Terma
Member
- Joined
- May 8, 2017
- Messages
- 1,063
I still can't properly reply on this forum, it's ******* gay. The only reason I do this is because I think this author (Abdulla) provides a decent summary about the current scientific consensus regarding the tryptophan kynurenine pathway, which is something @Travis had been talking about extensively, although he clearly did not approve of all this guy's ideas (I write that with respect to Travis; I think the main ideas put forward in this article are theoretical at best, but Abdulla provides a decent summary of the current scientific knowledge about the kynurenine pathway, and parts of this are very significant and contradict some of my own ideas - all subject to review).
Modulation of Tryptophan and Serotonin Metabolism as a Biochemical Basis of the Behavioral Effects of Use and Withdrawal of Androgenic-Anabolic Steroids and Other Image- and Performance-Enhancing Agents
If you read only the abstract, you're doing yourself a huge disservice, because it is the "Overview of Tryptophan Metabolism and Disposition" section that provides the best information. I'm not going to do like the amazon guy and highlight a bunch of quotes, I don't have the energy.
The last article that I'm aware by this author was: Kynurenine Pathway of Tryptophan Metabolism: Regulatory and Functional Aspects [edit: fixed second link]
Modulation of Tryptophan and Serotonin Metabolism as a Biochemical Basis of the Behavioral Effects of Use and Withdrawal of Androgenic-Anabolic Steroids and Other Image- and Performance-Enhancing Agents
Modulation of tryptophan (Trp) metabolism may underpin the behavioral effects of androgenic-anabolic steroids (AAS) and associated image and performance enhancers. Euphoria, arousal, and decreased anxiety observed with moderate use and exercise may involve enhanced cerebral serotonin synthesis and function by increased release of albumin-bound Trp and estrogen-mediated liver Trp 2,3-dioxygenase (TDO) inhibition and enhancement of serotonin function. Aggression, anxiety, depression, personality disorders, and psychosis, observed on withdrawal of AAS or with use of large doses, can be caused by decreased serotonin synthesis due to TDO induction on withdrawal, excess Trp inhibiting the 2 enzymes of serotonin synthesis, and increased cerebral levels of neuroactive kynurenines. Exercise and excessive protein and branched-chain amino acid intakes may aggravate the effects of large AAS dosage. The hypothesis is testable in humans and experimental animals by measuring parameters of Trp metabolism and disposition and related metabolic processes.
If you read only the abstract, you're doing yourself a huge disservice, because it is the "Overview of Tryptophan Metabolism and Disposition" section that provides the best information. I'm not going to do like the amazon guy and highlight a bunch of quotes, I don't have the energy.
The last article that I'm aware by this author was: Kynurenine Pathway of Tryptophan Metabolism: Regulatory and Functional Aspects [edit: fixed second link]
Regulatory and functional aspects of the kynurenine (K) pathway (KP) of tryptophan (Trp) degradation are reviewed. The KP accounts for ~95% of dietary Trp degradation, of which 90% is attributed to the hepatic KP. During immune activation, the minor extrahepatic KP plays a more active role. The KP is rate-limited by its first enzyme, Trp 2,3-dioxygenase (TDO), in liver and indoleamine 2,3-dioxygenase (IDO) elsewhere. TDO is regulated by glucocorticoid induction, substrate activation and stabilization by Trp, cofactor activation by heme, and end-product inhibition by reduced nicotinamide adenine dinucleotide (phosphate). IDO is regulated by IFN-γ and other cytokines and by nitric oxide. The KP disposes of excess Trp, controls hepatic heme synthesis and Trp availability for cerebral serotonin synthesis, and produces immunoregulatory and neuroactive metabolites, the B3 “vitamin” nicotinic acid, and oxidized nicotinamide adenine dinucleotide. Various KP enzymes are undermined in disease and are targeted for therapy of conditions ranging from immunological, neurological, and neurodegenerative conditions to cancer.
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