Mendelian randomization using 363 BMI-associated variants with consistent effects across ancestries indicates that higher body mass index causally raises blood sugar markers in both African and European adults. In UK Biobank, each 1 SD increase in BMI raised HbA1c by 0.26 SD in Africans (95% CI 0.07, 0.45) and 0.27 SD in Europeans (0.22, 0.32), with random glucose rising 0.21 SD and 0.15 SD respectively. Sensitivity analyses found no sign of unbalanced pleiotropy.
Observational data from sub-Saharan Africa have long linked adiposity to dysglycaemia, but confounding left causality open; this analysis shows the relationship is likely causal and similar in magnitude across ancestries. That matters for adults in populations where type 2 diabetes is rising fast yet trial evidence is scarce: weight management plausibly protects glycaemic control there as it does in Europe. Limits are real. The African sample was small (about 5,800 for HbA1c), producing wide intervals that cannot rule out meaningful ancestry differences, and the African-ancestry UK Biobank participants are mostly diaspora, not people living in Africa. HbA1c itself can be skewed by haemoglobin variants common in African populations. MR also estimates lifelong genetic exposure, not the effect of losing weight in midlife. This is a preprint that has not been peer reviewed, so figures may shift. Overall, it is a confirmatory, methodologically useful step toward including African ancestry in causal genetics.