Genetic influences on eight psychiatric disorders based on family data of 4 408 646 full and half-siblings, and genetic data of 333 748 cases and controls.

BACKGROUND: Most studies underline the contribution of heritable factors for psychiatric disorders. However, heritability estimates depend on the population under study, diagnostic instruments, and study designs that each has its inherent assumptions, strengths, and biases. We aim to test the homogeneity in heritability estimates between two powerful, and state of the art study designs for eight psychiatric disorders. METHODS: We assessed heritability based on data of Swedish siblings (N = 4 408 646 full and maternal half-siblings), and based on summary data of eight samples with measured genotypes (N = 125 533 cases and 208 215 controls). All data were based on standard diagnostic criteria. Eight psychiatric disorders were studied: (1) alcohol dependence (AD), (2) anorexia nervosa, (3) attention deficit/hyperactivity disorder (ADHD), (4) autism spectrum disorder, (5) bipolar disorder, (6) major depressive disorder, (7) obsessive-compulsive disorder (OCD), and (8) schizophrenia. RESULTS: Heritability estimates from sibling data varied from 0.30 for Major Depression to 0.80 for ADHD. The estimates based on the measured genotypes were lower, ranging from 0.10 for AD to 0.28 for OCD, but were significant, and correlated positively (0.19) with national sibling-based estimates. When removing OCD from the data the correlation increased to 0.50. CONCLUSIONS: Given the unique character of each study design, the convergent findings for these eight psychiatric conditions suggest that heritability estimates are robust across different methods. The findings also highlight large differences in genetic and environmental influences between psychiatric disorders, providing future directions for etiological psychiatric research.

Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index.

The maintenance of normal body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time. Prior to the onset of AN, premorbid body mass index (BMI) spans the entire range from underweight to obese. After recovery, patients have reduced rates of overweight and obesity. As such, loci involved in body weight regulation may also be relevant for AN and vice versa. Our primary analysis comprised a cross-trait analysis of the 1000 single-nucleotide polymorphisms (SNPs) with the lowest P-values in a genome-wide association meta-analysis (GWAMA) of AN (GCAN) for evidence of association in the largest published GWAMA for BMI (GIANT). Subsequently we performed sex-stratified analyses for these 1000 SNPs. Functional ex vivo studies on four genes ensued. Lastly, a look-up of GWAMA-derived BMI-related loci was performed in the AN GWAMA. We detected significant associations (P-values <5 × 10-5, Bonferroni-corrected P<0.05) for nine SNP alleles at three independent loci. Interestingly, all AN susceptibility alleles were consistently associated with increased BMI. None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2: CARF and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previously been associated with AN or obesity. Sex-stratified analyses revealed that the strongest BMI signal originated predominantly from females (chr. 10 rs1561589; Poverall: 2.47 × 10-06/Pfemales: 3.45 × 10-07/Pmales: 0.043). Functional ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fasting. Hypothalamic expression of Ctbp2 was increased in diet-induced obese (DIO) mice as compared with age-matched lean controls. We observed no evidence for associations for the look-up of BMI-related loci in the AN GWAMA. A cross-trait analysis of AN and BMI loci revealed variants at three chromosomal loci with potential joint impact. The chromosome 10 locus is particularly promising given that the association with obesity was primarily driven by females. In addition, the detected altered hypothalamic expression patterns of Ctbp2 and Nbeal1 as a result of fasting and DIO implicate these genes in weight regulation.

A Danish register-based study on involuntary treatment in anorexia nervosa.

OBJECTIVE: Involuntary treatment is controversial and widely debated, but remains a significant component of treatment for severe anorexia nervosa. Given how little is known about this topic, we describe the frequency of various involuntary measures in a national cohort of all patients diagnosed with anorexia nervosa. In a subsample of patients, we explored predictors of the first involuntary measure recorded. METHOD: Descriptive statistics and Cox proportional hazard analyses were conducted using the national registers of Denmark covering the total population. Data from the National Patient Register and the Psychiatric Central Research Register including all psychiatric visits from 1969 onwards were merged with data from the National Register on Coercion covering 1999 onward. Involuntary measures registered between 2000 and 2013 were analyzed. RESULTS: A total of 4,727 patients with a diagnosis of anorexia nervosa representing 16,592 admissions were included. Eighteen percent experienced at least one involuntary measure. A variety of measures were used with tube feeding being the most frequent followed by mechanical restraint, involuntary medication, physical restraint, constant observation, and sedative medication. A subsample of 2% of AN patients had more than 100 involuntary measures recorded. The first recorded involuntary measure was predicted by most but not all psychiatric comorbidities, especially schizophrenia, autism spectrum, and personality disorders, older age at first diagnosis, and previous admissions. DISCUSSION: It is important to develop a more granular understanding of patients at risk of requiring involuntary treatment and to determine how best to treat them effectively with minimal use of involuntary measures.

