Has any rationale been given for the use of nicotinic acid (flushing type, typically called niacin) rather than niacinamide (non-flushing type, also called nicotinamide)?
I'll urge you and anyone else considering it to be very cautious with high-dose nicotinic acid. It has been known to cause toxicity at 750mg, and even at 500mg if using sustained release forms (
ref;
ref2). Unless there is something specific about nicotinic acid to justify using it this way, niacinamide is much safer at high doses. Niacinamide doses up to 1000mg have been used safely (
Chen et al., 2015), and even up to 3000mg in one study (
Murray et al., 2001). Beyond 3000mg, niacinamide also produces toxicity (
Huber & Wong, 2020).
I've not watched it yet, but I'm curious why he is using it. In the setting of chronic infection, the kynurenine pathway would be expected to be driven at higher levels, which could shunt tryptophan away from its other important uses in the body, causing blood levels to drop (as has been shown in some CFS studies, but not all). It has been shown that high-dose niacinamide can restore blood tryptophan levels in HIV patients (
ibid.), possibly by putting backpressure on kynurenine pathways.
Also, there is some indication that niacinamide might have (in vitro) antiviral effects (
Moëll et al., 2009;
Murray & Srinivasan, 1995). It also may have anti-inflammatory immunomodulatory effects (
Hedman et al., 2006).
might be worth starting a thread about it.
