. (2014) Symeon the Holy Fool: patron of the mentally ill. British Journal of Psychiatry 205: 94.

7. Goh, B. T. (2005) Syphilis in adults. Sexually Transmitted Infections 81: 448–52.

8. Ha, T., Tadi, P., Dubensky, L. (2022) Neurosyphilis. StatPearls Publishing.

9. Harper, K. N. et al. (2011) The origin and antiquity of syphilis revisited: An appraisal of Old World pre-Columbian evidence for treponemal infection. Yearbook of Physical Anthropology 54: 99–133.

10. Iyassu, R. et al. (2013) Psychological characteristics of religious delusions. Social Psychiatry and Psychiatric Epidemiology 49: 1051–61.

11. Kenyon, C. R. et al. (2016) The global epidemiology of syphilis in the past century – A systematic review based on antenatal syphilis prevalence. PLOS Neglected Tropical Diseases 10: e0004711.

12. King, A. J., Catterall, R. D. (1959) Syphilis of Bones. British Journal of Venereal Diseases 35: 116.

13. Majander, K. et al. (2020) Ancient bacterial genomes reveal a high diversity of Treponema pallidum strains in Early Modern Europe. Current Biology 30: 3788–803.

14. McAvoy, L. H. (2013) Uncovering the ‘saintly Anchoress’: myths of Medieval anchoritism and the reclusion of Katharine de Audley. Women’s History Review 22: 801–19.

15. McIntyre, L. et al. (2022) The All Saints Anchoress? An Osteobiography. Medieval Archaeology 66: 368–99.

16. Nissanka-Jayasuriya, E. H., Odell, E. W., Phillips, C. (2016) Dental stigmata of congenital syphilis: a historic review with present day relevance. Head and Neck Pathology 10: 327–31.

17. Nunn, N., Qian, N. (2010) The Columbian Exchange: A History of Disease, Food, and Ideas. Journal of Economic Perspectives 24: 163–88.

18. Rowley, J. et al. (2019) Chlamydia, gonorrhoea, trichomoniasis and syphilis: global prevalence and incidence estimates. Bulletin of the World Health Organization 97: 548–62.

19. Schuenemann, V. J. et al. (2018) Historic Treponema pallidum genomes from Colonial Mexico retrieved from archaeological remains. PLOS Neglected Tropical Diseases 12: e0006447.

20. Swain, K. (2018) ‘Extraordinarily arduous and fraught with danger’: syphilis, Salvarsan, and general paresis of the insane. Lancet Psychiatry 5: 702–03.

21. Tang, Y. et al. (2022) Investigation of the immune escape mechanism of Treponema pallidum. Infection, doi.org/10.1007/s15010-022-01939-z

22. Tuddenham, S., Ghanem, K. G. (2018) Neurosyphilis: Knowledge Gaps and Controversies. Sexually Transmitted Diseases 45: 147–51.

23. Wolgemuth, C. W. (2015) Flagellar motility of the pathogenic spirochetes. Seminars in Cell & Developmental Biology 46: 104–12.

INDEX

A note about the index: The pages referenced in this index refer to the page numbers in the print edition. Clicking on a page number will take you to the ebook location that corresponds to the beginning of that page in the print edition. For a comprehensive list of locations of any word or phrase, use your reading system’s search function.

acromion 247–50, 252

Act of Supremacy (1534) 224

aDNA (ancient DNA). See DNA

Ælfgifu of Northampton 43, 44

Ælfgifu of York 43

Æthelberht, King of Kent 97–8

Æthelred II (‘Æthelred the Unready’), King of the English 12–13, 14–19, 20–22, 24, 25, 37, 38, 43, 44

Æthelstan, King of the English 14

Æthelwold, Bishop 80, 82

Africa 164, 180, 189, 190, 191, 201, 272, 273, 276, 280, 281

agriculture 42, 151–2, 205

Aldevrandus 75

Alexander II, Pope 98

Alexander III, Pope 104, 108, 110, 111

Alfred the Great, King of Wessex 12, 14, 92

All Saints church, Fishergate 263–7, 284–96

- anchoritism and SK3870 skeleton discovered at 286–96

- excavation of medieval church (2007) 263–4

- SK3870 skeleton discovered at 264–7

- SK3870 skeleton, historical records and investigation into 286–96

- SK3870 skeleton osteobiography 284–6

- syphilis and SK3870 skeleton discovered at 266–7, 284–5, 290–92

almshouses 48, 49, 50, 51

Alphege, St 103, 113–14

amelogenin 85–8

amputation 54, 84, 132, 239

Anarchy (1138–53) 99, 100, 103, 251

anchoritism 158, 286–96

Ancrene Wisse (guidebook for anchorites and anchoresses) 289

Anglo-Dutch Wars (1652–1784) 49–50

Anglo-Norman Church 99, 147–8

Anglo-Saxon Chronicle 12, 13, 15, 17, 18, 19, 23, 32

Anglo-Saxons 3, 114

- Anglo-Saxon Chronicle see Anglo-Saxon Chronicle

- burials 36

- diets 16, 27, 28, 31

- hospitals 50, 81

- Norman period and 42–6, 50, 81, 98, 147, 148

- Vikings and 12–25, 27, 28, 31, 32, 36

Annales de l’Institut Pasteur 183

Annan, Simon 258–9

Annebault, Admiral Claude d’ 226

Anthony Roll naval inventory 232

anthropology 2, 204, 237, 253, 257

antibiotics 62, 188–91, 271, 272, 273, 274, 284

antiserum 186, 188–9

apatite 155

archaeogenomics 4, 29, 205, 283, 297, 299. See also DNA; genetics and individual study or place name

archaeology 4, 5, 10, 12, 23, 25–6

- genetics and see genetics

- history and 2–3, 28, 38, 46, 71, 83–5, 151, 296, 297–8

- physical archives, importance of 173

- uneven nature of samples 172

archery/archer hypothesis, Mary Rose 6, 250–62, 297

- acromion and 247–52

- Assize of Arms (1242) 250–51

- Charles University study 254–8

- forearm bones and 258–9

- humerus and 252–3, 254, 255, 257, 258, 261

- longbow archers 250–52, 255, 258–61

- os acromiale and 247–52

- Skeleton 82 and 259

- Swansea University study 258–9

- University of Massachusetts experiment 253–6

Aretaeus 62–3

arsphenamine 270–71

arthritis 52, 68, 160, 167, 177, 241, 242, 265, 266

Assize of Arms (1242) 250–51

Audley, Katharine de 292–6

Audley, Nicholas de 294–5

Augustine, St 16, 97, 98, 109

Augustinians 148

Austin, George 125

Bale, John 137

Baltic Sea 30, 32, 33, 257

Bartonella quintana 210

Bec, Abbey of, Normandy 99

Becket, Thomas 99, 100–43

- appearance 100

- Archbishop of Canterbury and Pope John Paul II kneel and pray on site of murder

