Eating disorders are influenced by genes, with research showing moderate heritability across anorexia nervosa, bulimia nervosa, and binge eating disorder.
Large population studies demonstrate that genetic factors account for roughly 30 to 40 percent of risk, while environmental factors and their interaction with genetic predisposition shape the remaining liability.
This article explains how genetics contribute to eating disorders, what recent research reveals about inherited risk, and why family history matters for understanding and addressing these serious conditions.
Are Eating Disorders Genetic?
Yes, eating disorders are genetic to a significant degree. Population-wide registry studies across Denmark and Sweden, analyzing approximately 17 million individuals, found heritability estimates of 36 percent for anorexia nervosa, 39 percent for bulimia nervosa, and 30 percent for other specified eating disorders. These figures reflect the proportion of variation in eating disorder risk attributable to genetic differences in a population, confirming that genes play a meaningful but not deterministic role.
Twin studies conducted over several decades established the foundation for understanding eating disorder genetics. Early research reported heritability estimates ranging widely due to sample size and methodology, but more recent analyses using rigorous liability-threshold models have converged on moderate heritability. For anorexia nervosa, estimates from twin studies fall between 48 and 74 percent, while bulimia nervosa shows 55 to 62 percent and binge eating disorder approximately 39 to 45 percent.
Genome-wide association studies have taken genetic research further by identifying specific DNA variants linked to eating disorders. The largest anorexia nervosa study to date, involving 16,992 cases and 55,525 controls, identified eight genetic loci associated with the disorder and estimated SNP-based heritability at 11 to 17 percent. This figure represents the portion of heritability captured by common genetic variants measured in the study, explaining why it appears lower than family-based estimates that include all genetic influences.
How Genetics and Environment Interact?
Genetic predisposition does not guarantee someone will develop an eating disorder. Environmental factors such as dieting behavior, media exposure, trauma, peer influences, and life stress interact with genetic vulnerability to trigger onset. The Scandinavian registry studies showed that familial aggregation remained robust across different relationship types and birth cohorts, yet environmental factors still accounted for the majority of variance in liability for some eating disorder presentations, particularly purging disorder.
Understanding Genetic Risk Beyond Family History
Emerging research shows that eating disorder risk stems from complex genetic architecture that spans psychiatric and metabolic pathways, beyond simple family history patterns:
The Metabo-Psychiatric Architecture of Anorexia Nervosa
Anorexia nervosa exhibits a unique pattern among psychiatric disorders, one that researchers describe as metabo-psychiatric. Genetic correlation analyses reveal that anorexia nervosa shares genetic variation with psychiatric conditions like obsessive-compulsive disorder, schizophrenia, and neuroticism, while simultaneously showing genetic overlap with metabolic traits. Specifically, anorexia nervosa demonstrates positive genetic correlations with HDL cholesterol and physical activity, but negative correlations with body mass index, insulin, glucose, leptin, and type 2 diabetes.
Importantly, these metabolic genetic relationships persist even after accounting for BMI-associated genetic variants. When researchers used statistical methods to remove the influence of BMI-related genes, the genetic correlations with fasting insulin, leptin, insulin resistance, and lipid traits showed only mild attenuation. This finding suggests that shared genetic architecture between anorexia nervosa and metabolic biology operates partially independent of body weight genetics, pointing to deeper connections involving energy homeostasis, insulin signaling, and perhaps immune function.
The first genome-wide significant locus for anorexia nervosa, identified in 2017, sits in a chromosomal region previously implicated in type 1 diabetes and autoimmune diseases. While this particular variant did not replicate at genome-wide significance in the larger 2019 meta-analysis, the pattern of autoimmune and metabolic connections has been reinforced through multiple lines of evidence. Finnish national registry data showed elevated autoimmune disease prevalence in eating disorder patients, with odds ratios of approximately 1.7, driven primarily by type 1 diabetes and Crohn’s disease. Danish cohort studies found that autoimmune diagnoses in childhood were associated with 36 percent higher hazard for anorexia nervosa, 73 percent for bulimia nervosa, and 72 percent for other eating disorders.
Transdiagnostic Genetic Liability and Comorbidity
Eating disorders rarely occur in isolation. Research using genomic structural equation modeling has revealed a transdiagnostic genetic component that captures shared psychiatric liability across multiple disorders. In Swedish anorexia nervosa cases linked to national health registers, a shared psychopathology polygenic risk score predicted 9 to 39 percent higher risk across measures of clinical burden, including total number of diagnoses, psychiatric medication prescriptions, and inpatient hospitalization days. Disorder-specific genetic risk for anorexia nervosa added smaller, more selective effects on top of this broad psychiatric liability.
