NAD+ is a coenzyme found in every cell in your body. Its primary roles are helping your cells produce energy, repairing damaged DNA, and activating protective proteins that play a central role in how your body ages.*

The problem is that your body produces less NAD+ as you get older. Research shows that levels can decline by 40-60% between your 30s and 60s. As NAD+ falls, your cells become less efficient at generating energy, slower at repairing damage, and more vulnerable to the kind of accumulated stress that accelerates aging.*

What the research shows NAD+ supports:

Cellular Energy Production. Your cells produce energy through structures called mitochondria. Mitochondria depend on NAD+ to function. When NAD+ declines, energy output declines with it. Replenishing NAD+ targets the problem at its source – inside the cell.*

DNA Repair. Your DNA sustains thousands of hits per day from normal metabolic activity alone. Your body has dedicated repair systems that detect and correct this damage, but they require NAD+ to operate. When NAD+ is low, damage goes unaddressed, but when it's restored, repair resumes.*

Cognitive Performance. Your brain consumes more fuel than any other organ – roughly 20% of your body's total output. When cellular resources drop, you feel it as brain fog, slow thinking, and mental fatigue. Restoring NAD+ delivers what your brain needs to perform at full capacity.*

Cardiovascular Function. Your heart beats approximately 100,000 times per day without rest. Cardiac cells have among the highest power demands in the body. NAD+ helps sustain mitochondrial efficiency, which those cells depend on to perform under continuous load.*

Metabolic Function. NAD+ plays a direct role in how your body processes carbohydrates, fats, and proteins into usable fuel. When NAD+ levels are sufficient, these metabolic pathways operate efficiently. When they're not, conversion slows across the board.*

Inflammation and Cellular Aging. Visible aging is a downstream effect. The real process starts inside your cells – declining output, accumulating DNA damage, and persistent low-grade inflammation. NAD+ acts on all three of these root mechanisms.*

Scientific References:

1. Rajman, L., Chwalek, K., & Sinclair, D. A. (2018). Therapeutic potential of NAD-boosting molecules: the in vivo evidence. Cell Metabolism, 27(3), 529–547.
2. Verdin E. (2015). NAD⁺ in aging, metabolism, and neurodegeneration. Science (New York, N.Y.), 350(6265), 1208–1213.
3. Covarrubias, A. J., Perrone, R., Grozio, A., & Verdin, E. (2021). NAD+ metabolism and its roles in cellular processes during ageing. Nature reviews. Molecular cell biology, 22(2), 119–141.
4. Yoshino, J., Baur, J. A., & Imai, S. I. (2018). NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR. Cell metabolism, 27(3), 513–528.
5. 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), e42357.
6. Lautrup, S., Sinclair, D. A., Mattson, M. P., & Fang, E. F. (2019). NAD+ in Brain Aging and Neurodegenerative Disorders. Cell metabolism, 30(4), 630–655.
7. Hou, Y., Lautrup, S., Cordonnier, S., Wang, Y., Croteau, D. L., Zavala, E., Zhang, Y., Moritoh, K., O'Connell, J. F., Baptiste, B. A., Stevnsner, T. V., Mattson, M. P., & Bohr, V. A. (2018). NAD+ supplementation normalizes key Alzheimer's features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency. Proceedings of the National Academy of Sciences of the United States of America, 115(8), E1876–E1885.
8. Hou, Y., Wei, Y., Lautrup, S., Yang, B., Wang, Y., Cordonnier, S., Mattson, M. P., Croteau, D. L., & Bohr, V. A. (2021). NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS-STING. Proceedings of the National Academy of Sciences of the United States of America, 118(37), e2011226118.
9. de Picciotto, N. E., Gano, L. B., Johnson, L. C., Martens, C. R., Sindler, A. L., Mills, K. F., Imai, S., & Seals, D. R. (2016). Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice. Aging cell, 15(3), 522–530.

Yoshino, M., Yoshino, J., Kayser, B. D., Patti, G. J., Franczyk, M. P., Mills, K. F., Sindelar, M., Pietka, T., Patterson, B. W., Imai, S. I., & Klein, S. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science (New York, N.Y.), 372(6547), 1224–1229.