The Disease Model of Addiction Reconsidered
Another reason for clinicians' acceptance of the status quo was that the drug war, for all its excesses, never seriously endangered their ability to prescribe mood-altering drugs.
Richard DeGrandpre has criticized the division of the pharmacopeia into nonmedical 'devil' drugs and medical 'angel' drugs.
The latter, he argues, were protected and privileged by pharmaceutical interests, bureaucrats and medical researchers, including the NIDA brain disease establishment.
Whether or not current drug scheduling is actually irrational (or, for that matter, dichotomous), it has never been so aggressive that organized medicine felt it had to revolt.
On the contrary, many critics think that prescribing remains underregulated. Doctors, abetted by big-name researchers in the pay of pharmaceutical companies, have been prescribing far too many unproven and dangerous psychoactive drugs for far too many patients, including young children (DeGrandpre, 2006; Angell, 2009).
Finally, why were social scientists slow to embrace the NIDA paradigm? Some of them, like psychologists Stanton Peele (1998) and Bruce Alexander (2008), simply thought it was wrong on its merits, that it was reductively inattentive to individual values and social context. DeGrandpre has similarly argued that it is set and setting that matter, not just neurons pickled in a sea of exogenous toxins.
Beyond that, there were strong disciplinary biases at work. Social scientists have long been collectively suspicious of anything that smacks of biological essentialism. Biological explanations, after all, have a notorious dark side, having been used to stigmatize, exploit and exterminate minority groups. On one level, social-scientific skepticism about the NIDA paradigm was part of a broader post-World War II pattern of resistance against biological explanations of behavior, genetic research and the neo-Darwinian renaissance (Degler, 1991).
Although that resistance has recently shown signs of abating, it is still very much in evidence among social science's old guard. Troy Duster, an influential sociologist who has written on drugs, deviance, race and science, highlighted the concern in his 2005 presidential address to the American Sociological Association. He spoke frankly of the challenge of scientific authority and 'the attendant expansion of data bases on markers and processes "inside the body"?'. For Duster, reductionist science was the enemy at the gates, threatening to further defund and marginalize sociology, draw attention from the decisive social and economic forces, and dominate the policy process (Duster, 2006, p. 1).
Another way to say this is that both social scientists and neuroscientists still live in their own gated academic communities, that they engage in vigorous boundary maintenance, and that they champion their own disciplinary and subdisciplinary master variables. There is a lot more at stake in the brain disease debate than our understanding of addiction. At bottom, it is really a high-stakes argument about how we ought to understand human behavior, motivation and pleasure - and about what policies we should adopt to regulate it.
Yet such academic resistance in no way implies the failure of the brain disease theory. All new scientific paradigms encounter opposition, much of it socially or politically motivated. Paradigms that can both explain familiar problems and unresolved puzzles usually win out in the end, assuming the mantle of the new 'normal science' (Kuhn, 1970).
One of the NIDA paradigm's strengths has been its ability to shed light on fundamental research questions in other fields, such as the neuronal basis of learning and memory, or the nature of behavioral addictions.
Researchers have shown that reward cues 'light up' the same neural pathways in behavioral and drug addictions, and that opiate antagonists like Naltrexone have value in treating disorders like compulsive gambling (Vrecko, 2010).
These striking findings legitimate the idea that some people with bad habits are genuinely addicted.
They also reinforce the NIDA paradigm. Scientists favor theories that prove to be both parsimonious and unifying, such as Darwinian evolution. In fact, the NIDA paradigm extends evolutionary theory. 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 superneurotransmitters that can override the brain's control mechanisms. Drugs can stimulate reward neurons for minutes or hours instead of the usual milliseconds before reuptake. No wonder drugs and their cues make such a lasting impression on the memory, or have such potential to impair judgment (Kuhar, 2010).
This brings me to my own research.
Whatever defects I may have identified in its official history, I count myself among the beneficiaries of the NIDA paradigm. It guided me when I wrote Forces of Habit, a study of the spread and commercialization of the planet's psychoactive resources. I noticed that the most commercially popular drugs invariably affected, whether strongly or weakly, directly or indirectly, the reward system that neuroscientists now held to be central to both motivation and craving.
That could not be a coincidence. Dopamine reward helped explain why an exotic, bizarrely consumed, seemingly diabolical drug like tobacco, which often met with fierce official resistance, caught on wherever it was introduced in the early modern world. Dopamine reward also helped explain why exposure mattered so much, and why proximity to supply was by far the most important variable for explaining addiction rates in different countries.
Research on the ways drugs synergistically increased dopamine levels helped me understand why novel combination practices, like smoking tobacco while drinking spirits, had taken root together. 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 (Courtwright, 2001b, Chapter 5).
Of course, biology was not the whole story. Social influences, as when young people smoked in imitation of adults, also played important roles. But the larger point remains. Someone in an unrelated discipline, history, was able to draw on NIDA-sponsored research to gain insight and solve puzzles.
This suggests one final analogy. The NIDA paradigm and the neuroscience behind it may yet prove to be a scaled-down version of the manned space program. Even though NASA failed to achieve its central long-term objective - cheap, routine and dependable human access to space - it nevertheless demonstrated the possibility of travel beyond the atmosphere and produced any number of 'spinoffs'.
Among those claimed by NASA were programmable heart pacemakers, waste purification, solar energy, cordless appliances, laser surgery, liquid crystal displays, epoxy adhesives, portable computers, parallel processing and digital body imaging - the last, of course, a key tool for NIDA researchers (National Aeronautics and Space Administration, 1992).
Although it is too soon to pronounce judgment, it seems possible that NIDA's own brain disease research will follow a similar trajectory. That is, it can fail in its central political objective - the medicalization of a treatable disease - and yet still succeed in winning scientific converts and sparking innovations in other fields.
It would not, after all, be the first time that policy and science went their separate ways.
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About the Author
David Courtwright has written about the history of drug use and drug policy in such books as Addicts Who Survived (1989), Dark Paradise: A History of Opiate Addiction in America (2001) and Forces of Habit: Drugs and the Making of the Modern World (2001). He is currently Presidential Professor in the Department of History at the University of North Florida.
Source: BioSocieties (2010) 5, 137-147