The man who became the central figure in this diagnostic dispute was Hugh Trowell. Trowell first encountered children suffering from severe malnutrition in the early 1930s while stationed in the neighboring British colony of Kenya. Trowell was so inspired by the idealism of the interwar period and the creation of the League of Nations that he joined the colonial medical service immediately after completing his medical degree in the late 1920s. In Kenya, Trowell very quickly ran afoul of the settler politics limiting the provision of medical care, and he was transferred from his rural outpost to Nairobi where, in the context of the Great Depression, he expected to be dismissed from colonial service and sent home. A senior official who shared Trowell’s interest in public health instead put Trowell in charge of a newly created African medical training program. Training African medical personnel beyond the level of hospital assistant did not have the support in Kenya that it did in Uganda. Reluctance to allow Trowell’s medical students into the wards of the African hospital in order to obtain the necessary clinical experience forced Trowell to demand that he be given his own ward. When he first went to visit the pediatric department to which he’d been assigned, he found “about two children in each bed, and one underneath. Quite a number had brown hair. Some had swollen legs . . . and some were crying [and] moaning.” Trowell later looked back on this moment as the first time that he came face to face with children exhibiting the classic symptoms of severe acute malnutrition.9
The consensus in Kenya was that these children were suffering from parasitic infections, especially hookworm. The problem with this diagnosis was that deworming medications did little to improve their chances of survival. Treatment failure was not only the linchpin in efforts to nail down the condition’s etiology, but it also did little to encourage parents to bring their severely malnourished children to the hospital. Nor did it persuade parents to allow their children to be subjected to experimental procedures of limited apparent therapeutic value. In one of his earliest publications on the condition, Trowell reported that mothers were, as he put it, among “the greatest obstacles in the treatment. It proved necessary in these cases to separate completely the mother and child and to forbid suckling.”10 Only ten of the twenty-six children Trowell attempted to treat in this early study achieved a full recovery, and these were children brought to the hospital at an early stage of their illness. None of those who arrived severely malnourished survived. According to Trowell, five children “were discharged by impatient parents in an improved condition” but with an uncertain long-term prognosis, as “it usually proved impossible to detain them or secure their re-attendance.”11 Any resistance or reluctance on the part of parents is hardly surprising, given that Trowell later estimated he lost as many as three-quarters of his severely malnourished patients at this time. The largely futile attempts to treat the children in his care led Trowell to begin to suspect that he was dealing with a new disease.12 Postmortem examinations conducted with the limited resources at his disposal revealed only that the children had an enlarged liver that was infiltrated with fat.13
A colonial medical officer stationed across the continent also became convinced that she was dealing with a new illness. Cicely Williams observed that the severely malnourished children at a children’s hospital in present-day Ghana had been fed a diet deficient in protein and she was the first to propose that the condition was a form of severe malnutrition. Her seminal article on the condition documented how the provision of a milk-based, varied diet appeared to reverse many of the symptoms. In the end all but one of the children later died, but the visible improvement of their health in response to a high-protein diet led Williams to conclude that protein deficiency was to blame. Her hypothesis challenged the accepted diagnosis of experts in the burgeoning field of nutritional science. Hugh Stannus, who identified the condition as the vitamin B deficiency, pellagra, while working in present-day Malawi over a decade before, promptly published a review refuting Williams’s evidence.14 Williams responded with a second article in the preeminent British medical journal, the Lancet, delineating the significant distinctions between pellagra and the condition, which she then referred to as kwashiorkor, the local name for the condition in Ghana.15
The debate between Williams and Stannus reflected both the inconclusive therapeutic outcome of dietary treatments and the heightened interest in micronutrients following the wave of vitamin and mineral discoveries in the initial decades of the twentieth century.16 Yet there was also a political dimension, as the proposition that children living within a British colony suffered from a diet deficient in one of the major food groups, rather than a newly discovered vitamin or mineral, was, in the words of a leading figure in British nutritional science, “politically objectionable.”17 Whereas previously unknown vitamin and mineral deficiencies provided further opportunities for science to improve the lives of colonial subjects, protein malnutrition pointed to the poverty of colonial populations. Williams was not easily deterred and despite her transfer to Malaysia (and interment during World War II), she remained an ardent advocate of the protein hypothesis throughout her life.18
The small medical library in Nairobi where Trowell lived and worked at the time did not carry a subscription to the Archives of Disease in Childhood that published Williams’s first article advancing the protein hypothesis, and thus Trowell only learned of the debate through the refutation written by Stannus. Trowell then assembled a collection of photographs and tissue specimens and consulted with Stannus while on home leave in 1935. According to Trowell, Stannus only glanced over the photographs and then confidently reiterated that the condition was a form of pellagra. When pressed about the fat deposits in the liver, Stannus apparently refused to examine the liver specimens and sent Trowell away with an article on pellagra among African Americans.19 For a time, Trowell nonetheless followed Stannus, referring to the condition as a form of “infantile pellagra” in his first two publications on the condition.20
In fact, Trowell did not begin to suspect that the condition was not a form of pellagra until relocating to the neighboring colonial territory of Uganda. He first traveled to Uganda in order to assess and report on medical training at Makerere. His enthusiastic endorsement of the high level of African medical training in Uganda was not well received in Kenya. Antipathy to advanced medical training for African colonial subjects was so great among the white settlers that Trowell’s endorsement was met with a punitive relocation to a remote outpost in Kenya’s Northern Frontier District. Only through an invitation to join the teaching staff at the Makerere Medical School was Trowell able to avoid being demoted and separated from his wife and young children. Once in Uganda, Trowell was again placed in charge of pediatrics where he again found children suffering from severe acute malnutrition. His further efforts to determine the cause and devise a cure placed him at odds with many within the medical establishment in Uganda. The pathologist at Mulago Hospital, for instance, refused to thoroughly examine Trowell’s patients at autopsy.21 Albert Cook, who undoubtedly felt beleaguered by new legal restrictions on the services midwives could provide, which threatened CMS finances, was especially reticent to entertain the idea that the condition was not congenital syphilis.22 In fact, Cook never conceded that children previously diagnosed with congenital syphilis may have been severely malnourished, and severely malnourished children continued to be treated as cases of syphilis in the main CMS hospital until the mid-twentieth century.23
Isolated, but undeterred, Trowell created his own small laboratory and trained a Ugandan assistant, John Kyobe, to examine liver extracts and blood slides. When a cable arrived from the United States announcing the synthesis of a new B vitamin and its arrival on the next plane, Trowell dropped everything to get to the airport, retrieve the bottle of niacin, and begin treating the children suffering from severe malnutrition in his ward.24 Tragically, it was not known then that vitamin B therapies were harmful and dangerous to severely malnourished children, and eight of the ten children given the niacin died as a result.25 Trowell resumed his efforts to treat the children with other B vitamins before eventually abandoning