期刊
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
卷 38, 期 12, 页码 2907-2914出版社
WILEY-BLACKWELL
DOI: 10.1111/acer.12572
关键词
Childhood Adversity; ADH1B; Alcohol; African Americans
资金
- NIH [DA12849, DA00167, DA12690, AA017921, AA11330, AA13736]
- CTSA [KL2 RR024138]
- Robert E. Leet and Clara Guthrie Patterson Trust
- APA/Merck Early Academic Career Award Program
- VA CT and Philadelphia VA Mental Illness Research, Education, and Clinical Centers
BackgroundThe ADH1B gene has consistently been implicated in problem drinking, but rarely incorporated into gene by environment investigations of alcohol phenotypes. This study examined the joint effects of variation in ADH1B and childhood adversitya well-documented risk factor for alcohol problems and moderator of genetic liability to psychiatric outcomeson maximum drinks consumed in a 24-hour period (maxdrinks) and alcohol use disorder (AUD) symptoms. MethodsData were drawn from 2,617 African-American (AA) and 1,436 European-American (EA) participants (42% female) in a multisite genetic study of substance dependence. We tested the most significant ADH1B single nucleotide polymorphisms for alcohol dependence from a genomewide association study with this sample, ADH1B-rs1229984 (Arg48His) and ADH1B-rs2066702 (Arg370Cys), in EA and AA subsamples, respectively. ResultsOrdinal regression analyses conducted separately by sex and population revealed significant main effects for childhood adversity for both alcohol phenotypes in AA women and men and for maxdrinks in EA women. A significant rs1229984 by childhood adversity interaction was observed for AUD symptoms in EA men. Unexposed His-allele carriers reported a mean of 3.6 AUD criteria, but adversity-exposed His-allele carriers endorsed approximately the same number (6.3) as those without the protective allele (6.3 and 7.0 for adversity-exposed and -unexposed groups, respectively). ConclusionsResults suggest that under conditions of childhood adversity, the His allele does not exert its protective effects in EA men (OR=0.57, CI: 0.32 to 1.01; p=0.056). Findings highlight the robust risk effect conferred by childhood adversity and the importance of considering population and sex in genetically informative investigations of its association with alcohol outcomes.
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