Is addiction a disease, or is it a choice? To think clearly about this question, we need to make a sharp distinction between an activity and its results. Many activities that are not themselves diseases can cause diseases. And a foolish, self-destructive activity is not necessarily a disease.

With those two vital points in mind, we observe a person ingesting some substance: alcohol, nicotine, cocaine or heroin. We have to decide, not whether this pattern of consumption causes disease nor whether it is foolish and self-destructive, but rather whether it is something altogether distinct and separate: Is this pattern of drug consumption itself a disease?

Scientifically, the contention that addiction is a disease is empirically unsupported. Addiction is a behavior and thus clearly intended by the individual person. What is obvious to common sense has been corroborated by pertinent research for years (Table 1).

The person we call an addict always monitors their rate of consumption in relation to relevant circumstances.

For example, even in the most desperate, chronic cases, alcoholics never drink all the alcohol they can. They plan ahead, carefully nursing themselves back from the last drinking binge while deliberately preparing for the next one.

This is not to say that their conduct is wise, simply that they are in control of what they are doing. Not only is there no evidence that they cannot moderate their drinking, there is clear evidence that they do so, rationally responding to incentives devised by hospital researchers.

Again, the evidence supporting this assertion has been known in the scientific community for years (Table 2).

My book Addiction Is a Choice was criticized in a recent review in a British scholarly journal of addiction studies because it states the obvious (Davidson, 2001).

According to the reviewer, everyone in the addiction field now knows that addiction is a choice and not a disease, and I am, therefore, "violently pushing against a door which was opened decades ago." I'm delighted to hear that addiction specialists in Britain are so enlightened and that there is no need for me to argue my case over there.

In the United States, we have not made so much progress. Why do some persist, in the face of all reason and all evidence, in pushing the disease model as the best explanation for addiction?

I conjecture that the answer lies in a fashionable conception of the relation between mind and body. There are several competing philosophical theories about that relation.

Let us accept, for the sake of argument, the most extreme "materialist" theory: the psychophysical identity theory. Accordingly, every mental event corresponds to a physical event, because it is a physical event. The relation between mind and the relevant parts of the body is, therefore, like the relation between heat and molecular motion:

They are precisely the same thing, observed in two different ways. As it happens, I find this view of the relation between mind and body very congenial.

However, I think it is often accompanied by a serious misunderstanding: the notion that when we find a parallel between physiological processes and mental or personality processes, the physiological process is what is really going on and the mental process is just a passive result of the physical process.

What this overlooks is the reality of downward causation, the phenomenon in which an emergent property of a system can govern the position of elements within the system (Campbell, 1974; Sperry, 1969). Thus, the complex, symmetrical, six-pointed design of a snow crystal largely governs the position of each molecule of ice in that crystal.

Hence, there is no theoretical obstacle to acknowledging the fact that thoughts, desires, values and other mental phenomena can dominate bodily functions. Suppose that a man's mother dies, and he undergoes the agonizing trauma we call unbearable grief.

There is no doubt that if we examine this man's bodily processes we will find many physical changes, among them changes in his blood and stomach chemistry. It would be clearly wrong to say that these bodily changes cause him to be grief-stricken.

It would be less misleading to say that his being grief-stricken causes the bodily changes, but this is also not entirely accurate. His knowledge of his mother's death (interacting with his prior beliefs and values) causes his grief, and his grief has blood-sugar and gastric concomitants, among many others.

There is no dispute that various substances cause physiological changes in the bodies of people who ingest them. There is also no dispute, in principle, that these physiological changes may themselves change with repeated doses, nor that these changes may be correlated with subjective mental states like reward or enjoyment.

I say "in principle" because I suspect that people sometimes tend to run away with these supposed correlations.

For example, changes in dopamine levels have often been hypothesized as an integral part of the reward/reinforcement process. Yet research shows that dopamine in the nucleus accumbens does not mediate primary or unconditioned food reward in animals (Aberman and Salamone, 1999; Nowend et al., 2001; Salamone et al., 2001; Salamone et al., 1997).

According to Salamone, the theory that drugs of abuse turn on a natural reward system is simplistic and inaccurate: "Dopamine in the nucleus accumbens plays a role in the self-administration of some drugs (i.e., stimulants), but certainly not all" (personal communication, Nov. 26, 2001).

