Melissa A. Munn-Chernoff

Associations between body mass index, post-traumatic stress disorder, and child maltreatment in young women.

The objective of this study was to examine interrelationships between child maltreatment, post-traumatic stress disorder (PTSD) and body mass index (BMI) in young women. We used multinomial logistic regression models to explore the possibility that PTSD statistically mediates or moderates the association between BMI category and self-reported childhood sexual abuse (CSA), physical abuse (CPA), or neglect among 3,699 young women participating in a population-based twin study. Obese women had the highest prevalence of CSA, CPA, neglect, and PTSD (p<.001 for all). Although all three forms of child maltreatment were significantly, positively associated with overweight and obesity in unadjusted models, only CSA was significantly associated with obesity after adjusting for other forms of maltreatment and covariates (OR=2.21, 95% CI: 1.63, 3.00). CSA and neglect, but not CPA, were associated with underweight in unadjusted models; however, after adjusting for other forms of maltreatment and covariates, the associations were no longer statistically significant (OR=1.43, 95% CI: 0.90-2.28 and OR=2.16, 95% CI: 0.90-5.16 for CSA and neglect, respectively). Further adjustment for PTSD generally resulted in modest attenuation of effects across associations of child maltreatment forms with BMI categories, suggesting that PTSD may, at most, be only a weak partial mediator of these associations. Future longitudinal studies are needed to elucidate the mechanisms linking CSA and obesity and to further evaluate the role of PTSD in associations between child maltreatment and obesity.

Are there common familial influences for major depressive disorder and an overeating-binge eating dimension in both European American and African American Female twins?

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 3,226 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.

Genetic and Environmental Risk for Major Depression in African-American and European-American Women

It is unknown whether there are racial differences in the heritability of major depressive disorder (MDD) because most psychiatric genetic studies have been conducted in samples comprised largely of white non-Hispanics. To examine potential differences between African-American (AA) and European-American (EA) young adult women in (1) Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) MDD prevalence, symptomatology, and risk factors, and (2) genetic and/or environmental liability to MDD, we analyzed data from a large population-representative sample of twins ascertained from birth records (n = 550 AA and n = 3226 EA female twins) aged 18-28 years at the time of MDD assessment by semi-structured psychiatric interview. AA women were more likely to have MDD risk factors; however, there were no significant differences in lifetime MDD prevalence between AA and EA women after adjusting for covariates (odds ratio = 0.88, 95% confidence interval [CI]: 0.67-1.15). Most MDD risk factors identified among AA women were also associated with MDD at similar magnitudes among EA women. Although the MDD heritability point estimate was higher among AA women than EA women in a model with paths estimated separately by race (56%, 95% CI: 29-78% vs. 41%, 95% CI: 29-52%), the best fitting model was one in which additive genetic and non-shared environmental paths for AA and EA women were constrained to be equal (A = 43%, 33-53% and E = 57%, 47-67%). In spite of a marked elevation in the prevalence of environmental risk exposures related to MDD among AA women, there were no significant differences in lifetime prevalence or heritability of MDD between AA and EA young women.

Anorexia Nervosa, Major Depression, and Suicide Attempts: Shared Genetic Factors

The extent to which genetic and environmental factors influenced anorexia nervosa (AN), major depressive disorder (MDD), and suicide attempts (SA) were evaluated. Participants were 6,899 women from the Swedish Twin Study of Adults: Genes and Environment. A Cholesky decomposition assessed independent and overlapping genetic and environmental contributions to AN, MDD, and SA. Genetic factors accounted for a substantial amount of liability to all three traits; unique environmental factors accounted for most of the remaining liability. Shared genetic factors may underlie the coexpression of these traits. Results underscore the importance of assessing for signs of suicide among individuals with AN.

Prevalence of and familial influences on purging disorder in a community sample of female twins.

OBJECTIVE Purging disorder (PD) was recently included as an otherwise specified feeding or eating disorder (OSFED) in the DSM-5; however, limited information is available on its prevalence, and its etiology is unknown. METHOD Data from 1,790 monozygotic and 1,440 dizygotic European American female twins (age range = 18-29 years) from the Missouri Adolescent Female Twin Study were used to investigate prevalence and familial influences for PD. A structured clinical interview assessed lifetime DSM-IV criteria for eating disorders and PD. After adjustment for age, twin correlations and biometrical twin models were used to estimate familial (i.e., genetic plus shared environmental) influences on PD. RESULTS One hundred and twenty one (3.77%; 95% CI: 3.14, 4.49) women met criteria for lifetime PD. Twin correlations suggested that genetic, shared environmental, and nonshared environmental factors influenced liability to PD. Nonshared environmental factors accounted for 56% [35%, 79%] of the variance in PD. Although familial effects accounted for a significant proportion of variance (44% [21%, 65%]), it was not possible to disentangle the independent contributions of additive genetic effects (20% [0%, 65%]) and shared environmental effects (24% [0%, 57%]). DISCUSSION PD is a prevalent form of eating pathology. Familial factors are relevant to the development of PD but do not demonstrate the magnitude of heritable factors found for other eating disorders.