Genetic and environmental aspects in the association between attention-deficit hyperactivity disorder symptoms and binge-eating behavior in adults: a twin study.

BACKGROUND: Prior research demonstrated that attention-deficit hyperactivity disorder (ADHD) is associated with binge-eating behavior, binge-eating disorder (BED), and bulimia nervosa (BN). The aim of this study was to investigate these associations in an adult twin population, and to determine the extent to which ADHD symptoms and binge-eating behavior share genetic and environmental factors. METHODS: We used self-reports of current ADHD symptoms and lifetime binge-eating behavior and associated characteristics from a sample of over 18 000 adult twins aged 20-46 years, from the population-based Swedish Twin Registry. Mixed-effects logistic regression was used to examine the association between ADHD and lifetime binge-eating behavior, BED, and BN. Structural equation modeling was used in 13 773 female twins to determine the relative contribution of genetic and environmental factors to the association between ADHD symptoms and binge-eating behavior in female adult twins. RESULTS: ADHD symptoms were significantly associated with lifetime binge-eating behavior, BED, and BN. The heritability estimate for current ADHD symptoms was 0.42 [95% confidence interval (CI) 0.41-0.44], and for lifetime binge-eating behavior 0.65 (95% CI 0.54-0.74). The genetic correlation was estimated as 0.35 (95% CI 0.25-0.46) and the covariance between ADHD and binge-eating behavior was primarily explained by genetic factors (91%). Non-shared environmental factors explained the remaining part of the covariance. CONCLUSIONS: The association between adult ADHD symptoms and binge-eating behavior in females is largely explained by shared genetic risk factors.

Paternal age at childbirth and eating disorders in offspring.

BACKGROUND: Advanced paternal age at childbirth is associated with psychiatric disorders in offspring, including schizophrenia, bipolar disorder and autism. However, few studies have investigated paternal age's relationship with eating disorders in offspring. In a large, population-based cohort, we examined the association between paternal age and offspring eating disorders, and whether that association remains after adjustment for potential confounders (e.g. parental education level) that may be related to late/early selection into fatherhood and to eating disorder incidence. METHOD: Data for 2 276 809 individuals born in Sweden 1979-2001 were extracted from Swedish population and healthcare registers. The authors used Cox proportional hazards models to examine the effect of paternal age on the first incidence of healthcare-recorded anorexia nervosa (AN) and all eating disorders (AED) occurring 1987-2009. Models were adjusted for sex, birth order, maternal age at childbirth, and maternal and paternal covariates including country of birth, highest education level, and lifetime psychiatric and criminal history. RESULTS: Even after adjustment for covariates including maternal age, advanced paternal age was associated with increased risk, and younger paternal age with decreased risk, of AN and AED. For example, the fully adjusted hazard ratio for the 45+ years (v. the 25-29 years) paternal age category was 1.32 [95% confidence interval (CI) 1.14-1.53] for AN and 1.26 (95% CI 1.13-1.40) for AED. CONCLUSIONS: In this large, population-based cohort, paternal age at childbirth was positively associated with eating disorders in offspring, even after adjustment for potential confounders. Future research should further explore potential explanations for the association, including de novo mutations in the paternal germline.

Risk of eating disorders in immigrant populations.

