Anorexia nervosa and generalized anxiety disorder: Further explorations of the relation between anxiety and body mass index

We explore comorbidity of anorexia nervosa (AN) and generalized anxiety disorder (GAD) and their relation with body mass index (BMI) and evaluate the presence of fasting and excessive exercise which both have anxiolytic and weight loss effects. All participants were female: 32 with AN only, 607 with GAD only, 22 with AN and GAD (AN+GAD), and 5,424 with no history of AN or GAD (referent) from the Swedish Twin study of Adults: Genes and Environment (STAGE). Lowest adult BMI differed significantly (p < .001) and was lower in those with AN+GAD than those with AN only (p < .029). Those with AN+GAD were most likely to endorse fasting and excessive exercise, followed by women with AN only, women with GAD only, and the referent. Comorbid AN and GAD may be a particularly pernicious presentation influencing both BMI and proclivity to engage in behaviors such as fasting and exercise that serve both weight loss and anxiolytic goals

Understanding the Relation Between Anorexia Nervosa and Bulimia Nervosa in a Swedish National Twin Sample

We present a bivariate twin analysis of anorexia nervosa (AN) and bulimia nervosa (BN) to determine the extent to which shared genetic and environmental factors contribute to liability to these disorders

Effects of reducing the frequency and duration criteria for binge eating on lifetime prevalence of bulimia nervosa and binge eating disorder: Implications for DSM-5

We assessed the impact of reducing the binge eating frequency and duration thresholds on the diagnostic criteria for bulimia nervosa (BN) and binge eating disorder (BED)

Shared and unique genetic and environmental influences on binge eating and night eating: A Swedish twin study

We applied twin methodology to female and male twin pairs to further understand the nature of the relation between two behaviors associated with eating disorders—binge eating (BE) and night eating (NE) in an effort to determine the extent of overlap of genetic and environmental factors influencing liability to these behaviors. We calculated heritability estimates for males and females for each behavior and applied bivariate twin modeling to the female data to estimate the genetic and environmental correlation between these two traits. Data on BE and NE were derived from the Swedish Twin Study of Adults: Genes and Environment (STAGE) of the Swedish Twin Registry (STR; N = 11604). Prevalence estimates revealed sex differences with females more likely to endorse BE and males more likely to endorse NE. In males, we were only able to estimate univariate heritabilities due to small sample sizes: The heritability for BE was .74 [95% CI = (0.36, 0.93)] and for NE was .44 [95% CI = (0.24, 0.61)]. The best fitting bivariate model for females included additive genetic and unique environmental factors as well as the genetic correlation between BE and NE. Heritability estimates were 0.70 [95% CI = (0.26, 0.77)] for BE and 0.35 [95% CI = (0.17, 0.52)] for NE. The genetic correlation, 0.66 [95% CI = (0.48, 0.96)] suggests considerable overlap in the genetic factors influencing liability to BE and NE. In females, there is considerable overlap in the genetic factors that contribute to these traits, but the incomplete overlap allows for the influence of independent genetic and environmental factors as well. BE and NE in females are therefore best conceptualized as related but not identical traits

A behavioral-genetic investigation of bulimia nervosa and its relationship with alcohol use disorder

Bulimia nervosa (BN) and alcohol use disorder (AUD) frequently co-occur and may share genetic factors; however, the nature of their association is not fully understood. We assessed the extent to which the same genetic and environmental factors contribute to liability to BN and AUD. A bivariate structural equation model using a Cholesky decomposition was fit to data from 7,241 women who participated in the Swedish Twin study of Adults: Genes and Environment. The proportion of variance accounted for by genetic and environmental factors for BN and AUD and the genetic and environmental correlations between these disorders were estimated. In the best-fitting model, the heritability estimates were 0.55 (95% CI: 0.37; 0.70) for BN and 0.62 (95% CI: 0.54; 0.70) for AUD. Unique environmental factors accounted for the remainder of variance for BN. The genetic correlation between BN and AUD was 0.23 (95% CI: 0.01; 0.44), and the correlation between the unique environmental factors for the two disorders was 0.35 (95% CI: 0.08; 0.61), suggesting moderate overlap in these factors. Findings from this investigation provide additional support that some of the same genetic factors may influence liability to both BN and AUD

