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Preface and Key practice points

  • No NAD⁺ precursor is licensed by the MHRA or EMA for anti-ageing, “longevity” or healthspan extension. All such use is off-label / food-supplement use and should be framed as adjunctive care with explicit informed consent, or ideally within a research/registry framework.
  • Human RCTs consistently show biochemical target engagement (oral NR and NMN reliably raise blood/tissue NAD⁺ and metabolites) and good short-term tolerability, but effects on clinically meaningful ageing, metabolic, vascular and functional outcomes are heterogeneous and frequently null (Gallagher & Emmanuel 2026; Freeberg et al. 2023; Bhasin et al. 2023).
  • Do not infer hard clinical benefit from a rise in NAD⁺ or from surrogate biomarkers; that linkage is not established by robust human outcome data (Bhasin et al. 2023).
  • Two agents have genuine RCT-supported disease indications distinct from longevity: oral nicotinamide 500 mg twice daily for keratinocyte-carcinoma chemoprevention in high-risk immunocompetent patients (ONTRAC; Chen et al., NEJM 2015), and nicotinic acid (niacin) as a historical lipid agent — the latter now largely abandoned because AIM-HIGH and HPS2-THRIVE showed no cardiovascular benefit added to statins and net harm (2018 AHA/ACC systematic review).

1. Scope

Covered:

  • Oral NAD⁺ precursors used in longevity practice: L-tryptophan, nicotinic acid (niacin), nicotinamide (niacinamide), nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR).
  • Biological rationale, human evidence and GRADE-style certainty, patient selection, baseline work-up, dosing, monitoring, safety, contraindications and practical scenarios.

Not covered (or flagged as low-grade only):

  • Intravenous/intramuscular NAD⁺ infusions — no eligible controlled outcome trials exist for anti-ageing/wellness indications; evidence limited to short-term safety/PK data only (Gallagher & Emmanuel 2026). Not recommended outside research.
  • Preclinical (rodent/in-vitro) efficacy, presented separately as mechanistic context only.
  • Disease-specific licensed uses of niacin/nicotinamide are summarised only where they inform safety and dosing.

This document is adjunctive to, and not a substitute for, conventional primary/secondary care.

2. Background and pathophysiology

Biological rationale (human-relevant mechanism):

  • NAD⁺ is an essential redox cofactor and a consumed substrate for sirtuins, PARPs and CD38, linking it to DNA repair, mitochondrial function, inflammation, senescence and circadian biology (Strømland et al. 2021; Chini et al. 2024).
  • Tissue and circulating NAD⁺ decline with age in several organisms including humans, attributed to an imbalance between synthesis (reduced NAMPT) and increased consumption (PARP/CD38 activation) (Strømland et al. 2021).
  • Precursors feed NAD⁺ via distinct routes: tryptophan through the de novo kynurenine pathway; nicotinic acid via the Preiss–Handler pathway; nicotinamide, NR and NMN via the salvage pathway (Castro-Portuguez & Sutphin 2020; Yaku & Nakagawa 2023).
  • The geroscience hypothesis proposes that restoring NAD⁺ could mitigate multiple age-related diseases, but the relationship between NAD⁺ and senescence is complex and bidirectional and is not yet a validated therapeutic target in humans (Chini et al. 2024).

Robust human mechanistic evidence:

  • Oral NR (up to ~2000 mg/day) and NMN (250–2000 mg/day) reliably and dose-dependently raise NAD⁺ and related metabolites in blood and, for some, muscle (Martens et al. 2018; Gallagher & Emmanuel 2026; Yaku & Nakagawa 2023).
  • Importantly, a raised methyl-nicotinamide/NAD⁺ metabolite signature can occur without a measurable rise in skeletal-muscle NAD⁺ or improved mitochondrial function (Connell et al. 2021) — target engagement in blood does not guarantee tissue repletion.

