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Development and preliminary validation of a brief broad-spectrum measure of trauma exposure: The Traumatic Life Events Questionnaire.

Edward Kubany et al.Jan 1, 2000

This article describes the development and preliminary validation of a brief questionnaire that assesses exposure to a broad range of potentially traumatic events. Items were generated from multiple sources of information. Events were described in behaviorally descriptive terms, consistent with Diagnostic and Statistical Manual of Mental Disorders IV posttraumatic stress disorder stressor criterion A1. When events were endorsed, respondents were asked if they experienced intense fear, helplessness, or horror (stressor criterion A2). In separate studies with college students, Vietnam veterans, battered women, and residents of a substance abuse program, most items possessed adequate to excellent temporal stability. In a study comparing questionnaire and structured-interview inquiries of trauma history, the 2 formats yielded similar rates of disclosure. Preliminary data on positive predictive power are also presented.

Clinical Psychology

Psychology

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Evidence that ‘food addiction’ is a valid phenotype of obesity

Caroline Davis et al.Sep 6, 2011

There is growing evidence of 'food addiction' (FA) in sugar- and fat-bingeing animals. The purpose of this study was to investigate the legitimacy of this disorder in the human condition. It was also our intention to extend the validation of the Yale Food Addiction Scale (YFAS) – the first tool developed to identify individuals with addictive tendencies towards food. Using a sample of obese adults (aged 25–45 years), and a case–control methodology, we focused our assessments on three domains relevant to the characterization of conventional substance-dependence disorders: clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance. Results were strongly supportive of the FA construct and validation of the YFAS. Those who met the diagnostic criteria for FA had a significantly greater co-morbidity with Binge Eating Disorder, depression, and attention-deficit/hyperactivity disorder compared to their age- and weight-equivalent counterparts. Those with FA were also more impulsive and displayed greater emotional reactivity than obese controls. They also displayed greater food cravings and the tendency to 'self-soothe' with food. These findings advance the quest to identify clinically relevant subtypes of obesity that may possess different vulnerabilities to environmental risk factors, and thereby could inform more personalized treatment approaches for those who struggle with overeating and weight gain.

Internal Medicine

Clinical Psychology

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Bulimia nervosa in a Canadian community sample: prevalence and comparison of subgroups

Paul Garfinkel et al.Jul 1, 1995

Clinical Psychology

Demography

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Fluoxetine After Weight Restoration in Anorexia Nervosa

B. Walsh et al.Jun 13, 2006

NOREXIA NERVOSA IS A SERIous psychiatric illness with substantial morbidity and a lifetime mortality arguably as high as that associated with any psychiatric illness. 1 A major contributor to the poor prognosis of this illness is the high rate of relapse following initial treatment.Despite successful weight restoration, 30% to 50% of patients require rehospitalization within 1 year of discharge. 2,3 This discouraging experience has prompted interest in interventions aimed at preventing deterioration following weight restoration.Patients with anorexia nervosa often exhibit symptoms of other psychiatric disorders, 4 such as depression and obsessive-compulsive disorder, which are responsive to antidepressant medication, suggesting that pharmacological interventions might be of use.Surpris-ingly, virtually all of the controlled trials of medication (most of which have been conducted during the initial phase of treatment when patients are underweight) have shown no benefit of medication compared with placebo. 5,6 Despite this lack of evidence of effectiveness, a substantial number of pa-See also p 2659 and Patient Page.

Internal Medicine

Clinical Psychology

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Features associated with excessive exercise in women with eating disorders

Hemal Shroff et al.Apr 24, 2006

Excessive exercise and motor restlessness are observed in a substantial number of patients with eating disorders. This trait has been studied extensively among animal models of activity anorexia nervosa (AN) and may hold particular interest as an endophenotype for AN. We explored features associated with excessive exercise across subtypes of eating disorders.Participants were female probands and affected female relatives from the multi-site international Price Foundation Genetic Studies with diagnoses of AN, bulimia nervosa (BN), and both AN and BN or eating disorder not otherwise specified (ED-NOS) (N=1,857). Excessive exercise was defined based on responses to the Structured Interview for Anorexic and Bulimic Disorders (SIAB).Among the eating disorder diagnostic groups, excessive exercise was most common among the purging subtype of AN. Individuals who reported excessive exercise also reported lower minimum BMI, younger age at interview, higher scores on anxiety, perfectionism, and eating disorder symptom measures, more obsessions and compulsions, and greater persistence.Excessive exercise may be associated particularly with the purging subtype of AN as well as with a constellation of anxious/obsessional temperament and personality characteristics among women with eating disorders.

