Positive Living Newsletter

Can We Reduce Addiction to Brain Chemistry?

Geoff Thompson, PhD

Novelist Margaret Atwood pointed out that our modern world is obsessed with the concrete. Her example: Many people want to believe in the story of Noah’s ark in the Bible, but they really don’t. So, they’re desperately hoping an archeologist will dig up a piece of the ark, which will then make the story real to them. Today, most people see a story as fiction, as something not real. We privilege the concrete facts and figures of the physical sciences as the way to understand human nature.

Atwood’s observation fits well in the field of addiction studies. It is rare to find an expert who probes the ideas of playwright Eugene O’Neill or philosopher Francis Seeburger for their insights into why some people are so attracted to intoxication. Most focus on mainstream psychological science, and a growing number of experts now rely on the scientific study of the physical brain, which proposes that addiction is a chronic brain disease. The disease model is the foundation for research at the two American national institutes of health (NIH) that specialize in addictions and for the societies of addiction medicine (SAM). Beginning in the 1970s, even 12-step programs began embracing the disease model proposed by NIH and SAM, and by the mid-1990s had fully absorbed it. We call this the biomedical model, which states that addiction is a pathological condition in the brain.

A Primer on the Biomedical Model of Addiction

To explain addiction, the biomedical model focuses on neural networks, brain scans of the nucleus accumbens and associated structures (the brain’s reward center), and activity in the mesocorticolimbic system (the dopamine network connecting the reward center to the thinking part of the brain). Correlational studies of various alleles (different forms of a gene), such as genes for the D2 and GABA 2A receptors, provide evidence that those vulnerable to addiction share specific genetic mutations, which constitute a genetic predisposition for addictive drug use.

Why a person chooses a particular drug is often pinned to their neurobiological makeup. For example, a person suffering from Attention Deficit Disorder chooses stimulants to self-medicate their lack of dopamine stimulation in the prefrontal lobes.

According to the model, once drug use is initiated, the effects of the drug alter the structure and function of the reward center and prefrontal lobes, which then undermine voluntary control over drug use. Neuroscientist Anna Rose Childress (NIH, 29 January, 2008) even argues that relapse back into active addiction happens outside of conscious awareness. The addicted person is at the mercy of their brain chemistry, even if they don’t want to use drugs and even if they derive no pleasure from intoxication. In fact, this lack of control is the defining feature of addiction, which the influential addiction scientist Alan Leshner (1997) described as a “compulsion” (p. 45).

Treatment typically follows from theory, so the applied version of the biomedical model promotes medical technologies. Medications are prescribed to detoxify the addicted, inhibit drug cravings, and act as medically safe substitutes for a drug (such as buprenorphine for opioid addiction). Newer programs use medication-assisted therapies, such as micro-dosing psilocybin (a hallucinogen that affects serotonin pathways in the brain), and prescribe repetitive Transcranial Magnetic Stimulation (rTMS), a costly piece of medical equipment, which targets the brain’s limbic system with electromagnetic pulses to help clients reduce depression and feel a wider range of emotions.

Questioning the Biomedical Model of Addiction

The biomedical model is very concrete and thus neat and tidy. It doesn’t bother with all that messy human stuff, such as thoughts and emotions. Yet some addiction experts question how useful it is as a framework to understand and treat drug problems. Generally, they argue that the biomedical model has not led to any substantial improvements in our treatment of addiction, and many argue that it has not led to any substantial advancement in our understanding of the phenomenon.

Their complaints are too numerous and from too many disciplines to list them in a single article. Given this, here are a handful of objections.

Insufficient evidence

The most obvious problem with the biomedical model is that it has insufficient evidence to command general agreement. Most experts involved in the drug use section in DSM-5—the American psychiatric bible often used to diagnose addiction—lamented that we cannot rely merely on neuroscience research to make sense of addiction precisely because we have yet to identify all the relevant neural circuitry. This is likely the major reason why DSM continues to classify addiction (and other disorders) according to behavioral and not biological criteria.

Mistaken interpretation of the evidence

Neuroscientist Marc Lewis (2017) surveyed the neuroscience research and argued that addiction is not a disease but, rather, a problem of learning (neuroplasticity). Psychologist Gene Heyman (2009) examined the psychological research and concluded that it was a “disorder of choice.” Psychologist Stanton Peele (1998) complained that the lack of agency inherent in the biomedical model was motivated by a “compulsion to bypass human experience . . . [and that] lived human experience and its interpretation are central to the incidence, course, treatment, and remission of addiction” (p. ix).

How most experts view the model as stated

In fact, most addiction experts do not accept the biomedical model as stated. Fraser, Valentine, and Ekendahl (2018) surveyed addiction professionals in Europe and North America and reported that 95 percent of them did not agree with the brain disease model. The experts disagreed with the assumption that those suffering from addictions had no agency, because they were convinced that psychological and social factors were equally important.

Barnett et al. (2018) surveyed clinicians who reported they accepted the biomedical disease model. The authors concluded: “Among mixed findings of treatment providers’ support for the DMA [disease model of addiction], strong validity studies indicated treatment providers supported the disease concept and moral, free-will or social models simultaneously” (p. 697). This rather curious interpretation of the disease model suggests that even those who accept the model struggle with the idea that the addicted have lost voluntary control over drug use. Interestingly, clinicians with the most advanced education tended to dismiss the disease model.

