The Disease Model of Addiction Reconsidered
BioSocieties (2010) 5, 137-147
David T Courtwright?, Department of History, University of North Florida, Jacksonville, Florida, 32224-2645, USA. E-mail: firstname.lastname@example.org
The author has never applied for NIDA funding and has no conflicts of interest.
This article examines 'the NIDA paradigm', the theory that addiction is a chronic, relapsing brain disease characterized by loss of control over drug taking.
I critically review the official history of the National Institute on Drug Abuse (NIDA) paradigm and analyze the sources of resistance to it.
I argue that, even though the theory remains contested, it has yielded important insights in other fields, including my own discipline of history.
It is a commonplace in the history of science that new paradigms generate both opposition and unexpected insights. The National Institute on Drug Abuse (NIDA) paradigm of addiction as a brain disease has done both. The research behind it has expanded our knowledge of motivation and learning, of normal as well as abnormal behavior.
Yet it has also been met with indifference, suspicion, and, in some cases, open resistance. I am particularly interested in why politicians, clinicians and social scientists have been slow to embrace what the neuroscientific community generally regards as a major breakthrough.
The key elements of the NIDA brain disease paradigm can be simply stated. They are that addiction is a chronic, relapsing brain disease with a social context, a genetic (or, more precisely, a gene-environment-stress-interactive) component, and significant comorbidity with other mental and physical disorders.
Although drug use often begins voluntarily, and develops over time, users lose control with the onset of addiction. According to the former NIDA director, Alan Leshner, addiction is defined, not by physical withdrawal symptoms, but by 'uncontrollable, compulsive drug craving, seeking, and use, even in the face of negative health and social consequences'.
Persistent use leads to long-term changes in brain structure and function. Neurons become more responsive to the biochemical changes triggered by drug consumption. Imaging studies have shown specific patterns of abnormal activity in the brains of many addicts. In essence, addiction is a brain disease because addicts exhibit a behavioral disorder that can be linked to observable pathological changes in their brains. To again quote Leshner, addiction is 'the quintessential biobehavioral disorder' (Leshner, 2001).
Where did this paradigm come from? Here is the official version, from the NIDA publication Drugs, Brains, and Behavior: The Science of Addiction.
It bears the signature of Nora Volkow, the current NIDA director: "Throughout much of the last century, scientists studying drug abuse labored in the shadows of powerful myths and misconceptions about the nature of addiction. When science began to study addictive behavior in the 1930s, people addicted to drugs were thought to be morally flawed and lacking in willpower.
"Those views shaped society's responses to drug abuse, treating it as a moral failing rather than a health problem, which led to an emphasis on punitive rather than preventative and therapeutic actions. Today, thanks to science, our views and our responses to drug abuse have changed dramatically. Groundbreaking discoveries about the brain have revolutionized our understanding of drug addiction, enabling us to respond effectively to the problem. (National Institute on Drug Abuse, 2008, p. 1)"
The statement evokes the Whiggish history of psychiatry. Substituting 'mental illness' for addiction gives a textbook account of beneficent medicalization. We used to treat mentally ill people as wicked or possessed, but now, thanks to neuroscience, we treat them as patients. The paradigm shift was progressive in another way. It tidied things up.
Making the brain the affected organ, as historian Nancy Campbell has written, provided 'a unified framework for a problem-based field in conceptual disarray' and enabled addiction researchers to draw on the technical resources and social authority of neuroscience (Campbell, 2007, p. 200).
The political subtext of Volkow's statement is plain enough: keep funding our research. What may be less obvious is that virtually every historical claim in the statement is either factually incorrect or a form of wishful thinking. Let me start with the state of things before the 1930s, a decade presumably chosen because it corresponds to the opening of the federal narcotic hospitals and their research facilities.
Neither popular nor medical opinion then regarded all addicts as morally flawed. People distinguished between medical cases and nonmedical addicts with underworld or delinquent backgrounds. All junkies were addicts, but not all addicts were junkies.
There was also a good deal of scientific investigation before the 1930s. Psychiatrist Lawrence Kolb, whom one colleague called 'the Osler of drug addiction', and who labored longer and harder than anyone to establish that addiction was a true mental disease, began his federally funded researches in 1923. These involved lab work with monkeys as well as the systematic study of 230 human cases (Kolb, 1962; Courtwright, 2001a, Chapter 5; Acker, 2002, Chapter 5).
