Science-Backed Benefits of NMN for Health and Longevity
The summary below discusses the science-backed benefits of NMN (Nicotinamide Mononucleotide) for health and longevity.
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In June of 2018, the World Health Organization (WHO) released the 11th edition of its International Classification of Diseases, and for the first time added aging.1
Nutrient sensing systems have been an intense focus of investigation, including mTOR (the mammalian target of rapamycin) for regulating protein synthesis and cell growth; AMPK (activated protein kinase) for sensing low energy states; and sirtuins, a family of seven proteins critical to DNA expression and aging, which can only function in conjunction with NAD+ (nicotinamide adenine dinucleotide), a coenzyme present in all living cells.4
The slow process of aging has been described as a “cascade of robustness breakdown triggered by a decrease in systemic NAD+ biosynthesis and the resultant functional defects in susceptible organs and tissues.”6 Aging is marked by epigenetic shifts, genomic instability, altered nutrient sensing ability, telomere attrition, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and dysregulated intercellular communication.7,8
By middle age, our NAD+ levels have plummeted to half that of our youth.9 Numerous studies have demonstrated that boosting NAD+ levels increases insulin sensitivity, reverses mitochondrial dysfunction, and extends lifespan.10,11 NAD+ levels can be increased by activating enzymes that stimulate synthesis of NAD+, by inhibiting an enzyme (CD38) that degrades NAD+, and by supplementing with NAD precursors, including nicotinamide riboside(NR) and nicotinamide mononucleotide (NMN).12,13
A conceptual framework called NAD World, formulated over the last decade by developmental biologist Shin-ichiro Imai, MD, PhD, of Washington University School of Medicine, positions NMN (Nicotinamide Mononucleotide) as a critical, systemic signaling molecule that maintains biological robustness of the communication network supporting NAD+.6
NMN (Nicotinamide Mononucleotide) has been able to suppress age-associated weight gain, enhance energy metabolism and physical activity, improve insulin sensitivity, improve eye function, improve mitochondrial metabolism and prevent age-linked changes in gene expression.14
NMN (Nicotinamide Mononucleotide) is a NAD precursor and Sirtuin activator, the body’s anti-aging and longevity genes, so you may look and feel years younger. NMN also promotes new cellular growth and restores mitochondrial function to assist in fast recovery of muscle tissue and the immune system.
What is Nicotinamide Mononucleotide (NMN)?
Put simply, NMN is a naturally occurring molecule that helps power your body.
NMN is a type of molecule called a nucleotide. Nucleotides play many roles in your body, including as the building blocks of DNA.
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Within your cells, NMN is converted into another molecule known as nicotinamide adenine dinucleotide (NAD). Your body needs NAD for a variety of functions involved in metabolism and energy production.
You might think of NMN as raw material and NAD as the refined version that your body can actually use.
The amount of NAD your body can make depends on the amount of NMN available in your body.
NMN (Nicotinamide Mononucleotide) and NAD.
All the cells in your body use NAD and therefore require NMN, its precursor, to function properly. NAD helps cells regulate a number of essential functions that help keep your cells running smoothly.
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It’s essential that your cells have plenty of NMN to produce enough NAD to support these functions.
Your NMN levels naturally decline over time, and, as a result, your levels of NAD decline, too. This may contribute to some of the health effects you might experience during aging.
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Potential Benefits of NAD
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Since taking NMN may help your body produce more NAD, it’s also important to consider the research behind the benefits of NAD. Studies investigating NAD shed light on its potential benefits:
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It may increase longevity. In your cells, NAD activates a group of proteins called sirtuins, which help repair your DNA. The activity of sirtuins is linked to longevity. On the flip side, low-NAD levels are associated with age-related diseases.
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It may have protective effects on the brain. NAD is thought to regulate the production of a protein that helps guard cells against oxidative stress. These cellular stressors are related to some neurological diseases, including Alzheimer’s disease.