Substance use disorders in women with anorexia nervosa

Objective: We examined prevalence of in women substance use disorders (SUID) with: (1) anorexia nervosa (AN) restricting type (RAN); (2) AN with purging only (PAN); (3) AN with binge eating only (BAN); and (4) lifetime AN and bulimia nervosa (ANBN). Secondary analyses examined SUD related to lifetime purging behavior and lifetime binge eating. Method: Participants (N = 731) were drawn from the international Price Foundation Genetic Studies. Results: The prevalence of SUD differed across AN subtypes, with more in the ANBN group reporting SUD than those in the RAN and PAN groups. individuals who purged were more likely to report substance use than those who did not purge. Prevalence of SUD differed across lifetime binge eating status. Discussion: SUD are common in AN and are associated with bulimic symptomatology. Results underscore the het-erogeneity in AN, highlighting the importance of screening for SUD across AN subtype

Substance use disorders in women with anorexia nervosa

We examined prevalence of substance use disorders (SUD) in women with: (1) anorexia nervosa (AN) restricting type (RAN); (2) AN with purging only (PAN); (3) AN with binge eating only (BAN); and (4) lifetime AN and bulimia nervosa (ANBN). Secondary analyses examined SUD related to lifetime purging behavior and lifetime binge eating

Life beyond the eating disorder: Education, relationships, and reproduction

We investigated sociodemographic characteristics in women with and without lifetime eating disorders

Association of Candidate Genes with Phenotypic Traits Relevant to Anorexia Nervosa

This analysis is a follow-up to an earlier investigation of 182 genes selected as likely candidate genetic variations conferring susceptibility to anorexia nervosa (AN). As those initial case-control results revealed no statistically significant differences in single nucleotide polymorphisms, herein we investigate alternative phenotypes associated with AN. In 1762 females using regression analyses we examined: (1) lowest illness-related attained body mass index; (2) age at menarche; (3) drive for thinness; (4) body dissatisfaction; (5) trait anxiety; (6) concern over mistakes; and (7) the anticipatory worry and pessimism vs. uninhibited optimism subscale of the harm avoidance scale. After controlling for multiple comparisons, no statistically significant results emerged. Although results must be viewed in the context of limitations of statistical power, the approach illustrates a means of potentially identifying genetic variants conferring susceptibility to AN because less complex phenotypes associated with AN are more proximal to the genotype and may be influenced by fewer genes

A behavioral-genetic investigation of bulimia nervosa and its relationship with alcohol use disorder

Bulimia nervosa (BN) and alcohol use disorder (AUD) frequently co-occur and may share genetic factors; however, the nature of their association is not fully understood. We assessed the extent to which the same genetic and environmental factors contribute to liability to BN and AUD. A bivariate structural equation model using a Cholesky decomposition was fit to data from 7,241 women who participated in the Swedish Twin study of Adults: Genes and Environment. The proportion of variance accounted for by genetic and environmental factors for BN and AUD and the genetic and environmental correlations between these disorders were estimated. In the best-fitting model, the heritability estimates were 0.55 (95% CI: 0.37; 0.70) for BN and 0.62 (95% CI: 0.54; 0.70) for AUD. Unique environmental factors accounted for the remainder of variance for BN. The genetic correlation between BN and AUD was 0.23 (95% CI: 0.01; 0.44), and the correlation between the unique environmental factors for the two disorders was 0.35 (95% CI: 0.08; 0.61), suggesting moderate overlap in these factors. Findings from this investigation provide additional support that some of the same genetic factors may influence liability to both BN and AUD