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Genetics of Alcoholism

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Ties That Bind: Examining the Genetics of Alcoholism within the Context of a 
Body Mind Paradigm

J. Bowers
2005

    Ethanol abuse is an issue evoking a wide-variety of perspectives in determining its origins. Historically, alcohol abuse and its antecedents produced an array of labels and speculations. Early viewpoints observed those abusing alcohol as morally inept, incapable of functioning properly within the greater society. Other vantage points and systems pointed out that psychological factors predisposed and maintained faulty belief systems, entangling the excessive drinker in a web of defective thought patterns and emotional knots. Discovery and advances in medical science paved the way for a new model emphasizing the influence of genetics on human behavior. Genes represented a series of switches and manipulating these junctures possessed the potential for turning diseases on and off at will. Through all of the above conceptions, behavioral medicine recognizes that chronic illnesses, including alcoholism, emerge through a more comprehensive, epigenetic model (Giovanni & Sonino, 2000). 

     The emergence of a biopsychosocial paradigm incorporates a host of relevant health components, recognizing that no portion of this model stands independent of the others in promoting disease. White (2005) concurs with this formulation and outlines that new discoveries in the genetics of alcoholism expand, not reduce, the epigenetic view of alcoholism. Through the breakdown of ethanol addiction into its contributing parts, White (2005) demonstrates that each portion contributes toward a malady that is greater than the sum of its parts.

Biology

     White (2005) reiterates that the discovery of D2 receptors' potential role in alcoholism illuminates biology's impact in this complex process. Highlighting compelling evidence that deficient D2 receptors may create a potential for alcohol abuse is one significant piece of the addiction puzzle. Dopamine receptors appear integral in the cycle of alcohol craving and subsequent abuse (Hutchison, McGeary, Smolen, Angela & Swift, 2002). Recent scientific investigations (Bechtholdt & Cunningham, 2005) also uncovered relationships between alcohol and receptor sites, specifically opioid and GABA sites. Though this plethora of physical evidence beckons reductionism conclusion, White (2005) offers other elements contributing to alcoholism's body-mind outline.

Psychology

     Thinking patterns, emotional response, and self-control certainly appear as being manipulated by ethanol abuse (Stritzke, Patrick & Lang, 1995; Fishbein, Hyde, Eldreth, London, Matochik, Ernst, Isenberg, Steckley, Schech, & Kimes, 2005).  Aggression is one particular focus area in the psychological realm with studies revealing alcohol's exacerbation and perpetuation of hostility (Aviles, Earleywine, Pollock, Stratton, & Miller, 2005). Combined with the impaired cognition and inhibition mechanisms (Abroms & Fillmore, 2004)  cited in contemporary studies (Baumeister, DeWall, Ciarocco, & Twenge, 2005), this interaction of alcohol, physiology, and emotion creates a potential for serious consequences such as propensity for impulsive, misdirected and violent behavior (Assaad, Pihl, Sequin, Nagin, Vitaro, Carbonneau & Tremblay, 2003). These consequences may significantly impact one's social interactions.

Social 

     White (2005) includes the sum of an individual's environmental and interpersonal experiences into a comprehensive equation of alcoholism. Familial interactions solidify this notion (Eiden, Leonard, Hoyle & Chavez, F, 2004) where a child growing up in an alcoholic home is constantly exposed to behaviors, thoughts, and events that potentially lead to one's own adoption of problematic alcohol consumption. Resulting stigma and related behavioral patters of those struggling with the disease further alienate individuals from the support that one needs most (Baumeister, DeWall, Ciarocco & Twenge, 2005). 

     This social exclusion provides the fuel for continuing a set of self-defeating cognitions and behaviors. White (2005) acknowledges this impending loss of hope, referring to this concept within the context of an individual's sense of spirituality. Spirituality is a perception of being a part of something lager than the self. Faced with little hope and salvation for a positive outcome, the alcohol-addicted individual reduces one's world down into the confines of bottle. 

     White (2005) builds a strong foundation for alcoholism's inclusion in the paradigm of body-mind study. Integrating the biological realms of genetics and brain function together with emotion and experiential aspects, a clear interaction is observed. Avoiding reductionism, the author carefully attributes that the physiological and psychological underpinnings of addiction are symbiotic. Genetics influence how one responds to alcohol though predisposition, including genetic markers. However, one's emotions and experiences similarly exert some power over the biological systems as well.  One glaring piece of evidence, often overlooked in reductionism views, is the fact that one may be biologically inclined toward alcoholism, but do not succumb to the disease. This is due to better coping skills, adequate mastery of emotion and self control, and even the decision in avoiding alcohol exposure. 

     Though much more work remains in exploring the vast body-mind forces comprising addictive behaviors, one aspect remains clear. Independent, causative agents represent necessary, but not sufficient conditions influencing the disease of alcoholism.

References 

Abroms, B. & Fillmore, M. (2004). Alcohol-induced impairment of inhibitory mechanisms involved in visual search. Experimental and Clinical Psychopharmacology, 12(4), 243-250.

Assaad, J., Pihl, R., Sequin, J., Nagin, D., Vitaro, F, Carbonneau, R. & Tremblay, R. (2003). Aggressiveness, family history of alcoholism, and the heart rate response to alcohol intoxication. Experimental and Clinical Psychopharmacology, 11(2)158-166.

Aviles, F., Earleywine, M., Pollock, V., Stratton, J., & Miller, N. (2005). Alcohol's effect on triggered displaced aggression. Psychology of Addictive Behaviors, 19(1), 108-111. Retrieved May 7, 2005, from PsycARTICLES database. 

Bechtholdt, A. & Cunningham, C. (2005). Ethanol-induced conditioned place preference is expressed through a ventral tegmental area dependent mechanism.  Behavioral Neuroscience, 119(1), 213-223.

Baumeister, R. F., DeWall, C. N., Ciarocco, N. J., & Twenge, J. M. (2005). Social exclusion impairs self-regulation. Journal of personality and social psychology, 88(4), 589-604. Retrieved May 7, 2005, from PsycARTICLES database. 

Eiden, R. D., Leonard, K. E., Hoyle, R. H., & Chavez, F. (2004). A transactional model of parent-infant interactions in alcoholic families. Psychology of Addictive Behaviors, 18(4), 350-361. Retrieved May 7, 2005, from PsycARTICLES database. 

Fishbein, D., Hyde, C., Eldreth, D., London, E. D., Matochik, J., & Ernst, M., Isenberg, N., Steckley, S., Schech, B. & Kimes, A. (2005). Cognitive performance and autonomic reactivity in abstinent drug abusers and nonusers. Experimental and clinical psychopharmacology, 13(1), 25-40. Retrieved May 7, 2005, from PsycARTICLES database. 

Giovanni & Sonino (2000). Psychosomatic medicine: emerging trends and perspectives. Psychotherapy and Psychosomatics, 69(4), 184-197. 

Hutchison, K., McGeary, J., Smolen, A., Angela, B. & Swift, R. (2002). The DRD4 VNTR polymorphism moderates craving after alcohol consumption. Health Psychology, 21(2), 139-146.

Stritzke, W., Patrick, C. & Lang, A. (1995). Alcohol and human emotion: a multidimensional analysis incorporating startle-probe methodology. Journal of Abnormal Psychology, 104(1), 114-122.

White, G. M. (2005).  Alcoholism and the D2 receptors. An organism predisposed to alcoholism,current theory and treatment implications. Retrieved May 3, 2005 from the Center on Behavioral Medicine Website at: http://www.centeronbehavioralmedicine.com/