NAD+ (oxidised nicotinamide adenine dinucleotide)
Overview
Oxidised NAD is formed from beta-NMN and ATP by NMN adenylyltransferase [1]. Its redox state, cellular compartment and free or protein-associated pools must be distinguished.
Dietary Context
Dietary precursors can support NAD supply. A precursor amount is not an amount of NAD formed, and a blood response does not demonstrate delivery into every tissue or mitochondrial compartment. No direct food NAD-content edge is created here.
Foods
Recipes
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 NMNAT1, Q9HAN9. Entry version 202, Rhea 21360, retrieved 26 October 2026. Oxidised NAD reaction target, not a dietary efficacy study.
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. → 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