Daniel Shapiro’s Alcoholism Blog Project

On the surface, alcoholism seems like an evolutionary paradox (Gerald et al, 2002).  There is no apparent justification for the persistence of the over-consumption of alcohol as a phenotype when it appears to be detrimental to human survival and reproductive fitness (Gerald et al, 2002).  For millions in the contemporary global human population, alcohol is a devastating vice.  It’s a disease that negatively impacts the families, relationships, social lives, academic performance, professional careers, and health of people who suffer from it.  The U.S. alone has an estimated 14 million citizens who have a dependency on alcohol (Grohsman, 2009).    Alcoholism has come under the scope of science since it became accepted as a legitimate malady, but science has not yet come to a consensus on the root of the problem.  Some thinkers argue that alcohol dependency emerged as a maladaptive behavior resulting from adaptations that human ancestors made to their environments in order to survive, and others believe that the disease is the product of genetic variations.  However, the two explanations for how alcoholism came to be are not absolute opposites.  Rather, they are two sides of the same coin. They both explain how alcoholism connects to human evolution, so they both deserve a thorough analysis.

            Beginning with the argument that human ancestors set the precedent for contemporary alcoholism, the handicap theory of biologist Amotz Zahavi suggests that alcohol consumption was designed as an adaptive trait to assist our ancestors in their quest for reproductive success.  According to Zahavi (1993), animals attract mates with signals that display their genetic fitness.  Engaging in risky behaviors is one of these signals (Zahavi, 1993).  The excessive consumption of alcohol, in this context, provides a reliable signal our ancestors could have used to attract mating opportunities (Diamond, 1992).  In contrast, the capacity for individuals in contemporary society to consume alcohol in markedly large amounts is not an indicator that the individual will attract mating opportunities.  In reality, given the fact that alcohol over time deteriorates the body and mind, heavy drinkers are less likely to attract mates. Thus, this trait that modern humans have come into this world with as a result of ancestral actions is now maladaptive.

            Another theory for why alcohol consumption would emerge as an adaptive behavior in the ancestral environment and has persisted as a phenotype is that alcohol is found in high-energy foods, such as fruit, which played a significant role in the diets of ancient humans. (Dudley et al, 2004).  Graber (2008) tells us that creatures today still roam “forests in search of energy rich” foods like our predecessors did long ago.  For instance, the Malaysian pen-tailed tree shrew consumes fruit nectar that is “the equivalent of about nine alcoholic beverages a night” (Graber, 2008).  Some animals, like humans, eat fruit to obtain energy and thus increase the likelihood of survival.  For this reason, the cravings that humans developed for alcohol potentially developed as a result of eating food that was beneficial to our health, and just coincidentally contained alcohol.  The only problem with this data is that it doesn’t explain why only a select few of animals like alcohol and most animals don’t.  More studies on alcohol consumption in animals are needed.

            Most of the animals that actively seek out alcohol like human ancestors did are those who are closely related to us: primates (Graber, 2008).  Most animals, however, avoid substances containing high concentrations of alcohol as much as possible according to Graber (2008).  Rhesus monkeys, for instance, have shown that when given the opportunity to indulge in an un-limited supply of alcohol, they will not administer it excessively like other animals in captivity, such as chimps (Katner et al, 2007).  Why then do some animals and humans actively seek alcohol while others will not, especially if foods containing alcohol aid survival?  This is a question that has not been addressed by the environmental adaptation argument yet, but can be aptly answered by the argument that genetics are at the root of alcoholism.

            The enzymes that metabolize alcohol have genes that are found in all “living organisms” (Milton, 2004).  It has been hypothesized that the variations in the design and presence of these genes account for why some individuals (and animals) become alcoholics while others don’t.  One enzyme called “aldehyde dehydrogenase (ALDH2)” has gained notable attention from evolutionary biologists (Chai, 2005).  According to Chai (2005) individuals with the inactive allele of ALDH2 are less tolerant to alcohol, thus more prone to alcohol abuse, while individuals with the active allele of ALDH2 tolerate alcohol well and are thus protected against alcohol abuse.  To support this assertion, Chai (2005) showed that the active allele of the gene was overrepresented in the alcoholic proportion of his study.  In the study, 96% of alcoholics had an active ALDH2 genotype, and only 4% of alcoholics had an inactive ALDH2 genotype.  The 4% of alcoholics with an inactive gene create a weakness within this data.  However, this weakness can be remedied with the hypothesis that the majority of alcoholism is determined by genetics, and the minority of alcoholism is influenced by other factors such as psychological disorders or social pressures.  The effect size in this experiment appears large and indeed biologically relevant to alcoholism.  Although this study included only a small sample of alcoholics from a particular population, the implications it has for the argument that alcoholism has a significant genetic component are profound. 

