During the Second World War, Trowell also sent liver specimens to Professor Harold Himsworth at the University College in London. Himsworth became interested in Trowell’s work when, in the context of wartime rationing, he was asked to determine the dietary protein requirements of young children. As very little was then known about the repercussions of protein deficiency, Himsworth began conducting experiments with rats and found that, like Trowell’s patients, when deprived of protein they developed a fatty liver, discolored hair, and even slight edema.48 Himsworth then became a key advocate of Trowell’s work. Trowell preserved the liver specimens from his severely malnourished patients in his home refrigerator until they could be transported to England: “I would keep the bit refrigerated until I could take it to the plane, in the hope that it hadn’t ‘gone bad’, as you might say, by the time it got to London. I’d put some of it in pickle sometimes.”49 He would, of course, as he later explained, warn his wife by letting her know “look, you mustn’t let the boys cook this.”50 What the “boys” who cooked for Trowell and his family thought of the pickled liver specimens that were kept in the home refrigerator will probably never be known. It is, nonetheless, likely that such practices spurred scandalous rumors about the colonial medical officer conducting research on severely malnourished children.
The breakthrough in the search for the etiology of the condition finally came at the end of the Second World War when a new pathologist, Jack Davies, joined the staff at Mulago. Davies was already aware of Trowell’s nutritional research before he arrived in Uganda, and, unlike his predecessor, was eager to assist in future nutritional studies. He immediately agreed to conduct thorough postmortem examinations, and in the first child he examined, Davies found the long-awaited pathological link between the highly fatal condition and protein deficiency. The child’s pancreas was atrophied and the degenerate condition of the pancreatic cells indicated that the child’s pancreas had not been secreting digestive enzymes. This crucial discovery appeared to substantiate Williams’s protein hypothesis, as enzyme synthesis is dependent on adequate supplies of dietary protein. It was then that, in order to honor Williams and her foresight, Trowell began to refer to the condition as kwashiorkor. Pancreatic atrophy also explained why severely malnourished children were not easily treated. Even protein-rich foods like milk were of limited therapeutic value without sufficient protein to produce the digestive enzymes needed to breakdown and absorb essential nutrients. It was a vicious cycle: children suffering from severe acute malnutrition simply could no longer fully digest and absorb the food they consumed.51
To verify that the pancreatic atrophy occurred prior to death and not as part of a process of rapid decomposition, it was necessary to perform further autopsies within twenty minutes of the child’s death. This was not possible during the day when both Trowell and his colleagues were needed in the hospital wards. “It was possible at night if,” as Davies explained, he and Trowell “coordinated well.” Trowell would inform Davies that “he had a dying child expected to die in the night . . . [and Davies] would wait ready in the morgue . . . till a scuffle outside indicated Hugh’s arrival with the body of the sad victim he had pronounced dead only a few minutes before.”52 So little time had passed between when the children were pronounced dead and their delivery to the morgue that according to Davies, “usually the muscle twitched as [he] rapidly did a postmortem getting the essential organs into fixative as the time dictated.”53 Trowell and his colleagues were aware of the sensitivity that such work required and did take precautions. They would only remain in the morgue long enough to get the specimens into the fixative, and would wait until the next morning when they were delivered to the laboratory to analyze them. “For,” as Davies explained, “never were Europeans allowed by the staff to carry anything other than papers from the morgue. This was in deference to local feelings. . . . Autopsies performed by Europeans in Mulago Hospital were closely watched, as were the pathologists. It would have been a very upsetting thing if a new pathologist, lithe and slender had become stout for the darkest suspicions would be aroused.”54 In the end, as we will see, such precautions proved to be insufficient and did little to assuage a growing set of local concerns.
This important development in the long search for the etiology of kwashiorkor came at a significant moment in the rise of international medicine. In October 1949, an Expert Committee on Nutrition formed jointly by the United Nations Food and Agricultural Organization (FAO) and the World Health Organization (WHO) held its first meeting in Geneva. Kwashiorkor, described as “one of the most widespread nutritional disorders in tropical and sub-tropical areas,” was high on the agenda, and Trowell was asked to prepare a memorandum on the condition for the committee’s consideration.55 The committee resolved to conduct an investigation of kwashiorkor in sub-Saharan Africa beginning with a visit to Mulago Hospital in order to first consult Trowell and his colleagues in Uganda. The subsequent WHO report, Kwashiorkor in Africa, was based in large part on evidence from Mulago and became the seminal study in the growing international focus on protein malnutrition.56 A second meeting of the Joint FAO/WHO Expert Committee on Nutrition centered largely on discussions of this seminal report, concluding with a resolution to conduct further surveys.57 Delegations later sent to Central America and Brazil confirmed that kwashiorkor was a worldwide problem requiring immediate action.58
The pathological evidence that appeared to connect the condition to protein deficiency did not immediately gain widespread acceptance, however, especially in Uganda. The pancreatic atrophy explained why it was so difficult to treat severely malnourished children, but it did not provide a clear way to address this problem. Experiments with pounded steak and desiccated hog stomach were disappointing and, in Uganda, as Davies later explained, they simply “had no special high protein material to feed the children.”59 Ongoing therapeutic failure fueled doubts that were compounded when the pancreatic atrophy found at autopsy could not be independently verified. At the time it was not known that the changes to the pancreas were only visible in children who died prior to receiving any treatment. The rapid recovery of the pancreas in children given sufficient milk reversed the signs of pancreatic atrophy found by Davies and Trowell.60 The next step was to examine the secretion of pancreatic enzymes, and the British Medical Research Council (MRC), now headed by Himsworth, sent an expert who had been working on a new procedure to extract the contents of the small intestine from a tube inserted through the stomach with the guidance of an x-ray. The procedure furnished further evidence that the production of digestive enzymes was severely suppressed in children suffering from severe malnutrition. But before they had a chance to complete the analysis of their findings and publish the results, nutritional research in Uganda was swept up in a political insurrection with far-reaching consequences for future medical research in the region. As it turns out, this further extraction of fluids and tissues from severely malnourished children, who had very slim chances of survival, may have actually done more harm than good.
Muwazi and the Insurrection of 1949
On April 25, 1949, thousands of Ugandans gathered at the central palace of the kabaka, the king of Buganda. By 10:00 a.m., an estimated four thousand people were reportedly pressing against the palace gates. Leaders of the political organizations representing the protesters were allowed to enter the palace and present the kabaka with a set of demands, but tensions remained high, and more than a thousand people reassembled at the kabaka’s palace early the next morning. Attempts to disperse them with baton charges erupted in violence. Arson and looting spread rapidly throughout the Ugandan capital and into the outlying districts of the south-central Kingdom of Buganda and continued for several days.61 The violence explicitly targeted the property of specific individuals, including members of the Ganda chiefly class, elite Ganda officials, the Indian community, and a Ugandan doctor, Eria Muwazi.62 Muwazi was at the central Ugandan hospital on Mulago Hill when news broke that his property and home had been destroyed. Muwazi feared that he and his family were in imminent danger and unsuccessfully sought police protection.63 He believed he was “a marked man” because, as another medical officer reported, “Muwazi is said to kill children by taking blood.”64
Mounting dissatisfaction with the ongoing experimentation on severely malnourished children who continued to die converged, in the late 1940s, with political unrest, contributing to what