(ORDO NEWS) — It is generally accepted that depression is caused by a lack of the neurotransmitter serotonin, and it is with it that many modern antidepressants fight.
However, a new analysis of past work has shown that this hypothesis has never been proven experimentally.
Over the past decades, the chemical imbalance hypothesis has become dominant in explaining the nature of depression, which links it with disorders of serotonin metabolism.
Scientists rely on it, exploring depression, doctors, prescribing antidepressants, patients, taking such drugs.
However, there is no reliable evidence base for the hypothesis. This was demonstrated by a large review of past experiments on the connection of serotonin with depression.
Serotonin is a key hormone and inhibitory neurotransmitter involved in mood regulation. It is assumed that problems with the synthesis or transport of serotonin, with its release in synapses or the work of serotonin receptors are one of the factors in the development of clinical depression.
Modern antidepressants stimulate the work of this particular system: for example, they prevent the reuptake of serotonin, helping to accumulate it in synapses.
However, the experimental basis of these ideas turned out to be doubtful. This is shown by new work carried out by a team from University College London, led by Professor Joanna Moncrieff.
Scientists analyzed the results of many past experiments, the purpose of which was to find a connection between serotonin and depression. As a result, it turned out that this relationship was not shown reliably.
The authors point to a number of studies in which it was not possible to find any correlation between various aspects of the work of the serotonin system and the development of depression.
So, in one of the experiments, scientists compared the amount of serotonin and its metabolic products in the blood and in the brain in healthy people and patients with depression, but did not find a significant difference between them.
In several studies, the level of serotonin in volunteers was artificially lowered, using a diet depleted in tryptophan, the amino acid from which it is synthesized.
A careful analysis of such experiments showed that this does not always work and not all participants develop depression.
In some cases, when the authors of the studies actually managed to show a change in the work of the serotonin system in people with diagnosed depression, the scientists did not take into account the intake of antidepressants, which makes such conclusions unreliable.
Also, studies of patients with hereditary disorders of genes involved in the metabolism of serotonin did not give definite results. Some of them have indeed shown a connection, for example, between the work of the serotonin transporter protein and the risk of developing depression.
However, other works have refuted it. “The hypothesis of the development of depression as a result of reduced activity or concentration of serotonin does not receive confirmation,” the authors of the new article sum up.
“Patients should not be told that depression is due to a lack of serotonin or a chemical imbalance, or that antidepressants work by correcting these unproven abnormalities,” adds Professor Moncrief.
“We don’t understand exactly what antidepressants do in the brain.” “I have been taught all my life that depression is caused by low serotonin, and I myself teach this to students,” said another author of the work, Mark Horowitz. “Participation in this study opened my eyes, turning all past ideas upside down.”
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