The “hard problem” in consciousness studies

The multidisciplinary field of consciousness studies also questions the validity of the disease model. Philosopher David Chalmers (1996) proposed the “hard problem” in understanding consciousness. The hard problem asks how do brain chemicals give rise to personal experience? After all, brain chemicals have no motivations, intentions, goals, or desires; they simply act according to the laws of chemistry. So, the hard problem asks how did the chemicals in Shakespeare’s brain give rise to Hamlet and Macbeth? How did the chemicals in my brain give rise to the dream I had last night about a three-storey haunted house at the corner of Main and Hastings in Vancouver? How do the chemicals in an addicted person’s brain lead them to frequent bars or meet regularly with the drug dealer?

If we interpret humans as nothing more than their neurobiology, how do we overcome the hard problem? Of course, some consciousness experts argue that once we have figured out all the easy problems (the ones we know how to solve, such as how the visual system works or how the hippocampus aids in developing memory), we’ll discover there is no hard problem. For them, the mind is merely an epiphenomenon of the physical brain, a curious phenomenon of no real consequence. But this solution suggests we are essentially chemical robots. We may believe that we make choices, but we don’t. You and I are simply pawns of molecules floating about in our brains.


Philosophers who have studied addiction routinely dismiss the biomedical model because they say it is illogical. At the most basic level of reasoning, they point out that if the biomedical model was accurate—that addiction is a compulsion—then how would anyone quit drugs? At a more complex level of reasoning, they point out that agency must be present in addictive behavior. A philosopher’s typical definition of compulsion is that the individual lacks options. But compulsion does not apply to drug use because the individual always has options—unless some power holds a gun to the drug user’s head and threatens to pull the trigger if they don’t get intoxicated.

As an aside, this is an ongoing issue for philosophers who deal with neuroscientists. They criticize scientists for not providing rigorous definitions for terms such as “compulsion” or “undermining voluntary control.”

At a more sophisticated level, philosophers Stephens and Graham (2009) examined the experimental design of neuropsychologists Robinson and Berridge’s (2001) research on how rats become addicted. The neuroscientists concluded that the compulsive use of drugs arose from a drug-induced sensitization of the mesocorticolimbic pathways in the brain. The philosophers argued, however, that Robinson and Berridge could not logically conclude this. They pointed out that if neuroscientists propose that rats develop an addicted brain, this means that at one point they had a non-addicted brain. Logically, then, neuroscientists would need to specify what a normal [ie, non-addicted] brain is. Given the complexity of the brain and the fact that every brain is different, then this is an unrealistic objective. If we can’t specify a normal brain, then how can a neuroscientist argue that a brain is addicted? (FYI. Brain scans cannot detect an addiction.)


Neuroscience has given rise to the new discipline of neuroethics. Applied to addictions, neuroethicists ask how ethical it is for clinicians to treat clients based on the biomedical model, which denies human agency and has insufficient evidence to convince most experts (see, for example, Goldberg, 2020).

The Opioid Crisis as a Case Study of the Biomedical Model’s Limitations

The opioid crisis is an instructive case study on the validity of the biomedical model, because government policy and treatment are based on it. Most addiction experts interviewed in the media declare that opioid addiction is a brain disease. Yet despite this interpretation—and the staggering amount of money and resources devoted to it—we haven’t accomplished very much. In British Columbia (BC), Canada, where I live, the number of opioid overdose deaths in 2016 was 914 (of which 667 were fentanyl-related). A recent headline in the media announced, “B.C. sets new record with 1,455 drug deaths in the 1st 7 months of 2023” (C. Pawson, 29 August 2023). Since BC declared it a medical emergency in April 2016, the opioid crisis has claimed the lives of 12,739 British Columbians (as of September 2023).

Researchers have variously explained this failure as a lack of public education on the dangers of opioids, weak physician training, the prohibitionist ideology behind the war on drugs, poor social conditions, and so on (see, for example, Ning & Csiernik, 2022). But a consistent conclusion is that we have mistakenly relied on the biomedical model as the framework to understand and respond to the crisis.

Unlike disciples of the biomedical model, Hawre, Buchanich, Roberts, Balmert, Zhang, and Burke (2018) took a different approach. They showed that the opioid crisis is not a standalone, discrete event. Rather, it is the most recent manifestation of an exponential rise in American drug overdoses since 1979, which has included, at various times and places, cocaine, methamphetamine, and other drugs. Rather than focus on opioids, the authors called for elucidating the “‘deep’ drivers of the overdose epidemic” such as “despair, loss of purpose, and dissolution of communities” (p. 1188).

Yet the ideas of Hawre and colleagues and others have gained little traction. As Margaret Atwood suggested, the concreteness of the biomedical model is so attractive that we seem unwilling to shift our approach to the crisis, even though current efforts have failed.



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National Institutes of Health (29 January, 2008). Does the desire for drugs begin outside awareness? NIDA research reveals subconscious signals can trigger drug craving circuits. NIH News Releases. https://www.nih.gov/news-events/news-releases/does-desire-drugs-begin-outside-awareness

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Pawson, C. (29 August, 2023). B.C. sets new record with 1,455 drug deaths in 1st 7 months of 2023. CBC News. https://www.cbc.ca/news/canada/british-columbia/toxic-drug-deaths-july-2023-1.6950922

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