Race, environment and ischemic heart disease
nese men aged 55 to 64 years living in the United States have a CHD mortality less than a third of that of To the editor: I was extremely inter- white men of the same age living ested by Dr. R.J. Shephard's contribu- there.3 tion on this subject (Can Med Assoc J In South Africa, among whites, CHD 111: 1336, 1974). is more common in the Jewish than in As Dr. Shephard indicates, environ- the non-Jewish population: the differment rather than constitution is un- ence is not explicable on the basis of doubtedly the primary influencing fac- known differences in prevalence of risk tor in the development of coronary factors. In the South African Indian heart disease (CHD). I think that per- population CHD is almost as common haps there is insufficient appreciation as it is among whites, yet Indians are of the fact that the effects of the inter- far less affluent. Their percentage inaction of these two components, con- take of calories from fat is lower and stitution and environment, vary from their intake of sugar less. Also, the population to population. It is pre- peak mortality from CHD occurs a sumably this interaction that causes decade earlier in Indians than in whites. CHD rates to be higher or lower in In strong contrast, in South African some populations than would be ex- blacks, even in urban areas, CHD is pected.1 There is evidence too that par- virtually nonexistent.1 Yet observations ticular levels of environmental risk fac- we made in Soweto, Johannesburg 20 tors, such as hypercholesterolemia and to 25 years ago indicated that even at hypertension, evoke or are associated that time a significant proportion of with different responses in different black adults had high serum cholesterol populations; levels that are noxious in values, were hypertensive, obese, sedsome groups are apparently less noxi- entary, smoked (although not heavily) ous in others. and had a measure of job responsibilKeys and colleagues2 have carried ity. In Soweto there are nearly a milout extensive observations on CHD lion blacks. In some townships, for rates in groups of men in the United example, Dube, half the black families States and Europe (five countries). now employ full-time or part-time They stated that "Rules for clinical servants and there are about 25 cars judgements and EGG criteria and the per 100 families. I have calculated that details of the examinations and their in a white population of the same age spacing were identical, yet the US men and sex structure as the black populahad an incidence rate of hard GHD tion of Soweto at least 1200 episodes roughly double that of European men of CHD or sudden death would be of the same age, blood pressure, serum likely to occur annually. Yet the curcholesterol, and smoking habit. Even rent figure among these urban blacks considerations of relative body weight is about 20 to 50 per annum.4 This and of physical activity does (sic) not disparity in CHD incidence between change the discrepancy. The conclusion whites and urban blacks also prevails seems inescapable that the incidence in Durban.5 Thus, South African urban of CHD is strongly influenced by one blacks have far less CHD than would or more variables unrelated to any con- be expected. Their response to sophissidered in these studies." Also, Japa- tication of diet and manner of life obviously differs enormously from that Contributions to the Correspondence section are of the urbanized Alaskan Eskimos dewelcomed and if considered suitable will be published as space permits. They should be scribed by Dr. Shephard, among whom typewritten double spaced and should not exceed the CHD prevalence was stated to be 1½ pages in length. 1284 OMA JOURNAL/JUNE 7, 1975/VOL. 112
only a little lower than that among whites. The serum cholesterol value has different connotations with respect to CHD in different populations. In one study in Sydney, Australia the mean serum cholesterol value of male patients aged 40 to 60 years with CHD was 278 mg/dl.6 Yet in an urban area in India the mean serum cholesterol value of a corresponding group of male patients was 162 mg/dl.7 Actually, mean serum cholesterol values of groups of CHD patients within the same country have been found to differ. For example, in Norway, among male patients with infarction, aged 40 to 59 years, the following values were reported: in city dwellers in Oslo, 270 mg/dl; in fishing communities, 258 mg/dl; and in farming communities, 223 mg/dl.8 The evidence provided by Dr. Shephard, as well as the brief information given in this letter, underline the caution required in the prediction of prevalence of disease. It is these variations in biologic response that make epidemiologic studies so exciting; they would indeed be dull were all findings simply "comme ii taut". ALEXANDER R.P. WALKER, D Sc
MRC human biochemistry research unit, South African Institute for Medical Research Johannesburg, South Africi.
