MedicalResearch.com Interview with:
Marc Lewis, Ph.D.
MedicalResearch.com: What is the background for this study?
Response: According to the brain disease model, addiction is a chronic disease brought about by changes in brain systems that mediate the experience and anticipation of reward and higher-order systems underlying judgment and cognitive control. Its proponents propose that these changes are driven by exposure to drugs of abuse or alcohol. The brain disease model is the most prevalent model of addiction in the Western world.
The disease model’s narrow focus on the neurobiological substrates of addiction has diverted attention (and funding) from alternative models. Alternatives to the brain disease model highlight the social-environmental factors that contribute to addiction and the learning processes that translate these factors into negative outcomes. Learning models propose that addiction, though obviously disadvantageous, is a natural, context-sensitive response to challenging environmental contingencies, not a disease.
In this review I examine addiction within a learning framework that incorporates the brain changes seen in addiction without reference to pathology or disease.
MedicalResearch.com: What are the main findings?
Response: I examine four neurocognitive changes central to brain disease models. The first is the shift from impulsive behavior mediated by the ventral striatum to compulsive responses mediated by the dorsal striatum. The second change, which also supports the presumption of involuntary behavior, is a reduction in connectivity between the striatum and prefrontal cortex. The third change is increased and enduring sensitivity to cues predicting addictive rewards, underpinned by increased dopamine uptake. The fourth change is a decrease in sensitivity, caused by dopaminergic blunting, not only to alternative rewards but even to addictive rewards themselves.
I show that these neurocognitive changes are normal features of learning highly-motivating, repetitive and habitual behavior patterns. Highly-motivating pursuits, repeated frequently, shift activation to brain regions (e.g., dorsal striatum) responsible for triggering behaviors that bypass reflection and judgment mediated by the prefrontal cortex. These brain changes promote efficiency in reward pursuit, as well as sensitization to particular rewards, by entrenching synaptic pathways that represent a narrow subset of attractive goals (and engage dopamine circuitry). Thus, like falling in love, religious extremism, sports, wealth pursuit, and other self-perpetuating habits, addiction locks in familiar routines that become difficult to relinquish without effort and determination.
MedicalResearch.com: What should readers take away from your report?
Response: The entrenchment of particular synaptic pathways in the brain (at the expense of alternative pathways) goes hand in hand with reduced flexibility in the immediate social environment. As a result, the “narrowing” that characterizes addiction in the brain parallels a “narrowing” in the addict’s environment, such that alternative sources of relief and reward (e.g., meaningful relationships, educational pursuits) become less and less accessible. Given extremely high correlations between early social and emotional adversity and later addiction, we can view environmental impediments in childhood and adolescence as triggering addictive patterns that go on to constrain neural development as well as further environmental opportunities.
MedicalResearch.com: What recommendations do you have for future research and practice as a result of this study?
Response: Study the links between socioeconomic challenges, developmental diversity, developmental neuropsychology, and subjective experience. While many addicts recover without treatment, treatment (when necessary) should highlight developmental precursors as well as the potential for personal agency (empowerment) to make choices and shift behavioral patterns. Chemical dependency may be a medical matter, but addiction is a psychological (learning) process that interacts with progressive environmental limitations.
Marc Lewis, Ph.D.
October 18, 2018
N Engl J Med 2018; 379:1551-1560
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