I am suffering from both sleep deprivation and depersonalization (although I am used to the latter). My HSCRP is through the roof (although I have normal CRP and cytokines like IL6). It seems like my tryptophan is being converted into kynurenine due to inflammation and I might have high glutamate as well.
How does one stop the inflammation? Shouldn't I locate it? Does anyone know how to find where inflammation is?
I've been to several doctors and they've got nothing.
Are there any tests to verify having high glutamate or high kynurenine/low serotonin/tryptophan?
NMDA antagonists seem to have different results for me.
CBD (cannibidiol), lithium, 5HTP+EGCG and NAD boosters seem to help. Mag threonate made my sleep markedly worse. NAC either didn't help or made sleep worse.
Can anyone think of other NMDA antagonists or neuro antinflammatories?
I have heard naltrexone might help. Does anyone have experience with naltrexone and sleep/depersonalization?
Do the people with depersonalization have sleep disturbance/low serotonin? I wonder both are tied to the same inflammation process?
Adreno isn't posting anymore. I'm starting to become drunk so I'm going to post in his place. He doesn't endorse me posting this.
You basically can't prevent trytophan going down the kynurenine pathway. That basically amounts to curing the disease.
You can lower it by lowering cortisol and cortisol's effects on the liver. The biggest amount of kynurenine is generated in the liver by TDO which is cortisol driven (not immune-drive). Even if you can't prevent the IDO conversion by the immune system.
There's a limited amount of research on this, but it's possible that kynurenine itself (the first in the pathway) causes issues. This is actually solved by exercise (!) which increases the kynurenine -> kynurenic acid conversion. I suspect this is an issue since people with ME/CFS don't exercise. Also, this conversion can be prevented by low glutathione, which is fixed by NAC + glycine + theanine.
Otherwise, you might be like me and suffer from excessive NMDA antagonism. In part this can be caused by kynurenic acid, which is NMDA antagonist, as well as a cholinergic receptor modulator I forget which (lowers dopamine). Anyway, the only thing that can slow down the kynurenine -> kynurenic acid conversion I'm aware of is COX-2 inhibitors.
Downstream from that you could have issues with quinolinic acid (niacin precursor) and picolinic acid (zinc absorption factor), but I doubt they affect me so I didn't look that far into them.
The simplest thing to try for any of this is actually high dose transdermal magnesium chloride. It affects a few of the kynurenine metabolite conversions.
I might or might not be able to reply to this.