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Background: Identifying predictors of psychological outcome for patients with eating disorders may improve the effectiveness of treatment. Patients with different pre-treatment characteristics and symptoms may benefit from different therapies. This study aimed to identify potential predictors of treatment outcome in a large naturalistic cohort of patients with an eating disorder., Method: The study sample included patients (N = 1153) with all types of eating disorders who were receiving residential, day, or outpatient treatment. Remission was defined by means of four different indicators based on the Eating Disorder Examination-Questionnaire global score: 1. achieving reliable change; 2. showing a 50% reduction in baseline symptom severity; 3. reaching the clinical significance cut-off point; and 4. a combination of indicators 2 and 3. Potential predictor variables were investigated in univariate and multivariate Cox regression models., Results: Different predictors were found for the four outcome criteria. Patients with high levels of interpersonal distrust at baseline were less likely to have achieved reliable change in eating disorder psychopathology. Higher self-esteem and less body dissatisfaction at baseline was independently associated with a symptom reduction of more than 50% and/or reaching the clinical significance cut-off point. Contrary to our expectations, no differences in outcome were found between the eating disorder subtypes., Discussion: Clinically, it is important to reduce the risk of poor outcome and to achieve a rapid response in treatment using an intervention designed for this purpose, such as shared decision making or an intervention directed at self-esteem or body image, which may act as a catalyst for change. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2016; 49:863-873)., (© 2016 Wiley Periodicals, Inc.)

Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countries (15 sites) and 14 860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery data sets. Seventy-six (72 independent) single nucleotide polymorphisms were taken forward for in silico (two data sets) or de novo (13 data sets) replication genotyping in 2677 independent AN cases and 8629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication data sets comprised 5551 AN cases and 21 080 controls. AN subtype analyses (1606 AN restricting; 1445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01 × 10(-7)) in SOX2OT and rs17030795 (P=5.84 × 10(-6)) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76 × 10(-)(6)) between CUL3 and FAM124B and rs1886797 (P=8.05 × 10(-)(6)) near SPATA13. Comparing discovery with replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P=4 × 10(-6)), strongly suggesting that true findings exist but our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field.

Objective: The female preponderance and onset around puberty in the majority of eating disorders (EDs) suggest that sex hormones, like estrogens, may be involved in the onset of these disorders. An eight-SNP haplotype at the estrogen receptor I (ESR1) gene was found to be associated with anorexia nervosa (AN) (Versini et al., Neuropsychopharmacology, 35, 1818-1825, 2010) and three SNPs from this haplotype (rs726281, rs2295193, and rs3798577) were associated with AN and/or EDs. Our objective was to replicate these findings in an independent cohort of 520 patients with an eating disorder, of whom 244 had AN (142 restricting type) from the GenED study and 2,810 random women from the Netherlands Twin Registry., Method: The frequencies of the eight-SNP haplotype and three ESR1 SNPs were compared between patients with an eating disorder, with AN (restricting type), with bulimia nervosa (BN), and the control women., Results: Neither the haplotype nor the three ESR1 SNPs were associated with EDs, BN, AN, or restricting type AN., Discussion: Despite sufficient statistical power, the associations reported by Versini et al. (Neuropsychopharmacology, 35, 1818-1825, 2010) were not replicated., (Copyright © 2013 Wiley Periodicals, Inc.)

Twin studies suggest that genetic factors play a substantial role in anorexia nervosa (AN) and self-induced vomiting (SV), a key symptom that is shared among different types of eating disorders (EDs). We investigated the association of 25 single nucleotide polymorphisms (SNPs), capturing 71-91% of the common variance in candidate genes, stathmin (STMN1), serotonin receptor 1D (HTR1D), tryptophan hydroxylase 2 (TPH2) and brain-derived neurotrophic factor (BDNF), with AN and EDs characterized by regular SV. The first allele frequencies of all the SNPs were compared between a Dutch case group (182 AN, 149 EDs characterized by SV) and 607 controls. Associations rendering P-values < 0.05 from this initial study were then tested for replication in a meta-analysis with two additional independent ED case-control samples, together providing 887 AN cases, 306 cases with an ED characterized by SV and 1914 controls. A significant effect for the minor C-allele of tryptophan hydroxylase 2 rs1473473 was observed for both AN [odds ratio (OR) = 1.30, 95% CI 1.08-1.57, P < 0.003] and EDs characterized by SV (OR = 1.52, 95% CI 1.28-2.04, P < 0.006). In the combined case group, a dominant effect was observed for rs1473473 (OR = 1.38, 95% CI 1.16-1.64, P < 0.0003). The meta-analysis revealed that the tryptophan hydroxylase 2 polymorphism rs1473473 was associated with a higher risk for AN, EDs characterized by SV and for the combined group., (© 2010 The Authors. Genes, Brain and Behavior © 2010 Blackwell Publishing Ltd and International Behavioural and Neural Genetics Society.)

