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Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication...

Discussion in 'Other Health News and Research' started by anne_likes_red, Jan 1, 2014.

  1. Star-Anise

    Star-Anise Senior Member

    @Radio Awesome! Thanks so much. I have some reading to do... S:thumbsup:
    Radio likes this.
  2. pone

    pone Senior Member

    Just to play devil's advocate here:

    1) It is not necessarily that we have a failure to convert Tryptophan. We might have a dietary insufficiency, or alternatively we might have an absorption issue. People with fructose malabsorption have low levels of tryptophan in the blood, and fructose malabsorption affects one THIRD of all white people of European descent!! The tryptophan levels should be easy to test using any of the good nutritional eval tests? It's very worth noting that fructose malabsorption also affects folic acid levels!! Interesting that so many CFS patients have both the NAD+ production problem (maybe from tryptophan deficiency) but also have folic acid deficiencies. Interesting that those two symptoms get tied together here.

    2) Do we really want to be supplementing large doses of tryptophan? Some of that converts to serotonin and would strongly affect many other systems not just NAD+ production? Also, if we have a failure to convert tryptophan, how would supplying more tryptophan fix that?

    3) NADH is probably the one supplement you would NEVER want to take, The whole point of this paper was that the NADH is piling up in your body and is not able to convert back to NAD. As a result, the mitochondria are processing it in some very bad way that creates lots of free radicals. It would not only not solve the NAD+ problem to take NADH, but you would actually be making the damage to your body significantly worse, by increasing free radical production.

    4) The recommendation for R-lipoic acid makes great sense. This will help to process the backlog of NADH to NAD+. But the question is dosing. How much do we take, and how often do we take it? Is there any objective testing we can do for that?

    As some approximation for dosing, what kind of intravenous doses do the Europeans give of R-lipoic as a treatment for diabetic neuropathy? This might be used both to establish an upper limit for toxicity, as well as to help establish a range of effective oral doses.

    5) It seems to me the key recommendation should be for niacinimide, NMN (used in David Sinclair's mouse study), or Niagen / Nicotinamide Riboside (NR). I have read that NMN and NR may promote cancer so you use them at your own risk. What about niacinimide? I read one source that claimed studies show it is not only safer, but generates 20%+ more NAD+ conversion? I have yet to locate the original sources on this claim.

    And - the difficult question - what doses would be therapeutic? How often would we need to take it?

    6) Can you explain the riboflavin recommendation? I don't see how the MOA enzymes here would be deficient or needed.

    Point number 5) deserves its own thread. I can't believe this is not being discussed every day on this site. To me this looks like something very close to a potential cure.

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