            Taking the tolerance factor one step further is the study of Wang et al (2007), which found that fruit flies acquire “rapid tolerance” in response to alcohol sedation.  What happened to the flies virtually depicts what happens to all humans in varying degrees: after one exposure to alcohol, from that experience forward they will need a greater amount of alcohol in order to get as drunk.  This is dangerous for humans who have a genetic disposition to high tolerance, like fruit flies, because higher dosages of alcohol put users at higher risk for addiction.  Thus, through the building of tolerance, the process of addiction is augmented.

            Another genetic abnormality that has been linked to alcoholism is the A1 allele of the D2 Dopamine Receptor gene (Bergegren et al, 2006). The function that is commonly associated with this gene is the control of dopamine release in the limbic (reward) system of the brain. This gene has become associated with alcoholism because addicts are believed to have less dopamine flow than non-addicts, and this allele may hold the key to the variability of dopamine release.  One study found that the A1 allele of the dopamine receptor gene is “overrepresented” among alcoholics (Bergegren et al, 2006).  Although the effect size of this study was reported as small (Bergegren et al, 2006), DRD2’s role in alcoholism has been suspected since 1990 and documented in other studies.

            An additional study that focused on the presence of the DRD2 A1 allele in alcoholics also found that the gene was “overrepresented” in the alcoholic sample of the study (Blum et al, 1990).  Blum et al (1990) found that the A1 allele was present in 69% of the alcoholics in the study.  This indicates a relatively large, and biologically relevant, effect size.  However, there is also a weakness in this data because 31% of alcoholics in this study don’t have the A1 allele and still need to be accounted for.  Again, this inconsistency suggests that genes can’t be the sole cause of alcoholism.  For all the alcoholics who don’t have the A1 allele, or any other genes believed to be connected to alcoholism, other factors must be responsible for their malady (Blum et al, 1990).  Ultimately, more studies are needed to confirm genetic traits responsible for alcoholism and find other genes that make individuals susceptible to the addiction.

            The cause of alcoholism is not black or white, so to speak.  In other words, alcoholism does not seem to be rooted in the environmental adaptations of our ancestors nor genetics alone.  Rather, the disease seems to be the result of a mixture of factors.  Therefore, both arguments are correct to a certain degree.  There is strong evidence from our diets, observations of other animals, and our destructive tendencies that alcohol consumption emerged as an adaptive behavior in the ancestral environment long ago and has stuck around and become a maladaptive behavior in contemporary society.  There are also genetic studies that evince evidence of some individuals being more susceptible to alcoholism than others because of genetic variations.  A synthesis of the two arguments would serve a seeker of the truth better than the acceptance of one explanation over another.

            Our ancestors, for good reasons, drank alcohol and passed down this phenotype to us.  Even though their actions are negatively affecting us today, there is nothing that society can do to alter what has already happened.  What society can do, however, is focus on what it has to work with to change the way things are: genetics.  We know alcoholism has a strong genetic component, and the more we approach the disease biologically, the more we will be able to identify genes connected to it and be able to prevent people with an increased susceptibility to the disease from becoming alcoholics.  If we can find genes that are overrepresented in alcoholic populations, we can use these genes as indicators of the disease.  We can warn people of their potential to become alcoholics before they ever start drinking, and save many people from addiction to alcohol.  Alcoholism is a disease that can affect people regardless of race, religion, income, sex, etc.  Biologically understanding the disease will bring relief not just to a handful of people, but to millions of people all over the world, and the millions of children in generations to come.

 

 

 

Cited Sources

 

 

Secondary Sources:

 

Dudley, Robert, and Michael Dickinson. “The Comparative Biology of Ethanol Consumption: An Introduction to the Symposium.” 2004. Web. Oct. 2009. <http://sipddr.si.edu/dspace/bitstream/10088/6859/1/Dudley_and_Dickinson_2004.pdf>.

