NAD+
Nicotinamide Adenine Dinucleotide
NAD+ is a vital coenzyme present in every cell that plays crucial roles in energy metabolism, DNA repair, and cellular aging processes. As NAD+ levels naturally decline with age (by ~50% by age 50), supplementation through IV therapy or injections aims to restore cellular energy production, activate longevity pathways through sirtuin proteins, and support mitochondrial health. Research demonstrates significant improvements in cognitive function, physical performance, and biomarkers of aging.
NAD+ Mechanism of Action
The Complete Journey: From Injection to Results
NAD+ functions as an essential coenzyme in over 400 enzymatic reactions, primarily serving as an electron carrier in cellular respiration and energy metabolism. In mitochondria, NAD+ accepts electrons from metabolic substrates and transfers them through the electron transport chain for ATP synthesis. NAD+ also serves as a substrate for three major enzyme families: sirtuins (SIRT1-7), poly(ADP-ribose) polymerases (PARPs), and CD38/CD157. Sirtuin activation by NAD+ promotes deacetylation of key proteins involved in metabolism, stress resistance, and longevity, including PGC-1α for mitochondrial biogenesis, p53 for DNA repair, and FOXO transcription factors for stress response. PARP enzymes utilize NAD+ for DNA repair processes, while CD38 represents a major NAD+ consumer that increases with age, contributing to age-related NAD+ decline.
How NAD+ Works at the Molecular Level
Scientific Mechanism
NAD+ functions as an essential coenzyme in over 400 enzymatic reactions, primarily serving as an electron carrier in cellular respiration and energy metabolism. In mitochondria, NAD+ accepts electrons from metabolic substrates and transfers them through the electron transport chain for ATP synthesis. NAD+ also serves as a substrate for three major enzyme families: sirtuins (SIRT1-7), poly(ADP-ribose) polymerases (PARPs), and CD38/CD157. Sirtuin activation by NAD+ promotes deacetylation of key proteins involved in metabolism, stress resistance, and longevity, including PGC-1α for mitochondrial biogenesis, p53 for DNA repair, and FOXO transcription factors for stress response. PARP enzymes utilize NAD+ for DNA repair processes, while CD38 represents a major NAD+ consumer that increases with age, contributing to age-related NAD+ decline.
Simple Explanation
Think of NAD+ as your cellular battery charger and repair supervisor all in one. Every cell in your body needs NAD+ to turn food into energy - it's like the key that starts your cellular engines. But NAD+ does much more than just energy production. It also activates special 'longevity proteins' called sirtuins that work like a cellular maintenance crew, fixing damaged DNA, building new mitochondria (your cellular power plants), and helping cells resist stress and aging. The problem is that as we age, our NAD+ levels drop dramatically - by age 50, we have only half the NAD+ we had in our 20s. This is like having a car with a dying battery and a maintenance crew that's falling asleep on the job. NAD+ therapy aims to recharge this system, giving your cells the energy and repair support they need to function optimally.
The Simple Truth: Why It Works So Well
Medical Disclaimer
NAD+ therapy is currently in research phase and not FDA-approved for specific medical conditions. This information is for educational purposes and should not replace consultation with qualified healthcare providers. Individual results may vary significantly. Professional medical supervision is recommended for all NAD+ therapeutic protocols.