- (1982) 138

- Archbishop of Canterbury, elected 101

- burial 109–10, 127–8, 131, 132, 134, 136, 137

- Catholic mass held in Canterbury Cathedral to mark eighth centenary of death (1970)

- 138

- Cave examines bones associated with 134–6

- Chronicle of Battle Abbey 101

- coffin re-opened (1949) 134–6

- Constitutions of Clarendon and 102–3

- cult of 111–25, 137–43

- English Reformation and 123–5, 137–8

- France, exile in 103

- graves uncovered in Canterbury Cathedral (1888) and 125–34

- Henry II and 99, 100–105, 108, 110–12, 114, 128, 142, 250

- Henry VIII attacks cult of 6, 49, 123–5, 127–9, 132, 137–8, 142, 145

- John of Salisbury and 99–100, 101–2, 105, 106, 108–10

- murder 103–10

- Paris, studies in 100

- pilgrim destination of Canterbury and 112–13, 137–43

- reburial of remains (1951) 136

- relics of 116–17, 118–19, 129–30, 133, 137, 142

- resignation from chancellorship 101, 102

- return to Canterbury (1170) 103

- shifting loyalties 101–2

- Trinity Chapel, body transferred to shine in (1220) 116–17

- Trinity Chapel shrine 112–23, 131, 137, 139–42

bejel 277, 278

Bellay, Martin du 227

Benedictines 77

Beorhthelm 148

Bertelin, St 148

Bertha, Queen of Kent 97

Betjeman, John: The Church’s Restoration 95

Bible 16, 64, 72, 73

Birinus, St 92

Birkenhead, Thomas 149

Bishop’s Register 48–9

Black Death 179–214

- Africa and 180, 189, 190, 191, 201

- bubonic plague and 194, 209

- fourteenth-century pandemic 179–80, 191–4, 195–7, 201, 213

- Great Plague of London (1665) 199

- hospitals and 49

- inequalities and 188

- mass graves and 179–80, 194–8, 212–14

- Montpellier and 195–6

- mortality rates 181–2, 189, 190

- name 180

- Norton Priory and 148

- Osteological Paradox and 179, 180

- pathogen that causes, identification of 180–86 see also Yersinia pestis

- Pediculus humanus (human louse) and 209–11

- pneumonic plague and 209

- prevention 191

- Second Plague Pandemic and 199, 211

- rural communities, impact on/Thornton Abbey mass grave and 212–14

- Yersinia pestis and see Yersinia pestis

Blackwater River, Essex 14–15

Blick, Sarah 122

Bloodaxe, Eric 14

bog bodies 155

Boleyn, Anne 224

bone

- ancient DNA (aDNA) extracted from see DNA and genetics

- apatite and 155

- bone matrix 155–6, 158

- canaliculi and 154, 156–8

- collagen and 155, 166, 175

- diet and see diet

- disease read on 3–4, 58–9, 160–78, 179 see also individual disease name

- fish 32–6, 204

- gap junctions 157–8

- hydroxyapatite and 155

- lesions 5, 52, 84, 160, 166, 172, 173–4, 177, 241, 243, 255, 266, 267, 269, 277, 278, 281, 284

- metabolic disruption and 154

- osteobiography and 1, 5–6

- osteoblasts and 155–6, 158–9, 162–3, 165–6, 171, 177, 245, 254

- osteoclasts and 158–9, 166, 169, 170, 171, 175, 176, 177, 254

- osteocytes and 154–60, 177

- osteolysis and 159, 171

- palaeopathology and 3–4

- radiocarbon dating 2, 26, 27, 35, 51, 81, 82, 136, 174, 204, 213, 279, 283, 284, 287

- renewal and replacement of 154–60

- violent injury, signs of on 10–12, 27, 38, 39

- See also individual bone and disease name

Booth, Tom 198

Breamore, Anglo Saxon cemetery at 198–9

Breton, Richard le 105–6, 107, 126

Britain’s Most Historic Towns (television series) 82

British Sub-Aqua Club 230

Bronze Age 4, 26, 202–7

Brooke family 149–50

Bruno, St 73–4

bubonic plague 181–2, 190, 194, 203, 204, 209

burial ix, 3

- All Saints, Fishergate/syphilis and 284–90

- anthropomorphic grave 90

- Becket’s 109, 127, 131, 132, 133–4, 136–7

- boat burials 30

- Bronze Age 4, 206

- cemeteries and see cemeteries

- Charterhouse mass burial 206

- children 153–4

- double/multiple burials 198–9, 207

- East Smithfield burial ground 197

- Edix Hill burial grounds 197–8

- family ‘vaults’ 4

- graves and see graves

- Hospital of St Mary Magdalen/leprosy and 51–3, 67–8, 79, 83, 84, 85

- mass burial 26, 36–8, 197, 206–7

- Norton Priory/Paget’s disease and 152–4, 176–7, 178

- plague victims 194–9, 203–7, 213–14

- Rinnukalns burials 204–5

- Servicium Recludendi or Service of a Recluse and 287–8

- Seven Comfortable Acts and 76

- St James 91

- Viking 30, 39

Byrhtferth: Life of St Oswald 50

Byzantine Empire 4, 73, 75, 192, 193, 197, 201

Byzantium 73

Caffa 192

calcium phosphate 155

calculus 52, 90, 242, 265

calvarium, or skull-cap 11

canaliculi 154, 156–8

Canterbury

- Cathedral see Canterbury Cathedral

- established by Romans (Durovernum Cantiacorum) 96–7

- Henry II visits 111–12, 114

- leprosy hospital in 51

Canterbury Cathedral 98–145

- Archbishop of Canterbury and Pope John Paul II kneel and pray on site of Becket

