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5-HTP experiment to regain the magic

WSH

Bluelighter
Joined
Nov 30, 2012
Messages
360
My tolerance is such that a 120mg dose of MDMA gives me almost no effects at all (whereas one year ago the same batch affected me strongly, so it's not the quality).

I've read that high doses of 5-HTP are supposed to bring the magic back and that would make sense if MDMA tolerance was caused by serotonin depletion, because 5-HTP is a serotonin precursor.

So I tried it.

I took about 1500mg 5-HTP over a period of about one week.

Then i took 120mg MDMA and there were almost no effects again.

And so I'm reporting back that high-dose 5-HTP can be added to the long list of things that don't work to bring the MDMA magic back.
 
Taking 5-HTP in high doses regularly will increase your tolerance to MDMA. It doesn't reduce tolerance to MDMA, that is myth. It's only good for the come down and maybe the day after for the next day hangover.
 
Taking 5-HTP in high doses regularly will increase your tolerance to MDMA. It doesn't reduce tolerance to MDMA, that is myth. It's only good for the come down and maybe the day after for the next day hangover.

thats correct , 5 htp will make you roll less if you take it before you roll.

Moving on, I took it after 5-mapb and got serotonin syndrome quite bad. so no more 5-htp right after rolling for me.
 
Taking 5-HTP in high doses regularly will increase your tolerance to MDMA. It doesn't reduce tolerance to MDMA, that is myth. It's only good for the come down and maybe the day after for the next day hangover.

Yes, I also found 5-HTP to be effective in treating the hangover, so there's at least some use for it.

But for regaining the magic it didn't work, so now my theory is that it isn't caused by serotonin depletion, but by receptor desensitization.
 
Yes, I also found 5-HTP to be effective in treating the hangover, so there's at least some use for it.

But for regaining the magic it didn't work, so now my theory is that it isn't caused by serotonin depletion, but by receptor desensitization.
Or it could be that 5-HTP doesn't cross the blood-brain barrier and as such isn't readily converted to serotonin in the brain. This seems to be more likely to me. It doesn't have to be receptor downregulation, though it could very well be of course
 
Or it could be that 5-HTP doesn't cross the blood-brain barrier and as such isn't readily converted to serotonin in the brain. This seems to be more likely to me.

It does cross the blood-brain barrier using the same transporter as L-Dopa:

5-Hydroxytryptophan: a clinically-effective serotonin precursor
5-HTP is well absorbed from an oral dose, with about 70 percent ending up in the bloodstream. It easily crosses the blood-brain barrier and effectively increases central nervous system (CNS) synthesis of serotonin.
 
It does cross the blood-brain barrier using the same transporter as L-Dopa:

5-Hydroxytryptophan: a clinically-effective serotonin precursor


egcg causes 5-htp and l -dopa both to cross the bbb. Of course a good dose of egcg most be had, most green teas have very low egcg levels, like not enough to cause 5-htp to cross the brain blood barrier. When i took 5-htp after my roll I used about 350 egcg with 100 mgs of ro 5-htp..again I dont recommend this and most likely will never use 5-htp again after any roll
 
It does cross the blood-brain barrier using the same transporter as L-Dopa:

5-Hydroxytryptophan: a clinically-effective serotonin precursor

the question is if it is stays in the bloodstream long enough for a significant amount to reach the transporter and have an effect. 5-htp is broken down quickly in the gut and the bloodstream.

your paper said:
Some concern has arisen regarding whether 5-HTP should be used only in con- junction with a peripheral decarboxylase in- hibitor (PDI) such as carbidopa. The argument is essentially that without a PDI, 5-HTP will be converted into serotonin in the peripheral circulation, negating any potential CNS bene- fit from 5-HTP. However, this argument ignores scores of clinical studies in which 5- HTP was given alone and in which significant clinical benefit was seen, with no significant adverse effects.

if that is their only agrument that it reaches the brain, it's pretty much a non-argment considering that most of the studies done with 5-htp are not very good in design and have very few participants.

http://www.sciencedirect.com/science/article/pii/S016372580500135X said:
Definitive, large-scale studies of efficacy and safety have not been conducted for 5-HTP. In conducting our own review of the literature, we were able to identify 27 studies that evaluated the efficacy of 5-HTP for depression (total N = 990). Because these studies were heterogeneous in terms of design, duration, and dose, meta-analysis is not feasible. We therefore employed a descriptive approach, broadly categorizing these studies according to design.

Eleven of these studies were double-blind, placebo-controlled (DB-PC) studies (Table 1). Among the 11 DB-PC studies, the authors reported that 5-HTP was superior to placebo in 7 of them. However, the sample sizes in all these studies were quite small, and only 5 of these studies were able to show statistical significance. Of these, 1 was a monotherapy relapse prevention study (van Praag & de Haan, 1981), 3 were augmentation studies (Alino et al., 1976, Nardini et al., 1983 and Quadbeck et al., 1984), and 1 tested a 5-HTP/dopamine agonist combination against placebo, rather than 5-HTP alone (Rousseau, 1987).

if only 5 out of 11 studies reach significance it already looks pretty bad. if only one out of those used 5-htp as monotherapy things look even worse.

same paper as above said:
In a recent study of healthy volunteers, the addition of carbidopa resulted in a 14-fold increase in 5-HTP plasma levels (Gijsman et al., 2002)

so if you don't add a peripheral decarboxylase inhibitor such as carbidopa or egcg it seems as if >92% of the 5-htp you're consuming is already going down the drain...

of course this is in conflict with a study from 1980 where they found a bioavailibility of 70%, but most of the time it's advisable to rather trust studies done in the last few years more than ones that were done 35 years ago. the analytical methods as well as the standards for scientific work has definitely increased since then.
the authors of the my paper above think that said:
review of the literature reveals a lack of data on dosage and usage considerations.
 
5-htp shouldn't be taken in that high of a dose, and you should take 5-htp with omega 3 tuna oil and vitamins and a good diet, and it should be longer than just a week esp if your suffering bad serotonin depletion
 
Yes, I agree, combining it with a decarboxylase inhibitor would have been better, but I don't have access to carbidopa.

EGCG was mentioned, I don't know anything about it, is it a good decarboxylase inhibitor?

If so, I would try this serotonin repletion experiment again with sufficient decarboxylase inhibition and report back again.
 
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