Disordered eating and cardiometabolic risk factors in Chinese women: evidence from the China Health and Nutrition Survey.

Disordered eating (DE) is associated with elevated cardiometabolic risk (CMR) factors, yet little is known about this association in non-Western countries. We examined the association between DE characteristics and CMR and tested the potential mediating role of BMI. This cross-sectional study included 2005 Chinese women (aged 18-50 years) from the 2015 China Health and Nutrition Survey. Loss of control, restraint, shape concern and weight concern were assessed using selected questions from the SCOFF questionnaire and the Eating Disorder Examination-Questionnaire. Eight CMR were measured by trained staff. Generalised linear models examined associations between DE characteristics with CMR accounting for dependencies between individuals in the same household. We tested whether BMI potentially mediated significant associations using structural equation modelling. Shape concern was associated with systolic blood pressure (ß (95 % CI) 0·06 (0·01, 0·10)), diastolic blood pressure (DBP) (0·07 (95 % CI 0·03, 0·11)) and high-density lipoprotein (HDL)-cholesterol (-0·08 (95 % CI -0·12, -0·04)). Weight concern was associated with DBP (0·06 (95 % CI 0·02, 0·10)), triglyceride (0·06 (95 % CI 0·02, 0·10)) and HDL-cholesterol (-0·10 (95 % CI -0·14, -0·07)). Higher scores on DE characteristics were associated with higher BMI, and higher BMI was further associated with lower HDL-cholesterol and higher other CMR. In summary, we observed significant associations between shape and weight concerns with some CMR in Chinese women, and these associations were potentially partially mediated by BMI. Our findings suggest that prevention and intervention strategies focusing on addressing DE could potentially help reduce the burden of CMR in China, possibly through controlling BMI.

Shared Genetic Influences Between Loss-of-Control Eating and Body Mass Index in Adolescent Twins.

OBJECTIVE: Pediatric loss-of-control (LOC) eating is associated with high BMI and predicts binge-eating disorder and obesity onset with age. Research on the etiology of this common comorbidity has not explored the potential for shared genetic risk. This study examined genetic and environmental influences on LOC eating and its shared influence with BMI. METHOD: Participants were 499 monozygotic and 398 same-sex dizygotic twins (age = 17.38 years ± 0.67, BMIz = 0.03 ± 1.03, 54% female) from the Colorado Center for Antisocial Drug Dependence Study. LOC eating was assessed dichotomously. Self-reported height and weight were converted to BMIz. Univariate and bivariate twin models estimated genetic and environmental influences on LOC eating and BMIz. RESULTS: More girls (21%) than boys (9%, p < 0.001) reported LOC eating. The phenotypic correlation with BMIz was 0.03 in girls and 0.18 in boys. Due to the nonsignificant phenotypic correlation in girls, bivariate twin models were fit in boys only. Across all models, the best-fitting model included genetic and unique environmental effects. Genetic factors accounted for 0.51 (95% CI: 0.23, 0.73) of the variance of LOC eating in girls and 0.54 (0.18, 0.90) in boys. The genetic correlation between LOC eating and BMIz in boys was 0.45 (0.15, 0.75). DISCUSSION: Findings indicate moderate heritability of LOC eating in adolescence, while emphasizing the role of unique environmental factors. In boys, LOC eating and BMIz share a proportion of their genetic influences.

ARFID Genes and Environment (ARFID-GEN): study protocol.

BACKGROUND: The Avoidant Restrictive Food Intake Disorder - Genes and Environment (ARFID-GEN) study is a study of genetic and environmental factors that contribute to risk for developing ARFID in children and adults. METHODS: A total of 3,000 children and adults with ARFID from the United States will be included. Parents/guardians and their children with ARFID (ages 7 to 17) and adults with ARFID (ages 18 +) will complete comprehensive online consent, parent verification of child assent (when applicable), and phenotyping. Enrolled participants with ARFID will submit a saliva sample for genotyping. A genome-wide association study of ARFID will be conducted. DISCUSSION: ARFID-GEN, a large-scale genetic study of ARFID, is designed to rapidly advance the study of the genetics of eating disorders. We will explicate the genetic architecture of ARFID relative to other eating disorders and to other psychiatric, neurodevelopmental, and metabolic disorders and traits. Our goal is for ARFID to deliver "actionable" findings that can be transformed into clinically meaningful insights. TRIAL REGISTRATION: ARFID-GEN is a registered clinical trial: clinicaltrials.gov NCT05605067.

Shared Genetic Factors Contributing to the Overlap between Attention-Deficit/Hyperactivity Disorder Symptoms and Overweight/Obesity in Swedish Adolescent Girls and Boys.

