Industrial pollution doesn’t always look like a single visible disaster at first.

More often, it slowly seeps into ordinary life: through irrigation water, through fish that seemed safe to eat, or through air that quietly becomes dangerous to breathe.

That pattern ran through Japan’s four major pollution scandals across the 20^th century- and why they still matter now. The health costs of industrial growth are still so often borne by everyone except the industries that create them.

When industrial chemicals entered ordinary life

First identified in 1912, itai-itai disease began with industrial waste slowly contaminating a river.

In Toyama Prefecture’s Jinzū River basin, toxic waste released upstream from Mitsui Mining and Smelting Company’s Kamioka Mines contaminated water used to irrigate rice fields. Driven by surges in mining production of silver, zinc and lead to meet wartime demands, the contamination entered local food supplies and drinking water over several decades.

The result was cadmium poisoning (1). Chronic exposure damaged the kidney first, especially the renal tubules, disrupting the body’s ability to regulate minerals properly (2). That in turn caused severe bone softening, producing fractures and agonising pain that gave the disease its name: itai-itai, or “it hurts, it hurts”.

“The pains gnaw at my body. I want to throw out my stomach and intestines.” Takako Nakamura, a victim of itai-itai disease, quoted in Time (1971). Source: https://time.com/archive/6838618/environment-and-now-cadmium/

Itai-itai disease mattered because it showed how industrial pollution could become chronic harm in everyday life. Those most affected depended on that land and water for farming and daily life, while the mining industry treated them as a sink for waste.

A very public pollution scandal

Minamata disease revealed the same pattern again, but on the scale of a national scandal.

Officially identified in 1956 around Minamata Bay, the disease had been building for years through industrial discharge into the sea (3). At the Chisso chemical plant, methylmercury was produced as a by-product of acetaldehyde manufacturing, and an estimated 70 to 150 tons of contaminated wastewater was released over the years.

Fish and shellfish then bioaccumulated the toxin, turning an ordinary food source into a route of poisoning. Once ingested, methylmercury damaged the central nervous system, causing sensory disturbance, ataxia, and sight and hearing impairments (4). It could also cross the placenta, leading to devastating fetal injury (5). Officially, around 3,000 people were affected.

What made Minamata especially horrifying was the invisibility of the harm. Contaminated seafood looked no different from safe seafood, leaving almost no visible warning signs. The Minamata incident became a defining symbol of pollution-related health harm in post-war Japan.

“We came to understand that it was caused by methylmercury poisoning but we couldn’t really make it public that we were victims, because people thought that Minamata disease was contagious.” Masami Ogata, a Minamata disease survivor, recalling the stigma that surrounded the illness when its cause was still poorly understood. Source: https://www.unep.org/globalmercurypartnership/news/editorial/telling-tragic-story-mercury-poisoning-japan

But the pollution scandal didn’t end there. Less than a decade later, a similar methylmercury poisoning episode emerged in Niigata.

The scandal repeated

In 1965, a second methylmercury poisoning scandal was identified in the Agano River basin in Niigata Prefecture, linked to wastewater from Showa Denko’s Kanose factory. Fish and shellfish in the river system became contaminated, and Minamata disease returned much the same pathway as a decade before (6).

That repetition changed the meaning of the original Minamata scandal. By the mid-1960s, this was no longer a one-off disaster: the earlier scandal had failed to produce safeguards to prevent another. Corporate priorities were still placed above environmental safety and human health.

Economic growth itself became breathable as illness

In the post-war era, Yokkaichi became a major petrochemical and refinery city, promoted as part of Japan’s industrial transformation. But the prosperity it generated came with a heavy cost.

“Yokkaichi was gradually prospering, and our family was also running a business, so I thought it was good. I never dreamed that my own daughter would be affected by the industrial complex.” Teruko Tanida, whose daughter Naoko was a victim of Yokkaichi asthma (2022). Source: https://www.tokai-tv.com/tokainews/feature/article_20220811_20719

From the late 1950s into the 1960s, emissions from oil refineries, power plants and petrochemical facilities released large quantities of chemical dust, sulfur oxides and sulfuric acid mist. These pollutants accumulated over surrounding neighbourhoods, creating some of the country’s most notorious urban-industrial air pollution (7,8).

Residents living closest to the industrial zone paid for that pollution with their lungs. People developed bronchial asthma, chronic bronchitis, emphysema and related respiratory disease, which became a resulting cluster of illnesses known as Yokkaichi asthma. Unlike Minamata, this wasn’t poisoning through a single contaminated food source, but the slower impacts of ordinary air made toxic.

Yokkaichi widened the critique beyond a single factory or pollutant, showing how corporate expansion, fossil fuel development and permissive politics could make industrial harm part of everyday life.

Towards activism and compensation

What turned these pollution diseases into a national reckoning was organised activism by victims and communities. In Minamata, citizens’ groups helped turn the disaster into a national political issue by demanding legal accountability. But recognition and relief came slowly, often after years of corporate denial, lawsuits and campaigns. The incident also carried a wider legacy of the 2013 Minamata Convention on Mercury, an international treaty that aims to curb mercury pollution and its harms to human health and the environment. The treaty carried the name of a local catastrophe onto the global stage, but it could not undo the damage left behind.

Air pollution activism followed a similar path. In Yokkaichi, residents sued six major firms in the Yokkaichi Pollution Lawsuit, arguing that emissions from the petrochemical complex had caused severe respiratory illness. The case helped establish dirty air as a form of industrial harm for which companies could be held responsible.

Court rulings held corporations including Showa Denko and Mitsui Mining & Smelting responsible for measurable health damage, securing compensation for some victims and helping establish pollution as a harm that could be fought in court. Nationally, the Water Pollution Control Law of 1970 required factories to regulate hazardous effluent and explicitly linked pollution control to the protection of human health. Together with wider anti-pollution reforms in the early 1970s, these cases forced Japan’s courts and government to confront the human costs of post-war growth, though often only after ordinary communities had already borne them.

What Japan’s scandals tell us about corporate harms

Japan’s major pollution scandals reveal that corporate harm to health is often slow and denied. Uncertainty then became part of the harm itself. Victims were told to wait for better evidence or official recognition even when illness had already become impossible to ignore.

That pattern has hardly disappeared. Fossil fuel companies and allied industries help create the conditions in which pollution becomes normalised and politically protected. Air pollution is still associated with roughly 5.1 million premature deaths each year worldwide, making it one of the largest environmental threats to health (9). The same is true of hazards such as PFAS and asbestos, where industries can leave damage behind for years while regulation struggles to catch up.

Powerful industries will prioritise commercial and financial interests while the health costs are pushed outward onto workers, residents and communities living near extraction sites and power plants. As environmental protections are weakened in parts of the world, those risks become harder to contain.

Japan’s pollution crises is a warning about the consequences of neglect. Public health is undermined when corporations are allowed to shape the air, water and food that sustain life while avoiding responsibility for the damage they cause.

Sources and References:

Jepang, K.L.H., 2017. Lessons from Minamata Disease and Mercury Management in Japan. Jepang, diakses tanggal, 6. https://www.env.go.jp/content/900414989.pdf

Yorifuji, T., 2020. Lessons from an early-stage epidemiological study of Minamata disease. Journal of epidemiology, 30(1), pp.12-14. https://doi.org/10.2188/jea.JE20190089

Feng, D., 2021. Certification, Lawsuits and the Role of Epidemiology in the Yokkaichi Asthma Episode in the 1960s and 1970s: Lessons and Legacy. Social History of Medicine, 34(1), pp.118-140. https://doi.org/10.1093/shm/hkz058

Takemoto, Y., Takahashi, M., Kito, H. and Terazawa, T., 2017. History of Yokkaichi Asthma and Its Anti-pollution Measures. J. Mater. Sci. Eng, 7, pp.188-198. doi: 10.17265/2161-6213/2017.7-8.003

(1) Kasuya, M., 2000. Recent epidemiological studies on itai-itai disease as a chronic cadmium poisoning in Japan. Water science and technology, 42(7-8), pp.147-154. https://doi.org/10.2166/wst.2000.0563

(2) Aoshima, K., 2012. Itai-itai disease: cadmium-induced renal tubular osteomalacia. Nihon eiseigaku zasshi. Japanese journal of hygiene, 67(4), pp.455-463. doi:10.1265/jjh.67.455

(3) Harada, M., 1995. Minamata disease: methylmercury poisoning in Japan caused by environmental pollution. Critical reviews in toxicology, 25(1), pp.1-24. https://doi.org/10.3109/10408449509089885

(4) Ekino, S., Susa, M., Ninomiya, T., et al. 2007. Minamata disease revisited: an update on the acute and chronic manifestations of methyl mercury poisoning. Journal of the neurological sciences, 262(1-2), pp.131-144. https://doi.org/10.1016/j.jns.2007.06.036

(5) Sakamoto, M., Tatsuta, N., Izumo, K., et al. 2018. Health impacts and biomarkers of prenatal exposure to methylmercury: lessons from Minamata, Japan. Toxics, 6(3), p.45. doi: 10.3390/toxics6030045

(6) Maruyama, K., Yorifuji, T., Tsuda, T., et al. 2012. Methyl mercury exposure at Niigata, Japan: results of neurological examinations of 103 adults. BioMed Research International, 2012(1), p.635075. doi: 10.1155/2012/635075

(7) Yoshida, K., Oshima, H. and Imai, M., 1966. Air pollution and asthma in Yokkaichi. Archives of Environmental Health: An International Journal, 13(6), pp.763-768. https://doi.org/10.1080/00039896.1966.10664661

(8) Kitagawa, T., 1984. Cause analysis of the Yokkaichi asthma episode in Japan. Journal of the Air Pollution Control Association, 34(7), pp.743-746. https://doi.org/10.1080/00022470.1984.10465807

(9) Lelieveld, J., Haines, A., Burnett, R., et al. 2023. Air pollution deaths attributable to fossil fuels: observational and modelling study. bmj, 383. doi: https://doi.org/10.1136/bmj-2023-077784

At the Missouri river landing, the steamboat SS. St. Peter coughed smoke into the dusk. Crates of fur and clothing thudded onto the planks, along with something else nobody could see…

Within weeks, communities along the river were devastated.

On the Great Plains of North America, smallpox spread through a landscape reshaped by river trade and forts. The routes feeding a new American economy also carried the virus at speed, turning the paths of commerce into catastrophe.

But did it happen by accident, indifference, or design?

Steamboats, forts and routes that carried smallpox

Between 1836 and 1840, smallpox tore across the northern Great Plains in repeated waves, with multiple introductions and brutally uneven impact. The outbreak peaked after spring 1837, when the American Fur Company steamboat SS St. Peter travelled up the Missouri River, linking a chain of river landings and ports from the Midwest to the Upper Missouri.

The virus followed the infrastructure of expansion through trading posts like Fort Clark and Fort Union. The result was a mass epidemic that fell hardest on Indigenous nations, including the Siouan, Mandan, Hidatsa, Arikara, Blackfoot and Assiniboine nations. Estimates suggest over 17,000 deaths among Upper Missouri nations (1), and approximately 10,000 in the Northern Plains.

In the virus’s favour

The Great Plains smallpox catastrophe didn’t come out of the blue. The region had already been hit by an earlier epidemic in 1781–82, and the virus returned to a landscape where vulnerability had been building for years. Because smallpox came in intermittent waves, immunity was uneven, leaving some communities particularly exposed when it struck again.

The crisis accelerated once cases appeared. At Fort Clark, the trader Francis Chardon wrote that the dead were falling so fast it was impossible to keep account (2). Reconstructions of the 1837–38 epidemic suggest that crowded living, malnutrition and unsanitary conditions were linked to rapid spread (3).

“The Mandans & Rees gave us two splendid dances, they say they dance, on account of their Not having a long time to live, as they expect to all die of the small pox.” Francis Chardon, (2).

Prevention tools existed, but protection didn’t arrive evenly. Congress had funded Indigenous vaccination through the Indian Vaccination Act of 1832, but coverage on the Upper Missouri remained incomplete, early winter disrupted delivery, and the US Army judged that the Mandan was no longer important enough to the trade economy to prioritise vaccination (4). In Western Canada, Hudson’s Bay Company operations showed that more systematic vaccination could blunt disaster and prove that the scale of loss wasn’t inevitable (5).

The smallpox in the blanket accusation

In the aftermath, some Indigenous leaders framed the epidemic as a betrayal. The Mandan chief Four Bears, speaking as he lay dying in July 1837, condemned the traders for bringing smallpox into his nation.

“You know it, but to die with my face rotten, that even the wolves will shrink with horror at meeting me, and say to themselves, that is the Four Bears, the friend of the Whites…” Four Bears, translated from Mandan into English by Francis Chardon (2).

The most famous allegation was that smallpox had been spread deliberately through infected blankets presented as gifts. Some versions pinned the outbreak on an American Indian who supposedly stole a blanket from an infected passenger on the SS St. Peter (6). Others recast the blankets as a deliberate weapon.

“I have in my possession the certificate of a young man who was employed as one of the company; that they designed to communicate [smallpox] on a present of tobacco…or if such an opportunity should not offer, an infected article of clothing…Not long after this the Pawnees on the Great Platt River were most dreadfully afflicted with small-pox.” Isaac McCoy, in a letter he said was sent to President Andrew Jackson about alleged attempts by traders to spread smallpox (7).

Unlike the well-documented 1763 Fort Pitt incident, in which British officers reportedly gave Indigenous emissaries blankets and a handkerchief taken from a smallpox hospital during a siege parley, the 1837 Plains epidemic had no comparable paper trail, no explicit orders or admissions tying blanket distribution to a plan. Some historians have argued that the blanket story was developed to help shift blame onto Indigenous actors themselves (8).

Where the evidence is firmer is failed precautions. Illness was widely recognised on the Missouri River traffic at the time, yet attempts at isolation were inconsistently applied and frequently overridden (2). Some historians place particular blame on the SS St. Peter’s captain, Bernard Pratte Jr., for refusing to quarantine suspected cases (9).

Why Indigenous communities still bear the burden

Smallpox became catastrophic on the Great Plains in the 1830s because the infrastructure built to maintain commerce also enabled the outbreak to spread, while measures meant to prevent harm arrived late and were often overridden. Indigenous nations along these corridors bore the overwhelming burden.

The 1837 epidemic exposes an institutional failure, one that still shapes Indigenous health today. The US federal system charged with providing care to indigenous peoples, the Indian Health Service, remains structurally under-resourced relative to need. In 2023, per-capita spending for those people receiving care is half that of Medicaid. That gaps show up in everyday realities of long travel appointments, fewer clinicians and delayed treatment.

Those gaps are laid bare in crises. During the 2009 H1N1 influenza and COVID-19 pandemics, American Indian and Alaska Native communities had a death rate two to four times higher than other US adults. This disproportionate burden also shows up in diabetes, cardiovascular and liver disease- conditions closely tied to under-resourced care and living conditions shaped by policy. Layered on top are commercial determinants of health: tobacco industries having documented histories of targeting Indigenous communities to profit from harm.

The Great Plains epidemic shows how catastrophe is enabled not just by pathogens, but by the structural racism embedded in social and economic conditions. In 1837, the infrastructure that sustained commerce carried disease risk faster than prioritising protective measures, and Indigenous nations bore the consequences. Today, the same pattern persists when under-resourced care and delayed safeguards leave Indigenous communities exposed to disproportionate harm.

Then as now, structural failures helped determine whose lives were put at greater risk and whose protection came too late.

Sources and References:

North Dakota Studies. https://www.ndstudies.gov/curriculum/high-school/mandan-hidatsa-sahnish/documents-mha

Boyd, R., 1994. Smallpox in the Pacific Northwest: the first epidemics. BC Studies: The British Columbian Quarterly, (101), pp.5-40. https://pdxscholar.library.pdx.edu/anth_fac/141/

Ferch, D.L., 2020. Fighting the smallpox epidemic of 1837-38: The response of the American fur company traders. Museum of the Fur Trade Quarterly, 19, pp.2-7. https://jedediahsmithsociety.org/wp-content/uploads/2020/04/JSS-Castor-Spring-2020.pdf

Pearson, J.D., 2003. Lewis Cass and the politics of disease: The Indian Vaccination Act of 1832. Wicazo Sa Review, 18(2), pp.9-35. https://www.jstor.org/stable/1409535

Fenn, E.A., 2000. Biological warfare in eighteenth-century North America: beyond Jeffery Amherst. The Journal of American History, 86(4), pp.1552-1580. https://gwern.net/doc/history/2000-fenn.pdf

(1) Ray H Mattison, “The Indian Frontier on the Upper Missouri to 1865,” Nebraska History 39 (1958): 241-266 https://history.nebraska.gov/wp-content/uploads/2017/12/doc_publications_NH1958IndFrontier.pdf

(2) Chardon’s Journal at Fort Clark, 1834-1839. U of Nebraska Press. https://babel.hathitrust.org/cgi/pt?id=uc1.b3625047&seq=11

(3) Dollar, Clyde D. “The High Plains Smallpox Epidemic of 1837-38.” The Western Historical Quarterly 8, no. 1 (1977): 15–38. https://doi.org/10.2307/967216

(4) Vaccination—Indians. Letter from the Secretary of War. 22nd Cong., 2nd sess., H. Doc. 82. February 2, 1833. https://digirepo.nlm.nih.gov/ext/dw/101604565/PDF/101604565.pdf

(5) Hackett, F.P., 2004. Averting disaster: The Hudson’s Bay Company and smallpox in Western Canada during the late eighteenth and early nineteenth centuries. Bulletin of the History of Medicine, 78(3), pp.575-609. DOI: 10.1353/bhm.2004.0119

(6) Audubon, M. R. (1897). Audubon and His Journals, Volume Two. John Wilson and Son Cambridge, U.S.A. https://www.gutenberg.org/cache/epub/39979/pg39979-images.html

(7) Isaac McCoy 1840. History of Baptist Indian Missions: Embracing Remarks on the Former and Present Condition of the Aboriginal Tribes; Their Settlement within the Indian Territory; and Their Future Prospects https://archive.org/details/historyofbaptist00mcco

(8) Mann, Barbara Alice (2009). The Tainted Gift: The Disease Method of Frontier Expansion. Santa Barbara, CA.

(9) Ables, M.J., 2010. Smallpox: The American Fur Company Pox Outbreak of 1837-1838. Fairmount Folio: Journal of History, 12.

Some historical questions hinge on traces of evidence so elusive that they may as well be hidden inside a marble column.

One of them is whether lead poisoning played any role at all in the collapse of the Western Roman Empire. Yes, the title pun is trying to earn its keep.

The “lead hypothesis” isn’t an attempt to sack Rome all over again by blaming everything on plumbing. The usual cast of imperial misery still applies: war, financial strain, political instability and and men in togas making poor decisions. Lead is the more insidious possibility lurking in the background. If it was embedded deeply enough in daily life, could chronic exposure have quietly chipped away at health and resilience in ways nobody at the time could name or measure?

We now know that lead causes real harm in the body and across populations. So the hard question is what kind of evidence would justify saying that an invisible toxin helped tilt the odds of history.

What we mean by the “Fall of Rome”

Before we can ask whether lead contributed to the “fall of Rome”, we have to get clear about what exactly we mean by Rome and by fall.

In most historical writing, we are referring to the Western Roman Empire- the political system that ruled much of western Europe. It doesn’t mean Rome as a city (despite what popular culture often implies), and it doesn’t mean the Eastern Empire centred on Constantinople, which carried on for centuries after the West splintered.

And fall is really shorthand. The Western Empire didn’t topple like a single monument; it declined through overlapping crises. The third-century crisis brought rapid turnover of emperors, civil wars, and frontier pressures that strained finances and armies. Later shocks such as the defeat at Adrianople, the Rhine crossings by barbarians and the sacks of Rome in 410 and 455 CE made the weakening unmistakeable. The loss of North Africa in 439 CE was especially damaging economically. Adding a faltering tax system, military fragmentation, and periodic epidemics, imperial control shrank unevenly across the 4^th and 5^th centuries until what remained no longer functioned as an empire in the old sense.

Histories often point to the year 476 CE, when the last western Roman emperor was deposed, as an important endpoint. But it can also mislead. Any proposed factor such as lead has to be considered within this context of complex historical events.

How the lead hypothesis took shape

The lead hypothesis argues that Romans’ everyday reliance on lead- pipes, fittings, cookware, some cosmetics and even food-and-wine processing as sweeteners- may have created a low, steady dose of exposure that undermined health and, with it, the capacity for effective political judgement.

In the body, lead is a toxin that builds up over time. Children are especially vulnerable because lead can disrupt the developing brain, affecting attention and learning. In adults, long-term exposure is linked to high blood pressure, kidney damage, anaemia and cognition and mood effects. At higher or prolonged exposures, it can cause abdominal pain and gout. Lead can also harm fertility and pregnancy outcomes.

Ancient writers noticed at least part of the risk. Roman architect Vitruvius wrote that water carried clay pipes was healthier than water carried through lead. But the specific claim that lead exposure helped drive collapse of the Western Roman Empire is modern. It gained prominence after S. Colum Gilfillan’s 1965 essay “Lead Poisoning and the Fall of Rome”, which argued over-exposure to lead in elite societies- especially through wine-related practices- may have impaired leadership and reduced fertility (1).

From there, the lead hypothesis became a durable popular explanation, even as debate continued over how significant the exposure really was (2).

Lead pollution at scale

If the lead hypothesis is going to carry any weight, it has to clear the first hurdle: was there enough lead pollution in the Roman environment to matter? On that front, the evidence is fairly strong.

In Rome itself, geochemists have analysed harbour and river sediments and found lead isotopes that match the city’s extensive pipe network. The implication is that water moving through the system could pick up around 100 times more lead than water from local springs. That’s a signal of lead contamination, even if it doesn’t yet tell us what most people actually absorbed day to day (3).

There’s also some evidence of large-scale exposures to lead. A classic Greenland ice-core study showed that atmospheric lead levels rose several-fold above natural background during the peak centuries of Greek and Roman mining and smelting (4). This suggests that the empire’s metal economy loaded the atmosphere with lead across a huge region.

So the environmental case is relatively straightforward. Romans produced and moved a lot of lead, and it leaked into water supplies and the atmosphere.

From lead pollution to people

That gets us to the next trickier step- how much of that environmental lead pollution entered Roman bodies- and in what doses?

Here, some evidence exist. Lead can be measured in bones and teeth, which can preserve lifetime and childhood exposures. At one British archaeological site, researchers found markedly higher enamel lead in Roman-British burials compared with prehistoric graves, pointing to much higher exposure in at least some communities (5). A broader multi-country analysis similarly found children often carried higher enamel lead than adults, and that was associated with earlier death (6).

A 2025 modelling study tried to translate these environmental signals into an estimate of neurological harm. Using Roman-era lead preserved in Arctic ice, atmospheric models, and modern data on lead exposure, it suggested children across the empire may have lost about 2-4 IQ points on average (7). Still, the estimate depends on a major assumption. It moves from population-level data to individual health effects, a cross-level leap called ecological fallacy. So the result is suggestive, but not definitive.

The post-Roman Empire problem

One challenge to the lead hypothesis is that elevated exposure didn’t end with Roman decline. If anything, lead remained a persistent hazard across much of medieval and Renaissance Europe through mining, smelting, metalworking activities and everyday use; ice core (8) and archaeological burial evidence (5) support this.

If lead exposure was serious enough to help explain the collapse of the Western Roman Empire, it’s reasonable to ask why later societies living with similar hazards didn’t suffer similar outcomes. While this doesn’t disprove that lead was relevant, it does mean the evidence has to show more than exposure alone. It has to explain what made Roman exposure historically distinctive despite lead remaining a persistent hazard for centuries.

Inferring Roman collapse to lead

That’s why the biggest argument in the lead hypothesis is political, moving from lead exposure levels in Romans to weakened leadership and imperial collapse. For that to work, several things have to line up. Exposure would have to be high enough among people whose decisions mattered for the state. And those individual effects would somehow have to scale into institutional failure.

Hence the argument often focuses on elites (1). Senators, administrators and high-ranking officers may have had more contact with high-status routes of exposure- especially wine storage and processing (9). But direct evidence for elite overexposure is thin. We rarely have skeletal samples tied to identifiable office-holders with certainty, let alone direct lead measurements in them, so this aspect is usually inferred and not proven.

Some would go further and speculate about particular emperors- Claudius, Caligula, Nero, Tiberius, Galba and Commodus- suggesting that chronic lead exposure might have worsened mood instability and impulsivity (9). Physiologically, that’s not impossible. But historically it’s conjectural, and risks turning messy political histories into retrospective biomedical diagnoses built on guesswork rather than evidence. These rulers also lived centuries before the Western Empire’s collapse, so treating their behaviour as evidence of lead-driven elite dysfunction in the empire’s final decline is largely irrelevant.

