RESEARCH DIGEST / NAD+ & AGING
NAD+ is a coenzyme whose cellular brightness dims with age, read here through the precursor research.
A scholarly, scene-by-scene reading of the published NAD+ literature: what declines, why precursors like NMN and NR are studied to raise it, and what the trials actually measured — every figure cited.
The short version
NAD+ (a fuel-handling helper molecule every cell uses to turn food into energy) is not a drug and not a single product on a shelf. It is a coenzyme (a helper molecule an enzyme needs to do its job) that your body makes on its own, and its level in tissues slowly falls as you age. Most things sold as "NAD" are actually precursors (building blocks the body converts into NAD+ — NMN and NR are the common ones), because NAD+ itself is large and poorly absorbed when swallowed. This site is a reading list of the studies, not medical advice and not a place to buy anything.
What NAD+ is, and what the literature has established
NAD+ (nicotinamide adenine dinucleotide) is the cell's central redox carrier — "redox" being the electron-shuttling chemistry that releases energy from food. It moves electrons through glycolysis, the TCA cycle, and oxidative phosphorylation to make ATP, the molecule cells spend as energy [5]. It is also a consumed substrate: three enzyme families — the sirtuins (a family of cellular-maintenance enzymes that cannot work without NAD+), the PARPs (DNA-repair enzymes), and CD38 (an NAD-burning enzyme on cell surfaces) — spend NAD+ as they govern DNA repair, gene regulation, and inflammation [5]. Tissue NAD+ declines with age across yeast, worms, mice, and humans, a finding catalogued in a foundational 2021 review of NAD+ metabolism in ageing [5].
NAD+ is endogenous: every human cell synthesizes it from tryptophan (the de novo route), from nicotinic acid (the Preiss-Handler route), and — dominantly — from the salvage pathway, which recycles nicotinamide back into NAD+ through the rate-limiting enzyme NAMPT [5]. Its molecular weight is 663.43 Da and its registry identifier is CAS 53-84-9. NAD+ is not a peptide and not a protein; it is a dinucleotide built from a nicotinamide ring and an adenine ring joined by two bridging phosphates. This site reads that science one scene at a time, and it summarizes what NAD+ does in the body without recommending any product or dose.
NAD+ as a Dietary Supplement: Precursors, Not NAD+ Itself
The market sells "NAD" as a dietary supplement, but the regulatory and biochemical reality is narrower than the label suggests. NAD+ is not FDA-approved for any disease; it is a supplement, and oral NAD+ itself is poorly taken up by cells intact [6]. For that reason most experts treat precursors — nicotinamide mononucleotide (NMN), nicotinamide riboside (NR), and the older B3 vitamers niacin and nicotinamide — as the rational oral approach, and some argue plain oral "NAD+" capsules are largely ineffective [6].
The distinction matters for reading the evidence honestly: when a randomized trial reports raised blood NAD+, the participants almost always took a precursor, not NAD+ itself. NR at 100, 300, and 1000 mg/day for eight weeks raised whole-blood NAD+ by 22%, 51%, and 142% respectively in healthy overweight adults [4]. Oral NMN at 300-900 mg/day for 60 days raised blood NAD+ at days 30 and 60 across all doses in a multicenter double-blind trial [3]. None of those participants "took NAD+" — they took a building block their cells assembled into it. See NMN vs NR for the precursor-to-precursor comparison.
What the Research Has Measured (Not 'Benefits')
Search traffic asks for "NAD+ benefits," but the literature measures outcomes in specific studies, not benefits in general — and the honest summary keeps that frame. In prediabetic, postmenopausal women, 10 weeks of oral NMN at 250 mg/day increased skeletal-muscle insulin sensitivity, with no change in body composition or HbA1c [1]. In a middle-aged multicenter trial, 60 days of oral NMN raised blood NAD+ dose-dependently and improved six-minute walking distance versus placebo, with 600 mg/day identified as the optimal dose and no safety signal at any dose [3]. NR's signature result is pharmacodynamic: a clean, dose-scalable rise in whole-blood NAD+ without flushing [4].
The rodent record is broader and stronger than the human one. NMN and NR improved insulin sensitivity, glucose tolerance, and liver fat in metabolic mouse models [6], and NMN restored markers of fertility and mitochondrial function in aged mouse ovaries [9][10]. These are described findings, not endorsements — and crucially, the strongest anti-aging data remain in animals. A 2025 Nature Metabolism review of NAD+ precursor supplementation in human ageing concluded that human efficacy for hard clinical endpoints remains limited and that tissue-NAD+ data are still sparse [13]. The honest reading: precursors raise blood NAD+ reliably; what that buys a human is still being measured.
How to read this site
Each page is a scene in the NAD+ record. NAD+ and aging reads the decline itself — why tissue NAD+ falls and what the precursor research tries to restore. NMN vs NR sets the two leading oral precursors side by side. The research page covers mechanism, the human precursor trials, and the pharmacokinetics of injectable and IV NAD+. Doses used in the research reports what was administered, to which species, by which route — never a human recommendation. The FAQ answers the questions readers actually ask, and the full references and citations list resolves every figure on the site to a study you can open. Nothing here is dispensed, priced, or sold.