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 Essential for Life
NAD+ stands for nicotinamide adenine dinucleotide.

NAD+ is a molecule found in every cell in the body that is used to power metabolism, construct new cellular components1, resist free radical and DNA damage and send signals within the cells.2,3 It enables the mitochondria – the ‘powerhouses 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 processes.4,5

Healthy mitochondrial function, is an important component of healthy human aging. Our body naturally has the ability to make NAD+ from components in the food we eat. Research in laboratory animals and people shows that as we age, levels of NAD+ declines substantially. This decline leaves us at greater risk for neuro and muscular degeneration6, declines in our cardiometabolic health7 and our capacity for repair and resiliency.

Research suggests NAD+ is key to increasing the amount of time we spend in good health.4-7

What Environmental and Lifestyle Factors Can Impact NAD+ Levels?

Research in animal models suggests that there are a number of lifestyle and environmental factors that impact natural NAD+ levels:

Scientists at prestigious research institutions have been investigating NAD+ boosting strategies as a therapy for degenerative conditions related to aging. Research indicates that NAD+ plays a unique role in muscle and tissue protection, as well as increasing lifespan.4,8

How does NR boost cellular energy?


  1. Nature Education. (2014). Cell Energy and Cell Functions. Retrieved October 17, 2016, from
  2. Canto C, Auwerx J. NAD+ as a signaling molecule modulating metabolism. Cold Spring Harb Symp Quant Biol. 2011;76:291–298. doi: 10.1101/sqb.2012.76.010439.
  3. Ziegler M. New functions of a long-known molecule. Emerging roles of NAD in cellular signaling. Eur. J. Biochem. 2000;267:1550–1564.
  4. Belenky, P., Racette, F. G., Bogan, K. L., Mcclure, J. M., Smith, J. S., & Brenner, C. (2007). Nicotinamide Riboside Promotes Sir2 Silencing and Extends Lifespan via Nrk and Urh1/Pnp1/Meu1 Pathways to NAD. Cell, 129(3), 473-484. doi:10.1016/j.cell.2007.03.024
  5. Imai, S., & Guarente, L. (2014). NAD and sirtuins in aging and disease. Trends in Cell Biology, 24(8), 464-471. doi:10.1016/j.tcb.2014.04.002
  6. Frederick, D., Loro, E., Liu, L., Davila, A., Chellappa, K., Silverman, I., . . . Baur, J. (2016, August). Loss of NAD Homeostasis Leads to Progressive and Reversible Degeneration of Skeletal Muscle. Cell Metabolism, 24(2), 269-282. doi:10.1016/j.cmet.2016.07.005
  7. Gomes, A., Price, N., Ling, A., Moslehi, J., Montgomery, M. K., Rajman, L., . . . Sinclair, D. (2013). Declining NAD Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging. Cell, 155(7), 1624-1638. doi:10.1016/j.cell.2013.11.037
  8. Prolla, T., & Denu, J. (2014). NAD Deficiency in Age-Related Mitochondrial Dysfunction. Cell Metabolism, 19(2), 178-180. doi:10.1016/j.cmet.2014.01.005
  9. Mouchiroud, L., Houtkooper, R. H., & Auwerx, J. (2013). NAD metabolism: A therapeutic target for age-related metabolic disease. Critical Reviews in Biochemistry and Molecular Biology, 48(4), 397-408. doi:10.3109/10409238.2013.789479