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From: B. Harris)
Subject: 5-HTP + B6 = Trouble; Doc Harris Presents Green Banana Award (was: US 
	ban on tryptophan)
Date: 29 Dec 1996

Simon Friedman <>

Jack Challem wrote:
> If you look around, you will find a few companies now selling
tryptophan supplements to doctors in the US. The molecular
structure is slightly different, basically just the immediate
precursor molecule. I checked with my FDA contact, and he said
yes, it's true.<

>>You can also buy 5-hydroxytryptophan from at least 2 mail-order
outlets that I know of. 5-HTP is the next step in metabolism from
trypophan on its way to become serotonin.

    Comment: Yes, and in fact 5-HTP needs only one more step to
become serotonin-- a decarboxylation.  The sequence is:

Tryptophan --> 5-HTP --> Serotonin.

An exactly analogous sequence is:

Tyrosine --> L-DOPA --> Dopamine

   In both cases the end product neurotransmitter does not get
across the blood brain barrier very well, but all of the
precursor molecules above are transported by the brain's large
neutral amino acid pump, and they get into the brain fine.  Thus,
if you are a Parkinson's patient who wants to raise dopamine
levels, you must take L-DOPA, not dopamine.  Similarly, it would
do you no good to take serotonin-- you must take tryptophan or
5-hydroxytryptophan (5-HTP).

   Now for the complications. (Aren't there always complications
in life?)  The final reaction to the neurotransmitter in both the
case of dopamine and serotonin, is decarboxylation, and the same
enzyme (the aromatic L-amino acid decarboxylase) is involved in
both conversions.  This decarboxylase enzyme is present in the
liver, and it acts in the case of L-DOPA to convert the compound
to dopamine before it can make it into the brain (and if this
happens, the L-DOPA is wasted).  The decarboxylase enzyme uses B6
as a cofactor for this reaction, and for this reason a
Parkinson's disease patient taking L-DOPA cannot take more than
the RDA of B6, because doing so would act to neutralize
oral L-DOPA too quickly.  These days, almost all Parkinson's
patients on L-DOPA take the drug in a combination with an
artificial decarboxylase inhibitor, called Carbidopa (the
combination is called Sinemet).  But even with Carbidopa,
Parkinson's patients are advised not to exceed a daily dose of B6
of 25 mg, since more will overwhelm the Carbidopa effect, and
cause pharmacologic L-DOPA to be destroyed in the liver before it
can get into the brain.

   Now, Carbidopa, because it acts on the same metabolizing
enzyme in the liver, performs exactly the same preservative
service for 5-HTP as for L-DOPA.  For this reason, neurologists
have experimented with giving Carbidopa to people who needed to
take 5-HTP to raise brain serotonin (this in the days before
selective serotonin re-uptake inhibitor antidepressants like
Prozac were available).   The problem today with 5-HTP-selling
companies bypassing doctors and going to laymen, is that a lot of
health enthusiasts with problems who are enthusiastically taking
5-HTP are NOT taking Carbidopa, but they ARE taking a lot of B6
in one form or another.  Yet without Carbidopa, more than a few
milligrams of extra B6 per day would be expected to insure that
most dietary 5-HTP gets turned into serotonin before it can get
into the brain.

   Alas, one company I know packages their 5-HTP in 50 mg
capsules with 10 mg of B6.  They do this ostensibly so that 5-HTP
can be converted to serotonin in the brain.  Duh.  This insures
that any 5-HTP will get converted to serotonin in the liver
instead, and thus never make it to the brain.  Vitamin B6 is the
*LAST* thing you want in an 5-HTP product.

   At the very best, people who take B-vitamins with 5-HTP, or
who take 5-HTP products with B6, waste their money.  All this
would be merely humorous (caveat emptor) were it not for some
other facts.  At worst, ignorant people fooling with 5-HTP
actually risk their health, since serotonin in the peripheral
blood is not benign.  Serotonin causes not only harmless flushing
and diarrhea, but people with serotonin secreting tumors (hindgut
carcinoids) also have problems with fibrosis of the endocardium
and valves in their right hearts, which can cause heart failure.
This fibrosis is caused by the serotonin.  This effect can also
be seen with dietary intake of only modest amounts of serotonin,
and there has actually been described in the medical literature a
tribe of South Sea islanders with right heart fibrosis as a
result of eating green banana mash (matuki), which poisons them
with its serotonin content.  No, I'm not making this up.  The
hydroxylation of tryptophan is a rate-limiting step in the
peripheral production of serotonin, and one bypasses it at one's

   How much does it take?  Several hundred milligrams of 5-HTP
taken per day, if converted to serotonin, would result in a
urinary excretion of the serotonin metabolite 5-hydroxyindoleac-
etic acid (5-HIAA) of several hundred milligrams also-- an amount
well within the urinary excretion range of the average person
with a serotonin producing carcinoid.  Such a dose of 5-HTP
certainly would result in a serotonin blood load comparable to
that of green-banana-diet eating people who have
serotonin-induced heart valve disease.  Normally, people do not
excrete breakdown products of more than 10 mg of serotonin
metabolites per day.  If you take one capsule per day of 50 mg
5-HTP with 10 mg B6, however, you would be expected to go to at
least 50 mg per day of 5-HIAA in the urine.  Less metabolism in
the liver (less B6) would result in less 5-HIAA in the urine.  If
you are going to take 5-HTP, therefore, you probably need 5-HIAA
urine monitoring, to figure out just how big a dose of systemic
serotonin you're actually getting (and incidentally, how much
5-HTP you're wasting).  See a doctor!

