Prevalence over different periods

1700s/1800s: Despite several natural and man-made disasters over the 18th and 19th centuries^{(Reference Webster107)}, there is only one record of pellagra, namely, the outbreak of pellagra following the rinderpest epidemic of 1897^{(Reference Bender8)}. The dearth in reports could be due to the fact that most health care was, with exception of the Cape settlement, provided by traditional healers and, later on, missionaries. By the end of the 19th century, South Africa had a mere 650–700 Western trained medical doctors of whom more than 60 % lived in the Cape area^{(Reference Coovadia, Jewkes and Barron108,Reference Gilder109)} .

1900–1930: During the first three decades of the 20th century, several events occurred that gave rise to food shortages and malnutrition^{(Reference Nattrass110,Reference Jewell111)} , but are not reflected in reports on incidences of pellagra. This period also saw the creation of Black reserves through a series of discriminatory acts, e.g. the controversial Land Act of 1913 that made it illegal for Black Africans to purchase land except in demarcated reserves or to work as sharecroppers^{(Reference Nattrass110,112)} .

Over the three decades, three outbreaks of pellagra were recorded, but never nearly of the magnitude seen in Europe or the USA. The first outbreak (1906) occurred among prisoners of war when 150 pellagrins were identified by Dr LG Haydon among 3000 Zulu prisoners of war^{(Reference Cluver11)}. The second outbreak (1912–1913) occurred in the Pretoria Mental Institution where sixty inmates were diagnosed with pellagra^{(Reference Cluver11,87)} , and the third outbreak (1927–1928) involved sixty-four Black prisoners from three prisons in the Durban Prison Command diagnosed by Drs Rhodes and English^{(Reference Cluver11,15)} . An estimated fifty more sporadic cases were officially diagnosed, mainly from Zululand, Natal, the Transkei and a few from the Johannesburg area^{(Reference Cluver11)}. However, verbal reports, both from medical personnel and locals, suggest that pellagra may have been more prevalent^{(Reference Cluver11,Reference Mears22,65)} . There are also indications that subclinical deficiency of niacin may have been common in certain areas, especially in Black reserves^{(Reference Cluver11,113)} . According to census data, the population of South Africa numbered 16 928 580 in 1921^{(Reference Christopher114)}.

1931–1947: Over the following 17 years, the frequency of reports on the prevalence of pellagra, as well as the number of pellagrins for specific areas, increased^{(Reference Heiman17–Reference Suzman19,Reference Fox21,Reference Gillman and Gillman28,Reference Gillman, Gillman and Brenner29)} . In general, malnutrition and malnutrition-related diseases were by now common among the poor^{(Reference Hendriks, Mkandawire and Hall115–Reference Fox118)}. The increase in the number of reported pellagra cases may partly have resulted from the founding of community health centres^{(Reference Coovadia, Jewkes and Barron108,Reference Gluckman117,Reference Brown, Fee and Kark119)} ; an increase in the doctor:patient ratio from 1:3600 in 1930 to 1:2427 in 1946^{(Reference van Rensburg and Mans104)} and an increase in the number of community health surveys between 1930 and 1947^{(Reference Kark and le Riche20,Reference Hendriks, Mkandawire and Hall115,Reference Gluckman117)} . Pellagra was recorded in large community studies primarily focusing on Black children. The recorded prevalence in those studies varied widely between areas. For instance, in a 1938/1939 study by Kark and Le Riche^{(Reference Kark and Le Riche18,Reference Kark and le Riche20)} involving about 7000 Black schoolchildren in urban and rural areas of the Transvaal, Orange Free State, Natal and the Transkei, a total of 131 (1·87 % of 7000) cases of pellagra were reported, with figures varying between 0 % and 14·83 % for different regions. No such studies exist for adults.

