In them, addiction has been both criminalized and medicalized; addicts were labeled as sick individuals yet also punished for bad behavior as deviants. The authors conclude by advocating for a consilience of scientific perspectives—integrating neurobiology, behavioral science, economics, and public policy—to address addiction effectively. They emphasize the value of neurobiology in understanding addiction’s biological mechanisms and designing effective interventions. A multidisciplinary approach is crucial to improve outcomes and combat the ongoing stigma surrounding addiction. This article explains that addiction is a brain disease, addressing critiques while affirming its neurobiological basis.
- An addict may suffer an impairment, caused by a dysfunction of the dopaminergic system, and yet be able to maintain homeostasis.
- When first put forward, the brain disease view was mainly an attempt to articulate an effective response to prevailing nonscientific, moralizing, and stigmatizing attitudes to addiction.
- The roots of this insight date back to 1940, when Spragg found that chimpanzees would normally choose a banana over morphine.
- Addiction fits this definition, as demonstrated by significant impairment and distress in affected individuals.
ALTERNATE FRAME: HARM REDUCTION AND SOCIAL JUSTICE
Rather, in supportive environments, where the agent is buffered from many demands by social support, this impairment is fully compatible with pursuing a good life. Addiction makes it hard to make good choices, but people aren’t completely controlled by it. People with addiction have a harder time making good choices, like choosing to be healthy rather than take drugs.
Heterogeneity in choice models of addiction: the role of context
The authors provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, this paper argues that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, the authors propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.
In this editorial, we explore prospects of doing better by comparing US policies with a brief historical survey of Western European countries that have adopted medications for problem substance use while remaining skeptical of or agnostic toward the CRBD model. These examples show that the CRBD model is not the only or best way to fight stigma and provide treatment. Policies in these countries provide support and push back against stigma in a range of ways, the most effective of which incorporate aspects of harm reduction. We can learn from these successes and continuing challenges as we work to achieve effective policies in the United States.
- There are scientific accounts of addiction according to which it does not involve any brain pathology at all.
- In these conditions, there was no selective pressure for human beings to develop a specific self-control mechanism with regard to these substances.
- It originates from within the scientific community itself, and asserts that this conceptualization is neither supported by data, nor helpful for people with substance use problems.
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I would like to thank Jerome Wakefield and Richard Holton for very helpful comments on an earlier version of this paper. I am also grateful to the Australian Research Council for a generous grant supporting the work leading to this article. David Herzberg has served as a paid consultant and expert witness for the plaintiffs in opioid litigation in the United States. This work has been supported by the University at Buffalo, State University of New York; by the Thomas Jefferson Fund of the Embassy of France in the United States; by the FACE Foundation; and by the Norwegian Research Council (project ).
Astrocyte-neuron signaling in the mesolimbic dopamine system: the hidden stars of dopamine signaling
Neuroimaging, while not a primary diagnostic tool, provides crucial insights into underlying mechanisms and potential treatment targets. Studies consistently reveal alterations in brain structure and function, particularly within fronto-striatal circuitry, across various substances. Integrating data from human and animal studies provides a comprehensive understanding of addiction’s neurobiological basis, further acknowledging the impact of social and environmental factors.
Identification of THC impairment using functional brain imaging
Acknowledging these underpinnings promotes medicine, not moral judgment, as the way to understand and treat addiction. Dr. Kevin Sabet is a former three-time White House drug policy advisor and the president of Smart Approaches to Marijuana and the Foundation for Drug Policy Solutions. The rare good news in the decades-old addiction crisis was attributable mostly to a drop in deaths from synthetic opioids, chiefly fentanyl, said researchers at the National Center for Health Statistics, who compiled the numbers.
Instead, it asserts the critical role of neurobiology in understanding and treating addiction. Different levels of analysis—neurobiological, behavioral, and societal—are needed for a comprehensive understanding. Consilience, the integration of multiple scientific perspectives, is crucial for effective research, treatment, and policy development regarding addiction.
Dysfunction accounts come in two varieties, corresponding to the two competing philosophical analyses of function. On a selectionist account, expounded most influentially by Millikan (1984), a dysfunction occurs when something fails to play the role for which it was selected in the evolutionary history of the organism. On addiction as a brain disease revised: why it still matters, and the need for consilience pmc the systemic account, developed by Cummins (1975), it is not the role that something played in evolutionary history that gives it its function; rather, it is the role it (or its homologs) actually plays in a system. Rather, I shall focus on what the accounts have in common, arguing that neither entails that addiction is brain disease.
A common criticism of the notion that addiction is a brain disease is that it is reductionist and in the end therefore deterministic 81, 82. In his classic 1960 book “The Disease Concept of Alcoholism”, Jellinek noted that in the alcohol field, the debate over the disease concept was plagued by too many definitions of “alcoholism” and too few definitions of “disease” 10. He suggested that the addiction field needed to follow the rest of medicine in moving away from viewing disease as an “entity”, i.e., something that has “its own independent existence, apart from other things” 11. What is notable is the double standard regarding different levels of analysis in understanding addiction.
When the system is operating as it should, dopaminergic activation attenuates in response to expected reward. Dopamine response increases when the world is better than expected; when an expected reward is delivered, the world is exactly as expected and there ought to be no dopamine response. If drugs worked like natural rewards, we could expect them to trigger an initial dopamine response to consumption, but an attenuation of this response as consumption is repeated. At the same time, we ought to expect an increase in dopamine response to predictors of drug availability. Instead, what we find is dopamine response to predictors of drug availability and – because drugs of addiction drive up the dopamine response by their chemical action – continuing dopaminergic activity at consumption as well. In effect, the dopaminergic system responds to drugs with the signal that consumption is better than expected.
