Update on the Genetics of Alcoholism Alcohol Research: Current Reviews

alcoholism hereditary statistics

Hugo Bellen, a geneticist at Baylor College of Medicine in Houston, Texas, said the study «lays the foundation for a genetic approach to dissecting the acute, and possibly the chronic, effects» of alcohol in people. A study in Sweden followed alcohol use in twins who were adopted as children and reared apart. The incidence of alcoholism was slightly higher among people who were exposed to alcoholism only through their adoptive families. However, it was dramatically higher among the twins whose biological fathers were alcoholics, regardless of the presence of alcoholism in their adoptive families. A number of studies have looked at alcohol use among specific racial and ethnic populations, including Black, Indigenous, and People of Color (BIPOC) communities.

Linking risk genes to brain chromatin interaction

  • The above studies used the DSM-IV-TR criteria for alcohol dependence in order to define the phenotype.
  • To compare within- and cross-ancestry fine mapping, we performed within-ancestry fine mapping for the above 92 regions using the same SNP sets and EUR-only LD information (Fig. 2b,c).
  • For studies of rare variants, families are quite valuable for sortingout true positives from the background of individual variations that we allharbor.
  • Alcohol Use Disorder (AUD) is a chronic psychiatric illness characterized by harmful drinking patterns leading to negative emotional, physical, and social ramifications.
  • The estimated credible set containing the causal gene can be prioritized for functional assays.

Despite the evidence supporting the prominence of genetic factors in AUD’s etiology, the identification of genetic risk variants has been difficult and labor intensive. With recent advances in technology, the most promising results stem from recent GWAS, which have helped to identify new variants in the genetics of AUD. Among the variants identified, the most significant SNPs remain in the alcohol metabolism enzyme genes, ADH and ALDH. Importantly, the prevalence of the various isoforms of ADH and ALDH celebrities with fetal alcohol syndrome differs among ethnicities and populations. Therefore, lower alcohol consumption in certain populations, as a result of the protective effect of alcohol metabolism SNPs, may be due to gene-environment interactions. Another study investigating the heritability of assorted substance dependencies, including alcohol, tobacco, cannabis, and illicit drugs, used GCTA estimates to conclude that common SNPs contribute to at least 20% of the variance in substance dependence vulnerability (Palmer et al., 2015).

alcoholism hereditary statistics

Identification of novel genetic loci and candidate genes for progressive ethanol consumption in diversity outbred mice

  • These approacheshave been quite fruitful for some studies and need to be employed in analyses ofalcohol-related traits and phenotypes.
  • As the field of psychiatry transitions to the DSM-5 criteria for AUD, there may also be changes in the functional variants identified by GWAS.
  • Through our collaborative gene‐brain‐behavior paradigm, we aspire to address both the causes and consequences of heavy alcohol use and AUD, which still contributes annually to 3 million preventable deaths globally.
  • As whole exome and whole genome sequencingtechnologies come down in cost, they are being applied to identifying rarevariants.
  • The more family members (related by birth) you have with an alcohol problem, the higher your risk.
  • Independent genetic signals from the cross-ancestry meta-analysis were searched in OpenTargets.org37 for druggability and medication target status based on their nearest genes.
  • COGA investigators are doing additional genotyping of SNPs in and near candidate genes in the regions of linkage for further analysis of linkage and linkage disequilibrium (i.e., the nonrandom association of alleles).

Future GWAS should focus on the endophenotypes of AUD in order to better understand the genetic connections to specific behavioral symptoms. Likewise, it will be important to separate the role of genetic variants due other substance use disorders and to comorbid psychiatric disorders. Defining specific phenotypes and separating comorbid disorders will be useful in order to parse genetic variants involved in multiple disorders and addictions from those only involved in AUD. Future studies may also focus on pathway analysis in order to better understand the heterogeneous group of variants currently identified by GWAS.

alcoholism hereditary statistics

Within- and cross-ancestry causal variant fine mapping

Recent successes in genetic studies of AUDs will definetely motivate researchers and lead to better therapeutic interventions for this complex disorder. From its inception, COGA has focused on the importance of brain function and on developing novel brain intermediary phenotypes of risk for and consequences of alcohol use and AUD. This has been done through the examination of neuropsychological tests and noninvasively recorded brain electrical activity during resting state and cognitive tasks, and more recently, by deriving measures of neural synchrony and connectivity (3. Brain Function).

Twin studies

Reassuringly, many COGA findings have been replicated in other samples (e.g., References 76, 77, 78, 79). Although studies spanning multiple approaches have suggested a genetic basis for AUD, identification of the genetic risk variants has been challenging. Some promising results are emerging from GWAS studies; however, larger sample sizes are needed to improve GWAS results and resolution. As the field of genetics is rapidly developing, whole genome sequencing could soon become the new standard of interrogation of the genes and neurobiological pathways which contribute to the complex phenotype of AUD.

Sex-stratified analyses

1. Available genetic data, quality control, and imputation

alcoholism hereditary statistics