Having Too Much of This Could Lead to Depression
WHY YOU SHOULD CARE
Meds don’t always work. Maybe scientists aren’t targeting the right factor.
By Libby Coleman
Do you feel persistent sadness? Loss of interest? And you’re sure that your life isn’t just extremely boring and full of rain clouds and woe? While scientists don’t fully understand the causes of the mood disorder that affects more than 350 million people worldwide, there’s new illuminating evidence about depression. According to a recent study:
High levels of hippocampal FGF9 play an important role in the development or expression of mood and anxiety disorders.
Sure, we know insufficient serotonin levels get a bad rap when it comes to depression, but that’s like blaming one person in a full-scale riot. Depression isn’t caused by only one factor. In fact, study co-author Elyse Aurbach says we’re probably not getting to the core of why people are depressed because “the brain is immensely complex.” In this study, the research team conducted eight experiments (four on animal brains, four on brains of the deceased human kind) of varying sample sizes — from 20 to 90 brains in each — and found that the brains of deceased humans who’d been depressed had increased levels of hippocampal FGF9 and that live animals with increased FGF9 levels demonstrated depressive, anxious behavior. “This is not just a correlation,” study leader Huda Akil of the University of Michigan says. Less really may be more, at least when it comes to FGF9.
This finding is further evidence that mental health problems are not simply that: mental. Which could be good news for campaigns that want to decrease the stigma surrounding depression. With only a quarter of adults with mental health symptoms believing that people are sympathetic toward individuals with mental illness, according to a CDC study, fewer people seek treatment. Think about it this way: Depression is probably not one illness, “like when you have a fever,” Akil says. From genetics to trauma to having too much FGF9 — which regulates the growth of hair, lung and many other tissues, as well — there are many physical factors in depression.
This finding could be huge for the development of new antidepression drugs. While such drugs have been available and evolving for decades, millions of people still struggle; over time, some become resistant to the current solutions. There should be many depression treatments, just as there are many cancer treatments, Akil says. Targeting FGF9 levels is a new angle, but it will be a long and unpredictable road to the creation of a medication. In the meantime, the research team will continue to study how FGF9 impacts other brain regions and the exact ways its levels are increased or decreased.
The question remains: Will these results be consistent over time? While the study was well-designed, evolutionary psychologist Paul Andrews says other growth factors — like FGF2 and FGF3 — have been implicated in depression before but not consistently. He also warns that we ought to continue trying to determine whether depression has evolutionary benefits — helping with deep analytical thought, for example — before rushing to medicate. But according to a 2013 study by the National Institutes of Health, 7 percent of American adults had suffered depression over the previous year and not all of them want to live with depression — evolutionarily beneficial or not. Damn you, FGF9.