Introduction
In Sub-Saharan Africa (SSA) the prevalence of overweight/obesity is increasing rapidly1 in rural and urban populations that are experiencing lifestyle changes (ie, greater sedentary behaviour, tobacco smoking, alcohol consumption, unhealthy diets and urbanisation)2–6 and increasing life expectancy (due to reductions in child mortality7 and adult HIV-related mortality).8 However, the extent to which this transition is affecting the risk and burden of dyslipidaemia is little understood. Although recent Mendelian randomisation (using genetic variants as instrumental variables) and randomised controlled trial evidence challenge the role of low levels of high-density lipoprotein-cholesterol (HDL-C) in causing coronary heart diseases (CHD), high circulating total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C) and triglycerides (TG) are key causal risk factors for CHD,9 10 and are effectively and cost-effectively reduced by statins with clear benefits for primary and secondary CHD prevention. In populations of white European origin, higher body mass index (BMI), waist to hip ratio (WHR) and waist circumference (WC) are associated with higher TC, LDL-C and TG.11 In these populations, some studies have reported stronger associations of WHR or WC, than BMI, with CHD.12 13 However, in by far the largest study to date which included ~222 000 adults from 58 cohorts in an individual participant meta-analysis, similar magnitudes of association were found for BMI, WC and WHR (HR for CHD (95% CI) for a 1 SD greater BMI 1.23 (1.17 to 1.29), WC 1.27 (1.20 to 1.33) and WHR 1.25 (1.19 to 1.31).14 In that study, reproducibility was also shown to be greater for BMI than WHR (or WC). Prospective studies of children/adolescents in white European populations also find similar magnitudes of association between WC, WHR, waist to height ratio and BMI with blood pressure, fasting glucose and fasting lipids.15 16 Evidence on the association of adiposity and lipid profile in black SSA populations is limited. Most studies in SSA have been small or focused on HIV-positive individuals, and few have collected fasted blood samples and examined differences by sex and area of residence (urban/rural).17–20
Some evidence suggests that African women are more adipose than Europeans,21 yet people of African ancestry have also been shown to have a more favourable lipid profile.22 In a small cross-sectional study undertaken 20 years ago in Cameroon, higher BMI was associated with higher blood pressure and higher fasting insulin, glucose and TG (other lipids were not assayed) in urban residents, but with lower blood pressure and lower fasting insulin, glucose and TG in rural residents.17 The rapid epidemiological transition and the coexistence of insults such as infection and malnutrition (including undernutrition in early life and emerging overweight and obesity in adulthood),23 might influence manifestation of adiposity and its association with lipids in SSA populations that differ from those in European populations and this previous SSA study. For example, in Malawi, a very poor SSA country, affected by childhood undernutrition and food insecurity, nearly 25% of the adult population have raised total cholesterol (≥5.0 mmol/L).24
A better understanding of the extent to which the adiposity (total and central) associates with lipids in SSA, and whether any associations differ by sex and residency (urban/rural) is essential to inform the long-term impact of obesity and dyslipidaemia on the burden of CHD in SSA countries and the development of tools (including cardiovascular risk scores) and interventions appropriate for the setting.
Our aim was to explore whether there was evidence for a causal effect of BMI and WHR on adverse lipid profiles in a poor SSA country and whether any effect differed between women and men and by rural and urban areas. We acknowledge that the data that we are using (population representative data from urban and rural Malawi) is cross-sectional and likely biased by residual confounding (discussed in the limitations of the study). We have carefully considered and controlled for observed confounders, including several measures of socioeconomic position, and believe residual confounding will largely be due to reporting bias of behaviours, such as smoking and physical activity, and our inability to adjust for diet.