References 1. WALKER ARP: Coronary heart disease are there differences in racial susceptibility? Am I Epldemiol 90: 359, 1969 2. KEYs A, ARAVANIS C, BLACKBURN H, Ct al: Probability of middle-aged men developing coronary heart disease in five years. Circulation 45: 815 1972 3. GORDON T:. Further mortality experience among Japanese Americans. Public Health Rep 82: 973, 1967 4. WALKER ARP: The epidemiological emerpence of ischaemic arterial disease (E). Am Heart 1 89: 133, 1975 5. SEEDAT YK: Hypertension and myocardial infarction. Br Med 1 4: 346, 1974 6. PALMER AJ, BLAcKET RB, LEELARTKAEPHIN B: Hyperlipidaemia in a group of coronary subjects in Sydney. Med .1 Aust 2: 19, 1973 7. PAssc.sss C, Pints AS, MATHUR OC, et al: Serum uric acid and serum cholesterol relashionship in acute myocardial infarction. I Indian Med Assoc 50: 561, 1968 8. JERvELL A, MEYER K, WESThUND K: Coronary heart disease and serum cholesterol in males in different parts of Norway. Acta Med Scand 177: 13, 1965
nese men aged 55 to 64 years living in the United States have a CHD mortality less than a third of that of To the editor: I was extremely inter- white men of the same age living ested by Dr. R.J. Shephard's contribu- there.3 tion on this subject (Can Med Assoc J In South Africa, among whites, CHD 111: 1336, 1974). is more common in the Jewish than in As Dr. Shephard indicates, environ- the non-Jewish population: the differment rather than constitution is un- ence is not explicable on the basis of doubtedly the primary influencing fac- known differences in prevalence of risk tor in the development of coronary factors. In the South African Indian heart disease (CHD). I think that per- population CHD is almost as common haps there is insufficient appreciation as it is among whites, yet Indians are of the fact that the effects of the inter- far less affluent. Their percentage inaction of these two components, con- take of calories from fat is lower and stitution and environment, vary from their intake of sugar less. Also, the population to population. It is pre- peak mortality from CHD occurs a sumably this interaction that causes decade earlier in Indians than in whites. CHD rates to be higher or lower in In strong contrast, in South African some populations than would be ex- blacks, even in urban areas, CHD is pected.1 There is evidence too that par- virtually nonexistent.1 Yet observations ticular levels of environmental risk fac- we made in Soweto, Johannesburg 20 tors, such as hypercholesterolemia and to 25 years ago indicated that even at hypertension, evoke or are associated that time a significant proportion of with different responses in different black adults had high serum cholesterol populations; levels that are noxious in values, were hypertensive, obese, sedsome groups are apparently less noxi- entary, smoked (although not heavily) ous in others. and had a measure of job responsibilKeys and colleagues2 have carried ity. In Soweto there are nearly a milout extensive observations on CHD lion blacks. In some townships, for rates in groups of men in the United example, Dube, half the black families States and Europe (five countries). now employ full-time or part-time They stated that "Rules for clinical servants and there are about 25 cars judgements and EGG criteria and the per 100 families. I have calculated that details of the examinations and their in a white population of the same age spacing were identical, yet the US men and sex structure as the black populahad an incidence rate of hard GHD tion of Soweto at least 1200 episodes roughly double that of European men of CHD or sudden death would be of the same age, blood pressure, serum likely to occur annually. Yet the curcholesterol, and smoking habit. Even rent figure among these urban blacks considerations of relative body weight is about 20 to 50 per annum.4 This and of physical activity does (sic) not disparity in CHD incidence between change the discrepancy. The conclusion whites and urban blacks also prevails seems inescapable that the incidence in Durban.5 Thus, South African urban of CHD is strongly influenced by one blacks have far less CHD than would or more variables unrelated to any con- be expected. Their response to sophissidered in these studies." Also, Japa- tication of diet and manner of life obviously differs enormously from that Contributions to the Correspondence section are of the urbanized Alaskan Eskimos dewelcomed and if considered suitable will be published as space permits. They should be scribed by Dr. Shephard, among whom typewritten double spaced and should not exceed the CHD prevalence was stated to be 1½ pages in length. 1284 OMA JOURNAL/JUNE 7, 1975/VOL. 112
only a little lower than that among whites. The serum cholesterol value has different connotations with respect to CHD in different populations. In one study in Sydney, Australia the mean serum cholesterol value of male patients aged 40 to 60 years with CHD was 278 mg/dl.6 Yet in an urban area in India the mean serum cholesterol value of a corresponding group of male patients was 162 mg/dl.7 Actually, mean serum cholesterol values of groups of CHD patients within the same country have been found to differ. For example, in Norway, among male patients with infarction, aged 40 to 59 years, the following values were reported: in city dwellers in Oslo, 270 mg/dl; in fishing communities, 258 mg/dl; and in farming communities, 223 mg/dl.8 The evidence provided by Dr. Shephard, as well as the brief information given in this letter, underline the caution required in the prediction of prevalence of disease. It is these variations in biologic response that make epidemiologic studies so exciting; they would indeed be dull were all findings simply "comme ii taut". ALEXANDER R.P. WALKER, D Sc
MRC human biochemistry research unit, South African Institute for Medical Research Johannesburg, South Africi.
References 1. WALKER ARP: Coronary heart disease are there differences in racial susceptibility? Am I Epldemiol 90: 359, 1969 2. KEYs A, ARAVANIS C, BLACKBURN H, Ct al: Probability of middle-aged men developing coronary heart disease in five years. Circulation 45: 815 1972 3. GORDON T:. Further mortality experience among Japanese Americans. Public Health Rep 82: 973, 1967 4. WALKER ARP: The epidemiological emerpence of ischaemic arterial disease (E). Am Heart 1 89: 133, 1975 5. SEEDAT YK: Hypertension and myocardial infarction. Br Med 1 4: 346, 1974 6. PALMER AJ, BLAcKET RB, LEELARTKAEPHIN B: Hyperlipidaemia in a group of coronary subjects in Sydney. Med .1 Aust 2: 19, 1973 7. PAssc.sss C, Pints AS, MATHUR OC, et al: Serum uric acid and serum cholesterol relashionship in acute myocardial infarction. I Indian Med Assoc 50: 561, 1968 8. JERvELL A, MEYER K, WESThUND K: Coronary heart disease and serum cholesterol in males in different parts of Norway. Acta Med Scand 177: 13, 1965
