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5 htp and Heart Damage

Serotonin has a curious effect on the circulatory and cardiovascular systems: it acts as a growth factor to repair damaged tissue. Unfortunately, this repair sometimes creates more problem than harm. Find out if and how 5 HTP supplementation can cause sufficient damage to the heart and what you can do to prevent this from happening.
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5 HTP and Serotonin

5 HTP or 5-hydroxytryptophan is a naturally occurring amino acid synthesized from L-tryptophan, an essential amino acid.

Because 5 HTP is not found in food, it is widely sold as a dietary supplement. The 5 HTP used in such dietary supplements are obtained from the seeds of Griffonia simplicifolia, a plant native to Africa.

5 HTP is important in human health because it is the precursor of two important neurotransmitters: serotonin and melatonin. While 5 HTP is the immediate precursor of serotonin, it is merely an intermediate in the synthesis pathway of melatonin.

Unlike tryptophan, 5 HTP is easily taken up into the central nervous system since it does not compete with other essential amino acids for absorption. Since serotonin cannot cross the blood-brain barrier, 5 HTP is the supplement of choice to increase the level of serotonin in the brain.

Once 5 HTP gets through to the brain, it is converted to serotonin in one reaction that is catalyzed by a decarboxylase enzyme and vitamin B6.

Therefore, all the effects of 5 HTP, including both therapeutic effects and side effects, are due to its ability to increase serotonin levels in the body but especially in the central nervous system.

What Serotonin Does

In the central nervous system, serotonin is responsible for mood, sleep and appetite just as it also contributes to memory and learning. However, the effects of serotonin extends well beyond the brain.

In fact, 90% of the serotonin produced in the body is released outside of the brain by the enterochromaffin cells of the gastrointestinal tract.

In the gut, serotonin is responsible for intestinal motility.

The excess serotonin released by these specialized gut cells is then drained away by blood vessels around the intestines. Once it is inside blood vessels, serotonin is stored in platelets. Therefore, the platelets are responsible for transporting serotonin to various organs through the circulatory system.

The platelets release serotonin once they bind to clots. The released serotonin then controls the process of blood clotting and also serves as a vasoconstrictor and a healing factor.

All over the body, serotonin acts through its receptors. There are 7 classes of serotonin receptors numbered from 5 HT1 to 5 HT7.

When serotonin binds to these receptors, it can produce either inhibitory or excitatory response depending on the location and type of receptor. These receptors are also occupied by serotonin receptors such as antidepressants.

Through these receptors, serotonin controls the release of other neurotransmitters (e.g. GABA, glutamate, acetylcholine, dopamine, norepinephrine and epinephrine) and hormones (e.g. cortisol, vasopressin, oxytocin, prolactin and substance P).

On its own, serotonin can serve as a growth factor to help wound healing. It can also trigger the release of growth factors like insulin-like growth factor.

The ability of serotonin to serve as growth factor for tissue repair also involves serotonin receptors. For example, when the liver is damaged, more 5 HT2A and 5 HT2B receptors are produced. This increases the number of binding sites for the serotonin circulating in the blood and stored in platelets. The increased binding sites serve as the base for serotonin to increase cellular growth and repair the damaged liver.

A very similar process happens in the heart, and it is both a merit and demerit of serotonin in the cardiovascular system.

Serotonin and Fibrosis

When platelets are recruited to the site of damage, they release the serotonin they have bound up.

Therefore, serotonin release accompanies platelet binding to damaged tissue. The vasoconstriction that follows this release stops bleeding from the site of damage. It also speeds up healing by encouraging the growth of new muscle fibers (connective tissue) to cover the wound.

The vasodilatory action of serotonin results from the release of nitric oxide while the fibrotic growth is believed to be mediated by serotonin binding to 5 HT1B receptors.

While vasodilation is a welcome effect of serotonin in the cardiovascular system, fibrosis is mostly considered a side effect. Serotonergic fibrosis is not only restricted to serotonin; in fact, it is mostly experienced with drugs that affect the serotonergic system.

Major Serotonin Drugs Causing Fibrosis
  • Antimigraine drugs that act by causing vasoconstriction through serotonin such as ergotamine and methysergide
  • Appetite suppressant drugs such as fenfluramine
  • Drugs for Parkinson’s disease such as pergolide which bind to 5 HT2B receptors as a side reaction even though they bind to dopamine receptors to produce their therapeutic effect
  • Recreational drugs such as Ecstasy which binds to 5 HT2B receptors

These drugs can cause fibrosis in different parts of the body but especially fibrosis in the cardiac valve and peritoneum.

