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Genetics of Anorexia Nervosa.

ABSTRACT: 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.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.

SUBMITTER: Baker JH

PROVIDER: S-EPMC6139670 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Genetics of Anorexia Nervosa.

Baker Jessica H JH Schaumberg Katherine K Munn-Chernoff Melissa A MA

Current psychiatry reports 20170922 11

<h4>Purpose of review</h4>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.<h4>Recent findings</h4>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 ...[more]

PMID: 28940168

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Anorexia Nervosa Genetics Initiative (ANGI)

Project description:Anorexia Nervosa Genetics Initiative (ANGI)

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Anorexia Nervosa Genetics Initiative (ANGI)

Project description:Anorexia Nervosa Genetics Initiative (ANGI)

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Contemporary views on the genetics of anorexia nervosa.

Project description:Anorexia nervosa (AN) is a serious mental illness characterized by severe dietary restriction that leads to high rates of morbidity, chronicity, and mortality. Unfortunately, effective treatment is lacking and few options are available. High rates of familial aggregation and significant heritability suggested that the complex etiology of AN is affected by both genetic and environmental factors. In this paper, we review studies that reported common and rare genetic variation that influence susceptibility of AN through candidate gene studies, genome-wide association studies, and sequencing-based studies. We also discuss gene expression, methylation, imaging genetics, and pharmacogenetics to demonstrate that these studies have collectively advanced our knowledge of how genetic variation contributes to AN susceptibility and clinical course. Lastly, we highlight the importance of gene by environment interactions (G×E) and share our enthusiasm for the use of nutritional genomic approaches to elucidate the interaction among nutrients, metabolic intermediates, and genetic variation in AN. A deeper understanding of how nutrition alters genome stability, how genetic variation influences uptake and metabolism of nutrients, and how response to food components affects disordered eating, will lead to personalized dietary interventions and effective nutraceutical and pharmacological treatments for AN.

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The Anorexia Nervosa Genetics Initiative (ANGI): Overview and methods.

Project description:BACKGROUND:Genetic factors contribute to anorexia nervosa (AN); and the first genome-wide significant locus has been identified. We describe methods and procedures for the Anorexia Nervosa Genetics Initiative (ANGI), an international collaboration designed to rapidly recruit 13,000 individuals with AN and ancestrally matched controls. We present sample characteristics and the utility of an online eating disorder diagnostic questionnaire suitable for large-scale genetic and population research. METHODS:ANGI recruited from the United States (US), Australia/New Zealand (ANZ), Sweden (SE), and Denmark (DK). Recruitment was via national registers (SE, DK); treatment centers (US, ANZ, SE, DK); and social and traditional media (US, ANZ, SE). All cases had a lifetime AN diagnosis based on DSM-IV or ICD-10 criteria (excluding amenorrhea). Recruited controls had no lifetime history of disordered eating behaviors. To assess the positive and negative predictive validity of the online eating disorder questionnaire (ED100K-v1), 109 women also completed the Structured Clinical Interview for DSM-IV (SCID), Module H. RESULTS:Blood samples and clinical information were collected from 13,363 individuals with lifetime AN and from controls. Online diagnostic phenotyping was effective and efficient; the validity of the questionnaire was acceptable. CONCLUSIONS:Our multi-pronged recruitment approach was highly effective for rapid recruitment and can be used as a model for efforts by other groups. High online presence of individuals with AN rendered the Internet/social media a remarkably effective recruitment tool in some countries. ANGI has substantially augmented Psychiatric Genomics Consortium AN sample collection. ANGI is a registered clinical trial: clinicaltrials.govNCT01916538; https://clinicaltrials.gov/ct2/show/NCT01916538?cond=Anorexia+Nervosa&draw=1&rank=3.

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The Genetics of Anorexia Nervosa: Current Findings and Future Perspectives.

Project description:Anorexia nervosa is a perplexing illness with the highest mortality rate of any psychiatric disease. In this paper, we review the genetic research on anorexia nervosa (AN). Family studies have demonstrated that anorexia nervosa is familial, and twin studies have indicated that additive genetic factors contribute to the familial aggregation. Molecular genetic research, including genomewide linkage and case control association studies, have not been successful in identifying DNA variants that are unequivocally involved in the etiology of AN. We provide a critical appraisal of these studies and discuss methodological issues that may be implicated in conflicting results. Furthermore, we discuss issues relevant to genetic research such as the importance of phenotypic refinement, the use of endophenotypes, and the implications for nosology and genetic analysis. Finally, the future of genetic research for AN is discussed in terms of genomewide association studies (GWAS) and the need for establishing large samples.

