Nicotinamide riboside
Overview
Nicotinamide riboside (NR) is a pyridinium riboside. Human NRK1 phosphorylates it to NMN; NMN adenylyltransferase can then form oxidised NAD [1]. Cow-milk LC-MS analysis establishes dietary occurrence [2].
Dietary Context
Raw and commercial cow milk contained NR in the examined samples [2]. Single-dose NR-chloride supplementation altered blood NAD metabolism in a small human study [3]. Milk occurrence does not establish a food-effective dose or equivalent brain/mitochondrial delivery.
Foods
1 food
Milk
Dairy drink providing complete protein and calcium
Recipes
1 recipe containing this substance
Turmeric Milk
A warming drink combining turmeric (curcumin) with milk/fat for enhanced curcumin absorption
Biological Regulatory Systems
See the evidence-qualified precursor pathways connected to NAD metabolism. An intermediate or target identity does not create a dietary admission.
References
[1] UniProt Consortium (2026). Human NRK1, Q9NWW6. Entry version 170, Rhea 14017, retrieved 26 October 2026. Reaction provenance.
[2] Trammell et al. (2016). Nicotinamide Riboside Is a Major NAD+ Precursor Vitamin in Cow Milk. Primary composition analysis; milk form and sample variability remain.
[3] Trammell et al. (2016). Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Supplement pharmacokinetics; blood endpoints do not establish brain uptake.
Foods supply the named dietary input. They are not shown as containing the downstream metabolite. Conversion evidence does not establish a new downstream PM admission, effective dose or equivalent food intervention.
Nicotinamide riboside → Human NRK1 phosphorylates beta-NR to beta-NMN using ATP. → Nicotinamide mononucleotide
BRS4-FM1-PM2: Maintain NAD⁺ availability so redox reactions and mitochondrial signalling stay adequately powered.
Existing admission: Type A / derived; versioned-assessment. Production context for an already admitted substrate; no new metabolite-to-PM relationship is admitted.
Supplemental NR chloride at 100–1000 mg is not an effective milk dose. Blood responses do not establish neuronal or mitochondrial NAD delivery, redox flux, superiority to adequate niacin or clinical benefit. Intestinal metabolism and tissue salvage can differ from the displayed intracellular NRK route; other NAD precursors remain alternatives.
- Milk — supplies Nicotinamide riboside; verified; form not known. Raw cow milk from individual cows and commercial cow-milk samples, including skim milk
Composition provenance
An established intracellular route is not proof that all oral NR reaches each tissue intact; parallel degradation/salvage can contribute.
Dependencies: Functional NRK activity; ATP and divalent-metal availability; Tissue access to intact NR
Nicotinamide riboside → Human NRK1 phosphorylates beta-NR to beta-NMN using ATP. → NMN adenylyltransferase adenylates oxidised beta-NMN with ATP to form oxidised NAD. → NAD+ (oxidised nicotinamide adenine dinucleotide)
BRS4-FM1-PM2: Maintain NAD⁺ availability so redox reactions and mitochondrial signalling stay adequately powered.
Existing admission: Type A / derived; versioned-assessment. The complete derived relationship is admitted for this PM.
Supplemental NR chloride at 100–1000 mg is not an effective milk dose. Blood responses do not establish neuronal or mitochondrial NAD delivery, redox flux, superiority to adequate niacin or clinical benefit. Intestinal metabolism and tissue salvage can differ from the displayed intracellular NRK route; other NAD precursors remain alternatives.
- Milk — supplies Nicotinamide riboside; verified; form not known. Raw cow milk from individual cows and commercial cow-milk samples, including skim milk
Composition provenance
An established intracellular route is not proof that all oral NR reaches each tissue intact; parallel degradation/salvage can contribute.
Dependencies: Functional NRK activity; ATP and divalent-metal availability; Tissue access to intact NR
NMNAT1 establishes reaction identity; other isoforms/transport determine compartmental provision. No fixed dietary conversion yield or mitochondrial/brain endpoint is inferred.
Dependencies: Functional NMNAT activity; ATP availability; Compartment-specific precursor access