OBJECTIVE: The risk of certain psychiatric disorders is elevated among immigrants. To date, no population studies on immigrant health have addressed eating disorders. We examined whether risk of eating disorders in first- and second-generation immigrants differs from native-born Danes and Swedes. METHOD: All individuals born 1984-2002 (Danish cohort) and 1989-1999 (Swedish cohort) and residing in the respective country on their 10th birthday were included. They were followed up for the development of eating disorders based on out-patient and in-patient data. RESULTS: The risks of all eating disorder types were lower among first-generation immigrants compared to the native populations: Incidence-rate ratio (95% confidence interval) was 0.39 (0.29, 0.51) for anorexia nervosa, 0.60 (0.42, 0.83) for bulimia nervosa, and 0.62 (0.47, 0.79) for other eating disorders in Denmark and 0.27 (0.21, 0.34) for anorexia nervosa, 0.30 (0.18, 0.51) for bulimia nervosa, and 0.39 (0.32, 0.47) for other eating disorders in Sweden. Likewise, second-generation immigrants by both parents were at lower risk, whereas those with only one foreign-born parent were not. CONCLUSION: The decreased risk of eating disorders among immigrants is opposite to what has been observed for other psychiatric disorders, particularly schizophrenia. Possible explanations include buffering sociocultural factors and underdetection in health care.

Obstetric and gynecologic problems associated with eating disorders.

OBJECTIVE: This article summarizes the literature on obstetric and gynecologic complications associated with eating disorders. METHOD: We performed a comprehensive search of the current literature on obstetric and gynecologic complications associated with eating disorders using PubMed. More recent randomized-controlled trials and larger data sets received priority. We also chose those that we felt would be the most relevant to providers. RESULTS: Common obstetric and gynecologic complications for women with eating disorders include infertility, unplanned pregnancy, miscarriage, poor nutrition during pregnancy, having a baby with small head circumference, postpartum depression and anxiety, sexual dysfunction and complications in the treatment for gynecologic cancers. There are also unique associations by eating disorder diagnosis, such as earlier cessation of breastfeeding in anorexia nervosa; increased polycystic ovarian syndrome in bulimia nervosa; and complications of obesity as a result of binge eating disorder. DISCUSSION: We focus on possible biological and psychosocial factors underpinning risk for poor obstetric and gynecological outcomes in eating disorders. Understanding these factors may improve both our understanding of the reproductive needs of women with eating disorders and their medical outcomes. We also highlight the importance of building multidisciplinary teams to provide comprehensive care to women with eating disorders during the reproductive years.

Evidence for the role of EPHX2 gene variants in anorexia nervosa.

Anorexia nervosa (AN) and related eating disorders are complex, multifactorial neuropsychiatric conditions with likely rare and common genetic and environmental determinants. To identify genetic variants associated with AN, we pursued a series of sequencing and genotyping studies focusing on the coding regions and upstream sequence of 152 candidate genes in a total of 1205 AN cases and 1948 controls. We identified individual variant associations in the Estrogen Receptor-ß (ESR2) gene, as well as a set of rare and common variants in the Epoxide Hydrolase 2 (EPHX2) gene, in an initial sequencing study of 261 early-onset severe AN cases and 73 controls (P=0.0004). The association of EPHX2 variants was further delineated in: (1) a pooling-based replication study involving an additional 500 AN patients and 500 controls (replication set P=0.00000016); (2) single-locus studies in a cohort of 386 previously genotyped broadly defined AN cases and 295 female population controls from the Bogalusa Heart Study (BHS) and a cohort of 58 individuals with self-reported eating disturbances and 851 controls (combined smallest single locus P<0.01). As EPHX2 is known to influence cholesterol metabolism, and AN is often associated with elevated cholesterol levels, we also investigated the association of EPHX2 variants and longitudinal body mass index (BMI) and cholesterol in BHS female and male subjects (N=229) and found evidence for a modifying effect of a subset of variants on the relationship between cholesterol and BMI (P<0.01). These findings suggest a novel association of gene variants within EPHX2 to susceptibility to AN and provide a foundation for future study of this important yet poorly understood condition.

The expression of cytokines and chemokines in the blood of patients with severe weight loss from anorexia nervosa: an exploratory study.

Anorexia nervosa (AN) is a serious, potentially life-threatening disorder characterized by severe weight loss, dysregulated eating, and often excessive exercise. While psychiatric illnesses such as depression are associated with increased levels of pro-inflammatory mediators, evidence for such disturbances in patients with AN has been less clear. In an exploratory study of possible disturbances in immune responses in AN, we assayed a panel of cytokines and chemokines in the blood of patients undergoing inpatient treatment, testing the hypothesis that metabolic disturbances in this disease would lead to a pattern of immune disturbances distinct from that of other psychiatric diseases. For this purpose, we evaluated patients by the Beck Depression Inventory-II (BDI-II) and the Eating Disorders Examination-Questionnaire and assessed cytokines and chemokines by enzyme-linked immunosorbent assays. Patients reported a moderate level of depression (mean BDI-II = 22.6) but exhibited few immunologic abnormalities of the kind associated with major depressive disorder [e.g., increased interleukin (IL)-6]; RANTES showed the most frequent elevations and was increased in 4 of the patients studied. Together, these findings suggest that features of AN such as loss of adipose tissue and excessive exercise may attenuate cytokine production and thus modulate the experience of illness that impacts on core features of disease.