A recent review of the written, material and bioarchaeological record urge caution (10). Popular claims about empire-wide wine sweetening don’t always fit the evidence available, and enamel and bone lead datasets are variable and context-dependent. Lead may have been a real health stressor in parts of the empire, but the pathway from exposure to pollical collapse relies on speculations rather than solid evidence.

The attribution problem of Roman collapse

It’s tempting to treat the lead hypothesis as convincing: Romans used lead at scale, lead is a potent toxin, therefore lead helped topple an empire. But that’s where interpretation can outpace evidence. We’re on firmer ground in the early steps: Roman lead use was a case of early anthropogenic pollution that carried consequences for health. The harder steps are showing whether exposure was high enough in elite Roman society to affect imperial rule, and why this was uniquely consequential.

Even as lead did worsen health in some places, that wouldn’t by itself make it a driver of political collapse. That kind of claim sets a high evidence bar, because large historical outcomes rarely have a single cause and instead emerge from multiple interacting pressures.

That caution applies equally to the present. Modern epidemiology can show that lead exposure harms children and that air pollution increases cancer and cardiovascular risk. But quantifying how much specific exposures independently contribute, once poverty, nutrition, chronic stress and other risks are entangled, remains methodologically difficult.

The lead hypothesis debate shows that some evidence can be solid while the story we build from it overreaches. Real hazards rarely explain complex historical events on their own. More often, they accumulate, interact with other pressures, and quietly raise risk.

Sources and References:

Middleton GD. The Fall of the Western Roman Empire. In: Understanding Collapse: Ancient History and Modern Myths. Cambridge University Press; 2017:182-212. https://doi.org/10.1017/9781316584941.009

Saturnine Gout among Roman Aristocrats. 1983. N Engl J Med 1983;309:431. DOI: 10.1056/NEJM198308183090713

Vitruvius. On Architecture. Book 8. Translated by Frank Granger, Harvard University Press, 1931–1934. https://penelope.uchicago.edu/Thayer/E/Roman/Texts/Vitruvius/8%2A.html

Reddy, A. and Braun, C.L., 2010. Lead and the Romans. Journal of Chemical Education, 87(10), pp.1052-1055. https://doi.org/10.1021/ed100631y

(1) GILFILLAN, S C Ph.D.. Lead Poisoning and the Fall of Rome. Journal of Occupational Medicine 7(2):p 53-60, February 1965.

(2) Retief, F.P. and Cilliers, L., 2005. Lead poisoning in ancient Rome. Acta Theologica, 2005(sup-7), pp.147-164. DOI: https://doi.org/10.38140/at.v0i7.2086

(3) Delile, H., Blichert-Toft, J., Goiran, J.P., et al. 2014. Lead in ancient Rome’s city waters. Proceedings of the national academy of sciences, 111(18), pp.6594-6599. doi: 10.1073/pnas.1400097111

(4) Hong, S., Candelone, J.P., Patterson, C.C. and Boutron, C.F., 1994. Greenland ice evidence of hemispheric lead pollution two millennia ago by Greek and Roman civilizations. Science, 265(5180), pp.1841-1843. DOI: 10.1126/science.265.5180.1841

(5) Budd, P., Montgomery, J., Evans, J. and Trickett, M., 2004. Human lead exposure in England from approximately 5500 BP to the 16th century AD. Science of the Total Environment, 318(1-3), pp.45-58. https://doi.org/10.1016/S0048-9697(03)00357-7

(6) Moore, J., Filipek, K., Kalenderian, V., et al. 2021. Death metal: Evidence for the impact of lead poisoning on childhood health within the Roman Empire. International Journal of Osteoarchaeology, 31(5), pp.846-856. https://doi.org/10.1002/oa.3001

(7) McConnell, J.R., Chellman, N.J., Plach, A., et al. 2025. Pan-European atmospheric lead pollution, enhanced blood lead levels, and cognitive decline from Roman-era mining and smelting. Proceedings of the National Academy of Sciences, 122(3), p.e2419630121. https://doi.org/10.1073/pnas.2419630121

(8) McConnell, J.R., Chellman, N.J., Wilson, et al. 2019. Pervasive Arctic lead pollution suggests substantial growth in medieval silver production modulated by plague, climate, and conflict. Proceedings of the National Academy of Sciences, 116(30), pp.14910-14915. https://doi.org/10.1073/pnas.1904515116

(9) Nriagu, J.O., 1983. Saturnine gout among Roman aristocrats: did lead poisoning contribute to the fall of the Empire?. New England Journal of Medicine, 308(11), pp.660-663. doi: 10.1056/NEJM198303173081123

(10) Simpson RML, Garvie-Lok SJ. Lead exposure in the Roman Empire: a review of the written, material, and bioarchaeological evidence. Journal of Roman Archaeology. Published online 2026:1-35. DOI: https://doi.org/10.1017/S1047759426100646

I originally wrote this Substack post on 24th May 2025, but have since conceptually re-written the essay.

What makes medical practices last?

Most people would say brilliant doctors like Galen, or foundational textbooks like Gray’s Anatomy. Rarely do we focus on the institutions that preserve medical knowledge and carry it across generations.

During the Islamic Golden Age, Bimaristans were more than places for the sick. Across cities such as Baghdad, Damascus and Cairo under the Abbasid Caliphate (750 to 1258CE) and even for centuries beyond, they were living institutions that allowed medicine to outlast individual practitioners while treating nobles and beggars alike.

Here’s why Bimaristans mattered, and how they made medicine function as a system.

Bimaristans standardized care

Bimaristans were organized institutions with separate wards for different kinds of illness and injury, including internal medicine, infections, traumas and fractures (1). Within each ward was a clear hierarchy: senior physicians supervised care while training a team of junior doctors, allowing clinical judgement to be passed on through practice.

Medicines, too, came under institutional control, with adjoining pharmacies preparing and dispensing prescriptions. What a physician prescribed and what a patient actually received were connected by the health system.

Strict attention to hygiene and sanitation was central to how these hospitals worked. Sanitary inspectors kept wards clean, well-ventilated and ensured bedding was changed regularly. Some Bimaristans also had dedicated spaces for quarantine. This emphasis on cleanliness predated modern germ theory, but it was reinforced by a broader Islamic concern with ritual and physical purity.

Health innovations that Bimaristans made possible

The Bimaristans also created the conditions for medical innovation.

Al-Razi (Rhazes), for example, carefully distinguished smallpox from measles through close clinical observation. Ammar ibn Ali al-Mawsili innovated cataract removal surgery. And Ibn al-Nafis rejected the idea that blood passed through invisible pores in the heart’s wall, arguing instead that it moved through the lungs, an important step toward understanding pulmonary circulation (2).

These advances happened because Bimaristans concentrated medical practice, observation and teaching under one roof. Some also functioned as medical schools, with lectures and private libraries (3). They preserved and built upon Greek and Roman medicine while also drawing from Persian and Indian traditions. That pluralism also shaped who worked in Bimaristans, with Christian and Jewish physicians often playing prominent roles. Scholars like al-Razi and Ibn Sina (Avicenna) also synthesized influential medical encyclopaedias that shaped practice across the Islamic world, and remained influential in European medical education well into the Renaissance.

Bimaristans were also embedded in a wider culture of regulation and accountability. After a notorious fatal medical error in Baghdad in 931 CE, the Abbasid state introduced physician examinations and licensing, overseen by senior doctors and the muḥtasib, or public inspector. The aim was to limit harm and protect patients from unqualified practitioners, creating an early form of health governance alongside medical care.

Healing the body, mind and spirit

As well as medical innovations, Bimaristans embodied a wider ethical model of care, grounded in compassion, responsibility and respect for the patient. Islamic thinkers saw sickness as atonement, and relieving suffering was a physician’s duty to care for all patients.

“The physician, even though he has his doubts, must always make the patient believe that he will recover, for the state of the body is linked to the state of the mind.” al-Razi, Kitab al-Hawi (The Comprehensive Book on Medicine).

That ethic shaped a vision of care that attended to the whole person, not just to treat disease. Patients were given warm meals, and music could be used as part of treatment. Gardens and fountains formed part of the healing environment, reflecting a tradition shaped by both Islamic thought and Galenic medicine, in which mental and spiritual wellbeing were seen as inseparable from physical recovery.

“Insist upon their quiet and rest, for their limbs are weak;
Try to lift their spirit through welcoming words and pleasant company;
Give them sweet-scented perfumes and flowers;
Obtain happiness and music for them;
Spare them sombre thoughts and fatigue.”

Ibn Sina (Avicenna), Urjuzah fi al-Tibb (Poem of Medicine, page 62). https://archive.org/details/avicennaspoemonm0000avic/page/62/mode/2up

This approach was especially evident in the treatment of mental illness. Al-Razi, for example, wrote about mental illness in clinical terms and considered how a patient’s circumstances might shape their condition, rather than reducing it to bodily imbalance (4).

And healthcare didn’t necessarily end at discharge. Some Bimaristans sent patients home with clothing, food, or a small stipend- recognising that healing could easily unravel once a patient returned to poverty.

Healthcare access for all through waqfs

“The hospital shall keep all patients, men and women, until they are completely recovered. All costs are to be borne by the hospital whether the people come from afar or near, whether they are residents or foreigners, strong or weak, low or high, rich or poor, employed or unemployed, blind or sighted, physically or mentally ill, learned or illiterate… The entire service is through the magnificence of Allah, The Generous One.” Policy statement of the Bimaristan of al-Mansur Qalawun in Cairo, 1284 CE.

Bimaristans weren’t only centres of healing and innovation. They also widened access to care- treating healthcare as a public good at a time when, in many parts of the world, it remained a private privilege or depended on religious charity.

Many major Bimaristans were funded through waqfs- charitable endowments enshrined under Islamic law (5). These endowments weren’t mere acts of piety. They were legally binding social contracts that could fund salaries, medicinal supplies, or beds, often with written conditions that services remain free and open to all. Because a waqf was irrevocable and held in trust for public benefit, it gave Bimaristans a more stable foundation than temporary patronage or goodwill.

A Bimaristan architecture of health equity

While figures like Avicenna and al-Razi shaped medical history, it was the Bimaristans that allowed their practices to endure.

Even after the Abbasid Empire following the Mongol invasion, Bimaristans continued to thrive and expand under successor dynasties. The Mamluks, for instance, constructed the massive Bimaristan of al-Mansur Qalawun in Cairo in 1284 CE that remained a working hospital for centuries. The model was later adapted by the Ottoman Empire, which built expansive darüşşifas (houses of healing) like the Sultan Bayezid II complex in Edirne, cementing the institution's role in public health well into the early modern era.

An important feature of the Bimaristan model was that health equity was built directly into their institutions through the waqf system. That model is not purely historical- waqf-based healthcare is actively being revived across Malaysia, Indonesia and the Gulf, where endowment-funded clinics and hospitals continue to provide subsidised care today. At a time when many health systems still struggle with insurance gaps and funding volatility, the Bimaristan model suggests that access is not only a question of resources, but of how care is organised.

These institutions also challenge narrow ideas about how healthcare begins and ends. By providing discharge stipends, integrating gardens and music alongside orderly wards, health was understood to depend not only on treating the illness, but on a patient’s wider social and material conditions. That insight resonates with current debates on social determinants of health, even as systems struggle to act on it.

The history of the Bimaristans during the Islamic Golden Age shows that medical knowledge has never stood apart from the systems that sustain it. At a time when modern health systems too often reduce medicine to treatment alone, this history shows that continuity, access and care were built into medicine from the start.

Position statement

I write as a London-based editor working in public and global health (views my own), and approach issues in the Global South with a commitment to amplifying diverse histories, voices and perspectives. I recognise my position outside the communities I write about, and approach these histories with humility, curiosity, and respect for the people who lived and shaped them.

References and sources:

Al-Ghazal, S.K., 2007. The origin of Bimaristans (hospitals) in Islamic medical history. Foundation for Science Technology and Civilisation, pp.1-10.

The Medieval Islamic Hospital: Medicine, Religion, and Charity. Cambridge University Press; 2015:141-175.

Hemat, T. and Hamid, N.A., 2013. Medical Inventions in the Abbasid Caliphate and their Development in the Present Era. Journal of Health, Medicine, and Clinical Studies, 2(1), pp.16-30. DOI: https://doi.org/10.58425/jhmcs.v2i1.149

Ibn Sina (Avicenna). The Canon of Medicine. https://data.nur.nu/Kutub/English/Avicenna_Canon-of-Medicine_text.pdf

Al-Razi. Kitab al-Hawi fi al-tibb (The Comprehensive Book of Medicine).

Majeed, A., 2005. How Islam changed medicine. BMJ, 331(7531), pp.1486-1487. doi: https://doi.org/10.1136/bmj.331.7531.1486

The Islamic Roots of the Modern Hospital. 2017 https://www.aramcoworld.com/articles/2017/the-islamic-roots-of-the-modern-hospital

The bimaristan: How early Islamic hospitals pioneered treatments like eye surgery and music therapy. Middle East Eye, 2023, https://www.middleeasteye.net/discover/islam-hospitals-bimaristan-pioneered-eye-surgery-music-therapy

Abdel-Halim, R.E.S., 2014. The role of Ibn Sina (Avicenna)’s medical poem in the transmission of medical knowledge to medieval Europe. Urology annals, 6(1), pp.1-12. doi: 10.4103/0974-7796.127010

The Medieval Islamic Hospital. 2015, Cambridge University Press. https://doi.org/10.1017/CBO9781316271797

(1) Maravia, U. and Al-Ghazal, S.K., 2021. Bimaristans: services and educational role in Islamic medical history and their influence on modern medicine and hospitals. Journal of the British Islamic Medical Association, 8, pp.28-42. https://muslimheritage.com/bimaristans/

(2) West, J.B., 2008. Ibn al-Nafis, the pulmonary circulation, and the Islamic Golden Age. Journal of Applied Physiology, 105(6), pp.1877-1880 doi: 10.1152/japplphysiol.91171.2008

(3) Miller, A.C., 2006. Jundi-Shapur, bimaristans, and the rise of academic medical centres. Journal of the Royal Society of Medicine, 99(12), pp.615-617. Doi: https://doi.org/10.1177/014107680609901208

(4) Ahmed, J.O., Kakamad, K.K., Najmadden, Z.B., Saeed, S.I., Kakamad, K. and Najmadden, Z., 2024. Abu Bakr Muhammad ibn Zakariya al-Razi (Rhazes)(865-925): the founder of the first psychiatric ward. Cureus, 16(7). doi: 10.7759/cureus.64601

(5) Abbasi, M.Z., 2012. The classical Islamic law of Waqf: A concise introduction. Arab Law Quarterly, 26(2), pp.121-153. https://www.jstor.org/stable/23234650

A strange substance fell from the sky over the villages of Laos, Cambodia and Afghanistan in the mid-1970s. It spattered like raindrops, leaving yellow spots after aircraft passed overhead. Communities came to call it “Yellow Rain”.

Soon, reports followed of sudden illness- vomiting, bleeding and blisters- fuelling fears that a new kind of weapon was being used. Survivors carried those stories into refugee camps, where journalists and government officials began recording them.

When the testimonies reached the United States, this ambiguity hardened into a sweeping accusation that the Soviet Union was using biological warfare.

The wars that didn’t end

The Yellow Rain incident unfolded in a region still reeling from the Indochina and Soviet-Afghan wars.

Communist victories in Laos, Cambodia, and Vietnam since 1975 left behind a landscape of unresolved insurgencies. In Laos, the Pathet Lao takeover forced thousands of Hmong people- many of whom had fought alongside US covert forces- to flee into the mountains or across the Mekong. In Cambodia, the fall of the Khmer Rouge and Vietnam’s occupation in December 1978 triggered new guerrilla campaigns along the Thai border. In Afghanistan, the Soviet invasion of 1979 opened another brutal front, marked by aerial bombardment and counterinsurgency warfare that led to large refugee flows into Pakistan.

It was in this setting that reports of “Yellow Rain” emerged. Testimonies from Hmong villagers who had fled Laos to refugee camps in Thailand, and from Khmer soldiers operating along the Thai-Cambodia border, described more than 400 alleged attacks between 1975 and 1982 (1). Afghanistan entered the same story through refugee testimony, medical reports and a smaller body of disputed physical evidence, rather than the yellow residue samples found in Southeast Asia. The US Department of State expanded these claims further, describing thousands of casualties (2,3).

Independent verification of these figures was impossible. None of the alleged attacks was witnessed by Western observers, and access to sites and medical forensics was severely limited.

The bioweapons accusation

The “Yellow Rain” incident soon moved from disturbing refugee testimony into an official US allegation that the Soviet Union, either directly or through allied forces, was using a bioweapon (4). This allegation emerged when the Biological Weapons Convention had come into force from 1975, and chemical weapons were already a major subject of international dispute.

US officials focused on trichothecene mycotoxins, a group of fungal toxins known to cause gastrointestinal injury, irritation, and at high exposure, bleeding effects (2). Government and academic laboratories tested environmental and biomedical samples linked to some reports, and findings of toxin markers were publicly cited as evidence of deliberate toxin use. Two Soviet gas masks reportedly recovered from Afghanistan in late 1981 were also said to be contaminated with the same toxins (3). Together, these findings were used by the Reagan administration to support the case of Soviet involvement, and the issue was raised in international forums.

At the same time, technical questions were raised regarding how the evidence was interpreted: how samples had been handled, whether mycotoxin could have come from natural contamination in the environment or food, and how much weight should be placed on two contaminated Soviet gas masks, and whether the concentrations measured matched the symptoms being reported.

As the case unfolded, alternative explanations and new investigations entered the debate. “Yellow Rain” became not only a scientific controversy, but also a test of how states turn uncertain evidence into claims about prohibited bioweapons.

Evidence of bee-droppings

One of the most influential challenges to the toxin-weapon explanation came from Harvard biologist Matthew Meselson and his team, who approached “Yellow Rain” as a problem of natural history (5).

Their independent investigation point to ecology. In Southeast Asian forests, the giant honeybee Apis dorsata conducts mass defecation flights, during which swarms releasing yellow fecal spots over wide areas (6). The results showed a speckled pattern resembling a light spray settling on foliage- an explanation that matched the most consistent visual detail in the reports.

Meselson’s team supported this idea with several lines of scientific evidence: observations of bee flights, comparisons of droplet size and distribution with samples collected from alleged attack sites, and microscopic analysis showing pollen grains in the yellow material (7).

This doesn’t mean the reported symptoms were fabricated. Rather, it suggested that Yellow Rain itself may have been misidentified- and that the case for a Soviet bioweapon may have been built on that initial error.

Unresolved gaps remain

Even if Meselson’s bee explanation accounts for the yellow speckling itself, it doesn’t fully settle the “Yellow Rain” controversy.

The case was never only about what people saw on leaves and rooftops. Refugees also described sudden illness that, to outside observers, resembled toxic exposure. Those accounts cannot be dismissed outright, but nor are they easy to interpret clinically. They were collected in the midst of war and displacement, with little health information and documentation. Later analysis of refugee interviews found that the testimonies were more inconsistent than US official reports implied, making them less straightforward as solid evidence of a clearly defined chemical attack (7).

The difficulty deepens once Afghanistan is included. Meselson’s bee hypothesis was developed to explain the yellow, pollen-rich residue reported in Southeast Asia, but the Afghanistan allegations didn’t centre on that kind of visible speckling. Instead, they rested on more fragmentary evidence. The bee explanation for yellow rain cannot, on its own, resolve the wider set of claims.

Then there is the question of detection. Trichothecene mycotoxins were reported in some tested materials from US investigations, but independent testing from British, French and Swedish groups failed to confirm them in the samples they examined (4). And even positive findings don’t prove weapon use (8). Mycotoxins occur naturally in mouldy grain and damp environments- a Canadian government report found comparable trichothecene levels in samples to natural contamination in food supply (4). In settings where samples were collected under difficult conditions, background exposure could plausibly blur into evidence linked to a specific incident.

One possibility, then, is that more than one thing was happening at once: bee droppings produced the visible “rain”, while unrelated illness or harsh camp conditions shaped what people experienced and remembered. What has kept the case so difficult is this limited and conflicting evidence.

Some archival material has since been declassified, but many of the US documents remain restricted, adding another layer of opacity to a story already defined by what can no longer be fully recovered.

The politics of proof

The Yellow Rain incident is ultimately a case about how people come to believe something has happened. It shows how easily fragments of evidence can be drawn into narratives that feel certain long before they are proven, and how hard those narratives are to undo once they harden at diplomatic level.

In the US, those claims had policy force. The Reagan administration cited them as evidence of Soviet treaty violations and help build support for renewed binary nerve gas production, and the Yellow Rain accusations were never formally retracted even as the evidence remained contested.

That same process also shaped how testimony was understood. Hmong accounts described real suffering; the problem was how their experiences were interpreted through Cold War demands for attribution. For many Hmong communities, Yellow Rain is inseparable from the wider experience of post-1975 persecution and mass death that followed the Laotian civil war, not just a scientific dispute over evidence.

Most of all, the Yellow Rain incident shows how difficult attribution really is (9). Detecting a substance isn’t the same as proving intent, yet intent is what international law is meant to judge. The evidence used to identify who is responsible can be fragile and deeply sensitive to political context. Once an accusation gains political force, later evidence struggles to dislodge the narrative it helped create.

Two decades later, a strikingly similar pattern played out over Iraq’s alleged weapons of mass destruction. The case was built from fragmentary intelligence and unreliable defector testimony. As a result, the evidence produced a case that felt airtight until it collapsed- and, as with Yellow Rain, only after the policy consequences could no longer be undone.

History is full of moments where the need to act came before the ability to know. Yellow Rain was one of them, and it won’t be the last. The gap between action and certainty is a space where science moves more slowly than politics, and where decisions demand the humility and clarity to face what we do and don’t yet know.

Sources and References

Baird, I.G., 2025. The Transnational Politics of Laos After 1975. In Oxford Research Encyclopedia of Politics. https://doi.org/10.1093/acrefore/9780190228637.013.2184

Shultz, G.P. 1982. Chemical Warfare in Southeast Asia and Afghanistan: An Update (No. 104). US Department of State, Bureau of Public Affairs, Office of Public Communication, Editorial Division. https://foia.state.gov/DOCUMENTS/FOIA_Micro_Oct2024_10/F-1989-03991/DOC_0C09000001/C09000001.pdf

Yellow Rain. Harvard University Meselson CBW Archive. https://meselsonarchive.hsites.harvard.edu/yellow-rain

Pribbenow, M.L., 2006. “Yellow rain”: lessons from an earlier WMD controversy. International Journal of Intelligence and CounterIntelligence, 19(4), pp.737-745. https://doi.org/10.1080/08850600600656525

(1) Meselson, Matthew. “The Yellow Rain Affair: Lessons from a Discredited Allegation.” Stanford University Press, June 2008

(2) RW Wannemacher; SL Wiener (1997). “Trichothecene mycotoxins: in Medical Aspects of Chemical and Biological Warfare”. U.S. Army Medical Department. https://web.archive.org/web/20070622144523/http://www.bordeninstitute.army.mil/published_volumes/chemBio/Ch34.pdf

(3) Bowman, Steven R. Yellow Rain and Related Issues: Implications for the United States, report, September 29, 1983; Washington D.C.. (https://digital.library.unt.edu/ark:/67531/metacrs8829/), University of North Texas Libraries, UNT Digital Library.

(4) Tucker, J.B., 2001. The “yellow rain” controversy: Lessons for arms control compliance. The Nonproliferation Review, 8(1), pp.25-42. https://www.nonproliferation.org/wp-content/uploads/npr/81tucker.pdf

(5) Ashton, P.S., Meselson, M., Robinson, J.P. and Seeley, T.D., 1983. Origin of yellow rain. Science, 222(4622), pp.366-368. doi: 10.1126/science.222.4622.366.

(6) Nowicke, J., Meselson, M. Yellow rain — a palynological analysis. Nature 309, 205–206 (1984). https://doi.org/10.1038/309205a0

(7) T.D. Seeley, J.W. Nowicke, J. Guillemin and P. Akratanakul, “Yellow Rain”. Scientific American, September 1985, Vol. 253, pp 128‑137. https://meselsonarchive.hsites.harvard.edu/sites/g/files/omnuum7261/files/meselsonarchive/files/1985_scientific_american_yr.pdf

(8) Watson, S.A., Mirocha, C.J. and Hayes, A.W., 1984. Analysis for trichothecenes in samples from southeast Asia associated with ‘yellow rain’ https://doi.org/10.1093/toxsci/4.5.700

(9) Katz, R. and Singer, B., 2007. Can an attribution assessment be made for Yellow Rain? Systematic reanalysis in a chemical-and-biological-weapons use investigation. Politics and the Life Sciences, 26(1), pp.24-42. DOI: https://doi.org/10.2990/26_1_24

Author’s note: Devin Teichrow has previously written a biology-forward explainer of the competing syphilis origins hypotheses last year- When Did Syphilis Enter Europe? The Origins Debate. My aim here is different, to show why syphilis origins is partly a problem of definitions and evidence types.