Preclinical only (mechanistic plausibility — not a basis for clinical claims):

  • In rodents, NAD⁺ augmentation improves glucose/lipid metabolism, endothelial function, cardiac ischaemia-reperfusion, neurodegeneration models and healthspan/lifespan (Bhasin et al. 2023; Forman et al. 2023). These effects are frequently not reproduced in human outcomes and should not be extrapolated to patients.

3. Evidence base and grading

Evidence landscape:

  • The largest synthesis (PRISMA systematic review, Gallagher & Emmanuel 2026) identified 33 human intervention studies (28 randomised) plus 80 rodent studies. Human trials are typically small (tens of participants), short (weeks–months) and use surrogate/biomarker endpoints.
  • No adequately powered RCT has tested mortality, incident age-related disease, or validated composite healthspan endpoints for any precursor as a longevity intervention.

GRADE-style certainty and strength of recommendation by outcome:

NAD⁺ elevation / biochemical target engagement (NR, NMN)

  • Evidence: High-certainty evidence from multiple RCTs (e.g. Martens et al. 2018; Yoshino et al. 2021) shows reliable, dose-dependent increases in blood NAD⁺/metabolites.
  • Certainty: High. Consistent, direct, precise.
  • Recommendation: This is a pharmacodynamic finding only — not a clinical benefit. No recommendation for use can be based on it.

All-cause mortality / incident age-related disease / functional healthspan

  • Evidence: No adequately powered RCTs.
  • Certainty: Very low (no direct evidence).
  • Recommendation: Only in research.

Cardiovascular surrogates — blood pressure and arterial stiffness (NR, NMN)

  • Evidence: Martens et al. 2018 (n=24 crossover) found NR well tolerated with a non-significant trend to lower systolic BP/aortic stiffness, hypothesis-generating only. A 2025 pilot RCT (Lin et al., n=54) found NR + exercise was not superior to placebo + exercise for daytime systolic BP, with only post-hoc nighttime signals.
  • Certainty: Low (imprecision, small samples, inconsistency).
  • Recommendation: Conditional / only in research for CV endpoints.

Muscle insulin sensitivity / glucose metabolism (NMN)

  • Evidence: A single positive RCT (Yoshino et al., Science 2021; n=25 prediabetic postmenopausal women) showed improved muscle insulin sensitivity by clamp. However, meta-analyses of RCTs (Chen et al. 2024, 8 RCTs, n=342; largely healthy adults) found no significant effect on fasting glucose, insulin, HbA1c, HOMA-IR or lipids.
  • Certainty: Low (inconsistency, indirectness, imprecision).
  • Recommendation: Conditional against routine use for glycaemic benefit; only in research in prediabetes.

Muscle/physical function and liver enzymes (NMN)

  • Evidence: One RCT meta-analysis (Wang et al. 2024, 9 RCTs, n=412) reported small significant improvements in gait speed (SMD 0.34) and ALT (SMD −0.29). Findings are of uncertain clinical importance and at risk of small-study/publication bias.
  • Certainty: Low.
  • Recommendation: Conditional / only in research.

Mitochondrial and skeletal-muscle function (tryptophan + nicotinic acid + nicotinamide combination)

  • Evidence: RCT in physically compromised older adults (Connell et al. 2021, n=14 crossover) showed no improvement in mitochondrial respiration or exercise efficiency despite evidence of increased NAD⁺ turnover.
  • Certainty: Moderate for absence of benefit (direct, but small).
  • Recommendation: Recommend against this combination for muscle/mitochondrial benefit.

Keratinocyte (non-melanoma) skin cancer chemoprevention (nicotinamide)

  • Evidence: Phase 3 RCT (ONTRAC; Chen et al., NEJM 2015, n=386) — nicotinamide 500 mg BD reduced new non-melanoma skin cancers by 23% (95% CI 4–38) over 12 months in high-risk immunocompetent patients; benefit lost after stopping. Negative in organ-transplant recipients (two RCTs).
  • Certainty: Moderate–High in the immunocompetent high-risk population.
  • Recommendation: Strong recommendation to consider in that specific dermatological indication (a disease indication, not a longevity claim).

