Will guidelines on alcohol consumption be personalized by a genetic approach?
Ontology highlight
ABSTRACT:
SUBMITTER: Costanzo S
PROVIDER: S-EPMC7830050 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description: Not available
| S-EPMC3216427 | biostudies-literature
Project description:Multiple interindividual and intra-individual factors underlie variability in drinking motives, challenging clinical translatability of animal research and limiting treatment success of substance use-related problems. Intra-individual variability refers to time-dependent continuous and discrete changes within the individual and in substance use research is studied as momentary variation in the internal states (craving, stressed, anxious, impulsive and tired) and response to external triggers (stressors, drug-associated environmental cues and social encounters). These momentary stimuli have a direct impact on behavioural decisions and may be triggers and predictors of substance consumption. They also present potential targets for real-time behavioural and pharmacological interventions. In this review, we provide an overview of the studies demonstrating different momentary risk factors associated with increased probability of alcohol drinking in humans and changes in alcohol seeking and consumption in animals. The review also provides an overview of pharmacological interventions related to every individual risk factor.
| S-EPMC7429479 | biostudies-literature
Project description:We showed that F1 hybrid genotypes may provide a broader variety of ethanol drinking phenotypes than the inbred progenitor strains used to create the hybrids (Blednov et al. in Alcohol Clin Exp Res 29:1949-1958, 2005). To extend this work, we characterized alcohol consumption as well as intake of other tastants (saccharin, quinine and sodium chloride) in five inbred strains of mice (FVB, SJL, B6, BUB, NZB) and in their reciprocal F1 hybrids with B6 (FVBxB6; B6xFVB; NZBxB6; B6xNZB; BUBxB6; B6xBUB; SJLxB6; B6xSJL). We also compared ethanol intake in these mice for several concentrations before and after two periods of abstinence. F1 hybrid mice derived from the crosses of B6 and FVB and also B6 and SJL drank higher levels of ethanol than their progenitor strains, demonstrating overdominance for two-bottle choice drinking test. The B6 and NZB hybrid showed additivity in two-bottle choice drinking, whereas the hybrid of B6 and BUB demonstrated full or complete dominance. Genealogical origin, as well as non-alcohol taste preferences (sodium chloride), predicted ethanol consumption. Mice derived from the crosses of B6 and FVB showed high sustained alcohol preference and the B6 and NZB hybrids showed reduced alcohol preference after periods of abstinence. These new genetic models offer some advantages over inbred strains because they provide high, sustained, alcohol intake, and should allow mapping of loci important for the genetic architecture of these traits.
| S-EPMC3038337 | biostudies-literature
Project description:PurposeTo investigate the role of consumption phenotypes as genetic proxies for alcohol misuse and nicotine dependence.MethodsWe leveraged GWAS data from well-powered studies of consumption, alcohol misuse, and nicotine dependence phenotypes measured in individuals of European ancestry from the UK Biobank (UKB) and other population-based cohorts (largest total N = 263,954), and performed genetic correlations within a medical-center cohort, BioVU (N = 66,915). For alcohol, we used quantitative measures of consumption and misuse via AUDIT from UKB. For smoking, we used cigarettes per day from UKB and non-UKB cohorts comprising the GSCAN consortium, and nicotine dependence via ICD codes from UKB and Fagerström Test for Nicotine Dependence from non-UKB cohorts.ResultsIn a large phenome-wide association study, we show that smoking consumption and dependence phenotypes show similar strongly negatively associations with a plethora of diseases, whereas alcohol consumption shows patterns of genetic association that diverge from those of alcohol misuse.ConclusionsOur study suggests that cigarette smoking consumption, which can be easily measured in the general population, may be good a genetic proxy for nicotine dependence, whereas alcohol consumption is not a direct genetic proxy of alcohol misuse.
| S-EPMC8026738 | biostudies-literature
Project description:We investigate whether the serotonin transporter-linked polymorphic region (5HTTLPR), a gene associated with environmental sensitivity, moderates the association between smoking and drinking patterns at adolescents' schools and their corresponding risk for smoking and drinking themselves. Drawing on the school-based design of the National Longitudinal Study of Adolescent Health in conjunction with molecular genetic data for roughly 15,000 respondents (including over 2,000 sibling pairs), we show that adolescents smoke more cigarettes and consume more alcohol when attending schools with elevated rates of tobacco and alcohol use. More important, an individual's susceptibility to school-level patterns of smoking or drinking is conditional on the number of short alleles he or she has in 5HTTLPR. Overall, the findings demonstrate the utility of the differential susceptibility framework for medical sociology by suggesting that health behaviors reflect interactions between genetic factors and the prevalence of these behaviors in a person's context.
