(NaturalNews) Roughly half the population should never be prescribed antidepressant drugs because they are only likely to become more depressed, according to a new study conducted by researchers from Columbia University and the New York State Psychiatric Institute and published in the journal Neuron.
Scientists have known for some time that antidepressant drugs only work in about half of patients. Research has discovered that although the drugs are designed to raise circulating levels of the neurotransmitter chemical serotonin in the brain, they actually produce the opposite effect in large numbers of people.
"The more antidepressants try to increase serotonin production, the less serotonin [they] actually produce," researcher Rene Hen said.
An estimated 11 percent of U.S. women and 5 percent of men in non-institutionalized settings are currently taking antidepressants.
Genetic and brain imaging studies have led some scientists to believe that the explanation for this effect lies in the actual make up of the brain, specifically in the numbers of 1A serotonin receptors found in the raphe neurons deep in the brain's center. Although higher numbers of these receptors on raphe neurons are correlated with decreased responsiveness to antidepressants, scientists have had trouble testing the hypothesis directly.
In the new study, scientists genetically engineered mice to contain either high or low numbers of 1A receptors in their raphe neurons. They found that in mice with higher levels of receptors, antidepressants actually lowered serotonin levels rather than lowering them -- consistent with the effect seen in people whose bodies resist the drugs.
The researchers then lowered the number of receptors in these mice and re-tested them. The mice then became responsive to the drugs.
"By simply tweaking the number of receptors down, we were able to transform a non-responder into a responder," Hen said.
Rather than suggesting that antidepressant use be scaled back, however, Hen and colleagues expressed eagerness to find ways to suppress the activity of some of the 1A neurons in the raphe receptors of people who are resistant to the drugs, so that everyone can be treated with them equally.