63 replies to this topic

[niner]

I'll put in a plug for Slo Niacin, an OTC extended release formulation.  It's very cheap, and is occasionally on sale at places like Costco or Walmart.  I use 1g/day, split into two 500mg doses for my elevated lp(a).  It is coming down, and legend has it that niacin will continue to bring it gradually lower for years.  I don't know what happens if you stop, but I'd expect it would go back up.  Immediate Release niacin is said to be more effective for most lipid markers, but I've heard from a cardiologist that ER is actually better for lp(a).

[Jason30]

To be honest, HDL raising and triglyceride lowering interventions (including niacin) have had disappointing results on CVD outcomes (they're probably both coincident markers of other risk factors like low activity level and metabolic syndrome). NA offers significant reductions in cardiovascular events, but there's little association of this reduction with increased HDL levels.

 

I'm mostly interested in NA as an NAD⁺ precursor (hopefully synergizing with exercise, mild caloric restriction, salicylate, and CD38 inhibition by flavonoids), but I have noticed possible mild anti-inflammatory and photoprotective effects.

 

The therapeutic dose in cardiology is typically 1.5 to 3 g, generally taken these days in a prescription extended release form (eg Niaspan).

 

There are a number of over-the-counter niacins.  I mentioned the most common form, niacinamide, with caveat emptors above. Sustained release ("flush-free") niacins like inositol hexanicotinate are to be avoided: they're poorly absorbed, have little lipid effects, and at high doses, are hepatotoxic in some patients. I take 1 g of crystalline / immediate release nicotinic acid, but I have no elevated CVD risks.

 

I believe the Solgar is also nicotinic acid, but is at a dosage suitable only for ramping up to therapeutic levels.

 

 

Thanks again Darryl. I start with 50gram a day because of the flush, and will increase it slowly.

[Jason30]

I'll put in a plug for Slo Niacin, an OTC extended release formulation.  It's very cheap, and is occasionally on sale at places like Costco or Walmart.  I use 1g/day, split into two 500mg doses for my elevated lp(a).  It is coming down, and legend has it that niacin will continue to bring it gradually lower for years.  I don't know what happens if you stop, but I'd expect it would go back up.  Immediate Release niacin is said to be more effective for most lipid markers, but I've heard from a cardiologist that ER is actually better for lp(a).

 

Thanks for the suggestion, I will look into that when my bottle from Solgar is empty.

[LexLux]

Don't reduced NAMPT levels in aged individuals make nicotinamide riboside preferable for raising NAD+ levels in older people? 

 

NAD+ and sirtuins in aging and disease,

Shin-ichiro Imai, Leonard Guarente, Trends in Cell Biology, 29 April 2014, ISSN 0962-8924

 

Some points -

• NR can be converted to NMN  (NR-> NR Kinase -> NMN)
• NR boosts NAD+ " in worms and mice and can counter effects of aging 18 and 40. NR supplementation also increases mitochondrial NAD⁺ levels and stimulates SIRT3-mediated deacetylation of mitochondrial proteins [40]."
• Circadian Machinery declines with aging, results in less NAMPT and NAD+, meaning "...NMN and NR, rather than earlier NAD⁺ precursors like nicotinamide would be critical in enhancing NAD⁺ biosynthesis efficiently in aged individuals."
• Chronic inflammation could be to blame - TNF-? significantly reduces NAMPT and NAD+ and "...suppresses CLOCK/BMAL-mediated clock gene transcription in the liver and SCN of TNF-?-treated mice [43]. [...] If this is found to be true, strategies to suppress chronic inflammation and sustain NAD⁺ biosynthesis and circadian function with aging might be effective in maintaining sirtuin activity and possibly robust health [9]."
• "PARP, CD38, and the nuclear sirtuins all compete for the same pool of NAD⁺ and inhibition of PARP or CD38 has the potential to activate sirtuins. [...] A possible explanation for these findings is that aging is associated with an increase in chronic nuclear DNA damage, which leads to NAD⁺depletion by PARP (Figure 4, left). The fact that loss of SIRT1 or SIRT6 activity exacerbates DNA damage[12] may create an autocatalytic downward spiral in the nucleus, with NAD⁺ depletion as the nexus."

To be honest, HDL raising and triglyceride lowering interventions (including niacin) have had disappointing results on CVD outcomes (they're probably both coincident markers of other risk factors like low activity level and metabolic syndrome). NA offers significant reductions in cardiovascular events, but there's little association of this reduction with increased HDL levels.

 

I'm mostly interested in NA as an NAD⁺ precursor (hopefully synergizing with exercise, mild caloric restriction, salicylate, and CD38 inhibition by flavonoids), but I have noticed possible mild anti-inflammatory and photoprotective effects.

 

The therapeutic dose in cardiology is typically 1.5 to 3 g, generally taken these days in a prescription extended release form (eg Niaspan).

 

There are a number of over-the-counter niacins.  I mentioned the most common form, niacinamide, with caveat emptors above. Sustained release ("flush-free") niacins like inositol hexanicotinate are to be avoided: they're poorly absorbed, have little lipid effects, and at high doses, are hepatotoxic in some patients. I take 1 g of crystalline / immediate release nicotinic acid, but I have no elevated CVD risks.

 

I believe the Solgar is also nicotinic acid, but is at a dosage suitable only for ramping up to therapeutic levels.