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Why do tryptophan/serotonin levels dip in mood disorders? Here is what you can do.
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Your body takes all the protein you eat and breaks it into small nutrients for use. One such nutrient is tryptophan which is used to make serotonin in your brain. Serotonin is a chemical messenger that puts you in a good mood and helps you get refreshed sleep [1]. Foods like tofu, meat, and dairy products are good sources of tryptophan.
Why does tryptophan face challenges in serotonin production?
Tryptophan faces the following challenges:
- The body only allows 5% of the tryptophan extracted from your food to enter the brain [2]. It is first converted to a nutrient called 5-htp. Tryptophan is then used to produce serotonin from 5-htp
- Over 90% of the tryptophan that enters the brain passes through a pathway that protects the brain from inflammation[3]. This is called the kynurenine pathway and creates other chemicals instead of serotonin [4].
- Metabolism of tryptophan and serotonin is affected in mood disorders. Studies have found that those with mood disorders produce a higher level of toxic brain compounds (neurotoxins) from tryptophan [5]
How is tryptophan used in healthy vs depressed people?
In healthy individuals, 1-3% of tryptophan is converted to serotonin in the brain [6]. The kynurenine pathway creates protective brain compounds (neuroprotective) from tryptophan. In mood disorders, there is increased production of neurotoxins in the pathway and this causes inflammation which contributes to the onset of serious diseases.
A review of 101 studies with over 10,000 participants found that those with mood disorders had lower levels of neuroprotective compounds and higher levels of neurotoxins compared to healthy people [5]
How can you produce serotonin efficiently?
5-htp can freely cross into the brain for direct conversion to serotonin (chemically called 5-HT). It skips all the challenges faced by tryptophan [7]. It can be extracted from a plant called Griffonia Simplicifolia in supplemental form. Our 100mg 5-htp supplement is extracted and isolated from Ghanian Griffonia Simplicifolia seeds. 98% of the tablet is comprised of 5-htp making it the smallest, nutrient-dense tablet available and no unnecessary bulking agents. You can read more about it here.
References
- Carhart-Harris, R. et al. (2017). Serotonin and brain function: a tale of two receptors. Journal of Psychopharmacology, [online] 31(9), pp.1091–1120. doi:10.1177/0269881117725915.
- Bell, C. et al. (2001). Tryptophan depletion and its implications for psychiatry. The British Journal of Psychiatry: The Journal of Mental Science, [online] 178, pp.399–405. doi:10.1192/bjp.178.5.399.
- Davis, I. et al. (2015). What is the tryptophan kynurenine pathway and why is it important to neurotherapeutics? Expert Review of Neurotherapeutics, 15(7), pp.719–721. doi:10.1586/14737175.2015.1049999.
- Schwarcz, R., et al. (2012). Kynurenines in the mammalian brain: when physiology meets pathology. Nature Reviews Neuroscience, [online] 13(7), pp.465–477. doi:10.1038/nrn3257.
- Marx, W., et al. (2021). The kynurenine pathway in major depressive disorder, bipolar disorder, and schizophrenia: a meta-analysis of 101 studies. Molecular Psychiatry, [online] 26(8), pp.4158–4178. doi:10.1038/s41380-020-00951-9.
- Richard, D.M., et al. (2009). L-Tryptophan: Basic Metabolic Functions, Behavioral Research and Therapeutic Indications. International Journal of Tryptophan Research, [online] 2, p.IJTR.S2129. doi:10.4137/ijtr.s2129.
- Birdsall, T.C. (1998). 5-Hydroxytryptophan: a clinically-effective serotonin precursor. Alternative Medicine Review: A Journal of Clinical Therapeutic, [online] 3(4), pp.271–280. Available at: https://pubmed.ncbi.nlm.nih.gov/9727088/.
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