From records of hospitals and clinics, and from verbal reports by locals who referred to pellagra as kelaba, it appears that pellagra may have been endemic in areas of the Transkei such as Idutywa and in Tsolo where 418 cases were diagnosed in the 1940s^{(Reference Mears22,Reference Mears23,Reference Gillman and Gillman28)} . Pellagra was not uncommon in the Ciskei^{(Reference MacVicar16)}, but due to a scarcity of medical services, records are not available. Better records are available for Johannesburg which had far better medical services and a medical school. While only isolated cases were reported in the Johannesburg area during the 1900–1930 period, at least 500 patients were diagnosed with pellagra between 1935 and 1941^{(Reference Heiman17–Reference Kark and le Riche20)}, and according to our calculations, about 1000 cases over the 1942–1945 period (Table 1). However, Gillman and Gillman^{(Reference Gillman and Gillman30)} who were by then studying pellagra in South Africa and had access to unpublished data estimated that more than 2000 patients were treated for pellagra at Johannesburg Hospital over the 1942–1945 period. Based on their own observations and that of others, Gillman and Gillman^{(Reference Gillman and Gillman30)} further estimated 4000 cases of pellagra in South Africa between 1943 and 1947, which can be extrapolated to approximately 1000 per annum, mostly in the Black population.

1948–1994: When in 1948, the National Party came into power; it institutionalised and expanded on the apartheid policies of preceding decades. The Promotion of Bantu Self-Government Act of 1959 proclaimed the existence of eight African ethnic groups with the aim of developing self-governing Black Homelands (Bantustans), independent of White intervention^{(Reference Nattrass110,112)} . This culminated in two homelands for the Xhosa, namely, Ciskei and Transkei; Bophuthatswana for the Tswana people; KwaZulu for Zulu people; Lebowa for the Pedi and Northern Ndebele; Venda for Vendas; Gazankulu for Shangaan and Tsonga people and Qwa for Basothos^{(Reference Nattrass110,112,Reference Butler, Rotberg and Adams120)} . The Black homelands were characterised by poor economic conditions before and after establishment, lack of infrastructure, limited employment opportunities which forced many to become migrant labourers, large-scale corruption and the growth of a Black middleclass bureaucratic elite. These factors contributed to poverty and malnutrition in the general homeland populations^{(Reference Nattrass110,Reference Butler, Rotberg and Adams120,Reference Thompson121)} .

Confusion exists about the prevalence of pellagra during the ‘era of high apartheid’ (1948–1976). Uncorroborated reports^{(4,Reference Neser41,Reference Quass42,Reference Metz, Du Plessis and Bothwell77,122–Reference Latham124)} suggest that pellagra reached epidemic proportions throughout South Africa during the 1970s. We found, for this period, reliable sources for at least 4500 cases of pellagra out of 276 000 observations, an estimated prevalence of 1·63 % (Table 1). In 1960, in an attempt to estimate the national prevalence of pellagra, a questionnaire was sent by the National Research Institute to all registered medical practitioners, requesting information on patients seen over two 30-d periods, namely, a summer period and a winter period^{(Reference Potgieter and Fellingham67,Reference Potgieter, Fellingham and Nesser68)} . Two hundred and fifty-three correctly completed questionnaires (each questionnaire containing records of up to ten doctors) were returned. These appear to be mainly from doctors in areas where malnutrition and diseases of malnutrition were common, such as the Black reserve areas of Zululand, the Transkei and Northern Transvaal. Of the 195 175 patients documented in the survey, 3132 were diagnosed with pellagra, an estimated prevalence of 1·6 %.

We suspect that many cases of pellagra went unpublished, such as the 1949–1950 outbreak of pellagra at Mandhleni, Msinga District, in the then Zululand⁽³³⁾. Msinga is an isolated, poverty-stricken area, located in deep gorges of the Tugela and Buffalo Rivers in an area that later became part of the KwaZulu Homeland. We only found evidence on the Msinga outbreak in the National Archives, in letters to and from the medical superintendent at Tugela Ferry. During the Msinga outbreak, fifty-five families are said to have contracted pellagra with an unspecified number of fatalities⁽³³⁾.

From 1948 to 1994, the population more than trebled from 11 957 000 in 1948 to 38 631 000 by mid-1994⁽¹²⁵⁾. Over this period, an estimated 7000 cases of pellagra were officially documented, with a prevalence of 1·75 % among the more than 400 000 individuals surveyed (Table 1). Many of the surveys focused on areas and groups with known malnutrition, and figures can thus not be extrapolated to represent national prevalence. More unreported incidences probably occurred, especially in areas with inadequate medical services such as the Black homelands^{(Reference van Rensburg and Mans104,116)} . To illustrate, by 1962, only 2·8 % of fulltime medical doctors in South Africa worked in the homelands, which grew to 4·8 % by 1974. The doctor:population ratio in the homelands was estimated at 1:15 000, in contrast to 1:1969 in rest of South Africa^{(Reference van Rensburg and Mans104)}.