Biochemistry

Clinical Psychology

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Dopamine for “Wanting” and Opioids for “Liking”: A Comparison of Obese Adults With and Without Binge Eating

Caroline Davis et al.Mar 12, 2009

Obesity research suffers from an overinclusion paradigm whereby all participants with a BMI beyond a certain cutoff value (e.g., 30) are typically combined in a single group and compared to those of normal weight. There has been little attempt to identify meaningful subgroups defined by their salient biobehavioral differences. In order to address this limitation, we examined genetic and psychological indicators of hedonic eating in obese adults with ( n = 66) and without ( n = 70) binge eating disorder (BED). Our analyses focused on dopamine (DA) and opioid genetic markers because of their conjoint association with the functioning of brain reward mechanisms. We targeted three functional polymorphisms related to the D2 receptor ( DRD2 ) gene, as well as the functional A118G polymorphism of the mu‐opioid receptor ( OPRM1 ) gene. We found that significantly more obese controls had the “loss‐of‐function” A1 allele of Taq 1A compared to their BED counterparts, whereas the “gain‐of‐function” G allele of A118G occurred with greater frequency in the BED group. A significant gene–gene combination χ 2 analysis also indicated that of those participants with the gain‐gain genotype (G + and A1), 80% were in the BED group whereas only 35% with the loss‐loss genotype (G − and A1 + ) were in this group. Finally, BED subjects had significantly higher scores on a self‐report measure of hedonic eating. Our findings suggest that BED is a biologically based subtype of obesity and that the proneness to binge eating may be influenced by a hyper‐reactivity to the hedonic properties of food—a predisposition that is easily exploited in our current environment with its highly visible and easily accessible surfeit of sweet and fatty foods.

Genetics

Internal Medicine

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Identifying tissues implicated in Anorexia Nervosa using Transcriptomic Imputation

Laura Huckins et al.Feb 14, 2018

Anorexia nervosa (AN) is a complex and serious eating disorder, occurring in ~1% of individuals. Despite having the highest mortality rate of any psychiatric disorder, little is known about the aetiology of AN, and few effective treatments exist. Global efforts to collect large sample sizes of individuals with AN have been highly successful, and a recent study consequently identified the first genome-wide significant locus involved in AN. This result, coupled with other recent studies and epidemiological evidence, suggest that previous characterizations of AN as a purely psychiatric disorder are over-simplified. Rather, both neurological and metabolic pathways may also be involved. In order to elucidate more of the system-specific aetiology of AN, we applied transcriptomic imputation methods to 3,495 cases and 10,982 controls, collected by the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED). Transcriptomic Imputation (TI) methods approaches use machine-learning methods to impute tissue-specific gene expression from large genotype data using curated eQTL reference panels. These offer an exciting opportunity to compare gene associations across neurological and metabolic tissues. Here, we applied CommonMind Consortium (CMC) and GTEx-derived gene expression prediction models for 13 brain tissues and 12 tissues with potential metabolic involvement (adipose, adrenal gland, 2 colon, 3 esophagus, liver, pancreas, small intestine, spleen, stomach). We identified 35 significant gene-tissue associations within the large chromosome 12 region described in the recent PGC-ED GWAS. We applied forward stepwise conditional analyses and FINEMAP to associations within this locus to identify putatively causal signals. We identified four independently associated genes; RPS26, C12orf49, SUOX, and RDH16. We also identified two further genome-wide significant gene-tissue associations, both in brain tissues; REEP5, in the dorso-lateral pre-frontal cortex (DLPFC; p=8.52x10-07), and CUL3, in the caudate basal ganglia (p=1.8x10-06). These genes are significantly enriched for associations with anthropometric phenotypes in the UK BioBank, as well as multiple psychiatric, addiction, and appetite/satiety pathways. Our results support a model of AN risk influenced by both metabolic and psychiatric factors.

