NAD+ dosage, as studied — the figures from the trials, not a protocol.

Before the numbers

This page reports NAD+ dosage figures the way the studies reported them — what was given, to whom, for how long, and by which route. It is not a recommendation and contains no instruction to take anything. Two reminders carry the whole page. First, oral NAD+ itself is poorly absorbed; the figures below are mostly for precursors (NMN and NR), the building blocks the body turns into NAD+. Second, a dose that worked in a trial is a research observation in that population, not a dose for any individual. Numbers are tagged by route so an oral-precursor figure is never confused with an IV one.

Doses studied in the research literature

In human trials, NMN (a precursor) was studied at 250-900 mg/day orally, with 250 mg/day the most-replicated dose and up to 1200 mg/day examined; the multicenter dose-ranging trial spanned 300/600/900 mg/day and identified 600 mg/day as optimal for raising blood NAD+ ^[3]. The insulin-sensitivity trial used 250 mg/day for 10 weeks ^[11]. Nicotinamide riboside (NR, a precursor) was commonly studied at 250-1000 mg/day, with the 8-week dose-ranging trial at 100/300/1000 mg/day ^[4] and up to 3000 mg/day tested for safety in a Parkinson's-disease study (NR-SAFE). Plain nicotinamide has been studied at 500 mg twice daily for skin-cancer chemoprevention. For the injectable route, reported IV NAD+ protocols run roughly 250-1000 mg per session over several hours, and one pharmacokinetic study used a continuous 3 umol/min infusion over 6 hours ^[14]. These are doses observed in studies, presented as research figures only — not human dosing guidance.

How much NAD should I take?

This page reports doses studied in the literature — for example NMN 250-900 mg/day and NR 250-1000 and up to 3000 mg/day — rather than a recommendation ^[3][4]. It is informational only and is not human dosing guidance; whether, how, and how much to use is a decision for a qualified clinician, not this digest.

Why most oral products are precursors

NAD+ itself is a large, charged dinucleotide and is not freely taken up intact by most cells, so plain oral 'NAD+' is an inefficient way to raise the coenzyme. The body builds NAD+ through pathways that start from smaller molecules, and that is exactly where precursors enter. A precursor is a building block the body converts into NAD+ — NMN and NR are the common ones. NR is taken up and converted to NMN by NRK kinases, then to NAD+; NMN sits one step from NAD+ ^[5]. This is why nearly all of the strong oral human data come from NMN and NR rather than NAD+ capsules — they feed the salvage and NRK routes the cell already runs ^[4][7].

How long NAD+ and its precursors persist

NAD+ half-life depends entirely on route. Infused IV NAD+ is cleared from plasma rapidly — a pilot pharmacokinetic study found near-complete plasma removal within roughly the first two hours, with the infused NAD+ extensively metabolized before plasma NAD+ rose ^[14]. Oral precursors behave oppositely: absorbed and converted over time, they raise whole-blood NAD+ over days to weeks, and the elevation persists through chronic dosing in 8-12 week trials ^[4]. After stopping an oral precursor, blood NAD+ returns toward baseline over weeks. There is no single 'NAD+ half-life' figure — the coenzyme is endogenous and continuously synthesized and consumed; what the trials track is the whole-blood NAD+ level as a pharmacodynamic readout, not the clearance of a drug.

Routes studied

Oral capsules and powders of NMN, NR and nicotinamide carry the bulk of the controlled human evidence ^[4]. Intravenous NAD+ infusion is used in wellness settings with limited, mostly pilot or retrospective data ^[14]. Subcutaneous and intramuscular NAD+ injection is compounded with minimal peer-reviewed pharmacokinetics. Sublingual, intranasal, topical and transdermal-patch NAD+ products are marketed but have little controlled evidence behind them. A stability note matters for the injectable routes: NAD+ and NMN are hygroscopic and degrade with heat and moisture, and reconstituted injectable NAD+ should be kept cold and protected from light. Compounded injectables also carry contamination risk — the FDA has issued a Class I recall of a compounded NAD+ injection over elevated endotoxin.

Tolerability and adverse events reported in trials

In the cited oral-precursor trials, NAD+ side effects were generally mild and similar to placebo. The 8-week NR dose-ranging trial reported no flushing and no significant adverse-event difference from placebo at 100/300/1000 mg/day, and NR did not elevate LDL cholesterol ^[4]. The NMN trials at 300/600/900 mg/day and 250 mg/day reported good tolerability and no serious adverse events ^[3][11]. The clearest documented risks attach to the injectable and IV routes: the FDA Class I endotoxin recall of a compounded injectable NAD+, and transient infusion-related chest pressure, abdominal discomfort, flushing and nausea when an IV is run too fast, which resolve on completion of the infusion. A separate theoretical concern — that boosting NAD+ could support the metabolism of existing cancers — has prompted caution in cancer populations, because NAD+'s role in oncology is dual and context-dependent. This describes what studies and reports observed; it is not safety advice.