Late onset eating disorders in Spain: clinical characteristics and therapeutic implications.

OBJECTIVE: The literature on later age of onset (LAO) in women with eating disorders is scarce. We compared the severity of eating disorders, eating disorder subtype, and personality profiles in a clinical sample of consecutively assessed women with eating disorders with later age of onset (LAO, > = 25 years) to women with typical age of onset (TAO, <25 years). METHOD: All eating disorder patients met the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV) criteria and were admitted to the Eating Disorder Unit of the University Hospital of Bellvitge in Barcelona, Spain. Ninety-six patients were classified as LAO and 759 as TAO. ASSESSMENT: Measures included the Eating Attitude Test-40 (EAT-40), Eating Disorders Inventory-2 (EDI-2), Bulimic Investigatory Test Edinburgh (BITE), Symptom Checklist Revised (SCL-90-R), and the Temperament and Character Inventory-Revised (TCI-R), as well as other clinical and psychopathological indices. RESULTS: LAO individuals reported significantly fewer weekly vomiting episodes, fewer self-harming behaviours, less drug abuse, and lower scores on the BITE symptoms, the EDI-2 drive for thinness, and the TCI-R harm avoidance scales than TAO individuals. Conversely, the LAO group reported more current and premorbid obesity than the TAO group. CONCLUSION: LAO eating disorder patients in this sample presented with milder symptomatology and less extreme personality traits. Premorbid obesity may be more relevant to LAO than TAO eating disorders and should be routinely assessed and considered when planning treatment.

Update on the treatment of anorexia nervosa: review of clinical trials, practice guidelines and emerging interventions.

BACKGROUND: Anorexia nervosa is a potentially deadly psychiatric illness that develops predominantly in females around puberty but is increasingly being recognized as also affecting boys and men and women across the lifespan. The aim of this environmental scan is to provide an overview of best practices in anorexia nervosa treatment across the age spectrum. METHOD: A triangulation approach was used. First, a detailed review of randomized controlled trials (RCTs) for anorexia nervosa published between 1980 and 2011 was conducted; second, clinical practice guidelines were consulted and reviewed; third, information about RCTs currently underway was sourced. This approach facilitated a comprehensive overview, which addressed the extant evidence base, recent advances in evidence and improvements in treatment, and future directions. RESULTS: The evidence base for the treatment of anorexia nervosa is advancing, albeit unevenly. Evidence points to the benefit of family-based treatment for youth. For adults no specific approach has shown superiority and, presently, a combination of renourishment and psychotherapy such as specialist supportive clinical management, cognitive behavioral therapy, or interpersonal psychotherapy is recommended. RCTs have neither sufficiently addressed the more complex treatment approaches seen in routine practice settings, such as multidisciplinary treatment or level of care, nor specifically investigated treatment in ethnically diverse populations. Methodological challenges that hinder progress in controlled research for anorexia nervosa are explained. CONCLUSIONS: The review highlights evidence-based and promising treatment modalities for anorexia nervosa and presents a triangulated analysis including controlled research, practice guidelines, and emerging treatments to inform and support clinical decision making.

Remission, continuation and incidence of eating disorders during early pregnancy: a validation study in a population-based birth cohort.

