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Psychiatric Times. Vol. 18 No. 2
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Addiction and the Eating Disorders

By Caroline Davis, Ph.D. | February 1, 2001
Dr. Davis is associate research scientist in the department of psychiatry at the University Health Network at York University in Toronto. She is professor of psychology in the department of kinesiology and health science at the University of Toronto.

A key concept in current formulations about risk for addiction concerns individual differences in sensitivity to reward or the ability to experience pleasure-a concept firmly rooted in neurobiology. In recent years, theories of addiction have moved from an emphasis on physical dependence to a broader focus on motivational dependence and the importance of anhedonia and dysphoria as powerful incentives for the continuation of addictive behaviors (Di Chiara, 1999).

A large body of research has demonstrated that a relatively long-lasting anhedonic state can be induced by prolonged drug administration (Gamberino and Gold, 1999) and by exposure to chronic mild stress (Zacharko, 1994) and that this process is primarily mediated by DA receptor downregulation. Furthermore, anhedonia can also be an innate characterological trait associated with low DA availability; a factor that has consistently been associated with greater risk for a variety of addictions (Volkow et al., 1999).

Recently, we proposed that this concept has great utility for understanding certain differences between patients with anorexia nervosa (AN) and patients with bulimia nervosa (BN), viz that the former display a facility for self-starving and report a decreasing interest in food, while the latter have increasing difficulty resisting food and become compulsive overeaters (Davis et al., 2000). There is no doubt that these differences are influenced by a variety of cognitive factors relating to personal identity and a need for control as well as social reinforcement. As with addiction, there is good reason to believe that biologically based motivational effects relating to capacity for reward and the regulation of affective states are also influential. Given that food is the most basic natural reinforcer, our findings that patients with AN were significantly more anhedonic than those with BN offer support for the premise that individual differences in this characteristic contribute to the avoidance and approach relationships to food found in these two groups, respectively. The cross-sectional nature of our data raises the inevitable question of whether these differences reflect premorbid-and, therefore, potentially causal-characteristics, whether the stress of starvation experienced most acutely in the patients with AN induced their anhedonic state, or both. Recently it has been suggested that differences in the ability to experience the positive-incentive value of food may be diminished in response to an extended period of food deprivation, making it easier for patients with severe anorexia to starve themselves (Pinel et al., 2000).

Summary and Conclusions

There is a strong argument that the eating disorders are a form of addiction. Clinically, the behaviors that define eating disorders and substance abuse are very similar. Similar biological mechanisms account for the compulsively progressive nature of both disorders; in the case of alcohol(Drug information on alcohol) and other drugs, from recreational use to a state of pathological dependence; in AN, from casual dieting to a life-threatening refusal to eat; and, in BN, the increasing inability to resist large quantities of food. There is also support for a common psychobiological vulnerability and for the notion that individuals use a variety of rewarding behaviors to self-medicate their affective disturbances depending on the specific effects of each. But why do some individuals choose nicotine(Drug information on nicotine), others alcohol and others food (or its absence)? Environment, sociocultural factors and personality must play an important role. For example, one who is obsessional, anxious, conforming and female is more likely to be attracted to highly sanctioned behaviors like dieting and exercise, and to the enormous rewards associated with the pursuit of thinness in our culture, than to illicit drug use. In order to understand the motivation to continue these behaviors beyond the point of body-image improvements, we must look beyond psychosocial explanations. I suggest that the great strides which have occurred in our understanding of brain mechanisms in addiction also provide excellent insight into the processes that occur in the eating disorders. As such, they also offer a useful approach to improved methods of treatment.

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References

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Davis C, Woodside DB, Olmsted MP (2000), A study of anhedonia and excessive exercise in the eating disorders. Presentation at the 9th International Conference on the Eating Disorders. New York; May.

Davis C, Katzman DK, Kirsh C (1999), Compulsive physical activity in adolescents with anorexia nervosa: a psychobehavioral spiral of pathology. J Nerv Ment Dis 187(6):336-342.

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Volkow ND, Wang GJ, Fowler JS et al. (1999), Prediction of reinforcing responses to psychostimulants in humans by brain dopamine D2 receptor levels. Am J Psychiatry 156(9):1440-1443.

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Zacharko RM (1994), Stressors, the mesolimbic system, and anhedonia: implications for PTSD. In: Catecholamine Function in Posttraumatic Stress Disorder: Emerging Concepts. Murburg MM, ed. Progress in Psychiatry, No. 42. Washington, D.C.: American Psychiatric Press pp99-130.


 
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