Cardiovascular outcomes with nicotinic acid (niacin)

  • Evidence: AIM-HIGH (n=3414) and HPS2-THRIVE (n=25,673) — no reduction in cardiovascular events added to statins, with increased adverse effects including worsened glycaemic control (2018 AHA/ACC systematic review, Wilson et al. 2019).
  • Certainty: High.
  • Recommendation: Recommend against nicotinic acid for cardiovascular risk reduction / longevity.

Cross-cutting GRADE limitations: high risk of small-study bias and heterogeneity; substantial indirectness (disease populations, surrogate endpoints, short duration); imprecision from small samples; and plausible publication bias favouring positive biomarker findings.

4. Patient selection and indications

Who might reasonably be considered (all off-label unless stated):

  • Adults seeking preventive/longevity input who understand the intervention is experimental with unproven hard outcomes and who can give informed consent.
  • Middle-aged/older adults with cardiometabolic risk factors interested in low-risk adjuncts — noting the evidence for benefit is low-certainty (NR/NMN).
  • High-risk immunocompetent patients with recurrent keratinocyte carcinoma — nicotinamide 500 mg BD is evidence-based here (ONTRAC) and is the one genuinely supported indication among these agents.

Where benefit is least likely / avoid:

  • Frail multimorbid older adults expecting functional or muscle benefit — best RCT evidence (Connell et al. 2021) is null; use only in research.
  • Athletes expecting performance/longevity gains — no robust human ergogenic or healthspan data.
  • Anyone wanting cardiovascular protection from nicotinic acid — recommend against (AIM-HIGH, HPS2-THRIVE).
  • Solid-organ transplant recipients seeking skin-cancer prevention from nicotinamide — RCTs negative.

Exclusion / high-risk groups: see Section 8.

Regulatory/ethical status:

  • Off-label / food-supplement for all longevity uses. Best practice: document informed consent, provide balanced evidence, and where feasible enrol in trials/registries. Parenteral NAD⁺ should be research only.

5. Assessment and baseline work-up

History and examination:

  • Full cardiometabolic and medication history (including statins, antihyperglycaemics, antihypertensives, anticoagulants).
  • Alcohol, hepatic and renal history; personal/family history of gout and skin cancer.
  • Baseline symptom review (GI symptoms, flushing tolerance).
  • Validated tools as clinically indicated: cardiovascular risk (e.g. QRISK3), frailty assessment (e.g. Clinical Frailty Scale) in older adults.

Baseline investigations (tailor to agent and comorbidity):

  • FBC, renal profile, liver function tests (nicotinic acid and high-dose nicotinamide can cause hepatotoxicity; ALT is an outcome measure in NMN trials).
  • Fasting glucose/HbA1c and lipid profile (nicotinic acid worsens glycaemia).
  • Serum urate (nicotinic acid raises urate).
  • Blood pressure (ideally ambulatory if a vascular endpoint is being tracked).
  • Routine measurement of blood NAD⁺ is not validated for clinical decision-making and is not required; if measured for research, interpret cautiously.

Risk stratification:

  • Low risk: healthy adult, low-dose NR/NMN or nicotinamide, no interacting drugs.
  • Moderate risk: cardiometabolic disease, polypharmacy, hepatic/renal comorbidity — closer monitoring.
  • High risk: diabetes/impaired glucose tolerance or gout considering nicotinic acid; hepatic impairment considering high-dose nicotinamide; pregnancy/breastfeeding (avoid).

Baseline documentation: consent record, indication and off-label rationale, chosen agent/dose, baseline bloods/BP, and predefined stop criteria and review date.

