5-HTP & ecstasy

[Nagognog2]

Do NOT mention a store by name. Even if it seems harmless - NO sources means NO SOURCES. Zip. Nada. NOTA.

[radiometer]

Of all people to make such a silly mistake! Edited accordingly.

[napoleon in rags]

this is the stuff you want:



200mgHTP + 2000mg Vit C + 200mg Vit B6 for the preload

50mgHTP + 1000mg Vit C Halfway through the roll

8mg Melatonin + some soft tunes on my harp for the comedown to sleepyville*

*your results may vary

[napoleon in rags]

In the US, you can find 5-HTP at your friendly neighborhood chain store pharmacy. it just might be hard to find considering it's not really in high demand. I always find my stuff right there on the shelf, though!

You can also find it online for a couple bucks less

[psyche]

Since XTC causes oxidative stress, antioxidants should just do the trick. In blueberries, for instance, there is lots of them.

[psyche]

5-htp doesn't, as said many times, protect from any damage, but it really helps brain to recover. Ecstasy affects on serotonin like amphetamines act on dopamin: both releasing enormous amounts and blockin the re-uptake.

[bounz2dabeatz]

first off, very very little 5-htp will cross the bbb no matter what. that is y it is so inefficient. second, DO NOT TAKE LARGE DOSES OF 5-HTP. This can be very dangerous. The plant that most companies use to extract there 5-htp also contains another alkaloid that most companies do not take out. This substance is dangerous in large quantities. Be careful with 5-htp. Take it as the label suggests maybe even twice as much as it says, but not half the bottle after a rough weekend of rolling.
As for it actually working, i can say i have used it a few times and it minimally helps the hangover effects of mdma. Not to mention it gave me headaches so i never used it again.

[Alfa]

There is a lot of difference in quality between various 5-HTP products. Most are far from effective. It can provide a very good sleep.
What alkaloid of griffonia do you mean?

[bounz2dabeatz]

It's something that is being called "peak x". i found an article on erowid u can check out on the subject http://www.erowid.org/smarts/tryptop...n_info10.shtml

[Drunkken_Munkey]

Now look, I've taken 5-HTP before I roll and it didn't do nothing. I've taken 5-HTP sober, and it still didn't do anything. BUT!! I took it right as soon as I was coming down off a roll and whoa!!! I felt fucked up all over again!! In fact, I felt more fucked up than when I was rolling. I felt like I was so just so full of energy again. I was thinking that maybe the X hadn't worn off enough, and I was still kinda rolling a little bit when I took it and that's why I felt the way I did. Peepz, I don't recommend this, but you take a little bit as soon as you feel like your about to come down, you'll be in for one wild ride!!

Peace"

[Antidote]

5-HTP, in my experience, has been a godsend... any negative feelings in recovery time are negated by the seretonin boost, and as well the 5-HTP helps to make SWIM drowsy after rolling, inducing sleep, which is sometimes half the battle.

[Diego]

I´ve been taking vitamins, minerals, antioxidants, 5-htp, ginko, fishoils, etc. for years.
So far 5htp helps me to have a good sleep. I´ve tried the preloading with 5htp, with no noticeable effect.
Increasing the amount of my daily 5htp to 200mg daily two days before and saturday night I take 50 mg each hour 5 hours prior to my XTC, and I didn´t see any increase in the effects.
Actually, I feel the roll is smoother and the high not so high when I preload with 5htp, so I stopped the preloading and I take my daily 100 mg 5htp as a help for sleep and as antioxidant.

Do you want to increase the intensity of your XTC roll? well, try "popper" (amilnitrile inhalant). Inhalants are seen as "low class", but you can take a very small bottle with you and take a quick sniff now and a then. It has a very short duration, but the high and the rush are UNBELIVABLE.

Do you want to reduce the XTC hangover? Usually I roll from sturday night to sunday noon, almost every weekend. I use XTC, G, marijuana.
The best way I´ve found is to eat and sleep well sunday, monday, etc. and if you feel down on tuesday or wedensday, drink two beers. The best treatment for the "terrible tuesday" is BEER.

