The Pellagra Experiments: Orphanages, a Prison Farm and the Filth Parties

In February 1914 the United States Public Health Service handed Dr. Joseph Goldberger a disease that was killing thousands of people a year across the American South and that nobody could explain. Pellagra announced itself with a rough, burn-like rash on the backs of the hands, the neck and the feet, then brought diarrhoea, confusion and, in the worst cases, death. Most experts of the day believed it was an infection or a poison carried in spoiled corn. Within about four months Goldberger had reached a different conclusion: pellagra came from what people ate, and from what they could not afford to eat.

This page follows the experiments of 1914 to 1916 that turned that idea into evidence: the epidemiological clues he noticed in institutions, the diet trials in two Mississippi orphanages and a Georgia asylum, the 1915 experiment on volunteer convicts at the Rankin State Prison Farm, the “filth parties” of 1916 in which he and his colleagues tried and failed to infect themselves, and the survey of seven South Carolina cotton-mill villages that tied pellagra to family income and food supply. It ends with a plain account of who the subjects were and how they came to take part, judged by the record rather than by later rules. The man himself, the food science and the later discovery of niacin each have their own pages in this wing.

Table of Contents

  1. An Epidemic in the American South
  2. Pellagraphobia and the Rival Theories
  3. The First Clues of 1914
  4. Diet Trials in Mississippi Orphanages
  5. The Georgia State Sanitarium
  6. The Rankin State Prison Farm Experiment, 1915
  7. The Transmission Experiments of 1916
  8. Seven Cotton-Mill Villages with Edgar Sydenstricker
  9. Income, Food Supply and Pellagra
  10. Subjects, Consent and the Standards of the Time
  11. Key Research Papers
  12. Connections

1. An Epidemic in the American South

Pellagra was an old disease in Europe but a new one in the United States. Physicians in eighteenth-century Spain and Italy had described it among poor peasants who lived largely on maize, the corn plant brought from the Americas. In the United States the first reports came in 1902, and over the next two decades the disease spread into an epidemic across the Southern states. It was concentrated among the rural poor, tenant farmers, cotton-mill workers and the residents of orphanages, asylums and prisons.

Doctors summarised its course as the “four Ds”: dermatitis, a symmetrical rash on skin exposed to the sun; diarrhoea; dementia, ranging from depression and confusion to psychosis; and finally death. The rash was so characteristic that it gave the disease its name, from the Italian pelle agra, “rough skin”.

The scale of the epidemic is hard to overstate. The historian Harry Marks estimates that pellagra caused at least 100,000 deaths in the Southern United States between 1900 and 1940, and that about half of its victims were African American and more than two-thirds were women. Charles Bryan and Shane Mull, writing in 2015, put the toll at its peak at 7,000 or more deaths a year across fifteen Southern states. Many thousands more lived with recurring rashes, chronic digestive illness and mental decline, and state asylums filled with pellagra patients.

The disease returned with the seasons. Cases rose in late winter and spring, faded through summer and autumn, and came back the next year. That pattern, which looked like the behaviour of an insect-borne fever, was one reason so many investigators were convinced that pellagra was catching.

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2. Pellagraphobia and the Rival Theories

Because no one knew what caused pellagra, people feared it. Historians describe a “pellagraphobia” in the South of the 1910s: people with pellagra were shunned and isolated, as though the disease were catching. Kumaravel Rajakumar’s 2000 history of pellagra in the United States describes how the fear of contagion added social exclusion to the illness itself.

The spoiled-corn theory

The oldest explanation came from Italy. A school of Italian physicians held that pellagra was caused by a toxin in damaged or mouldy maize. The link with corn was real — pellagra followed maize wherever it became the staple of the poor — but the toxin was never found, and the theory could not explain why some corn eaters fell ill and others did not.

Sambon’s insect theory

Louis Sambon, a physician working in tropical medicine, argued instead that pellagra was an infection spread by an insect, much as malaria and yellow fever had recently been shown to be. David Gentilcore’s 2016 study in the Journal of the History of Medicine and Allied Sciences traces how Sambon’s theory clashed with the Italian maize school between 1905 and 1914 and how it found a sympathetic hearing in the United States. The seasonal pattern and the rural setting of the disease seemed to fit.

