TUESDAY, Sept. 30, 2003 (HealthDayNews) -- A Stanford University Medical Center study may offer new insight into why some people suffer side effects when taking common antidepressants while other people experience no problems.
The Stanford scientists identified a genetic marker that may play a role in a person's response to antidepressants.
They also concluded that a key liver enzyme involved in breaking down these antidepressants surprisingly played no role in causing side effects or in the efficacy of the drugs.
Their findings may help reduce side effects for people taking antidepressants. The study appears in the October issue of the American Journal of Psychiatry.
The study included an analysis of DNA samples from 246 people, aged 65 and older, with depression who were randomly assigned to take either the antidepressant paroxetine (Paxil) or mirtazapine (Remeron) for eight weeks.
The two antidepressants work in completely different ways but both do affect serotonin, a neurotransmitter that binds to specific receptors in the brain and nervous system. The Stanford team focused on one type of serotonin receptor called 5HT2a, believe to be involved in causing antidepressant side effects.
The study found that people with one variation of the 5HT2a gene were much more likely to discontinue taking paroxetine due to intolerable side effects than people with two other variations of the same gene.
This same gene variation didn't seem to affect the people taking mirtazapine.
The study was partially funded by Organon Pharmaceuticals Inc., the company that makes mirtazapine.
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