NAD+ (nicotinamide adenine dinucleotide) — clinical evidence
Assessed outcomes with certainty ratings, contributing trials and the reasoning for each rating.
§3Clinical evidence
§3.1Alcohol use disorder
Anchor outcome. Drinks per drinking day.
Effect as recorded. No assessable randomised evidence identified; —.[1,2]
Certainty. Very low certainty Intravenous NAD+ is offered commercially for substance-withdrawal indications with no controlled evidence base.
Contributing trials. None identified. The rating reflects an absence of controlled evidence rather than conflicting evidence.
Full evidence extract for alcohol use disorder · Indication assessment
§3.2Biological ageing and healthspan endpoints
Anchor outcome. Epigenetic age acceleration.
Effect as recorded. No randomised controlled human trial of administered NAD+ on any ageing endpoint identified; —.[2,3]
Certainty. Very low certainty Trials of the oral precursors nicotinamide riboside and nicotinamide mononucleotide exist and report raised blood NAD+ concentrations with limited functional effect. Those trials are not evidence for intravenous NAD+, and the Institute states the distinction because it is routinely elided in marketing.
Contributing trials. None identified. The rating reflects an absence of controlled evidence rather than conflicting evidence.
Full evidence extract for biological ageing and healthspan endpoints · Indication assessment
§3.3Cognitive performance and neuroprotection
Anchor outcome. Domain-specific cognitive test scores.
Effect as recorded. No assessable randomised evidence identified; —.[3,4]
Certainty. Very low certainty —
Contributing trials. None identified. The rating reflects an absence of controlled evidence rather than conflicting evidence.
Full evidence extract for cognitive performance and neuroprotection · Indication assessment
§3.4Primary mitochondrial myopathy and bioenergetic disorders
Anchor outcome. Six-minute walk distance.
Effect as recorded. No assessable randomised evidence identified for administered NAD+; —.[4,5]
Certainty. Very low certainty —
Contributing trials. None identified. The rating reflects an absence of controlled evidence rather than conflicting evidence.
Full evidence extract for primary mitochondrial myopathy and bioenergetic disorders · Indication assessment
References cited on this page
References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.
- Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism 2015;21(3):443–454. doi:10.1016/j.cmet.2015.02.009 · PMID 25738459
- Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. British Journal of Pharmacology 2014;171(8):2029–2050. doi:10.1111/bph.12461 · PMID 24117165
- United States Pharmacopeial Convention. General Chapter ⟨85⟩ Bacterial Endotoxins Test. United States Pharmacopeia — National Formulary (USP–NF) 2024;USP 2024 Issue 1. identifier not held by the Institute
- United States Pharmacopeial Convention. General Chapter ⟨71⟩ Sterility Tests. United States Pharmacopeia — National Formulary (USP–NF) 2024;USP 2024 Issue 1. identifier not held by the Institute
- International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use. ICH Q1A(R2) Stability Testing of New Drug Substances and Products. ICH Harmonised Tripartite Guideline 2003;Step 4 version. identifier not held by the Institute
Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.