Funk’s “vitamine” idea

A third possibility was new. In 1912 the biochemist Casimir Funk proposed that several diseases, beriberi and scurvy among them, were caused by the lack of tiny amounts of essential substances in food, which he called “vitamines”, and he included pellagra on his list. Bryan and Mull show that the same year the British physician Fleming Sandwith and the US Surgeon General Rupert Blue both put the “vitamine hypothesis” for pellagra into words in the United States, two years before Goldberger began his work. The idea existed; what it lacked was proof.

The Thompson-McFadden Commission

The most thorough American study before Goldberger was made by the privately funded Thompson-McFadden Pellagra Commission, whose investigators Joseph Siler, Philip Garrison and Ward MacNeal studied six cotton-mill villages around Spartanburg, South Carolina, between 1912 and 1914. According to the 2014 comparison by Stephen Mooney, Justin Knox and Alfredo Morabia, the Commission concluded that pellagra was probably an infectious disease. Bryan and Mull argue that the authority of this conclusion slowed the acceptance of the dietary explanation and cost lives in the years that followed; that is their judgement, and Mooney and colleagues give a more detailed account of why two careful investigations of the same villages reached opposite answers.

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3. The First Clues of 1914

Goldberger was directing a diphtheria study in Detroit in the winter of 1913–14 when Surgeon General Blue asked him to take over the Public Health Service pellagra programme. He was appointed in February 1914. He was an infectious-disease man by training — he had worked on yellow fever, typhus and measles — and nothing in his record suggested he would turn to diet.

He began by visiting the institutions where pellagra was rife and looking at who fell ill. The decisive observation was simple. In orphanages, asylums and prisons, inmates developed pellagra, sometimes in large numbers, but the nurses, attendants and staff who lived and worked beside them did not. If pellagra were an infection passed from person to person, or carried by insects through the wards, the staff would have caught it too. The difference between the two groups was not exposure; it was the food. Staff ate differently, while inmates lived largely on corn bread, corn grits, fat pork and molasses, with little fresh meat, milk or vegetables.

By June 1914, about four months after his appointment, Goldberger had reached his conclusion, and he set out his reasoning in his first pellagra paper, “The Etiology of Pellagra: The Significance of Certain Epidemiological Observations with Respect Thereto”, published in Public Health Reports that year. He argued that the disease was not communicable and that it was caused by a faulty diet, and that it could therefore be prevented by a better one. The paper was short and rested on observation, not experiment. The experiments came next.

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4. Diet Trials in Mississippi Orphanages

The first test was made in two orphanages in Jackson, Mississippi, from the summer of 1914. In his 2008 account in the Journal of the Royal Society of Medicine, the epidemiologist Alfredo Morabia records that by 15 September 1914 one of the two orphanages (labelled “MJ” in Goldberger’s reports) had had 79 cases of pellagra and the other (“BJ”) 130 cases.

The children’s diet was changed. Goldberger did not add a medicine. He increased the fresh animal and leguminous protein foods — milk, buttermilk, eggs, beans and peas — and reduced the share of corn. The rest of the children’s lives, including their housing and sanitation, was left as it had been.

The result, reported by Goldberger with C. H. Waring and David Willets in “The Treatment and Prevention of Pellagra” later in 1914 and followed up over the next year, was striking. Children who had had pellagra did not relapse in the following spring, the season when the disease usually returned, and virtually no new cases appeared. In institutions where pellagra had been a yearly event, a change of menu had made it disappear.

Goldberger recognised that an orphanage study had a weakness: it could show that a better diet prevented pellagra, but it could not by itself show that a poor diet caused it. That question shaped the prison-farm experiment the following year.

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5. The Georgia State Sanitarium

The second trial took place in the Georgia State Sanitarium, which Morabia describes as the largest asylum in the South, beginning in late 1914. Here Goldberger was able to make a comparison inside a single institution. Women patients who had had pellagra were divided between wards that received the improved diet and wards that continued on the usual asylum fare.