| S-EPMC3659161 | biostudies-literature
Project description:High alcohol consumption is a risk factor for morbidity and mortality, yet few genetic loci have been robustly associated with alcohol intake. Here, we use U.K. Biobank (n = 125,249) and GERA (n = 47,967) datasets to determine genetic factors associated with extreme population-level alcohol consumption and examine the functional validity of outcomes using model organisms and in silico techniques. We identified six loci attaining genome-wide significant association with alcohol consumption after meta-analysis and meeting our criteria for replication: ADH1B (lead SNP: rs1229984), KLB (rs13130794), BTF3P13 (rs144198753), GCKR (rs1260326), SLC39A8 (rs13107325), and DRD2 (rs11214609). A conserved role in phenotypic responses to alcohol was observed for all genetic targets available for investigation (ADH1B, GCKR, SLC39A8, and KLB) in Caenorhabditis elegans. Evidence of causal links to lung cancer, and shared genetic architecture with gout and hypertension was also found. These findings offer insight into genes, pathways, and relationships for disease risk associated with high alcohol consumption.
| S-EPMC6962045 | biostudies-literature
Project description:Investigating the association of alcohol and gene expression of breast tumors and tumor-adjacent tissues.
2017-08-31 | GSE93601 | GEO
Project description:Heavy drinking and diagnosis with alcohol use disorder (AUD) are consistently associated with risk for suicide attempt (SA). Though the shared genetic architecture among alcohol consumption and problems (ACP) and SA remains largely uncharacterized, impulsivity has been proposed as a heritable, intermediate phenotype for both alcohol problems and suicidal behavior. The present study investigated the extent to which shared liability for ACP and SA is genetically related to five dimensions of impulsivity. Analyses incorporated summary statistics from genome-wide association studies of alcohol consumption (N = 160,824), problems (N = 160,824), and dependence (N = 46,568), alcoholic drinks per week (N = 537,349), suicide attempt (N = 513,497), impulsivity (N = 22,861), and extraversion (N = 63,030). We used genomic structural equation modeling (Genomic SEM) to, first, estimate a common factor model with alcohol consumption, problems, and dependence, drinks per week, and SA included as indicators. Next, we evaluated the correlations between this common genetic factor and five factors representing genetic liability to negative urgency, positive urgency, lack of premeditation, sensation-seeking, and lack of perseverance. Common genetic liability to ACP and SA was significantly correlated with all five impulsive personality traits examined (rs = 0.24-0.53, ps < 0.002), and the largest correlation was with lack of premeditation, though supplementary analyses suggested that these findings were potentially more strongly influenced by ACP than SA. These analyses have potential implications for screening and prevention: Impulsivity can be comprehensively assessed in childhood, whereas heavy drinking and suicide attempt are quite rare prior to adolescence. Our findings provide preliminary evidence that features of impulsivity may serve as early indicators of genetic risk for alcohol problems and suicidality.
| S-EPMC10006209 | biostudies-literature
Project description:Purpose of reviewRecent advances in sequencing technologies have allowed for the identification of genetic variants within germline DNA that can explain a significant portion of the genetic underpinnings of prostate cancer. Despite evidence suggesting that these genetic variants can be used for improved risk stratification, they have not yet been routinely incorporated into routine clinical practice. This review highlights their potential utility in prostate cancer screening.Recent findingsThere are now almost 100 genetic variants, called single nucleotide polymorphisms (SNPs) that have been recently found to be associated with the risk of developing prostate cancer. In addition, some of these prostate cancer risk SNPs have also been found to influence prostate specific antigen (PSA) expression levels and potentially aggressive disease.SummaryIncorporation of panels of prostate cancer risk SNPs into clinical practice offers potential to provide improvements in patient selection for prostate cancer screening; PSA interpretation (e.g. by correcting for the presence of SNPs that influence PSA expression levels; decision for biopsy (using prostate cancer risk SNPs); and possibly the decision for treatment. A proposed clinical algorithm incorporating these prostate cancer risk SNPs is discussed.
| S-EPMC4281884 | biostudies-literature
Project description:Pharmacogenetic and adaptive treatment approaches can be used to personalize care for alcohol-dependent patients. Preliminary evidence shows that variation in the gene encoding the ?-opioid receptor moderates the response to naltrexone when used to treat alcohol dependence. Studies have also shown moderating effects of variation in the gene encoding the serotonin transporter on response to serotonergic treatment of alcohol dependence. Adaptive algorithms that modify alcohol treatment based on patients' progress have also shown promise. Initial response to outpatient treatment appears to be a particularly important in the selection of optimal continuing care interventions. In addition, stepped-care algorithms can reduce the cost and burden of treatment while maintaining good outcomes. Finally, matching treatment to specific problems present at intake or that emerge during treatment can also improve outcomes. Although all of these effects require replication and further refinement, the future of personalized care for alcohol dependence appears bright.
| S-EPMC6431083 | biostudies-literature