Scientist Smackdown: Can a Single Gene Really Predict Depression?

By Eliza Strickland | June 17, 2009 11:39 am

depressionFor six years, psychiatrists thought they had found a genetic clue as to what makes some people more prone to depression when they’re hit with an emotional blow: a single gene. A 2003 study created a sensation among scientists and the public because it offered the first specific, plausible explanation of why some people bounce back after a stressful life event while others plunge into lasting despair [The New York Times]. But now a broader analysis of 14 studies has found no link between the gene and the risk of depression, and researchers argue that the 2003 findings were prematurely heralded as a breakthrough. “I think what happened is that people who’d been working in this field for so long were desperate to have any solid finding” [The New York Times], says Kathleen R. Merikangas, one of the authors of the new study.

The so-called “depression gene” that researchers focused on in the 2003 study helps regulate levels of serotonin, a brain chemical that plays a major role in depression and is a key target of antidepressant drugs. Researchers … found from a long-term study of 847 people in New Zealand that those with a short version, or allele, of the serotonin transporter gene were more likely to become depressed by adverse life events than were those with only long alleles [ScienceNOW Daily News].

But the new study, published in The Journal of the American Medical Association, reviewed 14 studies involving 14,250 participants on the interaction between the serotonin-transporter gene and stressful life events, [and] found no such association with depression risk. The study goes on to caution that any potential use of [the gene] as a screening tool for depression risk would be invalid [Time]. The researchers say they believe that genetics and environmental triggers can each play a roll in depression, but argue that a single gene is unlikely to explain the mental ailment.

Unsurprisingly, the authors of the 2003 paper are challenging the new meta-analysis, which examined the results of 14 studies of different sizes and with different methodologies. The authors of the 2003 paper, Avshalom Caspi and Terrie Moffitt, note that the larger studies used in the analysis — which contained as many as 2,179 participants — assessed stressful life events and depression symptoms via phone or questionnaires, rather than in comprehensive interviews. “Not surprisingly, these big studies with weak measures did not find positive results, and this tilted the meta-analysis toward a null finding,” the scientists say [Science News].

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Image: iStockphoto

CATEGORIZED UNDER: Mind & Brain
  • http://alexfiles.com Alex

    Arguing that the large studies using objective measures are less accurate than smaller studies using interviews is a bit disingenuous for a scientist. While the comprehensive interviews may have been conducted in a scientifically rigorous manner, there’s no reason not to expect that an objective inventory correlating depressive episodes, health care, life events, etc. wouldn’t be equally scientific. The 2009 authors could just as easily call interviews a “weak measure,” unless the interviewers were all trained to interpret in the same way, and captured the same measurements across the board.

    Isn’t the goal not to cast stones at each other, but to take what’s useful from both studies and discover the truth?

  • imanism

    Well said!

    Besides, this issue is highly debatable anyway. The second study’s findings are more akin to common sense, really. No one will likely find a single gene responsible for depression, because the issue of emotional instability is not a two dimensional problem.

    Seriously, c’mon.

    A test of less than 1,000 people, long-term or no, that finds something remarkable like a smoking gun gene….

    I mean, that is a little suspect. Is it not?

  • YouRang

    It would have been nice if one of the articles quoted reported the supposed rate of incidence of major depression in each group and had reported the frequency of each of the two alleles worldwide. If the incidence of the gene is so low that it may cause SOME depression, then if the subsequent tests chose people at random, then both sides might be correct: THE GENE MAY HAVE A HIGH PROBABILITY OF CAUSING DEPRESSION IN ITS OWNERS: BUT OTHER CAUSES MIGHT ALSO BE IMPORTANT IN THE ONES WITHOUT THE GENE. Also were the people in the more recent phone interviews chosen at random or were they known to have depression or known not to have depression.

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