NMN supplementation reduced aging in mice (broad array of parameters) | David Sinclair

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Previous studies on nicotinamide mononucleotide, an NAD+ forerunner, showed that the particle is effective in enhancing NAD+ levels throughout several cells while enhancing the end result of a selection of age-related illness in rodents. Current study on rodents shows that nicotinamide mononucleotide improves frailty and also heart feature. Although these studies are promising in terms of rodent health and wellness, the inquiries of whether they work in people and at what dose continue to be unanswered. In this clip, Dr. David Sinclair discusses the current state of research on nicotinamide mononucleotide.

This clip was taken from the FoundMyFitness interview with Dr. David Sinclair found at https://youtu.be/5DtWqzalEnc

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Nicotinamide mononucleotide

Nicotinamide Mononucleotide (NMN) & Resveratrol

Original episode released on Nov 6, 2019

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  1. awesome??

  2. Send some NMN soon 🙂 !!

  3. Couple questions on timing. I always see NMN being taken in the morning. Is this during the fasting window? (For example) if someones feeding window is 11 am to 6 pm, would it be a good idea to take NMN early, say on waking at 5 am and then reverestral during the feeding window? I know Dr Sinclair takes the reverestral in the AM with yogart, but to my mind that is eating.

  4. NAD+ metabolism promotes cancer progression.
    (Notably, NMN treatment resulted in a significant decrease in the proportion of normal acinar area in pancreata compared to controls, indicative of an increase in the amount of precancerous and cancerous lesions).
    We next determined the effects of NAD+ metabolism-regulated proinflammatory SASP in vitro using a co-culture of the OIS IMR90 cells with TOV21G ovarian cancer cells. Compared with controls, OIS IMR90 cells stimulated the growth of the co-cultured TOV21G cancer cells (Fig. 4a). Notably, knockdown of HMGA1 or NAMPT or treatment with NAMPT inhibitor FK866 in the established OIS cells significantly suppressed the growth stimulation (Fig. 4a). We next determined the effects of NAD+ metabolism-regulating the proinflammatory SASP in vivo. To do so, we utilized a pancreatic cancer mouse model in which the proinflammatory SASP promotes tumor progression in a paracrine SASP-dependent and intrinsic senescence-associated growth arrest-independent manner 21. Specifically, mice expressing Cre recombinase-inducible Lox-STOP-Lox-K-RasG12D were crossed with mice expressing Cre under the control of the pancreas-specific p48 promoter (hereafter referred to as KC mice). These mice develop pancreatic intraepithelial neoplasia (PanINs), precursors to malignancy, which contain senescent cells 22. At 8 week of age, KC mice were given intraperitoneal injections of either vehicle control, 500 mg/kg NMN daily, or treated with 25 mg/kg FK866 daily for 13 days. Mice were sacrificed the day after the last injection and pancreata were harvested for analysis. Notably, NMN treatment resulted in a significant decrease in the proportion of normal acinar area in pancreata compared to controls, indicative of an increase in the amount of precancerous and cancerous lesions (Fig. 4b-c). Indeed, there was a significant increase in the amount of desmoplastic tissue in NMN-treated pancreata compared to controls, as indicated by Masson trichrome staining (Fig. 4d-e). This correlated with an increase in IL1β, IL-6, and IL-8 expression and an increase in immune cell infiltration (such as CD3- and F4/80-positive cells) in NMN-treated pancreata (Fig. 4f-j). Notably, NAMPT expression positively correlates with expression of a number of SASP genes in human PanINs (Supplementary Fig. 4). Consistent with the findings that NAMPT inhibition suppresses senescence at the time of initiation (Supplementary Fig. 2a-d), FK866 suppressed the expression of IL1β, IL-6, and IL-8 and senescence markers such as SA-β-gal, p16 and p21 (Fig. 4f and 4k-n). Indeed, FK866 did not decrease acinar area, Masson trichrome staining or immune cell infiltration compared with KC controls (Fig. 4b-j), suggesting tumor progression that is associated with overcoming senescence. In addition, the expression of the senescence markers such as SA-β-gal, p16 and p21 was not decreased by NMN treatment (Fig. 4k-n). Notably, nicotinamide (NAM), a substrate of NAMPT, stimulated TOV21G tumor growth in a xenograft mouse model and inducible NAMPT knockdown suppressed the observed growth stimulation (Fig. 4o-p). This suggests that the observed effects are due to growth of cancer cells. Taken together, these data support the notion that NMN treatment enhances the inflammatory environment in the pancreas to accelerate pancreatic cancer progression.
    (Fig. 4a-p) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448588/figure/F4/?report=objectonly
    Published online 2019 Feb 18. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448588/

  5. Yes…BUT! Can humans take NMN and not get CANCER!? No safety studies in large numbers followed over several years. Do we want to be lab rats because the manufacturer of supplements do not have to meet any standards???

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