At the end of the fifteenth century, Europe met a terrifying disease many believed was new. French soldiers returning from the Italian Wars arrived with bodies covered in ulcers, faces disfigured, and some had bones seemingly gnawed from within. The disease would later be called syphilis, and it spread faster than physicians could explain it.

The first response was to assign blame. Italians blamed the French. The French blamed Naples. Physicians and writers blamed foreigners, sex and sin. Within decades, syphilis was conveniently linked to the New World and Columbus’s voyages, solidifying into a powerful origin story in which Europe had been infected by the Americas.

But origin stories are rarely that simple. Only recently have tools like ancient DNA and evolutionary analysis made it possible to test these ideas directly. In doing so, they force a deeper question of whether “the origin of syphilis” is even a meaningful thing to look for.

Why syphilis defies simple categories

Biologically, syphilis belongs to a family of closely related bacterial infections known as treponemal diseases, which also includes yaws, bejel (alternatively called endemic syphilis) and pinta. On paper, they seem different- syphilis is primarily passed through sex (also called venereal syphilis), whereas yaws, bejel and pinta are spread through non-sexual skin contact, often in settings shaped by poverty, crowding, childhood exposure or particular climates.

In practice, those boundaries blur. Closely related treponema pallidum bacteria can produce different symptoms depending on environment, immune history, and patterns of contact. Syphilis itself is also famously called “the Great Imitator” that can mimic a wide range of other conditions including liver and heart disease.

What appears in the historical record as a single disease called “syphilis” may instead reflect similar pathogens expressing themselves differently or mistaken for other conditions. This ambiguity is why older evidence so often resists neat labels- and why identifying “syphilis” in the past is far more difficult than the word implies.

The competing origins hypotheses

Once we recognise how slippery “syphilis” is as a medical category, the question of where it came from becomes even harder to frame. Different definitions of syphilis produce different and testable hypotheses about where and how the disease emerged.

“Two things happened and are on this Island, which in the beginning were very painful for the Spaniards: one is the disease of buboes, which in Italy they call the French disease, and this, know for certain that it came from this Island, either when the first Indians came, when Admiral Christopher Columbus returned with the news of the discovery of these Indies, which I later saw in Seville, and these could have caught them in Spain, infecting the air or by another way, or when some Spaniards, already with the disease, went on the first return voyages to Castile, and this could have been from the year 1494 until the year 1496.” Bartolome de Las Casas, General History of the Indies, 1527-1561 (1).

The Columbian hypothesis proposes that sexually transmitted syphilis originated in the Americas and was introduced to Europe after 1492 through the voyages of Christopher Columbus. If true, Europe and Asia should show little or no evidence of syphilis before Columbus’s expeditions, while the Americas should display a deeper and more diverse past of treponemal infections.

The pre-Columbian hypothesis reverses that logic. It argues that syphilis already existed in the Old World but was confused with other disfiguring conditions such as leprosy. Supporting this would require convincing pre-1492 evidence from Europe or Asia- ideally well dated skeletons and, better still, ancient DNA that fits securely within the treponemal family tree.

A third idea is the unitarian hypothesis. Rather than a single point of origin, treponemal infections may have been widespread, with the apparent “new” disease reflecting shifts in transmission or different symptoms driven by changing environmental or social conditions.

What the historical sources doesn’t tell us

As the origin of syphilis depends on how it was defined, then historical witness accounts become a fragile form of evidence. When syphilis swept through Europe in the 1490s, observers wrote about it prolifically- but not in the way a modern clinician would. Physicians described eruptive “pox”, ulcers and rashes, sores, boils and frightening disfigurement, often wrapped in moral language about sin, divine punishment, and national blame (2). They were as much moral judgement and politics as describing medical symptoms.

“I will begin at the disposition of the firmament and will also not keep silent that this illness comes from the will of God as a punishment to mortals on account of sin.” Joseph Grunpeck, On the French Evil, 1496.

This makes retrospective diagnosis deeply uncertain. Conditions we now separate- syphilis, smallpox, or even leprosy- could overlap in how they were described. Some medieval manuscripts and artwork even framed genital disease through leprosy’s language, such as “venereal leprosy”, a category broad enough that syphilis could be misidentified (3). And because leprosy already carried centuries of stigma and social meaning, a new “pox” could easily be read through that same lens or rhetorically amplified in ways that heightened fear rather than clarified disease boundaries.

Even the sense of sudden appearance is tricky. A genuine biological shift is one possibility, but so are changes in how disease was observed and reported. The spread of the printing press in the fifteenth century, for example, allowed accounts to circulate faster and farther than before. Written sources capture the moment a society noticed the disease, but they don’t automatically prove when it truly began.

Bones didn’t settle the debate

This is where skeletons enter the story. In principle, human remains should offer biological evidence that written accounts couldn’t. For decades, that promise fuelled the search for evidence of “pre-1490s” syphilis in cemeteries. Yet the evidence wasn’t straightforward. Some older skeletons showed signs of treponemal disease, but these bone changes became much more common only after the syphilis epidemic of the 1490s began (4).

But skeletal evidence has a lot of limitations. Many treponemal infections never produce late-stage bone damage at all. And when they do, those changes usually appear years after infection as complications, meaning the archaeological record captures only advanced disease. Worse, similar skeletal patterns and marks can be caused by different infections or even physical injuries.

As a result, the bone evidence debate on pre-Columbian origins narrowed to questions of dating and diagnosis. When researchers re-tested famous “pre-1490” skeletons using stricter criteria and better radiocarbon dating, several claims became less convincing (4). Some remains turned out to be younger than originally thought, others couldn’t be confidently attributed to syphilis. A cautionary example is “The Syphilis Enigma”, a 2001 documentary later criticised for drawing sweeping conclusions from ambiguous skeletal evidence and an illustration of how easily conclusions can run ahead of the data (5).

If bone evidence can mislead, the obvious next step is to look for the pathogen itself.

Early modern Europe “syphilis” wasn’t simple

The syphilis-origins debate took a sharp turn in 2020, when researchers reported the recovery of treponemal DNA from early modern remains in Europe. By reconstructing four ancient Treponema pallidum genomes and comparing them with modern strains, they expected to find a single lineage corresponding to sexually-transmitted syphilis (6). Instead, they found a surprising variety: some lineages were linked to sexually-transmitted syphilis, others closer to yaws-like relatives, and one belong to a previously unknown branch of the family tree.

This mattered because it challenged the idea that the European epidemic began as a single, uniform infection imported after the 1490s. Molecular clock analyses also raised the possibility that some treponemal lineages had diverged before overseas contact, keeping the pre-Columbian hypothesis in play. On that reading, “syphilis” may have been a catch-all label for infections that looked similar to physicians at the time but weren’t genetically identical.

But the study couldn’t settle the origins question on its own. Because the samples came from after the epidemic had already emerged in Europe, the molecular clock estimates carried wide uncertainty intervals- broad enough to accommodate both pre-Columbian divergence and post-1490s importation.

Ancient DNA from the Americas also show deep diversity

A logical next step would be to look for earlier samples and to turn to the Americas, where the Columbian hypothesis places syphilis’s roots. Over the past few years, two major ancient-DNA studies have done exactly that, reshaping the debate once again.

The first recovered treponemal DNA from pre-contact Brazil, roughly 2,000 years old (7). This showed that treponemes were circulating in the Americas long before the 1490s. But the strains were closer to bejel than to the sexually transmitted syphilis we recognised today. That means the study still couldn’t answer when, where, and under what conditions syphilis became sexually transmitted.

The second, broader study added genomes from other parts of the Americas, spanning both pre-contact and contact periods, and compared them with modern strains (8). These ancient genomes sat near the base of the treponeme family tree, suggesting that the lineages leading to syphilis, yaws and bejel had already diversified in the Americas long before European contact. That keeps the possibility alive that some American-derived treponemes reached Europe in the 1490s, but it doesn’t explain how those strains spread rapidly and under what conditions.

Sampling remains the major caveat: a handful of genomes cannot represent entire continents. But together all of these studies make the point that ancient DNA can’t yet deliver a single, neat origin story.

The oldest treponeme genome discovered

This year, the syphilis-origins timeline was pushed back even further. Researchers reported a ~5,500 year old Treponema pallidum genome recovered from a hunter-gatherer’s remains on the Sabana de Bogota in Colombia (9). This is the oldest genetic evidence of this pathogen family so far.

The significance was where this genome sits on the evolutionary family tree. The ancient strain falls just outside all modern forms that cause sexually-transmitted syphilis, yaws and bejel- like an older relative that diverged before these categories emerged. This shows treponemal pathogens were already established and diversifying in the Americas before written records. But crucially, the skeletal remains showed no physical signs of treponemal disease, and we cannot know what clinical symptoms this hunter-gatherer had, if any.

With that, the debate shifts again. Rather than a single “Columbus moment”, the evidence points towards a much longer history, focused on what changed and when the modern treponemal disease variants evolved.

What really counts as “syphilis”?

The syphilis origins debate has always looked like a tug-of-war over geography and time- America versus Europe, the 1490s or before. But perhaps we should be asking a different question entirely: what, exactly, are we trying to locate in the past when we say “syphilis”? And what kinds of evidence are allowed to decide?

The problem is that “syphilis” in the past can mean at least three different things, each with its own timeline. It can mean a recognisable set of symptoms: the ulcerating, disfiguring “pox” that horrified Europeans in the 1490s. In that case, pamphlets, physicians’ accounts, and the narratives of its time matter most. The risk, however, is mistaking the moment a society noticed and recorded a pattern of disease for the moment it truly began. Diseases are usually “born” in language long after microbes have been circulating.

Or “syphilis” can mean the pathogen lineage itself- a particular species on the treponemal family tree that includes sexually-transmitted syphilis alongside yaws and bejel. Ancient genomes can help trace that deep evolutionary history, but the evidence remains sparse and uneven, and much depends on calibration and sampling. A family tree can show relatedness and rough timelines, but it cannot automatically map onto the disease categories people actually lived with.

Then perhaps “syphilis” means the mode of transmission, above all the sexually-transmitted disease that we are familiar with today. That definition drags behaviour and ecology into the frame, alongside immunity, hygiene, sexual networks, migration and warfare. For that, we may assume that the 1490s marked the shift into predominantly sexual transmission, but have the thinnest evidence for how that shift actually happened.

This reframes the puzzle of the 1490s epidemic itself. Even if treponemal lineages were ancient, why did a devastating outbreak erupt when it did? Ancient genomes can trace lineages through time, but they are less able to explain shifts in transmission- particularly when, and under what conditions, syphilis became predominantly sexually transmitted. Here, neither bones nor DNA can do the whole job, because the crucial variable isn’t just what the bacterium was, but what conditions made widespread human transmission possible.

Rather than debating where and when syphilis came from, perhaps we may need to define what we mean by “syphilis” in its historical and scientific context: the disfiguring “pox” recorded in the 1490s, the pathogen behind it, or the shift into sexual transmission. Depending on what you are looking for, they aren’t the same thing.

Sources and References:

Fracastoro, G., 1911. Hieronymus Fracastor’s Syphilis: From the Original Latin; a Translation in Prose of Fracastor’s Immortal Poem. Philmar Company. https://archive.org/details/hieronymusfraca00frac

Grünpeck, Joseph. Tractatus de pestilentiali scorra sive mala de Franzos (Augsburg: Johann Schaur, 1496).

Baker, B.J., Crane‐Kramer, G., Dee, M.W., et al. 2020. Advancing the understanding of treponemal disease in the past and present. American Journal of Physical Anthropology, 171, pp.5-41. https://doi.org/10.1002/ajpa.23988

Tognotti, E., 2009. The rise and fall of syphilis in Renaissance Europe. Journal of Medical Humanities, 30(2), pp.99-113. https://doi.org/10.1007/s10912-009-9079-3

Mikita, G., Lizoń, M.J., Gąsiorowska, J., et al. 2025. Diagnostic Methods Used in Detecting Syphilis in Paleopathological Research—A Literature Review. Diagnostics, 15(9), p.1116. https://doi.org/10.3390/diagnostics15091116

Czinn, A.B. and Hoenig, L.J., 2023. Poxes great and small: The stories behind their names. Clinics in Dermatology, 41(3), pp.459-462. doi: 10.1016/j.clindermatol.2023.03.014

(1) Bartolome de Las Casas, General History of the Indies, 1527-1561. https://www.gutenberg.org/files/53131/53131-h/53131-h.htm

(2) Arrizabalaga, J., Henderson, J. and French, R.K., 1997. The great pox: the French disease in Renaissance Europe. Yale University Press.

(3) Hudson EH. Diagnosing a case of venereal disease in fifteenth century Scotland. Br J Vener Dis. 1972 Apr;48(2):146-53. doi: 10.1136/sti.48.2.146 https://pmc.ncbi.nlm.nih.gov/articles/PMC1048293/pdf/brjvendis00074-0060.pdf

(4) Harper, K.N., Zuckerman, M.K., Harper, M.L., et al. 2011. The origin and antiquity of syphilis revisited: An Appraisal of Old World pre‐Columbian evidence for treponemal infection. American journal of physical anthropology, 146(S53), pp.99-133. https://doi.org/10.1002/ajpa.21613

(5) Armelagos, G.J., Zuckerman, M.K. and Harper, K.N., 2012. The science behind pre‐Columbian evidence of syphilis in Europe: Research by documentary. Evolutionary Anthropology: Issues, News, and Reviews, 21(2), pp.50-57. doi: 10.1002/evan.20340

(6) Majander, K., Pfrengle, S., Kocher, A., et al. 2020. Ancient bacterial genomes reveal a high diversity of Treponema pallidum strains in early modern Europe. Current Biology, 30(19), pp.3788-3803. https://doi.org/10.1016/j.cub.2020.07.058

(7) Majander, K., Pla-Díaz, M., du Plessis, L. et al. Redefining the treponemal history through pre-Columbian genomes from Brazil. Nature 627, 182–188 (2024). https://doi.org/10.1038/s41586-023-06965-x

(8) Barquera, R., Sitter, T.L., Kirkpatrick, C.L. et al. Ancient genomes reveal a deep history of Treponema pallidum in the Americas. Nature 640, 186–193 (2025). https://doi.org/10.1038/s41586-024-08515-5

(9) Bozzi, D., Broomandkhoshbacht, N.Z., Delgado, M., et al. 2026. A 5500-year-old Treponema pallidum genome from Sabana de Bogotá, Colombia. Science, 391(6783), p.eadw3020. DOI: 10.1126/science.adw3020

“Pursued by General Winter—General Storm—General Famine, aided by the brave and skilful Russian Generals, the finest army that the world ever saw was almost annihilated.” The Gleaner, 23^rd April 1813.

If you remember the 2023 Napoleon film starring Joaquin Phoenix (and I’m sure the historians among you have already torn your hair out over its historical accuracy)- it leans hard into the image of Napoleon as a doomed conqueror. Few scenes embody that image more powerfully than his march into Russia.

In June 1812, at the height of his power, Napoleon marched east with one of the largest armies Europe had seen: half-million men under the banner of the French Empire. By forcing Tsar Alexander I back into the continental system, Napoleon aimed to secure France’s supremacy in Europe.

Five months later, the “Grande Armée” (Grand Army) was barely an army at all. With supplies collapsing and winter closed in, the retreat became a catastrophe that marked a turning point in the Napoleonic Wars.

For nearly two centuries, it was assumed that the army perished from the cold- the hubris of empire punished by nature.

But that story is beginning to fray. Pathogen DNA found in soldiers’ remains point to infections that travelled with the troops, making the campaign’s end look far messier than the legend of “General Winter” suggests.

Beyond “General Winter”

A long-standing popular explanation for Napoleon’s catastrophe has been that the “General Winter” killed the Grand Army. Contemporary observers helped cement that view (1). Napoleon’s chief surgeon Dominique-Jean Larrey left vivid accounts of frozen limbs and the brutal realities of treating frostbite.

“The projecting parts of the body, grown insensible, or being frozen, and remote from the centre of circulation, were attacked by gangrene, which manifested itself at the same moment, and was developed with such rapidity, that its progress was perceptible by the eye…” Dominique-Jean Larrey (1).

But that emphasis on cold can mislead, because the army was already coming apart before the worst winter conditions arrived. One of the first systems to fail was logistics. As the advance pushed deeper into Russia, supply depots and transport collapsed under the pace and scale of the march, forcing soldiers to rely on foraging that could never sustain an army of that size.

The consequences of this failure were evident in the dead themselves. Stable carbon and nitrogen isotope analysis of soldiers from a mass grave in Vilnius, Lithuania showed markedly varied diets among soldiers- evidence of the uneven access to food during the retreat (2). Another archaeological study from the same burial site reports some evidence of trauma, but not mass combat casualties- pointing instead to hunger, cold, exhaustion and disease (3).

Typhus as a culprit?

In that setting, typhus was an obvious suspect. “Camp fever” was a common historical label for epidemic typhus, and it fits the crowded makeshift camps and harsh conditions of the retreat. Hallmark symptoms like high fever, delirium and rash were widely reported (1), even if they overlapped with many other infections common in malnourished, exhausted armies.

That long-standing assumption gained molecular support in 2006, when researchers used pathogen DNA testing (using polymerase chain reaction, PCR) on dental pulp from soldiers buried in a Vilnius mass grave, as well as to body lice recovered from the burial environment (4). They detected Rickettsia prowazekii, the agent of epidemic typhus, alongside Bartonella quintana, which causes trench fever. The findings provided direct biological evidence that louse-borne diseases were present during the retreat.

But these also came with limits. Only a subset of remains tested positive, and targeted PCR can confirm presence without revealing how widespread those infections were across the army. By design, it asks only whether a suspected microbe was there, not what else might have been circulating.

A more crowded disease landscape

The picture shifted again in 2025, when the Vilnius burial site were re-examined with a different toolkit (5). Instead of testing for a small set of suspected pathogens, researchers used shotgun metagenomic sequencing on dental pulp from thirteen soldiers, with phylogenetic analysis to authenticate what they found.

The result was unexpected. The clearest signals came from Salmonella enterica Paratyphi C- an agent of food and water borne paratyphoid fever- and Borrelia recurrentis, which causes louse-borne relapsing fever. In these victims, epidemic typhus or trench fever weren’t detected.

The caveats also matter, because thirteen individuals are a miniscule sample, and a single burial site cannot stand in for the whole campaign. But the implication isn’t that typhus was irrelevant. It’s that the retreat unfolded within a crowded infectious landscape- lice-borne diseases thriving in overcrowded conditions, enteric infections transmitted through contaminated food and water, all layered onto hunger, exhaustion and cold.

Interpreting these together, these studies look less like contradictions than snapshots taken with different lenses, each capturing part of a catastrophe too complex to reduce to a single cause.

Defining a very complex death toll

Before asking what killed Napoleon’s Grand Army, we have to pin down what “killed” can mean in a catastrophe stretched across time and distance. This wasn’t a single disastrous day on the battlefield, but a months-long unravelling in phases. Losses began on the summer advance into Russia, followed by weeks of stagnation in Moscow, the grinding losses of the autumn retreat, the chaos at the Berezina River crossings, and near-total breakdown around Vilnius.

That sequence of events matters because it resists any single-cause of death explanation. Each phase exposed soldiers to different risks, reshaping who survived long enough to face the next. Men weakened early by hunger encountered disease and cold differently later on. What appears as winter mortality at the end of the campaign cannot be separated from the attrition that came before and alongside it.

Scale and geography are equally important. Napoleon’s retreat stretched across nearly a thousand kilometres, funnelling a multinational army through roads, rivers and towns that became choke points. Charles Minard’s famous map captures the magnitude of loss at a glance, but at the cost of over-simplifying the realities into a single trajectory and cause.

How do we explain a mass catastrophe?

The important question raised by the 1812 mass catastrophe is how we assign causality when death is caused by multiple factors that amplify each other. The Grand Army is an early, well-documented case of compounding risks, when war collided with collapsing logistics, poor water and sanitation and disease. The same pattern recurs in modern crises. In Gaza, conflict-driven displacement, destroyed homes and infrastructure, high levels of malnutrition and recent winter conditions have turned cold and flooding into direct threats to life.

New methodologies sharpen the picture of such catastrophic events, but they rarely resolve them cleanly. Genomics can reveal pathogens invisible to historical observers, yet samples are limited and shaped by where bodies are recovered. Administrative records, then and now, often tally deaths without explaining why. Even today, in humanitarian emergencies, cause of death is often inferred indirectly- through tools such as verbal autopsies- under conditions of limited access, political constraints and data scarcity.

In these situations, “what caused a catastrophe?” often says as much about what could be measured and narrated as about what actually happened. As the fate of the Grand Army shows, focusing on single-cause explanations flattens the complex, interacting system of pressures into a misleadingly simple story.

References and Sources:

Logistics and Supply from Part III - Raising and Supplying the Armies. The Cambridge History of the Napoleonic Wars , pp. 231 – 254. DOI: https://doi.org/10.1017/9781108278096.013

Von Clausewitz, C., 1843. The Campaign of 1812 in Russia, Translated from German by John Murray.

Rivera‐Perez, J.I., Santiago‐Rodriguez, T.M. and Toranzos, G.A., 2018. Paleomicrobiology: a snapshot of ancient microbes and approaches to forensic microbiology. Environmental Microbial Forensics, pp.63-90. https://doi.org/10.1128/9781555818852.ch4

Duchêne, S., Ho, S.Y., Carmichael, A.G., Holmes, E.C. and Poinar, H., 2020. The recovery, interpretation and use of ancient pathogen genomes. Current Biology, 30(19), pp.R1215-R1231. https://doi.org/10.1016/j.cub.2020.08.081

Checchi, F. and Roberts, L., 2005. HPN Network Paper 52: Interpreting and using mortality data in humanitarian emergencies: a primer for non-epidemiologists. https://www.files.ethz.ch/isn/93870/networkpaper052.pdf

(1) LARREY, Dominque Jean Baron. Surgical Memoirs of the Campaigns of Russia, Germany, and France. Translated from the French by JC Mercer, Etc. Carey & lea, 1832. https://archive.org/details/55810930R.nlm.nih.gov/page/n21/mode/2up

(2) Holder, S., Dupras, T.L., Jankauskas, R., Williams, L. and Schultz, J., 2017. Reconstructing diet in Napoleon’s Grand Army using stable carbon and nitrogen isotope analysis. American journal of physical anthropology, 163(1), pp.53-63. https://doi.org/10.1002/ajpa.23184

(3) Signoli, M., Ardagna, Y., Adalian, P., Devriendt, W., Lalys, L., Rigeade, C., Vette, T., Kuncevicius, A., Poskiene, J., Barkus, A. and Palubeckaité, Z., 2004. Discovery of a mass grave of Napoleonic period in Lithuania (1812, Vilnius). Comptes Rendus Palevol, 3(3), pp.219-227. https://doi.org/10.1016/j.crpv.2004.02.003

(4) Raoult, D., Dutour, O., Houhamdi, L., Jankauskas, R., Fournier, P.E., Ardagna, Y., Drancourt, M., Signoli, M., La, V.D., Macia, Y. and Aboudharam, G., 2006. Evidence for louse-transmitted diseases in soldiers of Napoleon’s Grand Army in Vilnius. The Journal of infectious diseases, 193(1), pp.112-120. https://doi.org/10.1086/498534

(5) Barbieri, R., Fumey, J., Kabral, H., Scheib, C.L., Signoli, M., Costedoat, C. and Rascovan, N., 2025. Paratyphoid fever and relapsing fever in 1812 Napoleon's devastated army. Current Biology, 35(21), pp.5384-5391. DOI: 10.1016/j.cub.2025.09.047

Author’s note: This is a collaborative post between and . The same post will be published on Caroline’s Substack.

Wilfrid Voynich staggered through the vaulted archways of the Villa Mondragone. He lunged for the nearest manuscript he could see …

All right, this is not The Da Vinci Code, but it is the story of a real-life historical mystery and a cipher that might never be cracked.

In 1912 Voynich, a Polish rare-book dealer from Telšiai in what is now Lithuania, bought some volumes from the Jesuit seminary at the Villa Mondragone, just southeast of Rome. Among them was a curious vellum manuscript full of drawings of unidentifiable plants, astrological charts and people – mostly women – bathing in a network of tubs. A neat, looping script accompanied the illustrations, but couldn’t be linked to any known language or alphabet. A letter attached to the manuscript hinted that it was the work of 13th-century English polymath Roger Bacon (1).