- murder (1982) 138

- Becket assassinated in 103–10

- Becket becomes archdeacon of 100

- Becket burial and 109–10, 127–8, 131, 132, 134, 136, 137

- Becket coffin re-opened (1949) 134–5

- Becket elected Archbishop of 101

- Becket reclaims land and revenue of 102, 104

- Becket remains reburied in (1951) 136

- Becket returns to (1170) 103

- Becket shrine in 112–23, 131, 137, 139–42

- building of 98

- Catholic mass held in to mark eighth centenary of Becket’s death (1970) 138

- Chaucer’s Canterbury Tales and 142–3

- Constitutions of Clarendon and 102–3

- Corona shrine 113, 131

- cult of Becket and 111–25, 137–43

- east end destroyed in fire (1174) 112–13

- English Reformation/Dissolution of the Monasteries and 123–5, 137–8, 145

- Erasmus visits 117–21

- graves uncovered in (1888) 125–34

- Henry II visits 111–12, 114

- ‘Old Way’, launch of 142

- pilgrim destination 92, 112–13, 114, 115, 117–18, 137–43

- relics in 116–17, 118–19, 129–30, 133, 137, 142

- sublimity of 98

- Trinity Chapel 112–23, 131, 137, 139–42

Carew, Vice Admiral, Sir George 224–5, 227, 232

Carew, Peter 232

carrack 219, 227

Cathewic, Hugh de 152

Cave, Alexander 134–6

cemeteries

- All Saints, Fishergate/syphilis and 263–4, 280–81

- Hospital of St Mary Magdalen/leprosy and 47, 50–52, 59–60, 66, 67–8, 71, 72, 79, 81–2, 84–5, 88, 89–91

- Norton Priory/Paget’s disease and 152–3, 172–3

- plague and 195, 197, 198–9, 212

- Viking 39

Changing Faces 73

chantry 48–9

Charibert I, King of the Franks 97

Charles the Simple, King of West Francia 24

Charles University, Prague 254–8

Charles V, Holy Roman Emperor 124, 223–6

Charles VIII, King of France 276

Charterhouse, mass burial at 206–7

Chartres, siege of (911) 24

Chaucer, Geoffrey 5

- Canterbury Tales 142–3

children

- Mary Rose, evidence of among bones on board 240

- Norton Priory burials and 153–4

- plague and 181, 192, 195–6, 206–7, 213

- St Mary Magdalen skeletons/leprosy and 52, 54–5, 67, 68–9, 84–9

- syphilis and skeleton of 278

- tooth enamel analysis and 2, 36, 55, 88–9

Chronicle of Battle Abbey 101

Church, English

- Anglo-Saxons and 97–8

- Henry VIII and 6, 49, 96, 101–5, 108–9, 114–15, 123–5, 137, 138, 145, 224

- hospitals and 76–7

- Normans and 99, 147–8

Church of England 123–4

Claudian invasion (43 CE) 96

claw hand 57

cloaca 59

Cnut, King of England 25, 43–4

‘cockle amongst the wheat’ 15, 16, 25, 37

cod 33–4

Colet, John 118

collagen 155, 166, 175

Columbian hypothesis 276–84

Columbus, Christopher 276, 279, 281

Conrad II, Holy Roman Emperor 44

Constitutions of Clarendon (1164) 102–3

Cordelière 221

Corona shrine, Canterbury Cathedral 113, 131

Cranmer, Thomas 124

Cruveilhier, Jean 247

crypt, definition of ix

cystic lesions 160

Danegeld, or ‘Dane-yield’ 15

Danelaw 14, 28, 43

‘Danes’ 12–26, 32, 37, 45

DC-STAMP (dendritic cell-specific transmembrane protein) 170

Deane, John and Charles 230

‘Declaration of Faith, and a Justification of the Proceedings of King Henry VIII, in Matters of Religion, A’ 128–32

deep-sea navigation 32, 34

Delft, François van der 226–7, 232

Demaitre, Luke 71, 72

Denmark 21–2, 30, 43, 44, 55, 66, 89, 272

dental defects. See teeth and individual defect or disease name

dental pulp 86, 87, 194, 195

diet

anchoritism and 289

Norton Priory skeletons and 174, 177

Rinnukalns burials and 204

Viking 27–8, 32–6

Winchester pilgrim 91–2

disease. See individual disease name

dissolution of the monasteries (1536–41) 124, 145–7, 149, 152, 174, 225

DNA

- aDNA (ancient DNA) 2, 29, 32–4, 42, 85, 87, 136, 175, 176, 180, 196–7, 204–5, 208–9

