Over the last three decades, society has been receiving an avalanche of information suggesting that depression is caused by a “chemical imbalance” in the brain. To be more exact, an imbalance of a brain substance called serotonin. However, our latest research review calls this into question.
The theory of the role of serotonin in depression was first proposed in the 1960s of the last century. But the pharmaceutical industry didn’t start actively promoting it until the 1990s, when they began marketing a new range of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs.
They had the backing of official institutions such as the American Psychiatric Association, which has since launched the message to patients and their families that “differences in certain brain chemicals may contribute to symptoms of depression.”
It is the same message that thousands of doctors around the world have been repeating, both in their private practices and in the media. People accepted it as a maxim. And many started taking antidepressants because they believed that it would solve the problem. imbalance of your brain. Without going any further, they are currently prescribed to one in six adults in England.
Although many leading academics and psychiatrists have questioned whether there is sufficient evidence that depression is a consequence of abnormally low or inactive serotonin, until now there has been no comprehensive review that would allow firm conclusions to be drawn one way or the other.
SSRI-type antidepressants work
At first glance, that SSRI-type antidepressants act on the serotonin system seems to support the theory of the role of serotonin in depression. In effect, SSRIs temporarily increase the availability of this neurotransmitter in the brain. However, this does not necessarily imply that its decline is the cause of the disease.
Furthermore, there are pharmacological trials showing that the effects of antidepressants in depressed patients are barely distinguishable from a placebo (dummy pill). However, they do seem to have a numbing effect on emotions that can influence people’s moods.
First comprehensive review
Our team has been the first to carry out a review umbrella to identify and compile the results on any and all major research on serotonin and depression.
Among other things, we included research comparing the levels of serotonin and its breakdown products in blood or brain fluid. In this sense, there do not seem to be significant differences between people with depression and those who do not suffer from it.
Another area of research to highlight is that focused on serotonin receptors, proteins located at the ends of neurons to which serotonin binds and that can transmit or inhibit its effects. Most of the studies in this sense do not detect differences between people with depression and those who do not suffer from it. Furthermore, some work suggests that serotonin activity is increased in people with depression, just the opposite of what the serotonin theory predicts.
Research on the serotonin transporter also suggests that, if anything, there would be increased serotonin activity in people with depression. Of course, keep in mind that many of the participants in these studies had already used antidepressants. And that could influence the results.
We also review research focused on whether depression can be induced by artificially lowering serotonin levels. Two systematic reviews from 2006 and 2007, along with a sample of the 10 most recent studies, found that lowering serotonin did not induce depression in hundreds of healthy volunteers. One of the reviews, based on just 75 patients, showed very weak evidence of a slight effect in a small subgroup of people with a family history of depression. But it was insufficient.
And what about genetics? Data based on thousands of patients also found no difference in the frequency of varieties of the gene that contains the instructions for making the serotonin transporter between people with depression and healthy controls. Only one famous 2003 study found a link between that gene and stressful life events, which later studies ruled out.
The only thing that there is evidence of is the strong effect of stressful life events on people’s later risk of developing depression.
Not supported by evidence
At this point we can say that although the serotonin and depression theory has been one of the most influential and widely researched biological theories about the origins of depression, it is not supported by scientific evidence. That questions the use of antidepressants.
Most currently used antidepressants are assumed to act through their effects on serotonin. Some also affect another neurotransmitter, norepinephrine. But experts agree that the evidence for its involvement in depression is too weak.
There is no other accepted pharmacological mechanism to explain the effect of antidepressants on depression. If they work because of their placebo effect or by numbing the emotions, it must be doubted that they do more good than harm.
The stigma of chemical imbalance
Far from reducing stigma, viewing depression as a biological disorder appears to increase it. Furthermore, there is evidence that people who believe their own depression is due to a chemical imbalance are more pessimistic about their chances of recovery.
It’s important for people to know that the idea that depression is due to a chemical imbalance is just a hypothesis. And that at the moment we don’t even understand what exactly happens in the brain when antidepressants temporarily elevate serotonin.
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Patients need all this information to make informed decisions about whether or not to use these drugs. With the data we have, it is impossible to say that taking SSRI antidepressants is worth it. We can’t even say that it’s completely safe.
This article was originally published on The Conversation. Read the original.