Depression: more evidence refutes famous ‘serotonin theory’

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According to the famous “serotonin theory”, most depressed patients are usually treated with drugs aimed at increasing the level of the hormone in the brain. Paradoxically, the number of serotonin transporters increases at the end of antidepressant treatment, which seems to cast doubt on the real involvement of the neurotransmitter in the phenomenon of depression. Today, more recent research confirms this doubt by synthesizing previous research, gathering evidence that refutes the original theory. The results showed no difference in serotonin and transporter levels between “healthy” and depressed people. Moreover, the induced decrease in serotonin levels in healthy people does not necessarily cause depression. These new data have the potential to revolutionize understanding of the mechanisms of the disease and research into ways to treat it.

Since the 1960s, it has been generally accepted that depression is associated with an imbalance (particularly a drop) in the levels of serotonin in the brain. Since this neurotransmitter is involved in mood regulation, most treatments for depression aim to increase its levels in the brain, including selective serotonin reuptake inhibitors (SSRIs), which block molecules that transport the hormone away from neurons. Other therapies also target norepinephrine, but the scientific evidence that it causes depression is even weaker than those associated with serotonin.

While more and more research has debunked the serotonin theory, it continues to be widely accepted by medical institutions and the general public. SSRIs continue to be one of the main first-line drugs for the treatment of depression.

Some experts argue that there is insufficient evidence that abnormally low levels of serotonin can cause depression. Moreover, clinical trials of existing drugs would show little difference in efficacy from placebo. Antidepressants will have more “pain-relieving” effects, which can affect patients’ mood.

This lack of conclusive evidence for the serotonin theory is a major limitation of current antidepressant therapies. Because the real mechanism of depression is not fully understood, a new English study published in the journal Molecular Psychiatry is one of the first to synthesize studies that may or may not link serotonin to depression.

According to the study in question, the common belief about the neurochemical origin of the disease is most likely erroneous, and its origin may be more organic. The results do provide additional evidence to disprove the link between low serotonin and depression. Thus, this study may support decisions about taking antidepressants for patient safety.

No difference between healthy and sick controls

The first series of studies reviewed by English researchers concerns the comparison of levels of serotonin and its metabolites present in the blood or cerebrospinal fluid of people with or without depression. Overall, this study would show no difference between healthy and sick people.

What’s more, a sample of 10 studies involving hundreds of volunteers found that an artificially induced decrease in serotonin levels caused depression, on average, in only 1 in 75 participants.

Studies involving tens of thousands of patients have also accounted for genetic variations, such as regulation of the serotonin transporter precursor gene. Result: no difference was found in the frequency of this gene between healthy and diseased controls. Although a well-known preliminary study has shown some correlation between this gene and daily stress, others suggest the opposite and believe that such a connection does not exist.

In addition, comparison of levels of serotonin transporters has shown increased activity of the hormone in people suffering from depression. However, these people had previously taken conventional antidepressants. Thus, in the absence of treatment, the levels of these vectors will not differ whether a person is sick or not. On the contrary, some studies suggest that taking antidepressants may, on the contrary, cause a decrease in serotonin levels.

Molecular Psychiatry.

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