This hierarchical model helps explain why individuals with eating disorders frequently experience depression, anxiety, obsessive-compulsive disorder, and other psychiatric conditions. The genetic architecture includes both a general vulnerability to psychopathology and eating disorder-specific genetic factors that shape whether and how disordered eating emerges.
Population registry analyses have quantified familial co-aggregation across diagnostic boundaries. The Scandinavian register studies documented extensive positive genetic correlations between eating disorders and other psychiatric disorders, with the strongest association found with obsessive-compulsive disorder. Genetic correlations with cardiometabolic diseases, including heart failure and peripheral artery disease, were also positive, varying by relationship type and remaining stable across inpatient and outpatient ascertainment methods.
How Are Eating Disorders Genetic Across Different Diagnoses?
Genetic liability appears to cut across diagnostic categories, with polygenic risk shaping shared and divergent features of binge-type and restriction-type presentations:
Polygenic Risk Patterns in Adolescents
Polygenic risk scores, which aggregate the effects of thousands of genetic variants, have demonstrated that genetic liability for anorexia nervosa extends to dimensional eating disorder behaviors in young people. An Australian study of adolescent female twins used polygenic scores derived from large discovery studies and found significant associations with global disordered eating and specific behaviors after controlling for relatedness, ancestry, age, and BMI. The anorexia nervosa polygenic score predicted avoidance of eating, objective bulimic episodes, self-induced vomiting, and driven exercise, illustrating that genetic risk operates across a spectrum rather than only within diagnostic categories.
These findings support the view that eating disorders exist on a continuum and that genetic influences shape both clinical diagnoses and subclinical symptoms. However, the researchers emphasized that current polygenic scores capture only a small portion of variance and lack clinical predictive utility for individual risk assessment. The value lies in research applications that illuminate shared etiology and inform prevention strategies at the population level.
Divergent Patterns in Binge Eating and Restriction
While anorexia nervosa shows negative genetic correlations with body mass index and related metabolic traits, binge eating behavior and binge eating disorder exhibit the opposite pattern. Recent genome-wide studies identified six genetic loci for broadly defined binge eating and confirmed that binge eating and anorexia nervosa share positive genetic correlations with multiple psychiatric phenotypes but diverge sharply on anthropometric and metabolic traits. Binge eating shows positive genetic correlation with waist-to-hip ratio, body mass index, and obesity-related measures, whereas anorexia nervosa correlates negatively with these same traits.
This mirror-image relationship suggests that eating disorder subtypes arise from partially overlapping psychiatric genetic liability combined with oppositely directed metabolic and anthropometric genetic predispositions. The psychiatric vulnerability may be relatively uniform across eating disorders, manifesting as difficulties with impulse control, emotion regulation, or compulsive thinking, while metabolic genetic factors help determine whether an individual tends toward restriction and low weight or binge eating and higher weight.
Genetic Sharing with Metabolic and Immune Pathways
Advanced methods that test genetic correlations at the local level, rather than averaging across the entire genome, have uncovered heterogeneous patterns of genetic sharing. A study examining nine neuropsychiatric disorders alongside obesity, type 2 diabetes, and metabolic syndrome found significant local genetic correlations even when global correlations were null. For anorexia nervosa, local negative genetic correlations with type 2 diabetes appeared at several chromosomal regions, and gene set analyses implicated insulin processing, secretion, and signaling pathways.
These findings align with the broader metabo-psychiatric framework and suggest that insulin and energy metabolism represent priority mechanisms for understanding eating disorder biology. The genetic architecture links brain circuits involved in reward, habit formation, and executive control with peripheral systems regulating glucose homeostasis, fat storage, and inflammatory responses.
The Role of Development and Puberty
Genetic influences interact with developmental timing, especially puberty, to shape onset, symptom course, and neurobiological pathways implicated in eating disorders:
Pubertal Timing and Eating Pathology
Genetic influences on eating disorders interact with developmental stages, particularly puberty. Longitudinal research demonstrates that early pubertal timing in girls is associated with increased body dissatisfaction and elevated risk for disordered eating during adolescence. These developmental trajectories show small to moderate effect sizes at the individual level but become meaningful at population scale. Because pubertal timing itself is heritable, some of the apparent environmental effects of early puberty may actually reflect genetic influences operating through developmental pathways.
Group-based trajectory modeling from early adolescence through young adulthood reveals that eating disorder symptoms follow distinct developmental courses that differ by sex and symptom type. Onset and progression of purging, loss of control eating, and weight loss behaviors vary across the second decade of life, with adolescence representing a critical risk window. Integrating polygenic risk scores into these trajectory analyses could refine understanding of which developmental paths are most strongly linked to genetic liability.