6. Dosing regimens and practical implementation

Regimens with the most robust human tolerability/target-engagement data:

  • Nicotinamide riboside (NR): commonly 250–1000 mg/day; up to 2000 mg/day well tolerated in RCTs and effectively raises NAD⁺ (Martens et al. 2018; Freeberg et al. 2023). No established loading regimen; steady-state metabolite rise within days–weeks. Off-label.
  • Nicotinamide mononucleotide (NMN): 250–1000 mg/day (studied 250–2000 mg/day, up to 12 weeks); dose-related rise in NAD⁺ (Chen et al. 2024; Wang et al. 2024). Off-label; food-supplement regulatory status varies.
  • Nicotinamide (niacinamide): 500 mg twice daily is the RCT-validated dose for keratinocyte-carcinoma chemoprevention (Chen et al., NEJM 2015). Pharmacological tolerability demonstrated up to ~3.5 g/day, but hepatotoxicity risk rises at high doses (Jadeja et al. 2020). Does not cause flushing.

Regimens requiring caution / limited longevity rationale:

  • Nicotinic acid (niacin): flushing is dose-limiting; extended-release forms reduce flushing but carry hepatotoxicity risk. Given null CV outcomes and net harm added to statins, not recommended for longevity/CV use (Wilson et al. 2019; Jadeja et al. 2020). Retain only for specialist-directed lipid indications.
  • L-tryptophan: no robust human longevity efficacy data; combination with nicotinic acid/nicotinamide was null for muscle/mitochondrial outcomes (Connell et al. 2021). Not recommended as a standalone longevity NAD⁺ strategy.
  • IV/IM NAD⁺: no controlled outcome evidence — research only.

Titration: for nicotinic acid, if ever used, start low and up-titrate to limit flushing; for NR/NMN/nicotinamide no formal titration is required, though starting at the lower end and reviewing tolerability is reasonable.

Dose–response: NAD⁺ metabolite elevation is dose-dependent for NR/NMN, but a biomarker dose–response does not translate into a clinical outcome dose–response in current human data.

7. Monitoring, safety and follow-up

Monitoring plan:

  • Clinical: GI symptoms, flushing/pruritus (nicotinic acid), rash; in older adults monitor falls and function if relevant.
  • Laboratory: LFTs (especially nicotinamide >1–1.5 g/day and any nicotinic acid), fasting glucose/HbA1c and urate if using nicotinic acid; lipids if a metabolic endpoint is tracked.
  • Ageing/surrogate biomarkers: track only if part of a research/registry protocol and interpret as surrogates, not proof of benefit.

Suggested timepoints:

  • Short term (4–12 weeks): tolerability review; LFTs/glucose if using nicotinic acid or high-dose nicotinamide.
  • Medium term (3–6 months): reassess symptoms, bloods, BP, and whether to continue given absence of demonstrable benefit.
  • Long term (≥12 months): periodic bloods; explicit reappraisal of continued off-label use.

Adverse effects and safety profile:

  • NR and NMN: generally well tolerated over weeks–months; mild GI effects (nausea, bloating, diarrhoea, dyspepsia) and occasionally rash/pruritus, mostly grade 1–2 (Lin et al., Lancet Neurology 2026; Freeberg et al. 2023). No serious safety signal in short-term trials; long-term safety unknown.
  • Nicotinamide: well tolerated at 500 mg BD in ONTRAC with no notable excess adverse events; hepatotoxicity, nausea and (rarely) thrombocytopenia reported at high pharmacological doses.
  • Nicotinic acid: flushing/pruritus (very common), hepatotoxicity (especially sustained-release), hyperglycaemia, hyperuricaemia/gout, GI upset; increased adverse events without CV benefit in large RCTs (Wilson et al. 2019).
  • Serious but rare: high-dose nicotinamide/nicotinic acid hepatotoxicity; nicotinic acid can precipitate gout and worsen diabetes.

Actions for abnormal findings:

  • Rising transaminases: reduce dose or stop and re-check; investigate if persistent.
  • New hyperglycaemia/gout on nicotinic acid: stop.
  • Significant GI intolerance: dose-reduce or switch agent/stop.

