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Tryptophan

 Tryptophan (Trp) is one of the nine essential amino acids that need to be ingested daily in the diet. The adult male requirement for Trp in diet is 4.0 mg per kg body weight. The idea of using Trp to reduce mental stress and improve sleeping has been implemented since 1970s, since the time medical scientists discovered that Trp influenced the rate at which neuronal endings formed the neurotransmitter serotonin and that Trp was a precursor of melatonin. The brain Trp co-depends on the plasma supply of Trp and carbohydrates (Fernstrom, 1983 & 1991), and it is inversely affected by the circulating levels of other large neutral amino acids (LNAA: tyrosine, phenylalanine, leucine, isoleucine and valine), making the availability of Trp dependent on nutritional aspects. Deficiency of Trp dietary supply results in rapid and severe decline in the brain serotonin activity. Trp deficiency worsens seasonal depression, anxiety, carbohydrate craving, the premenstrual syndrome, and the ability to deal with daily stresses (Blokland et al., 2002).

Human applications of the Trp deficiency model have suggested that the negative results of the deficiency originate not only from serotonin deficiency, but mainly from complex interactions between monoaminergic systems (Reilly et al., 1997; Van der Does, 2001; Delgado, 2000). Yet, the controversy on Trp use in supplements continues. Controlled clinical studies indicate that Trp supplements, alone, or in a combination with carbohydrates, alleviate stress-induced mood (Maes et al., 1999), and some milder forms of cognitive deterioration (Markus et al., 2002).

Moreover, Trp is necessary for the production of vitamin B3 and requires B6, zinc as well as vitamin C to make the conversion enzyme. Some suggest that Trp or 5-hydroxytryptamine (the demi-product in the conversion of tryptophan to serotonin) may help in controling hyperactivity in children (Rucklidge et al., 2009).

Unfortunately, human research on the Trp supplements suddenly shrank 21 years ago, when nonprescription Trp preparations made by a single maker were linked to deadly outbreak of eosinophilia myalgia syndrome (EMS), most probably due to impurities caused by insufficient quality control management. Consequently, Trp was banned from the US and UK markets until 2005, when it was again reintroduced.

ICAAS is currently intensively working on quality control methods that would help in preventing such disasters in the future and provide the consumers with an access to potentially useful amino acid. In addition, ICAAS is supporting both animal and human research models that may help to establish the upper intake limits for Trp.

Finally, Trp tends to be deficient in livestock feed for chicken and pigs, if the feed is mainly composed of maize. Livestock farming productivity is therefore increased by fortifying Trp to maize feed.

 

References
  1. Blokland, A., Lieben, C. & Deutz, N. E. (2002). Anxiogenic and depressive-like effects, but no cognitive deficits, after repeated moderate tryptophan depletion in the rat. Journal of Psychopharmacology, 16, 39-49.
  2. Delgado, P. L. (2000) Depression: the case for a monoamine deficiency. Journal of Clinical Psychiatry, 61, 7-11.
  3. Fernstrom, J. D. (1991). Effects of the diet and other metabolic phenomena on brain tryptophan uptake and serotonin synthesis. Advances in Experimental Medicine and Biology, 294, 369-76.
  4. Fernstrom, J. D. (1983). Role of precursos availability in control of monoamine biosynthesis in brain. Physiological Reviews, 63, 484-486.
  5. Maes, M., Lin, A. H., Verkerk, R., Delmeire, L., Van Gastel, A., Van der Planken, M. & Scharpe, S. (1999). Serotonergic and noradrenergic markers of post-traumatic stress disorder with and without major depression. Neuropsychopharmacology, 20, 188-97.
  6. Markus, C. R., Olivier, B. & de Haan, E. H. F. (2002). Whey protein rich in lactalbumine increases the ration of plasma tryptophan to the sum of the other large neutral amino acids and improves cognitive performance in stress-vulnerable subjects. American Journal of Clinical Nutrition, 75, 1051-1056
  7. Reilly, J. G., MCTavish, S. F. & Young, A. H. (1997). Rapid depletion of plasma tryptophan: a review of studies and experimental methodology. Journal of Psychopharmacology, 11, 381-392.
  8. Rucklidge, J. J., Johnstone, J., Kaplan, B. J. (2009). Nutrient supplementation approaches in the treatment of ADHD. Expert. Rev. Neurother. 9, 461-76.
  9. Van der Does, A. J. (2001). The effect of tryptophan depletion on mood and psychiatric symptoms. Journal of Affective Disorders, 64, 107-119.
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