Mayosi, B. M.; Forrester, T.
Author Affiliation, Ana.
Commentary: ‘serum-cholesterol, diet, and coronary heart-disease in Africans and Asians in Uganda’ by AG Shaper and KW Jones
The International Journal of Epidemiology
Date of Publication
Shaper and Jones are to be lauded for identifying the central role of cholesterol in determining variation in risk of coronary disease among different ethnic groups in Africa as early as 1959.1 Their publication followed closely the 1957 Seven Countries Study by Ancel Keys, which established unequivocally the pathophysiological role of dietary saturated fats acting through serum cholesterol concentrations in the causation of atherosclerotic vascular disease.2 The prescience of Shaper’s study of coronary artery disease is thrown into sharp relief because it challenged the prevailing assumption then that variation in risk of disease in Africans compared with Caucasians was genetic in origin; Africans were considered to be almost ethnically immune to the development of coronary artery disease.3,4 In fact, Shaper and Jones avoided the ‘racial profiling’ that was prevalent at the time by focusing in their study on measuring key components of environmental exposure, i.e. dietary composition. They identified the contribution of two of the main components of the diet–heart hypothesis to risk of coronary disease in Ugandans of African origin and those from the Indian subcontinent: (i) the intake of total fats, and proportion of animal (saturated) and plant (unsaturated) fats in the diet; and (ii) intake of vegetables and unrefined staple foods (i.e. vegetables, pulses and ground provisions—such as yams). They also hinted at the conditioning effect on risk of other lifestyle attributes, such as physical activity, but omitted mention of tobacco use. Since then, a large and robust literature has confirmed that the relationships between common cardiovascular disease risk factors and acute myocardial infarction are similar throughout the world. 5 The surprising omission from their report was an index of obesity; there is no information on weight or height or any measure of body size or composition. The association between overweight and coronary disease was well established by then.6 Perhaps, the focus on cholesterol as a major risk factor modifiable by simple dietary changes was the sole aim of the communication. Perhaps, also, they were correct to ignore easily measured indices of obesity such as BMI because of the recognized variation in proportion of fat and lean mass at any BMI and the consequent variation in risk that is mechanistically associated with adiposity. Certainly, relative weight captured as the BMI and cardiovascular risk are not absolutely correlated, as has been demonstrated in the Seychelles and South Africa.7,8 Although obesity has increased in the Seychelles and South Africa, mortality from coronary artery disease appears to be falling in both African countries.9–11 A current enumeration of the main risk factors for coronary disease would not differ substantially therefore from Shaper’s early framework; thus, almost nothing significant has been observed about risk of coronary artery disease that is not in the article, except for cigarette smoking and the variation in underlying susceptibility to risk exposures that is conditioned by early life development.12 The initial recognition by Barker and the subsequent elaboration of understanding of this variation in underlying susceptibility to the pathogenetic force of risk factors arising from developmental modulation of individual form and function is a major advance in the understanding of disease risk.13 Ironically, it comes perilously close to rehearsing old fallacies of the genetic basis of observed ethnic differences in disease profile because of the divergence of ethnic biological phenotypes, driven by generations of environmentally entrained epigenetic control of development early in life.14....