Interactions:

  • Nicotinic acid + statins: increased myopathy risk historically flagged; no added CV benefit — avoid combination for longevity.
  • Nicotinic acid may impair glycaemic control — caution with antidiabetic regimens.
  • Data on NR/NMN drug interactions are limited; review anticoagulants and complex polypharmacy individually.

Special populations:

  • Pregnancy/breastfeeding: avoid all for longevity indications (insufficient safety data); nicotinamide within normal dietary/niacin-equivalent requirements is a separate matter handled in antenatal care.
  • Renal/hepatic impairment: caution and closer monitoring; avoid high-dose nicotinamide and nicotinic acid in significant hepatic impairment.
  • Frailty/extremes of age: best evidence shows no functional benefit (Connell et al. 2021); if used, low dose with monitoring.

8. Contraindications and cautions

Absolute:

  • Known hypersensitivity to the specific agent.
  • Active significant hepatic disease — avoid nicotinic acid and high-dose nicotinamide.
  • Pregnancy/breastfeeding for off-label longevity use.

Relative / specialist advice advised:

  • Diabetes or impaired glucose tolerance (nicotinic acid — worsens glycaemia).
  • Gout/hyperuricaemia (nicotinic acid).
  • Peptic ulcer disease (nicotinic acid).
  • Concomitant statin therapy where nicotinic acid is being considered — generally avoid; no benefit, added harm.
  • Complex polypharmacy or organ impairment — individualised review.

Harm likely to outweigh benefit with current evidence:

  • Nicotinic acid for cardiovascular/longevity purposes.
  • Nicotinamide for skin-cancer prevention in solid-organ transplant recipients (RCT-negative).
  • Any expectation of proven mortality/healthspan benefit from any precursor.

9. Practical management scenarios (CKS-style)

Scenario A — Middle-aged adult with multiple cardiometabolic risk factors

  • Decision: Consider low-dose NR or NMN only as an adjunct with informed consent (Conditional; low-certainty benefit), after optimising evidence-based cardiometabolic care (BP, lipids, glucose, weight, exercise, smoking). Avoid nicotinic acid.
  • Assessment: cardiovascular risk (QRISK3), baseline LFTs, glucose/HbA1c, lipids, BP.
  • Shared decision-making: state that RCTs show NAD⁺ rises but heterogeneous/often null clinical effects; benefit is unproven, harms low short-term, long-term unknown.
  • Initiation: NR 250–500 mg/day or NMN 250–500 mg/day; ensure guideline-based therapies (statin, antihypertensives) are prioritised.
  • Monitoring/follow-up: tolerability and bloods at 12 weeks and 6 months.
  • Escalate/stop: stop if intolerance, abnormal LFTs, or no defined patient-centred goal met; never substitute for statin/antihypertensive therapy.

Scenario B — Older, frail patient with multimorbidity

  • Decision: Restrict to research / generally avoid for functional or muscle benefit — best RCT evidence is null (Connell et al. 2021) and frailty increases susceptibility to adverse effects and polypharmacy harm.
  • Assessment: Clinical Frailty Scale, medication review, renal/hepatic function.
  • Shared decision-making: emphasise absence of demonstrated functional benefit and deprescribing priorities.
  • If patient still wishes to proceed: lowest-dose NR/NMN, single agent, clear stop criteria, close monitoring.
  • Escalate/stop: stop for any new symptom, LFT derangement, or added pill burden without benefit.

Scenario C — Adjunct in a patient already under specialist care

  • Decision: Consider only with specialist communication; verify no interaction with the primary treatment. For a high-risk immunocompetent patient with recurrent keratinocyte carcinoma under dermatology, offer nicotinamide 500 mg BD (Strong; ONTRAC) — this is an evidence-based dermatological indication, not a longevity claim.
  • Assessment: confirm indication, comorbidities, interacting drugs; baseline LFTs.
  • Shared decision-making: coordinate with the treating specialist; document consent and rationale.
  • Initiation/monitoring: nicotinamide 500 mg BD with periodic LFTs; dermatology follow-up for skin surveillance (benefit wanes on stopping).
  • Escalate/stop: stop if hepatotoxicity; review with specialist if the primary condition changes.

