One of the leading myths that unfortunately still circulates about clinical depression is that it’s caused by low serotonin levels in the brain (or a “biochemical imbalance”). This is a myth because countless scientific studies have specifically examined this theory and have come back universally rejecting it.
So let’s put it to rest once and for all — low levels of serotonin in the brain don’t cause depression.
Let’s find out why.
This isn’t the first time we’ve had to debunk this myth. We last did so in 2007, pointing out that most people’s (even doctor’s!) belief that low serotonin causes depression is a result of pharmaceutical companies’ successful marketing. It’s a message they repeatedly hammered home ((Only pointing out it was just one possible theory of depression in small print in their advertisements and marketing.)), making it one of the most successful marketing messages-turned-into-fact ever done on Madison Avenue.
However, you may be reading this article to get to the punch line: So if low serotonin levels don’t cause depression, what does? Here’s the short answer — researchers still don’t understand what causes depression. We have a lot of theories still in the mix and still being researched, but none of them have resulted in one, conclusive answer.
One of those theories that’s been tested — and tested time and time again — is the idea that our brains can sometimes run low on a neurotransmitter called serotonin. It is thought by prescribing a selective serotonin-reuptake inhibitor (SSRI) antidepressant medication like Prozac, Zoloft, and Paxil “fixes” this imbalance, bringing serotonin levels back to “normal.”
First, let’s tackle the whole “chemical imbalance” theory that underlines the serotonin theory of depression. In order for us to suggest an imbalance in anything, we’d have to understand what a perfectly balanced brain looks like. To date, no study or researcher has been able to show such a brain. It’s likely because it doesn’t exist.
The brain is the least-understood organ in the body today. What we do know about it is that it is constantly changing and in flux. Virtually any stimuli can alter its energy consumption temporarily. We don’t understand why the brain is structured the way it is, or even how it actually communicates internally (although, again, we have a lot of theories).
It’s hard to imagine, but physicians only began to understand what the heart’s purpose in the body was about 400 years ago. It’s no wonder we might need a few more decades (or longer) to understand how the body’s most complex organ operates.
Serotonin’s Role in Depression
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 serotonin ((More technically, mice lacking the gene for TPH2 are genetically depleted of brain 5HT serotonin. So the researchers bred mice that lacked the TPH2 gene to test their theory.)) 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.
If a doctor suggests this is the cause of your depression, and all you need is an antidepressant like Prozac, point them to this article. And please take a moment to share this on Facebook and twitter. It’s an widespread myth that dumbs down depression that we need to put to rest once and for all.
Read the full article: Mice Study Suggests Lack of Serotonin Not Behind Depression