The relegation of Kolb's work to the dustbin of prescientific history may not have been entirely accidental. His primary finding, that nonmedical addiction was rooted in psychopathy and other preexisting (and hard-to-treat) personality disorders, fit poorly with the politics of medicalization and the NIDA paradigm's foundational metaphor, that drugs could flip the addiction 'switch' in even normal brains.
Ultimately, it may turn out that the tension between the personality and brain disease models is more apparent than real. Recent research has found that impulsive, thrill-seeking individuals have fewer D2 and D3 dopamine receptors in the ventral midbrain region, which means they have less inhibition of dopamine and experience more reward when stimulated by risky behavior (Sanders, 2008).
The propensity to addiction and certain kinds of personality disorder may have genetic and/or epigenetic common denominators. This possibility also has been debated for a long time. Early twentieth-century researchers investigating cigarettes and health pondered whether the type of individual attracted to smoking might be as causally important in explaining the moral and physical harms of the habit as tobacco itself (Brandt, 2007, Chapter 4).
Other researchers - mostly asylum proprietors, psychiatrists and public-health physicians - were thinking systematically about the nature of addiction even before Kolb began his work in the 1920s. What happened in the late twentieth century was essentially the confirmation and recasting of a series of shrewd hypotheses that these pioneers ventured. They held that alcohol, tobacco and other drug addictions were related through a common pathological action on the nervous system, which was permanently altered by the repeated use of drugs.
Indeed, they often referred to nicotine and alcohol as 'narcotics' or 'deadly narcotics'. They believed that loss of control was the most important and troubling aspect of addiction. They knew how to get patients through withdrawal. The big challenge was how to prevent relapse. They postulated that some individuals were more vulnerable to addiction than others, whether through an inherited vulnerability or through an acquired, stress-related impairment of their nervous systems. In short, they believed that addiction was a chronic, recurrent nervous disease with both an environmental and hereditary component. What they lacked was the means to prove it (Courtwright, 2005).
The history of addiction as a brain disease looks a lot like the history of atoms or germs, insofar as these were all older and controversial ideas for which scientific confirmation later became available. Improved instrumentation and new laboratory techniques, together with the infusion of money and research talent into the field, made possible the fundamental discoveries in the second half of the twentieth century that served as the building blocks of the current NIDA paradigm.
Among these were the observation of intracranial self-stimulation in rats; the discovery of an endogenous opioid system; the mapping of specific receptors and description of their functions; an understanding of drug sensitization and dendritic morphology; the piecing together of a mesolimbic dopamine reward pathway that was distinct from the anatomical pathways responsible for physical dependence and withdrawal syndromes; and, more recently, the location of single-nucleotide polymorphisms ('snips', or minute variations in DNA sequences) that seem to correlate with the risk of becoming an addict.
Dramatic improvements in neuroimaging also made possible the equivalent of Giovanni Morgagni's clinico-pathological studies. Morgagni pioneered the anatomical concept of disease. He based his classic 1761 study, De Sedibus et Causis Morborum, on some 700 case studies that showed how diseases with characteristic symptoms affected particular organs that exhibited characteristic lesions on postmortem examination.
Imaging made it possible to show patterns of pre-mortem change on the primary organ that addiction afflicts, the brain. This idea is made explicit in Drugs, Brains, and Behavior, which juxtaposes positron emission tomography (PET) scans of a healthy and diseased heart with those of a healthy brain and the 'diseased brain' of a cocaine abuser. 'Addiction is similar to other diseases, such as heart disease', the caption explains. 'Both disrupt the normal, healthy functioning of the underlying organ, have serious harmful consequences, are preventable, treatable, and if left untreated, can last a lifetime' (National Institute on Drug Abuse, 2008, p. 5).
Some individuals do respond well to treatment. Yet the new paradigm has not led to a large increase in our ability to 'respond effectively to the problem', as Volkow claims. Here is the practical heart of the matter. The prevalence and incidence of drug abuse are largely determined by demographic variables like migration, family stability and birth cohort size, as well as social forces like drug-financed civil wars within failed states, pharmaceutical marketing strategies, bohemian fashion and generational learning (and forgetting) about the dangers of certain drugs.
Pathological understanding is still disconnected from disease control, which is unusual in the history of medicine and public health. As psychiatrist Sally Satel puts it, a disease concept is not of much use unless it leads to 'actionable etiology' (Satel, 2009).