Within the context of our society, drinking of alcohol is a perfectly normal activity. For most people drinking a moderate amount of alcohol can be beneficial, indeed studies suggest that moderate drinking may protect against coronary heart disease by improving insulin resistance (Gold, 1991). However, for a minority of people drinking alcohol is an activity that is fraught with danger and, for a very few, is akin to taking a poison that will almost inevitably ruin their lives. Henceforth, it is important for research purposes to define who an alcoholic is and what the effects of alcohol on that person are. An alcoholic is a person who drinks excessive amounts of alcohol habitually and whose pattern of drinking is uncontrollable and usually impulsive. Alcoholism is a chronic and usually progressive illness involving the excessive ingestion of ethyl alcohol, whether in the form of familiar alcoholic beverages or as a constituent of other substances. Furthermore, alcohol often effects the nervous, peripheral and gastric systems and is characterized by mental disturbances and muscular uncoordination, and may eventually leads to disorders such as cirrhosis of the liver (Goodwin, 1988). Alcoholism is thought to arise from a combination of a wide range of physiological, psychological, social, and genetic influences. It is characterized by an emotional and often physical dependence on alcohol and may often lead to brain damage or early death (Drews, 1992).
In the past, researchers from various different disciplines sought to pin down a single cause for alcoholism. There was the concept of addictive personality whereby it was suggested that anyone with a particular personality type was almost inevitably predestined to alcoholism. In a similar way, the presence of a close family member with a drinking related disorder was also considered to be a danger of almost epic proportions with various people suggesting that their lifestyles would undoubtedly ‘rub off’ on anyone unfortunate enough to live near them (Raistrick, 1985). Studies on aspects such as the individual’s environment suggest a certain type of environment may play a major contributing factor in developing alcoholism. It has been illustrated that children of alcoholics are at great risk of being exposed to an unhealthy family system. The more time a person spends in such a negative environment, the more susceptible he/she becomes to trying alcohol and in the long run of becoming alcoholics, marrying an alcoholic or doing both and so continuing the vicious cycle (Bowden, 1985).
Clearly, Alcoholism, as opposed to merely excessive or irresponsible drinking, has been variously thought of as a symptom of psychological or social stress or as a learned, maladaptive coping behaviour (Barrera et al., 1991). More recently, and probably more accurately however, it has come to be viewed that alcoholism is a complex disease entity in its own right. Alcoholism usually develops over a period of years. Early and subtle symptoms include placing excessive importance on the availability of alcohol. Ensuring this availability strongly influences the person’s choice of associates or activities. Furthermore, alcohol comes to be used more as a mood-changing drug rather than as a beverage served as part of a social custom or religious ritual. Initially, the alcoholic may demonstrate a high tolerance to alcohol, consuming more and showing less adverse effects than others. Subsequently, however, the person begins to drink against his/her own will and best interests, as alcohol comes to assume more importance than personal relationships, work, reputation, and most importantly their physical health. The person commonly loses control over drinking and is increasingly unable to predict how much alcohol will be consumed on a give occasion or, if the person is currently obtaining, when the drinking will resume again. Physical addiction to the drug may occur, sometimes eventually leading to drinking around the clock to avoid withdrawal symptoms (Gold, 1991).
The effects of alcoholism are direct and toxic as well as have sedative effects on the body. The effects on major organ systems are cumulative and include a wide range of digestive system disorders such as ulcers and inflammation of the pancreas. Furthermore, if the blood from the digestive tract, which flows through the liver before going back to the heart, contains alcohol it may kill liver cells as it passes through. Consequently, these dead and damaged cells are replaced by fibrous tissue, which over time can accumulate and form masses of scar tissue. This is a common disorder of the digestive system known as cirrhosis of the liver. Moreover, permanent damage to the central and peripheral nervous systems can also be prominent. Serious withdrawal symptoms, such as those marked by Delirium Tremens, can prove to be fetal even despite prompt treatment. Delirium Tremens is an acute disorder occurring as a symptom following withdrawal from intoxication. The seizures generally last from three to six days and are characterized by terrifying hallucinations, usually of small creatures, and violent tremors. The patient is disoriented and usually incoherent. This is in contrast to withdrawal from narcotic drugs such as heroin, which, although distressful, rarely results in death (Gold, 1991).
Recent evidence has shown that heavy and even moderate drinking during pregnancy can cause serious damage to the child. Evidently, pregnant women can transfer alcoholism to their unborn children by means of the umbilical cord. When the mother consumes alcohol during pregnancy, both she and her child experience its effects. Researchers have proven that alcohol is extremely toxic to the fetus since it can harm fetal cells as well as affect the placenta, the organ through which the fetus absorbs oxygen and other nutrients from the mother. The extend to which a fetus is damaged by exposure to alcohol depends on which stage of pregnancy the mother consumed the alcohol in, as well as on how much she consumed (Bowden, 1985). A study conducted on pregnant animals that were fed alcohol, led researchers to conclude that major physical defects in the human embryo can be caused by exposures to alcohol in the first trimester, that is the first three months of pregnancy. Brain damage, on the other hand, can result from exposures at any time during the pregnancy (Brown, 1992).
Researchers know that the more alcohol the mother drinks and the longer the fetus is exposed to its toxic effects, the more severe the child’s birth defects will be. Moreover, binge drinking or heavy alcohol consumption at one sitting, is particularly hazardous to the fetus, because very high levels of alcohol enter the mother’s blood stream and the alcohol is passed into the blood of the fetus through the placenta (Bowden, 1985).
Furthermore, a rare but severe expression of damage to the fetus by means of alcohol consumption is known as fetal alcohol syndrome (FAS). This disorder includes mild to severe mental and physical damage. FAS affects approximately 1 to 3 of every 1000 live births world wide, and is the leading known cause of mental retardation in the Western world. French researchers at the University of Nantes in 1968 were the first to make a connection between maternal use of alcohol during pregnancy and birth defects in children. Children with FAS are small in size and weight at birth and have slow growth rates throughout their entire development. A child with FAS has characteristic facial features that may include short eyelids, a flattened midface, a smooth and elongated space between the nose and the mouth, and a narrow upper lip. Specifically, these children show evidence of damage to the central nervous system that may be in the form of mental retardation, learning disabilities, developmental disabilities, seizures, or even 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.
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