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IN THIS ARTICLE Serotonin: when enough is enough   
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Rewards and Addictions Dean D. Krahn, M.D. Behind every craving or urge there exists, scientists have discovered, a powerful brain system that is as automatic and basic as hunger or thirst. This reward reinforcement system is involved in a wide variety of motivated behaviors.1 Though we haven't uncovered all the details, what we do know will help you better understand your own reactions if you are trying to lose weight or change some other addictive or impulsive behavior pattern. You will see the powerful internal forces that a friend or relative must struggle against as they seek to gain control over impulsive behaviors. One note of caution -- this is only a sketch of how this remarkable system operates. When talking about addictive or impulsive behavior it is easy to overlook the fact that, most of the time, humans do exercise some sort of choice over whether or not to engage in these behaviors. Most behaviors are not persistently or addictively pursued. Rather, the healthy individual tries to achieve a balanced variety of reinforcing behaviors. We may overeat or over-indulge in alcohol at our cousin's wedding but quickly return to our everyday, more moderate pattern of food and alcohol consumption. We are able to do this because we have the ability to balance two competing neurochemical systems -- the reward reinforcement system which finds the eating of delicious food and drinking of alcoholic beverages pleasurable and, therefore, reinforcing, and the reflectivity or control system which enables us to weigh the potential negative consequences of an action. The Dopamine Connection Neurotransmitters are brain chemicals necessary for the transfer of information within the nervous system. One neurotransmitter, dopamine, is crucial to the reinforcing effects from both natural and nonnatural reinforcers/rewards. The dopaminergic pathway, extending from the brain stem, an old and most primitive area of the brain, to the forebrain, a more developed area in higher vertebrates,2 is involved in the reward reinforcement system. Ingestion of a variety of substances of abuse, as well as food and water, results in an increase in dopamine levels.3,4 Cocaine and amphetamines act directly on dopaminergic neurons. Alcohol and heroin alter dopaminergic systems indirectly, but they alter it nonetheless. If tiny amounts of chemicals that inhibit the activity of dopamine (dopamine antagonists) are injected into the area between neurons where dopamine is released, it is possible to block reinforcement.1,2 In one experiment, the participants were asked to drink alcoholic beverages. The two groups were identical, except that one group was given a low dose of haloperidol, a drug that blocks the reception of the neurotransmitter dopamine's chemical messages of craving, while the other received a harmless placebo. In the haloperidol group, alcohol consumption decreased.5 Unfortunately, so far, scientists have not found a dopamine blocker suitable for treating drug addiction in humans because such drugs cause unacceptable side effects, such as tremors similar to those seen in Parkinson's disease (in which dopamine also plays a role). Another drug that works at a slightly different point in the chemical messaging process that communicates alcohol addiction is naltrexone. When naltrexone or placebo is given to alcohol-dependent subjects who have completed an alcohol treatment program, the naltrexone-treated patients relapse significantly less frequently and report less craving for alcohol than the placebo-treated patients.6,7,8 Additionally, the naltrexone-treated patients report less positive effects from sampling alcohol, a finding consistent with the hypothesis that naltrexone blocked the reinforcing/rewarding effects of alcohol. Some scientists have speculated that there may be inborn abnormalities in the dopaminergic pathway in alcoholics and other patients troubled by excessive use of reinforcers. While studies of animals genetically bred to self-administer alcohol do show differences in dopamine measures, genetically based human differences have not been found. Even though it has not yet been possible to determine if a faulty reward reinforcement pathway is the cause of addictive behaviors, it is clear that this pathway is operating in them. Animals that like highly palatable foods also prefer substances of abuse. Rats who prefer sweet solutions self-administered more alcohol than rats with low preferences for sweet solutions.9 Conversely, rats bred for high preferences for alcohol showed high preferences for sweet solutions while rats bred for low preferences for alcohol showed low preferences for sweet solutions.10 With such results in rats, it is not surprising that alcoholics who remained abstinent longest after treatment were