NAD+ (nicotinamide adenine dinucleotide) in primary mitochondrial myopathy and bioenergetic disorders — evidence extract
The Institute's graded assessment of NAD+ (nicotinamide adenine dinucleotide) for primary mitochondrial myopathy and bioenergetic disorders, with the contributing trials and the domain-by-domain certainty reasoning.
§1Evidence extract: Primary mitochondrial myopathy and bioenergetic disorders
§1.1Question and anchor outcome
- Population
- Genetically determined impairment of oxidative phosphorylation producing myopathy, exercise intolerance or multisystem disease.
- Intervention
- NAD+ (nicotinamide adenine dinucleotide), intravenous infusion, subcutaneous or intranasal in research contexts; oral precursors are a separate matter
- Comparator
- As used in each contributing trial; reported per trial rather than pooled across comparator types
- Anchor outcome
- Six-minute walk distance
Additional outcomes the Institute extracts for this indication: Primary mitochondrial myopathy symptom assessment; Muscle phosphocreatine recovery kinetics.
§1.2Contributing trials
No trial has been identified for NAD+ (nicotinamide adenine dinucleotide) in primary mitochondrial myopathy and bioenergetic disorders. The rating below reflects that absence.
§1.3Certainty assessment
Table 2. Reasoning recorded against each certainty domain.
| Domain | Rating | Reasoning |
|---|---|---|
| Risk of bias | No concern | No serious concern identified in this domain. |
| Inconsistency | No concern | No serious concern identified in this domain. |
| Indirectness | Very serious | The enrolled population differs materially from the population of the assessment question. |
| Imprecision | Serious | The event count falls below the optimal information size. |
| Publication bias | No concern | No serious concern identified in this domain. |
| Overall rating: Very low certainty. The Institute has very little confidence in the effect estimate. The true effect is likely to be substantially different from the estimate. In this series a very low rating most often reflects an absence of controlled human evidence rather than conflicting evidence. | ||
§1.4What this extract does not establish
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
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.