NAD+ (500mg)

NAD+ (500mg)

$150.00 – $275.00

NAD+ (nicotinamide adenine dinucleotide) is a vital coenzyme in all living cells, essential for metabolic processes and cellular function. It acts as a mediator of redox reactions, alternating between its oxidized (NAD+) and reduced (NADH) forms to facilitate electron transfer, crucial for energy production and sustaining life. Involved in over 500 enzymatic reactions, NAD+ is central to maintaining cellular homeostasis. Research shows that NAD+ may be beneficial in improving muscle function, protecting cells of the nervous system, and generally reducing the effects of aging.

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Description

NAD+, short for nicotinamide adenine dinucleotide, is the oxidized form of NADH. It’s main biological function is to carry electrons from one biochemical reaction to another, acting to shuttle energy within a cell and, in certain conditions, to extracellular locations as well. NAD+ also plays roles in enzyme activation/deactivation, posttranslational modification of proteins, and cell-to-cell communication. As an extracellular signaling molecule, NAD+ has been found to be released from neurons in blood vessels, the bladder, the large intestine, and from certain neurons in the brain.

NAD+ Effects

  • NAD+ is best thought of as a support molecule that is essential to cellular metabolism as well as extracellular communication. Research shows that NAD+ plays important roles in energy conversion, DNA repair, immune defense, and circadian cycles. Levels of the cofactor, however, are sensitive to disease state as well as age. NAD+ as the following effects that decline as a result of natural age-related decreases in the levels of the cofactor.
  • NAD+ activates sirtuins and other enzymes, liked Poly-ADP-ribose polymerases, involved in DNA repair and inflammatory processes. Sirtuins are the same enzymes linked to the life-extending benefits of calorie restriction.
  • NAD+ controls the production of the protein PGC-1-alpha, which protects neurons and other cells in the central nervous system from oxidative stress. Research in mice shows that this particular effect may be linked to improved memory, particularly with aging.
  • In mouse models, NAD+ helps to protect blood vessels against age-related hardening and the deposition of atherosclerotic plaques. In some studies, the cofactor even helps to reverse age-related dysfunction of the aorta.
  • Mice given NAD+ show increased rates of metabolism and improved lean body mass.
  • Increased NAD+ levels can increase muscle strength and endurance in older mice.
  • NAD+ has been linked to extracellular signaling, particularly for smooth muscle. It may be of benefit in GI function. This effect is likely responsible for NAD+ benefits on blood pressure[1], [2].

Product Usage:

This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabeled as a drug, food or cosmetic.

Research

Anti-Aging Research and NAD+

One of the primary results of the standard aging process is a decline in both the quality and activity of mitochondria. Mitochondria are the body’s power plants, producing the energy for everything from neuron firing to digestion and muscle function. A decline in mitochondrial functioning has been associated with normal aging, but is also a factor in a number of age-related disease processes. Research shows that mitochondrial aging contributes to cellular senescence, inflammation, and even changes in stem cell activity that reduce rates of healing and make it harder for the body to recover from injury in old age[5].

According to Nuo Sun of the Heart, Lung, and Blood Institute of the National Institutes of Health, mitochondria cannot simply be viewed as bioenergetics factories, but “rather as platforms for intracellular signaling, regulators of innate immunity and modulators of stem cell activity.” He goes on to explain that “mitochondria can be linked to a wide range of processes associated with aging including senescence, inflammation, as well as the more generalized age-dependent decline in tissue and organ function.” In other words, mitochondria are the lynch pin of cellular aging and understanding how to protect their function is a necessary first step in understanding how to slow, stop, or even reverse the aging process.

New research suggests that at least some of the age-related decline seen in mitochondria can be reversed through dietary supplementation with NAD+. This function of NAD+ was uncovered, or at least made popular in research circles, by David Sinclair of Harvard University. Sinclair is the same researcher who uncovered the anti-aging effects of reservatrol (a component of red wine). In 2013, Sinclair revealed that mitochondria in the muscle of mice could be restored to a more youthful state via injection of a precursor to NAD+[6].

Research completed in 2013 showed that declining levels of NAD+ leads to a pseudohypoxic state within cells. This, in turn, interrupts the normal signaling that takes place between the nucleus, where DNA resides, and the mitochondria. By supplementing old mice with NAD+, mitochondrial function is restored and the communication commences again[7].