10. Research gaps and future directions

Key uncertainties:

  • Whether raising blood NAD⁺ produces target-tissue repletion and any hard clinical benefit (mortality, incident disease, disability) remains unproven (Bhasin et al. 2023; Gallagher & Emmanuel 2026).
  • Optimal agent, dose, duration and responder phenotype are undefined; biomarker dose–response does not predict outcomes.
  • Discordance between a single positive NMN insulin-sensitivity RCT (Yoshino et al. 2021) and null meta-analytic glucose/lipid data (Chen et al. 2024) needs resolution.
  • Long-term safety of chronic NR/NMN and any theoretical oncological signals are unquantified.
  • Parenteral NAD⁺ has essentially no controlled outcome evidence.

Priority research questions:

  • Adequately powered, long-duration RCTs with prespecified clinically meaningful endpoints in defined at-risk populations (e.g. cardiometabolic risk, sarcopenia/frailty).
  • Head-to-head precursor comparisons and tissue-level pharmacodynamics.
  • Standardised, validated NAD⁺/ageing biomarkers linked to outcomes.

Where practice should be limited: all longevity/healthspan use of NAD⁺ precursors — and all parenteral NAD⁺ — should ideally occur within well-designed clinical trials or prospective registries with informed consent, rather than as routine care.

 

Footnote


A few points worth highlighting on how the evidence maps to the recommendations:

– The strongest, most consistent human finding is biochemical, not clinical. RCTs (e.g. Martens et al. 2018; Yoshino et al. 2021) show reliable NAD⁺ elevation, but the two systematic reviews conclude clinical effectiveness for anti-ageing remains inconclusive with heterogeneous, often null outcomes. The document deliberately separates target engagement from clinical benefit.[5][6][1][2][3]

– The clearest “recommend against” signals are well-evidenced. Nicotinic acid showed no CV benefit and net harm added to statins in AIM-HIGH and HPS2-THRIVE, and the tryptophan/nicotinic acid/nicotinamide combination was null for muscle/mitochondrial outcomes.[11][10]

– The one genuinely RCT-supported indication among these agents is dermatological, not longevity-related — nicotinamide 500 mg BD for keratinocyte-carcinoma chemoprevention in high-risk immunocompetent patients (ONTRAC), negative in transplant recipients. It is flagged as such to avoid conflation with anti-ageing claims.[7][12][13]

– NMN metabolic data conflict — one positive clamp RCT against null meta-analyses for glucose/lipids and only small functional signals — so it is graded low-certainty/conditional.[6][9][8]

Caveats: GRADE labels here are applied pragmatically to a small-trial, surrogate-heavy literature and reflect clinical-editorial judgement rather than a formal guideline panel. The regulatory framing (off-label/food-supplement, MHRA/EMA status) reflects general regulatory reality and should be confirmed against current MHRA guidance and your clinic’s indemnity/governance requirements before implementation.



Figure 2 Skin Cancer–Free Survival Among Patients With or Without Exposure to Nicotinamide When Initiated After 1 to 4 Skin Cancers Breglio KF, Knox KM, Hwang J, et al. Nicotinamide for Skin Cancer Chemoprevention. JAMA Dermatology. 2025;161(11):1140-1147. doi:10.1001/jamadermatol.2025.3238.

 

Figure 1 Overall Skin Cancer–Free Survival Among Patients With or Without Exposure to Nicotinamide Breglio KF, Knox KM, Hwang J, et al. Nicotinamide for Skin Cancer Chemoprevention. JAMA Dermatology. 2025;161(11):1140-1147. doi:10.1001/jamadermatol.2025.3238.

