Hip, a couple random questions---I figured out that I was getting dizzy every time I put selenium in my smoothie lately--I used to be able to tolerate a few drops pulsed on and off but was more religious about it the last couple months and apparently developed an intolerance to it. any thoughts on that?@Antares in NYC
What you might like to look into is the ability of quinolinic acid to produce brain lesions. Quinolinic acid, which is a potent neurotoxin, is created in the brain as part of the inflammatory process (during inflammation activated microglia convert L-tryptophan into quinolinic acid). 1
When quinolinic acid is experimentally injected into the brain, it causes lesions to appear. 1 And interestingly, poliovirus induces quinolinic acid, and apparently all the damage resulting from poliomyelitis can be prevented simply by blocking the activity of quinolinic acid. 1
Quinolinic acid has been found to be significantly elevated in Borrelia infection, with dramatically high levels found in Lyme patients with CNS inflammation. 1
There are several supplements and drugs that help protect against quinolinic acid-induced neurotoxicity, including:
selenium, 1 memantine, 1 verapamil, 1 rolipram, 1 minocycline, 1 acyclovir, 1 copper at low doses, 1 COX-2 inhibitors (eg: propolis), 1 ibuprofen, 1 dapsone, 1 saffron, 1 pyruvate, 1 S-allyl-cysteine (from garlic), 1 curcumin, 1 DHEA, 1 EGCG. 1
also am curious, have been able to try amantadine on and off the last 6 years and it makes me depressed---wondering if since memantine is related it could have some of the same properties. I was wondering if amantadine, with being part antiviral, increased quinolinic acid and thus depression.
huh, editing my response to add this, so you put acyclivor in there as quinolinic inhibitor, which confuses me---because another post of yours gave a theory about why depression can happen like with interferon treatment and its related to quinolinic acid---and I think the th 1 th 2 balance---
anything with antiviral properties makes me feel like hell......from valtrex(valcyclivor) to amantadine to lysine....catatonic hopeless mood and increased pain etc
doesnt it seem like immune system and quinolinic acid such a nuanced individualized situation that one person's meat could be another's poison? I was stoked at first tho to see you compiled list of QUIN inhibitors, I am wanting to find more info on that.
here is your post from http://forums.phoenixrising.me/inde...munomodulators-in-cfs.8447/page-6#post-782133
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Hip said: ↑
Yes, I am pretty sure that the depression is caused by the fact that: the antiviral Th1 response increases interferon gamma (IFN-γ), and IFN-γ then causes an increase in the enzyme indoleamine-2-3-dioxygenase (IDO) in the brain, and IDO breaks down tryptophan, and tryptophan is needed to make serotonin, the happiness neurotransmitter.
In summary:
Th1 Response ➤ Increased IFN-γ ➤ Increased IDO ➤ Reduced Tryptophan ➤ Reduced Serotonin ➤ Depression
(Note however that this study contradicts the above standard explanation of interferon-induced depression, and instead suggests an alternate explanation: that although raised IDO is still responsible for the depression, the mechanism of this depression is via IDO's ability to produce kynurenine and kynurenine metabolites such a quinolinic acid, which is linked to depression. In summary: Th1 Response ➤ Increased IFN-γ ➤ Increased IDO ➤ Increased Kynurenine and its Metabolites such as Quinolinic Acid ➤ Depression)
This type of interferon-induced depression is well-known: this very miserable depression occurs in many hepatitis C patients taking intravenous interferon as a treatment for the hep C virus. Also, Dr John Chia, in his study employing intravenous interferon for ME/CFS patients, found that although interferon was very effective, and was able to place many ME/CFS patients he treated into almost full remission for around 2 to 14 months (which is a spectacular result), he found that many of his patients suffered very significant depression during the treatment period. This problem with interferon-induced depression was one of the reasons I believe Dr Chia has largely stopped using intravenous interferon treatment for ME/CFS (that and the very high cost of intravenous interferon, which is in the order of $15,000 for a course of treatment).
I did try taking IDO inhibitors at the same time as taking my Th1 boosting cocktail, in the hope of preventing this depression from occurring, but this did not seem to help. Perhaps these IDO inhibitors were not potent enough, or perhaps I should have used much higher doses of these IDO inhibitors. (Or perhaps I should have heeded the alternate explanation of how IDO causes depression, and taken quinolinic acid inhibitors instead).
The antidepressant drugs paroxetine and low dose amisulpride have been shown to mitigate interferon-induced depression, so it is worth trying these drugs to combat the depression when you take a Th1 boosting cocktail.
But note that not everybody experiences depression from raised interferon levels, so many ME/CFS patients may be able to take the above Th1 boosting cocktail without getting any depression side effects, and thus may potentially experience an improvement in their ME/CFS symptoms from this antiviral Th1 boosting approach.
Apart from my depression (which I suffer from anyway), I did not get any other side effects from this Th1 boosting cocktail.
I am not sure why the various ME/CFS doctors, such as Dr Cheney and Dr Klimas, have not tried a Th1 boosting cocktail like the one I provided above. These doctors note that ME/CFS patients are stuck in the Th2 mode, and that they need to by shifted into the Th1 mode if they are going clear the viruses likely driving their ME/CFS. So it seems to make sense to try to shift your immune system over to Th1 using several Th1 boosting supplements and drugs, not just one supplement."
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