Summary
This Mendelian randomization study used 97 genetic variants for BMI and 49 for waist-to-hip ratio adjusted for BMI to establish causal effects on cardiometabolic disease across 14 prospective cohorts and major disease genetics consortia. Both general and central adiposity showed causal associations with coronary heart disease, though central adiposity showed stronger association with ischaemic stroke. Type 2 diabetes mellitus showed large effects from both measures, with BMI exhibiting a 98% increased odds and central adiposity a 82% increased odds per standard deviation increase.
UK applicability
The findings are relevant to UK public health policy and clinical practice, as they provide causal evidence supporting adiposity reduction as a preventive strategy for major cardiometabolic diseases. The study's use of multinational cohorts including UK participants (e.g. Whitehall II, UK Biobank-linked studies) strengthens applicability to UK populations, though the genetic causal estimates may have limited applicability to non-European ancestry populations.
Key measures
Odds ratios per 1 standard deviation increase in WHRadjBMI and BMI for CHD, ischemic stroke, and type 2 diabetes mellitus; secondary outcomes included left ventricular hypertrophy, glycemic traits, interleukin 6, carotid intima-media thickness, and circulating lipids
Outcomes reported
The study quantified causal associations between central adiposity (waist-to-hip ratio adjusted for BMI) and general adiposity (BMI) with coronary heart disease, stroke subtypes, type 2 diabetes mellitus, and 18 secondary cardiometabolic traits using genetic instrumental variables.
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