There are two major hypotheses regarding the etiology of anxiety and depression: the mono-amine hypothesis and the hypothesis of an abnormal stress response acting partly via reduced neurogenesis. Association studies have focused on genes involved in these processes, but with inconclusive results. This study investigated the effect of 45 single nucleotide polymorphisms (SNPs) in genes encoding for serotonin receptors 1A, 1D, 2A, catechol-O-methyltransferase (COMT), tryptophane hydroxylase type 2 (TPH2), brain derived neurotrophic factor (BDNF), PlexinA2 and regulators of G-protein-coupled signaling (RGS) 2, 4, 16. Anxious depression (A/D) symptoms were assessed five times in 11 years in over 11 000 adults with 1504 subjects genotyped and at age 7, 10, 12 and during adolescence in over 20 000 twins with 1078 subjects genotyped. In both cohorts, a longitudinal model with one latent factor loading on all A/D measures over time was analysed. The genetic association effect modeled at the level of this latent factor was 60% and 70% heritable in the children and adults, respectively, and explained around 50% of the total phenotypic variance. Power analyses showed that the samples contained 80% power to detect an effect explaining between 1.4% and 3.6% of the variance. However, no SNP showed a consistent effect on A/D. To conclude, this longitudinal study in children and adults found no association of SNPs in the serotonergic system or core regulators of neurogenesis with A/D. Overall, there has been no convincing evidence, so far, for a role of genetic variation in these pathways in the development of anxiety and depression., (© 2010 The Authors. Genes, Brain and Behavior © 2010 Blackwell Publishing Ltd and International Behavioural and Neural Genetics Society.)

In most assessment instruments, distinct items are designed to measure a trait, and the sum score of these items serves as an approximation of an individual's trait score. In interpreting group differences with respect to sum scores, the instrument should measure the same underlying trait across groups (e.g., male/female, young/old). Differences with respect to the sum score should accurately reflect differences in the latent trait of interest. A necessary condition for this is that the instrument is measurement invariant. In the current study, the authors illustrate a stepwise approach for testing measurement invariance with respect to sex in a four-item instrument designed to assess disordered eating behavior in a large epidemiological sample (1,195 men and 1,507 women). This approach can be applied to other phenotypes for which group differences are expected. Any analysis of such variables may be subject to measurement bias if a lack of measurement invariance between grouping variables goes undetected.

Objective: Prior studies suggest eating disorders and related characteristics are moderately to substantially heritable. We are interested in identifying the genes underlying disordered eating behaviour (DEB), and want to know how much of the genetic influence underlying DEB is attributable to genetic influences on body mass index (BMI)., Method: Bivariate analyses were performed, in adolescent twins and siblings, to estimate the genetic and environmental contributions for DEB, BMI, and their overlap., Results: Shared genetic risk factors explained the overlap between BMI and DEB (genetic correlation was 0.43 in women, 0.51 in men). DEB was highly heritable in women (a(2) = 0.65; a(2) independent of BMI = 0.53) and moderately heritable in men (a(2) = 0.39; a(2) independent of BMI = 0.29). BMI was highly heritable in both men (a(2) = 0.76) and women (a(2) = 0.80)., Conclusion: The entire correlation between DEB and BMI was explained by shared genetic risk, but the majority of genetic influences on DEB were due to genetic effects independent of BMI.

Substantial effort has been put into the exploration of the biological background of eating disorders, through family, twin and molecular genetic studies. Family studies have shown that anorexia (AN) and bulimia nervosa (BN) are strongly familial, and that familial etiologic factors appear to be shared by both disorders. Twin studies often focus on broader phenotypes or subthreshold eating disorders. These studies consistently yielded moderate to substantial heritabilities. In addition, there has been a proliferation of molecular genetic studies that focused on Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) AN and BN. Seven linkage regions have been identified in genome-wide screens. Many genetic association studies have been performed, but no consistent association between a candidate gene and AN or BN has been reported. Larger genetic association studies and collaborations are needed to examine the involvement of several candidate genes and biological pathways in eating disorders. In addition, twin studies should be designed to assist the molecular work by further exploring genetic determinants of endophenotypes, evaluating the magnitude of contribution to liability of measured genotypes as well as environmental risk factors related to eating disorders. In this manner twin and molecular studies can move the field forward in a mutually informative way.