Academic journal article Alcohol Research

Genetic Research: Who Is at Risk for Alcoholism?

Academic journal article Alcohol Research

Genetic Research: Who Is at Risk for Alcoholism?

Article excerpt

Evidence from archeological artifacts indicates that fermented beverages existed as early as 10,000 B.C. The excessive consumption of alcohol, however, results in dangers to the health and well being of the drinker and those around him or her. Today, the World Health Organization estimates that alcohol causes 1.8 million deaths (3.2 percent of all deaths) worldwide and 58.3 million (4 percent of total) disability-adjusted life-years (DALYs) (1) lost to disease ( facts/alcohol/en/index.html). In the United States, alcohol dependence (i.e., alcoholism) is a major health problem, affecting 4 to 5 percent of the population at any given time, with a lifetime prevalence of 12.5 percent (Hasin et al. 2007).

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) was founded 40 years ago to further understanding of the biological underpinnings of alcohol dependence. Early genetic studies were focused on delineating whether environmental factors, genetic factors, or both contributed to the risk for alcohol dependence. Once it was apparent that genetics did indeed play a role in alcohol dependence, NIAAA began to fund studies seeking to identify relevant genes. Since then, studies in humans and animals have used complementary approaches to understand the genetics of alcohol use and dependence. This overview summarizes the evidence supporting a role for genetic factors in alcoholism and describes how new genetic findings could affect our understanding of the causes and factors contributing to this debilitating disease and could potentially guide the development of improved treatments.

Evidence of a Genetic Contribution to Alcohol Dependence

Several study designs, including twin, family, and adoption studies, are used to determine whether relatively common diseases, such as alcohol dependence, are caused at least in part by genetic factors and to estimate the magnitude of the overall genetic contribution. Twin studies compare the similarity in disease status (i.e., concordance2) between identical (i.e., monozygotic) and fraternal (i.e., dizygotic) twins. If risk for a disease (e.g., alcohol dependence) is determined at least in part by genetic factors, monozygotic twins, who have identical genetic material (i.e., genomes), would be expected to have a higher concordance rate for alcohol dependence than dizygotic twins, who on average share only half their genome. Studies by several groups have indeed shown higher concordance rates for alcohol dependence among monozygotic than among dizygotic twins (Agrawal and Lynskey 2008). Family studies, which evaluate the members of a family (both alcoholic and nonalcoholic members) for the presence of the disease, also have provided convincing evidence that the risk for alcohol dependence is determined partly by genetic influences (Gelernter and Kranzler 2009). Overall, family, adoption, (3) and twin studies provide convergent evidence that hereditary factors play a role in alcohol dependence, with variations in genes estimated to account for 50 to 60 percent of the total variance in risk. These estimates suggest that although genetic factors are important, nongenetic factors also contribute significantly to the risk for alcohol dependence.

Strategies for Identifying Genes Contributing to Alcohol Dependence

Researchers have developed several strategies to identify genes that contribute to differences in the risk for alcohol dependence, including case--control studies and linkage analyses. These strategies depend on the premise that for a particular position in the DNA of these genes, more than one possible form exists. Each of these forms is termed an allele. The study methods used to identify genes that affect the risk for alcohol dependence assume that the presence of certain alleles increases the risk of alcoholism. These variants that affect risk can be located either directly within a gene or near a gene. …

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