Which foods or habits effectively raise NAD+ levels?
Supplementation with NR or NMN measurably raises NAD+, but convincing evidence in healthy people is still lacking. Ordinary food supplies small amounts of precursors, and eating less sugar is the best-supported habit for not actively lowering NAD+.
Diet supplies small amounts of NAD+ building blocks through vegetables, meat, milk and fermented products. How large that contribution actually is to your NAD+ levels has barely been measured. Milk also contains tryptophan, an amino acid that can serve as a roundabout raw material for NAD+, but again, its effect on your actual NAD+ levels has not been measured directly.
Supplementation with direct NAD+ precursors, such as NR or NMN, measurably raises NAD+ in the blood. The most compelling human data come from a small double-blind study in patients with Werner syndrome, a rare aging disease. In that study, 1000 mg of NR per day significantly raised NAD+ levels and also improved arterial calcification, skin ulcers and kidney function. That is a specific patient group, so you cannot simply extrapolate this to healthy people. Results for cognitive decline are mainly positive in animal research; in humans, the data are scarce and sometimes contradictory.
Exercise is described as a way to support NAD+ metabolism in muscles, but how large that effect actually is has not been quantified in the available studies. It is biologically plausible, though: as we age, NAD+ consumption increases while replenishment falls behind, and exercise helps to partially compensate for that.
What you are better off avoiding: too many simple sugars. In cells and in young mice, NAD+ dropped sharply within hours upon high glucose exposure, with damage to bone formation and mitochondria. That recovery may be possible with supplementation was also shown in the mouse model, but human data are still lacking. Vitamin B3 (niacin) is furthermore crucial as a basis for NAD+ production. A severe deficiency during pregnancy caused congenital abnormalities in virtually every organ in mice. In liver disease, niacin supplements look promising in the lab, but human studies show mixed results.
Nine claims based on studies with varying designs: one small double-blind RCT in humans (Werner syndrome), two review articles covering cognitive function and muscle function respectively, laboratory and mouse models for sugar/bone formation and pregnancy, and mechanistic/observational claims for dietary sources. The human RCT data are limited and derived from a rare patient population.