At least prat of the reason that NAD+ helps to offset the effects of aging is that it activates SIRT 1 function in the nucleus and prevents the normal age-related decline in expression of this particular gene. SIRT 1 is a gene encoding a protein known as sirtuin 1 (short for NAD-dependent deacetylase sirtuin-1). Sirtuin 1 is an enzyme that plays important roles in regulating proteins involved in cellular metabolism and processes linked to stress, longevity, and inflammation[8].

References:

  1. “NAD+ Science 101 - What Is NAD+ & Why It’s Important,” Elysium Health. [Online]. Available: https://www.elysiumhealth.com/en-us/knowledge/science-101/everything-you-need-to-know-about-nicotinamide-adenine-dinucleotide-nad. [Accessed: 25-Jul-2019].
  2. “Nicotinamide Riboside: Benefits, Side Effects and Dosage,” Healthline. [Online]. Available: https://www.healthline.com/nutrition/nicotinamide-riboside. [Accessed: 25-Jul-2019].
  3. R. T. Matthews, L. Yang, S. Browne, M. Baik, and M. F. Beal, “Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects,” Proc. Natl. Acad. Sci. U. S. A., vol. 95, no. 15, pp. 8892–8897, Jul. 1998. [PMC]
  4. “What You Need to Know About Resveratrol Supplements,” WebMD. [Online]. Available: https://www.webmd.com/heart-disease/resveratrol-supplements. [Accessed: 25-Jul-2019].
  5. N. Sun, R. J. Youle, and T. Finkel, “The Mitochondrial Basis of Aging,” Mol. Cell, vol. 61, no. 5, pp. 654–666, Mar. 2016. [PMC]
  6. D. Stipp, “Beyond Resveratrol: The Anti-Aging NAD Fad,” Scientific American Blog Network. [Online]. Available: https://blogs.scientificamerican.com/guest-blog/beyond-resveratrol-the-anti-aging-nad-fad/. [Accessed: 08-Jul-2019].
  7. A. P. Gomes et al., “Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging,” Cell, vol. 155, no. 7, pp. 1624–1638, Dec. 2013. [PMC]
  8. S. Imai and L. Guarente, “NAD+ and sirtuins in aging and disease,” Trends Cell Biol., vol. 24, no. 8, pp. 464–471, Aug. 2014. [PubMed]
  9. A. R. Mendelsohn and J. W. Larrick, “Partial reversal of skeletal muscle aging by restoration of normal NAD+ levels,” Rejuvenation Res., vol. 17, no. 1, pp. 62–69, Feb. 2014. [PubMed]
  10. C. Kang, E. Chung, G. Diffee, and L. L. Ji, “Exercise training attenuates aging-associated mitochondrial dysfunction in rat skeletal muscle: role of PGC-1α,” Exp. Gerontol., vol. 48, no. 11, pp. 1343–1350, Nov. 2013. [PubMed]
  11. S. Ringholm et al., “Effect of lifelong resveratrol supplementation and exercise training on skeletal muscle oxidative capacity in aging mice; impact of PGC-1α,” Exp. Gerontol., vol. 48, no. 11, pp. 1311–1318, Nov. 2013. [PubMed]
  12. A. Lloret and M. F. Beal, “PGC-1α, Sirtuins and PARPs in Huntington’s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All,” Neurochem. Res., May 2019. [PubMed]
  13. C. Shan et al., “Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson’s disease,” Prog. Neuropsychopharmacol. Biol. Psychiatry, vol. 94, p. 109670, Jun. 2019. [PubMed]
  14. D. C. Maddison and F. Giorgini, “The kynurenine pathway and neurodegenerative disease,” Semin. Cell Dev. Biol., vol. 40, pp. 134–141, Apr. 2015. [PubMed]
  15. A. Garten, S. Schuster, M. Penke, T. Gorski, T. de Giorgis, and W. Kiess, “Physiological and pathophysiological roles of NAMPT and NAD metabolism,” Nat. Rev. Endocrinol., vol. 11, no. 9, pp. 535–546, Sep. 2015. [PubMed]
  16. S. Yamaguchi and J. Yoshino, “Adipose Tissue NAD+ Biology in Obesity and Insulin Resistance: From Mechanism to Therapy,” BioEssays News Rev. Mol. Cell. Dev. Biol., vol. 39, no. 5, May 2017. [PMC]
  17. J. E. Humiston, “Nicotinamide Adenine Dinucleotide,” p. 68. [FDA]

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