Objective Although prior studies have demonstrated that depression is associated with an overeating-binge eating dimension (OE-BE), phenotypically, little research has investigated whether familial factors contribute to the co-occurrence of these phenotypes, especially in community samples with multiple racial/ethnic groups. We examined the extent to which familial (i.e., genetic and shared environmental) influences overlapped between Major Depressive Disorder (MDD) and OE-BE in a population-based sample and whether these influences were similar across racial/ethnic groups Method Participants included 3226 European-American (EA) and 550 African-American (AA) young adult women from the Missouri Adolescent Female Twin Study. An adaptation of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) was administered to assess lifetime DSM-IV MDD and OE-BE. Quantitative genetic modeling was used to estimate familial influences between both phenotypes; all models controlled for age. Results The best-fitting model, which combined racial/ethnic groups, found that additive genetic influences accounted for 44% (95% CI: 34%, 53%) of the MDD variance and 40% (25%, 54%) for OE-BE, with the remaining variances due to non-shared environmental influences. Genetic overlap was substantial (rg = .61 [.39, .85]); non-shared environmental influences on MDD and OE-BE overlapped weakly (re = .26 [.09, .42]) Discussion Results suggest that common familial influences underlie MDD and OE-BE, and the magnitude of familial influences contributing to the comorbidity between MDD and OE-BE is similar between EA and AA women. If racial/ethnic differences truly exist, then larger sample sizes may be needed to fully elucidate familial risk for comorbid MDD and OE-BE across these groups.

Aspects of disordered eating and personality traits, such as neuroticism are correlated and, individually, heritable. We examined the phenotypic correlation between binge eating episodes and indices of personality (neuroticism, extraversion, openness to experience, agreeableness, conscientiousness and control/impulsivity). For correlations ≥ |0.20|, we estimated the extent to which genetic and environmental factors contributed to this correlation. Participants included 3446 European-American same-sex female twins from the Missouri Adolescent Female Twin Study (median age = 22 years). Binge eating episode was assessed via interview questions. Personality traits were assessed by self-report questionnaires. There was a significant moderate phenotypic correlation between binge eating episode and neuroticism (r = 0.33), as well as conscientiousness (r=−0.21) while other correlations were significant but smaller (r ranging from −0.14 to 0.14). Individual differences in binge eating episodes, neuroticism and conscientiousness were attributed to additive genetic influences (38% [95% confidence interval: 21%–53%], 45% [38%–52%], and 44% [0.33–0.55] respectively), with the remaining variance due to individual-specific environmental influences. Covariance was attributable to genetic (neuroticism rg = 0.37; conscientiousness rg = −0.22) and individual-specific environmental (neuroticism re = 0.28; conscientiousness re = −0.19) influences. Personality traits may be an early indicator of genetic vulnerability to a variety of pathological behaviors including binge eating episode. Furthermore, prior research documenting phenotypic correlations between eating disorder diagnoses and personality may stem from etiological overlap between these personality traits and aspects of disordered eating, such as binge eating episode.

Objective We examined the association between 15 single nucleotide polymorphisms (SNPs) in HTR2A and characteristics of disordered eating, including weight/shape concerns, binge eating (with or without loss of control) and compensatory behaviors (purging and non-purging). Whether a lifetime history of major depressive disorder (MDD) moderated or mediated this association was also investigated. Method A sample of 1533 twin women of Caucasian descent that were part of the Missouri Adolescent Female Twin Study was used. Data were collected using self-report responses to a semi-structured interview. Logistic regression analyses were used to examine the association between weight/shape concerns, binge eating and compensatory behaviors and SNPs (where carriers of the minor allele were coded as 1). Results Two SNPs, rs6561333 and rs2296972, showed a protective influence against binge eating, with rs2296972 being significant at a trend level after application of the False Discovery Rate. The SNP was not associated with MDD nor did MDD moderate its putative relation with binge eating. Discussion Pending replication, our analyses provide preliminary evidence for intronic SNPs in HTR2A and their association with binge eating. Given the well-documented role of serotonergic dysfunction in eating psychopathology, this report warrants considerable further study.