Alcoholism and Genetics

Introduction.

According to the University of California, San Francisco (UCSF) Family Alcoholism Study, over 76 million people in the United States are affected directly or indirectly by alcoholism and 100,000 deaths that happen each year are caused by alcoholism making it the top third cause of anticipated deaths in the United States.  Alcoholism has always been a problem in this country and the causes have always been a controversial issue.  To deal with this issue, a better understanding of the basic facts and two of the major causes assumed by scientists of alcoholism, genetic and environment, with a conclusion of my own  of the cause of alcoholism will be discussed in this paper.

I.      Alcoholism.

Alcohol is a drug that acts as a depressant - a substance that decreases the nervous system’s ability to function normally and it affects all who consume it, but alcohol is a drug more unique than any other.  It’s a drug that only certain people can become dependent on.  Most people get intoxicated before they reach the addiction level, because their bodies have a protection against alcohol. But by chance 20 percent of the population don’t have this protection, just like certain people are good at singing or good at drawing, and therefore have a higher tolerance of alcohol.  Alcohol requires large amounts of consumption before one can become addicted and the tolerance allows the addiction to develop, which means a higher chance of becoming an alcoholic.  (Arterburn, 242).  Women have a lower rate of tolerance than men, therefore there are almost three times as less women (3.9 million) as men (9.8 million) who are problem drinkers. 

Although different people react to alcohol differently, the symptoms of an alcohol problem are all very similar in everyone.  The following table lists some of the signs.

Alcoholism hasn’t been a problem just for individuals, but it also has been a problem for families of the affected individuals, because often times it results in moving down the line to the rest of the members.  In recognizing such a result many studies have been produced to test the genetic aspects of alcoholism.

II.     Genetic.   

Rumor has always been that alcoholism runs in the family and statistics has shown that it does.  “An estimated 20-25% of sons and brothers of alcoholics become alcoholics,” as stated from the UCSF Family Alcoholism Study and “5% of daughters and sisters of alcoholics become alcoholics.”  “Cotton (1979), in her classic review of family studies, concluded that alcoholics were six times more likely than nonalcoholics to report a positive family history of alcoholism,” (Development, 1) are just some more examples of the family and alcoholism. 

Many studies have been conducted to support such a proposal and findings are leading toward specific chromosomes.  The second of two studies by the Collaborative Study of the Genetics of Alcoholism (COGA) of “987 individuals from 105 families containing at least three first-degree relatives with alcohol dependence” (Pirisi) suggests that there is a “strong linkage between chromosomes 1 and 7 and susceptibility to alcohol dependence, and weak evidence for linkage to chromosome 2.”  Another suspect of genes that was also looked at is a marker known as the dopamine D₂ receptor found by Blum and co-workers to exit more often in alcoholics than nonalcoholics. (Genetics).  When studied in animals, dopamine D₂ receptor “had been associated with brain functions relating to reward, reinforcement, and motivation,” (Genetics) and therefore is suspected to increase a person’s risk of alcoholism and other addictions.

Along with the genes that were looked at, to make sure that alcoholism is inherited, studies were produced to find genetic markers.  Genetic markers could be proteins, genes or DNA sequences, and “in linkage studies, genes potentially involved in a disease can be identified when they are transmitted from one generation to the next by studying genetic markers that are close enough on the same chromosome that they do not become separated at gametogenesis.” (Palmer, 195).  In 1988 Hill et al. discovered a linkage between the MNS blood group system on chromosome 4 and alcoholism.  On the same year, Tanna et al. found yet another, but weaker linkage between esterase D on chromosome 13 and alcoholism.  (Palmer, 196).

Another finding that is gene related, reported by psychiatrist Henri Begleiter of the College of Medicine at the State University of New York Health Science Center at Brooklyn, is “a genetically influenced brain wave, called the P3 wave.” (Holden).  He said that this brain wave is connected with recognition and attention and is often found in alcoholics and their close relatives.  Also in another research that’s not yet published by psychologist William Iacono of the University of Minnesota, Minneapolis, has found that “P3  deficits go not only with alcoholism and drug addiction but also with antisocial behavior and learning disorder,” Begleiter concluded that “we have evidence that [P3 deficit] is a good index of central nervous system disinhibition,” (Holden).

III.    Environment.

How important is the role of environment in alcoholism? “Over 6.6 million children under the age of 18 live in a household of at least one alcoholic parent.” (NCADD).  Could living with an affected parent be the risk of the development of alcoholism? When studies are made, genetic and environmental factors can be quite confusing to distinguish. 

