Enabled by advances in high throughput genomic sequencing and an unprecedented level of global data sharing, molecular genetic research is beginning to unlock the biological basis of eating disorders. This invited review provides an overview of genetic discoveries in eating disorders in the genome-wide era. To date, five genome-wide association studies on eating disorders have been conducted – all on anorexia nervosa (AN). For AN, several risk loci have been detected, and ~11–17% of the heritability has been accounted for by common genetic variants. There is extensive genetic overlap between AN and psychological traits, especially obsessive-compulsive disorder, and intriguingly, with metabolic phenotypes even after adjusting for body mass index (BMI) risk variants. Furthermore, genetic risk variants predisposing to lower BMI may be causal risk factors for AN. Causal genes and biological pathways of eating disorders have yet to be elucidated and will require greater sample sizes and statistical power, and functional follow-up studies. Several studies are underway to recruit individuals with bulimia nervosa and binge-eating disorder to enable further genome-wide studies. Data collections and research labs focused on the genetics of eating disorders have joined together in a global effort with the Psychiatric Genomics Consortium. Molecular genetics research in the genome-wide era is improving knowledge about the biology behind the established heritability of eating disorders. This has the potential to offer new hope for understanding eating disorder etiology and for overcoming the therapeutic challenges that confront the eating disorder field.

Previous research has suggested that prenatal testosterone exposure masculinises disordered eating by comparing opposite- and same-gender twins. The objective of the current study is to replicate this finding using a sample of 439 identical and 213 fraternal females, 461 identical and 344 fraternal males, and 361 males and 371 females from opposite-gender twin pairs. Disordered eating was compared across twin types using the Eating Disorder Inventory–2. Inconsistent with previous findings, a main effect of co-twin gender was not found. Our results raise questions about the validity of prior evidence of the impact of prenatal testosterone exposure on patterns of disordered eating.

Background. Traditional models of psychiatric epidemiology often assume that the relationship between individuals and their environment is unidirectional, from environment to person. Accumulating evidence from developmental and genetic studies has made this perspective increasingly untenable.

Method. Literature search using Medline, PsycINFO, article references and contact with experts to identify all papers examining the heritability of measures of environments of relevance to psychiatry/psychology.

Results. We identified 55 independent studies organized into seven categories: general and specific stressful life events (SLEs), parenting as reported by child, parenting reported by parent, family environment, social support, peer interactions, and marital quality. Thirty-five environmental measures in these categories were examined by at least two studies and produced weighted heritability estimates ranging from 7% to 39%, with most falling between 15% and 35%. The weighted heritability for all environmental measures in all studies was 27%. The weighted heritability for environmental measures by rating method was: self-report 29%, informant report 26%, and direct rater or videotape observation (typically examining 10 min of behavior) 14%.

Conclusion. Genetic influences on measures of the environment are pervasive in extent and modest to moderate in impact. These findings largely reflect ‘actual behavior’ rather than ‘only perceptions’. Etiologic models for psychiatric illness need to account for the non-trivial influences of genetic factors on environmental experiences.