This claim, however, has proved precarious. In 2011, radiocarbon dating situated the vellum in the early 15th century, ruling out Bacon’s involvement but deepening the puzzle of who created it – and why. Cryptographers, linguists and historians have wrestled with the mystery for decades. Could it be a medical book, an astrology manual … or even an intricate hoax?

Every so often, researchers bask in fifteen minutes of fame by claiming to have cracked the code, but scrutiny always sends them back into obscurity. So here’s what we know about this mysterious manuscript – and the many competing theories about what the book was meant to be.

The Voynich Manuscript’s six-part blueprint

The Voynich Manuscript looks, at first glance, like a late-medieval medical textbook because of its layout.

Of the roughly 240 surviving pages, these illustrations were grouped into six distinct clusters:

• A herbal section with large plant drawings (126 pages)

• An astronomical/astrological section with suns, moons, and zodiac-like wheels (17 pages)

• A biological or balneological section showing nude figures, often in baths or linked by tube-like tunnels (20 pages)

• A cosmological section of dense circular diagrams and foldouts (14 pages)

• A pharmaceutical section with apothecary-style jars and plant parts (16 pages)

• A final section with shorter text blocks, resembling recipes (25 pages)

That structure looks familiar enough to invite recognition, yet strange enough in ways that still deepen the mystery.

Herb recipe book in disguise?

One popular interpretation is that the Voynich manuscript is a herbal medicine manual- an illustrated guide to plants and their remedies. The strongest support comes from the manuscript’s overall structure. Nearly half its pages are devoted to plant drawings, as well as a section showing roots and leaves beside apothecary-style jars, and ending with short, recipe-like entries; the kind of progression seen in many late-medieval remedy books.

But arguments against this theory are just as compelling. Many “plants” don’t match any real species that we know, and some look like composites (2,3), which undermines their practical use. Other sections- zodiac wheels and bathing figures- sit awkwardly in a straightforward herbal medicine book.

Until the text is deciphered, the herbal recipe interpretation remains suggestive. But what if the Voynich isn’t about “what” remedies to take at all, but “when”?

An astro-medical or life cycle guide?

Another plausible theory is that the Voynich was meant as a medical astrology guide used for treatment and prevention. In late medieval and Renaissance Europe, physicians looked to the planets and zodiac to choose auspicious moments for bloodletting, purging, bathing, or taking particular remedies, and to interpret recurring patterns of illness (3).

Some of the manuscript’s content seems to fit. After the plant-heavy opening, it turns to pages of circular diagrams- sun, moon, star-like wheels- and zodiac-style figures, alongside bathing scenes that can be read as therapeutic routines. A classic parallel is the medieval “Zodiac Man”: mapping zodiac signs onto body parts to judge safer or riskier moments to treat (4).

A related idea references the cycles but shifts the focus from the sky to the body itself- reading the manuscript as a “Life Cycle” compendium. In this view, the manuscript’s repeated female figures and sequences of circular charts track stages of bodily change across time: adolescence, menstruation, fertility, pregnancy, birth and later life.

Still, without a deciphered text- and with illustrations that can’t be pinned down (the zodiac wheels don’t clearly function as calendars and the human figures’ life stages are ambiguous)- the manuscript may simply borrow the look of astro-medical or life-cycle guides without fully being either.

A secret health manual for women?

The Voynich manuscript’s repeated depiction of nude female figures, flowing liquids, and interconnected tubular forms have led some to suggest a women’s health manual, in the tradition of medieval gynaecology. It’s a plausible explanation, given the wide circulation of 12th-century texts such as the Trotula corpus – a group of three works associated with the Salerno Medical School, addressing menstruation, fertility, and cosmetics. There is an anatomical quality to some of the Voynich illustrations that could reflect some knowledge of the female reproductive system.

In 2017, researcher Nicholas Gibbs claimed to have translated parts of the Voynich manuscript to show that it was indeed all about women’s health. He argued that it drew heavily from the Trotula and other sources, encoding Latin abbreviations for common herbal treatments. Like most Voynich theories, however, Gibbs’s translations were immediately debunked.

If the manuscript were a women’s health manual, why write it in code? The Trotula, after all, wasn’t hidden. One possibility is professional secrecy. Medical knowledge, especially relating to fertility and birth control, could be commercially valuable. Encoding might protect proprietary remedies. Another possibility is that the author had reasons for finding female sexuality and reproductive medicine a socially delicate subject, particularly if discussed outside a formal academic context (5).

Some have put forward a convincing case for female authorship, while acknowledging that this is currently speculative. Although women’s literacy wasn’t widespread in 15th-century Italy, it was increasing, especially among the privileged sections of society. Court writer Christine de Pizan, for example, wrote about women’s important role in history and advocated for their education. The Voynich manuscript could therefore be the work of a literate noblewoman interested in the sciences but keen to avoid the usual backlash against women’s progress.

Are these baths or anatomy?

The bathing or balneological section of the Voynich, with its female figures, also invites a different reading as a therapeutic bath book.

Health texts of the medieval period point to the importance of bathing alongside humoral theory, astrology and herbal medicine (6). Returning to the Trotula, we can find discussions of the appropriate times, temperatures and herbal mixtures in which to bathe, depending on the patient’s condition. The Regimen Sanitatis Salernitanum which, like the Trotula, is associated with Salerno, discusses the therapeutic role of baths within a broader medical framework. It’s not a stretch to place the Voynich in this tradition, possibly rooted in northern Italy.

De Balneis Puteolanis, written by Peter of Eboli around the end of the 12th century and still popular in the 15th, celebrates the therapeutic properties of the thermal baths around Pozzuoli near Naples. It survives mostly as 14th-15th century copies illustrated in a variety of ways, so we don’t know what any original pictures looked like. Could the Voynich illustrations reflect this original, lost work?

Yet the Voynich imagery is more diagrammatic and fantastical than most known spa manuscripts. The pools interconnect like schematic systems rather than physical baths. Perhaps these tubes are symbolic, representing the anatomy of the blood vessels, digestive pathways, or reproductive structures. Without a decoded text, it remains uncertain whether these images describe hydrotherapy or function as diagrams of anatomy. The manuscript might even blend both traditions, using the visual language of baths to encode medical knowledge.

Was it made to fool people?

Some researchers in the cryptography field have argued that the Voynich Manuscript is simply a meaningless text wrapped in alluring pictures- a deliberate hoax (7). The case starts with the blunt fact that nobody could convincingly understand

it. The script doesn’t match known alphabets, and the “recipes” could be exactly the sort of medieval “secrets” a forger might invent to impress.

A key point in the hoax argument is that the Voynich’s strange text may not need meaning at all. Researchers have shown that a scribe could generate similar-looking writing using very simple methods- recombining word fragments (e.g. prefixes, stems, suffixes) repeatedly using a template- to produce pages of convincing pseudo-text (8-10). In other words, a manuscript can look complex without actually saying anything, so visual complexity alone doesn’t rule out fabrication.

Yet given its 15^th century origins, producing a hoax at this scale would have been extremely labour-intensive. Hundreds of pages, carefully planned cycles of illustrations, and a repeating internal structure look more like sustained authorship than a quick con-job. The text also shows non-random statistical patterns, consistent word lengths and repetition- that many researchers say fit better with a meaningful writing system than purely gibberish (11).

Whether it’s clever nonsense or meaning hidden in plain sight, the Voynich resists easy dismissal and exposes the limits of what we can truly know.

A medical worldview without translation

Even if the Voynich manuscript is never deciphered, it still contains important lessons for us. Not every historical question yields to persistence, technology, or desire. Somewhere in the early fifteenth century, a real person or people prepared vellum, mixed ink, created illustrations and carefully inscribed looping characters for reasons that made sense in their own world. This might well have been a very individual world rather than a generalised ‘medieval’ one. How many of us have devoted our time to a project that seemed baffling to everyone else?

The gap between effort and recoverable meaning is exactly what the Voynich exposes. Over the past century, the undecipherable writings have been declared a lost language, an alchemical code, a hoax, even an alien message – claims driven more by imagination and deduction than proof. The Voynich manuscript is a lesson in intellectual discipline; distinguishing between possibility and probability, between speculation and evidence. Amid today’s torrent of misinformation and confidently erroneous assertions, its silence is instructive. Mystery, too, has value: although the truth is out there, we simply don’t have the power to retrieve it.

But unreadable text doesn’t mean an empty one. Even without a translation, the plant drawings, bathing figures and zodiac-like symbols invite us to point toward a medical worldview. Late medieval healers saw health as shaped by humors, weather and seasons- and acting at the right moment, whether through astrological timing, herbs or bathing. We no longer treat astrology as science, yet modern medicine still studies biological timing: circadian clocks, menstrual and fertility cycles, even when a drug works best. The difference is that we now demand harder proof of which patterns are real, causal and clinically meaningful before acting on them.

And so the Voynich manuscript ends where good inquiry begins- with uncertainty. It asks us to test patterns before naming causes, and to admit what we don’t know. In history as in medicine, sometimes we need a dose of that rare remedy – humility.

Position statement

MY is an editor of a medical journal working in public health and epidemiology, and comments represented here are his own and not representative of the journal. CR is an independent historian and writer.

References and Sources:

1. D’Imperio, Mary E. The Voynich Manuscript: An Elegant Enigma. NSA/CSS (original 1978), page 20-22. https://www.nsa.gov/portals/75/documents/about/cryptologic-heritage/historical-figures-publications/publications/misc/voynich_manuscript.pdf

2. Tiltman, John H. (Summer 1967). “The Voynich manuscript: The most mysterious manuscript in the world” (PDF). NSA Technical Journal. XII (3).

3. Greenbaum, D.G. (2015). Astronomy, Astrology, and Medicine. In: Ruggles, C. (eds) Handbook of Archaeoastronomy and Ethnoastronomy. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6141-8_19

4. Clark, Charles (1982) “The Zodiac Man in Medieval Medical Astrology,” Quidditas: Vol. 3, Article 3. https://scholarsarchive.byu.edu/rmmra/vol3/iss1/3

5. Brewer K, Lewis ML. The Voynich Manuscript, Dr Johannes Hartlieb and the Encipherment of Women’s Secrets. Social History of Medicine. 2024;37(3):559-582. doi:10.1093/shm/hkad099

6. Ramazzina, E. (2024). Bathing in medieval Europe. In M. Cesario, H. Magennis, & E. Ramazzina (Eds.), The elements in the medieval world: interdisciplinary perspectives: water (pp. 99-139). (Elements, Nature, Environment: Multidisciplinary Perspectives from the Ancient to the Early Modern World; Vol. 1). Brill. https://doi.org/10.1163/9789004696501_005

7. Reddy, S. and Knight, K., 2011, June. What we know about the Voynich manuscript. In Proceedings of the 5th ACL-HLT workshop on language technology for cultural heritage, social sciences, and humanities (pp. 78-86).

8. Rugg, G., 2004. An elegant hoax? A possible solution to the Voynich manuscript. Cryptologia, 28(1), pp.31-46. https://doi.org/10.1080/0161-110491892755

9. Schinner, A., 2007. The Voynich manuscript: Evidence of the hoax hypothesis. Cryptologia, 31(2), pp.95-107 https://doi.org/10.1080/01611190601133539

10. Timm, T. and Schinner, A., 2020. A possible generating algorithm of the Voynich manuscript. Cryptologia, 44(1), pp.1-19 https://doi.org/10.1080/01611194.2019.1596999

11. Montemurro, M.A. and Zanette, D.H., 2013. Keywords and co-occurrence patterns in the Voynich manuscript: An information-theoretic analysis. PloS one, 8(6), p.e66344. https://doi.org/10.1371/journal.pone.0066344

Do you know your family history?

For most people, the answer comes easily- their names, origins, the stories that stitch their lives together. But for some Argentinians born in the late 1970s and early 1980s, that question opens into blank space…

In June 1978, Argentina projected unity. Buenos Aires was celebrating. Fireworks lit the Estadio Monumental stadium alight, as the Argentinian team surged toward a World Cup win. On screen, national identity was loud and seamless- even as individual identities were being quietly erased from the record.

Just blocks away, a different Argentina moved in silence.

Every Thursday, grandmothers wearing white headscarves circled around the Plaza de Mayo, clutching photographs of their disappeared family members. They searched for grandchildren taken during dictatorship- babies born in captivity, registered, and placed with new families.

Their weekly march asked a different question entirely: How do you reclaim a past that was taken from you?

White headscarves walking silent circles

Between 1976 and 1983, Argentina’s military dictatorship operated a system of clandestine detention and enforced disappearance. Human rights groups estimate around 30,000 victims were taken (1).

Among the regime’s shocking crimes was the theft of infants. Women who were arrested when pregnant gave birth in captivity- their babies were stolen and placed with families linked to the authorities.

In that landscape of erasure, a small group of women began gathering in the Plaza de Mayo. Wearing white headscarves stitched from babies’ nappies and risking arrest, they walked in circles in front of the presidential palace. Every Thursday, they returned with photographs and handwritten names, refusing to let absence harden into forgetting.

From these courageous acts, a distinct mission emerged. In October 1977, some formed a separate group to focus specifically on the stolen babies- the Grandmothers (Abuelas) of Plaza de Mayo. Their goals were clear: locate the missing grandchildren, restore their identities, and seek legal restitution.

“My granddaughter’s disappearance haunted my life. She was only eight months old when she was taken, and whenever I would see a little girl who looked like her, I would follow her, unable to stop until I saw her face.” Buscarita Roa, a grandmother of Plaza de Mayo who was eventually reunited with her granddaughter. 2025. Source: https://www.theguardian.com/global-development/2025/aug/06/grandmothers-argentina-disappeared-legacy-reunited

What began as mourning in a square under fear and intimidation grew into a movement for painstaking search.

When there’s no body to bury

The military dictatorship ended in 1983. But the terror didn’t vanish- it was still haunting families. Disappearance isn’t only a human-rights crime; it shatters the psychology of those left behind. With ambiguous loss, there is no body, no grave, no ritual, families are left to grieve and cope with uncertainty- sometimes for a lifetime (2).

Its effects spill across generations; siblings or grandchildren growing up with whole chapters of their story left blank. Testimony and counselling wouldn’t be enough to mend a stolen childhood. To restore identity- and to prosecute theft- needed proof.

DNA tests to search for truth

To identify who the missing children were, the Grandmothers needed science. Many of the parents were dead or still missing, and the children they were searching for had new identities.

So in the early 1980s, the Grandmothers turned to genetics. They enlisted US geneticist Mary-Claire King, who helped devise a “index of grandpaternity” (indice de abuelidad). The simple idea was that if you can’t test a child against their parents, you could compare genetic markers against grandparent(s). A grandchild inherits predictable portions of their DNA from each grandparent, so by comparing a child’s genetic markers with those of one or more grandparents- and running the results through a statistical model- scientists could calculate the probability the child belonged to that family (3).

This wasn’t a perfect yes/no “match” like a fingerprint. It was designed to rule out look-alikes and false leads. With the right samples and markers, the method could distinguish a true grandchild from a cousin or unrelated person with more than 99% accuracy. That breakthrough made it possible to restore identities even when an entire parental generation had been erased.

The first forensic DNA biobank

To safeguard these genetic records, the Banco Nacional de Datos Genéticos (BNDG) was established by the Argentinian civilian government in 1987. This was the first DNA biobank of its kind dedicated solely to restoring stolen identities.

Families of the disappeared donated blood samples to build a reference archive- essentially, a library of genetic markers- so that when a child was located, their DNA could be compared against potential relatives (4). Over time, the archive grew across generations, allowing courts to confirm kinship even when their relatives were gone, and enabling young adults to reclaim their birth names decades after they were taken.

For the first time, genetic evidence could be used as a tool of reparation- to correct the record when history itself had been falsified.

139 people learned their real names

“I didn’t want to die without hugging him, and now I will be able to hug him soon.” Estela Carlotto, founder of the Grandmothers of Plaza de Mayo, speaking in 2014 about reuniting with her grandson who had grown up under another name until a DNA test revealed his identity. Source: https://www.theguardian.com/world/2014/aug/06/argentinian-grandmothers-find-son-of-woman-murdered-under-dictatorship

What started out as weekly protest by grieving grandmothers became a global model for the world: forensic genetics in the service of human rights.

In Argentina, their clearest legacy is reconnection and restored truth. Through the BNDG and court orders, 139 people have learned their true names and families. The Grandmothers’ advocacy has also spurred the creation of CoNaDI- a state agency dedicated to finding missing children and enshrined the “right to identity” into Argentina’s constitution.

Around the world, family-led searches have applied Argentina’s approach in different political landscapes. Guatemala’s Fundación de Antropología Forense (FAFG), and similar efforts in Peru and Colombia use DNA and exhumations to identify victims of conflict. Spain has applied forensic work to investigate Franco-era disappearances and cases of stolen children, amid political resistance to reopening the past. Across these contexts, the principle is the same: science is to serve families under civic oversight.

But tools that restore identity in one context can harm in another. Genetic databases can advance human rights, yet without consent and safeguards, they risk becoming instruments of surveillance or criminalization. Argentina’s model stands out for its deliberately narrow purpose. Access to the BNDG is tightly regulated by law, and families help oversee how data is used.

These ethics debates matter beyond human rights. As DNA testing rebuilds genealogies, it is also transforming medicine- from predicting disease risk to advancing precision medicine. But genetic records hold identities, not just data (5). That raise enduring questions: who controls these records decades from now, and what happens as laws, politics and technologies change? The challenge is stewardship- keeping consent, privacy and access strong enough that science continues to serve people, rather than concentrate power.

The World Cup stadium gave Argentina noise. The Grandmothers gave Argentina names. A restored name cannot undo the past, but it can transform the life that follows. That is the path by which stolen children can come home.

Position Statement:

I write as a London-based editor working in public and global health (views my own), and approach issues in Argentina with a commitment to amplifying diverse voices and perspectives. I recognise my position outside the communities I write about, and approach these histories with humility, curiosity, and respect for the people who lived and shaped them.

References and Sources:

Argentina Declassification Project - The “Dirty War” (1976-83). https://www.cia.gov/readingroom/collection/argentina-declassification-project-dirty-war-1976-83

Things You Should Know About...The Madres y Abuelas de la Plaza de Mayo. https://www.latinolife.co.uk/articles/things-you-should-know-aboutthe-madres-y-abuelas-de-la-plaza-de-mayo

Penchaszadeh, V.B., 2015. Ethical, legal and social issues in restoring genetic identity after forced disappearance and suppression of identity in Argentina. Journal of community genetics, 6(3), pp.207-213. doi: 10.1007/s12687-015-0219-3

(1) Catoggio Maria Soledad, The Last Military Dictatorship in Argentina (1976-1983): the Mechanism of State Terrorism, Mass Violence & Résistance, 5 July, 2010. https://www.sciencespo.fr/mass-violence-war-massacre-resistance/en/document/last-military-dictatorship-argentina-1976-1983-mechanism-state-terrorism.html , ISSN 1961-9898

(2) Boss, P., 2002. Ambiguous loss in families of the missing. The Lancet, 360, pp.s39-s40. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2802%2911815-0/fulltext

(3) Di Lonardo, A.M., Darlu, P., Baur, M., Orrego, C. and King, M.C., 1984. Human genetics and human rights: Identifying the families of kidnapped children. The American Journal of Forensic Medicine and Pathology, 5(4), pp.339-347. doi:10.1097/00000433-198412000-00011.

(4) Penchaszadeh, V.B., 2021. Genetic testing to restore the human right to identity in post‐dictatorship Argentina: Ethical, legal, and social issues. In American Journal of Medical Genetics Part C: Seminars in Medical Genetics (Vol. 187, No. 3, pp. 329-336). https://doi.org/10.1002/ajmg.c.31905

(5) Wan, Z., Hazel, J.W., Clayton, E.W., Vorobeychik, Y., Kantarcioglu, M. and Malin, B.A., 2022. Sociotechnical safeguards for genomic data privacy. Nature Reviews Genetics, 23(7), pp.429-445. https://doi.org/10.1038/s41576-022-00455-y

Public health often celebrates clear victories, moments when a disease is declared eliminated or under control.

In the early 20^th century, colonial governments declared war on sleeping sickness in Africa. It drew scientists, microscopes and field expeditions, new drugs, and mobile clinics operating with the backing of colonial states determined to demonstrate that organized administration could outpace disease.

In some regions, case numbers fell- proof that modern medicine and surveillance worked.

But the sleeping sickness campaigns didn’t just chase parasites. Behind the success story were the actions that remade communities in the name of disease control.

Communities already understood sleeping sickness

African sleeping sickness (Human African Trypanosomiasis, not to be confused with encephalitis lethargica which I wrote about previously) is a parasitic disease spread by tsetse flies. It comes in two main human forms: a slow form (caused by T. b. gambiense) that mainly affects West and Central Africa, and a rapid form (caused by T. b. rhodesiense) in East and Southern Africa.

Long before it became a focus of colonial medicine, sleeping sickness was already part of everyday life in parts of Africa. Its spread was shaped by rivers, livestock, insects and human movement. It was recorded as early as the 14^th century in South Sudan- and appeared as local flare-ups rather than a single continent-wide epidemic (1).

For African communities, the disease wasn’t an inexplicable novelty. In southern Africa, people recognised a fly-linked wasting illness in animals known in Zulu as nagana, and understood that tsetse flies harmed both humans and cattle. Herders adjusted grazing routes, avoided known fly-infested areas, and sometimes set bushes on fire to reduce risk.

This practical understanding shaped how people tried to live with a feared, often deadly illness long before colonial powers reframed it as a medical emergency.

The sleeping sickness emergency

Around 1900, what changed was less about the disease so much as what it claimed to represent for colonial states. Administrators began to treat it as a threat that demanded extraordinary intervention.

This shift was driven by a series of fast-moving epidemics that collided with the anxieties of newly established colonial states. In Uganda, a major outbreak in 1901 along the shores and islands of Lake Victoria reported 200,000 deaths- roughly a third of the population (2). Similar outbreaks were reported elsewhere across equatorial Africa. In parts of the French Congo and in Ubangi-Shari (now the Central African Republic), European observers described high infection rates among fishermen and canoeists, disrupting river transport systems on which colonial economies depended.

These epidemics alarmed administrators because they feared depopulation, which threatened labour supply and the appearance of competence of colonial rule. In that context, the new scientific promise of germ theory- alongside occasional humanitarian concern- drew multiple European research missions to study and manage sleeping sickness.

Microscopes, quarantine and forced resettlement

Between 1901 and 1913, imperial governments sent 15 medical research commissions to Africa to study sleeping sickness. These included early British efforts- such as the Royal Society commissions to Uganda (1902-1903), later extended to the Nile Valley and Sudan (1903-1905)- as well as shorter expeditions by German, French and Belgian teams across East and Central Africa. Together, these missions promoted new tools such as microscopy-based diagnosis and mass screening, while normalising research practices that treated African populations as convenient test subjects for colonial rule.

The approaches colonial administrators used for disease control varied by region (3). Around Lake Victoria, British administrators used ecological and social approaches such as tsetse fly control and forced resettlement of lakeshore communities. In the Belgian Congo, control relied on repeated mass screenings, enforced surveillance and the quarantine of people classified as suspected cases.

“We must withdraw from the insects the source of their infection. The whole country must be depopulated. There seems to me to be no other course than to remove everyone from reach of the fly for an indefinite period.” Hesketh Bell, governor of Uganda in 1906.

By the interwar years, French authorities in Central Africa moved away from short-term missions towards permanent operations. Medical research was embedded into colonial administration through standing health services and mobile teams. Led by a colonial doctor and supported by African nurses and soldiers, these teams moved village to village to examine and treat entire populations, with forced participation and serious side effects treated as acceptable costs of control.

All of this unfolded amid considerable scientific uncertainty. Researchers debated whether the parasite hid behind wildlife reservoirs, and whether disease control meant altering entire ecological landscapes, not just treating people (4). In practice, sleeping sickness control blurred into coercive governance, imposing fear and harm on the communities it claimed to protect.

The numbers that left everything out

In campaign reports, success was expressed above all through numbers. In French Equatorial Africa, nearly 90,000 people were examined and over 5,000 cases were identified and treated (5). In Cameroon, up to 150,000 cases had been diagnosed and treated by 1930 (6). On Príncipe Island, the Portuguese colonial government claimed that tsetse flies were eliminated between 1910 and 1914 (7). Figures like these translated forceful interventions into a story of control.

These campaigns also reflected genuine scientific advances. Mass screening and field laboratories helped consolidate parasitological diagnosis, clarify the causes of sleeping sickness, and map its transmission through tsetse ecology and human mobility.