Forget about the 5htp as a helper for rolling or as a cure for the hangover.

[London_Bloke]

This following describes serotonin pathways and references studies that show that 5-HTP crosses the BBB. A couple of things to note: many of the studies here utilized patients with chronic depression and were drawn from a patient group diagnosed with Fibromyalgia Syndrome, because one common factor in FMS patients as a rule show very low serotonin levels. The studies did not use 5-HTP dosages the same way most of us would use common NSAIDS for pain relief, they were used as a daily maintenance medication. When 5-HTP is used only intermittently, whatever perceived relief or lack of relief can only be considered valid for the individual and is purely anecdotal. There does not appear to be any empirical evidence to support or document 5-HTP use in the ways described in the threads above.

The serotonin pathway begins with L-tryptophan. Of the eight essential amino acids, tryptophan is the least common, accounting for only about one percent of protein content. After absorption from the gut to the bloodstream, tryptophan is carried by proteins and in free form to peripheral sites, where typically 90 percent is used for protein synthesis, about one percent converted to serotonin, and the balance is used to produce niacin. It takes 60 mg of tryptophan to produce 1 mg of niacin. The enzyme tryptophan pyrrolase (tryptophan 2,3-dioxygenase) is the first enzyme in the conversion to kynurenine, picolinic acid, and niacin, and is inducible by cortisol and tryptophan.(Hindle AT. Recent developments in the physiology and pharmacology of 5-hydroxytryptamine. Br J Anaesth 1994;73:395-407) and (Birdsall TC. 5-Hydroxytryptophan: A clinically-effective Serotonin precursor. Altern Med Rev 1998;3:271-280).

In the formation of serotonin, tryptophan is hydroxylated to 5-hydroxy-tryptophan (5-HTP) by tryptophan hydroxylase, which is tetrahydrobiopterin dependent and the rate-limiting step in serotonin production. 5-HTP cannot be degraded to kynurenine, nor can it be borrowed to enhance niacin production or used as a substitute for tryptophan in protein production. 5-HTP is converted to serotonin by an aromatic amino acid decarboxylase enzyme, which is vitamin B6 dependent. Tryptophan is transported across the blood-brain barrier via a transport molecule which also carries leucine, isoleucine, and valine, and prefers leucine. 5-HTP easily crosses the blood-brain barrier and does not utilize this transport mechanism; thus, it does not compete for passage through the blood-brain barrier with these amino acids.
In the body, 5-HTP is converted directly to serotonin. It is not broken down by tryptophan pyrrolase, and it does not have to compete for transport across the blood-brain barrier. Unlike tryptophan, it is not produced commercially by a fermentation process. Instead, it is extracted from the seeds of Grifonia simplicifolia, a plant grown in West Africa. In studies utilizing 5-HTP in the treatment of depression, with dosages ranging from 200 to 3000 mg per day, it was found that, "5-HTP is of therapeutic value, particularly in the serotonin-deficient subgroup of vital depressions." (van Praag, HM. Management of depression with serotonin precursors. Biol Psychiatry 1981;16:291-310)

In a double-blind, placebo-controlled, comparative multicenter trial of 60 patients with depression randomly receiving either fluvoxamine (an SSRI) or 5-HTP orally three times per day for six weeks, outcomes were equivalent for improvements in depressive mood, anxiety, insomnia, and somatic pains. Adverse side-effects, including nausea, were higher in the fluvoxamine group. (Poldinger W, Calanchini B, Schwarz W. A functional approach to depression: serotonin deficiency as a target syndrome in a comparison of 5-hydroxytryptophan and fluvoxamine. Psychopathology 1991;24:53-81).

Reputation Comments on this post:

	Good contribution!
	most usefull info
	Thanks for the useful references!
	good stuff
	great info

[eltimmy]

I think serotonin precursors at night could be useful as a replacement for SSRI therapy; e.g., upregulating dopamine mechanisms. But not 5-HTP.

