Key Benefits
Biologic Description
Nicotinamide adenine dinucleotide (NAD⁺) is a vital coenzyme found in every cell of the human body. It plays a central role in redox reactions—acting as an electron shuttle during cellular respiration—as well as serving as a substrate for key enzymes involved in DNA repair, epigenetic regulation, circadian rhythm, and cell survival. NAD⁺ exists in two forms: NAD⁺ (oxidized) and NADH (reduced), forming a redox pair essential to mitochondrial ATP production.
Beyond energy metabolism, NAD⁺ is a critical signaling molecule. It serves as a required cofactor for sirtuins (SIRT1–7), PARPs (poly ADP-ribose polymerases), and CD38/CD157 ectoenzymes, all of which are deeply involved in aging, inflammation, and cell death pathways.
As we age, NAD⁺ levels decline significantly in tissues—by as much as 50% by middle age—leading to mitochondrial dysfunction, loss of genomic integrity, and impaired stem cell maintenance. This decline is thought to be one of the core biological underpinnings of aging itself.
Dosage Guidelines
NAD⁺ in powdered lyophilized form is used subcutaneously for metabolic support, mitochondrial repair, cognitive enhancement, and anti-aging research. Most research protocols use between 10mg to 100mg per injection, depending on goals and tolerance.
Lower doses (10–50 mg) may be used for cellular maintenance or combined with NMN/NR in metabolic protocols. Higher doses (50–100 mg) are reserved for repair-intensive goals such as neurological recovery or systemic inflammation mitigation.
Starting Dose
10-100 mg
5 Days on 2 Days Off
6-8 Weeks
Side Effects
While NAD⁺ is a naturally occurring molecule, supraphysiologic restoration or aggressive elevation may produce unintended effects, especially in methylation-sensitive individuals.
Observed research effects:
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Transient fatigue or flu-like symptoms (common with IV NAD⁺ drips)
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Nausea or cramping (when administered too quickly or via non-buffered routes)
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Methyl donor depletion leading to mood or detox issues
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PARP overactivation in certain cancer models (caution in oncology)
Additionally, overactivation of CD38, an NAD-consuming enzyme, has been linked to immunosenescence and may blunt the benefit of NAD⁺ elevation unless addressed concurrently (e.g., using apigenin or CD38 inhibitors in research).
References:
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Trammell, S. A., & Brenner, C. (2013). Targeting nicotinamide adenine dinucleotide (NAD⁺) metabolism to treat metabolic diseases and cancer. Nature Reviews Drug Discovery, 12(11), 741–760. https://doi.org/10.1038/nrd4148
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Grant, R., Berg, J., Mestayer, R., et al. (2019). A pilot study of the effect of high-dose intravenous NAD+ on metabolism and neurodegeneration. Scientific Reports, 9, 9772. https://doi.org/10.1038/s41598-019-46120-z
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Cantó, C., Menzies, K. J., & Auwerx, J. (2015). NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus. Cell Metabolism, 22(1), 31–53. https://doi.org/10.1016/j.cmet.2015.05.023
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Imai, S., & Guarente, L. (2014). NAD+ and sirtuins in aging and disease. Trends in Cell Biology, 24(8), 464–471. https://doi.org/10.1016/j.tcb.2014.04.002
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