Rainier
27th March, 2008, 03:30 PM
I actually did try it briefly, but stopped due to it bothering my stomach. This supposedly goes away, but now I'm afraid to try. I also saw those old posts from "Dr. Steven Harris" and it has worried me too. Some old meds such as Phen-Fen and supplements such as 5-HTP apparently raise blood serotonin levels in addition to those in the brain, which could be hard on organs such as the heart and lungs. So what level of extra serotonin in the blood is safe? As far as I can tell this still seems to be a matter of debate, although I would like to think that the recommened dosage is safe. On Wikipedia it says the following: (with credible foot notes from medical journals) By the way...the last sentence seems to be the most concerning.
Risks and Side Effects
5-HTP raises blood serotonin levels, and because of the risks associated with elevated levels it should only be taken under the advice of a medical professional (See Chronic diseases resulting from serotonin 5-HT2B overstimulation (http://en.wikipedia.org/wiki/Serotonin#Chronic_diseases_resulting_from_serotoni n_5-HT2B_overstimulation)). For instance, elevated blood serotonin levels are associated with cardiac valve failure and acute or chronic pulmonary hypertension.
Comprehensive clinical data on other side-effects of 5-HTP are not available. Nevertheless, some product marketers claim that it causes fewer side effects than traditional antidepressants. The basis for these claims are anecdotal and have not been verified scientifically. Side effects of 5-HTP may include nausea, constipation, gas, drowsiness, decreased sex drive, anxiety, numbness, paresthesia, breathing problems, palpitations, chest pain, hallucinations and insomnia. 5-HTP can also have adverse interactions with other natural and traditional drugs. [1] (http://www.wholehealthmd.com/refshelf/substances_view/1,1525,747,00.html)
Chronic diseases resulting from serotonin 5-HT<sub>2B</sub> overstimulation
<dl><dd> Main article: Cardiac fibrosis (http://en.wikipedia.org/wiki/Cardiac_fibrosis)
</dd></dl> In blood, serotonin stored in platelets is active wherever platelets bind, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic, to aid healing. Because of these effects, overdoses of serotonin, or serotonin agonist drugs, may cause acute or chronic pulmonary hypertension from pulmonary vasoconstriction, or else syndromes of retroperitoneal fibrosis (http://en.wikipedia.org/wiki/Retroperitoneal_fibrosis) or cardiac valve fibrosis (endocardial fibrosis (http://en.wikipedia.org/wiki/Endocardial_fibrosis)) from overstimulation of serotonic growth receptors on fibrocytes.
Serotonin itself may cause a syndrome of cardiac fibrosis when it is eaten in large quantities in the diet (the Matoki banana of East Africa) or when it is over-secreted by certain mid-gut carcinoid (http://en.wikipedia.org/wiki/Carcinoid) tumors. The valvular fibrosis in such cases is typically on the right side of the heart, since excess serotonin in the serum outside platelets is metabolized in the lungs, and does not reach the left circulation.
Serotonergic agonist (http://en.wikipedia.org/wiki/Agonist) drugs in overdose in experimental animals not only cause acute (and sometimes fatal) pulmonary hypertension (http://en.wikipedia.org/wiki/Pulmonary_hypertension), but there is epidemiologic evidence that chronic use of certain of these drugs produce a chronic pulmonary hypertensive syndrome in humans, also. Some serotinergic agonist drugs also cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis (http://en.wikipedia.org/wiki/Retroperitoneal_fibrosis), as well as right-sided cardiac valve fibrosis (http://en.wikipedia.org/wiki/Cardiac_fibrosis).
In the past, three groups of serotonergic drugs have been epidemiolgically linked with these syndromes. They are the serotonergic vasoconstrictive anti-migraine drugs (ergotamine (http://en.wikipedia.org/wiki/Ergotamine) and methysergide (http://en.wikipedia.org/wiki/Methysergide)), the serotonergic appetite suppressant drugs (fenfluramine (http://en.wikipedia.org/wiki/Fenfluramine), chlorphentermine (http://en.wikipedia.org/wiki/Chlorphentermine), and aminorex (http://en.wikipedia.org/wiki/Aminorex)), and certain anti-parkinsonian dopaminergic agonists, which also stimulate serotonergic 5-HT<sub>2B</sub> receptors. These include pergolide (http://en.wikipedia.org/wiki/Pergolide) and cabergoline (http://en.wikipedia.org/wiki/Cabergoline), but not the more specific lisuride (http://en.wikipedia.org/wiki/Lisuride). A number of these drugs have recently been withdrawn from the market after groups taking them showed a statistical increase of one or more off the side effects described.
Because neither the amino acid L-tryptophan (http://en.wikipedia.org/wiki/L-tryptophan) nor the SSRI (http://en.wikipedia.org/wiki/SSRI)-class antidepressants raise blood serotonin levels, they are not under suspicion to cause the syndromes described. However, since 5-hydroxytryptophan (5-HTP (http://en.wikipedia.org/wiki/5-HTP)) does raise blood serotonin levels, it is under some of the same scrutiny as actively serotonergic drugs.