Food and serotonin
Serotonin intervenes in the control of appetite and eating behavior, resulting in an early onset of satiety, a lower intake of carbohydrates in favor of proteins and a reduction, in general, in the amount of food ingested. Not surprisingly, many people who complain of a drop in mood (for example a pre-menstrual depression, see pre-menstrual syndrome) feel an important need for sweets (rich in simple carbohydrates) and chocolate (it contains and promotes the production of serotonin, because it is rich in simple sugars , as well as psychoactive substances). It is no coincidence, therefore, that some anorectic drugs useful in the treatment of obesity, such as fenfluramine, act by increasing the signal of serotonin.
The ingestion of many carbohydrates stimulates the secretion of insulin, a hormone that facilitates the entry of nutrients into cells, including amino acids with the exception of tryptophan. Consequently, after massive insulin secretion in response to hyperglycemia, the relative levels of tryptophan in the blood increase (because those of other amino acids drop). The relative increase in tryptophan facilitates its passage into the central nervous system, where it increases production. of serotonin; this triggers a classic negative feed-back mechanism that decreases the desire to consume carbohydrates. With a similar mechanism, serotonin levels also increase during physical exertion (which partly explains the antidepressant effects of motor activity); the excessive increase of this substance during strenuous and prolonged exertion is involved in the perception of fatigue.
After a meal rich in protein, and therefore in tryptophan, the concentration of this amino acid in the blood increases, without however changing the brain levels of Serotonin. This lack of effect is due to the fact that, at the same time, the concentration of other amino acids also increases in the blood which, so to speak, prevent the passage of tryptophan to the brain. For this reason, the intake of food containing tryptophan or a specific supplement does not significantly increase the level of serotonin; even the administration of the same is not possible because it is broken down before it can produce its effect.
Serotonin and intestine
Serotonin regulates motility and intestinal secretions, where "the presence of enterochromaffin cells containing serotonin is conspicuous; it causes diarrhea if present in excess and constipation if present in defect. This" action, in particular, is sensitive to the "interrelation between the" enteric nervous system "and the brain (Central Nervous System - CNS) and explains why important psychophysical stresses very often have repercussions on intestinal motility.
Serotonin and the Cardiovascular System
In the cardiovascular system, serotonin acts on the contraction of the arteries, helping to control blood pressure; it also stimulates the contraction of the smooth muscles of the bronchi, the bladder and the large intracranial vessels (a massive vasoconstriction of the cerebral arteries seems to trigger the migraine attack as well as an excessive vasodilation).
Serotonin is also present in platelets, of which it stimulates aggregation by exercising a vasoconstrictive and thrombogenic activity in response to the lesion of the vascular endothelium (for example in response to trauma).
Sexuality and Social Behaviors
The serotinonergic system is also involved in the control of sexual behavior and social relationships (low levels of serotonin appear to be linked to hypersexuality and antisocial aggressive behavior). It is no coincidence that some drugs that increase the release of serotonin and / or the activity of its receptors, such as ecstasy, induce euphoria, a sense of increased sociability and self-esteem. In addition to sexual behavior, serotonin has inhibitory effects on pain sensitivity, appetite and body temperature.
, after being released from the axon terminal, a part of serotonin interacts with the postsynaptic receptors, while the excess is degraded by MAO (monoamine oxidase) or reabsorbed (reuptake) by the presynaptic terminal, where it is stored in particular vesicles. MAO-inhibitor drugs cause an irreversible block of monoamine oxidase, increasing the concentration of serotonin and other cerebral monoamines in the CNS; they are therefore useful in the therapy of depression, even if their use is nowadays reduced due to the important side effects. At the level of the central nervous system, the serotonin present in the defect is in fact the cause of pathological drops in mood; a lack of serotonin can therefore cause depression, but also states of anxiety and aggression. Many antidepressants (such as prozac) act by blocking the reabsorption of serotonin, thus restoring and strengthening its signal, which in depressed people is particularly poor; the same action is covered by St. John's wort (or St. John's wort). Some of these drugs simultaneously increase the signal of serotonin and that of noradrenaline (serotonergic and noradrenergic effect, typical of duloxetine and venlafaxine). Some drugs with anti-migraine properties also increase the serotonin signal (they are serotinonergic receptor agonists, such as sumatriptan), while other drugs taken for the same purpose have the opposite effect (pizotifen and methysergide).
The existence of many drugs capable of interfering with the metabolism of serotonin carrying out partly diversified effects depends, as mentioned, on the presence of different receptors (there are at least 7 types), distributed in the various tissues of the body and with which their active principles.
Excess of Serotonin
An excess of serotonin causes nausea and vomiting and it is no coincidence that this is one of the main side effects of various antidepressant drugs, such as prozac (nausea arises in the first week of therapy and then subsides); ondansetron, a drug that acts as a serotonin receptor antagonist, is instead a powerful antiemetic (it prevents the gag reflex, particularly strong during chemotherapy cycles).
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