But what counted in these totals was narrow. On the ground, the burden fell heavily on communities, and resistance was visible. During Eugene Jamot’s mobile-team operations in Ubangi-Shari (1917-1919), inhabitants were required- often at gunpoint- to submit to examination, yet many fled into the bush when teams returned for follow-up checks and further injections (2).

The harms of treatment were also largely absent from the numbers. During Robert Koch’s expeditions to the Ssese Islands in Lake Victoria in 1906-07, research reached its most extractive form: people with suspected sleeping sickness were forcibly rounded up in concentration camps. These sites also conveniently concentrated large numbers of patients for experimental drug testing and other experiments aimed at investigating competing theories of disease. Robert Koch tested arsenic-based treatments such as Atoxyl at high doses despite knowing that it caused severe toxicity, blindness and death in roughly one in ten people (8).

Campaign statistics served political purposes too. Mission reports were used to demonstrate scientific competence and administrative authority. Counting wasn’t meaningless; without it, disease control would have been difficult, and untreated sleeping sickness was often fatal. But it does mean “success” functioned as an administrative achievement as much as a health outcome.

Success didn’t last

After the big colonial-era epidemics receded, sleeping sickness didn’t simply vanish. Mobile screening teams, case registers and routine laboratory work left a template for specialised services that ran alongside general healthcare. This infrastructure did drive cases down, to fewer than 5,000 annually across Africa by the mid-1960s. But as cases became rarer, surveillance and active case-finding lost priority. By the 1970s-1990s, the disease resurged in several areas amid weakened health systems and control activities lapsed.

The afterlife of these campaigns was social, too. Memories of coercion and medical harm shaped how later public health efforts were received, leaving mistrust that outlasted the programs themselves.

Today’s problems with global health

The sleeping sickness campaigns show how disease priorities are set. The disease rose to the top of colonial agendas because it threatened the machinery of colonial administration. Urgency emerged where disease met politics: some deaths became unacceptable because they interfered with governance.

To a lesser extent, global health still follows similar patterns today. Funding and attention often gravitate towards diseases framed as cross-border risks (such as dengue and HIV), usually with influence from donor countries and organisations. Less visible but still heavy burdens- mental health, women’s and children’s health, and paradoxically, neglected tropical diseases like sleeping sickness- still struggle to attract long-term investment.

These campaigns also reveal the consequences of top-down coercion. Evasion and avoidance by communities at the time weren’t simply ignorance, but rational responses to being acted upon in the name of disease control. Those practices also expose an early form of what we would now call ethics dumping: research and interventions carried out with minimal consent and a high tolerance for harm. Koch’s experiments would likely have faced greater scrutiny if they were done in Europe, but no such accountability exists in colonial Africa. Interventions that breached medical ethics eroded legitimacy, and without legitimacy, their effectiveness rarely lasted.

This history lay bare the fragility of external dependence. Sleeping sickness control relied heavily on itinerant expertise and imported resources designed to demonstrate results. That vulnerability persists whenever global health initiatives are built to satisfy upward reporting- funding cycles, meeting public health targets and publications- more than to embed lasting logistical capacity in laboratories, staffing, procurement and governance.

Under empire, campaigns showed how far a state could reach with microscopes and surveys, and what that reach felt like from the communities. If today’s programs want durable results, they have to build reciprocity and local capability, not just coverage.

Position Statement:

I write as a London-based editor working in public and global health (views my own), and approach issues in the Global South with a commitment to amplifying diverse histories, voices and perspectives. I recognise my position outside the communities I write about, and approach these histories with humility, curiosity, and respect for the people who lived and shaped them.

I acknowledge that debates around sleeping sickness campaigns in Africa may still be contentious. I welcome corrections and additional context from African scholars and communities to ensure these histories are told accurately and respectfully.

Sources and References:

Steverding, D., 2008. The history of African trypanosomiasis. Parasites & vectors, 1(1), p.3. https://doi.org/10.1186/1756-3305-1-3

Lowes, Sara, and Eduardo Montero. 2021. “The Legacy of Colonial Medicine in Central Africa.” American Economic Review 111 (4): 1284–1314. DOI: 10.1257/aer.20180284

Mbopi-Keou, F.X., Belec, L., Milleliri, J.M. and Teo, C.G., 2014. The Legacies of Eugene Jamot and La Jamotique. PLoS neglected tropical diseases, 8(4), p.e2635. https://doi.org/10.1371/journal.pntd.0002635

Coghe, S., 2020. Disease control and public health in colonial Africa. In Oxford Research Encyclopedia of African History. https://doi.org/10.1093/acrefore/9780190277734.013.620

Burri, C., 2020. Sleeping sickness at the crossroads. Tropical medicine and infectious disease, 5(2), p.57. https://doi.org/10.3390/tropicalmed5020057

(1) Bado JP (1996) Médecine coloniale et grandes endémies en Afrique, 1900–1960: lèpre, trypanosomiase humaine et onchocercose. Paris: Editions Karthala. pp. 36–52, 169–173. https://excerpts.numilog.com/books/9782307500421.pdf

(2) Headrick, D.R., 2014. Sleeping sickness epidemics and colonial responses in East and Central Africa, 1900–1940. PLoS neglected tropical diseases, 8(4), p.e2772. doi: 10.1371/journal.pntd.0002772

(3) Worboys M (1994) The comparative history of sleeping sickness in east and central Africa, 1900–1914. Hist Sci 32: 89–98. https://doi.org/10.1177/007327539403200103

(4) Ford, J., 1971. The role of the trypanosomiases in African ecology. A study of the tsetse fly problem.

(5) Jamot E (1920) Essai de prophylaxie médicale de la maladie du sommeil dans l’Oubangui-Chari. Bull Soc Pathol Exot 13: 343–376.

(6) Jamot E (1932) La lutte contre la maladie du sommeil au Cameroun. Ann Inst Pasteur 48: 481–539.

(7) Figueiredo Moura da Silva, Ewerton Luiz (2019) “Tropical Medicine behind Cocoa Slavery: A Campaign to Eradicate Sleeping Sickness in the Portuguese Colony of Príncipe Island, 1911-1914,” Bulletin for Spanish and Portuguese Historical Studies: Vol. 44 : Iss. 1 , Article 28. https://doi.org/10.26431/0739-182X.1316

(8) Robert Koch, 1907. “Schlußbericht über die Tätigkeit der deutschen Expedition zur Erforschung der Schlafkrankheit,”, Deutsche Medizinische Wochenschrift, Nr. 46. https://edoc.rki.de/bitstream/handle/176904/5218/534-546.pdf

In the winter of 1889, reports of a new illness- widely called influenza or la-grippe- began to spread across the Russian Empire and into Europe. At first glance, the pandemic seemed like a respiratory disease moving along the railways and shipping routes of a newly industrialising world. Yet many doctors were uneasy because of how strange the illness itself appeared.

More than a century later, that unease has resurfaced. During the COVID-19 pandemic, researchers have begun asking a question implausible in 1889: what if the “Russian flu” wasn’t influenza at all, but an early coronavirus pandemic- one whose descriptions look different once COVID taught us to revisit the question?

A devastating pandemic during the industrialised age

The “Russian flu” unfolded in a series of global pandemic waves between 1889 and 1894, returning over several winters. First widely reported in the Russian Empire, it moved rapidly across an increasingly interconnected Europe and North America (1).

A very large share of the world’s population fell ill. During peak waves, around 60% of people in many cities experienced symptoms, and modern estimates place total deaths at roughly one million- making it one of the deadliest pandemics of the late 19^th century.

At the time, doctors almost universally called the disease influenza because it best fit what they could observe: a fast spreading winter respiratory illness that arrived in waves and left clear signals in death records (2). This was the pre-virology era- with no viral tests or any way to confirm cases beyond clinical observations.

Was it really influenza?

Early laboratory efforts to find a cause emerged just as bacteriology was taking off. In 1892-93, the German bacteriologist Richard Pfeiffer reported isolating a bacterium from respiratory secretions of many influenza patients (43). He named it “Bacillus Influenzae”, later Haemophilus influenzae. For a time this was widely treated as confirmation of the disease’s cause.

We now know influenza is caused by a virus, and that H. influenzae is better understood as a common secondary invader that takes advantage of airway damage caused by the primary infection. But Pfeiffer’s claim mattered because it briefly gave “influenza” the authority of a laboratory explanation.

A different kind of evidence called seroarchaeology revived the influenza hypothesis decades later. In the mid-20^th century, researchers tested blood samples from older people, using antibody patterns as clues to the influenza strains they may have first encountered in childhood. The evidence is indirect but suggestive: people old enough to have been exposed around 1890 showed higher levels of antibodies that cross-reacted to later influenza viruses.

Early interpretations suggested that the Russian flu pandemic might have involved a H2N2 virus (4). But later re-analyses increasingly pointed to an H3 subtype (5), which suggested apparent immune protection from the 1968 H3N2 pandemic. This is the closest biological evidence supporting influenza as the culprit behind the Russian flu, in the absence of actual 1890 specimens.

How the coronavirus hypothesis fits

Decades later, a striking alternative explanation has emerged. In 2005, virologists sequencing and analysing human coronavirus OC43- one of the viruses linked to common colds- suggested that it might be connected to the Russian flu (6). The genome of OC43 is extraordinarily close to the bovine coronavirus, and molecular clock analyses estimate that they diverged around 1890, roughly around the time the Russian flu first appeared.

The timing drew further interest because the late 1880s also saw reports of respiratory disease outbreaks in cattle in western Siberia (7). Together with expanding cattle trade, this offers a plausible ecological setting for a zoonotic spillover of coronavirus from cattle to humans, even if the historical record remains fragmentary.

The hypothesis gained renewed traction during the COVID-19 pandemic because Russian flu seems to fit the SARS-CoV2 clinical profile. Contemporary accounts repeatedly described neurological symptoms- neuralgia, insomnia, loss of taste and smell- as well as cardiovascular, gastrointestinal symptoms and prolonged exhaustion that could persist long after the acute illness had passed (8). Its demographic pattern also stood out: unlike many influenza pandemics, severe disease appeared to weigh more heavily among older adults, with comparative milder effects in children.

To a post-COVID pandemic reader, the resemblance is hard to ignore.

The evidence problem

The coronavirus hypothesis is compelling because it offers a new virus identity for interpreting an unresolved pandemic. But how much evidence is enough to rewrite a pandemic’s past? The Russian flu sits in an uncomfortable middle ground between what we can plausibly infer and what we can confidently know.

Part of the problem is that what counts as evidence has evolved. In the 1890s, bacteriology was the new frontier; Pfeiffer’s Bacillus briefly seemed to prove influenza was bacterial, before it was recognized as a common secondary invader. By the mid-20^th century, seroarchaeology used antibody patterns in older people to guess which influenza strains circulated in the 1890s. Today, genomics adds another layer: the OC43 coronavirus hypothesis rests on its genetic closeness to bovine coronavirus and molecular clocks dating their split to the late 19^th century. Each method reflects its own era- they mature and improve, but also reveal their own blind spots.

Yet without preserved specimens from 1889, we’re left stitching together indirect clues that can feel more decisive than it really is. Molecular clocks can shift by years or even decades (as a 2023 reanalysis of OC43 coronavirus data makes clear (9)). Antibody signatures are blurred by cross-reactivity and immune imprinting. Symptom “fit” depends on records never meant to distinguish between respiratory viruses. And because winters host a crowded ecology of respiratory pathogens, clinical descriptions alone rarely point to a single virus. While multiple lines of evidence can point to the same direction, a coherent story can still be misleading when surviving records are incomplete.

We also rarely acknowledge how our experience of pandemics reshape the past we think we are reading. COVID-19 taught us to pay attention to long-term symptoms that earlier generations may have noted but didn’t centre. But it can also bias us by over-mapping “long COVID” onto a grab-bag of post-viral symptoms that may have had multiple causes in the 1890s. In this sense, the Russian flu reflects not only 19^th century disease, but 21^st century attention.

Whether the Russian flu was really an influenza or coronavirus, the point isn’t to pick a winner but to understand how pandemic memory is made. We inherit the past through whatever evidence that survives, interpreted through the categories of its own time, and then reframed again by the frameworks that each generation brings- shaped by their worldviews. Pandemics end, but the narratives that seem to explain them best often outlive the evidence itself.

References and Sources:

Kempińska-Mirosławska, B. and WoŸniak-Kosek, A., 2013. The influenza epidemic of 1889–90 in selected European cities–a picture based on the reports of two Poznań daily newspapers from the second half of the nineteenth century. Medical science monitor, 19, p.1131. doi: 10.12659/MSM.889469

Honigsbaum, M. and Krishnan, L., 2020. Taking pandemic sequelae seriously: from the Russian influenza to COVID-19 long-haulers. The Lancet, 396(10260), pp.1389-1391.

Charters, E. and McKay, R.A., 2020. The history of science and medicine in the context of COVID‐19. Centaurus, 62(2), pp.223-233. https://doi.org/10.1111/1600-0498.12311

Charters, E. and Heitman, K., 2021. How epidemics end. Centaurus, 63(1), pp.210-224. doi: 10.1111/1600-0498.12370

Erkoreka, A., Hernando-Pérez, J. and Ayllon, J., 2022. Coronavirus as the possible causative agent of the 1889–1894 pandemic. Infectious disease reports, 14(3), pp.453-469. https://doi.org/10.3390/idr14030049

Berche, P., 2022. The enigma of the 1889 Russian flu pandemic: A coronavirus?. La Presse Médicale, 51(3), p.104111. doi: 10.1016/j.lpm.2022.104111

(1) Valleron, A.J., Cori, A., Valtat, S., et al. 2010. Transmissibility and geographic spread of the 1889 influenza pandemic. Proceedings of the National Academy of Sciences, 107(19), pp.8778-8781. https://doi.org/10.1073/pnas.1000886107

(2) Parsons, H.F., 1891. Report on the influenza epidemic of 1889-90 (Vol. 6387). HM Stationery Office. https://archive.org/details/b20413361/page/n3/mode/2up

(3) Pfeiffer, R., 1892. Vorläufige mittheilungen über die erreger der influenza. DMW-Deutsche Medizinische Wochenschrift, 18(02), pp.28-28. DOI: 10.1055/s-0029-1198870

(4) Mulder, J. and Masurel, N., 1958. Pre-Epidemic Antibody against 1957, Strain of Asiatic Influenza in Serum of Older People living in the Netherlands. The Lancet, Apr. 19, 810-14 ref. 22.

(5) Dowdle, W.R., 1999. Influenza A virus recycling revisited. Bulletin of the World Health Organization, 77(10), p.820. PMID: 10593030

(6) Vijgen, L., Keyaerts, E., Moës, E., et al., 2005. Complete genomic sequence of human coronavirus OC43: molecular clock analysis suggests a relatively recent zoonotic coronavirus transmission event. Journal of virology, 79(3), pp.1595-1604. https://doi.org/10.1128/jvi.79.3.1595-1604.2005

(7) Ryazantsev, S.V. and Smirnov, A.V., 2023. The Pandemic of the “Russian Flu” of 1889–1890: Occurrence, Spread, Demographic Losses. Siberian Historical Research, (2), pp.27-54. DOI:10.17223/2312461X/40/2

(8) Brüssow, H. and Brüssow, L., 2021. Clinical evidence that the pandemic from 1889 to 1891 commonly called the Russian flu might have been an earlier coronavirus pandemic. Microbial biotechnology, 14(5), pp.1860-1870. doi: 10.1111/1751-7915.13889

(9) Shaw, B. and Gatherer, D., 2023. Candidate historical events for the emergence of Human Coronavirus OC43: A critical reassessment of the molecular evidence. PLoS One, 18(5), p.e0285481. https://doi.org/10.1371/journal.pone.0285481

A church side-room in Oakland, January 1969: folding tables. Paper plates. Groceries scraped together from donations. On the first morning, 11 kids sat down to eat eggs, bacon and toast before school. By Friday, there were 135. Soon, more hungry kids were fed than the state of California.

Then the counter-story began. Parents heard whispers that the food was “tainted”. The rumours didn’t come from nowhere; intimidation and threats to arrest shadowed the program from the start.

But children showed up fed. They went to school on time. Nothing happened- except that the line grew longer.

The Black Panthers learnt that real care generates trust in ways public health institutions still sometimes find hard to sustain.

Health neglect during segregation

Breakfast programs like these emerged from a health and welfare system that had already failed Black communities by the 1960s. In segregated neighbourhoods, healthcare was often inaccessible, while job-linked insurance left many Black families without reliable coverage. Encounters with the medical system were shaped by routine discrimination.

These consequences were measurable. Black patients used healthcare less often, chronic diseases went untreated or poorly managed, and infant mortality rates in Black neighbourhoods doubled those in white neighbourhoods by the 1970s (1). This was the cumulative effect of structural barriers that made care harder to reach.

For the Black Panther Party, this was the context in which “Survival programs” became a political strategy. Food, health screening, and basic care were immediate necessities, and as proof that communities could identify their own health needs and act collectively when institutions refused to do so.

Kids’ breakfast became public health

The Free Breakfast for Children Program, launched in January 1969, became one of the Panthers’ most visible Survival Programs. A child who begins the day hungry is more likely to struggle to learn at school and grow. These programs reframed food insecurity as a structural outcome of poverty and marginalisation, influencing health long before anyone reached a clinic.

Implementation made the program powerful. Black Panther Party members partnered with churches that families already trusted, recruited local volunteers, and built dependable food supplies through donations. The daily routine mattered, showing up on time and serving every morning in a programme the community built for itself.

Every clinic in the neighbourhood

The Panthers’ free medical clinics took the survival idea beyond food and into healthcare delivery, creating spaces where Black patients could seek care without discrimination.

In April 1970, Black Panther Party leader Bobby Seale issued a directive that called on Panther branches to establish local free health facilities, helping turn scattered efforts into a recognisable infrastructure of care (2). Volunteer doctors, nurses and sciences students along with trained community members offered basic check-ups, referrals, and health education. Rather than treating medicine as a gatekept service, these health clinics were community institutions by pairing healthcare with advocacy.

From that base, the Panthers moved from meeting immediate needs to targeting a specific form of medical neglect.

Sickle Cell and the politics of neglect

“Most recently we have begun a testing and research program on sickle-cell anaemia; and we know that 98 percent of the victims of this disease are Black. To fail to combat this disease is submit to genocide; to battle it is survival.” Huey Newton, leader and chief theoretician of the Black Panther Party. Source: To Die for the People, 1972.

Sickle cell disease became one of the Panthers’ clearest demonstrations of how medicine, education and power could be braided together. In the US, it disproportionately affected people of African descent, yet for decades it attracted limited public attention and funding.

Panthers framed that neglect as political. In 1971, they launched a national campaign of screening and education through their networks of free clinics and community events. The test itself was just a simple finger stick and blood sample was then processed with basic laboratory methods. The barrier was never technical capacity alone.

By pairing screening with community education, the Panthers pushed sickle cell disease into the realm of public policy. The campaign brought national attention, including passage of the 1972 Sickle Cell Anaemia Control Act, which expanded federal support for education, counselling and research.

At the same time, the Panthers exposed the hard truth that identifying risk wasn’t enough. Meaningful care still depended on access to a medical system that many families couldn’t reliably reach or trust.

A harsh crackdown

As the Panthers built breakfast programs and free clinics, they also attracted the attention of police departments and FBI COINTELPRO, which treated these services as acts of political subversion. A movement capable of feeding children, offer screenings and welcome patients with dignity was also capable of winning public trust- and why FBI director J. Edgar Hoover labelled the Black Panther Party a major security threat.

Repression followed. Breakfast sites were raided, volunteers and parents faced harassment and risk of arrest. Propaganda campaigns- most notoriously rumours that the food was poisoned- were designed to scare families away from programs that were visibly working (3). The clinics faced their own forms of disruption, including hostile inspections and police interference that made staffing and supplies harder to sustain.

By exposing the state’s failure to care for Back communities, the Panthers also provoked a repressive response. Over time, the cumulative burden of surveillance, intimidation and internal strain helped fracture the very infrastructure the Panthers had built.

The politics of care

“We talked about police brutality, now everybody knows it’s happening. We talked about the breakfast program, now public schools across America have breakfast programs.” Billy X Jennings, 2020. Source: Eater Archives https://www.eater.com/21293327/black-panther-party-free-breakfast-program-history-oakland-california

What the Panthers were putting into practice was a basic idea that health is a matter of social justice. Health shouldn’t depend on having the right job, the right insurance, or the right connections within systems shaped by structural racism. It’s a collective responsibility, and the test of that responsibility is straightforward. Are children fed? Is there a clinic people can walk into? Can someone get a test without being ignored or turned away?

The breakfast program in Oakland showed how narrow the gap really was between need and action. Hunger was widespread, yet responding to it required little more than political will once feeding children was a right rather than privilege. The program made bare the failure that while simple solutions existed, they weren’t prioritized for Black communities.

That legacy is visible today in renewed efforts to universalise school meals. When food is offered to all children without scrutiny or means-testing, this removes the stigma keeping families from using the support that exists. As of 2025-2026, eight US states have implemented “Health School Meals for All” including California, New York, and others. When infrastructure is built to meet everyday needs, trust grows through what people can rely on.

Sickle cell disease reveals the other side of health justice. The first gene therapies for sickle cell approved in the US in late 2023 marked a genuine medical milestone. Yet the absence of very simple sickle cell screening tests in the communities most affected showed that identifying disease and inventing cures doesn’t guarantee access to care. High costs and limited specialist centers risk reproducing neglect in new forms, turning breakthroughs into unevenly distributed resources.

Health justice then, isn’t just medicine, but about who gets to benefit from what already exists. The Panthers forced that question into public view. They also showed why doing so can inspire gratitude and provoke backlash. Effective care doesn’t just treat illness, it challenges the baseline of neglect that structural racism has made routine.

References and sources:

Newton, H., 1972. To die for the people. Vintage Books.

Largent, E.A., 2018. Public health, racism, and the lasting impact of hospital segregation. Public Health Reports, 133(6), pp.715-720. https://doi.org/10.1177/0033354918795891

Bassett, M.T., 2016. Beyond berets: the Black Panthers as health activists. American journal of public health, 106(10), pp.1741-1743. doi: 10.2105/AJPH.2016.303412

Bittker, B.M., 2020. Racial and ethnic disparities in employer-sponsored health coverage. Human. Rights., 45, p.18. https://www.jstor.org/stable/27181068

The Black Panthers: Ten Point Program. https://collectiveliberation.org/wp-content/uploads/2025/01/BPP_Ten_Point_Program.pdf

Pope, R.J. and Flanigan, S.T., 2013. Revolution for breakfast: Intersections of activism, service, and violence in the Black Panther Party’s community service programs. Social Justice Research, 26(4), pp.445-470. DOI 10.1007/s11211-013-0197-8

Morabia, A., 2016. Unveiling the Black Panther Party legacy to public health. American journal of public health, 106(10), pp.1732-1733. doi: 10.2105/AJPH.2016.303405

Hilliard, D. ed., 2008. The Black Panther Party: service to the people programs. UNM Press.

(1) MacDorman, M.F., 1993. Trends in infant mortality by cause of death and other characteristics, 1960-88 (No. 20). National Center for Health Statistics, Centers for Diseases Control and Prevention. https://www.cdc.gov/nchs/data/series/sr_20/sr20_020acc.pdf

(2) Nelson, A., 2011. Body and soul: The Black Panther Party and the fight against medical discrimination. U of Minnesota Press.

(3) Lateef, H. and Androff, D., 2017. Children Can’t Learn on an Empty Stomach: The Black Panther Party’s Free Breakfast Program. J. Soc. & Soc. Welfare, 44, p.3. DOI:10.15453/0191-5096.3883

Cancer is often talked about as if it’s one illness.

In reality, it isn’t. People live with cancer in very different ways, even when they share the same diagnosis. Much of that difference has little to do with cancer itself, and a great deal to do with the circumstances around it.

For many, cancer is woven into ordinary life rather than standing apart from it. It shows up in fatigue that never quite gets better, in bodies altered by surgery or treatment, and in medical appointments where decisions have to be made quickly, often with limited options. It affects work, wages, childcare, travel, relationships, fertility, pain and time. Two people can be given the same diagnosis but experience cancer entirely different, because their lives outside the clinic aren’t the same.

Recognising these unequal lived realities is the central idea behind United by Unique, the theme for this year’s World Cancer Day. Understanding why it matters means looking at how cancer came to be treated as a shared public cause, and how that changed once the voices of people living with cancer began to shape priorities rather than simply being counted.