According to Morabia’s account, none of the 36 Black women and 36 white women given the new diet had a recurrence of pellagra, whereas about 47 per cent of the comparable patients in the wards whose diet was left unchanged had a recurrence. Because both groups lived in the same building, under the same sanitation and with the same exposure to any insects or infection, the difference pointed squarely at the food.

The final institutional report, 1923

Goldberger kept the institutional studies running for years. In 1923, with Waring and W. F. Tanner, he published the final report, “Pellagra Prevention by Diet among Institutional Inmates”. Morabia summarises it: among 414 people who had had pellagra and 288 who had not, only a single recurrence was recorded while the improved diet was maintained. Morabia quotes two of the report’s conclusions: “Pellagra may be completely prevented by diet” and “The idea that pellagra is a communicable disease receives no support from this study.”

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6. The Rankin State Prison Farm Experiment, 1915

To show that a poor diet could cause pellagra in healthy people, Goldberger needed volunteers who would eat that diet under observation. He found them at the Rankin State Prison Farm in Mississippi. The Governor of Mississippi, Earl Brewer, agreed to offer pardons to white male convicts who volunteered for the experiment. Eleven healthy volunteers took part.

The men were placed on a restricted diet built on corn: corn bread, grits and other corn products, with fat meat and syrup, but without fresh meat, milk or fresh vegetables — essentially the diet of the poorest Southern households and institutions. The experiment ended in late October 1915.

A count that sources give differently

Some of the volunteers developed the skin lesions of pellagra, together with digestive and nervous complaints. Exactly how many is reported differently in the secondary literature: some accounts say five of the eleven, others six. What the accounts agree on is that pellagra appeared in roughly half of the men on the corn diet. Goldberger and G. A. Wheeler reported the experiment in Public Health Reports in November 1915, and a fuller account, “Experimental Pellagra in White Male Convicts”, appeared in the Archives of Internal Medicine in 1920. The result was also announced to the press in November 1915.

The experiment had limits that historians have pointed out. Bryan and Mull note confounding factors: the volunteers’ conditions included confinement indoors, and their diet included coffee, either of which could have played a part. Lucius Lampton’s 2005 article in the Journal of the Mississippi State Medical Association revisits the Rankin experiment and the 2003 biography by Alan Kraut that describes it in detail. The experiment did not settle the debate on its own, because it left open the possibility that an infection was also involved. Goldberger’s answer to that possibility was the transmission experiments of 1916.

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7. The Transmission Experiments of 1916

If pellagra were infectious, it ought to be possible to pass it from a patient to a healthy person. Between April and June 1916, Goldberger set out to test that directly, using himself and his colleagues as subjects. The sessions became known as the “filth parties”.

According to the account by the science writer Sam Kean for the Science History Institute, there were eight sessions with about seventeen participants in all (other sources give sixteen), including Goldberger, his wife Mary, and fellow Public Health Service physicians. Material from people with active pellagra was introduced into the volunteers by every route an infection might take. Blood from patients was injected; secretions from patients’ noses and throats were swabbed into the volunteers’ own; and scabs from pellagra rashes, together with urine and faeces from patients, were mixed with flour into pills and swallowed. Mary Goldberger received an injection of a patient’s blood.

None of the volunteers developed pellagra. Goldberger reported the results in Public Health Reports in November 1916 under the title “The Transmissibility of Pellagra: Experimental Attempts at Transmission to the Human Subject”. Leslie Klevay, revisiting the paper in 1997 in the Journal of Nutrition, gave his commentary the title “Pellagra is not infectious!”

The experiments were a negative result, and a negative result can never prove absolutely that a disease is not infectious. But together with the institutional trials and the prison-farm experiment they made the case for an infectious cause very hard to sustain. They are also among the best-known episodes of self-experimentation in the history of medicine — recorded here as history, not as a procedure.

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8. Seven Cotton-Mill Villages with Edgar Sydenstricker

The institutional studies showed what diet could do inside an orphanage or an asylum. The next question was whether diet explained pellagra in ordinary communities. In 1916 Goldberger, the Public Health Service physician G. A. Wheeler and the Service’s statistician Edgar Sydenstricker began a study of seven cotton-mill villages in the Spartanburg area of South Carolina — the same district the Thompson-McFadden Commission had studied.

