It turns out that the "feel good" chemical serotonin has a lot less to do with depression than we thought.
So, the way doctors are treating the 1 in 10 Americans who suffer from depression may be totally wrong, according to new research from the VA Medical Center and Wayne State University. For the past three decades, a common treatment for depression has involved prescribing patients a selective serotonin re-uptake inhibitor (SSRI) pill to prevent serotonin — otherwise known as the "happy" chemical — from being reabsorbed in the brain. When some people were given the drugs in the 1980s, their symptoms diminished. Scientists thought they'd nailed it. Hello, Prozac Nation.
But there was a problem: The drugs only worked in 30% to 40% of patients. Without a better alternative, most of the other 60% to 70% continued to suffer from full-fledged depression.
Here's where the new research comes in: Looking for an explanation of serotonin's role in the brain, the VA and Wayne State University scientists experimented on mice by creating a group of the rodents without the ability to produce the chemical in their brains. Instead of showing signs of depression, the serotonin-free mice behaved, well, normally. Even when put in stressful situations, they acted in the same way as the mice who did not receive the treatment. The scientists also tried giving them traditional antidepressants to see how they would react. Surprisingly, the serotonin-free mice responded to the serotonin-protecting drugs much in the way typical mice would.
So much for serotonin.
Three decades of misguided treatment? Recently, other research has helped shine some light on the serotonin myth. Rather than simply protecting the brain's reserves of a "feel good" chemical, traditional antidepressants also foster the growth of new brain cells. The new cells could help to alleviate symptoms of depression, as many depressed people have smaller and less dense sections of several key regions of the brain.
The new finding is the latest in a series of new developments that are challenging what we thought we knew about depression and helping doctors create new treatments that actually work.
We now know, for example, that:
Specific brain regions are affected by depression. A seahorse-shaped segment in the center of the brain is critical for helping us create memories and process emotions (the hippocampus) shrinks in the brains of depressed people. In stressful situations, the flow of blood to the region is stifled. Over time, the area dwindles.
Depression is genetic. People with a variation in one specific chunk of DNA are more vulnerable to depression. Since each of us has two copies of the gene (one from each parent), people with two copies of the affected gene are at the highest risk of developing the condition.
So despite having bungled the past few decades of depression treatment, this new research brings us one step closer to finding real treatments than ever before.