Associations Between Attention Deficit Hyperactivity Disorder Symptom Dimensions and Disordered Eating Symptoms in Adolescence: A Population-Based Twin Study.

Although bivariate associations between attention-deficit/hyperactivity disorder (ADHD) and eating disorders in adolescent girls and boys have been previously identified, the mechanistic link underlying the symptom-level associations remains unclear. We evaluated shared genetic and environmental influences on ADHD symptoms and disordered eating in 819 female and 756 male twins from the Swedish TCHAD cohort using bivariate models. Common additive genetic and unique environmental effects accounted for majority of ADHD and disordered eating associations in a differential manner. For girls, the strongest genetic correlation was observed for cognitive/inattention problems-bulimia (0.54), with genetic factors accounting for 67% of the phenotypic correlation. For boys, the strongest genetic correlations were observed for conduct problems-bulimia and hyperactivity-bulimia (~ 0.54), accounting for 83% and 95% of the phenotypic correlation, respectively. As per our findings, the risk of comorbidity and shared genetics highlights the need for preventative measures and specialized treatment for ADHD and disordered eating in both sexes.

Evaluating differences in setting expected body weight for children and adolescents in eating disorder treatment.

OBJECTIVE: Weight restoration or weight gain is a common goal in eating disorder treatment. However, approaches to determine expected body weight (EBW) vary. A standardized approach based on normative data for a patient's age and gender uses weight associated with median BMI (mBMI). An individualized approach predicts EBW based on a patient's individual growth trajectory. Little research has examined differences in these approaches. METHOD: Weight and clinical data were collected from patients ages 6-20 enrolled in virtual eating disorder treatment. EBW associated with mBMI was compared with EBW using the individualized approach. Linear mixed effects models examined differences in weight, eating disorder symptoms, depression, and anxiety, and whether EBW approach varied by patient characteristics. RESULTS: Patients (N = 609) were on average age 15.6 (2.29), 85% were cisgender female, and predominantly diagnosed with anorexia nervosa (83.1%). The individualized approach led to significantly higher EBW on average (mean difference = 8.4 lbs [SE: .75]; p < .001) compared to mBMI; 70% of patients had a higher EBW using the individualized approach. Notably, EBW varied based on gender and diagnosis and it took longer on average to achieve individualized EBW. Time was the strongest predictor of changes in psychosocial outcomes and there were no significant differences by EBW approach. DISCUSSION: Results from this study indicate that an individualized approach led to significantly higher EBWs compared with using mBMI. As underestimation of EBW may lead to higher risk of relapse, eating disorder professionals should consider using an individualized approach for setting EBW. PUBLIC SIGNIFICANCE: For eating disorder patients who need to gain weight, accurately estimating target body weight for eating disorder treatment is critical to recovery and preventing relapse. An individualized, patient-centered approach to estimating target body weight more accurately estimated target body weight than the standardized, median body mass index approach. Using an individualized approach to treatment may improve a patient's likelihood of full recovery.

Understanding comorbidity between eating disorder and premenstrual symptoms using a network analysis approach.

Eating disorder symptoms are associated with ovarian hormones and fluctuate predictably across the menstrual cycle. However, the specific symptoms that underlie these associations remain unclear. The current study aims to examine which specific eating disorder and premenstrual symptoms confer risk and maintain comorbidity using network analysis. Eating disorder and premenstrual symptoms were measured using the Eating Pathology Symptoms Inventory and the Daily Record of Severity of Problems, respectively, in a large sample of young adult females. Network analysis was used to explicate the structure of eating and premenstrual symptom networks separately and together. Eating disorder networks replicated previous literature and identified body dissatisfaction as a core feature, but was unique in identifying monitoring calories as an additional core feature. Central symptoms identified in the premenstrual symptom network were symptoms interference with daily life and activities and negative emotions brought on by hormone changes. Bridge symptoms between networks were identified as relating to eating behaviors, interference with daily activities, joint and muscle pain, and negative emotions brought on by hormone changes. This study suggests that the links between eating disorder and premenstrual symptoms extend past their individual effects on eating behavior and are indicative of a shared underlying mechanism.

Effectiveness of delivering evidence-based eating disorder treatment via telemedicine for children, adolescents, and youth.

