In the model of GR resistance and low TDO, the body has more tryptophan reserve for serotonin and also for IDO(as a compensating mechanism?). What I mean is, what if a person has got high levels of Kynurenine pathway metabolites such as Kynurenic acid and quinolonic acid, what would be the final outcome? High or low levels of anxiety?
Is it possible to get excitotoxic brain damage eventhough while absense of anxiety?
What I mean by damage is, permanent drop in intelligence/cognitive impairment. It's much different than brainfog. Also I have never had a remission from my disease.
Is it possible to get excitotoxic brain damage eventhough while absense of anxiety?
What I mean by damage is, permanent drop in intelligence/cognitive impairment. It's much different than brainfog. Also I have never had a remission from my disease.
Our results show that CHD patients with depression had higher levels of CRP, IL-6 gene expression, and VEGF compared with CHD non-depressed, as well as lower plasma and saliva cortisol levels. The CHD depressed group also exhibited a reduction in GR expression and sensitivity. Finally, tryptophan levels were significantly lower in patients with depression, who also showed an increased kynurenine/tryptophan ratio. In conclusion, CHD patients with depression had elevated levels of inflammation in the context of HPA axis hypoactivity, GR resistance, and increased activation of the kynurenine pathway. Reduced cortisol bioavailability and attenuated glucocorticoid responsiveness due to decreased expression and sensitivity of GR may lead to insufficient glucocorticoid signaling and thus elevation of inflammation in these patients
https://www.ncbi.nlm.nih.gov/m/pubmed/25683698/
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