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VNN1 : a new biomarker of anorexia nervosa

Project description:Anorexia nervosa (AN) is a psychiatric disorder with an estimated heritability of around 70%. Although the largest genome-wide association study meta-analysis on AN identified independent loci-conferring risk to the disorder, the molecular mechanisms underlying the genetic basis of AN remains to be elucidated. To explore AN, we ran a transcriptome profiling in peripheral blood mononuclear cells of 15 AN subjects and 15 healthy controls. We validated our mean results in a mouse model of chronic food restriction mimicking several aspects of AN. Through this exploratory study we identified 673 significantly differentially expressed genes in AN. Among these genes, we identified the Vanin-1 (Vnn1) gene that appears to play a major role in the regulation of multiple metabolic pathways. We confirmed an underexpression of Vnn1, especially in the liver, in a mouse model of chronic food restriction. These results indicate that quantitative food restriction affects Vnn1 expression, suggesting that this gene may contribute to the anorexic phenotype in the chronic food restriction mouse model as well as in patients affected by AN. We believe that this report highlights promising candidate genes and gene pathways for AN and reveals Vnn1 as a biomarker that may be used as molecular targets to predict and/or to understand AN.

2023-10-31 | GSE245978 | GEO

WTCCC3 Anorexia Nervosa

Project description:As part of the Genetic Consortium for Anorexia Nervosa (GCAN) and Wellcome Trust Case Control Consortium 3 (WTCCC3), we have amassed the largest anorexia nervosa (AN) sample in the world (~4,000). Following the WTCCC3 GWAS, we secured funding from the Klarman Family Foundation to extend the genetic analyses to variants on the exome chip (CoreExome array). This pre-lim relates to carrying out genotyping on the CoreExome array on up to a maximum of 580 new samples.

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Copeptin in anorexia nervosa.

Project description:OBJECTIVE:Antidiuretic hormone (ADH) is involved in the response to stress and in depression and anxiety. However, studies on ADH in anorexia nervosa (AN) show conflicting results. A major reason for this may be methodological challenges due to short half-life of ADH in circulation and rapid degradation in vitro. To overcome these obstacles, copeptin, the C-terminal fragment stemming from the ADH precursor, has been increasingly used as a stable clinical measure for ADH. Furthermore, copeptin has been recognized as a biomarker of insulin resistance in obesity. METHODS:We measured fasting copeptin in plasma from 25 normohydrated, stable women with AN (BMI 13.0 ± 2.0) and 25 age-matched women. RESULTS:No difference in copeptin levels was found (6.8 ± 1.8 vs. 5.5 ± 0.5 pmol/L). Confirmatory, copeptin concentrations were correlated to insulin resistance assessed by the homeostasis model assessment of insulin resistance. DISCUSSION:We report for the first time that copeptin level as a marker of ADH activity is not altered in fluid- and electrolyte-stabilized patients with severe AN patients, indicating that ADH may not be crucial in the pathophysiological involvement of psychologic stress in AN.

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Identification of adipose tissue metabolic memory of anorexia nervosa

Project description:Anorexia nervosa (AN) is a complex debilitating disease characterized by intense fear of weight gain and excessive exercise. It is the deadliest of any psychiatric disorder with a high rate of recidivism, yet its pathophysiology is unclear. The Activity-Based Anorexia (ABA) paradigm is a widely accepted mouse model of AN that recapitulates hypophagia and hyperactivity despite reduced body weight, however, not the chronicity. Here, we modified the prototypical ABA paradigm to increase the time to lose 25% of baseline body weight from less than 7 days to more than 2 weeks. We used this paradigm to identify persistently altered genes after weight restoration that represent a metabolic memory of under-nutrition and may contribute to AN relapse. We focused on adipose tissue as it was identified as a major location of metabolic memory of over-nutririon. We identified 300 persistently dysregulated genes, including Calm2 and Vps13d, which could be potential global regulators of metabolic memory in both chronic over- and under-nutrition. However, despite being on the opposite spectrum of weight perturbations, the majority of metabolic memory genes of under- and over-nutrition do not overlap, suggestive of the different mechanisms involved in these extreme nutritional statuses.

2023-08-23 | GSE229316 | GEO

Anorexia nervosa: 30-year outcome.

Project description:BACKGROUND:Little is known about the long-term outcome of anorexia nervosa. AIMS:To study the 30-year outcome of adolescent-onset anorexia nervosa. METHOD:All 4291 individuals born in 1970 and attending eighth grade in 1985 in Gothenburg, Sweden were screened for anorexia nervosa. A total of 24 individuals (age cohort for anorexia nervosa) were pooled with 27 individuals with anorexia nervosa (identified through community screening) who were born in 1969 and 1971-1974. The 51 individuals with anorexia nervosa and 51 school- and gender-matched controls were followed prospectively and examined at mean ages of 16, 21, 24, 32 and 44. Psychiatric disorders, health-related quality of life and general outcome were assessed. RESULTS:At the 30-year follow-up 96% of participants agreed to participate. There was no mortality. Of the participants, 19% had an eating disorder diagnosis (6% anorexia nervosa, 2% binge-eating disorder, 11% other specified feeding or eating disorder); 38% had other psychiatric diagnoses; and 64% had full eating disorder symptom recovery, i.e. free of all eating disorder criteria for 6 consecutive months. During the elapsed 30 years, participants had an eating disorder for 10 years, on average, and 23% did not receive psychiatric treatment. Good outcome was predicted by later age at onset among individuals with adolescent-onset anorexia nervosa and premorbid perfectionism. CONCLUSIONS:This long-term follow-up study reflects the course of adolescent-onset anorexia nervosa and has shown a favourable outcome regarding mortality and full symptom recovery. However, one in five had a chronic eating disorder.

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