Research on niacin and NAD+

• Low NAD+ Levels Are Associated With a Decline of Spermatogenesis in Transgenic ANDY and Aging Mice

  A study in mice found that niacin supplementation increased NAD+ levels in the testes, which led to an improvement in sperm count and sperm motility. NAD+ deficient mice have ~30% smaller testes (balls) than the control mice (~1.5g vs ~2.17g). NAD+ is essential for spermatogenesis and that NAD+ deficiency leads to male infertility.

• Supplementation of nicotinic acid and its derivatives up-regulates cellular NAD+ level rather than nicotinamide derivatives in cultured normal human epidermal keratinocytes

  In cultured skin cells, nicotinic acid supplementation 1.3-fold up-regulated intracellular NAD+ level significantly and its metabolites nicotinic acid mono nucleotide also increased NAD+ level by 1.5-fold with 100 μM application. Surprisingly, NAM and its derivatives could not up-regulate cellular NAD+ levels in keratinocytes.

• Antidepressants may lead to a decrease in niacin and NAD in patients with poor dietary intake

  Authors hypothesis that antidepressants tilt tryptophan metabolism towards making serotonin instead of niacin, which in turn can lead to niacin/NAD+ deficiency that exacerbates common psychiatric problems.

• NAD+ repletion rescues female fertility during reproductive aging

  Loss of fertility is associated with lower NAD+ levels. Restoring NAD+ in aged mice by putting nicotinamide mononucleotide (NMN) in their drinking water at 2g/L restored their fertility as well as the adverse effect of old age on the development of the embryo.

• Gut dysbiosis dysregulates central and systemic homeostasis via decreased melatonin and suboptimal mitochondria functioning: pathoetiological and pathophysiological implications.

  In depth review of how deficiency of butyrate and melatonin compromise gut and overall mitochondrial function and lead to lower levels of other key molecules in cellular metabolism like sirtuins, PGC-1α and NAD+.

• Pharmacological Intakes of Niacin Increase Bone Marrow Poly(ADP-Ribose) and the Latency of Ethylnitrosourea-Induced Carcinogenesis in Rats

  Rats fed high niacin diet and then poisoned with ethylnitrosourea (a potent mutagen) survived for longer and had increase amounts of NAD+ (1-1.5x) and ADP-ribose in their bone marrow.