Attention-deficit/hyperactivity disorder (ADHD) and obesity are positively associated, with increasing evidence that they share genetic risk factors. Our aim was to examine whether these findings apply to both types of ADHD symptoms for female and male adolescents. We used data from 791 girl and 735 boy twins ages 16-17 years to examine sex-specific phenotypic correlations between the presence of ADHD symptoms and overweight/obese status. For correlations exceeding .20, we then fit bivariate twin models to estimate the genetic and environmental correlations between the presence of ADHD symptoms and overweight/obese status. ADHD symptoms and height/weight were parent- and self-reported, respectively. Phenotypic correlations were .30 (girls) and .08 (boys) for inattention and overweight/obese status and .23 (girls) and .14 (boys) for hyperactivity/impulsivity and overweight/obese status. In girls, both types of ADHD symptoms and overweight/obese status were highly heritable, with unique environmental effects comprising the remaining variance. Furthermore, shared genetic effects explained most of the phenotypic correlations in girls. Results suggest that the positive association of both types of ADHD symptoms with obesity may be stronger in girls than boys. Further, in girls, these associations may stem primarily from shared genetic factors.

Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies.

Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [rg ], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (rg = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (rg = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (rg = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (rgs = -0.19 to -0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors.

Selective Inhibition of PDE4B Reduces Binge Drinking in Two C57BL/6 Substrains.

Cyclic AMP (cAMP)-dependent signaling is highly implicated in the pathophysiology of alcohol use disorder (AUD), with evidence supporting the efficacy of inhibiting the cAMP hydrolyzing enzyme phosphodiesterase 4 (PDE4) as a therapeutic strategy for drinking reduction. Off-target emetic effects associated with non-selective PDE4 inhibitors has prompted the development of selective PDE4 isozyme inhibitors for treating neuropsychiatric conditions. Herein, we examined the effect of a selective PDE4B inhibitor A33 (0-1.0 mg/kg) on alcohol drinking in both female and male mice from two genetically distinct C57BL/6 substrains. Under two different binge-drinking procedures, A33 pretreatment reduced alcohol intake in male and female mice of both substrains. In both drinking studies, there was no evidence for carry-over effects the next day; however, we did observe some sign of tolerance to A33's effect on alcohol intake upon repeated, intermittent, treatment (5 injections of 1.0 mg/kg, every other day). Pretreatment with 1.0 mg/kg of A33 augmented sucrose intake by C57BL/6NJ, but not C57BL/6J, mice. In mice with a prior history of A33 pretreatment during alcohol-drinking, A33 (1.0 mg/kg) did not alter spontaneous locomotor activity or basal motor coordination, nor did it alter alcohol's effects on motor activity, coordination or sedation. In a distinct cohort of alcohol-naïve mice, acute pretreatment with 1.0 mg/kg of A33 did not alter motor performance on a rotarod and reduced sensitivity to the acute intoxicating effects of alcohol. These data provide the first evidence that selective PDE4B inhibition is an effective strategy for reducing excessive alcohol intake in murine models of binge drinking, with minimal off-target effects. Despite reducing sensitivity to acute alcohol intoxication, PDE4B inhibition reduces binge alcohol drinking, without influencing behavioral sensitivity to alcohol in alcohol-experienced mice. Furthermore, A33 is equally effective in males and females and exerts a quantitatively similar reduction in alcohol intake in mice with a genetic predisposition for high versus moderate alcohol preference. Such findings further support the safety and potential clinical utility of targeting PDE4 for treating AUD.

Premenstrual symptoms as a marker of ovarian hormone sensitivity in eating disorders.

OBJECTIVE: Research indicates a link between ovarian hormones and eating pathology, suggesting that some women with an eating disorder may be ovarian hormone sensitive. Using premenstrual symptoms (PMS) as an indirect measure of ovarian hormone sensitivity, we investigated the association between 11 PMS domains and four core eating disorder symptoms: body dissatisfaction, binge eating, purging, and restriction. METHOD: Participants were young adult women (N = 455) who completed an online survey. PMS were assessed using the Daily Record of Severity of Problems and eating pathology with the Eating Pathology Symptoms Inventory. Pearson correlations were calculated between PMS domains and eating disorder symptoms followed by a stepwise regression to create a more refined model for each eating disorder symptom, including relevant covariates. RESULTS: Significant correlations between a majority of eating disorder symptoms and PMS emerged (r's = .13-.37; p < .01). Backward regression revealed significant PMS domain predictors for each symptom. The final models captured a small-to-moderate amount of variance for each eating disorder symptom (R2 = 0.06-0.25). DISCUSSION: Women who experience physical and psychological PMS may be at risk for eating disorder symptoms; PMS could be a marker of ovarian hormone sensitivity in women at risk for an eating disorder. Future studies should address mechanisms underlying this association.