   For all the reasons outlined above, I am presenting those
vitamin companies who sell 5-HTP with B6, or who sell it alone
but don't warn their customers about 5-HIAA monitoring or B6
intake, a special award: the Green Banana Award.  This honor is
for those supplement-sellers who monkey around with people's
health before consulting with some really good nutrition and
medical specialists to make sure they don't f*&% up and hurt
somebody.  Hopefully, companies which receive the Green Banana
Award will contemplate its message, and will thereby change their
behavior in order to avoid some of the less-coveted awards which
otherwise await them in the future: the Civil Damage Award, for
instance, or even the All-Expense-Paid Guest of the Federal
Government Award.

                              Steven B. Harris, M.D.

From: B. Harris)
Subject: Re: 5-HTP + B6 = Trouble; Doc Harris Presents Green Banana Award (was: 
	US ban on tryptophan)
Date: 30 Dec 1996

In <5a75t6$> (Robert A.
Walston) writes:

>Does anyone else have information regarding 5-hydroxy tryptophan and
>the heart fibrosis problem Dr. Harris discusses?  I just ordered some
>50 mg capsules (without B-6), and now I am hesitant to take them.
>Would the same warning apply to tryptophan itself?  Were all of us who
>received such wonderful relief from insomnia from tryptophan before
>the FDA took it off the market endangering our lives?  If tryptophan
>itself doesn't create excess serotonin in the bloodstream and 5HTP
>does, then maybe I should have ordered pharmaceutical grade tryptophan
>(available as a veterinary supplement) instead!  Also, is there a real
>risk from taking just 50 mg of 5HTP a night (and no supplemental B-6)?
>Any information would be appreciated.
>-Bob Walston

The same warning does NOT apply to tryptophan, because the
hydroxylation of tryptophan to 5-HTP is rate limiting, and happens
essentially only in nervous system tissue.  It's bypassing this by
eating 5-HTP or serotonin which is the problem.  Pure tryptophan is not

Whether taking 50 mg of 5-HTP will give you problems, I don't know, as
I do not know what is the lowest dose of serotonin which has been
reported to cause the cardiac fibrosis (I'll let you know after some
further research).  And also (again) whether all of a 50 mg dose of
5-HTP gets turned into serotonin in your liver, will depend on your
vitamin status.  If you don't take any supplements at all, you're in
much better shape in this regard, than if you do.  As I noted, the only
way to really be sure is to do a 24 hour urine collection for the
serotonin metabolite 5-HIAA (5-hydroxyindole acetic acid).

                                             Steve Harris, M.D.

From: B. Harris)
Subject: Re: Dumb Question? About Amino Acids prescription
Date: Fri, 31 Oct 1997

In <> neiGHBor <> writes:

>> Somebody's going to get valve damage from 5-HT and sue Life
>> Enhancement.   And I imagine the defence is going to be: "How could WE
>> have KNOWN??"
>You mean 5-htp also right? Since that turns into 5-ht. How much 5-htp
>would you consider safe? Is 50 mg per night with 10 mg b6 too much?
>Or maybe you meant 5-htp all along. Either way please tell me.

Yeah, these abbreviations are not standardized, and I mix them up.
5-hydroxytryptAMINE (= 5-HT = serotonin) is what causes heart damage.
Never eat it.  It doesn't get into the brain anyway, since it's not
transported by the large neutral amino acid transport system.

5-hydroxytrytophan (5-HTP) is what's sold as a serotonin brain
precursor.  It is taken up into the brain.  If you could keep if from
getting converted to serotonin in the liver, you'd be in great shape.
Taking 10 mg of B6 a day, however, is going to get most of it converted
to serotonin before it has a chance to get into the brain.  50 mg a day
without carbodopa is too much, since most of it will get converted to
serotonin, and 50 mg a day of "outside the brain" serotonin or so is
about the amount associated wtih heart damage in carcinoid syndrome.

                                         Steve Harris, M.D.

From: B. Harris)
Subject: Re: 5-HTP doesn't  seem to convert to 5-HT in the bloodstream, only in 
	the brain.
Date: Tue, 04 Nov 1997
Newsgroups: alt.dreams.lucid,,

In <> neiGHBor <> writes:

>But that study said that even when they put tryptophan in the blood,
>5-htp levels in the blood rose.
>Does tryptophan turn into 5-htp in the blood only when high amounts of
>tryptophan are put into the bloodstream? Otherwise shouldn't lots of
>5-htp be entering the brain in people with a normal diet?

I think this is correct-- otherwise normal tryptophan eating would
cause increases in 5-HTP and 5-HT and urine 5-HIAA (as in the paper).
But none of this happens to normal people, who excrete less than 10
mg/day of 5-HIAA, and don't have to be careful to eat low tryptophan
diets (for instance) when being checked for carcinoid by urine 5-HIAA
levels (they do have to avoid bananas and pinapples, though!).  All in
all, the paper you cite is a strange one, and I cannot explain the
results.  Must be some odd effect of super massive tryptophan loading.

>In the study where they put tryptophan into the bloodstream, 5-htp
>levels in the blood rose, so couldn't one look at the effect of diets
>high in tryptophan instead?  And wouldn't tryptophan with b6 be
>dangerous also?