Researchers, Hawkins, Catalano & Miller (1992) have listed the risks involved with adolescents’ development of alcoholism into three domains: “(1) home and environmental factors such as parental use/parental acceptance of alcohol/drug use, family bonding, family conflict, ease of obtaining alcohol, peer use, and peer attitudes towards alcohol/drug use; (2) child behavioral factors such as rebellion against parents, gaining of peer acceptance, stress reduction, enhancement of social competence, and self-treatment of mental health and/or academic problems; and (3) societal norms such as laws regarding alcohol use, prominence of alcohol in the community, neighborhood economic conditions, and neighborhood disorganization.” (Kuperman).  All of the above factors are influences of surroundings, not just in the home, but also from what are thought to be harmless daily environments like the school.  Such factors need to be recognized in order to avoid misleading information when conducting studies involving alcoholism. 

One way of measuring the environment influences of alcoholism is by using the behavioral genetic method.  This method uses the experiences of identical twins; one affected by alcohol, the other unaffected, to compare the differences.  By using this method Scarr and McCarney, 1983, have identified three mechanisms of the genetic process, Genotype-Environment Correlation.  (1) The passive g-e correlation: the role of a parent play in influencing the environment of their children, (2) evocative g-e correlation: behavioral influences from teachers, parents, and peers, and (3) active g-e correlation: influences from different experiences.  When measured, environmental influences are found to be critical in determining the development of alcoholism for individuals classified as Moderate Genetic Loading, “a subset of the population”.  (Development, 33).

IV.    Genetic?

Rumor has always been that alcoholism runs in the family, but does that define it as being inherited?  Or are Americans just trying to find an excuse to blame their lack of self-control?  Studies after studies have been administered to find this multi-gene that is supposed to be responsible for so many problems, but none has been successful.  As long as the idea of “alcoholism being heritable” still exists then whenever a father is seen drinking severely the son will be assumed to follow in his footsteps, because “’[the belief that heavy drinkers produce heavy drinkers] has deep roots that stem from the untested observations of clinicians who treat alcoholics, from flawed studies that seemed to support the idea, and the success of Alcoholics Anonymous in emphasizing the view of alcoholism as a disease’” said by Archie Brodsky, coauthor of The Truth About Addiction and Recovery, from the Boston Globe .  (Hubbard, 100). 

From all the genetic studies I’ve looked at, I couldn’t find one that didn’t either contain flaws, uncertainty about the results or the results’ numbers being too low to make a difference.  Studies that support genetic existence would first state their discovery with enthusiasm, then they would point out the weakness in their research, leaving the reader in doubt, like the six twin studies shown in table 5.1 below, from The Molecular Pathology of Alcoholism (185).  MZ in the table represents Monozygotic or “identical” twins and DZ stands for dizygotic or “non-identical” twins such as fraternal twins and as the table shows, there seems to be a genetic connection for the separated identical twins.  But before one can rely on the accurateness of the six studies, one must look over the criticisms of each author’s method provided in the table and in the summary of the table from the book.  A short sentence found in the summary that sums up the carelessness of the studies as a whole would be: “the current (published) evidence for a genetic effect in alcoholism is therefore weak as far as data from these studies is concerned.” (Palmer, 184).  More studies involving twins and in cases where their alcohol metabolisms are measured, results suggested a “significant, though variable, heritability (Vessel et al. 1971; Kopun and Propping 1977; Martin et al. 1985)”. (Palmer, 183).  “This,” as Ruth Hubbard would say “should give us pause.”

Adoption studies are also used quite often when researching for the genetic aspects of alcoholism.  Such studies disentangle “genetic and environment influences, since adoptees receive their genes from one set of parents and their family upbringing from another.” (Palmer, 184).  As perfect as they may sound, adoption studies also have many flaws.  In many cases, adopting parents who are similar to adoptees’ biological parents are selected to adopt, therefore adoptees’ environmental effects are put into question.  Other factors that also need to be consider for adoption studies are, (1) how much alcohol was the adopted child exposed to in the womb, which would build up the child’s tolerance to alcohol and (2) what was the age of the child when he/she was adopted, for possible home exposures to alcohol already. (Hubbard, 101).

Other studies that didn’t seem to have defects would contain weak conclusions like this one of NIAAA’s (National Institute on Alcohol Abuse) director Enoch Gordis, who stresses that alcohol “gene search is infinitely more difficult than that in a single-gene disease. Alcoholism genes are multiple, they interact in unknown ways, and they have incomplete penetrance, which means you can have the genes but not be an alcoholic,” and he adds that “these genes are for risk, not for destiny.” (Holden).  Gordis is claming that alcoholism is genetic, but the carrier of the gene could end up never becoming an alcoholic at all, which strangely should take genetics completely out of the picture, because in the end it’s still all up to choice.  Such findings not only leave the reader in doubt, but also leave the reader in complete confusion.

For studies that didn’t show any signs of defects and had credible results; the results ended up being too low to make any difference or to actually be considered as credible. The adoption studies discussed earlier would be a good example. After all the factors of similarities between adopting parents and biological parents, of exposures to alcohol in the womb, and of possible alcohol exposures in the home before adoption were considered, the final number was 18 percent.  That means only 18 percent of the sons with an alcoholic biological parent became alcoholics instead of the 5 percent who became alcoholics but didn’t have any alcoholic biological parent.  “Though these results may suggest some biological component, we must remember that 82 percent of sons with an alcoholic biological parent did not become alcoholics.  Even if we were to grant a genetic component in alcoholism, it clearly does not have a strong determining effect and could not be used to predict anything about a person’s relationship to alcohol.” (Hubbard, 101).  In other words, with such a low probability and only for risk, this once again brings us back to the matter of choice and should eliminate the genetic factor.

