NAD+

NAD+, nicotinamide adenine dinucleotide, is a coenzyme present in every cell. It carries electrons through the reactions that convert food into ATP, which makes it a hard requirement for energy production rather than a modifier of it.

It is also consumed, not just recycled, by two families of enzymes: the PARPs that carry out DNA repair, and the sirtuins associated with metabolic regulation. Both draw down the pool when they are active, which is the mechanism linking DNA damage and NAD availability.

NAD+ levels decline with age. That observation is well established. What follows from it, and how much can be changed by supplementation, is a considerably less settled question.

Below 62 ug/gHb indicates a low NAD+ pool. Fatigue that does not respond to rest is the effect most often reported, which follows from its role in energy production.

Drivers include oxidative stress, chronic inflammation, poor sleep and alcohol intake. Anything that raises DNA damage raises PARP activity, and PARP activity consumes NAD+.

Niacin, vitamin B3, is the dietary precursor, so intake matters, though frank dietary deficiency is uncommon in populations eating enough protein.

Between 62 and 160 ug/gHb your red cell NAD+ sits inside the reference range for this panel.

Being in range does not mean the level is static. NAD+ turns over quickly, and the demands on it change with sleep, training load and inflammatory state.

Above 160 ug/gHb is uncommon and usually reflects supplementation with NAD+ precursors.

A high result is not established as harmful, but it is also not established as beneficial. The honest position is that the long-term consequences of sustained supraphysiological NAD+ are not yet known.

If you are supplementing precursors and your result is above the range, that is a reasonable prompt to reconsider the dose rather than to continue raising it.

Oxidative stress, short sleep and chronic low-grade inflammation all increase the rate at which NAD+ is consumed. The Western pattern supplies all three at once.

Alcohol is a direct drain, since metabolising it consumes NAD+ in the process. Regular intake creates a standing demand on the same pool that DNA repair depends on.

Niacin-rich foods supply the precursor: turkey, chicken breast, tuna and mushrooms.

Time-restricted eating and periods without food activate the sirtuin pathways associated with NAD+ metabolism.

Polyphenol-rich foods, including berries, green tea, dark chocolate, red onions and turmeric, are commonly recommended here, though the evidence for the effect on NAD+ specifically is weaker than the evidence for the pathway.

Exercise, particularly high-intensity intervals and resistance training, raises NAD+ production. This is the best-supported intervention on the list.

NMN at 250 to 500 mg daily or NR at 300 to 600 mg daily are the direct precursors. Both reliably raise measured NAD+. Whether that translates into the outcomes people take them for is still being studied, and the honest summary is that the human evidence lags the enthusiasm.

Resveratrol at 250 to 500 mg with fat is often taken alongside for its effect on sirtuins.

Apigenin at around 50 mg inhibits CD38, an enzyme that degrades NAD+. CoQ10 as ubiquinol at 100 to 200 mg supports the mitochondrial chain that NAD+ feeds.