Sydenstricker brought an economist’s eye to the problem. In 1915 he had already published “The Prevalence of Pellagra: Its Possible Relation to the Rise in the Cost of Food”, linking the growth of the epidemic to rising food prices. The mill-village study was designed to measure the link household by household.

The main fieldwork ran from 16 April to 15 June 1916, the season when pellagra peaked, and the surveillance continued in the following years. The team visited every household, recorded each case of pellagra, and collected detailed information on what the family ate. Mooney, Knox and Morabia describe how food intake was estimated over fifteen-day periods, using the purchase records of the village stores where mill families bought their food, together with interviews with the women who ran the households. They also recorded household size, earnings, sanitation and housing.

The design was what modern epidemiologists would recognise as a population survey with a careful measure of exposure. Mooney and colleagues, contrasting it with the Commission’s work in the same villages, point to the quality of the dietary information as the key difference: the Commission had looked closely at sanitation and at contact between cases, while the Public Health Service team measured food.

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9. Income, Food Supply and Pellagra

The results were published in two papers in Public Health Reports in 1920. The first, on diet, found that pellagra was concentrated in households whose diet was poor in fresh meat, milk and other animal protein foods, and that households with a more varied supply of these foods had much less of it. The second, “A Study of the Relation of Family Income and Other Economic Factors to Pellagra Incidence in Seven Cotton-Mill Villages of South Carolina in 1916”, showed that pellagra fell steadily as family income rose. The poorest households had by far the most cases.

The team also looked at the factors the infectious theory relied on. According to Mooney and colleagues’ analysis of the study, sanitation did not explain the pattern. What mattered was whether a family could buy, or produce, fresh meat and milk: pellagra was tied to a limited local supply of these foods as well as to low income.

The study turned pellagra into a question of economics as well as nutrition. A family living on low mill wages, buying from a store that stocked mainly corn meal, fat pork and syrup, ate the diet that the Rankin volunteers had eaten — and fell ill in the same way. Elmore and Feinstein, writing in the Annals of Internal Medicine in 1994, called Goldberger an “unsung hero of American clinical epidemiology” largely on the strength of studies like this one.

Historians have also examined what the economic framing left out. Marks argues that Sydenstricker’s emphasis on income and food supply, influential as it was, tended to obscure the roles of race and gender in who got pellagra — including the fact that women made up the great majority of victims. The way that later research turned these findings into a named food factor, and finally into niacin, is told on the Corn, Brewer’s Yeast and the P-P Factor and Goldberger’s Legacy pages.

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10. Subjects, Consent and the Standards of the Time

The people in Goldberger’s experiments were, for the most part, people with little power over their own lives. The diet trials were carried out on orphaned children and on asylum patients, who could not refuse the arrangements made by the institutions that housed them. In those trials the change was an improvement — more milk, eggs, beans and peas — but the asylum comparison depended on patients in the other wards continuing on the diet that was thought to cause the disease, and nearly half of them had a recurrence.

The Rankin volunteers were convicts, and what they were offered in return for eating a diet expected to make them ill was their freedom. The pardons were promised by the governor in advance. The men agreed to take part, but the offer of release to prisoners is the kind of inducement that later codes of research ethics treat as a reason to question whether consent is freely given. Several of the men developed the disease the experiment was designed to produce.

The transmission experiments, by contrast, were carried out on willing professionals who understood the risk, starting with Goldberger himself. Self-experimentation was an accepted, even admired, tradition in the medicine of the time; Goldberger had already caught yellow fever, dengue and typhus in the course of his earlier field work.

Formal written codes for research on human subjects, with independent review and documented informed consent, came decades later. Goldberger’s studies were carried out under the rules of their own time, and the prison experiment depended on the governor’s offer. The record shows both things: experiments that settled the cause of a disease that was killing thousands each year, and subjects — children, asylum patients and prisoners — whose part in them was set by their circumstances.

