Furthermore, shared genetic factors have been identified among SUDs, suggesting a complex interplay of common and specific biological pathways that influence vulnerability 15. However, a comprehensive understanding of the common and distinct genetic mechanisms underlying AUD and OUD is lacking. 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.
Seeking the Connections: Alcoholism and Our Genes
- Although this approach to studying complex behaviors was first proposed in the 1970s by psychiatric researchers investigating schizophrenia, it has recently proved even more valuable with modern tools for assessing biologic processes and analyzing genetic data.
- But to scientists, that apparent heritability suggested that some genetic component underlying vulnerability to alcohol problems was being transmitted from generation to generation.
- Starting with the F1 animals, researchers can then use different breeding schemes for subsequent analyses.
- As it turns out, there is no “alcoholic” gene in the human genome, nor is there an absolute “AUD-causing” environment or situation.
For the F2 design, animals from the F2 generation are studied both for the trait under investigation and for their genetic makeup (i.e., genotype). https://ecosoberhouse.com/ These lines differ in the composition of the genetic material inherited from the progenitors. The genetic connection to addiction comes through inherited levels of dopamine, a neurotransmitter made in your brain.
- In summary, GWASs have been limited by difficulties in quantifying alcohol-related phenotypes and in obtaining large sample sizes, together with co-morbidity of alcoholism with other behavioral and neuropsychiatric disorders, gender effects and population admixture.
- In particular, there are marked differences in alcoholism by gender, parent-of-origin effects, ethnicity, and other epidemiological factors.
- Alcohol is widely consumed, but excessive use creates serious physical,psychological and social problems and contributes to many diseases.
- The AUDIT, a 10-item, self-reported test was developed by the World Health Organization as a screen for hazardous and harmful drinking and can be used as a total (AUDIT-T), AUDIT-Consumption (AUDIT-C) and AUDIT-Problems (AUDIT-P) sub-scores.
- While the co-occurrence of OUD and AUD is well documented, the potential causal relationship between these disorders remains unclear.
- The tendency to become dependent on alcohol has long been known to run in families, which for some only added to the social stigma attached to this complicated condition.
Genes contributing to the risk of alcohol dependence
- Through the development of congenic lines and transgenic and knock-out animals, candidate genes can be identified and evaluated for their role in alcohol preference.
- Linkage studies are relatively robust to populationdifferences in allele frequencies (because they test within-family inheritance), andcan find a signal even if different variants in the same gene or region areresponsible for the risk in different families.
- Take our free, 5-minute alcohol abuse self-assessment below if you think you or someone you love might be struggling with substance abuse.
- Revealing the biological processes that can build and reinforce alcohol addiction will most certainly help to better target existing treatments and devise new ones to break alcohol’s hold.
- Compared with an F2 sample, the backcross offspring will not be as diverse with respect to their genotype or their phenotype.
- To identify as yet unknown genes involved in alcoholism and other disorders, investigators can search the entire genetic material (i.e., genome) by testing for linkage between polymorphic markers and the expression of the disorder or a related behavior.
- Teasing these effects apart is challenging, and to date fewer than a dozen genes that influence one’s risk for alcoholism have been identified, although more surely exist.
Your genetics don’t only increase your risk of AUD — they may have protective elements as well. That doesn’t mean you’ll absolutely develop AUD if you have a family member living with the condition. You may have a higher genetic predisposition, but the underlying causes of AUD are multifaceted and complex. Many is alcoholism inherited factors are involved in the development of AUD, but having a relative, or relatives, living with AUD may account for almost one-half of your individual risk. This was a secondary analysis, utilizing data previously published, with ethical approval obtained for each of the original studies. Development of a congenic line in which a quantitative trait locus (QTL) from the donor line is being bred into the recipient line.
Figure 1: Relationship among recently published genome-wide association studies related to AUDs.
According to a review from 2016, genes that promote alcohol metabolism and the production of enzymes, such as alcohol dehydrogenase and aldehyde dehydrogenase, can be protective against AUD. We used Gene Ontology (GO) and pathway enrichment analysis to understand the differential functional characteristics of each OUD group. Both groups shared 23 enriched GO terms, comprising 7% of OUD1 GO terms and 16% of OUD2 terms (Fig. 1G).
Immediate early genes (IEGs) enrichment analysis
The strong connection between variations in basic physiology and an individual’s susceptibility to alcohol problems is well illustrated by the very first gene to be identified as affecting the risk of developing alcohol dependence. The inclusion of data from different ancestral groups in this study cannot and should not be used to assign or categorize variable genetic risk for substance use disorder to specific populations. As genetic information is used to better understand human health and health inequities, expansive and inclusive data collection is essential. NIDA and other Institutes at NIH supported a recently released report on responsible use and interpretation of population-level genomic data, by the National Academies of Sciences, Engineering, and Medicine. The techniques to identify alcohol-related genes described in the preceding sections are still being developed and have yet to realize their full potential and identify genes contributing to alcoholism susceptibility.