What is the relation between NAD+ and vitamin B3?
Vitamin B3 is the only dietary building block for NAD+ in your body -- that relationship is causal and well supported. Whether NAD+ supplements such as NMN or NR genuinely deliver health benefits has yet to be proven.
Your body does not simply produce NAD+ on its own. It needs vitamin B3 as a building block. Vitamin B3 is not a single substance but a family: niacin, nicotinamide, and more modern variants such as NMN and NR. All of these forms are raw materials that cells use to produce NAD+. An intake that is too low through diet leads directly to an NAD+ deficiency.
NAD+ is indispensable in hundreds of energy-generating reactions in your cells, including the functioning of the mitochondria -- the power plants of your cell. In addition, proteins that repair DNA damage and switch genes on and off consume NAD+ as a raw material. It is therefore both an energy molecule and a regulator of your cellular health.
NAD+ levels decline measurably with age. Whether that decline can be countered with vitamin B3 supplements, and whether doing so also reverses symptoms, has not yet been proven in humans. There is a great deal of positive research in mice, but the step toward solid evidence in humans is still small.
The more modern and more expensive variants NMN and NR are largely converted to nicotinamide in the liver before they reach other tissues. The route through your body therefore strongly determines what such a supplement actually does. Ordinary niacin showed promising results in mouse studies on muscle breakdown in cancer: it restored NAD+ in tissues and improved mitochondrial function in muscles.
In humans, the data are scarce. A small study involving 30 Parkinson's patients (1000 mg NMN-related supplement per day, 30 days) showed a variable increase in NAD+ in the brain, along with less inflammation and a mild improvement in participants who produced more NAD+1,2,3,4,5,6,7,8. In mouse studies on Alzheimer's disease, five months of supplementation reduced inflammation in the brain and improved memory. These are preliminary results -- not proof of efficacy. Too little is still known about long-term safety, and experts advise waiting for larger studies.
Based on multiple review articles and studies in humans (PMID 34041853, 29249689, 39026037, 33930322, 29685734, 37012289, 35235774, 34497121). The studies in humans are small and limited in number. Most of the functional evidence on disease treatment comes from mouse studies.