   As I say, it's never been seen with dietary tryptophan.  This must
be an odd effect of IV loading of massive amounts.

>What do you think is more likley:
>	That those Baganda banana mush eaters had high levels of
>serotonin in the blood and that that is necessary for the danger.
>	That even barely detectable increases in blood serotonin are

    I would guess, to tell the truth, that high levels of serotonin in
the blood are actually necessary.  Blood levels ARE elevated in the
carcinoid (the rebuttal paper you cite disputes this, but the latest and
best of all the carcinoid studies finds significantly elevated
serotonin levels in carcinoid patients with fibrosis, vs carcinoid
patients without it).

   Why didn't serotonin levels go up in the paper you cite?  I
suggested not enough B6.  Perhaps more important, however, is the fact
that serotonin will be made from 5-HTP in the liver, and THIS serotonin
may not make it though the lungs, which destroy it with monoamine
oxidase (to turn it into 5-HIAA), so it never gets to a peripheral vein
to be measured as serotonin/5-HT.  Thus, the serotonin exists ONLY in
the circuit between liver and lungs.  Unfortunately, that circuit
contains the right heart, which is where the valve disease is in
carcinoid, and in serotonin eaters.  And that's why the disease is NOT
in the left heart, and why urine 5-HIAA levels are a better correlate
of heart disease than peripheral serotonin levels, which don't reflect
right heart levels when the serotonin comes from liver or gut.  So
don't pay too much attention to this paper (or, rather, to the
conclusions that the 5-HTP sellers draw from it).

   Interestingly, the valve disease is apparently due to serotonin
stimulation of myofibrocytes, which proliferate and go crazy, and make
the valves stiff.  The process in serotonin-associated valve disease is
histopathologically identical to that seen in fenfluramine, ergotomine,
and methylsergide valve disease.  These latter drugs are one and all
serotonin receptor agonists.  But fenfluramine and dexfenfluramine
aren't susceptable to the lung monoamine oxidase system, and so they
(perhaps no surprisingly) produce valve disease on both sides of the

   This is all an interesting story, some of which has become untangled
in just the last few months.  Perhaps I should write all this up again
for posting here on Usenet.

                                         Steve Harris, M.D.

From: B. Harris)
Subject: Re: 5-HTP doesn't  seem to convert to 5-HT in the bloodstream, only in 
	the brai
Date: Wed, 05 Nov 1997
Newsgroups: alt.dreams.lucid,

In <>
(Syd Baumel) writes:

>No, the textbooks say that's the largest fraction in the body as a whole.
>To quote from a 1986 pharmacology textbook: "In humans, about 90 percent
>of the total serotonin in the body is in enterochromaffin cells in the
>gastrointestinal tract; the remaining 10 percent is primarily in the
>platelets and brain." As for the 10 mg figure, that's roughly how much
>serotonin there is in the entire body, including the CNS's 10%, according
>to a scholarly review on serotonin in Drug Topics, October 10, 1994.
>Mind you, I don't know to waht extent that 90% in the GI wall is normally
>segregated from the rest of the body; if it is, then the difference
>between 1 or so mg of serotonin normally present in the rest of the body
>and the 50 to 900 mg that the therapeutic dose range of 5-HTP could
>achieve is immense and perhaps, as you argue, more than the body can
>safely cope with.

   I'm astonished if it's really true that the stomach neurons have 10
times more serotonin than the brain (I shall check).  If the whole
system has only 10 mg in it, that's a turnover of the whole pool in 24
hours, since that's about how much is metabolised.  Hmmm.

>>> In light of the research in which high blood levels of 5-HTP seemingly
>>> didn't translate into high blood levels of serotonin, is it possible,
>>> perhaps, that the the platelets act as a buffer, soaking up excess
>>> plasma serotonin?
>>   You don't get high blood levels of serotonin if you take blood after
>>it's already been through the lungs.
>That's a good point -- darn it ;-) (yes, I read your follow-up post to
>neiGHBor after I posted the message you replied to here).  But you still
>leave hanging the question of whether the platelets could come to the
>rescue.  Fenfluramine is a serotonin releaser and reuptake inhibitor,
>actions which the body may have a harder time counteracting than merely
>having to keep a surge of serotonin in the liver from running amok.  Do
>you know if fenfluramine also releases serotonin from platelets?  I
>assume it at least prevents serotonin's reuptake by those platelets. If
>it does both, locally in the heart, lungs, etc., we're dealing with a
>much more pernicious influence than 5-HTP could possibly be.

   A good thought (since I throught of it also <g>), but it seems not
to be the case.  Mice given dexfen have LOWER serotonin levels in blood
generally.   Dexfen is a plenty good enough S2 agonist on its own,
without having to do it's other reuptake and release tricks (which is
probably what makes it a long lasting anorectic, when pure SSRI
antidepressants generally work only temporarily-- harder to adapt to
something that is also a pure agonist).  If you give a mouse an
overdose of Dexfen, you know what happens?  Death by acute pulmonary
hypertension and resp arrest in about 15 minutes.  The stuff acts
directly on lung capillaries via smooth muscle S receptors.   And
there's that fact that heart lessions with dexfen, like those with the
serotonin agonists methylsergide and ergotamine, are bilateral.  You
don't see that in carcinoid UNLESS the lesions are bronchial and
serotonin is making it into the left sided circulation via pulmonary

>But that doesn't mean that I'm ready to let 5-HTP off the hook.
>Considering how popular it's becoming, there's a crying need for research
>to be done to confirm or refute these concerns.  Not just the heart, but
>the lungs and perhaps skin tissue of people taking 5-HTP for any length
>of time should be examined for signs of fibrotic hardening/thickening.

