8 replies to this topic

[PeaceAndProsperity]

A while ago I posted about his experiences with using this supplement but it didn't gain much attention. Now I've been thinking that very high dosages (10g?) ONCE daily may prove to have even stronger anti-aging benefits. Note that by anti-aging I simply mean SLOWING aging, not necessarily reversing it.

 

According to numerous studies throughout 30+ years, nicotinic acid is only toxic if you are chronically exposed to it. So a too high dosage of the slow-release variety or a too high dosage more than once daily could prove to be toxic. Therefore, if you want to try nicotinic acid you might need to try multiple grams but only once daily.

 

My 70 year old relative has been taking 500mg of nicotinic acid daily for around a year. At some point he switched from 500mg once daily to twice daily morning and evening. It has:

1. Restored his hair color 70% or so, from gray to black (his natural color)

2. Increased his amount of scalp hair around 30%

3. Improved his skin quality mildly

4. Significantly reduced his blood bacteria count to zero (during medical examination)

5. Undoubtedly mildly improved his cognitive abilities (memory, clarity, reasoning)

 

 

[Dolph]

Well... I'm known as a great fan of NA, specifically for cholesterol control, but 10g is a very high dose by every standard. I take 3g daily at the moment and personally, without very close medical supervision I wouldn't go beyond this limit, which already could be considered to be rather agressive. 

[Turnbuckle]

10 g a day would be a good way to destroy both your liver and your stomach.

[PeaceAndProsperity]

10g has been tried before with no adverse effects as far as I've understood.

 

[Dolph]

Yes, as I wrote, under strict medical supervision. I wouldn't **** around with that kind of dose on the base of very sketchy assumptions.

[Turnbuckle]

 

10g has been tried before with no adverse effects as far as I've understood.

 

 

 

Insofar as niacin is working because it's a NAD+ stimulant, niacinamide would work better.

[PeaceAndProsperity]

Yes, as I wrote, under strict medical supervision. I wouldn't **** around with that kind of dose on the base of very sketchy assumptions.

You're overreacting, it's actually an extremely mild chemical. It's nowhere near as toxic as vitamin A is in high dosages. Yet, many people megadose vitamin A with no toxicity symptoms (maybe an analog or prodrug of it has no liver toxicity).

[PeaceAndProsperity]

On the note of the increased nad or its close chemical relatives, do you think it could have an effect on telomerase on telomere length? Otherwise in my mind it seems rather pointless to increase those as even if the cell begins working again it's still at critical telomere length--hayflick limit..

You'd want at least both an amelioration of the telomere senescence and whatever-senescence that NA may work against.

[Turnbuckle]

On the note of the increased nad or its close chemical relatives, do you think it could have an effect on telomerase on telomere length? Otherwise in my mind it seems rather pointless to increase those as even if the cell begins working again it's still at critical telomere length--hayflick limit..

You'd want at least both an amelioration of the telomere senescence and whatever-senescence that NA may work against.

 

 

The NAD+/NADH ratio is the signal that sets the mitochondrial quality control mechanism in motion and a healthy population of mitochondria is critical for cellular health. Dysfunctional mitochondria increase the ROS load in the cell and erode telomeres.

 

Mitochondrial dysfunction produces indiscriminate amounts of reactive oxygen species that may lead to oxidative damage to cellular constituents, including telomeric DNA, causing telomere shortening. In fact, primary mitochondrial dysfunction (for example respiratory chain disorders) and secondary mitochondrial dysfunction (such as metabolic diseases, neurodegenerative diseases, cardiovascular diseases, and mood disorders, among others) have been shown to have shorter telomeres than healthy individuals.

 

https://www.ncbi.nlm...pubmed/27814605

 

 

 

and--

 

Active autophagy coupled with rapid mitochondrial fusion and fission constitutes an important mitochondrial quality control mechanism and is critical to cellular health. In our previous studies, we found that exposure of cells to nicotinamide (NAM) causes a decrease in mitochondrial content and an increase in mitochondrial membrane potential (MMP) by activating autophagy and inducing mitochondrial fragmentation. Here, we present evidence to show that the effect of NAM is mediated through an increase of the [NAD+ ]/[NADH] ratio and the activation of SIRT1, an NAD+ -dependent deacetylase that plays a role in autophagy flux. 

 

http://www.jbc.org/c...363747.full.pdf