No abstract

THEROSCLEROSIS IS THOUGHTto begin in childhood and to develop silently for decades before clinical events such as myocardial infarction or stroke occur. Autopsy studies in children and adolescents have confirmed the presence of preclinical atherosclerotic lesions and shown their associations with antemortem vascular risk factors. [1][2][3] Studies using ultrasound imaging have demonstrated atherosclerotic wall thickening in the arteries of children with risk factors. [4][5][6] Longitudinal studies have shown that risk factor levels measured in childhood are predictive of risk factor levels in adulthood. [7][8][9] Moreover, levels of serum cholesterol measured in young adult men have been associated with cardiovascular disease in midlife. 10,11 Al-

No abstract

To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P<5 × 10−8), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk.