Addiction and free will

This one slipped by me late last year. It offers a great description of the neurobiological processes involved in addiction. It also tries to tackle frequently neglected questions about free will and addiction. All of this is great, but the description of the client with a “secondary” addiction and their intervention (rather, the absence of any intervention) leaves me wanting.

In the early stages of addiction, the free will of someone like Jack is relatively intact. I say relatively because emerging research suggests that Jack probably had a decreased number of D2 dopamine receptors, and this state of hypodopaminergic function increased his risk to excessively respond to the suprathreshold dopamine stimulation of drugs of abuse.4 As the addiction progresses, the main brain engines of free will are damaged and begin to malfunction, including the attentional and self-control mechanism of the anterior cingulate gyrus; the crucial orbital prefrontal cortex that associates emotional and motivational valence with environmental stimuli and cues; and the dorsolateral prefrontal cortex, the seat of executive function and as such, the true decision maker.

In the later stages of addiction, Volkow cautions, free will may be virtually devastated: “We have come to see addiction as a disease that involves the destruction of multiple systems in the brain that more or less are able to compensate for one another. When the pathology erodes the various systems, you disrupt the ability to compensate, and the addictive disease erodes and destroys the life of the individual.”5

In the new conceptualization, addiction is not so much a matter of dysregulation of the pleasure systems but of a distortion of goal direction expressed by the term “salience.” Evolution has wired the brain to seek out and respond to environmental factors, such as sex, food, money, and affection, that improve the chance of the survival and even thriving of the species. All of these natural incentives release dopamine, not so much to satisfy desire as once thought but as a way of neurochemically cementing the salience of these stimuli (ie, potentiating learning).

Tragically, drugs and alcohol have a massively more potent dopaminergic action than even the best gourmet meal, a good run on a beautiful fall morning, or the devotion of a wife and children. These new neurobiological explanations of addiction give molecular weight to the phenomenological DSM-IV-TR criteria for “continued [substance] use despite adverse consequence” by a dependent person.6 Given the extreme biological response to drugs of abuse compared with daily life and work, it is no wonder that “time spent in obtaining the substance replaces social, occupational or recreational activity.”6 Jack had a family who loved him, and he was resourceful enough to have been successful had he only employed the immense energy he spent on substance use in the service of more productive aims.

So complete is drugs’ usurpation of human priorities that what were once semivoluntary actions and reactions become conditioned responses. In an elegant experiment, Volkow and colleagues7 measured dopamine metabolism in 18 cocaine-dependent patients while they watched a nature video and a video of persons using cocaine. Not only was there a substantial dopaminergic surge in the addicted patients when watching the cocaine film, but even more alarming, it corresponded to their subjective experience of craving, which itself is a measure of the compulsive quality of addiction.

These results obviously underscore the challenge of relapse prevention when even otherwise neutral cues can elicit the intensity of intoxication. But more ominously for free will, what Volkow calls the plastic changes in brain structure and function suggest the entire apparatus of self-determination may have been commandeered.8



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