Commonly abused substances such as alcohol, nicotine and opiates affect the release and/or levels of the neurotransmitter dopamine (DA) within a complex neurocircuit known as the “pleasure circuit.” Thus, independent of the primary effects of the substance used, substance use is pleasurable and therefore positively reinforcing. However, with repeated use the pleasure circuit is usurped such that the DA response to substance use falls noticeably short in terms of pleasure. Sensations that oppose pleasure emerge, and the substance user takes the drug to prevent these negative sensations. Thus, pleasure gives way to misery, and the user becomes dependent on the substance just to feel well. The user becomes an abuser.
The more technical name for the pleasure circuit is the mesolimbic-cortical-dopaminergic system. It is a mouthful, but the name indicates the brain regions that are involved in the circuit. The meso– part refers to the mesencephalon, or midbrain. Within the midbrain lies a region known as the ventral tegmental area (VTA). The VTA is one of two primary brain regions that give rise to neurons that make and release DA.
The term limbic refers to the limbic system, which is a combination of structures rather than a sole region. A key part of the limbic system involved in the pleasure circuit is the nucleus accumbens. The nucleus accumbens processes stimulus valence and affects response to stimuli. With substance use, the nucleus accumbens plays a role in interpreting whether the pleasure payoff from use is worth repeating. Research has shown that with repeated substance use, the threshold for activation in the nuclear accumbens is changed such that more dopamine is needed to be processed as a pleasure payoff. This change appears to be the result of structural modification to nerve cells that affect function in long-lasting ways.
The next region in the pleasure circuit is the cortex, in particular the prefrontal cortex (PFC), which is located behind the forehead. The many functions regulated by this region are termed “executive functions” and include impulse control, emotion regulation, planning, cognitive flexibility and a general awareness of the body. Research has shown that substance abuse can actually reduce both the size and function of the prefrontal cortex. By usurping the pleasure circuit through substance use, the abuser experiences long-term changes in many important brain systems that influence the way one feels, acts and thinks. One part of the PFC, the orbitofrontal cortex (OFC), is implicated in compulsive drug-seeking behaviors that accompany addiction. Other recent research demonstrates that the OFC is preferentially activated during drug craving, and the strong desire to reduce craving likely underlies the compulsive search for another pleasure payoff reminiscent of the first “big win” associated with substance abuse.
Neurobiological investigations of mindfulness effects in addicts are lacking. Still, such investigations in healthy persons suggest brain changes worthy of exploration in the substance abuser. For example, in a study that has quickly become a classic in the field, Dr. Sara Lazar and her research team at Harvard University investigated anatomical brain changes in meditators compared to nonmeditators using magnetic resonance imaging (MRI). What Dr. Lazar found was that meditators had significantly more cortical thickness in the prefrontal region than the nonmeditators. She did not study addicts, but recalling that substance abuse may lead to reduced cortical thickness in the prefrontal cortex, Dr. Lazar’s findings, suggesting that something about being a meditator is associated with increased PFC thickness, are noteworthy.
Using another form of MRI, Dr. Britta Holzel and her research team at the University of Giessen in Germany investigated brain function during mindfulness meditation. Again, Dr. Holzel did not study addicts. However, it’s noteworthy that she found increased activity in a part of the PFC that modulates impulse control and emotional processing. Relapse among substance abusers can be triggered by negative emotions or stress, which in turn affects craving and impulsive acts. That mindfulness increases activity in a part of the brain that modulates emotional processing and impulsiveness is again very interesting and worthy of further investigation in addicts.
We simply don’t have the evidence yet to say explicitly whether mindfulness can structurally and functionally change the brain of an addict. Still, it is interesting and perhaps encouraging that preliminary evidence from healthy persons supports brain changes associated with mindfulness that at first glance appear to be in the opposite direction of many brain changes occurring with addiction. Presently, Dr. Judson Brewer and his research team at Yale University are in the midst of investigating the effects of mindfulness, including lovingkindness practice, on the addict’s brain. Given the evidence reported here suggesting potentially profound brain effects, Dr. Brewer’s results are greatly anticipated.