- see also genetics and individual disease, study or place name

- agarose gel electrophoresis and 86–7

- base pairs 64

- Becket and analysis of 136

- ‘capture’ 198

fish 32–4

genome and see genetics

incest and 42

- leprosy and 64, 65–6, 90

measuring length of 87

mitochondrial (mtDNA) 29

- nonhuman – metagenome 4

- obsolete 64

- Paget’s disease in Norton Priory skeletons and 169, 175, 176

- pathogen, ancient 4 see also individual pathogen name

- plague 180, 191, 194–7, 198–9, 204–5, 206–7, 213–14, 300

- Richard III skeleton and 136

- sex determination and 85–8

- syphilis and 274–5, 281, 282, 283, 284

- teeth, extracting from 86–7, 136

- Viking 29–30, 32–4

Domesday Book 81

donsk tunga (‘Danish tongue’) 31–2

droplet infection 60, 190, 209, 211

Duggan, Anne 123

Duncan, St 113–14

Dutton family 148–9, 152, 153, 177

Dutton, Sir Piers 149, 152

- Eadwig, King 114

- East Saxons 15

- East Smithfield burial ground 197

- Edith of Wessex 44

- Edix Hill burial grounds 197–8

- Edmund Ironside, King of the English 43

- Edward III, King of England 220

- Edward the Confessor, King of the English 44

- Ehrlich, Paul 270

- Eleanor of Aquitaine, Queen 111

- Elizabeth I, Queen of England and Ireland 138

- Emma of Normandy, Queen 13, 24, 25, 43–6

- enamelin 85

- English Channel 23, 45, 48, 104, 220, 221, 222, 225, 226

- English Civil War (1642–51) 49

- English Reformation 49, 123–5, 130, 132, 137–8, 145–6

- enthesophytes 242

- Erasmus, Desiderius: Colloquies 117–21, 122, 129

- erysipelas 68

- Etheldreda of Canterbury 139

- ethnic minorities 6, 15, 18, 24, 32

- Ezekiel, Book of 73

- facial disfigurement 52–3, 57, 59–60, 70, 72–5, 162, 278

- facies leprosa or rhinomaxillary syndrome 59–60

- Falys, Ceri 10–12, 26, 35, 37–8, 39

- Faroe Islands 28, 34

- Field of the Cloth of Gold 223

- finger bones 53–5, 57, 58, 85, 236

- First World War (1914–18) 47

- fish

- drying 33, 34

- extracting and sequencing DNA from fish bones 32–4

- fish event-horizon 27, 28

- fisheries 151–2

- Norton Priory skeletons and 174, 177

- Rinnukalns burials and 204

- stockfish 33, 34

- Vikings and 27–8, 32–4, 35–6

- Fitz Nigel, William 148

- FitzStephen, William 105–8

- FitzUrse, Reginald 105–7

- Fleming, Alexander 189

- Florence of Worcester 20

- foot drop 57

- Forkbeard, Sweyn 19, 21, 43

- Fountains Abbey 146

- Fournier’s molars 279

- Francis Crick Institute: Ancient Genomics Lab 4, 198

- Francis I, King of France 223, 225, 228

- French National Centre for Scientific Research 194

Galen 63–4

Galgedil cemetery, Funen 39

gap junctions 157–8

Gaston III of Foix: Livre de Chasse 260

Gelin, Marie-Pierre 113

General Paresis of the Insane 270, 285

genetics

- ancient DNA (aDNA) 2, 29, 32–4, 42, 85, 87, 136, 175, 176, 180, 196–7, 204–5, 208–9

- archaeogenomics 4, 29, 205, 283, 297, 299

- DNA see DNA

- fish 32–4

- genomes, extraction and sequencing entire ancient 2, 4, 29

- human genome, first working draft published (2000) 180

- leprosy and/Mycobacterium leprae genome 60–67, 85–93

- Mary Rose skeletons and 241, 245, 247

- Paget’s disease and 165, 169–71, 174–8

- plague and/Yersinia pestis genome 180, 194–209, 212–14

- sex determination and 85–93

- syphilis and/Treponema pallidum genome 273–5, 281–4

- Thousand Ancient Genomes project 4–5, 198–9, 206–8

- Viking 29–32, 39

Geoffrey of Vigeois 105

geophysical surveys 2, 48, 50, 212–13

Gerald of Wales, Archdeacon of Brecon 104–5

Germann, Lady Isabella 286–91, 293, 296

Giffard, John 294, 295

Godwin, Earl of Wessex 44–5

Godwinson, Harold 21, 44–5

Gordon, Bernard de: Lilium Medicinae 68–70, 72

Gospel of St Matthew 16

Gotland, island of 257–8

Grand Louise 221

granuloma 57, 266–7

graves

- anthropomorphic 90

- Becket’s see Becket, Thomas

- Black Death and 180, 194–8, 212–14

- Commonwealth war graves 47

- grave-fill 53–4

- grave goods 26, 54, 153

- mass graves see mass graves

- See also individual place name

Great Heathen Army 13–14, 23, 27

Great Plague of London (1665) 199

Greenland 28, 29, 31, 34

Gregoras, Nicephoros 192–3

Gregory, Pope 47

Grimbald, St 92

Grim, Edward 104, 106, 107

Gruber, Wenzel 247–8, 249

gummata 266–7, 270, 284

Gunhild 21

Gunnor 13, 24

- Hadrian IV, Pope 99–100

- Hadza bows 256

- Haithabu 33–4

- Harefoot, Harold 44

- Harper, Kristin 278, 279, 281

- Harthacnut, King of Denmark 44

- Hartsoeker, Nicolaas 210

- hate speech 6, 16

- Henry II, King of England 99, 100–105, 108, 110–12, 114, 128, 142, 250

- Henry III, King of England 116, 250, 294

- Henry V, King of England 220

- Henry VIII, King of England

- English Reformation and 6, 49, 123–5, 127–9, 132, 137–8, 142, 145

- Mary Rose and 215, 216, 218, 219, 220–26, 228, 230, 261

- Thomas Becket and 123–5, 127–9, 132, 137–8, 142, 145

- Henry of Blois, Bishop of Winchester 48

- Hildred, Alex 216, 261–2, 301

- hip dysplasia 240–41

- Hispaniola 276

- HIV 273, 274

- Holcomb, Richmond Cranston 68, 70

- Holinshed, Raphael 232

- Holy Roman Empire 44, 124, 220, 221, 223–4, 226

- Hong Kong, plague outbreak in (1894) 180–88, 201, 305–7

- hospitals, origin of 50–51, 81–2. See also St Mary Magdalen, Hospital of

- Howard, Admiral Sir Edward 221–2

- Howard, Admiral Thomas 222

- Hrólfr (or Rollo) 24, 43, 45

- Huggon, Martin 77, 78

- Hugh of Horsea 107, 133

- Hutchinson, Sir Jonathan 279

- Hutchinson’s incisors 279

- hydroxyapatite 85–6, 155

- Ice Age 255, 257

- Iceland 24, 28, 29, 31, 34, 117

- Icelandic sagas 24, 117

- immigration 16, 36, 37, 164

- incest 42

- inflammation 53, 57, 59, 90, 161, 163–4, 193, 202, 250, 266–7, 270, 285

- injuries 3–4

- facial 73–5

- leprosy and 52, 57, 58

- Mary Rose skeletons and 233–4, 239–43, 250, 257

- Oxford mass grave and violent 10–12, 26, 38, 39

- Thomas Becket’s 126, 128, 130, 132, 135

- Innocent III, Pope 115

- Ireland 14, 28, 29, 30, 31, 34, 42, 45

- Iron Age 26, 92, 96, 97, 203

- Isle of Ensay 249, 251

- Isle of Wight 13, 228

- isotope analyses 27, 34, 35, 36, 88–92, 174, 176

- Janibeg, Khan of the Golden Horde 192

- Jarman, Cat 23, 27

- Jesch, Judith 31–2

- Jesus 47, 291

- John Chrysostom, St 16–17

- John of Salisbury (‘Johannes Parvus’, Little John) 99–100, 101–2, 105, 106, 108–10