Serotonin and Cardiac Fibrosis

Cardiac fibrosis results from the thickening of cardiac muscles or heart valves. Fibrosis in the heart is caused by the abnormal increase in fibroblast.

The new cardiac muscles generated by such fibrosis is stiffer than and not as stretchable as normal cardiac muscles. This happens because the fibrocyte cells responsible for stitching together collagen for heart muscles are overstimulated by serotonin and serotonin drugs. Therefore, the muscles produced are thicker and less flexible than normal heart muscles.

Cardiac fibrosis can easily lead to heart failure by thickening some of the valves of the right side of the heart.

The most direct connection between blood levels of serotonin and cardiac fibrosis is the evidence gathered from people who consume foods rich in serotonin.

A prime example of such foods is matoke, a meal prepared from steamed, green bananas or plantains. Matoke is the national dish of Uganda and also eaten in Rwanda, and it supplies an excessive amount of serotonin. In the African countries where this food is a staple, right-sided cardiac fibrosis is quite common.

Tryptophan, 5 HTP, SSRIs and Cardiac Fibrosis

Although L-tryptophan increases blood serotonin levels, the risk of heart damage from its supplementation is considered low.

Ideally, tryptophan faces a stiff competition to cross into the brain since it shares the same transport mechanism with amino acids such as leucine, isoleucine and valine. Therefore, the amount of tryptophan that successfully gets to the brain from each dose of the supplement will be lesser than the actual dose.

The amount of tryptophan that is prevented from entering the brain can circulate around the body and be used to produce more serotonin which will then be stored in the platelets where it can cause cardiac fibrosis.

However, the utilization of L-tryptophan supplement in the production of serotonin outside the brain does not have big effect on the plasma level of serotonin in the body.

SSRIs (selective serotonin reuptake inhibitors) which are antidepressants and the most commonly prescribed serotonin drugs are also considered to produce lower risk of heart damage.

Since SSRIs amplify serotoninergic signals instead of initiate them, it is unlikely that they will cause cardiac fibrosis even though there is a potential risk for such to occur. SSRIs do not increase serotonin levels but allow the neurotransmitter to stay longer at the synapses where it acts.

Because SSRIs are mostly active at serotonin receptors in the central nervous system and heart damage is a serotonin effect produced outside the central nervous system, these drugs have a lower tendency to cause cardiac fibrosis.

5 HTP, on the other hand, can possible cause heart damage although there is no report of such association yet.

Since 5 HTP is a short jump to serotonin, it can increase serotonin blood level significantly and possible cause valve disease or heart fibrosis. However, it will require large doses and long supplementation with 5 HTP for this to happen.

By co-administering carbidopa with 5 HTP, it is possible to prevent the conversion of the amino acid to serotonin outside of the brain. Therefore, the use of carbidopa with 5 HTP will not cause serotonin blood levels to rise while still ensuring that serotonin levels in the brain rises. This action eliminates any risk of heart damage from 5 HTP supplementation.

The combination of carbidopa and 5 HTP is used in the treatment of Parkinson’s disease. The side effects of this combination are nausea, vomiting and a skin reaction resembling scleroderma.

The first 2 side effects can be reduced by administering granisetron.

Serotonin and Carcinoid Syndrome

Carcinoid syndrome refers to the set of symptoms caused by the continuous release of certain vasoactive substances from malignant tumors in the small intestine. These tumors may also be found in the rectum, appendix, pancreas and lungs.

The substances released from carcinoid tumors include serotonin, histamine, prostaglandins, bradykinin and polypeptide hormones.

Therefore, carcinoid syndrome can increase the level of serotonin in the blood.

The symptoms of carcinoid syndrome are due to high levels of the vasoactive substances released. The most common symptoms of this syndrome are abdominal cramps, flushed skin and diarrhea. If the carcinoid tumor is left in place, the sustained increased serotonin levels may cause heart damage (especially fibrotic right valve) after several years.

Since carcinoid syndrome can cause heart damage on its own, increasing serotonin levels by taking 5 HTP supplements will only worsen the problem.

Carcinoid syndrome effectively increases the risk of heart damage due to 5 HTP. Therefore, people with this form of tumor should refrain from taking 5 HTP supplements for any of its indicated uses





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