5-htp crosses the blood-brain barrier. It also causes dangerous rises in peripheral serotonin. For a similar effect SWIM would use quality-assured tryptophan.

More information: http://yarchive.net/med/5-htp.html

[London_Bloke]

Originally Posted by eltimmy

I think serotonin precursors at night could be useful as a replacement for SSRI therapy; e.g., upregulating dopamine mechanisms. But not 5-HTP.
More information: http://yarchive.net/med/5-htp.html

You are aware the link you posted is not to any study or cluster of studies, it is to one doctor's opinion on a message board, and does not reference even a single study?

Additionally, this doctor posted this on his "Doc Harris's Green Banana Award" bulletin board almost 10 years ago. It is not uncommon to cite slightly older studies when the study is well designed and has been subsequently validated in further testing. I'm sorry, but I don't consider a 10 year old opinion from one doctor to constitute "More information." In one of the earlier posts on the board the doctor says "Yeah, these abbreviations are not standardized, and I mix them up. 5-hydroxytryptAMINE (= 5-HT = serotonin)".

Mixes them up? How disquieting is that? I can only hope for his patient's sake he doesn't flub like that when he's prescribing blood pressure medication.

[eltimmy]

>You are aware the link you posted is not to any study or cluster of studies, it >is to one doctor's opinion on a message board

Indeed. However, please feel free to contest the actual facts of the matter:

a) 5-HTP causes notable & large rises in peripheral serotonin.
b) Abnormally high levels of peripheral serotonin seem to be problematic for several reasons and are implicated in heart valve dysfunction.

>>does not reference even a single study?

Look again?

J Clin Invest 1985 Oct;76(4):1485-90

Central serotonergic stimulation of aldosterone secretion.

Shenker Y, Gross MD, Grekin RJ

Serotonin stimulates aldosterone secretion both in vitro and in
vivo, and serotonin antagonism decreases plasma aldosterone
levels in patients with idiopathic aldosteronism. This study was
designed to assess the effects of the serotonin precursor,
5-hydroxytryptophan (5HTP), upon aldosterone secretion in
man, and to determine whether stimulatory effects of 5HTP are
mediated through the central nervous system. Oral 5HTP, admini-
stered as a single 200-mg dose, increased plasma aldosterone
levels from 4.7 +/- 0.6 to 13.3 +/- 2.8 ng/dl in dexamethasone-
-pretreated, normal volunteers. Peripheral inhibition of decar-
boxylation of 5HTP, achieved by pretreatment with carboxydopa, 25
mg three times daily for 3 d, significantly increased the
stimulatory effects of 5HTP on aldosterone levels (P less than
0.001). No change in aldosterone levels occurred in subjects who
received placebo after pretreatment with dexamethasone and
carboxydopa. Increased aldosterone was not accompanied by
increases in plasma levels of renin activity, potassium, or ACTH.
Plasma levels of 5HTP were markedly increased by carboxydopa
pretreatment [indicating significant liver metabolism to
serotonin in those not getting it], but peak plasma levels of
serotonin were not significantly altered [by carbidopa, not by 5-
HTP; papers below find both. Serotonin metabolism is fast enough
and platelet uptake fast enough that differences in metabolites
are all that are sometimes seen, and no difference in platelet
free plasma]. Four patients with idiopathic aldosteronism all had
an increase in plasma aldosterone levels after 5HTP administrati-
on, whereas the response in four patients with aldosterone-produ-
cing adenoma was variable. Incubation of isolated human and rat
adrenal glomerulosa cells with serotonin resulted in increased
aldosterone secretion by both sets of cells, whereas 5HTP was
ineffective in stimulating aldosterone secretion in vitro. We
conclude that central serotonergic pathways are involved in the
stimulation of aldosterone induced by administration of 5HTP.
This mechanism may be an important etiologic factor in the
hypersecretion of aldosterone that occurs in patients with
idiopathic aldosteronism.

PMID: 2997280, UI: 86034589

----------

Folia Psychiatr Neurol Jpn 1985;39(1):25-31

Endocrinological function in schizophrenic patients under
haloperidol treatment: plasma PRL, HGH and 5HT levels after
L-5HTP loading.