- Vita S. Thomae Becket 110

- John Paul II, Pope 138

- John VI Kantakouzenos, Emperor 193

- John, King of England 114, 115

- Judoc, St 92

- Justinianic Plague 4, 197–9, 201–2

- Katherine of Aragon, Queen of England 219, 223–4

- Keble College, Oxford University 10

- Keene, Derek 92–3

- Kent 13, 22, 96–7, 222

- Ketill Flatnose, King of the Isles 43

- King, Turi 136

- Koopmans, Rachel 139

lagophthalmos 57

Lambesc mass grave 194–5

Langton, Archbishop Stephen 117

Lateran Council, Rome (1215) 72

Lazarus 47

Lazarus of Bethany 47

Leofsy 13

leprosaria/leprosy hospitals 47, 50, 51, 66, 68, 70–93

- Becket relics and 116

- children and 52, 54–5, 67, 68–9, 84–93

- diversity of 80

- earliest-recorded in England 51

- facial disfigurement and 70, 72–5

- guests or hospites 79

- medical intervention in 83–4

- number of in Norman England 81

- origins 66, 70–76, 80–82

- patient origins/patients from outside of England in 89–93

- range of patients 68, 70, 89–93

- religious nature of/monastic tradition and 76–8

- social welfare function 79

- status quo, serve to preserve 78–9

- St Mary Magdalen, Hospital of, Magdalen Hill, Winchester see St Mary Magdalen, Hospital of, Magdalen Hill, Winchester

leprosy 5, 46–93

Aretaeus on 62–3

Becket and 115–16

children and 52, 54–5, 67, 68–9, 84–93

claw hand and 57

decline of, fourteenth-sixteenth centuries 66–7

diagnosis 68–70

early detection 62

facial disfigurement 52–3, 57, 59–60, 70, 72–5

facies leprosa or rhinomaxillary syndrome 59–60

finger bones and 53–5, 57, 58, 85

foot damage 52, 53–4, 57, 58–9, 84, 85

Galen on 63–4

genetic studies 64–7

granuloma and 57

hands and 52, 53, 54, 57, 58–9, 85

lagophthalmos and 57

lepromatous leprosy 56–7, 59–60, 65, 72, 88

leprosaria/leprosy hospitals see leprosaria/leprosy hospitals

manifestation of 56–7

medical intervention 83–4

Mycobacterium leprae (M. leprae) and 55–6, 58, 59, 60, 62, 64–6, 67, 89, 90

numbers living with leprosy-related deformities 61–2

origins of 64

osteologically identifiable 67–8

palliative care 54, 62, 83

Pasteur and 181

sensory nerve damage 52, 57–8

social stigma and 61–2, 71, 72, 74, 75

spread of across Europe, Middle Ages 66–7

syphilis and 270, 280, 290

tooth damage 52–5, 73, 84–5, 86, 87, 88–9, 90

toe damage 53–4, 90

traditional view of society’s response to in Middle Ages 71–2

transmission 60–61, 62, 67–9

treatments 61, 62–4

tuberculoid leprosy 56, 60

venereal disease and 68–70

Leviticus 72, 75

lice, plague transmission and 206, 208–11

Lisle, Admiral, Viscount 226, 228

Lofoten archipelago 33, 34

London 4, 15, 22, 125, 134, 172, 187, 197, 199, 212, 225, 230, 279, 300

longbow archers 216, 250–52, 255, 258–61

Longspee, earl of Salisbury, William de 294

Longspee, Maud de 294

Louis VII, King of France 115, 122

Louis XII, King of France 223

Louth Park Abbey 213

Magdalen Hill, Winchester 46–7, 81–2

Magdalene, St Mary 47–9

Magnus, prince of Norway 44

Maldon, Battle of (991 AD) 15

mandible (lower jaw) 11, 53, 236, 264–5

Marter, Phil 48, 50, 52, 75

Mary (of Bethany) 47

Mary I, Queen of England 138

Mary Rose 6–7, 215–62

- acromion in skeletons discovered on 247–52

- Anthony Roll naval inventory (1546) and 232

- archers on, longbow/archer hypothesis 250–62 see also archery/archer hypothesis,

- Mary Rose

- archive 215–16, 234

- carrack design 219, 227

- Charles V tours 223

- decommissioned 223

- distribution of bones on 238–9

- Field of the Cloth of Gold and 223

- guns 219, 221, 224, 226–7, 230

- Mary Rose Trust, creation of 231

- as mass grave 215–16, 218–19, 232

- McKee and British Sub-Aqua Club rediscover (1970) 230–31

- Mitchell study (2022) 239–44, 247

- Museum 231–2, 261–2

- name 219

- numbers of men lost on 232–9

- origins 219–20

- os acromiale in skeletons discovered on 247–52

- ossification of the ligamentum flavum (OLF) in skeletons discovered on 245–7

- rediscovered by John and Charles Deane (1836) 230

- renovations 224

- rescue operation (1545) 228–30

- rescue operation (1982) 216–18, 231

- Schmorl’s nodes in skeletons discovered on 243–4

- sinks in Solent (1545) 215, 216, 218–19, 226–8, 230–31, 232, 239

- Skeleton 82 259

- Stirland report on skeletons discovered on (1985) 233

- War of the League of Cambrai and 220–33

mass graves 249

- Black Death and 180, 194–5, 196, 197, 212–14

- Mary Rose as 215–16, 218–19, 232

- Oxford, mass grave in/St Brice’s Day Massacre and 10–12, 25–9, 36–9

mastoid process 11

Matthews, Hannah 234, 261–2

maxillae 52, 53, 59, 90

McAvoy, Liz 292–3, 294, 295–6

McIntyre, Lauren 263–6, 285–6, 290

McKee, Alexander 230

Meaux 213

medical intervention 83–4

mercenaries 18–19, 20, 22, 32, 37–8, 276

metabolic disruption 154

metagenome 4–5, 284

microbiology 86, 180, 181

migration 2, 4, 16, 28, 30–31, 33, 36, 37, 45, 46, 164, 203, 205

Mitchell, Emily 239–44, 247

mitochondrial DNA (mtDNA) 29

Molnar, Petra 257

monasticism 71, 76, 77–8, 84, 152–3, 174, 290

monks 20, 50, 75, 76, 77–8, 101, 106, 107–8, 109, 113, 114, 117, 127, 132, 133, 145, 147, 152, 156, 158, 213, 287, 293

