Biologic effects of mindfulness meditation: growing insights into neurobiologic aspects of the prevention of depression.

A recent paper in the Archives of General Psychiatry confirms that mindfulness-based cognitive therapy (MBCT) “offers protection against relapse/recurrence on a par with that of maintenance antidepressant pharmacotherapy.” It is a tribute to the accumulated wisdom of humankind that a traditional Buddhist meditation practice going back 2500 years, which was originally designed in part to deal with the problem of human suffering, has been successfully adapted to prevent the relapse of depression in the modern era. Buddhist meditation techniques were originally adapted by Jon Kabat-Zinn, founding executive director of the Center for Mindfulness in Medicine, Health Care, and Society at the University of Massachusetts Medical School (www .umassmed .edu /Content .aspx?id=43102), for mindfulnessbased stress reduction (MBSR). Reviews of MBSR studies suggest that it decreases depression, anxiety and psychologic distress in people with chronic somatic diseases and that it reduces stress, ruminative thinking and trait anxiety in healthy people. Mindfulness-based cognitive therapy is similar to MBSR and is designed to change some of the cognitions that are associated with depression. Mindfulness has been described as “paying attention in a particular way: on purpose, in the present moment, and nonjudgementally.” In contrast to traditional cognitive behavioural therapy in which dysfunctional thoughts are targeted, the objective of MBCT is to help individuals learn, at times, to become aware of thoughts, feelings and bodily sensations rather than trying to modify them or acting on them. A core skill learned in MBCT is how to recognize and disengage from self-perpetuating patterns of ruminative, negative thought through sustained attention and attention-switching exercises. This self-regulation of attention is thought to help recovered depressed individuals shift attention away from the rumination about dysfunctional cognitions, which may be reactivated during transient mood lowering, and thus allows them to process depression-related information differently. Dysfunctional cognitions, such as “If I do not do as well as other people in a particular task it means I am infer ior,” “My value as a person depends on what others think of me,” or “It is important that everyone likes me,” are risk factors for depression in adults and children. Mindfulnessbased cognitive therapy targets the ruminative thinking by enhancing awareness and monitoring of thoughts. This suggests that MBCT might not only decrease relapse in depression but also prevent the onset of the first episode of depression in susceptible people. As Insel and Scolnick have pointed out, “the great public health success stories of the past century are largely stories of prevention.” Insights into both psychologic and biologic factors that are associated with the prevention of depression should help in the long run to develop better strategies for prevention. I describe some of the biologic factors associated with dysfunctional cognitions and what is known about the biologic effects of MBCT. Finally, I suggest some possible research directions that may provide more information on the systems that MBCT influences when preventing the onset of depression. Different forms of meditation have been compared with various control interventions, some of which did not have similar intensity. As a result, the exact component of meditation that produces a beneficial effect is not clear, although the targeting of dysfunctional cognitions is probably the most plausible mechanism. In the rest of this editorial, different forms of meditation are assumed to have similar effects. The idea that serotonin is related to the control of mood persists, and a small portion of the literature relates serotonin function to dysfunctional attitudes. In one of the first studies of this type, dysfunctional attitudes decreased in healthy participants when they were treated with the serotonin-releasing drug fenfluramine. In depressed patients, one of the more common abnormalities reported using positron emission tom ography (PET) is an increase in serotonin 2A (5-HT2A) binding potential. In depressed patients, high 5-HT2A binding