Experts, in order to test the effectiveness of a medication, often tally its effect with that of a placebo. Placebos are usually sugar pills whose main purpose is to have “no treatment” in an analysis. Such pills are often used in order to gauge the effect of the actual medication. However, in spite of being a sham, the placebo is observed to have the same effect as the actual drug on some patients. It seems that the effect of placebos may vary from person to person; but the cause for this disparity in its effect is still quite misty.
Now, a team of experts have stated that apart from its combined biological and psychological factors, even genetics may hold an answer to the positive effect of placebos noticed in some patients. These UCLA experts have stated that in patients with major depressive disorder (MDD), their genes may influence the response of placebos.
These researchers believe that the genes which influence the brain’s reward pathways may play a role in determining the response of placebos in patients with the above mentioned disorder. Apparently, placebos are presumed to function by emitting monoamines (a class of neurotransmitters), which notably trigger the central reward pathways of the brain. The released monoamines, which are often dopamine and norepinephrine, are believed to be chemicals which make a person “feel good.”
Since monoamines’ chemical signaling is noted to be under a strong genetic control, these researchers feel that common genetic variations (known as genetic polymorphisms) between each person may determine the placebo effect.
For better evaluating this criterion, the experts were believed to have analyzed the blood samples taken from more than 80 people suffering from major depressive disorder. Some of these patients were notably provided with a placebo, while the rest were given medications.
Following this, the researchers evidently assessed the polymorphisms in genes that coded for two enzymes that regulate monoamine levels – catechol-O-methyltransferase (COMT) and monoamine oxidase A (MAO-A). Apparently, it was observed that the subjects with greatest enzyme activity within the MAO-A polymorphism seemed to have a lower placebo response as compared to those with other genotypes.
“Our findings suggest that patients with MDD who have specific MAO-A and COMT genotypes may be biologically advantaged or disadvantaged in mounting a placebo response, because of the activity of these two enzymes,” says researcher Dr. Andrew Leuchter, professor of psychiatry, UCLA Semel Institute for Neuroscience and Human Behavior.
Seemingly, this is noted to be the first analysis of its kind to have assessed the link between MAO-A and COMT polymorphisms and placebo response in MDD patients.
He further states that including the influence of genotype, along with biological and psychosocial factors, may provide a more potent testing of future treatments.
This research has been presented in the edition of the Journal of Clinical Psychopharmacology.