Disorders of the brain can exhibit considerable epidemiological comorbidity and often share symptoms, provoking debate about their etiologic overlap. We quantified the genetic sharing of 25 brain disorders from genome-wide association studies of 265,218 patients and 784,643 control participants and assessed their relationship to 17 phenotypes from 1,191,588 individuals. Psychiatric disorders share common variant risk, whereas neurological disorders appear more distinct from one another and from the psychiatric disorders. We also identified significant sharing between disorders and a number of brain phenotypes, including cognitive measures. Further, we conducted simulations to explore how statistical power, diagnostic misclassification, and phenotypic heterogeneity affect genetic correlations. These results highlight the importance of common genetic variation as a risk factor for brain disorders and the value of heritability-based methods in understanding their etiology.
The transition to college has been identified as a critical period for increases in overweight status. Overweight college students are at-risk of becoming obese adults, and, thus prevention efforts targeting college age individuals are key to reducing adult obesity rates. The current study evaluated an Internet intervention with first year college students (N = 170) randomly assigned to one of four treatment conditions: 1) no treatment, 2) 6-week online intervention 3) 6-week weight and caloric feedback only (via email), and 4) 6-week combined feedback and online intervention. The combined intervention group had lower BMIs at post-testing than the other three groups. This study demonstrated the effectiveness and feasibility of an online intervention to prevent weight gain among college students.
Over the past decade, considerable advances have been made in understanding genetic influences on eating pathology. Eating disorders aggregate in families, and twin studies reveal that additive genetic factors account for approximately 40% to 60% of liability to anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). Molecular genetics studies have been undertaken to identify alterations in deoxyribonucleic acid sequence and/or gene expression that may be involved in the pathogenesis of disordered eating behaviors, symptoms, and related disorders and to uncover potential genetic variants that may contribute to variability of treatment response. This article provides an in-depth review of the scientific literature on the genetics of AN, BN, and BED including extant studies, emerging hypotheses, future directions, and clinical implications.
To explore age differences in current and preferred silhouette and body dissatisfaction (current -preferred silhouette discrepancy) in women aged 25-89 years using figural stimuli (range: 1-very small to 9-very large). Data were abstracted from two online convenience samples (N = 5,868). t-tests with permutation-adjusted p-values examined linear associations between mean silhouette scores (current, preferred, discrepancy score) and age with/without stratification by body mass index (BMI). Modal current silhouette was 5; modal preferred silhouette was 4; mean discrepancy score was 1.8. There was no significant association between current silhouette and age, but a positive linear association between preferred silhouette and age remained after stratification by BMI. A significant inverse linear association of silhouette discrepancy score and age was found only prior to stratification by BMI. Body dissatisfaction exists in women across the adult life span and is influenced by BMI.
The purpose of this invited review is to summarize the state of genetic research into the etiology of schizophrenia (SCZ) and to consider options for progress. The fundamental uncertainty in SCZ genetics has always been the nature of the beast, the underlying genetic architecture. If this were known, studies using the appropriate technologies and sample sizes could be designed with an excellent chance of producing high-confidence results. Until recently, few pertinent data were available, and the field necessarily relied on speculation. However, for the first time in the complex and frustrating history of inquiry into the genetics of SCZ, we now have empirical data about the genetic basis of SCZ that implicate specific loci and that can be used to plan the next steps forward.
Objective We assessed the impact of reducing the binge eating frequency and duration thresholds on the diagnostic criteria for bulimia nervosa (BN) and binge eating disorder (BED). Method We estimated the lifetime population prevalence of BN and BED in 13,295 female twins from the Swedish Twin study of Adults: Genes and Environment employing a range of frequency and duration thresholds. External validation (risk to co-twin) was used to investigate empirical evidence for an optimal binge eating frequency threshold. Results The lifetime prevalence estimates of BN and BED increased linearly as the frequency criterion decreased. As the required duration increased, the prevalence of BED decreased slightly. Discontinuity in co-twin risk was observed in BN between at least four times per month and at least five times per month. This model could not be fit for BED. Discussion The proposed changes to the DSM-5 binge eating frequency and duration criteria would allow for better detection of binge eating pathology without resulting in a markedly higher lifetime prevalence of BN or BED.
Most measures of eating disorder symptoms and risk factors were developed in predominantly White female samples. Yet eating disorders affect individuals of all racial and ethnic backgrounds. Black women appear more vulnerable to certain forms of eating pathology, such as binge eating, and less susceptible to other eating disorder symptoms and risk factors, such as body dissatisfaction, compared with their White peers. Despite concern that extant measures do not adequately assess eating concerns among Black women, the construct validity of scores on most of these measures has not been adequately examined within this population. This study included 2,208 Black and White women who completed the following: the Binge Eating Scale (BES), the Eating Disorder Diagnostic Scale (EDDS), the Eating Attitudes Test-26 (EAT-26), the Eating Disorder Inventory Body Dissatisfaction and Drive for Thinness subscales, the Bulimia Test-Revised (BULIT-R), the Multidimensional Body-Self Relations Questionnaire-Appearance Evaluation subscale (MBSRQ-AE), and the Objectified Body Consciousness Scale (OBCS). Most measures yielded internally consistent scores in both races. Confirmatory factor analyses indicated that loadings for some measures, including the EAT-26 and EDDS, were not invariant across groups and thus do not assess equivalent constructs in White and Black women. However, others, including the BULIT-R, BES, OBCS, and MBSRQ-AE, exhibited factorial invariance in both races. Results suggest scores are likely not equivalent across races for several popular measures of eating disorder symptoms and risk factors. Thus, it is recommended that researchers and clinicians obtain additional information regarding racial/cultural factors when using these instruments with Black women.
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 9 SNP alleles at 3 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 to 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.
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