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A family-based association study of the HTR1B gene in eating disorders.

ABSTRACT: OBJECTIVE:To explore the association of three polymorphisms of the serotonin receptor 1D? gene (HTR1B) in the etiology of eating disorders and their relationship with clinical characteristics. METHODS:We analyzed the G861C, A-161T, and A1180G polymorphisms of the HTR1B gene through a family-based association test (FBAT) in 245 nuclear families. The sample was stratified into anorexia nervosa (AN) spectrum and bulimia nervosa (BN) spectrum. In addition, we performed a quantitative FBAT analysis of anxiety severity, depression severity, and Yale-Brown-Cornell Eating Disorders Scale (YBC-EDS) in the AN and BN-spectrum groups. RESULTS:FBAT analysis of the A-161T polymorphism found preferential transmission of allele A-161 in the overall sample. This association was stronger when the sample was stratified by spectrums, showing transmission disequilibrium between the A-161 allele and BN spectrum (z = 2.871, p = 0.004). Quantitative trait analysis showed an association between severity of anxiety symptoms and the C861 allele in AN-spectrum participants (z = 2.871, p = 0.004). We found no associations on analysis of depression severity or preoccupation and ritual scores in AN or BN-spectrum participants. CONCLUSIONS:Our preliminary findings suggest a role of the HTR1B gene in susceptibility to development of BN subtypes. Furthermore, this gene might have an impact on the severity of anxiety in AN-spectrum patients.

SUBMITTER: Hernandez S

PROVIDER: S-EPMC7194274 | biostudies-literature | 2016 Jul-Sep

REPOSITORIES: biostudies-literature

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A family-based association study of the HTR1B gene in eating disorders.

Hernández Sandra S Camarena Beatriz B González Laura L Caballero Alejandro A Flores Griselda G Aguilar Alejandro A

Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) 20160701 3

<h4>Objective</h4>To explore the association of three polymorphisms of the serotonin receptor 1Dβ gene (HTR1B) in the etiology of eating disorders and their relationship with clinical characteristics.<h4>Methods</h4>We analyzed the G861C, A-161T, and A1180G polymorphisms of the HTR1B gene through a family-based association test (FBAT) in 245 nuclear families. The sample was stratified into anorexia nervosa (AN) spectrum and bulimia nervosa (BN) spectrum. In addition, we performed a quantitative ...[more]

PMID: 27579596

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Project description:ObjectiveMisconceptions around which patients will and will not benefit from family-based treatment (FBT) for adolescent eating disorders (EDs) limit referrals and access to this treatment modality. The present study explored whether common demographic and clinical factors that may prevent referral to FBT predict treatment outcomes in adolescent anorexia nervosa (AN) and bulimia nervosa (BN).MethodThe following predictors of treatment outcomes were assessed: baseline family and diagnostic factors (socioeconomic status, comorbidity, illness duration, parent feelings of self-efficacy, family status, prior treatment, sex and prior hospitalizations) in a combined sample of adolescents receiving FBT compared to those randomized to other treatment conditions, across six clinical trials in the United States and Canada (total n = 724, ages 12-18, 90% female across both diagnoses). AN and BN samples were examined separately.ResultsAny prior ED treatment emerged as the only predictor of outcome in AN and BN, such that having no prior treatment predicted better outcomes in FBT for AN, and in both FBT and other treatment modalities for BN. No other sociodemographic or clinical variables predicted outcomes for AN or BN in FBT or in other evidence-based treatment modalities.ConclusionsThe findings of this exploratory analysis suggest that commonly assumed factors do not predict outcome in FBT. Specifically socioeconomic and demographic factors or clinical variability in families seeking treatment do not predict treatment outcomes in FBT, or other evidence-based treatment modalities, with the exception of prior treatment. Providers should consider referring to FBT even when these factors are present.Public significanceThis manuscript reports that commonly assumed family, sociodemographic and diagnostic factors do not predict outcome in FBT or other evidence-based treatment modalities, with the exception of prior treatment. This data may be helpful for providers when considering referrals to FBT in the context of variability in these variables.

Project description:Suicidal behavior (SB) has a complex etiology of genes, environment or both. One of the genetic components in SB could be copy number variations (CNVs), since CNVs are implicated in a range of neurodevelopmental disorders. However, a recently published genome-wide and case-control study failed to observe a significant role of CNVs in SB (see E-MTAB-3519). Here we complement those initial observations by conducting a brief CNV-association study, for the first time in a family-based trio-sample with severe suicide attempt (SA) outcome in offspring (n=660 trios; the \GISS\ sample, see http://www.ncbi.nlm.nih.gov/pubmed/23422793 and refs therein). For association testing, we here used the FBAT-CNV methodology (http://www.ncbi.nlm.nih.gov/pubmed/18228561), which allows for CNV association testing directly on the raw intensity values (Illumina \log R ratio\), evaluating any type of CNVs (e.g. de novo or inherited) without reliance on CNV calling algorithms and robust to control selection biases. Here we have deposited these raw logR-values for 88,450 on-chip CNV-loci of the HumanOmni1-Quad_v1 chip, arranged in a standard pedigree format used as input for FBAT-CNV analysis in SVS software (goldenhelix.com): column 1 is the family ID, column 2 is the Subject type (1 = offspring, 2 = mother, 3 = father), column 3 is the father ID (? for missing), column 4 is the mother ID (? for missing), column 5 is the sex (1 = female, 0 = male), column 6 is the affection status (1 = suicide attempt, 0 = not affected) and columns 7 and onward are the logR-values for each CNV-loci as is listed in the header row. We observed experiment-wide significant association (P ≤ 5.6 x 10-7) of two proximal CNVs at chromosome 14 (Illumina markers cnvi0108946 and cnvi0118308, with NCBI 36.3 start positions 22794779 and 22582820). However, these CNV-associations mapped to T-cell receptor regions, and therefore most likely reflect inter-individual variation in somatic rearrangements occurring in white blood cells (as our source of DNA was blood), rather than association with SA. In conclusion, our results did not suggest any major role of CNVs in SA etiology, in line with the results of the recent case-control study (see E-MTAB-3519).

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A family-based association study of the HTR1B gene in eating disorders.

Publications

A family-based association study of the HTR1B gene in eating disorders.

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