FREE ESSAY ON ALCOHOLOSM

ALCOHOLOSM

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. 
Bibliography
References
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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:
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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.
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