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It may help with jet lag. Research suggests NAD may help adjust your internal clock, potentially helping ease jet lag or other circadian rhythm disorders.​​
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Restored growth of new blood vessels for improved circulation and reversal of vascular atrophy
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Boost Immunity & Immune System Health
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Powerful Anti-Aging Support
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Promotes DNA Repair Through SIRTUIN Gene Activation
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Supports Cardiovascular Health
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Boost Energy Levels, Metabolism & Endurance
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Helps Reduce Stress & Fatigue​​
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It’s important to note that these benefits were found for NAD, not for NMN specifically. More research on the benefits of NMN and NAD is needed. Recent research has found that taking NAD as a supplement doesn’t lead to the same potential benefits — but taking NMN can.
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References:
1. Zhavoronkov A, et al. Classifying aging as a disease in the context of ICD-11. Front Genet. 2015. November (Classifying aging as a disease in the context of ICD-11 - PMC (nih.gov)
2. Blagosklonny MV. Disease or not, aging is easily treatable. Aging (Albany NY). 2018. November 17;10(11):3067-3078 (Disease or not, aging is easily treatable | Aging (aging-us.com)
3. Editorial. Opening the door to treating ageing as a disease. Lancet Diabetes Endocrinol. 2018. August;6(8):587 (Opening the door to treating ageing as a disease - The Lancet Diabetes & Endocrinology)
4. López-Otín C, et al. The hallmarks of aging. Cell 2013;153(6):1194-1217 [PMC free article] [PubMed] [Google Scholar] (The Hallmarks of Aging: Cell)
5. Schultz MB, et al. Why NAD+ Declines during Aging: It’s Destroyed. Cell Metab. 2016. June 14; 23(6): 965–966 (Why NAD+ Declines during Aging: It’s Destroyed | Request PDF (researchgate.net)
6. Imai S. The NAD World 2.0: the importance of the inter-tissue communication mediated by NAMPT/NAD+/SIRT1 in mammalian aging and longevity control. NPJ Syst Biol Appl. 2016. August 18;2:16018. The NAD World 2.0: the importance of the inter-tissue communication mediated by NAMPT/NAD+/SIRT1 in mammalian aging and longevity control | npj Systems Biology and Applications (nature.com)
7. Conboy IM, et al. Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature 2005; 433: 760–764. (Conboy-et-al-(2005)-Nature.pdf (glennfoundation.org)
8. de Magalha~es JP, et al. Meta-analysis of age-related gene expression profiles identifies common signatures of aging. Bioinformatics 2009: 25: 875–881. Meta-analysis of age-related gene expression profiles identifies common signatures of aging (dntb.gov.ua)
9. Zhu XH, et al. In vivo NAD assay revels the intracellular NAD contents and redox state in healthy human brain and their age dependences. Proc. Natl. Acad. Sci. 2015; 112:2876–2881 In vivo NAD assay reveals the intracellular NAD contents and redox state in healthy human brain and their age dependences | PNAS
10. Suave AA. NAD+ and vitamin B3: from metabolism to therapies. J Pharmacol Exp Ther. 2008. March;324(3):883-93 [PDF] NAD+ and Vitamin B3: From Metabolism to Therapies | Semantic Scholar
11. Lee CF, et al. Targeting NAD+ Metabolism as Interventions for Mitochondrial Disease. Sci Rep. 2019. February 28;9(1):3073. JCI Insight - Mitochondrial and NAD+ metabolism predict recovery from acute kidney injury in a diverse mouse population
12. Camacho-Pereira J, et al. CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metab. 2016. June 14;23(6):1127-1139 [PMC free article] [PubMed] [Google Scholar] CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism — Mayo Clinic (elsevierpure.com)
13. Longo VD, et al. Interventions to Slow Aging in Humans: Are We Ready? Aging Cell 14(4): 497-510. Interventions to slow aging in humans: Are we ready? — Research Profiles at Washington University School of Medicine (wustl.edu)
14. Mills KF, et al. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metab. 2016. December 13;24(6):795-806 Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice — Research Profiles at Washington University School of Medicine (wustl.edu)