References

  1. NAD⁺ Supplementation for Anti-Aging and Wellness: A PRISMA-guided Systematic Review of Preclinical and Clinical Evidence. Gallagher C, Emmanuel OO. Ageing Research Reviews. 2026;116:103057. doi:10.1016/j.arr.2026.103057.
  2. Dietary Supplementation With NAD+-Boosting Compounds in Humans: Current Knowledge and Future Directions. Freeberg KA, Udovich CC, Martens CR, Seals DR, Craighead DH. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2023;78(12):2435-2448. doi:10.1093/gerona/glad106.
  3. Nicotinamide Adenine Dinucleotide in Aging Biology: Potential Applications and Many Unknowns. Bhasin S, Seals D, Migaud M, Musi N, Baur JA. Endocrine Reviews. 2023;44(6):1047-1073. doi:10.1210/endrev/bnad019.
  4. Impact of Geroscience on Therapeutic Strategies for Older Adults With Cardiovascular Disease: JACC Scientific Statement. Forman DE, Kuchel GA, Newman JC, et al. Journal of the American College of Cardiology. 2023;82(7):631-647. doi:10.1016/j.jacc.2023.05.038.
  5. Chronic nicotinamide Riboside Supplementation Is Well-Tolerated and Elevates NAD+ in Healthy Middle-Aged and Older Adults. Martens CR, Denman BA, Mazzo MR, et al. Nature Communications. 2018;9(1):1286. doi:10.1038/s41467-018-03421-7.
  6. Nicotinamide Mononucleotide Increases Muscle Insulin Sensitivity in Prediabetic Women. Yoshino M, Yoshino J, Kayser BD, et al. Science (New York, N.Y.). 2021;372(6547):1224-1229. doi:10.1126/science.abe9985.
  7. A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention. Chen AC, Martin AJ, Choy B, et al. The New England Journal of Medicine. 2015;373(17):1618-26. doi:10.1056/NEJMoa1506197.
  8. Effects of Nicotinamide Mononucleotide Supplementation on Muscle and Liver Functions Among the Middle-Aged and Elderly: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Wang JP, Wang L, Wang T, et al. Current Pharmaceutical Biotechnology. 2025;26(13):2141-2152. doi:10.2174/0113892010306242240808094303.
  9. Effects of Nicotinamide Mononucleotide on Glucose and Lipid Metabolism in Adults: A Systematic Review and Meta-Analysis of Randomised Controlled Trials. Chen F, Zhou D, Kong AP, et al. Current Diabetes Reports. 2024;25(1):4. doi:10.1007/s11892-024-01557-z.
  10. NAD+-Precursor Supplementation With L-Tryptophan, Nicotinic Acid, and Nicotinamide Does Not Affect Mitochondrial Function or Skeletal Muscle Function in Physically Compromised Older Adults. Connell NJ, Grevendonk L, Fealy CE, et al. The Journal of Nutrition. 2021;151(10):2917-2931. doi:10.1093/jn/nxab193.
  11. Systematic Review for the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Wilson PWF, Polonsky TS, Miedema MD, et al. Journal of the American College of Cardiology. 2019;73(24):3210-3227. doi:10.1016/j.jacc.2018.11.004.
  12. Keratinocyte Carcinoma. Wehner MR. JAMA. 2025;:2840731. doi:10.1001/jama.2025.18749.
  13. Sunscreens: Updates on Sunscreen Filters and Formulations. Ziglar J, Mohammad TF, Gilaberte Y, Lim HW. Photodermatology, Photoimmunology & Photomedicine. 2025;41(3):e70026. doi:10.1111/phpp.70026.
  14. Nicotinamide for Skin Cancer Chemoprevention. Breglio KF, Knox KM, Hwang J, et al. JAMA Dermatology. 2025;161(11):1140-1147. doi:10.1001/jamadermatol.2025.3238.