Decline in the prevalence of pellagra

Indications from clinics and hospital records are that the prevalence of pellagra in urban areas started to decline towards the 1970s. However, attendance records at dermatological services suggest that the number of patients suffering from pellagra in metropolitan areas already began to decline in the late 1960s. In large hospitals in the Pretoria area, the proportion of dermatological patients suffering from pellagra declined from 6·3 % in 1962 to 3 % in 1968, to below 1·7 % over the 1974–1980 period^{(Reference Park45,Reference Schultz55,Reference Schulz, Findlay and Scott56)} . The proportion of Black dermatological patients diagnosed with pellagra at Chris Hani Baragwanath Hospital, the largest hospital in Africa, declined from 2·2 % between 1968 and 1969 to 1·98 % between 1969 and 1972^{(Reference Dogliotti49,Reference Dogliotti50)} . The early decline observed in metropolitan areas may merely reflect differences in nutritional status between rural and urban populations^{(Reference Vorster126)}. Elsewhere, pellagra continued to occur, especially in the Black homelands. In 1975, a 2-week survey of twelve hospitals in the Ciskei and Transkei found 127 pellagrins out of 8684 patients (1·46 %)^{(Reference Rose, Dowler and Daynes54)}. A retrospective study of ten hospitals in rural KwaZulu-Natal found that 514 pellagrins were admitted over a 9-year period from 1975 to 1984^{(Reference Ndaba61)}. It is important to note that the figures only reflect those who attended hospitals.

All indications are that, by the late 1980s, early 1990s, the prevalence of pellagra was declining throughout South Africa. In a 1995 review of nutrition-related diseases, Walker^{(Reference Walker127)}, perhaps a little too optimistically, wrote ‘In the past this deficiency disease was common in rural areas. Its current prevalence is much lower. In big towns it is no longer seen’. By the end of the 20th century, very few papers even mentioned pellagra. In 1999, a retrospective study of 7029 dermatology patients at five academic hospitals in the Johannesburg area showed a pellagra incidence of 0·2 % for Black patients and 0 % for the White, Coloured and Indian populations^{(Reference Hartshorne80)}. In KwaZulu-Natal, no cases were diagnosed among 6664 Black private practice patients over 7 years between 2003 and 2010^{(Reference Dlova, Mankahla and Madala64)}, or among 3818 dermatological patients seen over 3 months at public referral hospitals in 2013^{(Reference Dlova, Chateau and Khoza81)}. Mortality data from Statistics SA showed decreased mortality due to pellagra, from eighty-six cases in 1997, to twelve cases in 2010, remaining below ten per year from 2012 to 2016⁽¹⁰⁶⁾.

Several factors probably contributed to a decline in the prevalence of pellagra as diagnosed by dermatological symptoms. Improvement in the socio-economic circumstances and social grants, as well as the food fortification initiatives and social and food security programmes, undoubtedly had a positive impact. For more information on the many food security initiatives, the reader is referred to a document from ‘Feed the Future Innovation Lab for Food Security Policy’^{(Reference Hendriks, Mkandawire and Hall115)}. A brief account on the South African food fortification initiatives, particularly the fortification of maize meal, can be found in the section dealing with pellagra and the consumption of maize in South Africa.

Subclinical levels of niacin

Subclinical (sub-pellagra) levels of niacin deficiency in South Africa were inferred as early as late 1920s to early 1930s. Deficiencies were implied by the rapidity with which some prisoners in Natal gaols developed pellagra when subjected to inadequate prison diets^{(Reference Cluver11)}, and by the appearance of pellagra symptoms when newly arrived migrant labourers from Black reserve areas started to work on the mines⁽¹¹³⁾. The first problem was remedied by a change in prison diets^{(Reference Cluver11)} and the second, by a period of rest on nutritionally adequate diets before engaging in the labour of mining⁽¹¹³⁾.