When cancer became sayable

“In 1999, when I was diagnosed, cancer was alien to most people in Uganda, and those who knew about it associated it with death. During my treatment, other kids were afraid to play with me. The adults in my community were the biggest contributors to the cancer stigma because they told their kids that they would get cancer from playing with me.” Moses Echodu, who lived through Burkitt lymphoma as a child and is now director for the Uganda Child Cancer Foundation. Source: https://www.ncdipoverty.org/blog/mosess-story

The road to United by Unique started with an earlier achievement: building a shared public language for cancer.

In the early 1900s, anti-cancer organisations began building campaigns that made cancer sayable at scale, at a time when the word itself evoked fear and denial (1). Through pamphlets, lectures and fundraising drives, they educated the public about cancer while framing it as something a community could face together.

In the United States, a group of 15 doctors and laypeople created a charity that would later become the American Cancer Society gave cancer advocacy a national reach. In Britain, Macmillan’s founding in 1911 by Douglas Macmillan, after witnessing his father’s death from cancer, reflects a parallel mission that moved from raising awareness to providing practical support for patients and families.

These charities helped break taboos and gave a sense of solidarity for cancer, even as lived experience remained far more complex than any single message could hold.

A War on Cancer

“Once the treatments are over, one achieves the status of “survivor,” which is how the women in my local support group identify themselves, A.A.-style, as we convene to share war stories and rejoice in our “survivor-hood”. Barbara Ehrenreich, with lived experience of Breast Cancer. Source: Welcome to Cancerland.

By the interwar years, cancer had moved beyond charity into something closer to a national public-facing campaign culture. One of the most striking examples was the Women’s Field Army, launched in 1936, which mobilised a legion of volunteers with the sole purpose of waging war on cancer.

The turning point came in 1971 with the National Cancer Act under the Nixon administration, which granted special funds for the National Cancer Institute and expanded federal investment in cancer research (2). Over the decades that followed in the US, screening and early detection became part of routine life, and survival rates improved for many cancers (3).

But what made the “war” message powerful also set its limits. Progress was often tallied in incident curves and mortality statistics, while the day-to-day reality of living through cancer sat at the margins (4). Inequities to cancer treatment were often treated as secondary rather than central problems.

People with cancer benefited from this progress, but were rarely invited to shape it.

Who gets to define survival?

“I have been to war, and still am. So has every woman who had had one or both breasts amputated because of the cancer that is becoming the primary physical scourge of our time. For me, my scars are an honorable reminder that I may be a casualty in the cosmic war against radiation, animal fat, air pollution, McDonald’s hamburgers and Red Dye No. 2, but the fight is still going on, and I am still a part of it.” Audre Lorde, The Cancer Journals, 1980.

Advocacy didn’t arrive as a single movement. It grew from shared frustration that too often, people with cancer were expected to endure decisions made about them, not with them. As survival improved from the 1970s onward, people began to ask questions about who gets to define “success”.

Breast cancer activism became one of the clearest signs of that shift. Advocates began pushing back against deeply paternalistic surgical practices and demanding choice and bodily autonomy that patients had long been denied. Rose Kushner, herself diagnosed with breast cancer, publicly challenged the routine practice of “one-step” biopsy followed by radical mastectomy- an extensive, life-altering surgery- and insisted that informed consent was a right, not a courtesy (5). Audre Lorde went further, insisting that cancer was politically inseparable from power, and whose lived experience must be taken seriously (6).

By the 1990s, this energy became organised force. The National Breast Cancer Coalition founded in 1991 trained advocates to engage with science and influence funding priorities. Alongside this, Breast Cancer Action pushed back against the commercialisation of awareness- termed “Pinkwashing”. Through campaigns like Think Before You Pink (launched 2002), they questioned whether visibility alone was meaningful progress when some corporate sponsors also contributed to the very disease they claimed to raise awareness about.

This shift redefined progress: not only more money, but accountability- and lives worth living during and after cancer.

Cancer has always been global

“A cancer diagnosis is tough under any circumstances, but I was facing mine in Syria in 2019, in a country torn apart by war, where the healthcare system was fragile, under-resourced, and mere safety was a luxury that few could afford.” Amr Sibai, who was diagnosed with cancer in Syria. Source: https://www.knowledge-action-portal.com/en/news_and_events/news/10388

As advocacy reshaped cancer politics in high-income countries, its ideas didn’t stay contained. Who gets timely diagnosis and treatment are global questions, felt most sharply where resources are scarce and care is inequitable.

Today, cancer advocacy is organised less around one flagship campaign than around networks that connect very different realities. The Union for International Cancer Control, founded in 1933, links cancer societies, patient groups, clinicians, researchers and governments across more than 170 countries. Its role reflects a shift from awareness alone to coordinating how diagnosis, treatment and survivorship can be stronger within very different health systems.

World Cancer Day, established in 2000 and marked each 4^th February, is the moment when these priorities briefly line up. It renews an old challenge from the earliest advocacy battles: how to act together without flattening difference.

United by Unique

“Don’t worry, the future is incredibly happy. I’m still living a passionate, rich life, just as seriously as ever.” Miho Suzuki, Japan- writing to her 10 years ago self. Source: https://onconnectla.com/cancer-survivor-quotes/

United by Unique captures the core promise of global cancer advocacy: one shared purpose, built across unequal systems of care and profoundly different lives.

Early cancer charities rallied the public with a single, galvanising message of fighting cancer. That unity mattered. It made cancer sayable, fundable, and public. But patient movements pushed the story further. Cancer has never been one experience. Cancer type and stage matter, but so do age, gender, race, geography, money, family responsibilities and disability. These differences shape what illness costs, what choices are available, and what survival even looks like.

This is why uniqueness isn’t only personal. A diagnosis lands differently in a well-resourced clinic than in a conflict zone, or a place where stigma delays care. Cancer advocacy is now translating solidarity into action. This means making early detection reach the excluded, ensuring treatment doesn’t impoverish, supporting survivorship beyond the last appointment, and treating palliative care as a right.

Unity is a shared demand for dignity. Unique is to build care around real lives.

Position Statement:

I write this as an editor working in public and global health, and who particularly works in cancer control. I don’t have lived experience of cancer, but as someone who has watched a parent go through cancer twice. Constructive comments from clinicians and people with lived experience are welcome.

Sources and References:

Rose Kushner, Breast Cancer: A Personal History and an Investigative Report (1975). ISBN 10: 0151225699 https://www.abebooks.com/9780151225699/Breast-cancer-personal-history-investigative-0151225699/plp

Barbara Ehrenreich. Welcome to Cancerland, 2001. https://pinkribbonblues.org/wp-content/uploads/2010/08/Ehrenreich-2001-WelcomeToCancerland-Harpers.pdf

Santora, Emily, Darby, Alexis, “Women’s Field Army (1936–1948)“. Embryo Project Encyclopedia ( 2021-07-31 ). ISSN: 1940-5030 https://hdl.handle.net/10776/13294

Moscucci, O., 2010. The British fight against cancer: Publicity and education, 1900–1948. Social History of Medicine, 23(2), pp.356-373. https://doi.org/10.1093/shm/hkp050

Smith, T.K., 2020. How Audre Lorde’s Experience of Breast Cancer Fortified Her Revolutionary Politics. Literary Hub. https://lithub.com/how-audre-lordes-experience-of-breast-cancer-fortified-her-revolutionary-politics/

(1) Holland JC, Gooen-Piels J. Historical Perspective. In: Kufe DW, Pollock RE, Weichselbaum RR, et al., editors. Holland-Frei Cancer Medicine. 6th edition. Hamilton (ON): BC Decker; 2003. Available from: https://www.ncbi.nlm.nih.gov/books/NBK12903

(2) Surh, Y.J., 2021. The 50-year war on cancer revisited: should we continue to fight the enemy within?. Journal of Cancer Prevention, 26(4), p.219. doi: 10.15430/JCP.2021.26.4.219

(3) Siegel, R.L., Kratzer, T.B., Giaquinto, A.N., Sung, H. and Jemal, A., 2025. Cancer statistics, 2025. CA: a cancer journal for clinicians, 75(1), p.10. https://doi.org/10.3322/caac.21871

(4) Stovall, E., Greenfield, S. and Hewitt, M. eds., 2005. From cancer patient to cancer survivor: lost in transition. National Academies Press. https://canceradvocacy.org/wp-content/uploads/2013/01/From-Cancer-Patient-to-Cancer-Survivor-Lost-in-Transition-Summary-.pdf

(5) Lerner, B.H., 2001. No shrinking violet: Rose Kushner and the rise of American breast cancer activism. Western Journal of Medicine, 174(5), p.362. doi: 10.1136/ewjm.174.5.362

(6) Audre Lorde. The Cancer Journals, San Francisco: Aunt Lute Books. 1980. https://monoskop.org/images/1/16/Lorde_Audre_The_Cancer_Journals_2nd_ed_1980.pdf

We all know about the Black Death. It erased a third of Europe. It led to the decline of serfdom in Western Europe, the Peasant’s Revolt in England in 1381, and a legacy of social upheaval. It was one of the most consequential plague pandemics in history.

We thought we knew where it began too: at the ports of Venice and Genoa- simply because that’s where the first written records about the disease appeared. But everything else we know before that blurred into speculation. Maybe it arrived on flea-ridden ships, or perhaps it began with infected bodies hurled over city walls during a siege.

Except… it didn’t come from nowhere.

A wave of discoveries in the past few years has turned the Black Death into a forensic investigation. Advances in ancient DNA, evolutionary biology and climate history are tracing the plague’s early life: where it emerged, when it diversified, and how it became a pandemic.

Piece by piece, the evidence now lets us follow the Black Death’s trail.

Where the Black Death began

In 2022, the Black Death’s origin story gained a crucial piece of evidence. Researchers sequenced Yersinia pestis DNA from the teeth of people buried in 1338-1339 near Lake Issyk-Kul, in the Tian Shan mountains of modern-day Kyrgyzstan (1). Those sites stood out because the burial dates on tombstones suggest a sudden spike in deaths, implying a local crisis unfolding as the community recorded it.

The genomes recovered from those teeth provided a breakthrough. The Issyk-Kul strain sits just before the explosive “big bang” moment when it diversified and spawned the Black Death lineages later seen across Europe and the Middle East. In evolutionary genetics terms, this is as close as we can get to the pandemic’s ground zero.

The ecology reinforces the picture. The plague strains found there today still circulates among wild rodents- especially marmots- and they remain the closest living relatives of the medieval plague pathogen.

The Black Death didn’t arrive from some unknown source. Current evidence points to Central Asia.

Black Death got a new time stamp

Once scientists placed the Issyk-Kul genomes onto the plague family tree, they were able to pinpoint the approximate timing. Using those 1338-1339 samples as reference points, they could estimate when the plague’s major branches first split apart. The divergence falls within a narrow window in the early-to-mid 1300s (1,2).

This detail matters because for years it was thought that the Black Death was just a late resurgence of an old pathogen that had been lingering quietly for centuries (3,4). The new dating makes that hypothesis less tenable. The bacterium diversified just decades before the first outbreaks struck Europe.

Seen this way, the Black Death looks like a new emergent force. Its global wave began just after the lineage fractured into its different forms, right before it reached the Mediterranean.

It couldn’t have “lived” in Europe

For a long time, it was tempting to speculate the Black Death as a European disease that simply kept flaring up on its own soil (5). But a modelling study suggests Europe never really had the right ecological conditions for plague to settle permanently (6). Compared to places where plague still circulates today, Europe seems to lack the combination of soil conditions and diverse rodent species that allow the bacterium to establish a long-term home.

If that’s true, Europe wasn’t plague’s natural reservoir- it was simply where the disease kept arriving. Genetic evidence also points in the same direction. A large study suggests that the Black Death entered Europe as a relatively uniform strain, which is what you would expect from a recent introduction rather than a pathogen that had been circulating locally for centuries (7). Only after arrival did the strain diversify as it spreads across the continent. Rather than lingering quietly in Europe, plague appears to have been repeatedly reintroduced from Asia via trade routes and human movement (8).

That brings us back to the Tian Shan mountains: a landscape where plague has long circulated in wildlife, and where in the 1300s we can see hints of the spillover event that set the Black Death in motion.

Volcanos, grain routes and how plague entered Italy

If Europe couldn’t sustain plague on its own, the real question becomes: what kept bringing it back?

Climate shocks have long been suspected to help set the stage of the Black Death. In particular, a recent modelling study suggests that a mid-1340s volcanic-driven climate downturn helped trigger crop failures and rising famine pressure in Italy (9). Major port cities like Genoa, Venice and Pisa responded the way any state would do when prices spike: they bought grain in bulk, increasingly from Black Sea trade routes.

Grain trade turned out to be an ideal vehicle for plague. In this reconstruction, plague arrived as part of a supply chain: rodents carrying fleas sheltering in sacks of grain, disembarking with the cargo into crowded harbours and storage warehouses at exactly the wrong moment.

Then this suggests that the Black Death wasn’t a single dramatic event but as a product of stressed systems colliding- a combination of climate shocks, food shortages, shifting trade routes and dense urban hubs where people and plague were suddenly brought together.

We still don’t know everything

We have to be mindful that when we reconstruct how the Black Death unfolded, big gaps remain.

Ancient DNA may give us crucial clues, but never a full narrative. We have only a handful of early plague genomes, and vast regions and decades are still unsampled (1). That means alternative routes and missing intermediate outbreaks may yet come to light. Even the molecular clocks used to estimate dates have limits: plague evolves at different speeds in different contexts, so timelines carry huge uncertainty even when they seem precise (2).

Ecological models rely on modern data and assumptions about medieval landscapes, rodent communities and land use that we can’t fully verify (7). Any historical reconstructions- like the grain-trade pathway- depend on patchy archival records and on inferred mechanisms like rats and flea transmission that were rarely documented directly.

Most of all, we still can’t compare the relative importance of different pathways. How much of the plague spread through ports versus overland routes? How often was plague reintroduced from elsewhere, and for how long did it linger locally? The exact sequence of events remains out of reach.

What the Black Death teaches about spillovers

What we know about how the Black Death began shows that spillover is rarely a single leap from one species to another. It’s usually a chain reaction through ecological, social and economic conditions that align just long enough for a local outbreak to escalate into a full-blown continental crisis.

Reservoirs are central to that story. Plague had long circulated in wild rodent communities across Central Eurasia. The deaths near Issyk-Kul look less like an isolated anomaly and more like a brief, visible flare from a much larger wildlife cycle. In the 1300s, nobody was watching for such signals. Today, understanding where pathogens quietly persist in animals and what pushes them towards people is why surveillance is so important for early action.

We see this in bird flu as an emerging disease threat. When the influenza virus strain like H5N1 keeps turning up in wild-birds and poultry outbreaks keep recurring, it signals sustained circulation in a wildlife reservoir and highlights a set of predictable interfaces for spillovers: farms, bird-markets, transport routes, and workers who move between them.

The real danger is when the response falters- delayed actions, weak reporting, or policies that prioritise short-term continuity over reducing transmission. That’s the systems lesson the Black Death seems to teach: a pathogen with a reservoir becomes a continent-scale disaster when stressed supply chains and crowded hubs create the bridges it needs. Spillover risk rises not only because a pathogen evolves, but because human systems open the door. And as climate extremes become more erratic, those spillovers will appear more often.

We now have a far clearer picture of how the Black Death began. It no longer looks like a sudden, inexplicable catastrophe, but the product of interacting pressures that built over time. That perspective helps clarify how spillovers occur- and how to manage pandemic threats we face today and tomorrow.

References and Sources:

The Spread of the Black Death: How the Plague Devastated Medieval Europe. Medieval Chronicles. https://www.medievalchronicles.com/medieval-life/medieval-diseases/black-plague/how-did-the-black-plague-spread/

Wheelis, M., 2002. Biological warfare at the 1346 siege of Caffa. Emerging infectious diseases, 8(9), p.971. https://doi.org/10.3201/eid0809.010536

Gaul, E. and Spyrou, M.A., 2025. Historical plague pandemics: perspectives from ancient DNA. Trends in Microbiology, 33(1), pp.7-10. DOI: 10.1016/j.tim.2024.10.008

Pauciullo, S., Zulian, V., La Frazia, S., Paci, P. and Garbuglia, A.R., 2024. Spillover: mechanisms, genetic barriers, and the role of reservoirs in emerging pathogens. Microorganisms, 12(11), p.2191. doi: 10.3390/microorganisms12112191

Plowright, R., Parrish, C., McCallum, H. et al. Pathways to zoonotic spillover. Nat Rev Microbiol 15, 502–510 (2017). https://doi.org/10.1038/nrmicro.2017.45

(1) Spyrou, M.A., Musralina, L., Gnecchi Ruscone, G.A. et al. The source of the Black Death in fourteenth-century central Eurasia. Nature 606, 718–724 (2022). https://doi.org/10.1038/s41586-022-04800-3

(2) Eaton, K., Featherstone, L., Duchene, S. et al. Plagued by a cryptic clock: insight and issues from the global phylogeny of Yersinia pestis. Commun Biol 6, 23 (2023). https://doi.org/10.1038/s42003-022-04394-6

(3) Green, M.H., 2020. The four black deaths. The American Historical Review, 125(5), pp.1601-1631. https://doi.org/10.1093/ahr/rhaa511

(4) Hymes, R., 2015. Epilogue: a hypothesis on the East Asian beginnings of the Yersinia pestis polytomy. The Medieval Globe, 1(1), pp.285-308.

(5) Carmichael, A.G., 2014. Plague persistence in Western Europe: a hypothesis. The Medieval Globe, 1(1), p.8. Available at: https://scholarworks.wmich.edu/tmg/vol1/iss1/8

(6) Stenseth, N.C., Tao, Y., Zhang, C., et al. 2022. No evidence for persistent natural plague reservoirs in historical and modern Europe. Proceedings of the National Academy of Sciences, 119(51), p.e2209816119. https://doi.org/10.1073/pnas.2209816119

(7) Spyrou, M.A., Keller, M., Tukhbatova, R.I. et al. Phylogeography of the second plague pandemic revealed through analysis of historical Yersinia pestis genomes. Nat Commun 10, 4470 (2019). https://doi.org/10.1038/s41467-019-12154-0

(8) Bramanti, B., Wu, Y., Yang, R., Cui, Y. and Stenseth, N.C., 2021. Assessing the origins of the European Plagues following the Black Death: A synthesis of genomic, historical, and ecological information. Proceedings of the National Academy of Sciences, 118(36), p.e2101940118. doi: 10.1073/pnas.2101940118

(9) Bauch, M., Büntgen, U. Climate-driven changes in Mediterranean grain trade mitigated famine but introduced the Black Death to medieval Europe. Commun Earth Environ 6, 986 (2025). https://doi.org/10.1038/s43247-025-02964-0

“Since then you do not permit it [opium] to injure your own country, you ought not to have the injurious drug transferred to another country, and above all others, how much less to the Inner Land! Of the products which China exports to your foreign countries, there is not one which is not beneficial to mankind in some shape or other.” Lin Zexu, in a letter written to Queen Victoria in 1839 (1).

Lin Zexu’s letter to Queen Victoria reads like a question we still haven’t answered: when those with power decide a drug is too dangerous, what makes it acceptable to sell it to someone else for profit?

In the late 1830s, opium had become a mass market in China, sustained by imperial supply chains and defended for commercial interests. The nation experienced a drug crisis so vast it reshaped a society.

But when officials tried to shut the market down, Britain sent gunboats.

The Opium Wars are usually remembered as a historical period of imperial humiliation and decline in China. Less often told is that an empire went to war to protect a drug market, trading human lives in the pursuit of profit.

Wars over trade profits

The Opium Wars began as a trade dispute, but they also delivered a public health disaster enforced at cannon range. Britain’s demand for Chinese tea and goods created a persistent trade imbalance. To settle it without silver, British merchants turned to opium grown from India to be sold illegally into China. By 1830s, tens of thousands of chests of opium were entering China each year (2).

Qing authorities condemned the trade as a threat to social order and tried to shut it down. In 1839, the imperial commissioner Lin Zexu escalated enforcement, seized and destroyed over 20,000 chests of opium at Humen, south China.

Britain’s traders lobbied fiercely for military protection, and the government responded with force. China’s defeat in the First Opium War led to the 1842 Treaty of Nanjing: heavy indemnities to be paid by the Qing government, the cession of Hong Kong, and the opening of treaty ports to foreign trade. A second war between 1856-1860 brought further “unequal treaties” which effectively normalised and safeguarded the opium trade with foreign protection, to the point that opium was intertwined with China’s economic and political structures (3).

The wars locked China’s market access by force, and helped entrench an opioid economy whose social and health costs would unfold as a long-term public health catastrophe.

Tens of millions exposed

By the mid-19^th century, opium use in China had spread far beyond its earlier medical and elite circles to become a national crisis. Once imported, opium became cheaper and widely available. Opium didn’t respect class- it was used by officials and merchants, but also labourers and rural workers least able to afford the cost of dependence. Many used them to dull their fatigue from work, provide pain relief, to induce sleep or suppress hunger.

Estimates suggested that by the 1880s, tens of millions of people were using opium or morphine, with roughly 15-30 million people experiencing heavy dependence (3, 4). This meant 3-10% of China’s population.

The crisis didn’t stop at China’s borders. Opium use spread across East and Southeast Asia, following trade routes and migrant networks, and was widely reported among Chinese communities overseas. Exposure reached a scale that made denial impossible, and turned opium to an issue of international concern.

Towards the first international opium regulations

By the early 1900s, China’s opium crisis could no longer be dismissed as a domestic failure. Faith leaders and activists from human rights and temperance movements argue that the opium epidemic was not simply China’s burden, but the product of an immoral international system that profited from the crisis (4).

That critique found unexpected allies. The United States, grappling with opium use in its Philippines colony and seeking to improve relations with China- helped push the issue onto the diplomatic agenda. In February 1909, delegates from major powers met at the Shanghai Opium Commission, the first-time governments examined the scale of global opium trade. They gathered evidence and called for the suppression of non-medical opium use.

The commission had no legal force, but it did reframe opium as a problem requiring international regulation. That shift fed directly into the 1912 Hague Opium Convention, and later into League of Nations mechanisms that laid the foundations for modern international drug control.

This was one of the first moments major powers treated opium harms as an international problem shaped by cross-border incentives and supply chains, because the trade’s instability, geopolitics and reputational costs were becoming hard to manage.

The long shadow of opium in China

For China, the Opium wars hardened into national memory. Opium became a symbol for foreign domination and above all, the loss of sovereignty. Across the late Qing, Republican, and early Communist periods that came afterward, drugs were repeatedly framed as threats to social order and state survival. Eradication was a political necessity.

That legacy still shapes China’s drug laws today. Drug possession and trafficking carry severe penalties, including long prison sentences and, in some cases, capital punishment for large-scale trafficking (5). People identified as drug users are placed in compulsory detention for rehabilitation, subjected to routine drug testing and registration with local police (6).

Harm-reduction measures such as methadone maintenance do exist. But they operate within a system that prioritises abstinence, surveillance and deterrence over people’s autonomy (7). As a result, drugs are regulated less as a public health issue than as a matter of social order and state security.

Understanding this history helps explain why China’s approach diverges so sharply from public-health led models elsewhere- and why debates over drug policy remain inseparable from the country’s imperial past.

Opium’s modern echoes, worldwide

The Opium Wars show how profit-driven commercial systems can be enforced through power- forcing markets open and leaving societies to bear the consequences. That hasn’t disappeared. What has changed are the ways states tolerate or enable drug economies whose harms fall elsewhere.

In the late 1990s and early 2000s, prescription opioids were increasingly used for chronic pain, alongside a broader push to treat pain more aggressively. After OxyContin was launched by Purdue Pharma in 1996, it was heavily marketed, with promotional messaging that downplayed risks of dependence. Prescribing expanded rapidly over the decade- faster than regulations or safeguards could keep up- and by around 2010, opioid prescribing in the US had tripled compared to levels a decade earlier (9).

The consequences were devastating. By 2023, the US recorded around 105,000 drug overdose deaths, with nearly 80,000 involving opioids. As the scale of harm became impossible to ignore, responsibility was increasingly displaced. A system that had normalised widespread exposure to dependent drugs was reframed as a problem of individual misuse alone.

In other settings, this operates across borders. Narco-export economies have emerged in which drug production and trafficking are intertwined with state conflict and regime survival. Until recently, Captagon production in Syria had expanded alongside war and sanctions, with trafficking networks reportedly connected to figures and security forces in the Assad regime. In Myanmar, prolonged conflict and fragmented sovereignty have enabled large-scale production of synthetic drugs for regional export in Southeast Asia, protected by armed groups and corrupt officials.