Garris et al. (1999) reached similar conclusions: "Dopamine may therefore be a neural substrate for novelty or reward expectation rather than reward itself." They concluded:
[T]here is no correlation between continual bar pressing during [intracranial self-stimulation] and increased dopaminergic neurotransmission in the nucleus accumbens.our results are consistent with evidence that the dopaminergic component is not associated with the hedonistic or 'pleasure' aspects of reward.Likewise, the rewarding effects of cocaine do not require dopamine; mice lacking the gene for the dopamine transporter, a major target of cocaine, will self-administer cocaine. However, increased dopamine neurotransmission in the nucleus accumbens shell is seen when rats are transiently exposed to a new environment. The increase in extracellular dopamine quickly returns to normal levels and remains there during continued exploration of the new environment.dopamine release in the nucleus accumbens is related to novelty, predictability or some other aspects of the reward process, rather than to hedonism itself.

Perhaps, then, some people have been too ready to jump to conclusions about specific mechanisms. Be that as it may, chemical rewards have no power to compel--although this notion of compulsion may be a cherished part of clinicians' folklore. I am rewarded every time I eat chocolate cake, but I often eschew this reward because I feel I ought to watch my weight.

Experience with addiction treatment must surely make us even more dubious about the theory that addiction is a disease. The most popular way of helping people manage their addictive behavior is Alcoholics Anonymous (AA) and its various 12-step offshoots.

Many observers have recognized the essentially religious nature of AA. The U.S. courts are increasingly regarding AA as a religious activity. In United States v Seeger (1965), the U.S. Supreme Court stated that the test to be applied as to whether a belief is religious is to enquire whether that belief "occupies a place in the life of its possessor parallel to that filled by the orthodox belief in God" in religions more widely accepted in the United States.

This requirement is met by members of AA and other secular programs that help people with addictive behaviors and encourage their members to turn their will and lives over to the care of a supreme being. What kind of disease is this for which the best available treatment is religion (Antze, 1987)?

Clinical applications are based on explanations for why the behavior occurs. An activity based on a religious belief masquerading as a clinical form of treatment tells us something about what the activity really is--an ethical, not medical, problem in living.

What passes as clinical treatment for addiction is psychotherapy, which essentially consists of various forms of conversation or rhetoric (Szasz, 1988). One person, the therapist, tries to influence another person, the patient, to change their values and behavior. While the conversation called therapy can be helpful, most of the conversation that occurs in therapy based on the disease model is potentially harmful.

This is because the therapist misleads the patient into believing something that is simply untrue--that addiction is a disease, and, therefore, addicts cannot control their behavior. Preaching this falsehood to patients may encourage them to abandon any attempt to take responsibility for their actions.

The treatment of drug effects, at the patient's request, is well within the domain of medicine, what passes as evidence for the theory that addiction is a disease is merely clinical folklore.


Aberman JE, Salamone JD (1999), Nucleus accumbens dopamine depletions make rats more sensitive to high ratio requirements but do not impair primary food reinforcement. Neuroscience 92(2):545-552.

Antze P (1987), Symbolic action in Alcoholics Anonymous. In: Constructive Drinking: Perspectives on Drink From Anthropology, Douglas M, ed. New York: Cambridge University Press, pp149-181.

Campbell DT (1974), 'Downward causation' in hierarchically organized biological systems. In: Studies in the Philosophy of Biology: Reduction and Related Problems, Ayala FJ, Dobzhansky T, eds. London: Macmillan.

Davidson R (2001), Conspiracy, cults and choices. Addiction Research & Theory 9(1):92-92 [book review].

Garris PA, Kilpatrick M, Bunin MA et al. (1999), Dissociation of dopamine release in the nucleus accumbens from intracranial self-stimulation. Nature 398(6722):67-69.

Nowend KL, Arizzi M, Carlson BB, Salamone JD (2001), D1 or D2 antagonism in nucleus accumbens core or dorsomedial shell suppresses lever pressing for food but leads to compensatory increases in chow consumption. Pharmacol Biochem Behav 69(3-4):373-382.

Salamone JD, Cousins MS, Snyder BJ (1997), Behavioral functions of nucleus accumbens dopamine: empirical and conceptual problems with the anhedonia hypothesis. Neurosci Biobehav Rev 21(3):341-359.

Salamone JD, Wisniecki A, Carlson BB, Correa M (2001), Nucleus accumbens dopamine depletions make animals highly sensitive to high fixed ratio requirements but do not impair primary food reinforcement. Neuroscience 105(4):863-870.

Sperry W (1969), A modified concept of consciousness. Psychol Rev 76(6):532-536.

Szasz TS (1988), The Myth of Psychotherapy: Mental Healing as Religion, Rhetoric, and Repression. Syracuse, N.Y.: Syracuse University Press.

United States v Seeger, 980 US 163 (1965).


Psychiatric Times October 2002 Vol. XIX Issue 10

See source page on Dr. Schaler's site for additional material.

Dr. Schaler is a Professor at American University in Washington, D.C., and Executive Editor of the journal Current Psychology.

Site of Jeffrey A. Schaler, Ph.D:

One of his books is Addiction is a Choice
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