those who used the most table sugar.11 This substitution of one activator (sugar) of the reward system for another (alcohol, which, of course, also contains a great deal of sugar) may explain other recent findings in humans. In unpublished results, our group has shown that alcoholics, early in abstinence, report increased likelihood of binge eating and increased preferences for sweet food. Another group of researchers has shown that, during the early phases of abstinence, more alcoholics report maximum preferences for highly sweet solutions than do nonalcoholic people.12 It appears that humans who are trying the stop the use of one reinforcer are turning to another reinforcer to activate the reward pathway their drinking or drug-taking once activated. It remains to be shown whether these substitutions are beneficial to subjects in the long run. Knowing When Enough Is Enough: The Role of Serotonin Given how physiologically reinforcing this system is, it is amazing that animals or humans who are using a positive reinforcer ever stop the use of that reinforcer. Why don't all of us just keep eating or drinking if it tastes or feels so good? How do animals and humans make choices about the use of one reinforcer versus another? How do they come to realize they've had enough? It appears that serotonin, another neurotransmitter, is importantly involved in both reflection on the use of reinforcers and in satisfaction. Serotonin levels are lower in people who are impulsive. Patients who attempt compulsive suicides and impulsive homicidal behavior, and those with severe early-onset alcoholism as well as bulimia, all have low levels of serotonin.13 On the opposite side, we have also seen that patients who are obsessive (i.e., those who reflect excessively prior to performing a behavior which might be wrong) are characterized by high metabolic rates in their frontal areas of their brain and by high serotonergic measures. At this point, we can only guess that good mental health derives from the neurochemical balance between impulse and reflection systems. An individual with an excessively active dopaminergic reward system and an underactive serotonergic control system might be prone to excessive use of reinforcers which could have negative effects on health. Conversely, if one is characterized by low dopaminergic and high serotonergic function in the relevant areas of the brain, then excessive obsessing (sitting around and thinking about it endlessly) and too little action for the best possible function might be your pattern. In the future, we may learn how to maximize the effect of talk therapy and drug interventions on these neurochemical systems. In the meantime, we can perhaps use this newly found knowledge to view addiction and impulsive behaviors with more enlightened compassion.
References 1. Stellar JR and Stellar E. The Neurobiology of Motivation and Reward Springer-Verlag, New York, 1985. return 2. Wise RA (1987) The role of reward pathways I the development of drug dependence. Pharmac. Ther. 35:227-263. return 3. Hernandez L, Hocbel BG (1988) Food reward and cocaine increase extracellular dopamine in the nucleus accumbens as measured by microdialysis. LifeSci 42:1705-1712. return 4. Pothos EN, Gruse I, Hoebel BG Restricted eating with weight loss selectively decreases extracellular dopamine in the nucleus accumbens and alters dopamine response to amphetamine, morphine, and food intake. The Journal of Neuroscience, Oct.1995,15(10):6640-6650. return 5. Modell JG, Mounts JM, Glaser FB, Lee JY. Effect of haloperidol on measures of craving and impaired control in alcoholic subjects. Alcohol Clin Exp Res 1993 Apr, 17(2):234-40. return 6. O'Malley SS, Jaffe AJ, Chang G, et al. Naltrexone and coping skills therapy for alchohol dependence: a controlled study. Arch Gen Psychiatry 49:881,1992. return 7. O'Malley SS, Jaffe AJ, Chang G, et al. Six month follow-up of naltrexone and psychotherapy for alcohol dependence. Arch Gen Psychiatry 53:217,1996. return 8. Volpicelli JR, Alterman AL, Hayashida M, et al. Naltrexone in the treatment of alcohol dependence. Arch Gen Psychiatry 49:876,1992. return 9. Gosnell BA, Krahn DD. The relationship between saccharine and alcohol intake in rats. Alcohol 9:203-206,1992. return 10. Sinclair JD, Kampov-Polevoy A, Steart R, Li TK. Taste preferences in rat lines selected for low and high alcohol consumption. Alcohol 9:155-160,1992. return 11. Lieblich I, Granchow JR, Blass EM, Bergmann F. Morphine tolerance in genetically selected rats induced by chronically elevated saccharine intake. Science 2211:871-873,1983. return 12. Carroll ME and Boe IN. Increased intravenous drug self-administration during deprivation and other reinforcers. Pharmacol Biochem Behav 17:563-567,1982. return 13. Oldham JM, Hallander E, Skodal AE. Impulsivity and Compulsivity. American Psychiatric Press, Inc., 1990. return |
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