   Yes, and the sort of peritoneal fibrosis seen in carcinoid and
chronic serotinergic agonist drug toxicity (not SSRIs).

>Given the fenfluramine experience, a large sample size wouldn't be
>necessary, at least as far as the heart damage is concerned -- in fact,
>any doctor who prescribes it to more than a handful of patients could
>potentially come up with useful data.



From: B. Harris)
Subject: Re: 5-HT and Heart Risk (was: Vitamin Vultures (was Re: Life Extension 
	HIV protocol)
Date: 3 Dec 1998 18:57:58 GMT

In <744uqe$> "kean" <>

>Steve Harris, said:
><(for example, they don't sell 5-HT because of me), but otherwise their
>supplement division is planned and run by other folks.>
>If you don't mind me asking, why did you not want them to sell 5-HTP?
>Maureen in Mukilteo


   5 hydroxytryptophan or 5-HTP (but not so much tryptophan) is
converted in the liver to 5-hydroxytryptamine/serotonin (5-HT), which
is not something you should have a lot of in your blood (it's nice to
keep it behind the blood brain barrier).   Chronic use of drugs that
act on serotonergic receptors on cardiac myocytes (ergotomine,
methylsergide) have been known to cause fibrosis and pulmonary
hypertension from vessel constriction, and also (more
dangerously) a hypertrophic proliferation of endocardial cells that
causes valve problems. Serotonin itself does all this if it gets into
the blood in quantity, and people with (carcinoid) mid-gut tumors that
dump serotonin into the blood, sometimes get this kind of (easy to
diagnose on autopsy) valve disease.  As ALSO do West Africans who eat
too much matoki, a green banana staple full of serotonin.  (That pretty
much does it for the argument that the carcinoids are making something
else which causes the valve problems-- if they do, it's something also
in green bananas BESIDES serotonin.  Which would be something that
would rack up as up there with the worst bad coincidences in medicine
to date; and that's not all--- read on)

   Not long ago there was a diet drug called fenfluramine which was
(among other properties) a direct serotonin agonist (as shown by its
ability to cause instant overdose death in animals by pulmonary
hypertension), just like the ergot drugs and serotonin itself-- but not
like SSRI antidepressants that raise serotonin levels only indirectly,
and then only in th brain, not the blood (they actually lower levels in
blood).  Fenfluramine caused pulmonary hypertension, and -- surprise--
myocyte proliferative valve disease.  "Gosh," said the doctors and the
FDA--- "who would ever have guessed it would do THAT?"  Duh.

   Fenfluramine is off the market.  But 5-HTP (unregulated by the FDA
right now becaues it appears in bananas and can therefore be claimed to
be a food supplement) is typically recommended to be given in doses
about equivalent to the serotonin amounts excreted into the blood in
people with carcinoid tumors who get heart disease (50 mg a day).  If
most of the ingested supplement 5-HTP is turned into serotonin/5-HT
before it can be taken up by the brain (which can't take up serotonin
directly), then there are potential problems.  Extra B6 and no
carbidopa (the way 5-HTP is often given) should exacerbate this
premature liver metabolism.  If people taking 5-HTP for years for
depression or sleep eventially come down with cardiac disease, I know a
lot of people who will say "Gosh, who could have guessed this danger"?
I've been going on about it on the net, and even managed to get a
mention of the problem in a popular book (Ray Sahalian's book on
5-HTP).  But he doesn't mention my name, and he doesn't look carefully
at the arguments.  Poor research on that.  I think he'll be one of the
ones screaming the loudest if the worst happens.

                                        Steve Harris, M.D.

From: B. Harris)
Subject: Re: 5-HTP (was: Ignorant Steve B. Harris)
Date: 23 Feb 1999 00:23:59 GMT

In <> writes:

>>   In all cases where valve problems are associated with high blood
>>serotonins, the daily amounts of serotonin released into the
>>bloodstream needed to do the nasty [deed] (judged by urine metabolites)
>>is about 50 mg a day.
>	Egad! You mean my love of chocolate could lead to MVP? Nooooo!

   Don't think there's much in chocolate. That's phenylethylamine.

>On a more serious note (and more lines to keep up with netiquette),
>has anyone done a correlation between taking tryptophan and pulmonary
>hypertension and/or cardiac valve problems? MAOIs? Conceivably,
>someone could be doing a lot of damage to themselves with the wrong
>diet while on an MAOI or if they take tryptophan as, say, a natural
>(read organic) sleep aid.
>Pete Womack, MT(ASCP).

   No, probably not.  Tryptophane, at least if uncontaminated, is
probably pretty safe.  Even the FDA agrees, since they still (very
covertly) approve it being added to infant formulas.  But their excuse
for taking it off the market due to contamination some years ago (a
problem now fixed) continues to be an excuse for a more restrictive

   You know: remember when that airliner bound for France was
supposedly blown up by a bomb a couple of years ago?  Which got us all
those restrictions about having to show a driver's licence before you
can fly, so that some computer somewhere has a record of everywhere
you've traveled by air, and when?  Well, turns out the airliner was
never proved to have been anything other than a mechanical failure (of
what sort never determined, but probably a fuel tank explosian).  But--
guess what-- you still have to show that driver's license and answer
those questions.  And the sniffers that sniff for nitrates now can be
built to sniff for anything.  Coming soon:  ID necessary to travel by
bus.  And smart highways which tell what cars go where and when.