Hoshino Y, Kaneko M, Kumashiro H, Tachibana R

In order to examine 5HT metabolism in the hypothalamo-pituitary
(HP) system of chronic schizophrenic patients taking haloperidol
for a short or long period, chronological changes of blood 5HT,
PRL and HGH were measured after an oral loading dose of L-5hyd-
roxytryptophan (L-5HTP), a precursor of 5HT. The subjects consis-
ted of 8 male patients with chronic schizophrenia, who were
divided into the following two groups. The 1st group--4 patients
taking haloperidol (5.6 mg/day) for 8 months on an average
(short-term treatment). The 2nd group--4 patients taking halop-
eridol (4.8 mg/day) for 7.5 years on an average (long-term
treatment). The control group was made up of 9 healthy male
volunteers. As a result, the basal level of blood 5HT in the 1st
group was significantly higher than that in the control group.
The blood 5HT levels in the 1st and 2nd groups showed an equally
remarkable increase as compared with the control group. The
basal level of plasma PRL in the 2nd group was significantly lowe
than that in the control group. Moreover, in the 2nd group, an
increase in the plasma PRL level after the loading was suppress-
ed, but it showed less suppression in the 1st group. There was no
significant difference in the basal HGH levels among the control,
1st and 2nd groups. After the loading, an increase in the plasma
HGH was suppressed in the 2nd group, but the suppression was less
in the 1st group.

PMID: 3876974, UI: 86031640

----------


Eur J Clin Pharmacol 1982;23(1):81-6
Human pharmacokinetics of long term 5-hydroxytryptophan combined
with decarboxylase inhibitors.

Magnussen I, Van Woert MH

L-5-Hydroxytryptophan (5HTP) and its major metabolites 5-hydroxy-
tryptamine (5HT) and 5-hydroxyindoleaceticacid (5HIAA) were
measured in blood and cerebrospinal fluid from neurological
patients receiving steady state treatment with 5HTP. There was
accumulation of 5HT in blood platelets and 5HIAA in plasma
in all patients, despite concomitant administration of the
L-aromatic amino acid decarboxylase inhibitors, carbidopa and
benserazide. There was no correlation between the 5HTP dose and
the circulating concentrations of the aminoacid or its metabolit-
es. Preliminary comparison of the biochemical and therapeutic
effects of carbidopa versus benserazide suggest that 5HTP:
carbidopa is superior to 5HTP: benserazide. A direct proportiona-
lity between plasma 5HTP concentrations and the levels of 5HTP in
the lumbar cerebrospinal fluid was found. The binding to serum
proteins of 5HTP in the clinically relevant concentration range
of 10 to 100 microM was investigated; 19% of circulating 5HTP was
bound to serum proteins. 5HTP did not displace protein-bound
tryptophan in serum.

PMID: 6182005, UI: 83027497

----------

N Engl J Med 1980 Oct 2;303(14):782-7

Development of a scleroderma-like illness during therapy with
L-5-hydroxytryptophan and carbidopa.

Sternberg EM, Van Woert MH, Young SN, Magnussen I, Baker H,
Gauthier S, Osterland CK

A scleroderma-like illness developed in a patient treated with
L-5 hydroxytryptophan (L-5HTP) and carbidopa for intention
myoclonus. The patient had high plasma kynurenine levels that
remained high when the L-5HTP-carbidopa combination was discon-
tinued, However, levels rose futher on drug rechallenge, suggest-
ing that the drug unmasked an abnormality in one of the enzymes
that catabolize kynurenine. Plasma kynurenine was also determined
to be high in seven of 15 patients wth idiopathic scleroderma,
but not in eight patients with intention myoclonus treated with
L-5HTP and a decarboxylase inhibitor and in whom scleroderma did
not develop or in 10 patients with Parkinson's disease treated
wth L-dopa and carbidopa. Our data and studies in the literature
suggest that two factors may be important in the pathogenesis of
some scleroderma-like illness: high plasma serotonin and the
abnormality associated with elevated kynurenine.

