While researchers found a strong link between the number of stressful life events subjects endured and risk of depression, they found no significant link between depression and that HTTLPR gene.
Back in 2003, depressed people had something other than bad parenting to blame for their mental malaise. At that time, a well-publicized study announced that a link had been found between a gene called 5-HTTLPR and depressive illness. The research postulated that people with a variant of that gene didn’t carry serotonin to their brain cells effectively. Since serotonin seems to allay depression, the scientists suspected that those with the gene variant would get depressed when life became difficult. And sure enough, the study found that those subjects who had the gene did get more profoundly depressed after traumatic life events than the subjects lacking the gene.
The mental health industry was all abuzz at the news, which seemingly explained why some people fall apart under stress while others just keep truckin’. As might be expected, the pharmaceutical companies, too, latched onto the results to use in concocting anti-depressant formulations. But now a new study punches big holes in the “genes-cause-depression” theory.
The study involved researchers from the National Institutes of Mental Health (NIMH) and six universities, who reviewed the original research plus 13 subsequent studies involving 12,500 people. While they found a strong link between the number of stressful life events subjects endured and risk of depression, they found no significant link between depression and that HTTLPR gene. In fact, divorce or a similar event raised depression risk by 40 percent, compared to the zero percent conferred by the gene.
“Even though our re-analysis did not confirm an association between the serotonin gene and depression, the finding that the environmental factor was strongly associated with depression in several studies reminds us that environmental factors are also involved in the complex pathways leading to mental disorders,” said study director Kathleen Merikangas.
It would seem time to score one for nurture versus nature, except that the scientists still think nature plays a big role. They believe that they just haven’t found the right gene yet — or combination of genes. “Knowing whether or not you have this gene is irrelevant,” said Dr. Merikangas, but she suggests that future studies should look at the interaction of many genes instead of focusing on just one.
But since it’s easier to study one gene than to study many genes interacting, the search for the magic-bullet genetic saboteur continues. As co-author, Dr. Neil Risch of the University of California, San Francisco, says, “Identifying gene-environment interactions is most successful when studies can focus on a single gene with a major effect…” Meanwhile, the author of the original study, Dr. Avshalom Caspi, insists that the HTTLPR gene is being maligned and it really does cause depression. “The article ignores the complete body of scientific evidence,” says Caspi, at the same time ignoring all of the new evidence himself.
Even though the scientists can’t agree, it hasn’t stopped the original findings implicating the suspected malfeasant gene from having a walloping impact. As Dr. Risch says, “A more serious concern … is that the findings of this [earlier 2003 study] and other non-replicated genetic associations are now being translated to a range of clinical, legal, research, and social settings such as forensics, diagnostic testing, study participants, and the general public.” There’s also the fact that if antidepressant formulations attempt to address the genetic issue based on that study, it’s no wonder that they so often don’t work.
Already, at least several genetic-testing companies evaluate patient samples for the errant gene in order to recommend a particular antidepressant drug. Also, companies have been working on home tests for the depression gene, to be marketed to the public. [Isn’t the allure of money wonderful?]
But why would people want to test for the depression gene? So that potential partners could screen each other to see if they might have depressed kids before committing to marriage? So that employers might start testing applicants to see who will show up in the morning chipper and fun, versus who just might be a daily drag? So that insurance companies might know who will require a regimen of pharmaceutical antidepressants for decades on end, and thus should be excluded from coverage?
Already psychiatrists have a blood test to diagnose depression in patients — which again brings up the question of why? Are shrinks really not capable of diagnosing depression without a blood test? I mean, aren’t they learning anything useful during all those years of schooling and hands-on training? The dark underside of all this genetic testing for depression is that it certainly will be used and has been used to justify dispensing drugs that often don’t work and that often have nasty side effects.
Instead of waiting for science to discover the gene that makes you feel morose or popping some very dangerous pharmaceutical drugs to get you through the day, you might want to explore some alternatives as detailed in my newsletters and blogs on depression.