Alcoholosm

.. ven a small head size. Furthermore, FAS children may develop hearing problems, heart defects and physical and behavioural problems. Researchers have also found that some children who were exposed to alcohol during fetal development show only some of the characteristics of FAS, these children are diagnosed as having fetal alcohol effects (FAE). However, both FAS and FAE individuals may have some degree of brain damage (Brent, 1991). Clearly, in addition to physiological, social, and psychological factors which all play a role in contributing to alcoholism, recent studies reveal that there may be a genetic predisposition to alcoholism.

More specifically, medical research indicates that alcoholism is hereditary and gives support to those who believe that children of alcoholics have a greater chance of become alcoholics themselves. This argument is supported by Lieber, chief researcher of a research program on liver disease, who discovered that the mitochondria in the liver of alcoholics are unable to convert acetaldehyde into acetate like those of non-alcoholics. This being evident even at the early stages of heavy alcohol consumption suggests that even before the alcoholic started to drink his/her lover cells were altered. To add to this, Psychiatrist Mark Schuleit, who studied children of alcoholics, found that metabolic abnormalities exist prior to heavy drinking. Like their parents, their children were unable to convert acetaldehyde at regular speed (Miliam & Ketchman, 1981). Furthermore, Researchers claim to have been able to separate hereditary influences from environmental one’s by testing children who had been put up for adoption at birth by their alcoholic parents.

Findings affirm that the adopted children had a high rate of alcoholism and thus conclude children of alcoholics have a much higher risk of becoming alcoholics themselves. Specifically, they are four times more likely to succumb to alcoholism (Goodwin, 1981). Researchers at the Portland Alcohol Research Center have recently mapped three gene regions in mice that influence the susceptibility to physical dependence on alcohol. According to Kari Buck, Ph.D.,”This is an important breakthrough because it is the first time that scientists have identified discrete gene regions involved in physical dependence on alcohol .. ” (p.22). Specifically Buck’s team has shown that mice carrying three gene regions are at greater risk for acute physical dependence on alcohol than mice without these genes.

Because of the importance of alcohol withdrawal in clinical manifestations of alcoholism, and because of similarities between the mouse and human genome, Buck feels that “the study will contribute significantly to the ultimate development of new treatments” (p.22). Although, Buck realizes that both genes and the environment influence alcohol dependence in humans, she manages to confirm that there is clearly an increased risk of alcohol-related problems in children of alcoholics (Gold, 1991). Furthermore, a collaborate study on the Genetics of Alcoholism, sponsored by the National Institute on Alcohol Abuse and Alcoholism, has examined regions of the human chromosome that that correspond to the genetic markers identified in mice. In addition, the study also found evidence for a gene on the human chromosome 1 that appears to be involved in alcohol dependence. In addition, it has been stated that the same region of the chromosome appears to contain more GABA receptor genes. Previous studies suggested that alcoholics appear to have more brain GABA receptors than non-alcoholics.

GABA is one of the brain’s most important chemical messengers, carrying signals to neighboring nerve cells and docking on receptor molecules embedded in the membrane of the cell (Vaillant, 1995). On a similar note, Kenneth Blum began formulating a theory of the cause of alcoholism in the 80’s that involved several factors including a biological predisposition. In a recent revision of this earlier theory (Blum, Cull, Braverman & Comings, 1996) he and his colleagues have expanded their theory to include various behavioural disorders including alcoholism, substance abuse, smoking, compulsive overeating, attention deficit disorder, Tourette’s syndrome and even pathological gambling. The authors state: “We believe that these disorders are linked by a common biological substrate, a ‘hard-wired’ system in the brain (consisting of cells and signaling molecules) that provides pleasure in the process of rewarding certain behavior” (Blum et al., 1996 p.132). A theory that would integrate this many previously different syndromes would be clearly extremely important as it could lead to similar methods of prevention and treatment.

Moreover, Blum believes that the common thread running through these behaviors is a dysfunction in the brain’s pleasure and reward system, one involving the neurotransmitter Dopamine usually present in the limbic system. Essentially he suggests that the use of several drugs and the expression of several compulsive behaviours are caused by the brain’s attempt to compensate for a deficient, hypoactive reward system. Furthermore, Blum believes that the genetic site that leads to the dopamine deficiency is the ‘A1’ allele. Henceforth, he suggests that the best hope of preventing these disorders is to increase genetic testing so that individuals who have the A1 allele can be counseled early on in life to avoid behaviour that could put them at risk (Blum et al., 1996). Clearly, as science and medicine have advanced in their understanding of genetics, it has become clear that many complex problems such as alcoholism, there is usually more than one gene responsible for the problem. Furthermore, identifying the genes that lead to alcoholism and drug addiction in humans has been difficult, since humans express more than 100,000 genes. Henceforth, the invention of gene mapping, which shows that often there are a number of different genes responsible for behaviours, related to alcoholism.

As a group these are referred to as QTL’s (quantitative trait loci). Moreover, understanding how they all fit together and more specifically how they influence behaviour of alcoholics is a subject of a great deal of long term research (Vaillant, 1995). Clearly, alcoholism is a complex phenomenon and it is most likely that all physiological, environmental, psychological, and genetic factors equally influence the cause of the disease. We live extraordinarily complex lives and we are acted upon by a multitude of variables affecting all aspects of our activities, henceforth, it would appear nonsensical to suggest that a single factor can cause a problem such as alcoholism. Bibliography References Barrera, M., Chassin L., Royosh, F. (1991). Substance use and symptomatology among adolescent children of alcoholics.

Journal of Abnormal Psychology, 100, 449-463. Black, C. (1987). Children of Alcoholics: It will never happen to me. New York: Ballantine. Blum, K., Braverman, E.

& Comings, D. (1996). Reward Deficiency Syndrome. American Scientist, 2, 84, 132-146. Bowden, D., Gravitz, L. (1985). Recovery: A Guide for Adult Children of Alcoholics.

New York: Simon and Schuster. Brent, E., Sher, K., Walitzer, K., Wood, P. (1991). Characteristics of Children of Alcoholics. Journal of Abnormal Psychology, 100, 427-448. Brown, S. (1992).

Safe Passage. Toronto: John Wiley and Sons. Drews, T. (1983). Getting Them Sober.

New Jersey: Bridge Publishing Inc. Gold, M. (1991). The Good News about Drugs and Alcohol: Curing, Treating, and Preventing Substance Abuse in the New Age of Biopsychology. New York: Villard Books. Goodwin, W. (1981).

Alcoholism: The Facts. New York: Oxford University Press. Raistrick, D. (1985). Alcoholism and Drug Addiction. New York: Churchill.

Vaillant, G. (1995). The natural History of Alcoholism Revisited. Cambridge: Harvard University Psychology Essays.