Associations between eating expectancies and Eating disorder symptoms in men and women.

Eating expectancies, or learned expectations that an individual has about eating, prospectively predict eating disorder (ED) symptoms. Most studies examining eating expectancies have focused on one or two eating expectancies and their relation with bulimic symptoms. In addition, these studies have been conducted mostly in women. Thus, it is unclear whether: 1) associations between eating expectancies and ED symptoms vary between men and women, and 2) extend to ED symptoms other than bulimic symptoms. The current study (N = 197 undergraduate men and 246 undergraduate women) investigated sex variance in a model of eating expectancies and ED symptoms, including factors associated with ED symptoms (i.e., negative urgency, negative affect, alcohol use, drug use, and body mass index). Sex variance was tested using path analysis in a model including eating expectancies and associated factors, with excessive exercise, negative attitudes toward obesity, restricting, cognitive restraint, binge eating, purging, muscle building, and body dissatisfaction as dependent variables. Unconstrained (i.e., unconstrained paths across men and women) and constrained (i.e., constraining paths across men and women) models were tested. The unconstrained and constrained models differed significantly, indicating that the models varied by sex. For both sexes, eating expectancies were uniquely associated with ED symptoms. For men, Eating Manages Negative Affect was significantly associated with the most ED symptoms. In contrast, for women, Eating Leads to Feeling Out of Control was associated with the most ED symptoms. Previous findings regarding eating expectancies and ED symptoms in women may not generalize to men. Intervening on eating expectancies in a sex-specific way may help reduce specific ED symptoms.

Associations Between Alcohol Involvement and Drive for Thinness and Body Dissatisfaction in Adolescent Twins: A Bivariate Twin Study.

BACKGROUND: Alcohol involvement has familial associations with bulimic symptoms (i.e., binge eating, inappropriate compensatory behaviors), with several studies indicating a genetic overlap between the two. It is unclear whether overlapping familial risk with alcohol involvement extends to other eating disorder symptoms. Understanding the genetic overlap between alcohol involvement and other eating disorder symptoms may aid in more targeted interventions for comorbid alcohol use-eating disorder symptoms. Thus, we investigated associations between alcohol involvement and 2 core eating disorder symptoms: drive for thinness and body dissatisfaction in adolescent female and male twins. METHODS: We assessed 3 levels of alcohol involvement: alcohol use in the last month, having ever been intoxicated, and alcohol intoxication frequency via self-report. The Eating Disorder Inventory-II assessed drive for thinness and body dissatisfaction. Sex-specific biometrical twin modeling examined the genetic overlap between alcohol involvement and eating disorder symptoms. RESULTS: Phenotypic associations between alcohol involvement, drive for thinness, and body dissatisfaction were significantly greater in girls compared with boys. A majority of the associations between alcohol involvement, drive for thinness, and body dissatisfaction in girls, but not boys, met our threshold for twin modeling (phenotypic r > 0.20). Moderate genetic correlations were observed between the 3 aspects of alcohol involvement and drive for thinness. Moderate genetic correlations were observed between alcohol use and intoxication frequency and body dissatisfaction. CONCLUSIONS: Together with the literature on alcohol involvement and bulimic symptoms, these findings suggest a generalized association between alcohol involvement and eating disorder symptoms in girls, whereas this association may be symptom specific in boys. Genetic correlations indicate that the amount and direction of this genetic overlap differs across specific symptoms. When intervening on comorbid alcohol involvement and eating disorder symptoms, it may be important to target-specific eating disorder symptoms.

Genetics of Anorexia Nervosa.

PURPOSE OF REVIEW: Genetic factors contribute to the etiology of anorexia nervosa (AN). This review synthesizes the current state of knowledge about the genetic etiology of AN, provides directions for future research, and discusses clinical implications for this research. RECENT FINDINGS: Candidate gene meta-analyses indicate serotonin genes may be involved in the genetic etiology of AN. Three genome-wide association studies have been conducted and one genome-wide significant locus was identified. Cross-disorder analyses suggest shared genetic risk between AN and several psychiatric, educational, and medical phenotypes. Much has been learned about the genetic etiology of AN over the past 3 decades. However, to fully understand the genetic architecture, we must consider all aspects including common variation, cross-disorder analysis, rare variation, copy number variation, and gene-environment interplay. Findings have important implications for the development of treatment and prevention approaches and for how AN, and psychiatric and medical diseases in general, are conceptualized.

The Science Behind the Academy for Eating Disorders' Nine Truths About Eating Disorders.

