Almost all antidepressants currently in the market have an effect in serotonergic synapsis (neuronal connections which work with a neurotransmitter called serotonin). The serotonergic hypothesis is one of the most popular among psychiatrist and pharmaceutics industries, according to which depression is caused by a deficit in the serotonin neurotransmitter. In other instances, the hypothesis claims the existence of structural changes in many brain regions that inhibits serotonergic transmission. Another popular hypothesis is the monoaminergic one, that claims that attest 3 neurotransmitters are involved in depression, which are: dopamine, noradrenaline and serotonin, assuming that serotonin has a special relevance.
Said hypothesis, despite the fact that they are very popular, have more holes than a strainer. Some of the hypothesis inconsistences are:
-Typically, the efficacy of the pills is used as evidence of the hypothesis (inhibitors of serotonin reuptake). This claim has 2 main issues: 1- Erroneous conclusion; the fact the chemotherapy reduces or eliminates a form of cancer, doesn’t mean that said cancer was caused by the lack of those chemicals in our blood. The fact that a headache is reduced after we take an aspirin, doesn’t mean that our headache was caused by the lack of aspirin in our organism; it does sound ridiculous when put this way ¿right? 2- The reported efficacy has been severely question; when you quantify the effect taking in consideration both published and unpublished results (which are generally unfavorable) the efficacy is considerably lower; additionally, a considerable part of the effects are explained by the placebo effect.
-The repletion of serotonin reserves doesn’t cause depression in healthy subjects. Neither does it increment depressive symptom in those already depressed.
-It has been found that many depressives patients have an elevated serotonergic transmission.
-Some measurements of serotonin (which is really really hard methodologically speaking, the direct measure is usually impossible in adult subjects, it requires invasive methods), have not shown decreased levels of the neurotransmitter in depressive patients. The same is true for dopamine and noradrenaline.
In general, the biomedical hypothesis of the so called mental illness have as much failures as the president of Venezuela.
So, if depression isn’t caused by a deficit or reduction in serotonergic transmission (or monoaminergic) what causes depression? That’s a question for another time, but its worth mentioning that the question is itself a trap. In certain instances, scientific progression is not defined by how many questions you can answer, but what question do you ask.
In the movie “I Robot” when Detective Spooner asks Doctor Lanning Hologram some questions, he says “my answers are limited, you must ask the right questions”. Like Detective Spooner we must ask the right questions, its not about how many questions we ask nature, first we must figure out what the right questions are.
I will only say that the word “cause” and the way we define “depression”, are important issues that condition the question we ask in the research field of “depression”.
References
-Principles of psychopharmacology for mental health professionals. Cap 3 Mood Disorders 37-66
-Pathophysiology of depression: do we have any solid evidence of interest to clinicians?
-Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies.
-Serotonin and Depression: A Disconnect between the Advertisements and the Scientific -Literature.
-Is serotonin an upper or a downer? The evolution of the serotonergicsystem and its role in depression and the antidepressant response
PD: There might me some mistakes, English is not my main language.