Half-siblings have also been used to study the genetic aspects of alcoholism.  In 1972, 164 half-siblings of 69 alcoholics were used by Schuckit et al. to show the genetic effects of alcoholism.  His results seemed to have a positive genetic effect on alcoholism because “it seemed to make little difference whether the half-sibs were raised by an alcoholic parental figure or not, since the same proportion of both groups became alcoholic.” (Palmer, 188).  But problems were later detected that 81 percent of the half-sibs lived in an unhealthy home, which could be used to argue for a positive environmental effect.

The genetic markers that were presented earlier also have a problem of their own.  Their linkage to alcoholism was too weak and didn’t “reach the usually accepted threshold of statistical significance.” (Palmer, 196).  Both markers were also protein markers, which is another weakness, because DNA markers have a better guarantee of future linkage studies.

Another finding that also should be closely examined is Blum and co-workers’ discovery of the dopamine D₂ receptor being found in alcoholics as mentioned earlier in the genetic section, the same article, The Genetics of Alcoholism from Alcohol Alert, went on to discuss that “a number of researchers have been unable to duplicate the results of Blum’s study” and it continued with the suggestion that “the dopamine D₂ association continues to be interesting, but it does not seem to be transmitted in families in such a way that it is responsible for alcoholism; its role, if any, has yet to be determined.” (Genetics).

Conclusion

          Over 76 million Americans are affected by alcoholism (UCSF), 40 percent being young adults of the age of 18-29 who started drinking before turning 15. (Kuperman).  As a result of it affecting so many people and because of its many visual symptoms of addiction alcohol has been labeled as a disease and that it’s inheritable. “Despite the fact that nicotine is six to eight times as addictive as alcohol and elicits withdrawals symptoms, smoking has escaped the disease label.” (Hubbard, 99).  And despite the fact that every study ever conducted to find the genetic aspects of alcoholism had failed or had too many flaws to determine anything, alcoholism is still considered inheritable.

The next time when a father is seen drinking severely, one can assume that his son will probably follow in his footsteps, but before insisting that alcoholism is genetic one should first live in the boy’s home for just one week to test out one’s hypothesis.  As one is examining the boy’s environment also consider the possibility of choice that he has.  Whether he might have been born with a higher tolerance of alcohol or whether he grew up with an abusive father, taking the first drink is still completely his choice and so is continuing to drink.  In reality genetic is not the true cause of alcoholism and either is the environment (but it may contribute more than genetic), because both are “for risk, not for destiny”.  To be an alcoholic or not to be an alcoholic is all up to choice. 

Bibliography

Arterburn, Stephen. Hand-Me-Down Genes and Second-Hand Emotions.  Nashville: Oliver-Nelson, 1992.

Holden, Constance. "Science." New clues to alcoholism risk. 29 May 1998. 13 Mar. 2002 <http://ehostvgw11.epnet.com/ehost.asp?key=204.179.122.140_8000_1898358314&site=ehost&return=n&profile=web>. 

Hubbard, Ruth, and Elijah Wald.  Exploding the Gene Myth. Boston: Beacon, 1997.

Kuperman, Samuel, et al. "Risk domains associated with an adolescent alcohol dependence diagnosis."  Addiction  Apr. 2001. 12 Mar. 2002 <http://ehostvgw6.epnet.com/ehost.asp?key=204.179.122.140_8000_1729570444&site=ehost&return=n&profile=web>. 

National Council on Alcoholism and Drug Dependence. Home Page. 14 Mar. 2002 <http://www.ncadd.org/>. 

Palmer, T. Norman, ed. The Modern Pathology of alcoholism. Oxford: Oxford University Press, 1991. 

Pirisi, Angela. "New insights gained into genetics of alcoholism." Lancet 30 May 1998. 12 Mar. 2002  <http://ehostvgw2.epnet.com/ehost.asp?key=204.179.122.140_8000_-1880294534&site=ehost&return=n&profile=web>. 

UCSF Family Alcoholism Study.  Home Page. 1 Aug. 2000. 14 Mar. 2002. <http://www.familystudies.org/Default.htm>.

 U.S. Department of Health and Human Services. National Institute on Alcohol Abuse and Alcoholism.  The Development of Alcohol Problems: Exploring the Biopsychosocial Matrix of Risk. Ed. Robert Zucker, Gayle Boyd, and Jan Howard. 

U.S. Department of Health and Human Services. National Institute on Alcohol Abuse and Alcoholism.  The Genetics of Alcoholism. Oct. 1992: No. 18 PH 328. 

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