BACKGROUND: We internally validated previously published rates of remission, continuation and incidence of broadly defined eating disorders during pregnancy in the Norwegian Mother and Child Cohort (MoBa) at the Norwegian Institute of Public Health. METHOD: A total of 77 267 pregnant women enrolled at 17 weeks gestation between 2001 and 2009 were split into a training sample (n = 41 243) from the version 2 dataset and a validation sample (n = 36 024) from the version 5 dataset who were not in the original study. Internal validation of original rate models involved fitting a calibration model to compare model parameters between the two samples and bootstrap estimates of bias in the entire version 5 dataset. RESULTS: Remission, continuation and incidence estimates remained stable. Pre-pregnancy prevalence estimates in the validation sample were: anorexia nervosa (AN; 0.1%), bulimia nervosa (BN; 1.0%), binge eating disorder (BED; 3.3%) and eating disorder not otherwise specified-purging disorder (EDNOS-P; 0.1%). In early pregnancy, estimates were: BN (0.2%), BED (4.8%) and EDNOS-P (<0.01%). Incident BN and EDNOS-P during pregnancy were rare. The highest rates were for full or partial remission for BN and EDNOS-P and continuation for BED. CONCLUSIONS: We validated previously estimated rates of remission, continuation and incidence of eating disorders during pregnancy. Eating disorders, especially BED, during pregnancy were relatively common, occurring in nearly one in every 20 women. Pregnancy was a window of remission from BN but a window of vulnerability for BED. Training to detect eating disorders by obstetricians/gynecologists and interventions to enhance pregnancy and neonatal outcomes warrant attention.

Disordered eating and suicidal intent: the role of thin ideal internalisation, shame and family criticism.

OBJECTIVE: We explored the effect of thin ideal internalisation, shame proneness and family criticism on disordered eating and suicidal intent in female Mexican adolescents. METHOD: We studied a probabilistic sample of 2537 high school students in central Mexico, stratified by marginalisation status and migratory intensity. We used a generalised logistic regression model to estimate the odds of disordered eating and suicidal intent across scores for three predictors: Internalisation of the thin ideal, shame and family criticism. RESULTS: Disordered eating was reported by 4.2% (95% CI = 0.9-7.5%) and suicidal intent by 13.2% (95% CI = 12.0-14.4%) of girls. The unadjusted odds ratios of any disordered eating for thin ideal internalisation, shame proneness and familial criticism were 1.2, 1.1 and 3.2, respectively. The positive association between thin ideal internalisation and disordered eating remained even after controlling for shame proneness and familial criticism. The association of these variables with suicidal intent was weaker. DISCUSSION: Results support stronger effects for disordered eating than suicidal intent across the three unadjusted predictors. It also highlights the presence of the relationship of criticism and disordered eating in female adolescents from low and middle socio-economic backgrounds.

Five-year outcome of cognitive behavioral therapy and exposure with response prevention for bulimia nervosa.

BACKGROUND: Few data exist examining the longer-term outcome of bulimia nervosa (BN) following treatment with cognitive behavioral therapy (CBT) and exposure with response prevention (ERP). METHOD: One hundred and thirty-five women with purging BN received eight sessions of individual CBT and were then randomly assigned to either relaxation training (RELAX) or one of two ERP treatments, pre-binge (B-ERP) or pre-purge cues (P-ERP). Participants were assessed yearly following treatment and follow-up data were recorded. RESULTS: Eighty-one per cent of the total sample attended long-term follow-up. At 5 years, abstinence rates from binging were significantly higher for the two exposure treatments (43% and 54%) than for relaxation (27%), with no difference between the two forms of exposure. Over 5 years, the frequency of purging was lower for the exposure treatments than for relaxation training. Rates of recovery varied according to definition of recovery. Recovery continued to increase to 5 years. At 5 years, 83% no longer met DSM-III-R criteria for BN, 65% received no eating disorder diagnosis, but only 36% had been abstinent from bulimic behaviors for the past year. CONCLUSIONS: This study provides possible evidence of a conditioned inoculation from exposure treatment compared with relaxation training in long-term abstinence from binge eating at 5 years, and the frequency of purging over 5 years, but not for other features of BN. Differences among the groups were not found prior to 5 years. CBT is effective for BN, yet a substantial group remains unwell in the long term. Definition of recovery impacts markedly on recovery rates.

A twin study of specific bulimia nervosa symptoms.

