The Collaborative Study on the Genetics of Alcoholism: An Update PMC

Our research group recently discovered, for example, that variation in a gene encoding a receptor involved in taste perception, known as hTAS2R16, is significantly linked to alcoholism in the COGA subjects. The risk variant, which causes decreased sensitivity to many bitter taste compounds, is uncommon in European Americans, whereas 45 percent of African-Americans carry this version, making it a much more significant risk factor in that population. What this means for family members of alcoholics is that you are not necessarily going to misuse alcohol yourself. Factors like your environment and ability to handle situations triggering dependency are just as important as genetics. These are things that we can remain mindful of as we continue to develop an understanding of alcoholism on a personal basis. A study in Sweden followed alcohol use in twins who were adopted as children and reared apart.

Overview of COGA participants across data modalitiesa including the Semi‐Structured Assessment for the Genetics of Alcoholism (SSAGA), genome‐wide association study (GWAS) and electroencephalography (EEG) data. People who meet criteria for dependence often have multiple cases of alcoholism in their families. 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. But to scientists, that apparent heritability suggested that some genetic component underlying vulnerability to alcohol problems was being transmitted from generation to generation. Researchers at the University of California at San Francisco (UCSF) are using fruit flies to find the genetic causes of alcoholism. According to scientists, drunken drosophila fruit flies behave the same way humans do when they are drunk.

Data from the LSS and CFS studies also allow us to examine the association between alcohol problems in the adoptive family and the occurrence of alcoholism in the adoptee. It should be noted, however, that because alcohol problems in the adoptive families could include problems experienced by siblings, analysis could overestimate the influence of the adoptive parents on the adoptees’ outcomes. By using archival records, the Stockholm study was able to obtain data on the entire sample of adoptees.

Alcohol Use Disorders Identification Test (AUDIT)

Having a close family relative, such as a parent, can account for up to 60% of your risk of developing AUD. 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. By Buddy TBuddy T is a writer and founding member of the Online Al-Anon Outreach Committee with decades of experience writing about alcoholism. Because he is a member of a support group that stresses the importance of anonymity at the public level, he does not use his photograph or his real name on this website. The sensitive mice tend to lose their inhibitions and pass out rather quickly, earning them the nickname "long sleepers." "Short sleepers" are mice that are genetically less sensitive to alcohol.

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. Understanding the genetic basis of alcoholism is crucial to characterize individuals' risk and to develop efficacious prevention and treatment strategies. Environmental factors also account for the risk of alcohol and drug abuse.2 Scientists are learning more about how epigenetics affect our risk of developing AUD. If a person grows up in a house with a parent who abuses drugs, struggles with mental illness, suffers a major financial setback or similar stress, and the child has a gene linked to alcohol use disorder, they are very likely to develop this condition later in life. Prevention and education programs can address this risk as part of regular medical checkups.

1. 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.
2. Because the diagnosis of an AUD requires the presence of a set ofsymptoms from a checklist, there are many different ways one could meet thecriteria.
3. Scientists have learned through studies of identical and non-identical twins that alcohol use disorder is heritable, with genetic factors accounting for about half of the risk of alcohol dependence.

The risks of smoking were first widely publicized by the Surgeon General's Report of 1964, and the combination of that medical information and social pressure has reduced the prevalence of smoking over the subsequent decades. An individual's awareness of personal genetic medical risks may similarly change his or her choices. The broader health and social effects of this new type of information may not be seen quickly, but they could be quite profound over time. "These genes are for risk, not for destiny," stressed Dr. Enoch Gordis, director of the National Institute on Alcohol Abuse and Alcoholism.

Antisocial personality disorder (ASPD), conduct disorder (CD) and attention deficit hyperactivity disorder (ADHD)] 1,7,16. Twin studies reveal consistently the existence of shared genetic influences between alcoholism and externalizing disorders 17-20. Longitudinal studies have shown that externalizing disorders of childhood such as CD and ADHD are important risk factors for the subsequent development of alcoholism 21.

The Neurobiology of Addiction: Dopamine Reward Circuitry and Interacting Stress Response Systems

If genetic influences, in particular, are important, a significantly higher risk ratio should occur in MZ compared with DZ twin pairs. Analyses of 987 people from 105 families in the initial sample provided evidence that regions on 3 chromosomes contained genes that increase the risk for alcoholism (Reich et al. 1998). The strongest evidence was for regions on chromosomes 1 and 7, with more modest evidence for a region on chromosome 2. The DNA regions identified through these analyses were broad, as is typical for studies of complex genetic diseases, and therefore are likely to contain numerous genes. Much additional work is required to narrow the regions and attempt to determine which specific gene or genes play a role in affecting the risk for alcoholism.

Results of Genetic Analyses

The goal of this series of reviews is to describe the study design, highlight the multi‐modal data available in what is sunrock weed the Collaborative Study on the Genetics of Alcoholism (COGA), and document the insights that these data have produced in our understanding of the lifecourse of AUD. COGA is an interdisciplinary project with the overarching goal of understanding the contributions and interactions of genetic, neurobiological and environmental factors towards risk and resilience over the developmental course of AUD, including relapse and recovery. In this overview, we outline the motivation behind and design of COGA as a multi‐modal project. However, the fundamental strength of COGA has been our ability to integrate across these domains in a cohort of families with whom we have established a robust research relationship for over three decades. Within both the U.S. and Scandinavian studies, no significant gender differences were found in the genetic contribution to alcoholism risk. In the Scandinavian data, genetic factors appear to be more important in women than in men (a pattern that is seen in both the Swedish adoption and Swedish twin studies), but no statistically significant difference exists.

Behavior genetic studies can establish the origins of comorbidity and evaluate the extent to which liability to different diseases is shared or unshared. This is conducted by looking at the cross-inheritance of different diseases within families and in twin pairs. Twin and family studies on alcoholism have revealed that genetic factors acting on alcoholism include both alcohol-specific genetic factors as well as genetic factors that are shared with other addictions (for review see Goldman & Bergen) 8. For example, results from several twin studies 9-13 have detected consistently a considerable overlap in the genetic liability to alcoholism and nicotine dependence, particularly in individuals who drink or smoke heavily. Rates of smoking are declining; however, studies reported during the past 20 years have indicated that as many as 80% of alcohol-dependent individuals are heavy smokers 14,15. Approximately 50% of the genetic vulnerability to nicotine dependence is shared with alcoholism, whereas 15% of the genetic vulnerability to alcoholism is shared with nicotine dependence 9.

Family TiesAt coga's outset, researchers at sites around the country sought to identify families severely affected by alcoholism. Previous twin, adoption and family studies had indicated that alcohol problems are strongly heritable--indeed, more than 50 percent of the overall risk for alcoholism is attributable to inherited factors, which makes family groups a powerful resource for tracking specific traits and linking them to the relevant genes. Variants of each of the known genes only modestly alter an individual's vulnerability to alcohol, but many are common in the general population and may have wider effects on drinking habits, on other addictions or problematic behaviors, and on disorders such as depression and anxiety.