Experts have debated for decades what causes mental illness, with the primary contenders being bad parenting, bad environment, and bad genetics. Those who believe that biology is to blame typically advocate drugs as the intervention of choice, holding that a physical problem needs a physical antidote. The nurture camp on the other hand, tends to favor psychotherapy, arguing that helping patients to figure out what trauma caused their distress (something to do with trains, tunnels, and mothers, I believe) will make the psychological problems go away. But when it comes to treating the most common mental disorder, depression, the medical establishment rarely advocates psychotherapy anymore. Rather, doctors pull out the prescription pad, believing that when somebody gets depressed, their biochemistry is askew and a pill can patch it up. And so, we’ve become a “Prozac nation,” with one in every ten people in the US over the age of six now taking an antidepressant.1
But as I’ve written before, antidepressants have a notoriously poor track record in combating depression. In fact, studies show that at absolute best, antidepressants do the job only half the time. That fact doesn’t stop doctors from prescribing the pills to everyone who complains that it’s been a crummy day. The rate of antidepressant use has just about doubled in the past 14 years, leading to over $11 billion a year in sales worldwide. That’s right — $11 billion in sales for a remedy that has only a coin-flip’s chance of working. Given the fact that the pills make so much money for industry and yet work so poorly and come with such ugly side effects, it would make sense that the pharmaceutical companies would worry that sometime soon the game will be up. This is even more true considering that so many things work better at combating depression than the pills do — including magnets, exercise, working on the farm, and meditating, not to mention the newest kid on the block, cognitive-bias modification.2
Perhaps to justify the continued reliance on antidepressants, and perhaps also to improve their effectiveness, scientists have been scrambling to find a “depression gene.” As I’ve described before, back in 2003, scientists found a link between a gene called 5-HTTLPR and depressive illness. The research back then postulated that people with a variant 5-HTTLPR didn’t carry serotonin to their brain cells, and that resulted in a tendency toward depression. That finding was good news for the pharmaceutical industry, because if genes cause depression, the thinking went, then there must be a way to pharmaceutically intervene. But sadly for industry and medical establishment, 14 subsequent studies found no link whatsoever between the gene and depression.
Now, though, like Lazarus, the issue has risen from the grave. New research, reviewing 54 previous studies, concludes that, in fact, there is a depression gene after all.3 An article published in the Archives of General Psychiatry reports that those 54 studies show that people with the gene variant are more vulnerable to depression than people without it. But there’s a trick to it. The gene “turns on” only when the individual carrying it goes through certain life events. For instance, those who experienced early childhood trauma and have the gene stand a greater chance of getting depressed later in life compared to those who don’t have the gene but also had traumatic childhoods. Also, those who carry the gene have a greater risk of depression when seriously ill, but not when they go through other stressful life events. The gene itself doesn’t cause depression, the researchers say, but rather, it creates a vulnerability that makes those carrying the gene more likely to get depressed if they experience certain stressful life events.
“This is the final word,” says Dr. Srijan Sen, a University of Michigan psychiatry professor. “A lot of resources and money have gone into looking at this one specific gene and whether it has an association with risk of depression, and now we can move as a field to look more broadly across the human genome to find other genes involved in depression.”
Dr. Sen acknowledges, however, that the gene is just one small factor contributing to depression, and that much more research needs to be done to map all the genetic determinants at play. “Ideally we would like to find a panel of different genetic variations that go together to help us predict who is going to respond poorly to stress, and who might respond well to specific types of treatment as opposed to others,” he says.
In fact, in the months since Dr. Sen’s study came out, two new studies have been published that came up with the same results, identifying DNA regions linked to depression. In the case of these studies, both published in The American Journal of Psychiatry, the researchers found a significant link between deviations in the chromosome called 3p25-26 and depression.
Already, the scientists are clamoring to use the findings to rewrite antidepressant recipes. WebMD predicts, for instance, that “discoveries like this one will help usher in the era of personalized medicine for the treatment of depression.” Sounds like they’re thinking about creating made-to-order pills, or specific combinations of existing pills, to match a patient’s particular chromosomal abnormalities.
While it would be wonderful if medical science did in fact come up with a happy pill that actually works and that causes little damage in the process, the track record is not encouraging. Plus, researchers say it will take at least 12 years before they develop new drugs using the findings.
But in the meantime, if you want to beat the blues, pause for a moment to comprehend what all these studies “really” are saying. Cut through the mumbo-jumbo, and the message is simply that outside circumstances affect us. By implication, if trauma can affect our genes to switch in one direction, other circumstances are just as likely to switch them in another direction. Proper diet could affect the gene switch. Exercise could affect the gene switch. Meditation could affect the gene switch. In other words, we’re right back where we started. If genes can be switched both on AND off, then we still can’t say for sure whether depression is the result of nature or nurture — despite Dr. Sens’s claims to the contrary. So with that in mind, check out Jon Barron’s newsletter on Stress and Depression for a complete list of all-natural, gene-switching, depression-busting options.
1 Smith, Douglas A. “Book Review: Prozac Nation.” The Antipsychiatry Coalition. 25 May 2011. <http://www.antipsychiatry.org/br-pro-n.htm>
2 “Therapist-free therapy.” 3 March 2011. The Economist. 26 March 2011. <http://www.economist.com/node/18276234>
3 Mann, Dennis. “‘Depression Gene’ Linked to Response to Stress.” 4 January 2011. WebMD. 25 May 2011. <http://www.webmd.com/depression/news/20110104/depresssion-gene-linked-to-response-to-stress>