Mont-aux-Malades, leproserie at 116

Montpellier, Black Death and 195–6

Moon, Henry 279

Moon’s molars 279

mortality rates 181–2, 189, 190

Morville, Hugh de 105–6

Most Likely Number of Individuals (MLNI) 237–8

murder 19, 20, 21, 100, 102, 103–11, 116, 117, 127, 132, 133, 138, 139

mycobacterium 55–6, 58, 59, 60, 62, 64–6, 67, 89, 90

Mycobacterium leprae (M. leprae) 55–6, 58, 59, 60, 62, 64–6, 67, 89, 90

Mycobacterium tuberculosis 56

- Neolithic era 26, 42

- archers in 255–6, 257, 258

- earthworks 10

- long barrows 4

- plague in 202, 205–6, 208

- neurosyphilis 284–5, 291

- nitrogen-15 35

- Normans/Norman period 13, 21, 22, 24–5, 37, 42–4, 45, 48, 50, 51, 294

- Church in England and 92, 99, 114, 147–8

- hospitals in 48, 50, 51, 81–2

- Norman Conquest 21, 44–6, 81–2, 147–8, 250

- origins of 42–6

- North Sea 12, 22, 23, 33, 44, 45

- North Sea Empire 44

- Norton Priory, Cheshire 145–54, 172–8

- abbot’s lodging 146, 149, 151

- agriculture as main business of 151–2

- archaeological investigation of begins (1970) 152–3

- Brooke family and 149–50

- construction of 150–52

- dissolution of the monasteries and 149, 152

- fisheries 151–2

- foundations 146

- graves/burials at 152–4

- Norton Priory Museum and see Norton Priory Museum

- origins of 146–9, 150, 152

- Paget’s disease and skeletons discovered at 147, 172–8

- radiocarbon-dating skeletons at 174

- SK101skeleton discovered at 175

- St Christopher statue 150–51

- Norton Priory Museum 146–7, 150, 153

- Norway 21, 23, 29, 30–34, 39, 43–4, 89, 244, 272

- obligate parasites 55–6

- Oholibah 73

- Orkney 28, 30, 35

- os acromiale 247–52

- Osage orange wood 256

- ossification of the ligamentum flavum (OLF) 245–7

- osteoarthritis 160, 167, 241, 242, 265, 266

- osteobiography 1, 5–7, 284, 296

- osteoblast 155–6, 158–9, 162–3, 165–6, 171, 177, 245, 254

- osteochondritis dissecans 241

- osteoclast 158–9, 166, 169, 170, 171, 175, 176, 177, 254

- osteocyte 154–60, 177

- Osteological Paradox 179, 180

- osteolysis 159, 171

- osteomyelitis 52

- osteoporosis 160, 163, 164, 244, 266

- osteosarcoma 168, 171, 173, 174

- othering 9

- Outer Hebrides 29, 43, 249

- Owen, Nick 258–9, 261

- Oxford, mass grave under St John’s College in 10–12, 25, 26, 27, 35–9

- oxygen isotope 36, 38, 88, 89

Paget’s disease 160–78

Paget, Sir James 160–72

Paget, Sir William 228

palaeopathology 3–4, 178, 254, 297

Pallig 19

Parable of the Tares 16

parietal bone 10

Pasteur Institute 181, 183, 186

Pasteur, Louis 181

pathogens

- aDNA, using to identify 4, 180–214

- leprosy see Mycobacterium leprae

- plague see Yersinia pestis

- syphilis see Treponema pallidum

Paul III, Pope 130–31, 132

Pawlo, Peter or Peter Paule 230

PCR testing 60–61, 62, 90, 195, 196

Peckham, Robert 183–4

Pecten maximus (Atlantic scallop) 91–2

Pediculus humanus (human louse) 209–10

pelvis 11, 38, 39, 135, 167, 174, 264–5, 266

penicillin 188–9, 271, 272, 273, 274

periosteum 58, 59, 167

Peter of Celle, Abbot 110

Peter Pomegranate 218–20, 224

phalanges 53, 236

phrenology 126

Pictish genomes 30

pla (plasminogen activator) 203

plague

- Black Death see Black Death

- bubonic plague 181–2, 190, 194, 203, 204, 209

- First Pandemic/Justinianic Plague (sixth century) 4, 197–9, 201–2

- Great Plague of London (1665) 199

- Hong Kong outbreak (1894) 180–88, 201, 305–7

- lice, plague transmission and 206, 208–11

- pneumonic plague 190, 191, 203, 206, 209

- Third Pandemic (nineteenth century) 199, 200–201, 208–9

- Yersinia pestis and see Yersinia pestis

Plath, Sylvia: Lady Lazarus 41

pneumonic plague 190, 191, 203, 206, 209

Poppa of Bayeux 43

pottery 4, 54, 150

pre-Columbian hypothesis 276–83

Prontosil 189–90

Protestant movement 123, 138

p62 (protein) 169, 175–6

psoriasis 68

- radiocarbon dating 2, 26, 27, 35, 51, 81, 82, 136, 174, 204, 213, 279, 283, 284, 287