   In any case, to return to the subject, tryptophan is not metabolized
to serotonin peripherally to any large extent, because the rate
comitting step or for that is the 5-hydroxylation, done by an enzyme
found in neural tissue (I think perhaps exclusively).  The chemists
have bypassed this regulatory step with 5-HTP.  Serotonin is supposed
to be confined behind your blood brain barrier, where 99% or something
of it is.  A little leaks out of neural tissues in your gut and gets
taken up by platelets, and performs a few odd functions, but mostly,
it's not supposed to eaten in large quantities, and the same goes for
the neural precursor 5-HTP (since your liver then easily converts this
to serotonin, which does your brain no good since it cannot get in).

                                     Steve Harris, M.D.

From: B. Harris)
Subject: Re: 5-HTP (title respectfully changed)
Date: 23 Feb 1999 00:54:33 GMT

In <>
shapere@aol.comicrelief (Shapere) writes:

>In article <7ar6ur$>,
> B. Harris) writes:
>>Because it gets turned into serotonin in your liver, and dumped into
>>your blood (depending on your B6 status, in part).  Same enzyme does
>>the job which does it for L-dopa (so it goes to worthless dopamine
>>before it can get across the blood brain barrier).  Your system is not
>>built to handle much serotonin in the blood.  SSRI's don't increase
>>serotonin levels in blood (only in the brain), but fenfluramine, as
>>well as methysergide and ergotomine, are all direct serotonergics (as
>>shown by their direct pulmonary hypertension on toxicity studies).
>I have a question...can you reassure me and provide a good rationalization for
>why MAOIs wouldn't do this too? (I mean, since MAO is *everywhere*.) Is there
>no serotonin whatsoever outside the CNS (under normal conditions)?

    Very little.  Though you have to count neuroendocrine-like cells in
the gut (enterochromafiin cells) as CNS (they really aren't, but act in
many of same ways).  So ar as your blood and tissues go, there's just a
scosh that leaks out of such neurons and neuron-like cells, in the gut.
Serotonin is metabolized by MAO, so in theory, your levels could go up
with an MAO inhibitor, indeed.  Don't know if this has been described
(another medline search required).  Such drugs have yet to be
associated with heart valve problems, so my guess is that you're okay
unless you eat too many green bananas (ie, they are a staple in your

>How extensively is 5-HTP usually metabolized by the liver, anyway?

   That depends entirely on your B6 status, and how much your
decarboxylase enzymes are occupied by other jobs.  So I can't say.  So
far as I can tell, nobody has yet done the critical experiment of
measuring urine 5-HIAA (the ultimate serotonin metabolite) in the urine
of people taking 5-HTP.  For people experimenting with the stuff, it
might be a good idea, though.

>>But serotonin does more than just cause pulmonary hypertension.  It
>>also causes direct proliferation of myocytes, which grow where they are
>>not supposed to, and cause heart valve deformities.
>That's interesting...I suppose serotonin syndrome could cause mitral valve
>prolapse too, then?

   More rarely.  Serotonin per se mostly does not make it through the
lungs (where it's metabolized), which is why left heart problems are
rare in serotonin eaters and in gut-carcinoid tumors, (unless,
interestingly, you actually have tumor metastases in the lungs).  No, I
have no idea what effect MAO inhibitors have on that.  Interestingly, a
lot of the serotonin-agonist left heart pathology is due to
non-serotonin chemicals which ACT like serotonin, but are not
metabolized in the lungs.  Fenfluramine being one.

>(Nobody ever found a murmur or anything until after I'd had CSS (4/97) -
>I'd never made the connection. Interestingly, I never had panic attacks
>before then either.)
>Any recommended reading on this subject? (Bearing in mind that I'm just a
>clueless pre-med?)

    None that I can put my finger on.  Somebody needs to write a review
of the various ways of getting serotonin-agonist valve syndrome.  I had
to put my own synopsis together from a number of rare and rather
unlikely sources (the Matoki-eater heart pathology literature is all
from the 50's and 60's).  The fact that such a review has not been done
is probably one reason why a lot of people still don't quite believe in
this pathological mechanism.  Even after fenfluramine.

                                   Steve Harris, M.D.

From: B. Harris)
Subject: Theoretical Dangers of 5-HTP (was Re: [Fwd: L-5-hydroxy Tryptophan 
Date: 7 Apr 1999 14:06:10 GMT
in Message-ID: <7edpba$g8q$>

In article <>, wrote:
> Go to http://www.dejannews then to Power Search, then enter
HTP-5 in the subject column and in the
poster's colum and this newsgroup in the newsgroup column.
You'll get them.<

>I did this. I got 37 posts. I sampled about 15 at random. Not a
single citation in one of them, nor even a reference to an
author. Harris makes a few allusions to serotonin conversion in
the liver.

>Did a Medline search on (5-HT or 5-HTP) and liver and convert.
Got two articles, one using yeast, one in rats, neither partic-
ularly relevant to the topic at hand.

>Did another Medline search on (5-HT or 5-HTP) and liver and B6.
One citation, about leucine, and only tangentially about seroton-
in, but only about brain serotonin, not serum serotonin.

