AHA Scientific Sessions 2026 AbstractNov 9, 2026, 01:14 GMT

Clinical obesity has genetic links beyond body mass index

Of 127 genetic regions linked to clinical obesity, 63 had no significant link to body mass index in an analysis across five ancestry groups.

Paper by Sohail Zahid, Seraj N. Grimes, April Kim, +6Alexis J. Battle · Johns Hopkins University

Enlarged fat cells sit beside a narrowed artery and dense lipid particles, while smaller gray fat cells sit near an open artery.

Our read

Mechanisms

Studied:: Genetic association study of people with and without clinical obesity (Independent replication)
What changed:: Of 127 independent loci linked to clinical obesity, 63 did not associate with body mass index
The catch:: Did not measure whether changing lipoprotein lipase activity changes heart disease risk

Editor of record: Boris Djordjevic · AgingResearch.News

Paper

People with clinical obesity—151,642 cases—and 128,874 controls without obesity were included in an observational genetic analysis across five ancestry groups. Participants came from the All of Us Research Program and UK Biobank. Clinical obesity describes excess body fat with impaired fat-tissue function, beyond body mass index, a measure based on weight and height.

The strongest mismatch between genetic links to clinical obesity and body mass index involved a DNA variant in LPL, the gene for lipoprotein lipase, an enzyme that processes fats. In independent cohorts, carriers had higher odds of coronary artery disease, which affects the heart’s blood supply. Reported odds ratios ranged from 1.048 to 1.069; an odds ratio of 1 would indicate no difference.

Why it matters

The authors suggest that lipoprotein lipase biology contributes to cardiovascular disease, an age-related health concern.

Caveats

The genetic associations did not test whether changing lipoprotein lipase activity would change heart-disease risk. The results were reported in a conference abstract.