Draft:Serotonin Hypothesis

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The serotonin hypothesis is a popular, medical and layperson hypothesis that depression or other mental disorders are caused by or highly correlated with a, "loss", or, "deficiency", of the hormone serotonin in the brain.

This view is widely held among American psychiatrists and was the basis for the development and prescription of SSRIs to treat depression. The hypothesis is probably wrong, suggesting there should be more oversight into the approval of drugs in the USA. 13% of Americans ingest SSRIs daily without knowing the mechanism of action, assuming SSRIs are clinically (ie not just statistically) significant at all beyond placebo.[1]

Serotonin and depression[edit]

It is notoriously hard to measure serotonin in the brain, which is partly why there has been some debate over the matter of serotonin and the brain.[2]

SSRIs were meant to cover up failure of benzos[edit]

In the late 1980s, after controversy resulting from mass dependence to benzodiazepine drugs, there was a coordinated effort to supplant benzodiazepines with a serotonergic drug: "buspirone". Central idea to the marketing of the first serotonergic psychiatrics drugs was that such drugs raised serotonin levels to, "normal", levels, implying an deficiency of serotonin in the brain.[3]

There probably isn't a serotonin deficiency in depression[edit]

Depressed patients may have increased serotonin[edit]

A 2008 paper for the Archives of General Psychiatry found evidence that there is increased serotonin activity in depressed patients.[4] This is in direct contradiction to the original theory that there is a, "deficit of serotonin in the brain", and the reason for prescribing drugs which decrease the reuptake of serotonin in the brain (increase serotonin in the brain).

Academic response to new evidence[edit]

Academics Jeffrey Lacasse and Jonathan Leo conducted an academic literature review of studies which analyze serotonin levels with respect to depression levels. According to them, the bulk of recent academia on the serotonin hypothesis of depression, deems the hypothesis as more likely false than true.

Contemporary scientific research has failed to confirm any serotononic lesion in any mental disorder, and has in fact provided significant counterevidence to the explanation of a neurotransmitter deficiency —Serotonin and depression, Plos Medicine[5]

The researchers also completely rejected the idea that there is a correct "balance" of serotonin, that could hint at any currently known imbalance associated with depression.

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…"
—Lacasse and Leo, PLOS medicine[6]

The clinically significant effects of SSRIs as larger than antidepressive effects[edit]

Academics such as David Antonuccio and David Healy challenge the notion that SSRIs even qualify as antidepressants in the first place, writing in the Scientifica journal that the "side effects" of SSRIs have a clinical significance that outweighs any possible anti-depressant effect. These academics half-joked that antidepressants should instead be called "anti-aphrodisiacs" or "agitation enhancers".[7]

References[edit]

See also[edit]