real effect. Patients with a certain copy of a serotonin gene showed less activity in the amygdala ( left ), indicating the reduced anxiety after treatment with placebo .
T. Furmark et al. Journal of Neuroscience
For a drug to market, pharmaceutical companies must demonstrate that it works better than a placebo. But sometimes the placebo is just as powerful as the real thing. Just why our bodies react so strongly to fake drugs has long been a mystery, but researchers are a step closer to solving this puzzle, after choosing a particular gene that may be responsible for a type of placebo effect.
The placebo effect works because patients believe they are actually receiving treatment. Expecting treatment is similar to anticipate the reward, studies have shown, and the anticipation of reward triggers the release of dopamine, a neurotransmitter in the brain, which can help relieve the symptoms of chronic pain and depression. But what about placebo effects for other conditions
Tomas Furmark, a psychologist at the University of Uppsala in Sweden, suspected that a different neurotransmitter plays a role in placebo responses to an anxiety disorder social (SAD) - an abnormal fear of being judged by others. Brain imaging studies have shown that the amygdala, a brain area that regulates the response of fear, is particularly active in patients with SAD. In addition, healthy people with certain variations in two genes that regulate the neurotransmitter serotonin amygdalas were more active
Based on these results, Furmark and colleagues -., In collaboration with the company pharmaceutical GlaxoSmithKline - ran a placebo-controlled trial with 108 patients who had been previously diagnosed with SAD. The volunteers were randomly assigned to receive either a new drug serotonin or a sugar pill for 8 weeks. Early in the trial, patients had to prepare and deliver a speech to a small group of people - a trigger anxiety event - while the researchers tracked their amygdala activity using positron emission tomography. The technique allows researchers to track blood flow - and thus activity - in different brain regions. The study participants had to give a similar speech at the end of the treatment period, so that researchers can determine if their brain activity patterns had changed.
Even sugar was enough to defeat some cases of SAD. Of the 25 patients who received placebo, 10 reported reduced anxiety by the end of the study. (Figures for the treatment group are not released because the trial is ongoing.) Brain scans during the second speech showed their amygdalas were also less active. Genetic analysis revealed that eight people who got a placebo had relief of a particular version of a gene that regulates serotonin production called hydroxylase-2 promoter tryptophan (TPH2), the researchers report tomorrow in the Journal of Neuroscience . This is one of the same genetic variants linked to increased activity of the amygdala in healthy people. TPH2 is the first genetic marker linked to a placebo response, reports the team.
Find genetic markers for the placebo effect could raise ethical questions about how companies design their clinical trials, Furmark said. For example, "it might be tempting to screen all individuals ... and select only those with [the] nonresponsive phenotype [for the trial]."
psychiatrist Helen Mayberg of Emory University in Atlanta, Georgia, who has studied the placebo effect in depression, admits that the results could have important implications for the design of the research. But first, more research is needed to determine if genetic markers for SAD placebo relief can be generalized to other diseases, and what other genes may contribute to the phenomena, she said.
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