An Evolutionary Genetic Perspective of Eating Disorders

Abstract

Eating disorders (ED) including anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) affect up to 5% of the population in Western countries. Risk factors for developing an ED include personality traits, family environment, gender, age, ethnicity, and culture. Despite being moderately to highly heritable with estimates ranging from 28 to 83%, no genetic risk factors have been conclusively identified. Our objective was to explore evolutionary theories of EDs to provide a new perspective on research into novel biological mechanisms and genetic causes of EDs. We developed a framework that explains the possible interactions between genetic risk and cultural influences in the development of ED. The framework includes three genetic predisposition categories (people with mainly AN restrictive gene variants, people with mainly BED variants, and people with gene variants predisposing to both diseases) and a binary variable of either the presence or absence of pressure to be thin. We propose novel theories to explain the overlapping characteristics of the subtypes of AN (binge/purge and restrictive), BN, and BED. For instance, mutations/structural gene variants in the same gene causing opposite effects or mutations in nearby genes resulting in partial disequilibrium for the genes causing AN (restrictive) and BED may explain the overlap of phenotypes seen in AN (binge/purge).

Food Addiction and Binge Eating: Lessons Learned from Animal Models

“…Although the genetic study of BED is still in early stages and there are no enough genome-wide association studies (GWAS) focused exclusively on BED, preliminary evidences suggests that could there be predisposing risk factors [ 171 , 172 , 173 , 174 ]. In fact, there are good evidences that heritable factors make a significant contribution to the risk of developing eating disorders [ 175 ]. Patrono et al showed that exposure to environmental conditions induces compulsion-like eating behaviour, depending on genetic background.…”

Gain‐of‐function variants in the melanocortin 4 receptor gene confer susceptibility to binge eating disorder in subjects with obesity: a systematic review and meta‐analysis

“…Multiple genes responsible for monogenic syndromic and non‐syndromic, oligogenic and polygenic forms of obesity have been identified . However, it is unclear as to which genes may predispose individuals to BED . Genetic variants and mutations in and near the melanocortin 4 receptor gene ( MC4R ) locus are linked with polygenic forms of leanness and monogenic, oligogenic and polygenic forms of obesity .…”

“…Both BED and obesity have strong genetic underpinnings (9)(10)(11). Heritability estimates for BED and obesity range from 41% to 57% and from 25% to 90% (12,13).…”

“…Patients with BED also report comorbid mental disorders and other chronic conditions, decreased health‐related quality of life and increased utilization of healthcare services . A better understanding of the aetiology of BED – and its possible implications for obesity – is expected to improve prediction, prevention and management of the illness .…”

Underlying Susceptibility to Eating Disorders and Drug Abuse: Genetic and Pharmacological Aspects of Dopamine D4 Receptors

“…Over the last few years, considerable progress has been made to understand the neurobiological mechanisms that underlie ED, converging that genetic factors and gene/environment interactions could contribute to the potential development of these disorders [ 186 , 187 , 188 , 189 ]. One of the possible candidates that may contribute to the dysregulation of feeding patterns in ED and risk of weight gain, leading to obesity, is the polymorphism of DRD4 gene.…”