The serotonergic hypothesis of depression

Depression is, together with anxiety disorders, one of the most frequent and known disorders or psychopathologies worldwide throughout history. The investigation referring to what exactly it is and what causes it has is therefore something very relevant for the scientific community and for the population in general. Based on the data reflected by the research, a large number of explanatory models have been proposed that take into account both biological and environmental factors.

Within the former, attempts to explain depression as a product of balance problems or the levels of certain neurotransmitters. And among these hypotheses, one of the most popular and recognized we find the serotonergic hypothesis of depression.

• You may be interested in: "Major Depression: Symptoms, Causes, and Treatment"

serotonin

Serotonin is one of the main and best known neurotransmitters present in the brain. This hormone, which in addition to the nervous system can be found in other body systems (in fact the largest part of the serotonin in our body is found outside the nervous system, especially in the digestive tract), was

one of the first neurotransmitters to be identified. It is synthesized from tryptophan, which in turn can enter the body through the diet.

Among the numerous functions it performs, it is considered linked to the regulation of circadian rhythms and energy levels (especially due to its important presence in the suprachiasmatic, ventromedial and paraventricular nuclei), thermal control, appetite, libido, relaxation and feelings of well-being and comfort. It is also considered one of the main hormones linked to mood maintenance, being altered in those people who have depressive-type problems.

• Related article: "Serotonin: 6 effects of this hormone on your body and mind"

Serotonergic hypothesis of depression

The serotonergic hypothesis of depression is one of the best known biological hypotheses that attempt to explain the causes of depression. He proposes that the causes of depression are a deficit or lack of serotonin in the brain. This theory is based on the role of serotonin in regulating mood, indicating that a decrease in levels of serotonin in the nervous system or in key points such as the limbic system would be responsible for the symptoms depressive.

Likewise, the so-called permissive hypothesis of serotonin indicates that the alteration and decrease of serotonin at the brain level generates a dysregulation of other neurotransmission systems, such as that of norepinephrine. It is part of the monoaminergic hypotheses, which suggest that the mental alterations characteristic of depression are due to a malfunction, synthesis or transmission of neurotransmitters such as serotonin, catecholamines (dopamine and norepinephrine).

Pharmacological treatments

When treating depression, different models and techniques have been used, both at the psychotherapy level and at the pharmacological level. In this last aspect, the main psychoactive drugs used for the pharmacological treatment of depression are those that regulate or alter monoamine levels, being especially used those that increase serotonin levels.

Specifically today, the most common psychoactive drugs when it comes to combating depression are SSRIs, Specific Serotonin Reuptake Inhibitors. This is a group of drugs whose main mechanism of action is (as its name says) to prevent presynaptic neurons to reuptake or absorb the serotonin they have released, so that it remains in the synaptic gap and the level of this neurotransmitter in the brain is generally increased.

Despite this, it must be taken into account that serotonin is not the only neurotransmitter involved, and that there are alternatives that focus on stimulating the levels of other substances, either secondary or major. For example, drugs that, in addition to serotonin, are increasingly successful norepinephrine levels increase, the ISRN, generating an equivalent level of symptomatic improvement.

Nor should we forget that drug treatment generates changes in the brain that reduce symptoms, but generally do not treat the basic problem that the person himself links to depression (for example, the absence of reinforcers, low perception of control, stress or anxiety prolonged). Psychological therapy has been shown to be more effective in the long term., which suggests that depression is not a merely serotonergic problem.

Caution: we are talking about a hypothesis

The existence of alterations in serotonin levels in the brain is somewhat documented, and it is assumed that one One of the main neurobiological problems that patients with depression present is a deficit of serotonin. It has also been observed that the decrease in the levels of this hormone generates depressive symptoms.

However, it is still true that these deficits are simply linked to depressive symptoms, without necessarily being the cause. In fact, the causes of depression are not yet fully known, being generated by the combination of biological and socio-environmental elements. Likewise, other neurotransmitters related to depressive symptoms or that may participate in their improvement have been found, such as norepinephrine, dopamine or GABA.

Thus, it should not be assumed that the serotonergic hypothesis describes the ultimate cause of depression, since there are many factors that play a role in its genesis. That is why today the serotonergic hypothesis has lost power and it has come to be seen not as a cause of depression but as a generator of a biological vulnerability to it.

The serotonergic hypothesis and the use of medications such as SSRIs have received much criticism, among other aspects for the fact that excessive attention has been focused on them and have greatly limited the development of other models and drugs. The debate about the actual effectiveness of antidepressants when it comes to treating the problem itself is also widely known.