The Opium Wars reveal a public health crisis engineered by incentives governments create or tolerate. When commercial interests outrun regulation- whether enforced by coercion, protected by political influence or enabled by state fragility- health disasters aren’t accidents. They are the predictable results of political design.

Sources and References:

The Opening to China Part I: the First Opium War, the United States, and the Treaty of Wangxia, 1839–1844. https://history.state.gov/milestones/1830-1860/china-1

First China War. National Army Museum. https://www.nam.ac.uk/explore/first-china-war-1839-1842

Kaufman, A.A., 2010. The “century of humiliation,” then and now: Chinese perceptions of the international order. Pacific Focus, 25(1), pp.1-33. https://doi.org/10.1111/j.1976-5118.2010.01039.x

Gilmore, A.B., Fabbri, A., Baum, F., Bertscher, A., Bondy, K., Chang, H.J., Demaio, S., Erzse, A., Freudenberg, N., Friel, S. and Hofman, K.J., 2023. Defining and conceptualising the commercial determinants of health. The Lancet, 401(10383), pp.1194-1213. DOI: 10.1016/S0140-6736(23)00013-2

(1) Zexu, L., 2015. Letter to Queen Victoria, 1839. From The Chinese Repository, vol. VIII, no 10 (February 1940): 497-503. https://media.bloomsbury.com/rep/files/Primary%20Source%2013.0%20-%20Lin.pdf

(2) Purdue, P.C. The First Opium War, The Anglo-Chinese War of 1839-1842. https://visualizingcultures.mit.edu/opium_wars_01/ow1_essay01.html

(3) Dikötter, F., Laamann, L. and Xun, Z., 2002. Narcotic culture. a social history of drug consumption in China. British Journal of Criminology, 42(2), pp.317-336. https://doi.org/10.1093/bjc/42.2.317

(4) Pietschmann, T., Tullis, M. and Leggett, T., 2009. A century of international drug control. United Nation Office on Drugs and Crime. https://www.unodc.org/documents/data-and-analysis/Studies/100_Years_of_Drug_Control.pdf

(5) 2015. Anti-Drug Law of the People’s Republic of China. https://english.court.gov.cn/2015-07/17/c_761568.htm

(6) Lin, M., Sun, N. and Amon, J.J., 2022. No exit: China’s state surveillance over people who use drugs. Health and human rights, 24(1), p.135. PMID: 35747288

(7) Meng, J. and Burris, S., 2013. The role of the Chinese police in methadone maintenance therapy: A literature review. International journal of drug policy, 24(6), pp.e25-e34. DOI: 10.1016/j.drugpo.2013.03.010

(8) Van Zee, A., 2009. The promotion and marketing of oxycontin: commercial triumph, public health tragedy. American journal of public health, 99(2), pp.221-227. doi: 10.2105/AJPH.2007.131714

(9) Guy, G.P., 2017. Vital signs: changes in opioid prescribing in the United States, 2006–2015. MMWR. Morbidity and mortality weekly report, 66.

On the morning of 6 April 1979, Dr. Margarita Ilyenko, chief physician at Hospital 24 in Sverdlovsk, arrived for what she thought would be a normal shift (1, prologue). She dropped her bag in her office, pulled on her white coat, and walked onto the ward.

She froze.

“There are dead bodies, people still alive, lying together. I thought, this is a nightmare. Something is very, very wrong.”

Within days, dozens of men from the factory district downwind of a military compound crowded her wards.

Dr. Ilyenko began a private record in a school notebook: names, ages, addresses, and a blunt tally: “358 got sick. 45 died. 214 in Hospital 40.”

The security services seized the official autopsy protocols, but somehow missed the notebook in her flat. Years later, its cramped lines would help prove that the killer was an airborne plume of anthrax from Compound 19, not contaminated meat.

Case I: Aralsk, 1971

Sverdlovsk wasn’t the first incident. Eight years earlier, the Soviet bioweapons programme had already spilled into civilian life.

This first happened in July 1971, when an open-air test of weaponized smallpox was carried out on Vozrozhdeniya Island in the Aral Sea- the Soviet Union’s most secret bioweapons range (2). According to a later testimony by Dr. Pyotr Burgasov, then chief sanitary physician of the USSR, 400 grams of variola virus were detonated in an aerosol trial.

“I called Andropov, who at that time was chief of the KGB, and informed him of the exclusive recipe of smallpox in use on Vozrozhdeniye Island. He ordered that not another word be said about it. This is a real biological weapon! The minimum radius of contamination was 15 kilometers. One could imagine what would have happened if instead of one laboratory technician, there had been 100 to 200 people.” Pyotr Burgasov, November 2001 (2).

Days later, a research vessel, the Lev Berg, passed closer to the island than permitted. On board was a 24-year-old female fisheries technician who collected plankton from the open deck. Within days of returning home to the port city of Aralsk (in present-day Kazakhstan), she developed fever and rash and became the index case of a smallpox outbreak.

Over the following weeks, ten people fell ill. Three unvaccinated victims- a young woman and two small children- died from haemorrhagic smallpox. Once the diagnosis was recognised, the response was swift and militarized: houses were quarantined, all traffic in and out of Aralsk was halted, nearly 50,000 residents were vaccinated in under two weeks and a hundred people were isolated in a makeshift facility on the city’s edge.

Aralsk showed that even the Soviet Union’s most controlled experiments could spill into civilian life. And yet, the lesson went unheeded.

Case II: Sverdlovsk, 1979

More than a thousand kilometres from Aralsk, a far deadlier accident unfolded in the closed industrial city of Sverdlovsk.

On 2 April 1979, during shift change at a military microbiology facility, a clogged filter was removed and its replacement delayed. For several minutes, aerosol from an anthrax drying unit vented directly into the air.

In the weeks that followed, at least 60 people died. They were mostly male factory workers.

The official explanation blamed contaminated meat. Internal records were altered, and physicians were pressed to certify a diagnosis that contradicted their own autopsy findings.

A decade later, when the Soviet state loosened its grip, American and Russian investigators overlaid weather data with victims’ addresses and uncovered what the government had denied: a plume of weaponized spores of anthrax from the military compound had drifted along a narrow, four-kilometer strip of city blocks and industrial yards (3). This was later confirmed through genetic analyses of autopsy samples (4).

What made those accidents inevitable

Aralsk and Sverdlovsk weren’t isolated incidents. They were visible leaks from an apparatus built in the early 1970s, when the Soviet Union- having just signed the Biological Weapons Convention- set up Biopreparat, a new “civilian” biotechnology network that in practice extended its offensive capabilities.

Biopreparat quickly moved to the centre of the world’s largest covert biological weapons program, coordinating the research, testing and mass production of agents including anthrax, plague, Q-fever, tularemia and smallpox. At its peak, the wider complex encompassed 40-50 major facilities and roughly 60,000 staff, many concealed in closed cities or remote industrial zones linked by dedicated rail lines and guarded perimeters. Among its most secret sites was Vozrozhdeniya Island in the Aral Sea, where open-air pathogen trials continued for years.

Inside this system, success was counted in outputs and production targets, not safe working conditions (5). Outbreaks and accidents were treated first as political incidents and second only as health crises, with reports rewritten to fit the authorised narrative.

“A thorough investigation of what had happened in Compound 19 would raise too many awkward questions even inside our own government about our activities. This was further proof that secrecy was valued above all else in our system-even if it endangered our own safety… Our coverup virtually guaranteed further disasters.” Kanatzhan Alibekov (Ken Alibek), former deputy director of Biopreparat later defected to the US (6).

The real hazard wasn’t just pathogens themselves. It was the secrecy and command structures built around them.

The quiet risks of high-risk biology

The Soviet bioweapons programme shows with unsettling clarity how high-risk biology goes wrong. The Aralsk and Sverdlovsk incidents weren’t caused by scientific ignorance, but of institutions that prized output over candour and made secrecy a condition of work.

Today’s high-containment labs operate under different but related pressures. Over the past two decades, BSL-3 and BSL-4 facilities have expanded across Europe, North America, Asia and the Middle East, many supporting public health preparedness and legitimate dual-use research (6). But some states- including Russia and North Korea- are still assessed in international reports as remaining out of compliance and maintaining covert offensive capabilities.

Even in well-regulated and legitimate systems, failures can occur. In 2007, live foot-and-mouth virus escaped from a UK research site at Pirbright, triggering outbreaks in nearby farms. In 2019, a brucellosis leak from a vaccine plant in Lanzhou, China infected over 10,000 people (7). Such incidents are rare. High-containment labs handle vast numbers of samples safely each year. But when breaches happen, rapid detection and transparent disclosure are really decisive to contain the consequences.

Outbreaks thrive in silence. The Soviet system institutionalised that silence by burying accidents. Today’s biological research operate under a much more regulated environment, but whenever secrecy or prestige trumps transparency and oversight, this risks happening again. Aralsk and Sverdlovsk endure as warnings- not because today’s labs resemble them, but because the incentives that produced them can return.

References and Sources:

Frischknecht, F., 2003. The history of biological warfare: Human experimentation, modern nightmares and lone madmen in the twentieth century. EMBO reports, 4(S1), pp.S47-S52. doi: 10.1038/sj.embor.embor849

Zilinskas, R.A., 2016. The Soviet biological weapons program and its legacy in today’s Russia. National Defense University Digital Commons @ NDU https://digitalcommons.ndu.edu/cgi/viewcontent.cgi?article=1000&context=wmd-occasional-papers

Enserink, M., 2002. Did bioweapons test cause a deadly smallpox outbreak?(Biowarfare). Science, 296(5576), pp.2116-2118. doi: 10.1126/science.296.5576.2116.

Cook, Michelle S., and Amy F. Woolf. Preventing proliferation of biological weapons: US assistance to the former Soviet states. CRS Report for Congress. No. CRSRL31368. 2002.

(1) Hoffman D.E. 2009. “The Dead Hand: The Untold Story of the Cold War Arms Race and Its Dangerous Legacy.” New York: Doubleday, 2009. Prologue: https://www.vpm.org/npr-news/2009-10-07/excerpt-the-dead-hand

(2) Tucker, J.B. and Zilinskas, R.A. eds., 2002. The 1971 smallpox epidemic in Aralsk, Kazakhstan, and the Soviet biological warfare program (No. 9). Center for Nonproliferation Studies, Monterey Institute of International Studies.

(3) Meselson, M., Guillemin, J., Hugh-Jones, M., Langmuir, A., Popova, I., Shelokov, A. and Yampolskaya, O., 1994. The Sverdlovsk anthrax outbreak of 1979. Science, 266(5188), pp.1202-1208. doi: 10.1126/science.7973702.

(4) Sahl, J.W., Pearson, T., Okinaka, R., Schupp, J.M., Gillece, J.D., Heaton, H., Birdsell, D., Hepp, C., Fofanov, V., Noseda, R. and Fasanella, A., 2016. A Bacillus anthracis genome sequence from the Sverdlovsk 1979 autopsy specimens. MBio, 7(5), pp.10-1128. https://doi.org/10.1128/mbio.01501-16.

(5) Alibek, K. and Handelman, S. (1999) Biohazard: The Chilling True Story of the Largest Covert Biological Weapons Program in the World. New York: Random House. https://www.nlm.nih.gov/nichsr/esmallpox/biohazard_alibek.pdf

(6) Muluneh, A.G., Moa, A., Lim, S. et al. Mapping biosafety level 3 (BSL-3) and BSL-4 laboratories for public health threats reduction. J Public Health (Berl.) (2025). https://doi.org/10.1007/s10389-025-02492-3

(7) Pappas, G., 2022. The Lanzhou Brucella leak: the largest laboratory accident in the history of infectious diseases?. Clinical Infectious Diseases, 75(10), pp.1845-1847. doi: 10.1093/cid/ciac463

“When I was born, I was born with a deformity but for unknown reasons. In fact, it wasn't until 2000 when we were given a health check to receive allowance from the government that we knew it was due to dioxin poison.” Pham The Minh, second generation victim of Agent Orange. Source: Antiatom.org, https://www.antiatom.org/english/world_conference/pdf/2021/TESTIMONY%20OF%20PHAM%20THE%20MINH.pdf

On 30 April 1975, the Vietnam War ended. US forces withdrew, and a conflict that had dominated global headlines began to recede into history. For governments and militaries, “post-war” meant reconstruction- and closure.

For those exposed to Agent Orange, it meant something else entirely.

The herbicide campaign had treated chemicals as temporary tools of war: sprayed from the air, assuming to do their work and disappear. Instead, it created a long-term public health problem nobody agreed to own.

What does “post-war” really mean when a chemical doesn’t stop acting?

A population exposed but never counted

Beginning in the early 1960s, the US military launched a large-scale herbicide campaign across South Vietnam, Laos and Cambodia. Aircraft sprayed roughly 18 million gallons of herbicides to strip forest cover and destroy crops believed to help opposing forces (1).

The program relied on a family of formulations known as the “rainbow herbicides”, named for the coloured bands painted on their barrels. Agent Orange- a mixture of two common phenoxy weedkillers- was the most heavily used.

The campaign was framed as tactical and temporary. Once spraying ended, the chemicals were assumed to break down quickly, leaving no lasting consequences beyond the battlefield.

In practice, the sprayed herbicides didn’t respect military boundaries. Villages, rivers, farmland and forest edges were sprayed indiscriminately (2).

Although some components degraded rapidly, the contaminated dioxins didn’t. They persisted for years to decades in the soil, contaminating fish and livestock, and returning through food and breast-milk in hotspot areas.

These created conditions that made the science itself harder. Epidemiology depends on knowing who was exposed, when, and to what degree. Yet in post-war Vietnam, the infrastructure to answer those questions was never built at scale. There were no exposure registries, little baseline health data, and few cohorts established early enough to follow families over time. Civilian exposure was just treated as collateral.

This structural failure meant that a vast exposed population was never formally defined, leaving limited infrastructure needed to observe long-term harm of Agent Orange and herbicides.

Epidemiology arrived, years too late

The failure to count early meant that by the time epidemiology began to take hold, exposure had already stretched across decades and geography. People had moved, families had aged, and the clear starting point required for long-term follow-up no longer existed.

Researchers responded by narrowing the frame. They focused on a small number of heavily contaminated sites- former herbicide storage and handling sites such as Da Nang and Bien Hoa- where exposure could be anchored to place, even if time remained uncertain (3). There, teams enrolled mothers and infants living nearby, measured dioxin levels in breast milk as a marker of early-life exposure, and followed children as they developed (4).

These studies revealed consistent patterns. In Da Nang cohorts, higher perinatal dioxin exposure was associated with altered early growth trajectories and differences in neurodevelopment detectable as early as 4 months of age (5). Another study around Bien Hoa extended these observations at roughly 2 years, suggested neurodevelopmental effects that persisted beyond infancy (6).

Even with findings in hotspots, the overall causal picture remains contested because exposure histories were incomplete. The uncertainty that remained is often framed as a failure to prove harm. This was the cost of arriving late.

Care in the absence of closure

“When the war is over for a long time, but the Vietnamese victims, they are suffering, and nobody here makes any — has any responsibility towards them.” Dang Hong Nhut, 2008- who was born with disabilities as a result of Agent Orange exposure. Source: Democracy Now, https://www.democracynow.org/2008/12/4/vietnamese_agent_orange_victims_demand_accountability

Even where the science remains scattered, living with the consequences of herbicide exposure has never been optional. An estimated 4.8 million people may have been affected (2), including at least 150,000 children and 35,000 grandchildren born with birth defects- figures that, however imprecise, hint at why this is a social burden of lived experiences as much as a biomedical one (7).

For families raising children with disabilities, daily life depends on whether support exists. The Vietnamese government now spends more than VND 10 trillion ($400 million) annually on monthly allowances for those exposed to Agent Orange and their families, supporting over 320,000 beneficiaries alongside health insurance and free treatment.

Civil societies also filled some gaps. The Vietnam Association for Victims of Agent Orange/Dioxin counts more than 400,000 members nationwide for long-term care: health check-ups, social protection, financial and educational support over years.

But Vietnam’s recovery remains partial and contested. US funded clean-ups at major hot spots address the most concentrated contamination, but they don’t settle questions about responsibility. Neither the US nor Vietnam wanted to revisit this past. Vietnamese advocacy groups continued to pursue legal action against herbicide manufacturers, pressing for accountability and compensation.

Whatever the mechanism of exposure- the aftermath of Agent Orange is still there, leaving systems to manage harm without closure.

The afterlife of temporary decisions

The herbicide campaign in Vietnam is often treated as a by-product of a particular war and era. It’s a recurring failure of short-term decisions whose biological consequences unfold far more slowly.

Warfare continues to starkly expose this failure. Burn pits in Iraq and Afghanistan, the re-emergence of chemical agents in the Syrian civil war- military technologies are authorised as temporary measures to achieve short-term strategic goals. Their long-term health consequences, from respiratory diseases to cancers and developmental harm, surface years later, without systems designed to track or manage them.

We also see this in civilian life. Forever chemicals such as PFAS were used because of their stability; their persistence in water, soil and human blood were a design feature left ungoverned (8). Agricultural pesticides like organophosphates are approved on the basis of short-term toxicity data, while cumulative neurodevelopmental and carcinogenic effects emerged only after decades of widespread use, long after tracing their cause for harm became difficult (9).

Agent Orange wasn’t dangerous only because it was toxic. It was dangerous because nobody wanted to be responsible for what came after use ended. Public health failures arise when systems plan for immediate goals and abandon long-term consequences. The result is decades of preventable illness, disability and care borne by families.

Post-war is a political word. For chemical exposures, it marks the end of attention, not the end of harm.

Position statement

I write as a London-based editor working in public and global health (views my own), and approach issues in the Global South with a commitment to amplifying diverse voices and perspectives. I recognise my position outside the communities I write about, and approach these histories with humility, curiosity, and respect for the people who lived and shaped them.

I welcome corrections and additional context from scholars and communities from Vietnam to ensure these histories are told accurately and respectfully.

References and Sources:

Normile, D., 2025. Fifty years after the Vietnam War, researchers are still struggling to document the long-term health effects of the massive spraying of Agent Orange and other herbicides. Science, doi: 10.1126/science.ady4158.

Science, 2025. In Vietnam, the health effects of Agent Orange remain uncertain 50 years later. https://www.science.org/content/article/vietnam-health-effects-agent-orange-remain-uncertain-50-years-later

Scientific American, 2016. Is Agent Orange Still Causing Birth Defects? https://www.scientificamerican.com/article/is-agent-orange-still-causing-birth-defects/

(1) Buckingham, W. A., Jr. (1982). Operation Ranch Hand: The Air Force and herbicides in Southeast Asia, 1961–1971. Office of Air Force History, United States Air Force. U.S. National Agricultural Library Special Collections. https://www.nal.usda.gov/exhibits/speccoll/files/original/5463ce5acea0dc40921b9f9a1da6efc3.pdf

(2) Stellman, J., Stellman, S., Christian, R. et al. . Nature 422, 681–687 (2003). https://doi.org/10.1038/nature01537

(3) Tuyet-Hanh, T.T., Minh, N.H., et al., 2015. Environmental health risk assessment of dioxin in foods at the two most severe dioxin hot spots in Vietnam. International Journal of Hygiene and Environmental Health, 218(5), pp.471-478. https://doi.org/10.1016/j.ijheh.2015.03.014

(4) Nishijo, M., Anh, N.T.N., et al., 2013. Dioxin exposure in breast milk and infant neurodevelopment in Vietnam. Occupational and Environmental Medicine, 70(9), pp.656-662. doi: 10.1136/oemed-2012-101021

(5) Nishijo, M., Tai, P.T., et al., 2012. Impact of perinatal dioxin exposure on infant growth: a cross-sectional and longitudinal studies in dioxin-contaminated areas in Vietnam. PloS one, 7(7), p.e40273. https://doi.org/10.1371/journal.pone.0040273

(6) Pham, N.T., Nishijo, M., Pham, T.T., et al. 2019. Perinatal dioxin exposure and neurodevelopment of 2-year-old Vietnamese children in the most contaminated area from Agent Orange in Vietnam. Science of the Total Environment, 678, pp.217-226. https://doi.org/10.1016/j.scitotenv.2019.04.425

(7) Truong Van Quoc and Nguyen Tong Minh, 2024. Ensuring the rights of Agent Orange victims https://en.baoquocte.vn/ensuring-the-rights-of-agent-orange-victims-289203.html

(8) Kahn, L.G., Philippat, C., Nakayama, S.F., Slama, R. and Trasande, L., 2020. Endocrine-disrupting chemicals: implications for human health. The lancet Diabetes & endocrinology, 8(8), pp.703-718. doi: 10.1016/S2213-8587(20)30129-7.

(9) Eskenazi, B., Bradman, A. and Castorina, R., 1999. Exposures of children to organophosphate pesticides and their potential adverse health effects. Environmental health perspectives, 107, p.409. doi: 10.1289/ehp.99107s3409

January is a good month for reflections. We look back- over the past year, then back further, sometimes pondering on the beginning of things (maybe that’s just me). In public health, that instinct leads to a deceptively simple question: when did pandemics begin?

Ask a historian for the first pandemic, and they’ll probably say the Plague of Justinian. Look up the Guinness World Records, and it’s the Plague of Athens.

These are great answers because they sound like certainty. But that certainty starts to wobble once you do the annoying epidemiologist thing and ask: what do we actually mean by a “pandemic”, exactly?

Today, the term has a clear definition- the worldwide spread of a new disease. But in the ancient world, nobody was thinking in those terms. The label has to be applied retrospectively, pieced together from clues like: how far did the outbreak spread? how disruptive was it?, or whether anyone wrote about it (and whether that survived)?

For a long time, those reconstructions relied almost entirely on written records. Now, that picture is more complicated. Ancient DNA is revealing far older disease events- prehistoric outbreaks that unfolded thousands of years before anyone wrote about them. If outbreaks spread widely in these deep pasts, they may have left no stories at all- only genetic traces in teeth and bones.

Which means our familiar pandemic timeline may be less like a straightforward history of disease and more like a history of what became visible. And the absences- the outbreaks nobody recorded- may tell us just as much about how pandemics occur.

A traceable pandemic of global scale

“During these times there was a pestilence, by which the whole human race came near to being annihilated.” Procopius, Byzantine historian of the 6^th century. Source: History of the Wars.

One outbreak that left a prominent mark was the Plague of Justinian. From 541 to 549 CE, it swept across the late antique world from the Mediterranean to Western Europe, the Middle East and North Africa- disrupting societies along the way.

People at the time tried to capture its impact: Procopius described of bubonic swellings and rapid death, while John of Ephesus wrote of entire villages falling silent. Later historians argue that the outbreak deepened existing cracks in the Roman Empire, adding political, economic, and military strain.

For centuries, these vivid accounts were all historians had. That changed with ancient DNA research, which identified Yersinia pestis- the bacterium behind Bubonic plague- as the culprit (1). Genetic evidence now suggests the Justinian plague may mark the beginning of the so-called “First Plague Pandemic”- a series of regional recurrences and outbreaks that unfolded over nearly 200 years (2). Climate shocks and trade routes likely amplified its reach: volcanic eruptions in 536 CE cooled the climate and strained harvests, while busy trade routes carried rodents and fleas across vast distances (3).

In that sense, the Justinian plague was the earliest event we can trace at a global scale using both written testimony and scientific evidence- that we can document with confidence.

A pandemic during systemic collapse

“The pain in the eyes, the attack of the fevers, and the ailment of all the limbs are the same among us and among the others, so long as we share the common flesh of this age.” Cyprian of Carthage describing the symptoms of the plague and their indiscriminate nature towards Pagans and Christians alike Source: De mortalitate (“On Mortality”), quote from (4).

The Plague of Cyprian is often cited as an example of how disease can accelerate a society already under pressure. It unfolded during the Third-Century Crisis (235-284 AD), a period marked by political fragmentation, recurring coups and economic turmoil across the Roman Empire. During this time, breakaway regimes such as the Gallic and Palmyrene Empires emerged as Rome’s central authority weakened.

Whether this event should be called a pandemic, however, is much harder to pin down. The outbreak seems to have spread less widely than the Justinian plague (5), and most surviving descriptions came from Cyprian of Carthage and later Christian writers who recorded intense suffering and social breakdown. But no pathogen has been identified, and proposed diseases remain speculative. No evidence exists to allow the outbreak’s scale to be measured with confidence.

For that reason, the Plague of Cyprian’s historical importance lies less in proving a pandemic than revealing how disease has always exploited vulnerability, turning existing strain into collapse in an interconnected world.

Pandemic in the imperial world

The Antonine Plague is often described as the first outbreak to sweep across an entire imperial world. Emerging in the late second century around 165 AD, it moved along the dense roads and trade networks that bound the Roman Empire together (6). Within a few years of its appearance, the disease was reported thousands of kilometres apart.

