A few weeks back, I reported on a new study that pounded yet another nail in the coffin of the theory that depression is caused by low serotonin. You can read that original post here as well as the follow up post wherein I responded to a question from a reader asking if I was trying to say that people who suffered with depression were to blame for their struggles (short answer: no.)
Over at PsychCentral, one of the most popular psychology news portals on the web, the director, Dr. John Grohol has an excellent piece summarizing the growing case against the low serotonin theory of depression. He writes….
Back in 2005, Lacasse and Leo pointed out in the journal PLOS Medicine that there was a huge disconnect between what we knew about serotonin’s role in depression from the medical research, and what pharmaceutical advertisements were claiming we knew:
Regarding SSRIs, there is a growing body of medical literature casting doubt on the serotonin hypothesis, and this body is not reflected in the consumer advertisements. In particular, many SSRI advertisements continue to claim that the mechanism of action of SSRIs is that of correcting a chemical imbalance, such as a paroxetine advertisement, which states, “With continued treatment, Paxil can help restore the balance of serotonin…” .
Yet […] there is no such thing as a scientifically established correct “balance” of serotonin. The take-home message for consumers viewing SSRI advertisements is probably that SSRIs work by normalizing neurotransmitters that have gone awry. This was a hopeful notion 30 years ago, but is not an accurate reflection of present-day scientific evidence.
New research that we reported on last month confirms the role of serotonin in depression is not well-understood. In that mice study, removing the stuff in the brain that creates serotonin2 did not create a bunch of depressed mice.
Other research confirms it’s not as simple as a serotonin deficit. As Whitaker (2010) noted, the 1976 Asbert study is still relevant. Asbert looked at levels of a metabolized result of serotonin (something called 5-HIAA) in spinal fluid. If low-levels of serotonin cause depression, then all people suffering from depression should have significantly lower levels of 5-HIAA in their spinal fluid than people without depression.
What Asbert found, however, wasn’t a clean result. In fact, it clearly shows how complicated depression as a disease process is. In both groups of people studied — both a depression group and a control group — about 50 percent had “regular” levels of 5-HIAA, about 25 percent had really low levels, and another 25 percent had really high levels.
If serotonin were really an important part of the picture in depression, we’d expect that group to look significantly different than the control group. In this study, at least, the two groups looked largely the same.
As we said back in 2007, serotonin may play some small, not-yet-well-understood role in depression. But if it does, it looks nothing like the simplistic “low levels of serotonin cause depression” hypothesis that was all the rage ten to twenty years ago. READ MORE.
Of course, none of this means that depression medication can’t be helpful but only, as I reported before, that it should never be the first course of treatment for depression. Research shows that meds are best when they play a supportive role to therapy. Meds alone do not represent the best standard of care for treating depression. If you are on medication for depression but not currently in counseling, talk to your doctor about getting a referral to a therapist in your area, or contact the Pastoral Solutions Institute to learn more about you can benefit from our Catholic-integrated, telephone counseling practice. Let us help you find effective, faithful solutions to the tough emotional challenges you are facing.