 

 

 

Graber, Cynthia. “Fact or Fiction?: Animals Like to Get Drunk.” Www.scientificamerican.com. Scientific American, 28 July 2008. Web. Oct. 2009. <http://www.scientificamerican.com/article.cfm?id=animals-like-to-get-drunk>.

 

 

 

Grohsman, B. “Alcoholism Statistics.” Www.treatment-center.net. 10 Sept. 2009. Web. 5 Nov. 2009. <http://www.treatment-centers.net/alcoholism-statistics.html>

 

 

Milton, Katharine. “Ferment in the Family Tree: Does a Frugivorous Dietary Heritage Influence Contemporary Patterns of Human Ethanol Use?” 2004. Web. 21 Oct. 2009. <http://www.cnr.berkeley.edu/miltonlab/pdfs/fermentfamily.pdf>.

 

 

Zahavi, Amotz. “The Fallacy of Conventional Signaling.” The Royal Society, 1993. Web. Oct. 2009. <http://www.jstor.org/pss/55797>.

 

Diamond, J.  1992.  The Third Chimpanzee: The Evolution and Future of the Human Animals.  HarperCollins.  New York, NY.

 

Primary Sources:

Chai, Young-Gyu, Dong-Yul Oh, Eun Kee Chung, Gil Sook Kim, Leen Kim, Yu-Sang Lee, and Ihn-Geun Choi. “Alcohol and Aldehyde Dehydrogenase Polymorphisms in Men With Type I and Type II Alcoholism.” Www.ajp.psychiatryonline.org. American Psychiatric Association, May 2005. Web. Oct. & nov. 2009. <http://ajp.psychiatryonline.org/cgi/content/full/162/5/1003>.

 

Blum, Kenneth, Ernest Noble, Sheridan Peter, Montgomery Anne, Terry Ritchie, Pudur Jagadeeswaran, Harod Nogami, Arthur Briggs, and Jay Cohn. “Allelic Association of Human Dopamine D2 Receptor Gene in Alcoholism.” Www.jama.ama-assn.org. The Journal of American Medical Association, 18 Apr. 1990. Web. 5 Nov. 2009. <http://jama.ama-assn.org/cgi/reprint/263/15/2055?ijkey=b3857c11c6da841e98214d1ab6de1ffd054e6259>.

 

Berggren, Ulf, Claudia Fahlke, Erik Aronsson, Aikaterini Karanti, Matts Eriksson, Kaj Blennow, Dag Thelle, Henrik Zetterberg, and Jan Balldin. “The TAQ1 DRD2 A1 Allele Is Associated With Alcohol-Dependence Although Its Effect Size Is Small.” Www.alcalc.oxfordjournals.org. Oxford University Press on behalf of the Medical Council on Alcohol, 2 June 2006. Web. Oct. & nov. 2009. <http://alcalc.oxfordjournals.org/cgi/content/full/41/5/479?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=%28DRD2+AND+allele+AND+1+AND+alcoholism%29&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT>.

 

Wang, Yan, Harish R. Krishnan, Alfredo Ghezzi, Jerry CP Yin, and Nigel S. Atkinson. “Drug-Induced Epigenetic Changes Produce Drug Tolerance.” Www.plosbiology.org. PLOS Biology, 16 Oct. 2007. Web. Oct. & nov. 2009. <http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050265>.

 

Katner, Simon N., Stefani N. Von Huben, Sophia A. Davis, Christopher C. Lay, Rebecca D. Crean, Amanda J. Roberts, Howard S. Fox, and Michael A. Taffe. “Robust and Stable Drinking Behavior Following Long-Term Oral Alcohol Intake In Rhesus Macaques.” Www.ncbi.nlm.nih.gov. NIH Public Access, 12 July 2007. Web. 9 Nov. 2009. <http://www.ncbi.nlm.nih.gov:80/pmc/articles/PMC2231844/>.

 

Gerald, M. S., and J. D. Higley. 2002. Evolutionary underpinnings of excessive alcohol

consumption. Addiction 97:415-425.


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One Response to “Daniel Shapiro’s Alcoholism Blog Project”

  1. Well it’s always great to have another person’s point of view on things isn’t it? Causes you to begin to think properly and freely, and so i appreciate your slant on things, despite the fact that I might not go along with all you say.