Publication Types:
Clinical trial


PMID: 6997735, UI: 81011891

----------


Neuropsychobiology 1979;5(4):232-40

L-5HTP treatment and serum 5-HT level after L-5-HTP loading on
depressed patients.

Kaneko M, Kumashiro H, Takahashi Y, Hoshino Y

Based on 5-HT hypothesis, L-5-HTP (150 or 300 mg/day) was given
orally to 18 depressed patients. The global estimates were 2 very
much improved; 8 much improved; 3 minimally improved, and 5
unchanged. The action of L-5-HTP was usually rapid. The elevation
of the serum 5-HT level 1 week after L-5-HTP administration was
relatively lower in the 5-HTP nonresponder group, compared
with the responders. The chronological change of the serum 5-HT
level in depressed patients after an oral loading dose of 3 mg/kg
of L-5-HTP showed a gradual and slight elevation, compared with
manic and normal groups. It seemed that the therapeutic effect of
L-5-HTP on responders was related to lower 5-HT level in the
brain for their pathogenesis, and that there was a metabolic
disturbance of L-5-HTP into 5-HT in some depressed patients.

PMID: 312470, UI: 79178849

----------

N Engl J Med 1977 Jan 13;296(2):70-5
Long-term therapy of myoclonus and other neurologic disorders
with L-5-hydroxytryptophan and carbidopa.

Van Woert MH, Rosenbaum D, Howieson J, Bowers MB Jr

We evaluated the therapeutic effect of L-5-hydroxytryptophan
(L-5HTP), the precursor of serotonin (5-hydroxytryptamine),
combined with carbidopa, a peripheral decarboxylase inhibitor, in
patients with intention myoclonus and examined the serotonin
metabolites in spinal fluid, blood and urine before and
during therapy. In 18 patients with intention myoclonus due to
anoxia or other brain damage, 11 derived more than 50% overall
improvement during treatment with L-5HTP and carbidopa. Spinal-
-fluid 5-hydroxyindoleacetic acid was 35% lower in patients with
intention myoclonus than in controls (P less than 0.05). Therapy
with L-5HTP and carbidopa increased the concentration of
serotonin metabolites in urine and spinal fluid. We postulate
that a deficiency of brain serotonin is causally related to
intention myoclonus and that the therapeutic effect of L-5HTP and
carbidopa may be due to the repletion of serotonin in regions of
the brain where serotoninergic neurons have degenerated.

PMID: 401457, UI: 77056277

-----

Hey, I'll even throw you one I found in "0.16 seconds" on google.

© 2005 FASEB
A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor-independent ROS generation
Pascale Bianchi*, David R. Pimentel*, Michael P. Murphy{dagger}, Wilson S. Colucci* and Angelo Parini{ddagger},1

* Cardiovascular Medicine Section, Boston University Medical Center, Boston, Massachusetts, USA;
{dagger} Medical Research Council Dunn Human Nutrition Unit, Cambridge, UK; and
{ddagger} INSERM U388, CHU Rangueil, Toulouse, France

1Correspondence: INSERM U388, Institut Louis Bugnard-CHU Rangueil-Bât. L3 TSA 50032, Toulouse 31059, France. E-mail: parini@toulouse.inserm.fr

SPECIFIC AIMS

Reactive oxygen species (ROS) play a critical role in cardiac hypertrophy. We have recently shown that the serotonin-degrading enzyme monoamine oxidase A (MAO A) is an important source of hydrogen peroxide in rat heart. The aim of the present study was to define whether hydrogen peroxide generated by MAO A contributes to the hypertrophic effects of serotonin in cardiac myocytes.

