65 replies to this topic

[ironfistx]

 

[1] Ines Sanchez-Roman et al, Regulation of longevity and oxidative stress by nutritional interventions: Role of methionine restriction Experimental Gerontology Volume 48, Issue 10, October 2013, Pages 1030?1042

 

 

Dietary restriction (DR), around 40%, extends the mean and maximum life span of a wide range of species and lowers mtROSp and oxidative damage to mtDNA, which supports the mitochondrial free radical theory of aging (MFRTA). Regarding the dietary factor responsible for the life extension effect of DR, neither carbohydrate nor lipid restriction seems to modify maximum longevity. However protein restriction (PR) and methionine restriction (at least 80% MetR) increase maximum lifespan in rats and mice. Interestingly, only 7weeks of 40% PR (at least in liver) or 40% MetR (in all the studied organs, heart, brain, liver or kidney) is enough to decrease mtROSp and oxidative damage to mtDNA in rats, whereas neither carbohydrate nor lipid restriction changes these parameters. In addition, old rats also conserve the capacity to respond to 7weeks of 40% MetR with these beneficial changes. Most importantly, 40% MetR, differing from what happens during both 40% DR and 80% MetR, does not decrease growth rate and body size of rats. All the available studies suggest that the decrease in methionine ingestion that occurs during DR is responsible for part of the aging-delaying effect of this intervention likely through the decrease of mtROSp and ensuing DNA damage that it exerts.

 

 

In diets rich in carbohydrates, growth

factors stimulate cellular glucose uptake and the production of energy is carried out through

glycolysis. In this context, the NAD+/NADH ratio decreases, in turn inhibiting, in theory,

sirtuins in the cytoplasm (Sirt2) and nucleus (Sirt1, Sirt6 and Sirt7). In fact, low Sirt1 and

Sirt6 activity generates a global increase in protein acetylation.

 

Maybe we should be eating more animal fat, less carbs and less proteins, like these guys http://high-fat-nutrition.blogspot.ca/ 

 

Also, trying to put everything together it seems that substances increasing methylation (methionine, B9, B12, etc) and acetylation (Apple cider vinagar, ALCAR, etc) make you feel better but live shorter, while substances that act as methyl sinks (NA, NAM, NR, NMN, etc via their metabolism) and deacetylators (NA, NAM, NR, NMN, etc via boosting NAD+) give you a long, miserable life. 

 

 

Wait ALCAR makes you not live as long?

[Tom Andre F. (ex shinobi)]

I'm not sure I could take high dose Niacin, I get mega flushing even at 100mg. 

 

Even normal doses can be associated with feeling warmth, redness, itching or tingling of the face, neck, arms or upper chest. This is called "flushing". In most cases, this problem will get better after taking niacin on a regular basis for a while. To prevent flushing, do not drink hot beverages or alcohol at the same time you take niacin (source: https://www.nlm.nih....cle/002409.htm)

The flushing means some positive effect too according to the studies on the first page of this thread.

 

The dosage :

 

Dietary Reference Intakes for Niacin:

Infants

• 0 to 6 months: 2* milligrams per day (mg/day)
• 7 to 12 months: 4* mg/day

*Adequate Intake (AI)

Children (RDA)

• 1 to 3 years: 6 mg/day
• 4 to 8 years: 8 mg/day
• 9 to 13 years: 12 mg/day

Adolescents and Adults (RDA)

• Males age 14 and older: 16 mg/day
• Females age 14 and older: 14 mg/day, 18 mg/day during pregnancy, 17 mg/day during lactation

 

https://www.nlm.nih....icle/002409.htm

 

so should try even lower dose such as 50mg on a regular basis

[Climactic]

It is absolutely true that hot beverages will make a flush a lot more likely. Nevertheless, it doesn't happen to me with 100mg x1 of niacin, but it does with 100mg x2. I certainly won't give up drinking hot tea or coffee. I can understand that once in a while the flush happens to people with 100mg; these people should definitely try 50mg instead as is noted in the prior post.

 

There is just no way I would exceed 100mg niacin. I tried it for over a month and the flushing never went away for me.

[newgenduder]

Recently found a straight NAD+ supplement -  I had been looking for one, for a few years, after NOW foods canceled their product. I use NAD+ to lower histamine levels, through methylation; NAD+ is the cofactor to folic acid's conversion to THF, which degrades histidine. 

https://squareup.com...e/LIASresearch/ this is the product I'm using. It's working for me. It's also providing a little bit of mental clarity. I'm taking 25mg once per day, lozenge. I personally can't tolerate Niagen, because it's sooo closely related to niacin, it liberates histamine. I believe this is why people get the side-effects they do on Niagen(pains and such) , because histamine is closely related to inflammation. 

[ryukenden]

Recently found a straight NAD+ supplement -  I had been looking for one, for a few years, after NOW foods canceled their product. I use NAD+ to lower histamine levels, through methylation; NAD+ is the cofactor to folic acid's conversion to THF, which degrades histidine. 

https://squareup.com...e/LIASresearch/ this is the product I'm using. It's working for me. It's also providing a little bit of mental clarity. I'm taking 25mg once per day, lozenge. I personally can't tolerate Niagen, because it's sooo closely related to niacin, it liberates histamine. I believe this is why people get the side-effects they do on Niagen(pains and such) , because histamine is closely related to inflammation. 

 

It looks quite interesting product. Anyone else using it? Which is better between it and Niagen?
 

[Oakman]

Not sure about humans, but in rats this study shows that NAD+ is eventually turned into NR. So why bother when you can start with NR, and it's cheaper?

 

http://nadh.wiki/wp-...-of-the-Rat.pdf

 

Digestion and Absorption of NAD by the Smail Intestine of the Rat1 CAROL J. GROSS ANDLxVELL M. HENDERSON2 Department of Biochemistry, University of Minnesota, 1479 Gartner Avenue, St. Paul, MN 55108 ABSTRACT

 

A number of preparations of varying complexity have been used in an effort to elucidate the reactions by which NAD is hydrolyzed to nicotinamide during intestinal digestion. NAD labeled with 14Cin the adenine or pyridine moiety was the substrate used with perfused rat intestine, live rats, perfused live rats, with collection of portal flow, intestinal contents, mucosa! tissue, or pancreatic juice. The conclusions reached are that a pyrophosphatase present in the intestinal juice and to a much lesser extent in the pancreatic juice releases 5'-AMP and nicotinamide ribonucleotide. The 5'- AMP was rapidly converted to adenosine then to inosine by bacteria-free intestinal contents. Perfused or intact intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed. J. Nutr. 113: 412-420, 1983.

Edited by Oakman, 10 July 2017 - 02:48 PM.