Niacin. Your thoughts?: I didn't find... - Advanced Prostate...

Advanced Prostate Cancer

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Niacin. Your thoughts?

17 Replies

I didn't find any hard evidence. Part of niacin converts into NAD+. I don't think that would be good. And the proven HDL increase doesn't seem to make much difference in actual cardiac risk (perhaps HDL is a marker and artificially changing it doesn't affect the root contributors to cardiac risk?).

Niacin perhaps a poor choice for BRCA positive PCa, perhaps beneficial for others:

Nicotinic acid: A case for a vitamin that moonlights for cancer? - PMC

ncbi.nlm.nih.gov/pmc/articl...

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17 Replies
cesces profile image
cesces

That's a B vitamin.

I think generally B vitamins aren't good for prostate cancer

in reply to cesces

Is that all B vitamins? I thought that it was primarily supplementing higher levels of B-12 and folate. But it's probably a bad idea to add high doses of most anything without some good rationale and data supporting it.

Yes. It was pretty weak. I didn't find any good studies. NAD+ seems like it might be contraindicated for PCa. Please post what you find out. Very appreciated.

Most people hate the niacin flush. I love it and it puts me to sleep. Every once in a while I succumb and take 500 mg or so of niacin. If I knew that it wasn't bad for me I'd take it once a week (more often and my body habituates and I need more and more to satisfy my niacin-flush addiction).

Russ

Higsby profile image
Higsby

I believe it is niacinamide ( 25 to 50 mg TID), not niacin, that is a precursor to NAD+. See video ‘The Role of NAD+ IN Optimal Health’ Nichola Conlon, Ph.D. | duration: 1:18 hoursbitchute.com/video/bJ7AtJ9C...

Higsby

in reply to Higsby

Correct me if I'm wrong, Nal. Nicotinic acid is a precursor. (Nicotinic acid is niacin)

timotur profile image
timotur

I take 100mg niacin at breakfast every other day to help control high cholesterol, and get about a 10-20% reduction in TC, but ratios stay about the same. Cheese and/or caffeine seems to transport more to the bloodstream— making more of a flushing effect.

in reply to timotur

Good to know. Thanks.

Miccoman profile image
Miccoman in reply to timotur

I have found that time release niacin does not give me the flush. I take it at dinner with my statin per my doctors (told me that cholesterol is made at night so you should take cholesterol fighting drugs in the evening). The combination has been very good a lowering overall cholesterol, boosting HDL and dramatically lower triglycerides. YMMV

in reply to Miccoman

He's right. Most of cholesterol is made at night. I take my statin during the day though to prevent insomnia (a rare side effect). I love the flush (weird) so prefer immediate release.

Justfor_ profile image
Justfor_

Is this Video relevant?

youtube.com/watch?v=JS4r4Tq...

in reply to Justfor_

Yes, but defeating cancer is sometimes at odds with longevity.

Given that I have PCa, I probably don't want to increase NAD+.

Purple-Bike profile image
Purple-Bike

Nal, I look forward to your research on this! I was going to start taking Nicotinamide Riboside/niagen, an alternative form of B3 and a precursor to NAD+, for promising anti-aging effect. But with PCa and BRCA+ this is perhaps a bad idea?

I have also been thinking about Apigenin, inhibitor of CD38 which will increase NAD+ but I suppose that could also be a bad idea....

Niacin is a precursor. My question is how much niacin converts to NAD+. Like many things, perhaps not something to mess around with until we know more.

NAD Metabolism in Cancer Therapeutics - PMC

ncbi.nlm.nih.gov/pmc/articl...

"NAD+ depletion leads to degenerative diseases, including aging, while an increase in the NAD+ pool has been related to tumorigenesis. Cancer cells shift from normal OXPHOS to glycolysis metabolism to obtain a faster ATP production rate, maintain redox balance and synthesize nucleic acids, proteins and fatty acids. This reprogramming metabolism, also called the Warburg effect, leads to tumor proliferation and cancer progression. To satisfy their high glycolytic demands, cancer cells have increased NAD+ levels and an upregulated NAD+ salvage biosynthesis pathway, the main source of NAD+ in cells. It is not surprising to find upregulated NAMPT, the rate-limiting enzyme of this pathway, in several human tumors. NAMPT has been proposed as a potent oncogene capable of promoting cell proliferation by increasing the NAD+ pool and, consequently, enhancing SIRT1 and PARP1 activation."

NAD+ metabolism, stemness, the immune response, and cancer - PMC

ncbi.nlm.nih.gov/pmc/articl...

Purple-Bike profile image
Purple-Bike

Great post, Russ. I was just going to start supplementing with Nicotinamide Riboside, a precursor to NAD+, for it most promising anti-aging potential. I am BRCA2+, and after studying this article I will probably refrain from doing this. It is not certain that NR/NAD+ will aggravate my cancer, but I can hardly dare take the risk without clarifications. Hopefully Nalakrats will come up with something.

in reply to Purple-Bike

Better safe than sorry.

Purple-Bike profile image
Purple-Bike

Nal, may I remind you, is there any chance you can get something on NAD+/Nicotinamide Riboside/Niagen. Seems so promising for anti-aging, but is there a downside for PCa

Purple-Bike profile image
Purple-Bike

PS Nal From a post a year ago by Patrick "CD38 as good guy and as bad guy",,, indications of NAD+ not being a good supplement for PCa

CD38 as the Good Guy.

(2018, Wake Forest, U.S.) [5]

CD38 Inhibits Prostate Cancer Metabolism and Proliferation by Reducing Cellular NAD+ Pools

Nicotinamide Adenine Dinucleotide (NAD+)

"Tumor cells require an available pool of NAD+ for appropriate metabolic control and post-translational protein modification, among other functions, to support survival and proliferation."

"NAD+ turnover in cancer cells is dramatically increased relative to non-proliferating healthy cells, making NAD+ metabolism an attractive therapeutic target.

"NAD+ levels can ... be modulated by enzymatic consumption. ... CD38 is the primary NAD’ase in mammalian cells"

CD38 drives down NAD+, &, hence, the proliferation rate.

"Although we and others have demonstrated that CD38 expression is reduced in PCa, the mechanism by which CD38 expression is decreased is unknown."

"... the data suggest that strategies to induce CD38 expression could be one mechanism to decrease NAD+ in PCa and perhaps affect therapeutic response and hint that there are epigenetic or other elements in CD38 that regulate its expression."

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