Barriers limit access to eating disorder treatment. Evidence-based treatment delivered using telemedicine could expand access. This study determined the effectiveness of enhanced Family-Based Treatment (FBT+) delivered using telemedicine for children and adolescents with eating disorders. Participants had a confirmed eating disorder diagnosis, lived in states where treatment was available, and lived with a family member willing to participate. Virtual FBT+ was administered by a five-person team including a therapist, dietitian, medical provider, peer mentor, and family mentor for up to 12 months. Measures were recorded at baseline and varying frequencies throughout treatment. Weight was self-reported. Eating disorder symptoms were assessed with the Eating Disorder Examination-Questionnaire Short Form (EDE-QS) and depression and anxiety were measured using the Patient Health Questionnaire-9 (PHQ-9) and General Anxiety Disorder-7 (GAD-7). Caregiver burden and self-efficacy were measured using the Burden Assessment Scale, and Parent Versus Eating Disorder scale. The majority of patients (N = 210; 6 to 24 years old [mean 16 · 1 years]) were cisgender female (83%) White, (71%), required weight restoration (78%), and had anorexia nervosa, restricting type (63%). After 16 weeks, patients on weight restoration gained on average 11 · 3 [9 · 86, 12 · 8] pounds and the average change in EDE-QS score was -6 · 31 [-8 · 67, -4 · 10] points. Similar reductions were seen for depression (-2 · 62 [-4 · 24, -1 · 04]), anxiety (-1 · 44 [-1 · 12, 0 · 78]), and caregiver burden (-4 · 41 [2 · 45, 6 · 31]). Caregiver self-efficacy increased by 4 · 56 [3 · 53, 5 · 61] points. Patients and caregivers reported satisfaction with treatment. Virtual FBT+ for eating disorders can transcend geographical and psychosocial treatment barriers, expanding access to evidence-based eating disorder treatment.

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.

Recommendations to encourage participation of individuals from diverse backgrounds in psychiatric genetic studies.

We present innovative research practices in psychiatric genetic studies to ensure representation of individuals from diverse ancestry, sex assigned at birth, gender identity, age, body shape and size, and socioeconomic backgrounds. Due to histories of inappropriate and harmful practices against marginalized groups in both psychiatry and genetics, people of certain identities may be hesitant to participate in research studies. Yet their participation is essential to ensure diverse representation, as it is incorrect to assume that the same genetic and environmental factors influence the risk for various psychiatric disorders across all demographic groups. We present approaches developed as part of the Eating Disorders Genetics Initiative (EDGI), a study that required tailored approaches to recruit diverse populations across many countries. Considerations include research priorities and design, recruitment and study branding, transparency, and community investment and ownership. Ensuring representation in participants is costly and funders need to provide adequate support to achieve diversity in recruitment in prime awards, not just as supplemental afterthoughts. The need for diverse samples in genetic studies is critical to minimize the risk of perpetuating health disparities in psychiatry and other health research. Although the EDGI strategies were designed specifically to attract and enroll individuals with eating disorders, our approach is broadly applicable across psychiatry and other fields.

Genetics of eating disorders in the genome-wide era.

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.

The Eating Disorders Genetics Initiative (EDGI): study protocol.

BACKGROUND: The Eating Disorders Genetics Initiative (EDGI) is an international investigation exploring the role of genes and environment in anorexia nervosa, bulimia nervosa, and binge-eating disorder. METHODS: A total of 14,500 individuals with eating disorders and 1500 controls will be included from the United States (US), Australia (AU), New Zealand (NZ), and Denmark (DK). In the US, AU, and NZ, participants will complete comprehensive online phenotyping and will submit a saliva sample for genotyping. In DK, individuals with eating disorders will be identified by the National Patient Register, and genotyping will occur using bloodspots archived from birth. A genome-wide association study will be conducted within EDGI and via meta-analysis with other data from the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED). DISCUSSION: EDGI represents the largest genetic study of eating disorders ever to be conducted and is designed to rapidly advance the study of the genetics of the three major eating disorders (anorexia nervosa, bulimia nervosa, and binge-eating disorder). We will explicate the genetic architecture of eating disorders relative to each other and to other psychiatric and metabolic disorders and traits. Our goal is for EDGI to deliver "actionable" findings that can be transformed into clinically meaningful insights. TRIAL REGISTRATION: EDGI is a registered clinical trial: clinicaltrials.gov NCT04378101 .

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.

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.

Weight suppression and weight elevation are associated with eating disorder symptomatology in women age 50 and older: Results of the gender and body image study.

