The news last month that serotonin deficiency in the brain does not explain depression surprised many. But the MenningerClinic argues that SSRIs may continue to have a role in treating depression—even if it's not exactly how we once thought.
So why did it persist, even if experts knew it was, if not wholly wrong, at least inadequate? Like many imperfect explanations, it survived because it had utility for modeling the role of monoamine chemicals in the brain, especially for drug development. After all, the first antidepressants all worked by increasing the level of monoamines in the brain. Although effective, they were not targeted and had many side effects.
Researchers then began concentrating on a specific monoamine, serotonin, as a target for drugs. What followed was a revolution in antidepressant treatment. Fluoxetine was the first SSRI, or serotonin reuptake inhibitor introduced in the US. Approved in 1987, it was an almost immediate success, and a flurry of other serotonergic drugs followed. Even today, nearly all drug treatments for depression target one or more monoamines, and serotonin is usually one of those.
Even if most mental health experts understood that the monoamine hypothesis was inadequate, it became one way to explain to patients what might be causing depression. It was not uncommon for doctors to tell patients that they had a “chemical imbalance.” This biological explanation was perceived less stigmatizing for most patients, who tended to blame themselves for something outside their control.
As Dr. Montcrieff fairly points out in a blog discussing her study, “even if leading psychiatrists were beginning to doubt the [serotonin hypothesis]…no one told the public.” Many of us thought, “what is the harm.” Even if not exactly true, the point of the explanation is well intended: that depression is a biological disease, not a moral failing or, in some other way, the patient’s
France Dernières Nouvelles, France Actualités
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