PRINCIPAL FINDINGS

1. Serotonin stimulates cardiac myocyte hypertrophy by receptor independent and receptor-dependent mechanisms
Exposure of myocytes to serotonin for 48 h increased 3H-leucine incorporation and total cellular protein content. The effect was observed at 1 µM and reached a maximum at 5 µM (3H-leucine incorporation: +43%; total protein content: +22%) (Fig. 1 A). To define the mechanism responsible for myocyte hypertrophy by serotonin, we investigated the ability of various compounds to modulate the serotonin effect. The effect of serotonin on both 3H-leucine incorporation and total protein content was prevented by pretreatment with the amine transporter inhibitor, imipramine, or the irreversible MAO inhibitor, pargyline (Fig. 1B ). Previous studies showed that hypertrophic effect of serotonin requires stimulation of 5-HT2B receptors. In accordance with these results, we observed that SB 206553, a 5-HT2B receptor antagonist, reduced the serotonin stimulated 3H-leucine incorporation only by 30% (P<0.001). Similar results were observed using the 5HT2 receptor antagonist ketanserin (data not shown). These results show that, in addition to the receptor-mediated hypertrophic effect, serotonin induces cardiomyocyte hypertrophy by a mechanism requiring its internalization into myocytes and degradation by MAOs.


>Mixes them up? How disquieting is that? I can only hope for his patient's sake >the doesn't flub like that when he's prescribing blood pressure medication.

Irrelevant to this discussion. Feel free to address the actual meat of the issue, or don't.

[London_Bloke]

I am not required to prove or disprove your point. You are. If you post using Doc Harris's Banana Blog, be prepared to defend your position.

[eltimmy]

I already offered you references. It is well-established that:

a) Abnormally high levels of peripheral serotonin are implicated in a number of health issues, including the gradual hardening of certain heart valves.
b) Ingestion of 5-HTP results in abnormally high levels of peripheral serotonin, excreted in urine.

Proceed from there -- at your caution.

[dnb warrior]

SWIM has taken 5-htp a number of times, usually about 2 per day, usually a few days before and after a roll... he has noticed no noticeable effect and vowed to stop wasting stupid amounts of money on this placebo.


but how would he even know if it was having an effect or not? it might just be that he is in a slightly better mood for reasons that actually
relate to the real world rather than the chemicals he puts into his body.

[Powder_Reality]

This post is a little old, but SWIM will add his 2 cents. SWIM has done MDMA both with 5-HTP and without 5-HTP.

Personally, SWIM didn't notice much of an increase in the effects from pre-loading. However, he did notice quite a positive effect from post-loading. He used 2 other vitamins as well though. SWIM was in attendance of a music festival, and had consumed that night: 5 beer and 2 lines of cocaine before dropping his MDMA. (*Note: Do not mix cocaine and alcohol with MDMA. SWIM learned the hard way that it drastically blurs the effects of the MDMA, not to mention the increased health problems.) Throughout the course of about 4-5 hours, SWIM proceded to consume about 400-500 mg of MDMA. (This is only a rough estimate. SWIM was buying molly in capsules, and they appeared to be roughly 100mg each). SWIM also smoked a little weed throughout the night, although not very much.

By the end of the night, SWIM felt (understandably) very drained, and returned to his car to get some sleep. He had been drinking water steadily throughout the night, and forced himself to eat some bread and an apple before falling alseep. Before falling alseep, he consumed 100mg of 5-HTP, 1000mg of Alpha-Liphoic Acid, and 1000mg of Vitamin C. (SWIM should point out that the recommended dose for Aplha-Liphoic Acid after MDMA use was 100mg, but he read the sheet wrong in his state). SWIM put his headphones on and was able to fall asleep very easily. The only problem was that he kept waking up every 1-2 hours. He woke up about 5 hours later and had a chat with his car neighbour, before cosuming another dose of all his vitamins. He fell back asleep for about another 5 hours and woke up feeling...pretty much fine.

SWIM would've thought that the high amount of MDMA and other chemicals he had consumed would have left him feeling extremely "fried" and sketchy, as they usually do. But this time he woke up feeling basically fine. He felt a little spaced out and "blank", but besides that he had a nice afterglow and felt quite pleasant.

