Shared and distinct genetic architectures of eating disorders and obesity: From monogenic causes to polygenic risk.

Abstract

Eating disorders and obesity are severe health conditions arising from an impaired body weight regulation. Both are strongly influenced by genetic factors. Accordingly, obesity can be broadly classified as either monogenic, caused by mutations in a single gene, or polygenic, resulting from the cumulative effects of numerous variants, each exerting modest effects on body weight. Although the genetic architecture of obesity is relatively well characterized, novel mutations underlying monogenic obesity are still being uncovered, and the mechanisms linking polygenic variants to the phenotype are not fully elucidated. In contrast, the genetic basis of eating disorders is considerably less well understood. Among these, anorexia nervosa has been the most intensively studied, with several genomic regions already associated with disease susceptibility. The present review summarizes the current knowledge about the genetics of obesity and anorexia nervosa, highlighting shared and distinct mechanisms and discusses emerging research directions.