Brain Circuitry and Neurobiological Mechanisms
Neuroimaging studies across eating disorders implicate altered connectivity and activation in reward circuits, including the ventral striatum and orbitofrontal cortex, as well as in executive control networks like the anterior cingulate and dorsomedial prefrontal cortex. These brain regions show blunted or dysregulated reward anticipation and altered habit-related processing, features that overlap with obsessive-compulsive disorder and depression and may represent neurobiological pathways through which genetic risk is expressed.
Some connectivity alterations normalize with weight restoration, suggesting they are secondary to malnutrition, while other trait-like features persist. Longitudinal imaging in adolescent cohorts shows that low ventral striatal activation during reward tasks predicts later depressive symptoms, hinting that reward circuitry dysfunction serves as a shared pathway across multiple psychiatric outcomes, including eating disorders, and could mediate the expression of transdiagnostic polygenic liability.
Four single-gene loci have been mapped with confidence in anorexia nervosa genome-wide studies: CADM1, MGMT, FOXP1, and PTBP2. These genes are expressed in the brain and have functions related to neuronal adhesion, DNA repair and epigenetic regulation, neurodevelopmental transcription, and RNA splicing. Their involvement points toward mechanistic candidates in synaptic connectivity, developmental programming, and neuronal plasticity rather than primarily metabolic or immune processes, though these domains are not mutually exclusive.
Key Findings from Genetic Research
Below is a summary of heritability estimates and genetic correlations from major studies:
| Eating Disorder | Population Heritability | Key Genetic Correlations |
| Anorexia Nervosa | 36% (30–41%) | Positive: OCD, schizophrenia, HDL cholesterol, physical activityNegative: BMI, insulin, glucose, type 2 diabetes |
| Bulimia Nervosa | 39% (32–46%) | Positive: psychiatric disordersMixed or positive: anthropometric traits |
| Other Eating Disorders | 30% (20–40%) | Positive: psychiatric and cardiometabolic diseases |
| Binge Eating Behavior | Emerging data | Positive: psychiatric disorders, BMI, waist-to-hip ratioOpposite to anorexia nervosa for metabolic traits |
These estimates come from Scandinavian population registries spanning 1972 to 2016 and genome-wide association studies through 2025. The figures represent the proportion of variation in eating disorder liability attributable to genetic differences at the population level, not individual determinism.
Limitations and Future Directions
Current genetic research on eating disorders faces several limitations. Discovery studies remain heavily weighted toward European ancestry populations, limiting generalizability to other groups. Anorexia nervosa has far greater statistical power than bulimia nervosa, binge eating disorder, or avoidant/restrictive food intake disorder, leaving genetic understanding of these conditions less developed. Diagnostic heterogeneity and crossover between eating disorder categories complicate interpretation, though transdiagnostic approaches are addressing this challenge.
Polygenic risk scores explain only a modest proportion of individual variance and lack clinical utility for diagnosis or individual prediction at present. Their value lies in research contexts, including identification of biological pathways, stratification of research cohorts, and testing hypotheses about shared etiology across conditions. The gap between population-level heritability estimates and SNP-based heritability reflects the contribution of rare genetic variants, gene-environment interactions, and unmeasured genetic variation that current methods cannot capture.
Future research aims to expand sample sizes, increase ancestral diversity, refine phenotyping to capture dimensional symptoms and longitudinal transitions, and integrate genetic findings with brain imaging, metabolic biomarkers, and immune measures. Efforts like the Eating Disorders Genetics Initiative 2 are working to recruit approximately 20,000 new participants across multiple countries with enhanced representation of underrepresented populations and inclusion of avoidant/restrictive food intake disorder. These advances will enable more precise mapping of genetic risk, better understanding of how genetic factors interact with environment and development, and ultimately translation into prevention and treatment strategies.
Why Genetics Matter for Treatment and Recovery?
Understanding the genetic basis of eating disorders has several practical implications. It reinforces that these are serious brain-based illnesses, not choices or failures of willpower, which can reduce stigma and self-blame. Family history serves as a meaningful risk indicator, allowing earlier identification and intervention for at-risk individuals. Genetic research illuminates biological pathways, such as reward circuitry, insulin signaling, and immune function, that may become targets for novel medications or behavioral interventions.
However, genetic risk is neither necessary nor sufficient for developing an eating disorder. Environmental factors, including access to treatment, social support, coping skills, and life circumstances, profoundly influence outcomes. Evidence-based interventions remain effective regardless of genetic background, and recovery is possible for all individuals. Genetics provides one piece of a complex puzzle, informing a more complete understanding of etiology and guiding more personalized approaches to care.
If you or someone you care about is struggling with an eating disorder, reaching out for our professional support is an essential step toward recovery. Summit’s comprehensive evidence-based treatment addresses the biological, psychological, and social dimensions of these conditions, offering pathways to healing that work with your unique needs and circumstances.
