Tryptophan-Kynurenine Metabolism - Inflammation and Immune System Function
Added 2021-04-04 21:24:04 +0000 UTCQuinine and its derivatives have nothing to do with its proposed function of a zinc ionosphere, but it certainly wouldn’t hurt to include.
Quinine inhibits tryptophan metabolism or more specifically, serotonin metabolism via inhibiting Tryptophan hydroxylase 2 enzyme in tryptophan-serotonin metabolism.
Islahudin, F., Tindall, S., Mellor, I. et al.
The antimalarial drug quinine interferes with serotonin biosynthesis and action. Sci Rep 4, 3618 (2014). https://doi.org/10.1038/srep03618
Studies suggest this induces tryptophan starvation, but commonly prescribed pharmacological dosages are overdosed and inhibit tryptophan metabolism near entirely.
Excess AND deficient systemic serotonin and low NAD+/high NADH are implicated in inflammation and immune system dysfunction.
Sorgdrager FJH, Naudé PJW, Kema IP, Nollen EA and Deyn PPD (2019) Tryptophan Metabolism in Inflammaging: From Biomarker to Therapeutic Target. Front. Immunol. 10:2565.
doi: 10.3389/fimmu.2019.02565
In more natural amounts found in food medicine and herbal medicines, it still inhibits tryptophan-serotonin metabolism, but force shifts tryptophan metabolism to Tryptophan-Kynuernine metabolism.
The end product of this pathway is Niacin, NAD+, and NAADP, the two molecules implicated as adjuvant therapies for recent viruses. Re: Dr. Dmitry Kats/@NiacinIsHealth on Twitter
High dose Niacin or Nicotinic acid also targets this same pathway.
https://twitter.com/niacinishealth/status/1372986426074234896?s=21
R. Miller, A.R. Wentzel, G.A. Richards,
COVID-19: NAD+ deficiency may predispose the aged, obese and type2 diabetics to mortality through its effect on SIRT1 activity,
Medical Hypotheses, Volume 144, 2020, 110044, ISSN 0306-9877,
https://doi.org/10.1016/j.mehy.2020.110044.
Pitt SJ, Funnell TM, Sitsapesan M, et al.
TPC2 is a novel NAADP-sensitive Ca2+ release channel, operating as a dual sensor of luminal pH and Ca2+. J Biol Chem. 2010;285(45):35039-35046. doi:10.1074/jbc.M110.156927
