Dyslipidemia in type 2 diabetes typically comprises hypertriglyceridemia and reduced HDL cholesterol, usually associated with hypercholesterolemia (1). Relatively little is known about its occurrence in developing African communities, where the prevalence of type 2 diabetes may escalate dramatically (2). This is important because dyslipidemia constitutes a major risk factor for coronary artery disease (CAD) in type 2 diabetes (3). We therefore assessed serum lipids of South African blacks with type 2 diabetes of differing socioeconomic status and compared levels with those of patients two decades earlier. Our initial expectations were that dyslipidemia would be substantially greater in the higher socioeconomic group due to affluence and that lipids would have risen considerably over time because of increasing urbanization.
Our low socioeconomic community comprised 445 black African patients (241 women and 204 men) with recently diagnosed type 2 diabetes studied between 1994 and 1996. They attended the diabetes clinic at Johannesburg Hospital and were mostly domestic workers, laborers, and pensioners who were overweight and not undergoing lipid-lowering therapy. The higher socioeconomic cohort consisted of 82 patients (32 women and 50 men), also with recently diagnosed type 2 diabetes studied during 2001–2003. They attended a private diabetes clinic in the same city and were mainly civil servants, clerks, and executives. Again, the majority was overweight and not receiving hypolipidemic drugs. Finally, we reevaluated lipid data from 47 African patients (mainly women, mean age 55 years) with type 2 diabetes who attended Johannesburg Hospital complex in 1976; they were predominantly domestic workers.
Venous blood was collected at ∼0800, and although not formally fasting, most subjects had not eaten overnight. Serum was analyzed for total cholesterol, HDL cholesterol, and triglycerides by automated enzymatic methods (4). LDL cholesterol was calculated using the Friedewald formula. (These differed from the 1976 automated techniques .) Long-term diabetes control was assessed by HbA1c concentrations. Statistical analysis of data between patient groups utilized the unpaired t test, with P < 0.05 after Bonferonni adjustment being significant.
Biochemical data (Table 1) showed unimpressive dyslipidemia in women with no significant differences, although total and LDL cholesterol tended to be lower and triglycerides higher in the higher socioeconomic cohort. For men, similar trends emerged (P < 0.05 for triglycerides). In both sexes, diabetes control was significantly worse in the Johannesburg Hospital setting.
Comparing mean total cholesterol and triglyceride concentrations in African diabetic patients (three-quarters of them women) from the 1976 survey with African diabetic women attending the same clinic two decades later, serum cholesterol had risen from 4.8 ± 1.1 to 5.3 ± 1.3 mmol/l (P < 0.01). Serum triglycerides, however, had not changed significantly (1.2 ± 0.5 to 1.5 ± 1.1 mmol/l).
Dyslipidemia in the higher socioeconomic cohort of South African blacks with type 2 diabetes was unimpressive and not substantially greater than in their less sophisticated counterparts, apart from mild hypertriglyceridemia; importantly, total and LDL cholesterol tended to be lower. This was our first misconception to be corrected and is explainable by two factors: tighter metabolic control and the likelihood that they had more affordable access to a prudent diet containing reduced saturated fat and refined carbohydrates.
Their higher triglyceride levels, significant in men despite better glycemia, could reflect greater insulin resistance in these subjects who likely were less physically active than the less affluent subjects. By contrast total cholesterol levels may have risen significantly, if not dramatically, over two decades, reflecting a relatively small impact of westernization.
Our protocol revealed methodological limitations: the automated techniques for lipid assays differed in the 1976 study, the nonfasting collection of some serum samples may have influenced triglyceride concentrations, and the absence of formal dietary histories limited our interpretation of the lipid data. Nevertheless, these findings have implications for evolving CAD in Africans with type 2 diabetes. Their CAD prevalence remains low but may be increasing among urban dwellers (6). If subsequently confirmed, this suggests that prolonged exposure to only modest dyslipidemia, particularly when combined with other risk factors such as hypertension, smoking, and hypercoagulability, is the key atherogenic stimulus.
We thank Greg Distiller for statistical help, Dr. Vanessa Panz for initial data processing, and Terry Newfield for secretarial assistance.
W.J.K. was formerly the head of the Diabetic Clinic, Johannesburg Hospital, Johannesburg, South Africa.