Wednesday, June 23, 2010
The Disease Model Reconsidered
Historian looks at resistance to the “NIDA paradigm.”
The history of addiction as a brain disease “looks a lot like the history of atoms or germs, insofar as these were older and controversial ideas for which scientific confirmation later became available,” writes historian David Courtwright, author of Forces of Habit: Drugs and the Making of the Modern World.
In a recent issue of the social science journal BioSocieties, Courtwright surveys the history of the disease paradigm of drug addiction, and, in doing so, brings into focus several key dilemmas related to what former National Institute on Drug Abuse (NIDA) director Alan Leshner once characterized as the “quintessential biobehavioral disorder.”
The scientific evidence available to us at present largely supports a statement like Leshner’s. Researchers have documented long-term changes in brain structure and function due to drug abuse, and neuroimaging technologies have resulted in maps of the abnormal neuronal activity addicts exhibit. Courtwright cites the discovery of the endogenous opioid system, the mapping of receptor pathways, and the growing understanding of the mesolimbic dopamine reward pathway as evidence of clinical confirmation of theories about addictive disease that has been floating around in one form or another for many years.
Why then, Courtwright asks, does the medical profession largely stay clear of issues having to do with our law enforcement-driven drug war? Why are clinical professionals not on the front lines of revolt over this issue? “If addiction was beyond the individual’s control, then criminal punishment was as inappropriate as jailing a schizophrenic who wandered into an emergency room,” the author writes.
The most obvious reason for this conundrum, says Courtwright, is that “the brain disease model has so far failed to yield much practical therapeutic value.” The disease paradigm has not greatly increased the amount of “actionable etiology” available to medical and public health practitioners. “Clinicians have acquired some drugs, such as Wellbutrin and Chantix for smokers, Campral for alcoholics or buprenorphine for heroin addicts, but no magic bullets.” Physicians and health workers are “stuck in therapeutic limbo,” Courtwright believes. “The drug-abuse field is characterized by, at best, incomplete and contested medicalization.”
Moreover, unlike the current situation in the case of, say, diabetes or schizophrenia, “at least four important groups continue to wrestle for control of the addiction field.” (Medical personnel, police, social scientists, and political officials.) Social scientists, in particular, are frequently skeptical about the NIDA disease paradigm “as part of a broader post-World War II pattern of resistance against biological explanations of behavior, genetic research and the neo-Darwinian renaissance.”
Social scientists and neuroscientists “still live in their own gated academic communities,” Courtwright alleges. “There is a lot more at stake in the brain disease debate than our understanding of addiction.”
However, these problems do not mean that valuable findings in one area--addictive disease theory--cannot produce innovations in other research fields as well. In fact, such spinoffs happen all the time. Courtwright points to advancements in our understanding of evolution: “Michael Kuhar has argued that, because the brain co-evolved with neurotransmitters, it can usually manage its internal chemistry quite well. But it did not co-evolve with drugs, understood as recently introduced and wholly exogenous super-neurotransmitters that can override the brain’s control mechanisms.”
The author also cites spinoffs in economic studies: “The permanent alteration of neurons and the development of addiction in some, but not all, users also helped explain the commercial and tax appeal of drugs, insofar as they were nondurable goods with relatively inflexible demand curves. Even non-addicted users tended to consume more over time, because of tolerance.”
In the end, it is just possible to contemplate some sort of fusion, or meeting of the minds, over the disease model. As Courtwright speculates, “it may turn out that the tension between the personality and brain disease models is more apparent than real.” He cites as evidence such connections as the fit between impulsive, thrill-seeking behavior and an associated paucity of dopamine D2 and D3 receptors in the midbrain region. The result? Such people “have less inhibition of dopamine, and experience more reward when stimulated by risky behavior.” A nice fit. And the number of nice fits between social science and brain science continues to accumulate.
“If the brain disease model ever yields a pharmacotherapy that curbs craving, or a vaccine that blocks drug euphoria, as some researchers hope,” Courtwright says, “we should expect the rapid medicalization of the field. Under those dramatically cost-effective circumstances, politicians and police would be more willing to surrender authority to physicians.”
Graphics Credit: http://alcoholanddrugabuse.org