Decline in NAD Level with Age
Graph based on data from Massudi, H., Grant, R., Braidy, N., Guest, J., Farnsworth, B., & Guillemin, G. J. (2012). Age-Associated Changes In Oxidative Stress and NAD Metabolism In Human Tissue. PLoS ONE, 7(7). doi:10.1371/journal.pone.0042357
NAD is Necessary for Life
NAD stands for nicotinamide adenine dinucleotide.
It is a molecule found in every cell in the body. NAD is used to power metabolism by enabling the mitochondria – the ‘power stations’ of the cell to convert the food we eat into the energy our body needs to sustain all its functions. It is also required to “turn off” genes implicated in accelerating aging processes1,2.
NAD helps maintain healthy mitochondrial function – an important component of healthy human aging. Research shows that as we age levels of NAD decline substantially. This decline leaves us at greater risk for neuro and muscular degeneration, declines in our cardiometabolic health and our capacity for cellular repair and resiliency.3, 4
Today, scientists believe NAD is key to increasing the amount of time we spend in good health.1-4
When was NAD discovered?
Scientists at prestigious research institutions have been investigating NAD boosting strategies as a therapy for degenerative conditions related to aging. Pre-clinical research indicates that NAD plays a unique role in muscle and tissue protection, as well as increasing lifespan1,13
- Belenky, P., et al., Nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+. Cell, 2007. 129(3): p. 473-84.
- Imai, S. and L. Guarente, NAD+ and sirtuins in aging and disease. Trends Cell Biol, 2014. 24(8): p. 464-71.
- Frederick, D.W., et al., Loss of NAD Homeostasis Leads to Progressive and Reversible Degeneration of Skeletal Muscle. Cell Metab, 2016. 24(2): p. 269-82.
- Gomes, A.P., et al., Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 2013. 155(7): p. 1624-38.
- Trammell, S.A., et al., Nicotinamide Riboside Opposes Type 2 Diabetes and Neuropathy in Mice. Sci Rep, 2016. 6: p. 26933.
- Josiane Ménissier de Murcia, C.N., Carlotta Trucco, Michèle Ricoul‡, Bernard Dutrillaux‡, Manuel Mark§, F. Javier Oliver, Murielle Masson, Andrée Dierich, Marianne LeMeur, Caroline Walztinger, Pierre Chambon, and Gilbert de Murcia, Requirement of poly(ADP-ribose) polymerase in recovery from DNA damage in mice and in cells. Proceedings of the National Academy of Sciences of the United States of America, 1997. 94(14): p. 7303-7307.
- Circu, M.L. and T.Y. Aw, Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med, 2010. 48(6): p. 749-62.
- Sasaki, Y., T. Araki, and J. Milbrandt, Stimulation of nicotinamide adenine dinucleotide biosynthetic pathways delays axonal degeneration after axotomy. J Neurosci, 2006. 26(33): p. 8484-91.
- Nakahata, Y., et al., Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1. Science, 2009. 324(5927): p. 654-7.
- Ramsey, K.M., et al., Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis. Science, 2009. 324(5927): p. 651-4.
- Massudi, H., et al., Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLoS One, 2012. 7(7): p. e42357.
- Hugo Theorell, R.B. The Mechanism of Alcohol Dehydrogenase Action. 1951 [cited 2017 October 17]; Available from: http://actachemscand.org/pdf/acta_vol_05_p0329.pdf
- Mouchiroud, L., R.H. Houtkooper, and J. Auwerx, NAD(+) metabolism: a therapeutic target for age-related metabolic disease. Crit Rev Biochem Mol Biol, 2013. 48(4): p. 397-408.