The article by Peciña and colleagues1 in this issue of JAMA Psychiatry reports the results of a study evaluating with a neuroimaging paradigm the neurochemical mechanisms underlying the formation of placebo effects in patients with major depressive disorder (MDD). Their study involved performing a single-blinded 2-week crossover randomized clinical trial of 2 identical oral placebos (described as having either active or inactive fast-acting antidepressantlike effects), followed by a 10-week open-label treatment with an antidepressant. The participants with MDD were studied with positron emission tomography and the μ-opioid receptor–selective radiotracer [11C]carfentanil after each 1-week inactive and active oral placebo treatment. In addition, 1 mL of isotonic saline was administered intravenously within sight of the volunteer during positron emission tomographic scanning every 4 minutes over 20 minutes only after the 1-week active placebo treatment. Reductions in depressive symptoms after 1 week of active placebo treatment, compared with the inactive placebo treatment, were associated with increased placebo-induced μ-opioid neurotransmission in a network of regions implicated in emotion, stress regulation, and the pathophysiology of MDD, namely, the subgenual anterior cingulate cortex, nucleus accumbens, midline thalamus, and amygdala. Their findings have numerous implications.
Fava M. Implications of a Biosignature Study of the Placebo Response in Major Depressive Disorder. JAMA Psychiatry. 2015;72(11):1073–1074. doi:10.1001/jamapsychiatry.2015.1727
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