What NAD+ Is
Nicotinamide adenine dinucleotide, written NAD+, is a coenzyme present in every living cell. It performs two distinct jobs.
Electron carrier. NAD+ accepts electrons during the breakdown of glucose, fatty acids, and amino acids, becoming NADH in the process, then delivers them to the mitochondrial electron transport chain where the majority of cellular ATP is generated. This shuttle runs constantly in every cell that produces energy.
Enzyme substrate. NAD+ is consumed, not just recycled, by two enzyme families. Sirtuins are involved in regulating metabolism, mitochondrial function, and cellular stress responses. PARPs participate in DNA repair. Both use NAD+ as a required substrate rather than borrowing it, which means their activity draws down the available pool.
That second role is why NAD+ became a focus of aging research. Cellular processes that consume NAD+ compete with the metabolic processes that depend on it.
Where NAD+ Comes From
The body produces NAD+ through several routes. The salvage pathway recycles nicotinamide back into NAD+ and accounts for most production. NAD+ can also be synthesized from niacin, from nicotinamide riboside and nicotinamide mononucleotide, and from the amino acid tryptophan.
Every approach to raising NAD+ levels works by supplying one of those inputs, or by administering NAD+ directly.
The Decline With Age
NAD+ levels fall with age across multiple tissues. That observation is well documented and is the starting point for most of the interest in the molecule.
The proposed explanations include increased consumption by DNA repair enzymes as damage accumulates, reduced activity in the salvage pathway, and increased activity of enzymes that degrade NAD+.
What the Human Research Supports
Being accurate here matters, because claims about NAD+ circulate far ahead of evidence.
The biology is solid. NAD+ is essential to cellular metabolism, levels decline with age, and in laboratory and animal models raising NAD+ availability produces measurable effects on mitochondrial function and cellular repair pathways.
Human clinical evidence is early. Most published human research has studied oral precursors, meaning nicotinamide riboside and nicotinamide mononucleotide, rather than NAD+ itself. Those studies generally confirm that blood NAD+ levels can be raised. What raising them accomplishes clinically in humans remains largely unestablished, and the studies are mostly small and short.
Intravenous NAD+ has less supporting data still. It was first described clinically in 1961 in the context of addiction treatment and has since become widely available through wellness clinics, but published human data examining it as a health-modifying intervention remains limited.
Anyone stating that NAD+ slows aging or protects neurons in humans is describing a hypothesis under investigation.
Where NAD+ Is Available
NAD+ can be received by infusion, by self-injection, or by nasal spray. The routes differ in dose, time commitment, and the amount of evidence behind them. A comparison of all three is available on the NAD+ Therapy page.
