By your reasoning, tomatoes, peppers, lettuce, green onions, milk, meat, and countless other products should be banned from the market because of outbreaks of illness.

This is pseudo-science and propaganda down to the last punctuation.

I am not against all drugs but people need to have options. Quit polarizing a situation that needs as many possible remedies as are available.

Are you a pharmaceutical rep, by chance?

In the late 1980s 37 people died and over 1500 were permanently disabled after consuming L-T produced by a Japanese company, Showa Denko.

It was determined these people were affected by a contaminate in the ‘Peak’ group, most probably Peak-X, which caused Eosinophilia-Myalgia Syndrome. This appears to be an intrinsic contaminate of L-T, and possibly also its metabolites, 5-HTP (5-OH-trp=5-HTP) and melatonin.

The focus at the time was on a particular batch, or batches, however, while these may have been more contaminated than usual, there is evidence that Peak contaminates are intrinsic to L-Tryptophan and its metabolites.

Reports of some 50 new cases unrelated to the 1988-9 event were still be reported to the FDA’s Special Nutritional Adverse Event Monitoring System until the system was shut down in 2002. The brands listed included: General Nutrition Corporation (GNC) Twin Labs Fedco Tishcon Corporation Tyson & Assoc Ltd Trimedia Natrol Inc

The fact that a particular brand is not on the above list does not mean it is necessarily any safer. Ajinomoto U.S.A of Raleigh, North Carolina is the only FDA licensed L-Tryptophan importer. They distribute it to supplement manufacturers, compound pharmacies, veterinary suppliers etc, so most brands contain L-Tryp from the same source.

The Showa Denko plant has since changed ownership, but it still produce more than 60% of the supplemental L-T available world wide and is believed to be Ajinomoto’s supplier.

That L-T made after the 1989 incident continues to be contaminated with Peak molecules was confirmed by a 1998-9 German study.

The FDA’s 2001 Information Paper on L-tryptophan and 5-hydroxy-L-tryptophan contains more information on the current thinking about these supplements.

There is also evidence that L-T may be involved in the formation of some cancers: http://tinyurl.com/ioo3, http://tinyurl.com/iooa.

However, the main problem with L-T use is that despite the popular mythology, antidepressants (ADs) do not increase brain serotonin levels or synthesis, they actually decrease it, or it remains unchanged. I’m listing some the studies showing this below [1].

Actually, this should not come as a complete surprise to most. Serotonin levels are increased within an hour or so of taking the first antidepressant, but instead of this easing anxiety levels most patients initially experience more anxiety.

However, the greatest indication that serotonin levels in either the synapses or the brain generally is not what affects anxiety/depression is the French antidepressant Tianeptine which is a Selective Serotonin Re-uptake Enhancer. That is it enhances the uptake of serotonin instead of inhibiting it as the SSRIs do. If you take both it and a SSRI at equivalent effective doses they cancel each other out. Yet Tianeptine seems to be as effective as any of the SSRIs and tends to begin working earlier.

HTH

Ian

[1] (Note 5-HT=serotonin)

Stenfors C, Yu H, Ross SB. (2001) “Pharmacological characterisation of
the decrease in 5-HT synthesis in the mouse brain evoked by the
selective serotonin re-uptake inhibitor citalopram.” Naunyn
Schmiedebergs Arch Pharmacol, vol 363(2):p 222-32
http://tinyurl.com/ka7xm

Alvarez JC, Sanceaume M, Advenier C, et al. (1999)”Differential changes in brain and platelet 5-HT concentrations after steady-state achievement and repeated administration of antidepressant drugs in mice.”
Eur Neuropsychopharmacol, vol 10(1):p 31-6
http://tinyurl.com/hdxhc

Moret C, Briley M.
“Ex vivo inhibitory effect of the 5-HT uptake blocker citalopram on 5-HT synthesis.”
J Neural Transm. 1997;104(2-3):147-60.
http://tinyurl.com/l7wzd

Zangen A, Overstreet DH, Yadid G. (1997) “High serotonin and
5-hydroxyindoleacetic acid levels in limbic brain regions in a rat model of depression: normalization by chronic antidepressant treatment.”
J Neurochem, vol 69(6):p 2477-83
http://tinyurl.com/egyza

Trouvin JH, Gardier AM, Chanut E, et al. (1993)
“Time course of brain serotonin metabolism after cessation of long-term fluoxetine treatment
in the rat.”
Life Sci, vol 52(18):p PL187-92
http://tinyurl.com/esqqt

Caccia S, Fracasso C, Garattini S, Guiso G, Sarati S.
“Effects of short- and long-term administration of fluoxetine on the monoamine content of rat brain.”
Neuropharmacology. 1992 Apr;31(4):343-7.
http://tinyurl.com/pveto