- Reformation 6, 49, 123–5, 127–9, 130, 132, 137–8, 142, 145–6

- refugees 17, 211

- Regent 221

- relics 146, 290

- St James 91

- St Thomas Becket 96, 116–17, 118–19, 123, 129–30, 133, 137, 142

- rheumatoid arthritis 68, 177

- Richard I of Normandy, King (Richard the Fearless) 13, 22, 24

- Richard I, King of England 114, 115

- Richard III, King of England 136

- Rinnukalns burials 204–5

- Roffey, Simon 48, 50–52, 67, 70, 75, 81, 82, 91–2

- Roman Empire 3, 26, 42, 77, 92, 110, 112

- Britain exits from 97

- leprosy in 63–4

- St Augustine’s visit to Britain and 97–8

- Rouen 22, 24, 116

- Routledge, Reverend Charles Francis 130, 131, 133, 134

- Royal Commissioners for the Destruction of Shrines 124, 127, 132, 149

- Rule, Margaret 216–17, 218, 230–31, 233

- Runcie, Archbishop of Canterbury, Robert 138

- Runcorn 146, 148, 150–51, 152

- Runcorn Development Corporation 162

Salme, Estonia 30

Salvarsan 270–72

Sámi populations 30

Santiago de Compostela, Spain, shrine of St James at 91

SARS-CoV-2 60

Scandinavia 13, 15, 23, 24–5, 28, 30–32, 34, 36–7, 39, 164, 209

Schmorl’s nodes 243–5

Schnebbelie, Jacob 50

Schwann cells 56, 57

seafaring, developments in 32–4

Seliger, Leonie 140

sepsis 52, 58, 190–91, 203, 206, 210

Servicium Recludendi (Service of a Recluse) 287–8

Seven Comfortable Acts/corporal Acts of Mercy 76

sex determination 26, 28, 29, 84–90, 153, 240, 264–5

sexually transmitted disease 69–70, 267, 271, 273, 274, 277, 282

Shibasaburo, Kitasato 183, 185

Shi Daonan, The Death of Rats 200

Sievers, Carl George Count 204

Simond, Paul-Louis 186–7, 208

Simpson, William 187

Skinner, Patricia 75

Skoglund, Pontus 4, 198

skulls

- All Saints Church, Fishergate, discovered at 264

- Mary Rose, discovered on 230, 233, 236, 242, 264

- Oxford mass grave, discovered at 10–11, 39

- Paget’s disease in Norton Priory skeletons and 161–3, 167–8, 172, 174, 175

- plague and 196, 204, 264

- St Mary Magdalen cemetery, discovered at 52, 53, 59–60

- Thomas Becket’s 107, 113, 117, 118, 126–30, 132–5

Smythe, Sir John 259–60

social stigma 61–2, 71, 72, 74, 75, 264, 291

Solent 215, 216, 218–19, 226–8, 230–31, 232, 239

spears 10, 11, 252, 255

spina bifida 242

spirochaete 267, 269

Staphylococcus aureus 189

St Brice’s Day Massacre (1002) 6, 9–39, 42, 43, 88–9

- earliest accounts of (1004) 15–21, 26, 37, 38

- origins of 12–15

- othering and 9

- Oxford mass grave, link to 10–12, 25–39

- Sweyn Forkbeard’s reaction to 21–2, 43

- Viking battles for control of the seas and 22–5

Stephen, King of England 48, 99–100, 103

St Frideswide, charter of (1004) 15–19, 26, 37, 38

Stirland, Ann: The Men of the Mary Rose: Raising the Dead 233–4, 236, 240, 242, 243, 244, 247, 248, 249–53, 257–8

St James and St Mary Magdalene Hospital cemetery, Chichester 67–8

St John Timberhill leprosarium cemetery, Norwich 67–8

St John’s College, Oxford University, mass grave underneath 10–12, 25, 26, 27, 35–9

St John’s hospital, Bridgwater 80

St John’s hospital, Cambridge 80

St Mary, abbey of, Norton 146–78. See also Norton Priory

St Mary Magdalen, Hospital of, Magdalen Hill, Winchester 46–93

- amelogenin analysis on skeletons discovered at 85–8

- Anglo-Dutch Wars and 49–50

- cemetery at 47, 50–52, 59–60, 66, 67–8, 71, 72, 79, 81–2, 84–5, 88, 89–91

- child skeletons discovered at 52, 54–5, 67, 84–6

- Civil War and 49

- discovery of 46–7

- excavation campaign, Roffey and Marter’s 50–52

- foundation of 47–8, 50–51, 66, 81–2

- graves at, nature of 71–2

- leprosy and skeletons discovered at 52–5, 59, 66, 67–8, 70–71, 78, 80, 81, 84, 85, 88–93

- see also leprosy

- name 47

- origins of individuals in cemetery at 88–90

- Pecten maximus (Atlantic scallop) found in cemetery at 91–2

- Reformation and 49

- sex determination of skeletons discovered at 84–90

- Skeleton 19 52–3, 59, 84

- Skeleton 27 90

- surgical intervention, evidence of at 84

- Time Team investigation 48

- Winchester pilgrimage site and 91–3

- Winton Domesday book and 48, 82

streptomycin 190

strontium 36, 38, 88, 89

Suffolk, Charles Brandon, Duke of 228–9

sulphonamide 189

Swali, Pooja 4–5, 198–9, 206–8

Swansea University 258

Sweden 30, 32, 35, 55, 66, 136

Swithin, St 92

synthesising approach 31

syphilis 5, 68, 70, 267–96

- All Saints, Fishergate skeleton SK3870 and 263–70, 284–96

- ancient evidence of in human skeletons 276–83

- bejel and 277, 278

- Columbian hypothesis and 276–84

- congenital syphilis 278–9, 282

- diagnosis 270

- Fournier’s molars and 279

- genetic studies of modern syphilis 273–5

- genomic evidence of treponemal infection in archaeological skeletons, first 281–3

