Candidate Genes

Genes that are suspected to be involved in the development of alcoholism are referred to as candidate genes, genes that are candidates for involvement in the condition. They encode for some brain chemicals and permit the interaction between neurons. Two candidate genes are a gene for the dopamine D2 receptor, DRD2 (Edenberg et al. 1998a), and a transporter gene for serotonin, HTT (Edenberg et al. 1998b). Both genes have been studied for a link to alcoholism. Researchers involved with the Collaborative Study on the Genetics of Alcoholism (COGA) systematically screen all human chromosomes for genes potentially involved with alcoholism.

No link has been found. We know that there is a strong relationship between serotonin dysfunction and behavior disorders, including alcoholism. A genetic factor that involves the reuptake of serotonin is known to be involved in this relationship. Other connections have been found between addictive behavior and genes. The genetic analyses of the COGA participants identified four regions, on chromosomes 2, 5, 6, and 13, that appear to contain genes affecting the amplitude of the P3 (Begleiter et al.

1998), so there is some evidence that genetics play a role in alcohol dependence. The P3 wave may be involved in other addictive behaviors as well. Also, Williams et al. (1999) found evidence that a region exists on chromosome 4 that protects against alcohol dependence. This region occurs with different frequency in different ethnic groups. Edenburg (2000) found that it occurs frequently in Asian populations, but is rare in Caucasian populations. Other genes that protect against alcohol dependence may also exist (NCADD). XIII.

Chromosome Regions The total DNA in a cell is packaged into smaller genetic units called genes. Chromosomes are composed of DNA material that makes up the smaller regions on the chromosomes are called genes. Chromosomes are the cellular components that contain genetic material called genes, the specific sequences of nucleotides in DNA or RNA located on a chromosome. Genes are the functional units of inheritance that control the transmission and expression of one or more traits by specifying the structure of a particular protein chain.

Nucleotides are the combination of sugar and complex molecules (called pyrimidines and purines) contained in genes. Pyrimidines or purines combine with sugar to form the nucleotides DNA and RNA respectively. The DNA or RNA without sugars is called nucleosides. Pirisi proposed that chromosomes 1 and 7 (Reich et al. 1998) are linked to alcohol dependence. Hill et al. (1988) later discovered a link between chromosome 4 and alcoholism and Tanna et al found a link between alcoholism and chromosome 13. Some chromosome regions have been connected with alcoholism.

COGA researchers have found certain regions of chromosomes 1, 2, 3 and 7 appear to increase the risk of becoming alcoholic (ref) or influence symptoms of the condition. Ultimately, there is no doubt that regions on some chromosomes are involved in the alcoholic condition, but the data cannot demonstrate that alcoholism is caused by these regions. XIV. Protective Regions While some regions of chromosomes can be associated with the symptoms and conditions of alcoholism, other regions appear to protect against the condition.

One such region has been identified on chromosome 4 near the region of the gene for the enzyme alcohol dehydrogenase (ADH). Therefore, it is clear that while some areas of the human genome may code for conditions connected with the alcoholic state, other chromosomal regions have the opposite effect. These genes protect the carrier against becoming alcoholic and thus reduce the risk for the condition. Protective genes are more common in some groups than in others. Asians, for example, have a high likelihood of carrying protective genes whereas Caucasians have a low likelihood.

Individuals and groups with higher levels of the dopamine D2 receptor, DRD2, appear to have greater protection against alcoholism. These dopamine receptors are thought to trigger protective behaviors in response to the presence of alcohol. XV. The P3 Wave Many studies have considered and investigated a possible genetics explanation for alcoholism. One component of an event related potential (ERP) is a brain wave called P3 (or P300) wave which is also viewed as a specific gene marker. Genes for the P3 wave can be found on regions of chromosomes 2, 5, 6 and 13 (Begleiter et al.

1998) It is connected with recognition and attention and is commonly observed in alcoholics and their close relatives. The P300 wave typically occurs 300 milliseconds after a stimulus and has been connected with addictive behavior in a number of studies. The P300 wave is an aggregate wave composed to two ‘wavelets’ known as P3a and P3b. These wavelets originate from the frontal lobe and the temporal-parietal lobes respectively and have been associated with attention, learning and memory. The amplitude of the P300 wave tends to decrease in alcoholism and may be affected in other addictive behaviors (George et al, 2004).