>I've done all this before, with different Medline searches, and
can find no citations to the things that Dr. Harris is talking
about. He won't provide any references, just uncited essays.

>I'm still waiting for citations. If Dr. Harris is basing his
speculation about heart problems from 5-HTP supplementation, he
*must* have some references.

Greg Nigh
Student, National College of Naturopathic Medicine
(, for whom I do not pretend to

Comment from Harris:

I have lots of references, but do not have all of them at hand at
this very moment.  However, let me suggest that you naturopathic
students learn to use MEDLARS a little more creatively.  The
thing is a computer program and it doesn't know what you're
trying to ask or find out, and it won't spoon feed you.  It's not
safe to do a couple of text word searches off the top of your
head, and conclude that I, or anybody else in biomedicine, must
therefore be talking out of my hat.  If you do that, I'm probably
going to rub your nose in it when I get around to it.

If you're having a problem finding papers which show that 5-HTP
administration raises serotonin blood levels a lot (and levels of
the serotonin metabolite 5-HIAA a lot also), I have included 5 of
them below, all human studies.  They aren't the only ones out
there, but these have this information in the abstract
itself.  Now, go back and find them (and the others) yourself, on
medline.  I leave this as an exercise for the student, because
I'm not going to spoonfeed you, either, so long as you decide not
to act like a student.

If you persist in being unpleasant,
grasshopper, you get the up-your-nose treatment instead.


For those joining this debate late, the subject is what nastiness
serotonin-agonist drugs (drugs which act directly on serotonin
receptors), and of course serotonin itself, do to the heart.  It
has been known for some time that serotonin causes proliferation
of cardiac myocyte cells, and that such a proliferation appears
to be what causes the syndrome of stiffening, thickening,
whitening, and dysfunction of heart valves in people taking
serotonergic agonists such as methylsergide and ergotamine
(identical pathology in these cases).  Exactly the same odd and
distinctive pathology as an effect of a drug was recently
discovered (surprise) in the serotonergic agonist
dexfenfluramine, which problem caused it to be removed from the

This may have been a shock to the public, but The Powers That Be
knew very well beforehand that dexfenfluramine was a direct
serotonin agonist (and not just a brain active neuronal re-uptake
inhibitor, which it is, also), since it has long been known to
have direct serotonin-like vasoconstrictive effects in the lungs,
as do all drugs in this direct agonist class.  For example,
injection of an overdose of dexfenfluramine in mice causes death
in minutes from acute pulmonary hypertension, something that will
never happen with Prozac or Zoloft (which raise serotonin levels
in the BRAIN, not the blood-- and even then not for weeks).  And
the FDA knew very well, long before the valve thing (duh...) that
dexfenfluramine occasionally caused pulmonary hypertension in
humans, too.  The rest should have been pretty much a yawner when
it finally showed up.  But as we heard, it just shocked the FDA.
Who knew?,  they said.

Well, a few people guessed, and did say.  So why was the stuff
kept on the market for so long?  First, because many of these FDA
folks are apparently idiots (see my discussion of government).
The FDA does not exactly hire the top researchers in the country.

Second, because nothing else worked, long term, in this class,
for weight loss, and there was a lot of economic push to keep the
fen in fen-phen.  For some reasons not well understood, appasta-
tic neurons adapt to the high serotonin levels caused by SSRIs,
and the weight loss effects caused by them disappear about the
time they really start to work on depression.  And probably this
isn't coincidence, since the same slow receptor changes probably
mediate both effects.  But since dexfenfluramine had another and
more direct action, its effects were harder to turn off.
Nevertheless, it's now gone off the market.  People don't want to
get thin as in _The Thin Man_.

Are we out of danger as regards this odd valve syndrome caused by
serotonin-acting drugs?  Well, consider that cardiac myocytes
weren't designed by Mother Nature to proliferate in response to
dexfenfluramine.  They respond to natural serotonin in
development, and possibly also to it as a trophic and injury
repair factor in platelets, when small amounts of damage occur,
and platelets adhere to the site (platelets take up serotonin
from the blood and are loaded with it-- they dump it on anything
they stick to).  And there are two separate lines of evidence
that excess (supra-physiologic) blood serotonin itself causes
this same valve syndrome.

First, the very same syndrome is seen in people with midgut
carcinoid tumors, that secrete serotonin into the blood.  And it
is seen only in the right side of the heart, consistent with
serotonin being oxidized in the lungs and not reaching the left
heart (the exception is when tumors have metastasized to the
lungs and thus bypass them).  Not all studies have shown that the
amount of serotonin secreted by such tumors correlates with
serotonin blood levels and urine serotonin metabolites (5-HIAA),
but the largest and more carefully done ones DO find a signific-
ant correlation.  That's hard to ignore.  Correlation is not
causation, to be sure, but on the other hand, as in the case of
smoking and lung cancer, we do have a mechanism, and many other
disparate examples.  Nevertheless, there are a few diehards in
cardiology who propose that other bad things from carcinoid
tumors are doing the dirty deed.  Like bradykinin.