During the second half of the 20th century, the existence of subclinical niacin deficiency was confirmed by urine analysis. Over the period 1962–1965, the nicotinic acid status based on urinary excretion of N¹-methyl nicotinamide (N¹-Me) and N¹-methyl-2-pyridone-5-carboxylamide (2-pyridone) was determined in 2105 urban schoolchildren between the ages of 7 and 15 years in the Pretoria area^{(Reference Du Plessis, de Lange and Viviers70,Reference Du Plessis71)} . A 2-pyridone:N¹-Me ratio of <1was considered as indicative of latent nicotinic acid deficiency^{(Reference Du Plessis, de Lange and Viviers70,Reference Du Plessis71)} . The study included the four main racial groups and found, depending on the area, latent niacin deficiency in 5·6–14·1 % White, 24·6–28·7 % Indian, 28·7–32 % Coloured and 35·6–53·1 % Black children^{(Reference Du Plessis, de Lange and Viviers70,Reference Du Plessis71)} . Other studies on primary schoolchildren showed niacin and riboflavin deficiencies^{(Reference Du Plessis71,Reference De Lange and Joubert73)} for Black, but not White children. We found only two studies investigating niacin levels in adults. The first, a 1969 study of 500 Venda men reported a fair nutritional status, but suboptimal nicotinamide levels in 60 % (151/253) rural and 47 % (116/247) urban Venda men^{(Reference Nel, Du Plessis and Fellingham48)}. The second study conducted in August 1970 and March 1971 reported low niacin status in 77 % (157/204) rural adult Pedi men from Mohlaletsi, Ehlanzeni District, Mpumalanga Province, and in 50 % (120/239) urban adult Pedi men from Katlehong Township, Ekurhuleni, Gauteng Province^{(Reference Louw, Du Plessis and Laubscher51)}. Studies conducted in the 1970s showed that fortification of maize meal with niacin and riboflavin could alleviate subclinical niacin deficiency^{(Reference Du Plessis, Groonhof and Laubsher128)}.

It is important to note that the above subnormal levels of niacin reported were generally found in populations with no visible dermatological symptoms of pellagra. Today, the diagnosis of pellagra and epidemiological estimates of niacin deficiency are still largely based on the dermatological symptoms of the disease. In view of the fact that niacin is the precursor of the all-important coenzyme NAD and that niacin and NAD deficiencies can influence virtually all physiological processes, from cerebral functions to genomic stability, this is rather disconcerting.

Pellagra and consumption of maize in South Africa

As a nutrition deficiency disease, pellagra is primarily associated with a deficiency in niacin. In Europe, the USA and Egypt, outbreaks of pellagra were often observed when maize became the staple food in near monophagic diets of the poor^{(Reference Viljoen, Bipath and Roos5)}. Most of the niacin present in maize is found in the aleurone, germ and endosperm, bound up in a hemicellulose complex that is nutritionally unavailable to humans. These niacin-containing fractions are lost during industrialised milling processes^{(Reference Viljoen, Bipath and Roos5,Reference Suri and Tanum129)} . Maize, furthermore, contains a limited amount of bio-available tryptophan, the precursor for in vivo synthesis of niacin.

As elsewhere, an association has been observed in South Africa between pellagra and nutritionally inadequate maize-based diets^{(Reference Cluver11,Reference Kark and le Riche20,Reference Fox21,Reference Gillman and Gillman28,Reference Gillman and Gillman30,Reference Prinsloo, Du Plessis and Kruger43,Reference Marshall and Heyl72,Reference Fox118)} . However, there are several noteworthy differences. Maize apparently became the primary staple food much later in South Africa than in Europe, and marginally later than in the USA^{(Reference Viljoen, Bipath and Roos5,Reference Cluver11,Reference Webster107)} . In KwaZulu-Natal, millet, as part of a multi-crop food source, was still the primary grain by the middle of the 19th century^{(Reference Webster107)}. At the turn of the century, maize had become the dominant crop in KwaZulu-Natal^{(Reference Cluver11)}, and the major grain in the Transkei by 1936^{(Reference Webster107)}. In South Africa, the practice of crude stone grinding, instead of industrialised milling, has been suggested to contribute to the relatively low incidence of pellagra in the 19th and early 20th centuries^{(Reference Cluver11)}. In addition, consumption of green maize, boiled or roasted, in which the endosperm is still soft and the nutrition bio-availability higher, forms an important part of maize consumption in Africa. Furthermore, traditional African food preparation processes such as fermentation and roasting increase the bioavailability of niacin^{(Reference Kodicek, Muller and Carpenter130,Reference Lay and Fields131)} . Fermented maize, for instance, has almost double the riboflavin and niacin content of unfermented maize^{(Reference Steinkraus132)}. Many fermented foods are traditionally consumed in Africa^{(Reference Ekpa, Palacious-Rojas and Kruseman133)}, including non-alcoholic beverages such as Mahewu, and alcoholic beverages such as Umqombothi^{(Reference Ekpa, Palacious-Rojas and Kruseman133–Reference Idowu, Fadahunsi and Onabiyi135)}. Drinks, made from fermented maize, are consumed by both adults and schoolchildren and in certain cultures are used as a weaning food for infants^{(Reference Ekpa, Palacious-Rojas and Kruseman133–Reference Idowu, Fadahunsi and Onabiyi135)}.