A Primer on the Genetics of Comorbid Eating Disorders and Substance Use Disorders

Eating disorders (EDs) and substance use disorders (SUDs) frequently co-occur; however, the reasons for this are unclear. We review the current literature on genetic risk for EDs and SUDs, as well as preliminary findings exploring whether these classes of disorders have overlapping genetic risk. Overall, genetic factors contribute to individual differences in liability to multiple EDs and SUDs. Although initial family studies concluded that no shared familial (which includes genetic) risk between EDs and SUDs exists, twin studies suggest a moderate proportion of shared variance is attributable to overlapping genetic factors, particularly for those EDs characterized by binge eating and/or inappropriate compensatory behaviours. No adoption or molecular genetic studies have examined shared genetic risk between these classes of disorders. Research investigating binge eating and inappropriate compensatory behaviours using emerging statistical genetic methods, as well as examining gene-environment interplay, will provide important clues into the aetiology of comorbid EDs and SUDs.

Genetic overlap between alcohol use disorder and bulimic behaviors in European American and African American women

BACKGROUND Despite substantial evidence that alcohol use disorder (AUD) and bulimic behaviors (i.e., binge eating and compensatory behaviors) co-occur, insufficient information exists regarding a possible shared etiology. Moreover, although numerous twin studies of European ancestry individuals have reported moderate heritability estimates for AUD and bulimic behaviors, with little evidence for shared environmental factors, research on genetic and environmental risk in African American (AA) individuals is lacking. METHODS We investigated specific and overlapping genetic and environmental influences on AUD and bulimic behaviors in 3232 European American (EA; 55.38% monozygotic) and 549 AA (42.81% monozygotic) young adult female twins from the Missouri Adolescent Female Twin Study (age range=18-29 years). A structured clinical interview assessed lifetime DSM-5 AUD (minus craving) and bulimic behaviors. Biometrical twin modeling was conducted to generate age-adjusted estimates of genetic and environmental influences on AUD, bulimic behaviors, and their comorbidity. RESULTS Estimates of genetic and environmental contributions on AUD and bulimic behaviors could be equated across EA and AA women. Additive genetic effects accounted for 59% (95% CI: 50%, 66%) and 43% (33%, 52%) of the variance in AUD and bulimic behaviors, respectively, with the remainder due to non-shared environmental effects. Shared genetic factors (rg=.33 (.18, .49)) were solely responsible for the correlation between phenotypes; the non-shared environmental correlation was not significant (re=.10 (-.05, .25)). CONCLUSIONS Findings indicate similar magnitudes of genetic and environmental effects on AUD and bulimic behaviors for EA and AA women and implicate common genetic mechanisms underlying liability to these problem behaviors.

Is the Relationship Between Binge Eating Episodes and Personality Attributable to Genetic Factors

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 3,446 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% CI: 21-53%], 45% [95% CI: 38-52%], and 44% [95% CI: 0.33-0.55%] respectively), with the remaining variance attributed to individual-specific environmental influences. Covariance was attributable to genetic (neuroticism r g = 0.37; conscientiousness r g = -0.22) and individual-specific environmental (neuroticism r e = 0.28; conscientiousness r e = -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 have stemmed from etiological overlap between these personality traits and aspects of disordered eating, such as binge eating episode.

Bulimic Behaviors and Early Substance Use: Findings from a Cotwin-Control Study

BACKGROUND Bulimic behaviors (i.e., binge eating and compensatory behaviors) and substance use frequently co-occur. However, the etiology underlying this association is poorly understood. This study evaluated the association between bulimic behaviors and early substance use, controlling for genetic and shared environmental factors. METHODS Participants were 3,540 young adult women from the Missouri Adolescent Female Twin Study. A telephone adaptation of the Semi-Structured Assessment for the Genetics of Alcoholism interview assessed DSM-IV bulimic behaviors, substance use, and other psychological characteristics. Lifetime bulimic behaviors were examined in twin pairs concordant and discordant for early substance use. Logistic regressions were adjusted for the nonindependence of twin data, zygosity, age, body mass index, early menarche (onset before age 12), and early sex (first consensual sexual intercourse before age 15). RESULTS In the entire study population, women who reported early use of alcohol or nicotine were more likely to engage in bulimic behaviors after adjusting for covariates. In 53 pairs of monozygotic twins discordant for alcohol experimentation before age 15, the twin who reported early alcohol experimentation had 3.21 (95% confidence interval = 1.54 to 6.67) times higher odds of reporting bulimic behaviors than the cotwin who did not report early alcohol experimentation, even after adjustment for covariates. CONCLUSIONS Findings suggest that early alcohol experimentation may contribute to the development of bulimic behaviors via mechanisms extending beyond shared vulnerability, including individual-specific environmental experiences or causal pathways.

Preliminary evidence for the role of HTR2A variants in binge eating in young women

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 nonpurging). Whether a lifetime history of major depressive disorder (MDD) moderated or mediated this association was also investigated. A sample of 1533 twin women of White descent that were part of the Missouri Adolescent Female Twin Study was used. Data were collected using self-report responses to a semistructured 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). 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. 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.