OBJECTIVE: In 2015, the Academy for Eating Disorders collaborated with international patient, advocacy, and parent organizations to craft the 'Nine Truths About Eating Disorders'. This document has been translated into over 30 languages and has been distributed globally to replace outdated and erroneous stereotypes about eating disorders with factual information. In this paper, we review the state of the science supporting the 'Nine Truths'. METHODS: The literature supporting each of the 'Nine Truths' was reviewed, summarized and richly annotated. RESULTS: Most of the 'Nine Truths' arise from well-established foundations in the scientific literature. Additional evidence is required to further substantiate some of the assertions in the document. Future investigations are needed in all areas to deepen our understanding of eating disorders, their causes and their treatments. CONCLUSIONS: The 'Nine Truths About Eating Disorders' is a guiding document to accelerate global dissemination of accurate and evidence-informed information about eating disorders. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.

Genetic and environmental components to self-induced vomiting.

OBJECTIVE: We examined the association between the genetic and environmental factors contributing to the liability to having ever engaged in self-induced vomiting (SIV initiation) and the genetic and environmental factors contributing to regular SIV behaviors (weekly or daily) for weight control. METHOD: SIV was assessed in 3,942 women from monozygotic twin pairs and 2,790 women from same-sex dizygotic twin pairs, aged 20-47, from the Swedish Twin study of Adults: Genes and Environment. A causal-contingent-common pathway model assessed the extent to which genetic and environmental factors that influence initiation of SIV also influence regular SIV behaviors. RESULTS: In the best-fit model, genetic and individual-specific environmental factors influenced liability to SIV initiation. The genetic factors influencing regular SIV behaviors were the same as the genetic factors influencing SIV initiation. Additional individual-specific environmental factors that were unrelated to SIV initiation influenced regular SIV behaviors. DISCUSSION: Our findings provide evidence that the underlying liabilities for SIV initiation and regular SIV lie on the same continuum given the degree of overlap in risk between SIV initiation and regular SIV behaviors. Further, the lack of specific genetic factors and the importance of individual-specific environmental factors for regular SIV behaviors highlight the significance of environmental factors in the etiology of eating disorder symptomatology and the non-deterministic nature of genetic factors. Finally, our results suggest that when it comes to preventing individuals from developing regular SIV behavior, intervening at an environmental level is warranted.

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.

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.

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.

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.

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.

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.

Shared genetic risk between anorexia nervosa and cardiovascular disease events: Evidence from genome-wide association studies.

OBJECTIVE: Cardiovascular complications occur in up to 80% of patients with anorexia nervosa (AN), yet the underlying mechanisms warrant further investigation. We assessed the genetic correlation (rg ) between AN and cardiovascular disease (CVD) events to inform whether elevated cardiovascular risk among individuals with AN is due to shared genetic effects. METHOD: We used genome-wide association study summary statistics for AN (N = 72,517), AN with binge eating (N = 12,630), AN without binge eating (N = 12,516), and six CVD events (N = 390,142 to 977,323). We calculated the rg s via linkage disequilibrium score regression and corrected for multiple testing using false discovery rate. RESULTS: Significant rg s emerged between AN with heart failure (rg  = -0.11, SE = 0.05, q = .04) and myocardial infarction (rg  = -0.10, SE = 0.03, q = .01). AN with binge eating had a significant rg with myocardial infarction (rg  = -0.15, SE = 0.06, q = .02). No significant rg emerged between AN without binge eating and any CVD event. DISCUSSION: Some loci affect the liability to AN and CVD in opposite directions and the shared genetic effects may not be consistent across all CVD events. Our results provide further evidence suggesting that the elevated cardiovascular risk in AN may not be due to shared genetic underpinnings, but more likely a downstream consequence of the disease.

An examination of the representativeness assumption for twin studies of eating pathology and internalizing symptoms.

Little research has investigated whether the twin representativeness assumption (that results from twin research generalize to singletons) holds for eating pathology and internalizing symptoms. This study compared disordered eating, depression, and anxiety among young adult female twins versus singletons. Participants included 292 twins and 997 singletons in three samples. Questionnaires included the Minnesota Eating Behavior Survey, Eating Disorder Examination Questionnaire, Beck Depression Inventory, and State-Trait Anxiety Inventory. We examined mean differences between twins' and singletons' scores, after adjusting for age, body mass index, and ethnicity. We found statistically significant mean differences on psychopathology, with twins reporting less disordered eating and internalizing symptoms compared with singletons. Effect sizes of these mean differences were small to moderate. Our results suggest that twins report less disordered eating and internalizing symptoms than singletons, which, combined with the generally small effect sizes, indicate that results from twin samples generalize to singletons.