BACKGROUND: Twin studies have suggested that additive genetic factors significantly contribute to liability to bulimia nervosa (BN). However, the diagnostic criteria for BN remain controversial. In this study, an item-factor model was used to examine the BN diagnostic criteria and the genetic and environmental contributions to BN in a population-based twin sample. The validity of the equal environment assumption (EEA) for BN was also tested. METHOD: Participants were 1024 female twins (MZ n=614, DZ n=410) from the population-based Mid-Atlantic Twin Registry. BN was assessed using symptom-level (self-report) items consistent with DSM-IV and ICD-10 diagnostic criteria. Items assessing BN were included in an item-factor model. The EEA was measured by items assessing similarity of childhood and adolescent environment, which have demonstrated construct validity. Scores on the EEA factor were used to specify the degree to which twins shared environmental experiences in this model. RESULTS: The EEA was not violated for BN. Modeling results indicated that the majority of the variance in BN was due to additive genetic factors. There was substantial variability in additive genetic and environmental contributions to specific BN symptoms. Most notably, vomiting was very strongly influenced by additive genetic factors, while other symptoms were much less heritable, including the influence of weight on self-evaluation. These results highlight the importance of assessing eating disorders at the symptom level. CONCLUSIONS: Refinement of eating disorder phenotypes could ultimately lead to improvements in treatment and targeted prevention, by clarifying sources of variation for specific components of symptomatology.

Binge eating disorder: a symptom-level investigation of genetic and environmental influences on liability.

BACKGROUND: Recent behavioral genetic studies have emphasized the importance of investigating eating disorders at the level of individual symptoms, rather than as overall diagnoses. We examined the heritability of binge eating disorder (BED) using an item-factor analytic approach, which estimates contributions of additive genetic (A), common environmental (C), and unique environmental (E) influences on liability to BED as well as individual symptoms. METHOD: Participants were 614 monozygotic and 410 dizygotic same-sex female twins from the Mid-Atlantic Twin Registry who completed a self-report measure of BED symptoms based upon DSM-IV criteria. Genetic and environmental contributions to BED liability were assessed at the diagnostic and symptom levels, using an item-factor approach. RESULTS: Liability to BED was moderately heritable; 45% of the variance was due to A, with smaller proportions due to C (13%), and E (42%). Additive genetic effects accounted for 29-43% of the variance in individual items, while only 8-14% was due to C. CONCLUSIONS: Results highlight the relevance of examining eating disorders at the symptom level, rather than focusing on aggregate diagnoses.

Patterns of co-morbidity of eating disorders and substance use in Swedish females.

BACKGROUND: Little is known about the association of eating disorder subtypes across multiple categories of substance use in population-based samples. We examined the association between eating disorders and substance use in a large population-based sample. METHOD: Female participants (n=13 297) were from the Swedish Twin Registry [Lichtenstein et al., Twin Research and Human Genetics (2006) 9, 875-882]. Substance use was examined in four defined groups - (1) anorexia nervosa (AN); (2) bulimia nervosa (BN); (3) AN and BN (ANBN); and (4) binge eating disorder (BED) as well as a referent group without eating disorder (no ED). Secondary analyses examined differences between restricting AN (RAN) and binge and/or purge AN (ANBP). RESULTS: In general, eating disorders were associated with greater substance use relative to the referent. The AN group had significantly increased odds for all illicit drugs. Significant differences emerged across the RAN and ANBP groups for alcohol abuse/dependence, diet pills, stimulants, and polysubstance use with greater use in the ANBP group. Across eating disorder groups, (1) the BN and ANBN groups were more likely to report alcohol abuse/dependence relative to the AN group, (2) the ANBN group was more likely to report diet pill use relative to the AN, BN and BED groups, and (3) the BN group was more likely to report diet pill use relative to the no ED, AN and BED groups. CONCLUSIONS: Eating disorders are associated with a range of substance use behaviors. Improved understanding of how they mutually influence risk could enhance understanding of etiology and prevention.

Is season of birth related to disordered eating and personality in women with eating disorders?

We assessed the relation between season of birth and eating disorder symptoms and personality characteristics in a sample of 880 women with eating disorders and 580 controls from two Price Foundation Studies. Eating disorder symptoms were assessed using the Structured Interview of Anorexic and Bulimic Disorders and the Structured Clinical Interview for DSM-IV. Personality traits were assessed using the Temperament and Character Inventory and the Frost Multidimensional Perfectionism Scale. Date of birth was obtained from a sociodemographic questionnaire. No significant differences were observed 1) in season of birth across eating disorder subtypes and controls; nor 2) for any clinical or personality variables and season of birth. We found no evidence of season of birth variation in eating disorders symptoms or personality traits. Contributing to previous conflicting findings, the present results do not support a season of birth hypothesis for eating disorders.