So in SWIM's experience, a dosage of the said vitamins in combination with some fresh fruit and a good night's sleep can do wonders for his comedown. SWIM also attributes the smooth comedown to taking pure MDMA instead of the plethora of adulterated (albeit cheaper) pills floating around the camp area.

*The report that SWIM read to figure out which vitamins to take can be found here: http://www.erowid.org/chemicals/mdma...article3.shtml

[eltimmy]

>Would regular 5-HTP use lead to a chemical dependancy, and possible inhibit >the brain's normal production of seratonin, instead relying on the supplements?

Yes and in my opinion this is one way serotonin-based antidepressants work.

Check it:

Dopaminergic mechanism of antidepressant action in depressed patients
Willner P, Hale AS, Argyropoulos S.
Department of Psychology,
University of Wales Swansea,
Swansea SA2 8PP, UK.
J Affect Disord. 2005 May;86(1):37-45

ABSTRACT

Clinical studies have not yet determined a common mechanism of action for antidepressant drugs, which have primary sites of action on a variety of different neurotransmitter systems. However, a large body of evidence from animal studies demonstrates that sensitisation of D2-like dopamine receptors in the mesolimbic dopamine system may represent a 'final common pathway' in antidepressant action. The present study aimed to determine whether, consistent with data from animal studies, the clinical antidepressant action of selective serotonin reuptake inhibitors (SSRIs) is reversed by acute administration of a receptor antagonist selective for D2-like receptors in the mesolimbic dopamine system. The participants were patients diagnosed with major depressive disorder (n=8) who had been treated successfully (Hamilton Depression Scale<10) with selective serotonin uptake inhibitors (fluoxetine, citalopram or paroxetine); and age-matched, non-depressed, untreated volunteers (n=10). They attended a psychiatric research ward on an out-patient basis, and received double-blind acute administration of either placebo, or a low dose of the selective dopamine D2/D3 receptor antagonist sulpiride (200 mg), in a counterbalanced order. Mood and psychomotor effects were assessed using visual analogue scales and the Fawcett-Clark Pleasure Capacity Scale. Sulpiride slightly improved subjective well-being in the control group, but in the antidepressant-treated patients, sulpiride caused a substantial reinstatement of depressed mood. These data are consistent with the hypothesis that sensitisation of D2-like receptors may be central to the clinical action of SSRIs.

>e has noticed no noticeable effect and vowed to stop wasting stupid >amounts of money on this placebo.

The effects are meant to arise with extended use.

Again I would like to suggest tested, high-quality tryptophan over 5-htp for interested parties .

[GForce]

If 5-HTP is long lasting enough to knock SWIM out for over half a day and still have him feel groggy when he wakes up, I doubt there is an over-the-counter stimulant they could add to 5-HTP. They could always put caffiene or something in it but it wouldn't really be of any use after an hour.

[London_Bloke]

They don't put anything in caffeine tabs to help you sleep or keep you from getting jittery because it's advertised as a stimulant. 5-HTP is marketed as a sleep aid and appetite suppressant.

Don't know if either of those statements are really true - and really neither does the FDA as they are not required to validate claims on dietary supplements.

[Beeker]

I take 200mg of 5-HTP at night then 800mg of DL-phenylalamine in the morning with 200mg of caffiene and 10mg D-amphetamine and have done so for a while. It has almost completely cured my bi-polar depression.

[MadShroomer]

Swim's 2 cents. 5-htp boost seritonin levels and can help with depleted seritonin after having Seritonic chem's in the brain. Vitamine c helps prevent "brain damage" wich is shown in mdma research and Vitamine B is neccessary for N20 indulgance. SWIM thinks that Zoloft or st.Johns wort would be good to take after the experience and personally aregular 100mg of zoloft a day won't effect the experience of MDMA and other Tryptamines but is shown to reduce negative 'effects' on the brain.
Vitamine c (500-1000mg) upon injestion and again 5 hours later.
Water (h2O) ascorbic acid is a dyeretic so hydration is important.
Vitaine b (supplement combo) for the hang over type (sleep is good on this stuff)
5-htp (or turkey :P) to increase the day after levels in the brain