Except that in the 1950's and early 60's (second line of
evidence) this syndrome was ALSO described in matoki eaters in
West Africa.  Matoki is a kind of green banana used as a dietary
staple in these populations, which get this same odd right sided
valve disease, which looks as though they all have carcinoid
tumors or are taking dexfenfluramine.  Except they aren't.  But
it just so happens that matoki contains the largest amount of
serotonin of any natural food.  Not bradykinin, or dexfenfluram-
ine or ergotamine, etc.  And the levels of serotonin metabolite
5-HIAA in the urine of this population are about the same
elevated levels (50 mg a day) as carcinoid patients who develop
right heart valve disease.  Nobody else gets this much from a
natural food.  At some point the coincidences start to pile up.
No, scientists haven't been able to reproduce this in animals.
But they haven't been able to reproduce lung cancer by cigarette
smoke, either.

Do we in the West eat serotonin?  No, not much.  Serotonin isn't
even a good dietary supplement to raise levels in the brain,
because it doesn't cross the blood brain barrier, which
transports amino acids and their analogs.  Serotonin is a simple
amine and lacks the carboxyl group to look like an amino acid.
So nobody sells it as a dietary supplement.

Tryptophane, the amino acid, does get into the brain and raise
serotonin after being hydroxylated to 5-hydroxytryptophan (5-
HTP), then decarboxylated by the aryl amino acid decarboxylase in
the brain, which is B6 dependent.  But tryptophane was taken off
the market by the FDA due to contamination problems about a
decade ago, and hasn't been seen since.  It's still added to baby
formula, so the FDA must figure the problems with manufacture
have been fixed.  But they aren't about to give you the power to
mess with your brain serotonin levels.  Who do you think you are,

Tryptophane isn't converted to much serotonin in blood (toxic
stuff there!) because the body wisely puts the committed step
enzyme, the 5-hydroxylase, behind the blood brain barrier, where
any serotonin made doesn't leak out again to nail your heart.  So
tryptophane is a natural food, but a safe one, when pure.

Alas, with tryptophane gone, health food stores now 5-HTP in
place of it, with the idea that you can do that 5-OH step
yourself in a chemlab, and not in your neurons, to get serotonin.

And they get away with it as a "food supplement," because there
is some 5-HTP in bananas, too (though not much).  The problem is
that unlike tryptophane, 5-HTP really DOES raise blood levels of
serotonin, since the liver contains a good aryl decarboxylase
(also B6 dependent) which turns 5-HTP to serotonin in varying
amounts and dumps it into your blood.  From where it cannot get
into your brain, and thus no doubt chews on your heart valves
some before you can metabolize it in the MAO systems in your
lungs, into 5-HIAA.  If metabolized in the liver to any large
extent, amounts of 5-HTP being given for depression and other
problems are enough to easily give the critical toxic 50 mg a day
of 5-HIAA which marks people at risk for valve disease.

And there is reason to believe that it is metabolized to a large
extent, especially if you take B6 (actually included in some 5-
HTP supplements, go figure).  We know serotonin levels go way up
in blood on 5-HTP, and that's from liver metabolism.  And so do
5-HIAA levels, and that's from metabolism of serotonin which
never made it too your brain.  And we know the situation with
liver decarboxylation of 5-HTP should be expected to be much the
same as for people with Parkinson's disease who take L-DOPA.  L-
DOPA is an amino acid analog (a hydroxylated tyrosine) which is
decarboxylated in the liver by the *very same aryl decarboxylase
that 5-HTP uses*, into dopamine (rather than the counterpart
serotonin) before IT can get into the brain.  That's a side
effect, and something you don't want to happen.  This dopamine is
stuck, also, and just hangs around raising your blood pressure
and doing nothing good.  So these people with Parkinson's who
take L-DOPA must take liver carboxylase inhibitors (carbidopa, as
in Sinemet) and stay away from too much B6.  I think even the
naturopaths have gotten this far.

But not to the next step, which is that it follows that, at
minimum, people taking 5-HTP should for the same reasons also do
these things that Parkinson' patients do (take carboxylase
inhibitors and no B6).  Except that few do.  And few monitor
their uninary 24 hour 5-HIAAs to see how much they are converting
to toxic serotonin outside the brain, either.  But yet this is a
widely available lab test, which any large lab will do (it's a
medical test for carcinoid tumors, but can as easily see green
banana craving and 5-HTP mis-metabolism.)

My guess is that we are headed for the same problems with 5-HTP
that we had with dexfenfluoramine, and that these will be used as
an excuse to further regulate the supplement industry, just as
happened with tryptophane.  I would suspect a giant plot to do
this, in fact, if I thought these people at the FDA were that
sophisticated.  But they aren't.  They're merely ignorant and
overworked and arrogant, and the healthfood people are greedy and
arrogant, and the consumer-- well, the consumer had better be on
the nets, these days.  Or be very, very conservative about new
health food products.  These days you may not die of a misprint,
as Twain said, but from lack of biochemistry knowledge and
ability to search medline.  Scary, but there you are.  And since
your doctor never learned any nutrition, you won't get any help
there.  And it doesn't look like the naturopaths are taking up
the slack, if Mr. Nigh and the rest of the yokels I see writing
pamphlets in health food stores are any indication.  5-HTP is
naturopathy's answer to Prozac, don't you know-- and they're not
going to give it up easily.  For the same reasons doctors didn't
give up dexfenfluramine.

So it looks bad all over, in the complicated future.  The bottom
line is that if you don't read, read, read, you're going to
suffer, suffer, suffer.  Probably best in that case to hoe your
beans and try to simplify, simplify, simplify.