Yet calling this a pandemic rests on inference rather than certainty. The physician Galen described fevers and skin eruptions- symptoms now often associated with a smallpox-like disease- but the pathogen itself remains unproven (6). What can be understood instead are the inferred population loss through disruptions to military recruitment, taxation and local labour supplies.

The Antonine plague matters as an example of how pandemics take shape, where interconnected political systems allowed disease to resurface across regions and over time.

When narrative outranks geography

“The sacred places also in which they had quartered themselves were full of corpses of persons that had died there…men, not knowing what was to become of them, became utterly careless of everything, whether sacred or profane.” Thucydides, whom wrote of the social disorder that occurred during the Plague in Athens. Source: History of the Peloponnesian War (7).

The Plague of Athens, which struck the city in 430 BCE during the early years of the Peloponnesian War, is sometimes included in lists of ancient “pandemics”, largely because it was described in such vivid detail.

Thucydides, who lived through the outbreak himself, wrote of sudden fevers, rashes, unquenchable thirst, delirium and violent spasms, along with profound social unravelling (7). The human cost was immense- perhaps a quarter to a third of the city’s population died within a few years (8).

Yet despite its severity, there’s little evidence that the disease spread far beyond the eastern Mediterranean. Its reach was more consistent with a devastating local or regional epidemic than with the kind of wide-ranging spread we now associate with a pandemic. Its prominence in pandemic histories owes more to the survival of powerful written account than to the scale of outbreak itself.

A neolithic plague pandemic?

Could something resembling a pandemic have unfolded thousands of years before the Plague of Justinian- quietly moving through Neolithic villages and Bronze Age farmsteads, long before anyone wrote it down?

Ancient DNA now shows that Yersinia pestis was circulating across Eurasia thousands of years before the first written pandemics. Some of the earliest recovered plague genomes- dating from around 5,000 to 2,800 years ago- have been found across a vast area, from the Eurasian steppe to Central and Western Europe (9). Later analyses of Neolithic and Bronze Age burials suggest these early strains persisted for centuries, resurfacing in multiple communities across the Baltic and beyond (10).

This has led some researchers to propose a “Neolithic plague pandemic” (11). As farming, herding and long-distance mobility expanded, early plague lineages appear to have spread and diversified, at a time when many regions showed signs of sharp population decline. In this view, plague may have quietly reshaped human societies long before written history began.

But there’s a catch. Many early Y. pestis strains lacked key genes that later enabled flea-borne, explosive outbreaks associated with bubonic plague (9), though this remains debated. A recent large survey of ancient pathogens instead found a patchy pattern of infection, suggesting a disease circulating mainly in animal reservoirs that occasionally spilled into human groups- causing devastating local or regional outbreaks rather than a single continent-wide pandemic (12).

For now, the evidence can support both interpretations. What is clear is that plague was already shadowing human societies millennia before it entered the historical record- whether as a slow persistent threat or a hidden driver of prehistoric population change.

How ancient pandemics shape our understanding of the next

If there’s a single lesson running through these early outbreaks, it’s that the “first pandemic” is rarely the first- only the first one we can see. What looked like an origin point is often the moment a disease becomes visible. Plague moved through prehistoric communities long before anyone recorded it, just as the Justinian plague was spreading before Procopius described deaths in Constantinople. SARS-CoV-2 followed the same pattern, circulating quietly in late 2019 before pneumonia cases in Wuhan drew global attention (13).

That visibility is not neutral. The historical record is an uneven detection system shaped by literacy and preservation. Empires that taxed, counted and wrote things down leave traces; outbreaks in less documented societies, or documents that didn’t survive often disappear from view. New scientific tools like ancient DNA can sometimes recover fragments of what was missed, but only partially and unevenly. Missing records doesn’t mean the absence of disease, only the absence of institutions able to register it in ways that researchers can recover. Public health today has its own thresholds of visibility too, based on what gets detected, reported and believed.

If the record shapes what we notice, the outbreaks themselves show what drives spread once it begins. Pandemics scale along lines of connection. Roman military routes and grain fleets were the logistical arteries of their world, much as flight networks, commuter lines and supply chains structure spread today. The routes people build determine how fast and how far it travels.

Networks alone, though, wouldn’t guarantee catastrophe. Amplification of an outbreak happens where vulnerability already exists. Volcanic cooling in 536AD, Roman political crises, and shifts in Neolithic settlement all created conditions for disease. Today’s climate crisis, ecological disruption, conflict and urban crowding do the same- making societies more vulnerable with unequal consequences.

Rather than crowning “a first pandemic” from a biased archive, it’s more revealing to recognise recurring patterns of visibility and spread. Each pandemic begins in obscurity, become visible only when institutions can detect them, spread along networks that connect populations together, and do the worst damage when societies are already under strain. The past offers a pattern of seeing, and that pattern is still shaping the outbreaks we face now.

Sources and References:

Harper, K. The Fate of Rome 2017. Princeton University Press.

Flemming, R., 2023. Pandemics in the ancient mediterranean world. Isis, 114(S1), pp.S288-S312. https://doi.org/10.1086/726988

Eisenberg, M. and Mordechai, L., 2020. The Justinianic plague and global pandemics: The making of the plague concept. The American Historical Review, 125(5), pp.1632-1667. https://www.jstor.org/stable/27156075

Swamy R. Adapa et al, Genetic Evidence of Yersinia pestis from the First Pandemic, Genes (2025). DOI: 10.3390/genes16080926

Procopius, History of the wars, 2,22-33. (Describes the Plague of Justinian 541-2 A.D). https://plagueanthology.com/2020/04/26/procopius-describes-the-plague-of-justinian-541-2-a-d/

John of Ephesus describes the Justinianic plague. https://www.plu.edu/studyaway/wp-content/uploads/sites/222/2020/09/john-of-ephesus-for-glst.pdf

(1) Wagner, D.M., Klunk, J., Harbeck, M., et al. 2014. Yersinia pestis and the Plague of Justinian 541–543 AD: a genomic analysis. The Lancet infectious diseases, 14(4), pp.319-326. DOI: 10.1016/S1473-3099(13)70323-2

(2) Keller, M., Spyrou, M.A., Scheib, C.L., et al. 2019. Ancient Yersinia pestis genomes from across Western Europe reveal early diversification during the First Pandemic (541–750). Proceedings of the National Academy of Sciences, 116(25), pp.12363-12372. https://doi.org/10.1073/pnas.1820447116

(3) Zonneveld, K.A., Harper, K., Klügel, A., et al. Climate change, society, and pandemic disease in Roman Italy between 200 BCE and 600 CE. Science advances, 10(4), p.eadk1033. DOI: 10.1126/sciadv.adk1033

(4) Harper, K., 2015. Pandemics and passages to late antiquity: rethinking the plague of c. 249–270 described by Cyprian. Journal of Roman Archaeology, 28, pp.223-260. DOI: https://doi.org/10.1017/S1047759415002470

(5) Huebner, S.R., 2021. The “Plague of Cyprian”: A revised view of the origin and spread of a 3rd-c. CE pandemic. Journal of Roman Archaeology, 34(1), pp.151-174. DOI: https://doi.org/10.1017/S1047759421000349

(6) Littman, R.J. and Littman, M.L., 1973. Galen and the Antonine plague. The American Journal of Philology, 94(3), pp.243-255.

(7) Thucydides, History of the Peloponnesian War, 7, 52-53. https://antilogicalism.com/wp-content/uploads/2017/07/history-pelo-war.pdf

(8) Littman, R.J., 2009. The plague of Athens: epidemiology and paleopathology. Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine. 76(5), pp.456-467. https://doi.org/10.1002/msj.20137

(9) Rasmussen, S., Allentoft, M.E., Nielsen, K., et al. 2015. Early divergent strains of Yersinia pestis in Eurasia 5,000 years ago. Cell, 163(3), pp.571-582. doi: 10.1016/j.cell.2015.10.009. Epub 2015 Oct 22.

(10) Valtueña, A.A., Mittnik, A., Key, F.M., et al. 2017. The Stone Age plague and its persistence in Eurasia. Current biology, 27(23), pp.3683-3691. DOI: 10.1016/j.cub.2017.10.025

(11) Rascovan, N., Sjögren, K.G., Kristiansen, K., et al. 2019. Emergence and spread of basal lineages of Yersinia pestis during the Neolithic decline. Cell, 176(1), pp.295-305. DOI: 10.1016/j.cell.2018.11.005

(12) Sikora, M., Canteri, E., Fernandez-Guerra, A. et al. The spatiotemporal distribution of human pathogens in ancient Eurasia. Nature 643, 1011–1019 (2025). https://doi.org/10.1038/s41586-025-09192-8

(13) Pekar, J.E., Magee, A., Parker, E, et al. 2022. The molecular epidemiology of multiple zoonotic origins of SARS-CoV-2. Science, 377(6609), pp.960-966. doi: 10.1126/science.abp8337



30 comments on PubPeer (by: Michael B. Weissman, Poecilimon Heroicus, Neoacanthoparyphium Echinatoides, Rubeotermes Jheringi, Aspergillus Australensis, Nebrioporus Baeticus, Diradops Nishidai, Guatteria Galeottiana, F. Débarre, Macrosiphoniella Ludovicianae)

In the gloomy winter of 1904, tuberculosis was killing one in three people in Denmark. Children coughed blood in handkerchiefs. Families quarantined sick relatives in back rooms, watching them deteriorate over months. The disease had seeped into every corner of life, from schoolrooms and kitchens to the cold sanatoriums that overflowed.

A cure wasn’t coming. Governments offered little help.

Behind his post office counter, postal clerk Einar Holbøll watched families mail Christmas letters they could barely afford. What if each letter- each tiny gesture of holiday goodwill- could help fight the epidemic?

His idea became the first Christmas Seal- a simple stamp that would change how the world funded and raised awareness of TB and lung disease.

Seals for tuberculosis awareness

Holbøll’s first Christmas Seal was humble- a small 2-øre stamp, barely larger than a thumbnail, featuring Queen Louise and the word “Julen” (Christmas). It wasn’t legal postage; it was an extra stamp, a voluntary gesture you added to your holiday letters. Its proceeds went toward building a tuberculosis sanatorium for poor children in Kolding.

Buying one cost almost nothing. That was the point. Yet people bought it eagerly. Some were moved by pity for children dying of tuberculosis, others saw it as a gentle collective act at a time when governments offered little protection. And many simply liked the idea that a holiday letter could carry hope along with good wishes.

Holbøll had shown something profound: ordinary people wanted to help. They just needed a way that felt manageable, seasonal and hopeful.

The idea crossed borders. Christmas Seals, with the double-barred red cross, became one of the world’s earliest micro-donation models: tiny, affordable, and emotionally resonant (1). In the United States, the campaign was spearheaded by Emily Bissell, a Delaware social reformer, who adapted the idea to raise funds for a tuberculosis sanatorium. The National Tuberculosis Association later scaled and professionalized the movement, turning seals into a brand with celebrity endorsements (including by President Roosevelt) and school programs where children learned disease prevention and anti-spitting hygiene.

The funds reshaped public health. They built hospitals, hired visiting nurses, supported research and case finding, and plastered cities with health promotion campaigns (2). It became a movement that, over the decades, raised tens of millions of dollars worldwide- $26 million in the US by 1955 alone- helping to build the basic infrastructure of modern TB control (3).

Art, national identity and politics of a Seal

As Christmas Seals spread across more than 70 countries, each place reimagined them in its own cultural language and popular culture. The designs became mini cultural artifacts- tiny canvases where art, nationalism and medicine converged.

In the US, seals featured religious symbols, cheerful families, and messages framing TB as civic duty.

In Korea, seals often showed children in hanbok or flying kites. Even in illness, there is joy, tradition, and resilience.

China’s designs, produced amid war and displacement, carried a stark urgency. Here, the seal wasn’t just fundraising- it was symbol of national survival: insisting that public health mattered in an era of strife.

These weren’t just pretty pictures. They were visual arguments about what mattered: Was TB a medical problem? A moral duty? A threat to the nation? A test of community solidarity? The seals answered differently in each place- and those answers tell us how societies understood disease, responsibility and hope in their moment.

A quiet legacy from TB to today

Over time, as tuberculosis rates fell in many countries, Christmas Seals quietly shifted focus. The same small stickers that once funded sanatorium beds now support a wider portfolio of lung health: asthma care, smoking cessation and clean air advocacy (4). In Denmark, they now help fund child-welfare services to address bullying, loneliness, and low self-esteem (5). It’s a natural evolution as health priorities shifted.

But TB never fully vanished. It remains one of the world’s leading infectious killers- over 1 million people a year and striking hardest in communities with the fewest resources. Countries worldwide, as members of the International Union against Tuberculosis and Lung Disease, still use seals to fund screening programs and treatment support in high-burden regions. A Christmas Seal’s worth of funding could mean the difference between an early diagnosis and a missed case- between life and death.

Yet the spirit behind Christmas Seals transformed the world.

The idea that millions of small contributions can drive major medical and public-health efforts has grown into a global ecosystem of micro-giving: the Ice Bucket Challenge’s surge of support for ALS, Movember’s seasonal moustaches funding men’s health, (RED)’s micro-purchases supporting HIV/AIDS programs, and one-click donations on WeChat, Alipay and GoFundMe that mobilise millions in moments of crisis. Even telethon traditions like Comic Relief, Red Nose Day, and Stand Up To Cancer still draw on the same collective energy first sparked by those early holiday stamps.

What ties them together is the power of seasonal giving. We respond to rituals: a Christmas letter, a holiday challenge, a familiar symbol that appears only once a year. When generosity is woven into a shared moment; we join in, carried by the feeling that we’re part of something larger than ourselves.

In those darkest winters, progress against TB didn’t rest on wealthy philanthropy alone- it grew from the quiet generosity of ordinary people. Small acts, repeated across each season, slowly bent the course of a disease once believed unbeatable. The same generous care still holds the power to shape what comes next.

And you can be part of it.

Christmas charity appeals 2025:

The Big Give: https://biggive.org/christmas-challenge/

The Patients Association: https://www.patients-association.org.uk/appeal/helpline-christmas-appeal-2025?StartAt=10

UNICEF: https://help.unicef.org/en/doneaza-de-craciun

Baby Lifeline: https://www.babylifeline.org.uk/christmas-appeal-2025

Sense: https://www.sense.org.uk/get-involved/support-us/christmas-appeal-2025

Save the Children Christmas Jumper Day: https://www.savethechildren.org.uk/christmas-jumper-day

Box of Hope: https://www.boxofhope.org/en/

Great Ormond Street Hospital charity: https://www.gosh.org/donate/christmas/

References and Sources:

Edward Wawrzynczak. Tuberculosis, Philately and the history of the ‘Christmas seal’, 29 December 2019. https://bshm.org.uk/tuberculosis-philately-and-the-history-of-the-christmas-seal/

Einar Holbøll. Danish Biographical Lexicon. https://biografiskleksikon.lex.dk/Einar_Holb%C3%B8ll (in Danish)

Loytved, G., 2006. Christmas seals. Pneumologie (Stuttgart, Germany), 60(11), pp.701-710.

The American Lung Association Crusade, University of Virginia Library. https://exhibits.hsl.virginia.edu/alav/index.html

(1) Emerson, K. (1939). The power of the Christmas seal. The Sanitarian, 2(6/7), 10. https://www.jstor.org/stable/26315853

(2) Christmas Seals. (1922). The American Journal of Nursing, 23(3), 229. https://www.jstor.org/stable/3407453

(3) Long, E. R. (1957). Development of the voluntary health movement in America as illustrated in the pioneer National Tuberculosis Association. Proceedings of the American Philosophical Society, 101(2), 141–170. https://www.jstor.org/stable/985505

(4) American Lung Association. https://www.lung.org/get-involved/ways-to-give/christmas-seals/history

(5) JULEMÆRKE FONDEN. https://icapcharityday.com/charities/2022-julem%C3%A6rke-fonden

I first stumbled on the term by accident- “Christmas disease”, buried in some haematology journal during a routine literature search. It sounded festive, almost whimsical, the sort of label invented for a holiday fundraiser.

But the name wasn’t about the season at all. It belonged to a real boy: Stephen Christmas, born in 1947, whose childhood unfolded in hospital wards across Britain and Canada (1).

Stephen bruised easily. An accident with a toy would be enough to leave his hand grotesquely swollen. Winters often meant hospital rather than holidays; instead of playgrounds and snow, there were wards, night-time checks, and parents trying to make sense of a diagnosis that kept changing.

Stephen was treated as just another unfortunate child in a system that barely recognised rare diseases at all. There were few specialists, no registries, no coordinated pathways of care- only a worried family and a boy confronting a condition that defied the medical knowledge of the day.

The case of an impossible clot

Stephen’s case, at first, seemed routine- another child with haemophilia, another family bracing for a lifetime of hospital visits. But when his blood reached the coagulation labs of the 1950s (2), the mystery began.

These labs were spare, improvised spaces: water baths, stopwatches, hand-mixed reagents, and scientists relying as much on intuition as on equipment.

And almost immediately, Stephen’s blood refused to behave.

The available treatments that corrected clotting in other haemophilia patients did nothing for him. Technicians added the usual Factor VIII preparation.

Still no clot.

So they tried a different experiment: cross-mixing studies- combining the plasma of different patients to see which samples corrected what. That was the turning point. The blood of some haemophilia patients fixed Stephen’s clotting… while Stephen’s blood corrected theirs.

The implication was extraordinary: this “single” disease was, in fact, at least two. Stephen wasn’t missing Factor VIII at all, but a different clotting factor entirely.

“Case 1.— The patient was a boy named Christmas, aged 5 years. There was no history of haemorrhage in other members of the family. He had numerous episodes of haemorrhage dating from the age of 20 months, mostly resulting from injuries during play. He was transfused on numerous occasions; each transfusion resulted in abrupt cessation of bleeding”. (2).

It was far more than an oddity from a clinical case. It was a boy with a name, who rewrote the definition of haemophilia itself.

From family curse to health system

For most of history, haemophilia lived in the shadows. It was already whispered about in Europe’s royal houses as “the royal disease”. Through Queen Victoria’s descendants, it appeared in princes of Britain, Russia, and Spain. Families knew it as a hidden inheritance: boys who bruised and bled, mothers and sisters carrying a risk they couldn’t see. Most historians now think that the royal form was the same broad family as Stephen’s- haemophilia B, or “Christmas disease” (3).

For decades though, all haemophilia was lumped together. Stephen’s blood helped reveal that it wasn’t. Haemophilia A is caused by a deficiency in Factor VIII. Stephen belonged to a smaller group missing Factor IX. Clinically the two looked similar, but biologically they were distinct- different genes, different laboratory tests, different treatment needs.

Once doctors could distinguish haemophilia A from B, the disorder became something that could be classified, tracked, and planned for.

By the 1960s and 70s, new factor concentrates transformed treatment. People who once faced years in hospital could return to school and work. But those “miracle” products forced health systems to reform too. Who needed which treatment? Which families carried which subtype? Countries began building specialist haemophilia treatment centers, hiring multidisciplinary teams- nurses, physiotherapists and genetics counsellors- and, crucially, creating registries like the UK National Haemophilia Database in 1968 to keep track.

A rare, almost mythic “family curse”, from palaces to council houses, was slowly becoming a public health category- something that required planning, surveillance, and lifelong follow-up, not just hospital care.

The gift carried a virus

By the late 1970s, haemophilia treatment had shifted to small vials of concentrated clotting factor that patients could use at home. It was practical and life-changing. But these concentrates were made from large pooled batches of donated plasma- a manufacturing breakthrough that carried a hidden danger.

If even one donation contained an undetected virus, the entire batch- and everyone treated from it- was at risk.

And that’s exactly what happened. In the late 1970s and early 1980s, two viruses slipped silently into global blood supplies: HIV and hepatitis C. Screening tests didn’t yet exist. Donor-risk policies were patchy, inconsistent and often politically fraught. As the epidemic spread, some 10,000 people with haemophilia- including those same children finally been given a chance to live their normal lives- became some of the earliest and hardest-hit victims.

Stephen Christmas was among them. The treatment that had transformed his livelihood ultimately infected him with HIV. He died in 21^st December, 1993, four days short of seeing another Christmas.

The blood scandal that called for change

The scandal that followed was immense. In the UK, France, Japan, Canada, and the US, families demanded answers. Inquiries that lasted years uncovered delays, denial, and slow adoption of safety measures. Governments had underestimated the risk; manufacturers failed to act decisively; health systems had no real mechanisms for early warning or transparency.

But out of that tragedy came sweeping reforms. Those once assumed safe were subjected to universal blood screening, stricter donor deferral policies, and expanded surveillance systems (4). Patients information and consent- long treated as afterthoughts- were finally taken seriously.

A small patient community had paid a terrible price. But their fight reshaped global blood safety, protecting millions who might never know their names.

The meaning of Christmas disease

Today, haemophilia B stands at the edge of another transformation. Gene therapies delivering Factor IX promise to replace the weekly blood infusions that once defined patients’ lives (5). Some trials report near-normal clotting after a single dose. But these breakthroughs raise a familiar question: who gets access first? (6). In many countries, only a minority of people with haemophilia ever reach a specialist center, let alone a gene-therapy program. The promise of a one-time cure risks becoming another story of privilege rather than progress.

Blood safety, too, can never be taken for granted. Emerging viruses continue to test the systems built after the contaminated-blood scandals (7). Climate change, political instability and fragile supply chains can make even well-designed infrastructures brittle. Complacency remains the greatest threat to a safe blood supply.

And then there’s memory. Many clinicians know “Christmas disease”, but few know the boy behind the name- or that he died after contracting HIV from the very treatment meant to protect him. His story is a reminder that only patient-centered care keeps innovation aligned with the people it’s meant to serve.

Christmas disease is the echo of one child’s life. Every diagnostic label began with a person, and the systems we build should honour their experiences. As gene therapies and new biologics reshape medicine again, we cannot lose sight of the patient behind the science.

Sources and References:

Mannucci, P.M., 2023. Hemophilia treatment innovation: 50 years of progress and more to come. Journal of Thrombosis and Haemostasis, 21(3), pp.403-412. https://doi.org/10.1016/j.jtha.2022.12.029

Hemophilia: From Plasma to Recombinant Factors. American Society of Hematology, 2008. https://www.hematology.org/about/history/50-years/hemophilia

Lee, C.A., 2009. The best of times, the worst of times: a story of haemophilia. Clinical medicine, 9(5), pp.453-458. doi: 10.7861/clinmedicine.9-5-453

Kumanan Wilson, M.D., 2007. The Krever Commission-10 years later. Canadian Medical Association. Journal, 177(11), p.1387. DOI: https://doi.org/10.1503/cmaj.071333

Can another infected blood scandal be averted?. The Lancet. Infectious diseases, 24(7), 2024. p.665.

(1) From eponym to advocate: The story of Stephen Christmas. Hektoen International. https://hekint.org/2020/01/22/from-eponym-to-advocate-the-story-of-stephen-christmas/

(2) BIGG, R., Douglas, A.S., MACFARLANE, R., DACIE, J., PJTITOY, W., MERSKEY, C. and O’BRIEN, J.R., 1952. Christmas disease; a condition previously mistaken for hemophilia. BMJ, 2, p.137S. https://doi.org/10.1136/bmj.2.4799.1378

(3) Rogaev, E.I., Grigorenko, A.P., Moliaka, Y.K., Faskhutdinova, G., Goltsov, A., Lahti, A., Hildebrandt, C., Kittler, E.L. and Morozova, I., 2009. Genomic identification in the historical case of the Nicholas II royal family. Proceedings of the National Academy of Sciences, 106(13), pp.5258-5263. https://doi.org/10.1073/pnas.0811190106

(4) de Jonge, L.L., Wiersum-Osselton, J.C., Bokhorst, A.G., Schipperus, M.R. and Zwaginga, J.J., 2022. Haemovigilance: current practices and future developments. Annals of Blood, 7, p.6918. doi: 10.21037/aob-22-2

(5) Pipe, S.W., et al. 2023. Gene therapy with etranacogene dezaparvovec for hemophilia B. New England Journal of Medicine, 388(8), pp.706-718. DOI: 10.1056/NEJMoa2211644

(6) Mahlangu, J., 2025. Haemophilia and access to gene therapy. EBioMedicine, 115.

(7) Almeida, F.J., Pacheco, J.T., Farias, C.G.A., de Matos, S.F., de Morais, C.O., Guerra, G.G., Dos Santos, A.C.C., Jarovsky, D., Bezerra, R.F., Furlanetto, B.H.S. and Oliveira, D.B.L., 2025. Dengue: a hidden threat in blood transfusions amidst Brazil’s largest outbreak?. The Lancet Infectious Diseases, 25(1), p.e10.