The oral cavity and esophagus aredirectly exposed to those levels, and the liver is exposed to high levels from theportal circulation. Thus it is not surprising that diseases of the GI system,including cirrhosis, pancreatitis, and cancers of the upper GI tract are affected byalcohol consumption80-86. AUD isn’t directly caused by genetics, but genetics may predispose you to developing AUD later in life. This risk is considered hereditary and may be passed down to you if you have a family history of AUD. Your genetics can influence how likely you are to develop AUD, but there’s currently no evidence of a specific gene that directly causes AUD once you start drinking.
Associated Data
- With the advent of microarrays that can measure hundreds of thousands tomillions of single nucleotide polymorphisms (SNPs) across the genome,genome-wide association studies (GWAS) have provided a relatively unbiased wayto identify specific genes that contribute to a phenotype.
- This paper provides an overview of different approaches that are being integrated increasingly to advance our knowledge of the genetic bases of alcoholism.
- Estimates of genetic and environmental effects did not appear to vary significantly within the group of U.S. studies or the group of Scandinavian studies.
- This is conducted by looking at the cross-inheritance of different diseases within families and in twin pairs.
- For women, Koskenvuo and colleagues (1984) found no same-sex twin pairs in which both twins had an alcoholism discharge code, making it impossible to estimate a risk ratio.
Thus, when investigating the biology of alcoholism, researchers must carefully define the problem–for example, distinguishing between true dependence on alcohol and alcohol abuse, which is a less medically severe syndrome. This ALDH1 gene variant has since been found to be common in Asian populations–seen in 44 percent of Japanese, 53 percent of Vietnamese, 27 percent of Koreans and 30 percent of Chinese (including 45 percent of Han Chinese)–yet it is rare in people of European descent. As might be expected, people with this slow-metabolizing gene variant also have a decreased risk, by up to sixfold, for alcoholism, so it is an example of a genetic variation that can protect against developing the disorder. As is true of many other human disorders, alcoholism does not have a single cause, nor is its origin entirely genetic. Genes can play an important role, however, by affecting processes in the body and brain that interact with one another and with an individual’s life experiences to produce protection or susceptibility. 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.
Although studies now include Hispanic, African-American, Asian, and other minority groups, most earlier studies predominantly used samples of European ancestry. The generalizability of findings in populations of non-European ancestry remains to be determined. As we’ve learned more about how genes play a role in our health, researchers have discovered that different factors can affect the expression of our genes. NIAAA’s “Core Resource,” although intended for health care professionals, has helpful information for the public as well. One NIAAA-supported study, the Collaborative Study on the Genetics of Alcoholism Project (COGA), explores how genes affect vulnerability to AUD, and has an easy-to-understand web resource about alcohol and genetics.
The COGA investigators also evaluated electrophysiological variables, such as EEGs and ERPs, from study participants. EEGs measure overall brain activity, whereas ERPs are brain waves elicited in response to specific stimuli (e.g., a light or sound). Analysis of such electrophysiological data may reveal a subset of genes that affect these quantitative, biological phenotypes related to alcoholism (Porjesz et al. 1998, 2002).
However, this could be an artifact of differences in research methodology, as no studies led by the same investigators and using a common research methodology have been conducted in both Scandinavia and the United States. Second, two studies appear to be outliers, producing results at variance with the general trend. The estimate of the shared environmental contribution to alcoholism risk from the Kaij (1960) study is much greater than in all other studies. The reasons for this are unknown, although it is possible that in the work by Kaij some registrations were accidentally overlooked. However, once one twin from a pair was identified with a registration, the records were searched more thoroughly to determine whether the co-twin also had been registered. Cadoret’s study of four adoption agencies (Cadoret 1994; Cadoret et al. 1995) has yielded a high estimate of the genetic contribution to variability in alcoholism risk, which does not differ significantly from a probability of 100 percent (i.e., complete heritability).
Other Addictive Behavior
Tabakoff et al. 122 compared the mRNA expression profiles of mouse strains displaying marked differences in acute tolerance to alcohol and results from this study indicate the importance of a signal transduction cascade that involves the glutamatergic pathway. How can results across different studies or even within studies (e.g., between men and women) be compared? Risk-ratio estimates cannot simply be pooled because of differences in the estimated rates of alcoholism.
Seek Help For An Alcohol Use Disorder
With rapid advances over the past 10 years in technologies for discovering and analyzing the functions of genes, researchers are now increasingly able to get at the biological roots of complex disorders such as substance abuse and addiction. The power to examine patterns of inheritance in large populations, and to survey hundreds of thousands of tiny variations in the genomes of each of those individuals, enables investigators to pinpoint specific genes that exert strong or subtle influences on a person’s physiology and his or her resulting risk for disease. Besides other addictions, alcoholism also coexists frequently with other psychiatric diseases, including both internalizing disorders (e.g. depression and anxiety) as well as externalizing disorders