What cannot be denied is that maize is, and has long been, a staple food in the country^{(Reference Cluver11,Reference Kark and le Riche20,Reference Fox21,Reference Gillman and Gillman28,Reference Gillman and Gillman30,Reference Prinsloo, Du Plessis and Kruger43,Reference Marshall and Heyl72,Reference Fox118)} and that inadequacies of a diet over-dependent on maize can contribute to nutritional deficiencies such as pellagra^{(Reference Viljoen, Bipath and Roos5)}. In South Africa, provisional maize meal enrichment programmes started as early as the 1960s^{(Reference Fehrsen136)} and in the 1970s studies were conducted which showed that fortification of maize meal with niacin and riboflavin could indeed alleviate subclinical niacin deficiency^{(Reference Du Plessis, Groonhof and Laubsher128)}. Attempts to remedy the inadequacies of a diet over-dependent on maize by voluntary fortification by industries have met with some success, but maize meal samples sourced during the last quarter of 1986 from stores in the erstwhile Transvaal, Orange free State, Natal, Eastern Cape Province and Transkei showed concentrations of nicotinic acid and riboflavin to be well below the recommended levels^{(Reference Aggett, Van der Westhuyzen and Kuyl137,Reference Danster-Christians138)} . In April 2003, regulations regarding mandatory fortification of all maize meal and wheat flour were printed in the Government Gazette, published under Act No 54 of 1972⁽¹³⁹⁾. Fortification of maize meal and wheat flour with vitamin A, thiamine (vitamin B₁), riboflavin (vitamin B₂), niacin (vitamin B₃), pyridoxine (vitamin B₆), folic acid (vitamin B₉), Fe and Zn became mandatory on the 7 October 2003, with cyanocobalamin (vitamin B₁₂) later added to the list. Despite indications from post-implementation studies that suggest suboptimal compliance with statuary fortification requirements at mills^{(Reference Danster-Christians138,Reference Yusufali, Sunley and De Hoop140)} , indications are that fortification of maize meal markedly improved the intake of micronutrients such as niacin^{(Reference Danster-Christians138,Reference Steyn, Wolmarans and Nel141)} .

Causes of pellagra in the South African population

Although pellagra is generally associated with diets inadequate in niacin, niacin is also synthesised from the essential amino acid tryptophan via the kynurenine pathway^{(Reference Bipath, Levay and Viljoen142)}. Such de novo synthesis of niacin decreases with protein malnutrition, and deficiencies in Fe, riboflavin and pyridoxine^{(Reference Bipath, Levay and Viljoen142,Reference McCormick143)} . South Africa has a long history of malnutrition, including micronutrient deficiencies^{(Reference Hendriks, Mkandawire and Hall115)}. From the reviewed literature, we can feasibly assume malnutrition, particularly malnutrition associated with maize as the staple in nutritionally inadequate diets, to be the main cause of pellagra.

Alcoholism may have been the second major cause of pellagra. Alcohol can cause or aggravate niacin deficiency by causing malnutrition, gastrointestinal disturbances, B vitamin deficiencies, and by suppression of de novo synthesis of niacin^{(Reference Badawy144)}. According to the WHO, South Africa has among the highest per capita alcohol consumption rates in the world⁽¹⁴⁵⁾. According to the Institute for Health Metrics and Evaluation, alcohol ranked among the top three risk factors that accounted for the 2010 disease burden in South Africa^{(Reference Lim, Vos and Flaxman146)}. In fact, alcohol consumption is a historical problem in South Africa. Between 1895 and 1909, the Natal Government Asylum, cited ‘intemperance in drink’ as the most frequently identified cause of insanity amongst male patients^{(Reference Parle147)}. A 1942 study in the Transkei found that the much higher incidence of pellagra in the Pondomisi tribe, compared to the Fingo tribe, was due to a higher alcohol intake^{(Reference Mears23)}. Pellagra, as well as suboptimal niacin levels, were linked to higher alcohol intake in Venda men^{(Reference Ross44,Reference Nel, Du Plessis and Fellingham48)} . In late 1970s, malnutrition and alcohol were implicated as causes of pellagra in admissions to psychiatric hospitals^{(Reference Marks and Andersson123)}. Pellagra has also been linked to alcohol consumption in dermatological patients visiting Baragwanath Hospital during 1969–1972^{(Reference Dogliotti50)}. In a 1984 overview of poverty and development in KwaZulu-Natal, a strong association is described between incidences of pellagra and alcoholism^{(Reference Ndaba61)}.