- global prevalence of 271–3

- ‘Great Exchange’, and 275–6

- Hutchinson’s incisors and 279

- Moon’s molars and 279

- neurosyphilis 284–5, 291

- origins 274–7

- patients’ experience of untreated syphilis 284–5

- pre-Columbian hypothesis 276–83

- pregnancy and 272

- primary phase of infection 267, 269

- record of, first 276

- secondary 269

- sexually transmitted 267, 271, 273, 274, 277, 282

- sign of infection, first 267

- syphilitic insanity 270

- tertiary 270, 278, 285

- treatment, first effective 270–71

- Treponema pallidum and 267–71, 273, 277–8, 281–4

- Treponema pallidum endemicum and 277, 281

- Treponema pallidum pertenue and 277, 282, 283

- treponemal diseases and 277–83

- Unitarian hypothesis 281–2

- yaws and 277, 278, 281, 282, 283

tares 16–17

teeth

- All Saints Church, Fishergate skeleton SK3870/syphilis and 264–5, 278–9

- calculus 52, 90, 242, 265

- childhood location, analysis of uncovers 2, 36, 55, 88–9

- defects see individual defect or disease name

- enamel analysis 36, 85, 88–9, 279

- facial disfigurement and 73

- hygiene, dental 53, 242, 266

- isotope analysis and 36, 92

- lesions in and poor health as a child 84–5

- Mary Rose, evidence of poor dental hygiene discovered on 242

- Oxford mass grave, stable isotope analysis on teeth at 36

- plaque, dental 53

- plague and 194–6, 198, 206

- pulp, dental 86, 87, 194, 195

- sex determination and 86, 87

- St Mary Magdalen skeletons/leprosy and 52–3, 54, 55, 84–5, 86, 87, 88–9, 90

- Thomas Becket’s, location of 125, 127, 136

Thames Valley Archaeological Service 10, 25–6

Theobald of Bec, Archbishop 99–101, 108

Thietmar, Bishop of Merseburg 73, 74–5

Thómas saga Erkibyskups (‘Saga of Archbishop Thomas’) 117

Thornton Abbey mass grave 212–14

Thornton, William Pugin 125–30, 132

Thousand Ancient Genomes project 4–5, 198–9, 206–8

Time Team (television series) 48

toe bones 53–4, 90

Tokesen, Pallig 21

Toti 37

Towton, Battle of (1461) 249, 251

Tracy, William de 105–7

transmission, disease

- leprosy 60–69

- plague 184, 186–8, 190, 203, 206–11, 307

- sexually transmitted disease 69–70, 267, 271, 273, 274, 277, 282

- syphilis 267, 271, 273, 274, 277, 282

Treaty of Alfred and Guthrum (886) 14

Treponema pallidum 267–71, 273, 277–8, 281–4

Treponema pallidum endemicum 277, 281

Treponema pallidum pertenue 277, 282, 283

treponemal disease 277–83

tuberculosis (TB) 38, 56–7, 60, 67, 85, 194, 202, 205

Tucker, Katie 38, 52, 55

- ulnae 236–8, 255

- unitarian hypothesis 281–2

- University of Massachusetts 253–6

- University of Nottingham 31

- University of the Mediterranean, Marseille 194

- University of Winchester 46, 48, 52

- vertebrae 11, 39, 125, 135, 243–6, 264, 265

- Vestfjord 33

- Vikings 3, 103

- Anglo-Saxons and 13–14, 15, 23–34, 43–4, 45

- Danegeld, or ‘Dane-yield’ 15

- Danelaw and 14, 28, 43

- ‘Danes’ and 12–26, 32, 37, 45

- diaspora, origins of 25–32

- diet 27–8, 32–4, 35–6

- genomes, study of Viking Age 29–39

- Normandy and 13, 24–5

- Oxford mass grave and 27–39

- St Brice’s Day Massacre and see St Brice’s Day Massacre

- term 23–4

- Viking Age 29–30, 33–4, 39

- víkingar (Icelandic sagas) 24

- Virchow, Rudolf 204

- Vitalis, Orderic: Historia Ecclesiastica 74

- Walchelin 74–5

- War of the League of Cambrai (1508–16) 220–23

- Welsh rebellion (1264–65) 294

- West Francia 24, 43

- William I, ‘William the Conqueror’, King of England 21, 24, 45, 99, 103

- William I, King of Scotland 111, 112

- William of Jumièges 19–22

- William of Malmesbury 20–22

- William of Sens, Archbishop 110

- William of Wykeham, Bishop of Winchester 49

- Williams, Emily: Notes on the Painted Glass of Canterbury Cathedral 140–41

- Willmott, Hugh 212, 213

- Wilm, Staff Surgeon 181–2

- Winchester 22, 46, 48, 49, 50, 51, 52, 66, 67, 78, 81, 89, 92–3. See also St Mary Magdalen, Hospital of, Magdalen Hill, Winchester

- Winton Domesday book 48, 82

- Wipert 73–5

- Witan 45

- Wolsey, Cardinal 222, 223

- Wordsworth, William: ‘St Catherine of Ledbury’ 292–4

- World Health Organization (WHO) 61–2, 271–2

- Wriothesley, Charles 227

- Wriothesley, Thomas 131, 132, 227

- X-chromosome 87

- X-rays 55, 60, 164, 165, 167, 168, 172, 173–4

- yaws 277, 278, 281, 282, 283

- Y-chromosome 29, 87

- Yersin, Alexandre 181–8, 201, 301, 305–7

- Yersinia pestis

- bubonic and pneumonic plague transmission routes and 190

- Black Death, as causative agent for 194–202

- Breamore Anglo Saxon cemetery and 198–9

- Britain, earliest evidence of in 206–7

- discovery of 182–3

- Edix Hill burial ground and 197–8

- evolution of 199–211

- Hong Kong plague outbreak (1894) and 180–88, 201, 305–7

- lice and transmission of 206, 208–11

- molecular detection of in archaeological human remains 194–208, 211, 283, 300

- naming of 183

- origins/ancient 197, 202–8

- pandemics and see Black Death

- pla (plasminogen activator) and 203

- rural communities and 212–14

- transmission routes 190, 208–11

- virulence, identification of genes associated with 203–11, 283

- Yersinia pseudotuberculosis and 202

- ymt gene and 203–9

- zoonotic disease 187–8

- ymt gene 203–9

- zoonotic disease 170, 187–8, 206, 211

CHAPTER ILLUSTRATIONS

- Page 1  Skeleton 27 from the St Mary Magdalen, Winchester site – the possible pilgrim with a scallop shell.

- Page 9  The mass grave at St John’s College, Oxford.

- Page 41 Skull from Skeleton 19 from the St Mary Magdalen cemetery – showing classic facies leprosa features.

- Page 95 Drawing of alabaster sculpture depicting the murder of Becket, c. 1450.

- Page 145 The head-niche stone coffins at Norton Priory.

- Page 179 Drawing of a detail of The Triumph of Death by Pieter Bruegel the Elder, c. 1562.

- Page 215 The Mary Rose being lifted from the Solent.

- Page 263 The grave of the possible anchoress from All Saints Church, Fishergate, York.

First published in Great Britain by Simon & Schuster UK Ltd, 2024

Copyright © Alice Roberts, 2024

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Hardback ISBN: 978-1-3985-1923-7

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