Genetics

Clinical Psychology

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Genome-wide copy number variation association study in anorexia nervosa

Alicia Walker et al.Nov 12, 2024

Abstract This study represents the first large-scale investigation of rare (<1% population frequency) copy number variants (CNVs) in anorexia nervosa (AN). Large, rare CNVs are reported to be causally associated with anthropometric traits, neurodevelopmental disorders, and schizophrenia, yet their role in the genetic basis of AN is unclear. Using genome-wide association study (GWAS) array data from the Anorexia Nervosa Genetics Initiative (ANGI), which included 7414 AN case and 5044 controls, we investigated the association of 67 well-established syndromic CNVs and 178 pleiotropic disease-risk dosage-sensitive CNVs with AN. To identify novel CNV regions (CNVRs) that increase the risk of AN, we conducted genome-wide association studies with a focus on rare CNV-breakpoints (CNV-GWAS). We found no net enrichment of rare CNVs, either deletions or duplications, in AN, and none of the well-established syndromic or pleiotropic CNVs had a significant association with AN status. However, the CNV-GWAS found 21 nominally associated CNVRs that contribute to AN risk, covering protein-coding genes implicated in synaptic function, metabolic/mitochondrial factors, and lipid characteristics, like the CD36 (7q21.11) gene, which transports long-chain fatty acids into cells. CNVRs intersecting genes previously related to neurodevelopmental traits include deletions of NRXN1 intron 5 (2p16.3), IMMP2L (7q31.1), and PTPRD (9p23). Overall, given that our study is well powered to detect the CNV burden level reported for schizophrenia, we can conclude that rare CNVs have a limited role in the etiology of AN, as reported for bipolar disorder. Our nominal associations for the 21 discovered CNVRs are consistent with AN being a metabo-psychiatric trait, as demonstrated by the common genetic architecture of AN, and we provide association results to allow for replication in future research.

Genetics

Biochemistry

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White matter microstructure in women with acute and remitted anorexia nervosa: an exploratory neuroimaging study

Amy Miles et al.Dec 17, 2018

Anorexia nervosa (AN) is a highly heritable psychiatric disorder characterized by starvation and emaciation and associated with changes in brain structure. The precise nature of these changes remains unclear, as does their developmental time course and capacity for reversal with weight restoration. In this exploratory neuroimaging study, we sought to characterize changes in white matter microstructure in women with acute and remitted AN. Diffusion-weighted MRI data was collected from underweight women with a current diagnosis of AN (acAN: n=23), weight-recovered women with a past diagnosis of AN (recAN: n=23), and age-matched healthy control women (HC: n=24). Image processing and analysis were performed with Tract-Based Spatial Statistics, part of FSL, and group differences in voxel-wise, brain-wide fractional anisotropy (FA) and mean diffusivity (MD), indices of white matter microstructure, were tested with nonparametric permutation and threshold free cluster enhancement. No significant main effect of group on FA was identified. A significant main effect of group on MD was observed in a large cluster covering 9.2% of white matter and including substantial portions of the corpus callosum, corona radiata, internal capsule, and superior longitudinal fasciculus, and post hoc analyses revealed similar effects of group on axial diffusivity (AD) and radial diffusivity (RD). Cluster-wise MD was significantly higher in acAN participants (+3.8%) and recAN participants (+2.9%) than healthy controls, and the same was true for cluster-wise AD and RD. Trait-based increases in diffusivity, consistent with atypical myelination and impaired axon integrity, suggest a link between altered white matter microstructure and vulnerability to AN, and evidence of reduced oligodendrocyte density in AN provides further support for this hypothesis. Potential mechanisms of action include atypical neurodevelopment and systemic inflammation.

Physiology

Internal Medicine

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Shared Genetic Risk between Eating Disorder- and Substance-Use-Related Phenotypes: Evidence from Genome-Wide Association Studies

Melissa Munn‐Chernoff et al.Aug 23, 2019

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 (BN) 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 BN 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 (MDD). Total sample sizes per phenotype ranged from ~2,400 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 non-diagnostic 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 MDD loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships between these behaviors.

Genetics

Biochemistry

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Genetics

Biochemistry

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