Please read this article:
https://kclpure.kcl.ac.uk/portal/files/73267822/2017_Russell_Alice_Elizabeth_1064415_ethesis.pdf (Read especially
p. 38-43 and
p.65-66)
I have a question, did you have a traumatic event or a stressful event before POIS?
or/and did you have infection before POIS?
"The major non-protein route of TRP metabolism is formation of KYN, catalyzed by rate-limiting enzymes: indoleamine 2,3-dioxygenase (IDO) or TRP 2,3- dioxygenase (TDO)"
"TDO is inducible by stress hormones, e.g., cortisol, prolactin, and by substrate, TRP" and
"IDO is activated by pro- inflammatory factors, e.g., interferon-gamma (IFNG), tumor necrosis factor-alpha, IL-1 beta, and lipopolysaccharide" (
https://openaccesspub.org/article/51/jbd-13-218.pdf)
Some of the thetryptophan catabolites (TRYCATs), like 3-HK and QUIN have noxious effects including neurotoxic, excitotoxic, cytotoxic and pro-oxidative effects.
Pathogens can take advantage of this imbalance. For example EBV (Epstein?Barr virus), "{...} EBV-transformed B-cells express elevated levels of IDO causing Trp degradation to Kyn, which ? in turn ? suppressed the expression of the activating receptor NK group 2, member D (NKG2D) receptor on the surface of NK cells (63). This might be important since NK cells have been suggested to control the proliferation of EBV-infected B-cells in the acute phase. In the same report, it was shown that IL18 suppressed the effect of Kyn on NKG2D expression. It might be speculated that the suppression of NK cell activation by IDO-expressing EBV-infected B-cells serves as an escape strategy of the virus. Recently, it was shown that in vitro generated macrophages expressed IDO after infection with EBV and displayed T-cell suppressive activities" (
https://www.frontiersin.org/articles/10.3389/fimmu.2014.00384/full)
I don't speak English very well, so i't s difficult to explain and make a complete summary, but please read also this article:
-
https://goo.gl/eJeBzJ (TRYCATs and gut microbiota)
Personally, I believe that POIS begins, with a stressful/traumatic event or with an infection in conjunction with gut dysbiosis or irritable bowel syndrome (IBS) (maybe there are also genetics predispositions). Stress can induce TDO. EBV is present in 90% of population, and can take advantage of the imbalance and go in parts of the body where normally does not, the virus stay in a particular latent form and become activated by orgasm or ejaculation. This pathogen elevate IDO causing Tryptophan depletion, the consequence is that there is an imbalance between Tryptophan and Kynurenine, this imbalance provoke
insomnia,
cognitive and
emotional symptoms of POIS (symptoms vary because of genetic and diet). Kynurenic acid acts in astrocytes and block glutamate and dopamine release wich causes cognitive dysfunction. In some cases is possible that the virus causes also an autoimmune reaction to the semen,
but not always! (EBV is linked to a lot of autoimmune diseases, chronic fatigue syndrome too). Our immune system does not recognize this virus because of immunosuppression caused by IDO.
Also
read this:
https://www.frontiersin.org/articles/10.3389/fimmu.2018.00229/fullI'm sure that POIS is a particular form of chronic fatigue syndrome! The infection theory of Pois can explain the heterogeneity of this disease and at the same time explain a more complex autoimmune disease (provoked by the pathogen) of what thought by Waldinger. Yes because I'm sure that people with POIS have also antibodies to β adrenergic and muscarinic cholinergic receptors (and not only) like persons with chronic fatigue syndrome.