A number of drugs^{(Reference Bilgili, Calka and Altun148–Reference Li, Yu and Wang150)} may influence niacin levels, but most are probably not used on a scale that would significantly influence the local prevalence of pellagra, except anti-tuberculosis agents. South Africa has a high incidence of tuberculosis and HIV-tuberculosis co-infection. According to the WHO, about 57 % (258 000) of the 45 400 patients with incident tuberculosis in 2015 were HIV positive⁽¹⁵¹⁾. The anti-tuberculosis drug, isoniazid, interferes with the conversion of tryptophan to niacin by producing a deficiency in pyridoxine coenzymes required for de novo synthesis of niacin. Several authors have reported pellagra symptoms in patients treated with isoniazid, especially poorly nourished patients, and at least one paper called to the fact that pellagra encephalopathy may occur in patients without pellagra-associated skin lesions^{(Reference Bilgili, Karadag and Calka152,Reference Ishii and Nishihara153)} . Niacin deficiency has occasionally been linked to HIV infection, and South Africa has a very high incidence of HIV. However, it is debatable whether niacin deficiency occurs as a result of HIV infection per se as the high pro-inflammatory activity associated with HIV infection stimulates de novo niacin synthesis at the cost of tryptophan levels^{(Reference Bipath, Levay and Viljoen142)}. Above normal de novo, niacin synthesis then scales down when the inflammatory activity normalises in response to anti-retroviral therapy^{(Reference Bipath, Levay and Viljoen142)}. Nevertheless, the niacin status of HIV-positive patients may be adversely affected by the malnutrition and malabsorption often observed in HIV-positive patients^{(Reference Griffin154)}.

The end of pellagra or niacin deficiency in South Africa?

The prevalence of pellagra, as diagnosed by dermatological symptoms, declined with improvement in socio-economic conditions, food fortification, social grants and food security programmes. Despite numerous food security programmes, the prevalence of deficiencies in several other micronutrients remains unacceptably high^{(Reference Hendriks, Mkandawire and Hall115)}. Currently, most micronutrient deficiencies are diagnosed using biochemical assessments, often in the absence of their respective deficiency syndromes. In contrast, niacin deficiency is still mainly diagnosed based on dermatological symptoms of pellagra, disregarding potential subclinical deficiency. Niacin levels may even be kept within normal range by de novo synthesis, at the cost of tryptophan levels.

Although few papers reported incidences of pellagra in South Africa since the end of the 20th century, outbreaks have recently been reported in specific regions of neighbouring countries. Regrettably, admissions to a clinic at Kuito in the Bie Province of central Angola showed that the incidence of clinical pellagra has not decreased since the end of the civil war in 2002^{(Reference Seal, Creeke and Dibari155)}. In Malawi, between July 2015 and April 2016, a total of 691 pellagrins were seen at a local Kasese catchment area clinic in Dowa. The clinic serves approximately 30 000 people, largely of the Chichewa tribe^{(Reference Matapandeu, Dunn and Pagels156)}. In central Mozambique, an outbreak of pellagra, following the March 2019 hit by Cyclone Idai, is reported to affect almost 4000 people in the Sofala and Manica provinces, with the numbers still increasing⁽¹⁵⁷⁾. In Zimbabwe, 2007 pellagra cases were recorded by village health workers between January and October 2020 and the numbers are expected to increase as food insecurity intensify⁽¹⁵⁸⁾. In Lesotho, pellagra is said to have been the most common dietary deficiency disease with 8600 cases in 1959^{(Reference Conz159)}. By 1964, the numbers started to decline, but indications are that it never really disappeared^{(Reference Conz159)}.

Limitations

Very few of the early papers and records could be traced through structured literature searches and were only uncovered through electronic hand searches and in library and other archives. Despite enormous efforts to discover all credible records on incidences of pellagra in South Africa, we suspect that some must have been overlooked.