I take about 250-300 mgs a day. It does more than my meds. Like having the zyprexa on hand for when ■■■■ gets serious, but that usually involves a 6 hr nap.
I used to take it. It’s very subtle. Less is definitely more. I was afraid to take it long term.
Just a serotonin supplement. Perhaps their might be a dependency issue. It’s pretty cheap though. Pulls me out of the low times.
Should be pretty harmless it’s a natural tryptophan precursor.
50mg would be a normal dose, 250 is a heroic dose, I’m not sure I’d personally risk a dose that high. Unless you take it once in a while instead of regularly.
It’s not all at once. The body doesn’t even use most of it.
It definitely works though. I took it when I was off meds. I became optimistic and felt the optimism was all my idea, it was that subtle. At least at 50mg. I wouldn’t take it now as I’d be afraid it might somehow interact with my meds.
Also it’s reported to stop working after about 2 years of regular use anyway.
I haven’t really followed the use of 5 htp. Here is some info on it for people:
5-Hydroxytryptophan (5-HTP), also known as oxitriptan, is a naturally occurring amino acid and chemical precursor as well as a metabolic intermediate in the biosynthesis of the neurotransmitter serotonin. 5-HTP is sold over the counter in the United States, Canada, the Netherlands, and the United Kingdom as a dietary supplement for use as an antidepressant, appetite suppressant, and sleep aid. It is also marketed in many European countries for the indication of major depression under the trade ...
More related research:
Considering each group as a whole, the only significant changes in rated psychosis consisted of an increase in the first group consequent to coming off neuroleptic medication and an increase in psychosis scores associated with adding L-5HTP to chlorpromazine . Neuroleptics apparently sensitize the central nervous system to the effects of L-5HTP loading. Acute exacerbations of psychosis induced by L-5HTP can be reversed by neuroleptics.
LB Bigelow, P Walls, JC Gillin and RJ Wyatt,
Biological psychiatry , Feb 1979
L-5-Hydroxytryptophan (L-5HTP) and the peripheral decarboxylase inhibitor carbidopa were administered to chronic schizophrenic patients in three separate experiments using a double-blind placebo-controlled crossover design. The three experiments were: (i) L-5HTP administration to 15 patients who had been withdrawn from all neuroleptic medication; (ii) L-5HTP administration to seven patients maintained on haloperidol; (iii) L-5HTP administration to nine patients maintained on chlorpromazine. Although the groups were diagnostically homogeneous, individual responses were highly variable. Considering each group as a whole, the only significant changes in rated psychosis consisted of an increase in the first group consequent to coming off neuroleptic medication and an increase in psychosis scores associated with adding L-5HTP to chlorpromazine. Neuroleptics apparently sensitize the central nervous system to the effects of L-5HTP loading. Acute exacerbations of psychosis induced by L-5HTP can be reversed by neuroleptics. Our experience does not give encouragement to the hypothesis that schizophrenic illnesses arise consequent to a deficit of serotonergic function that can be treated by giving a serotonin precursor in pharmacological quantities.
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K Fukuda,
Medical hypotheses , Jan 2014
To pose a new hypothesis of schizophrenia that affirms and unifies conventional hypotheses.Outside the brain, there are 5-HTP-containing argyrophil cells that have tryptophan hydroxylase 1 without l-aromatic amino acid decarboxylase. Monoamine oxidase in the liver and lung metabolize 5-HT, rather than 5-HTP, and 5-HTP freely crosses the blood-brain barrier, converting to 5-HT in the brain. Therefore I postulate that hyperfunction of 5-HTP-containing argyrophil cells may be a cause of schizophrenia. I investigate the consistency of this hypothesis with other hypotheses using a deductive method.Overactive 5-HTP-containing argyrophil cells produce excess amounts of 5-HTP. Abundant 5-HTP increases 5-HT within the brain (linking to the 5-HT hypothesis), and leads to negative feedback of 5-HT synthesis at the rate-limiting step catalysed by tryptophan hydroxylase 2. Owing to this negative feedback, brain tryptophan is further metabolized via the kynurenine pathway. Increased kynurenic acid contributes to deficiencies of glutamate function and dopamine activity, known causes of schizophrenia.The 5-HTP hypothesis affirms conventional hypotheses, as the metabolic condition caused by acceleration of tryptophan hydroxylase 1 and suppression of tryptophan hydroxylase 2, activates both 5-HT and kynurenic acid. In order to empirically test the theory, it will be useful to monitor serum 5-HTP and match it to different phases of schizophrenia. This hypothesis may signal a new era with schizophrenia treated as a brain-gut interaction.
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5-HTP Overview and Side Effects
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