OBJECTIVE: Weight suppression (WS), the difference between highest past non-pregnancy weight and current weight, predicts negative outcomes in eating disorders, but the impact of WS and related weight constructs are understudied in nonclinical, midlife populations. We examined WS (current weight < highest weight) and weight elevation (WE), the opposite of WS (current weight > lowest weight) and their associations with eating psychopathology in women aged 50+. METHOD: Participants were a community-based sample (N = 1,776, Mage = 59) who completed demographic and eating psychopathology questions via online survey. WS, WE, and WS × WE were tested as predictors of outcome variables; BMI and medical conditions that affect weight were controlled for. RESULTS: Individuals that were higher on WS and WE were most likely to engage in current weight loss attempts, dieting in the past 5 years, and extreme lifetime restriction. Individuals with higher WS were more likely to experience binge eating, greater frequency of weight checking, overvaluation of shape and weight, and lifetime fasting. Individuals with higher WE were more likely to report negative life impacts of eating and dieting. Higher WS and WE each predicted higher levels of skipping meals over the lifetime. DISCUSSION: This novel study investigated WS in midlife women and introduced a new conceptualization of weight change (WE) that may be more relevant for aging populations given that women tend to gain weight with age. The findings implicate the utility of investigating both WS and WE as factors associated with eating psychopathology in midlife women.

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.

Reproductive and Appetite Hormones and Bulimic Symptoms during Midlife.

Eating disorders and related symptoms occur during midlife; however, little is known about their aetiology. It has been hypothesised that perimenopause represents a window of vulnerability for the development or exacerbation of eating disorder symptomatology because, like puberty, perimenopause is a period of reproductive hormone change. We compared symptoms of bulimia nervosa (bulimic symptomatology) assessed via mean scores on a self-report questionnaire in premenopausal and perimenopausal women. We also examined the association between hormone concentrations (reproductive/appetite) and bulimic symptomatology. No mean differences in bulimic symptomatology were observed between premenopause and perimenopause. However, there was a significant positive association between leptin and binge eating. Although no significant associations between reproductive hormones and bulimic symptomatology were observed, additional research is needed to provide definitive information. It is essential to learn more about the aetiology of eating disorders and related symptomatology across the lifespan in order to develop age-relevant treatment and prevention programs. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.

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.

Active ghrelin and the postpartum.

Postpartum depression (PPD) occurs in 10-15 % of women. The appetite hormone ghrelin, which fluctuates during pregnancy, is associated with depression in nonpregnant samples. Here, we examine the association between PPD and active ghrelin from pregnancy to postpartum. We additionally examine whether ghrelin changes from pregnancy to postpartum and differs between breastfeeding and non-breastfeeding women. Sixty women who participated in a survey examining PPD and had information in regard to ghrelin concentrations were included in the study. The Edinburgh Postnatal Depression Scale was used to assess symptoms of PPD. Raw ghrelin levels and ghrelin levels adjusted for creatinine were included as outcomes. Women screening positive for PPD at 12 weeks postpartum had higher pregnancy ghrelin concentrations. Ghrelin concentrations significantly decreased from pregnancy to 6 weeks postpartum and this change differed based on pregnancy depression status. Finally, ghrelin levels were lower in women who breastfed compared with women who were bottle-feeding. No significant findings remained once ghrelin levels were adjusted for creatinine. Although results do not suggest an association between PPD and ghrelin after adjusting for creatinine, future research should continue to explore this possibility extending further across the postpartum period with larger sample sizes.

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.

Risk for self-reported anorexia or bulimia nervosa based on drive for thinness and negative affect clusters/dimensions during adolescence: A three-year prospective study of the TChAD cohort.

OBJECTIVE: This study explored the cross-sectional and predictive effect of drive for thinness and/or negative affect scores on the development of self-reported anorexia nervosa (AN) and bulimia nervosa (BN). METHOD: K-means were used to cluster the Eating Disorder Inventory-Drive for Thinness (DT) and Child Behavior Checklist Anxious/Depressed (A/D) scores from 615 unrelated female twins at age 16-17. Logistic regressions were used to assess the effect of these clusters on self-reported eating disorder diagnosis at ages 16-17 (n = 565) and 19-20 (n = 451). RESULTS: DT and A/D scores were grouped into four clusters: Mild (scores lower than 90th percentile on both scales), DT (higher scores only on DT), A/D (higher scores only on A/D), and DT-A/D (higher scores on both the DT and A/D scales). DT and DT-A/D clusters at age 16-17 were associated cross-sectionally with AN and both cross-sectionally and longitudinally with BN. The DT-A/D cluster had the highest prevalence of AN at follow-up compared with all other clusters. Similarly, an interaction was observed between DT and A/D that predicted risk for AN. DISCUSSION: Having elevated DT and A/D scores may increase risk for eating disorder symptomatology above and beyond a high score on either alone. Findings suggest that cluster modeling based on DT and A/D may be useful to inform novel and useful intervention strategies for AN and BN in adolescents.