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Key Research Papers

  1. Goldberger J. The Etiology of Pellagra: The Significance of Certain Epidemiological Observations with Respect Thereto. Public Health Reports. 1914;29(26):1683. DOI: 10.2307/4570920
  2. Goldberger J. The etiology of pellagra. 1914. Public Health Rep. 2006;121 Suppl 1:77-9; discussion 76. (2006 reprint of the 1914 paper.) PubMed PMID: 16550768
  3. Goldberger J, Waring CH, Willets DG. The Treatment and Prevention of Pellagra. Public Health Reports. 1914;29(43):2821. DOI: 10.2307/4571457
  4. Goldberger J, Waring CH, Tanner WF. Pellagra Prevention by Diet among Institutional Inmates. Public Health Reports. 1923;38(41):2361. DOI: 10.2307/4576901
  5. Goldberger J, Wheeler GA. Experimental Pellagra in the Human Subject Brought about by a Restricted Diet. Public Health Reports. 1915;30(46):3336. DOI: 10.2307/4572984
  6. Goldberger J. Experimental Pellagra in White Male Convicts. Archives of Internal Medicine. 1920;25(5):451. DOI: 10.1001/archinte.1920.00090340002001
  7. Goldberger J. The Transmissibility of Pellagra: Experimental Attempts at Transmission to the Human Subject. Public Health Reports. 1916;31(46):3159. DOI: 10.2307/4574262
  8. Sydenstricker E. The Prevalence of Pellagra: Its Possible Relation to the Rise in the Cost of Food. Public Health Reports. 1915;30(43):3132. DOI: 10.2307/4572933
  9. Goldberger J, Wheeler GA, Sydenstricker E. A Study of the Relation of Diet to Pellagra Incidence in Seven Textile-Mill Communities of South Carolina in 1916. Public Health Reports. 1920;35(12):648. DOI: 10.2307/4575517
  10. Goldberger J, Wheeler GA, Sydenstricker E. A Study of the Relation of Family Income and Other Economic Factors to Pellagra Incidence in Seven Cotton-Mill Villages of South Carolina in 1916. Public Health Reports. 1920;35(46):2673. DOI: 10.2307/4575780
  11. Morabia A. Joseph Goldberger’s research on the prevention of pellagra. J R Soc Med. 2008;101(11):566-8. PubMed PMID: 19029358
  12. Mooney SJ, Knox J, Morabia A. The Thompson-McFadden Commission and Joseph Goldberger: contrasting 2 historical investigations of pellagra in cotton mill villages in South Carolina. Am J Epidemiol. 2014;180(3):235-44. PubMed PMID: 24966221
  13. Bryan CS, Mull SR. Pellagra Pre-Goldberger: Rupert Blue, Fleming Sandwith, and The “Vitamine Hypothesis”. Trans Am Clin Climatol Assoc. 2015;126:20-45. PubMed PMID: 26330657
  14. Gentilcore D. Louis Sambon and the Clash of Pellagra Etiologies in Italy and the United States, 1905-14. J Hist Med Allied Sci. 2016;71(1):19-42. PubMed PMID: 25740951
  15. Rajakumar K. Pellagra in the United States: a historical perspective. South Med J. 2000;93(3):272-7. PubMed PMID: 10728513
  16. Marks HM. Epidemiologists explain pellagra: gender, race, and political economy in the work of Edgar Sydenstricker. J Hist Med Allied Sci. 2003;58(1):34-55. PubMed PMID: 12680009
  17. Klevay LM. Pellagra is not infectious! (Goldberger, 1916). J Nutr. 1997;127(5 Suppl):1032S-1034S. PubMed PMID: 9164297
  18. Lampton L. “Goldberger’s War” in Mississippi: the 1915 Pellagra Experiment at Rankin State Farm and a new book. J Miss State Med Assoc. 2005;46(2):44-7. PubMed PMID: 15816234
  19. Elmore JG, Feinstein AR. Joseph Goldberger: an unsung hero of American clinical epidemiology. Ann Intern Med. 1994;121(5):372-5. PubMed PMID: 8042827
  20. Hegyi J, Schwartz RA, Hegyi V. Pellagra: dermatitis, dementia, and diarrhea. Int J Dermatol. 2004;43(1):1-5. PubMed PMID: 14693013

PubMed Topic Searches

  1. Goldberger pellagra
  2. Pellagra history
  3. Pellagra epidemiology, South Carolina
  4. Niacin deficiency and pellagra

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Connections