Previous studies have found that the amplitude of the P300 wave is reduced in a heritable phenotype that correlates with alcohol dependence and psychiatric disorders (Porjesz et al. 1998). Further study is needed to determine how other forms of addiction affect the P300 wave. P3 deficits appear to be common in addiction to alcohol and other drugs as well in antisocial behavior and learning disorders. (Begleiter et al. ,1998) XVI. Consensus View Overall, these studies reach a general consensus view that genetics is somehow related to alcoholism.

However, as the NCADD points out, the results of these studies and conclusions are muddled by the idea, never adequately addressed, that an alcoholic’s environment rather than genetics might be the overriding influence in the habit of excess drinking. Some individuals with the same genetic traits do not become alcoholics, and many alcoholics do not have these traits. Also, even though these traits are interesting and statistically significant, perhaps the most significant statistic is that they do not explain the alcoholic tendencies (of consuming or not consuming alcohol) for about 80 percent of the population.

Plomin et al. (1980) point out that the incidence of alcoholism is 22 percent in individuals with alcoholic parents as compared to 4. 4 percent in control groups, so it is reasonable to reject the idea that genetics plays no role in alcohol consumption. Further evidence for a genetic involvement in alcohol consumption comes from the observation that antagonists at the opioid receptor decrease alcohol consumption without altering food or water intake. (Froelich, 1995) Still, the question of nature vs. nurture is not entirely clear.

The unstated and possibly false conclusion to reach from the genetics research literature and the general interpretive approach taken throughout the literature is that the genetic factors associated with alcoholism contribute to the habit of problem drinking rather than to the subsequent health problems. This may be true, but it is unlikely. Yet, we have no choice but to take this approach since that is the general approach taken in the literature. The best we can do is to repeatedly point out this muddled interpretation at various strategic points throughout our discussion. XVII. Summary and Conclusion

The information presented is not entirely conclusive as to the role genetics play in alcoholism and alcoholic behavior. Certainly, one of the greatest stumbling blocks to determining a role for genetics is the fact that we cannot reach an agreed upon definition for alcoholism. Alcoholics Anonymous presents the idea that alcoholic behavior constitutes alcoholism and that the behavior itself is a disease. Researchers do not necessarily agree, but the issue is hotly debated and cannot be adequately resolved, so no one can be absolutely certain to what one is referring when they mention the word ‘alcoholism’.

That issue aside, it is clear that excessive alcohol consumption leads to diseases and genetic factors may increase the likelihood of contracting some diseases associated with the alcoholic condition. Genetic factors certainly are involved, but ultimately, if excessive drinking is the disease or leads to the diseases associated with alcoholism, the general suspicion is that excessive drinking is a matter of personal choice rather than genetics. While genetics may contribute to the health effects that arise from over consumption, it is difficult to connect any genetic factors with the behavior.

Somehow, we must find a way to agree upon what constitutes ‘alcoholism’ so that we can move on from there. Until we reach some consensus agreement on the definition of alcoholism, we certainly will not be able to determine what causes the condition. You cannot attribute a cause to an uncertain, phantom condition.

References Alcoholism and Genetics, http://web. pdx. edu/~hue/alcoholism_and_genetics. htm. Alcoholism (2004). Reviewed By: Simon, Harvey. http://www. healthandage. com/html/well_connected/pdf/doc56. pdf Begleiter, H. , Porjesz, B.

, Reich, T. , et al. (1998). Quantitative trait loci analysis of human event-related brain potentials: P3 voltage. Electroencephalography and Clinical Neurophysiology 108, 244–250. Bohman, M. , Sigvardsson, S. , & Cloninger, C. R. (1981). Maternal inheritance of alcohol abuse: Cross-fostering analysis of adopted women. Archives of General Psychiatry 38, 965-969. Cadoret, R. J.. Cain, C. A. , & Grove, W. M. (1980). Development of alcoholism in adoptees raised apart from alcoholic biologic relatives. Archives of General Psychiatry 37, 561-563.

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