As for the naturopaths, I suggest they rethink 5-HTP some.  It's
going to hurt when it hits.  When physicians got caught by
dexfenfluramine, they had the FDA to blame, which in turn was
mighty lax about letting the public know how much evidence was in
the literature beforehand to predict the kind of problem they
eventually had.  Golly, they said, who would've thunk it?  The
journalists didn't exactly go pull out 1960's articles on matoki
and pore over textbooks of cardiology about carcinoid tumor.  So
everybody had somebody or something to blame, and they got away
with it.  Naturopaths, by contrast, have nothing-- and won't get
away with it.  The FDA won't back them on 5-HTP, because the FDA
will never approve it.  So naturopathy will be caught by 5-HTP
with their pants down and their fingers up their noses.  And just
about that time, the New England Journal of Medicine will be
discovering why the health food hucksters should have known it
biochemically all along.  Due to our new experience with fen-
phen, don't you know.  And they'll be passing all this new
insight on to the newspapers, so they won't have to read
textbooks, something that journalists never ever do.

                                  Steve Harris, M.D.


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


Hiroshima J Med Sci 1976 Sep;25(2-3):135-40

On the tryptophan-serotonin metabolism in manic-depressive
disorders. Changes in plasma 5-HT and 5-HIAA levels and urinary
5-HIAA excretion following oral loading of L-5HTP in patients
with depression.

Amamoto T, Sarai K

PMID: 1088369, UI: 77187367


From: "Steve Harris" <>
Subject: Re: 5-HTP side effect
Date: Thu, 7 Mar 2002 09:57:36 -0800
Message-ID: <a689kv$47d$>

Baron Blackfang wrote in message
>I recently gave 5-HTP (5-hydroxytryptophan) a try as a sleep aid. I consumed
>2, 50 mg caps twice a day.  I didn't find any relief from insomnia, and I
>found that my anxiety increased rather than decreased.
>5-HTP is supposed to be the active metabolite of tryptophan, which was used
>in the past as an antidepressant until it was banned by the FDA.

Do not take 5-HTP. It's converted (to variable extent) by the liver aryl
amino acid decarboxylase to serotonin (5-HT or 5-hydroxytryptamine), which
is a bad thing to have in your blood in large quantities. It causes cardiac
myocytes to proliferate, and that causes proliferate valve disease (a
problem seen in methylsergide overdose, old-time fenfluramine users, and
victims of midgut carcinoid tumors that make a lot of serotonin). And, BTW,
any serotonin that is made by the liver never gets into the brain, so it
does you no good there. Some 5-HTP does get into the brain (the same
transporter that gets tryptophan gets it in, but that doesn't work without
the COOH group) and is converted to serotonin there.  But you pay for that
with serotonin made outside the brain, which you want strictly controlled.

Free serotonin outside the CNS is nasty stuff. It causes instant
vasoconstriction, which is one reason why platelets sop it up and store it
as a sort of nature's wound vasoconstrictor anti-bleeding agent. An
overdose, however, causes enough pulmonary vasoconstriction to cause
pulmonary hypertension. Give an animal an overdose of serotonin and they die
of pulmonary hypertension. The same is true of an overdose of fenfluramine--
death follows in minutes from that mechanism. Serotonin is also a growth
factor for smooth muscle cells, which aids in wound healing when platelets
dump it on small areas of damage. But again, too much of a good thing causes
proliferation in smooth muscle cells where you don't want it, and that's the
valve disease.

There is some irony in the fact that tryptophan, which does not raise
peripheral serotonin levels, and is a fairly safe way to raise brain
serotonins, is illegal to sell without prescription. But 5-HTP, which
bypasses the APUD cell enzyme that converts tryptophan to 5-HTP, is still
available over the counter.


From: "Steve Harris" <>
Subject: Re: 5-HTP side effect
Date: Sat, 9 Mar 2002 15:43:31 -0800
Message-ID: <a6e6lq$v9u$>

Alex wrote in message ...
>"Steve Harris" <> wrote:
>> Do not take 5-HTP. It's converted (to variable extent) by the liver aryl
>> amino acid decarboxylase to serotonin (5-HT or 5-hydroxytryptamine), which
>> is a bad thing to have in your blood in large quantities.
>Steve, do you think there might be risks in taking one 50 mg capsule
>of 5-HTP once a *week*?

I would guess not. The average person with carcinoid heart disease is
excreting around 50 mg 5-HIAA a day, as I remember from one study,
suggesting that it takes around that much serotonin dumped into your blood
to do this to you.  In turn suggesting it's probably only people taking
upward of 50 mg 5-HTP who are going to get into trouble. But who knows where
there total safety limits are?

>>I have read that B6 is needed for the conversion to serotonin, so I
>take care *not* to mix it with a B6-containing supplement, to minimize
>probability of conversion taking place in the gut on the bloodstream.
>BTW, a brand of 5-HTP, I think from Nature's Way, comes with a hefty
>dose of B6.  I'd never buy it.

It does seem the ultimate stupidity to put these together into a supplement.
Duhhhhr (it's about like taking L-DOPA and B6 for your Parkinson's-- you're
not gunna get much dopamine into your brain THAT way).  But remember that if
you take B6 at all, you're probably loaded with it. In other words, just
because you take B6 today and 5-HTP tomorrow, that doesn't mean you're not
getting as good conversion as your body can do.  How long do you have to
wait for B6 washout?  I have no idea.  Which is why it's best to limit the
5-HTP intake, unless you're going to regularly measure your urine 5-HIAA's.


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