Vitamin B3 comprises niacin (nicotinic acid) and niacinamide (nicotinamide), precursors to NAD⁺/NADPH, central to mitochondrial energy metabolism. Niacinamide redirects here.

Vitamin B3
Niacin (vitamin B3) molecular structure
Niacin (vitamin B3) molecular structure
Vitamin name Niacin (nicotinic acid) / Niacinamide (nicotinamide)
Chemical formula
Solubility Water-soluble
Discovery year
Daily requirement (RDA)
Upper limit
Rich food sources Liver, poultry, fish, coffee; endogenous from tryptophan
Ray's verdict

Ray Peat preferred niacinamide over nicotinic acid for supplementation: nicotinic acid raises histamine, serotonin and prostaglandins, all inflammatory, while niacinamide is active in cells without releasing them.[1]

Dosing

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Peat community protocols often use small niacinamide doses (tens of mg, sometimes ~100 mg); megadosing is rarely necessary. See Harm reduction. Dietary sources include liver, poultry, and Coffee. Email notes treat niacinamide as usable alone; a full B-complex stack is not required for that form.[2]

Niacinamide has a wide therapeutic index; reversible liver toxicity has appeared only at very high doses, and minor liver-enzyme changes are infrequent.[3] Twice-daily topical 5% niacinamide for 12 weeks reduced fine lines, wrinkles, hyperpigmented spots, and red blotchiness versus vehicle on the other side of the face.[4]

Peat quotes (niacinamide)

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A four-week vinegar RCT in overweight adults improved PHQ-9 depression scores and raised circulating nicotinamide with upregulated NAD+ salvage metabolism on metabolomics profiling.[5]

Niacinamide, used in moderate doses, can safely help to restrain the excessive production of free fatty acids, and also helps to limit the wasteful conversion of glucose into fat.

— Ray Peat[6]

The competition between fatty acids and glucose, which has been called the "Randle cycle" for about 50 years, can be applied to the treatment of diabetes and other degenerative/stress problems by adjusting the diet, or by using supplements such as niacinamide and aspirin, which improve glucose oxidation by lowering the free fatty acids in the serum.

— Ray Peat[7]

Niacinamide and Aspirin are the two most practical agents for lowering circulating free fatty acids and stopping the stress reaction, which protects glucose oxidation in the Randle cycle.[8]

Mechanism

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Nicotinamide riboside boosted the mitochondrial unfolded-protein response and preserved mitochondrial oxygen consumption in stressed cardiomyocytes; human heart-tissue data correlated higher UPRmt activation with better function, a rationale for NAD+ precursor therapy in heart failure.[9] PARP-driven extracellular poly(ADP-ribose nucleated vascular and soft-tissue calcification; PARP inhibition blocked mineral deposition, a pathway niacinamide is known to inhibit at gram-scale doses.[10] Nicotinamide reversed restraint-induced depressive behavior in mice while restoring hippocampal ATP, supporting NAD+-linked bioenergetic failure as a driver of stress-related depression.[11] Oral pyruvate and niacinamide restored retinal pyruvate and NAD+ in glaucoma-prone mice, reversed metabolic deficits, and combined subtherapeutic doses lowered optic-nerve degeneration risk more than either alone.[12] Ten weeks of 250 mg daily NMN improved skeletal muscle insulin sensitivity and upregulated genes involved in muscle structure in postmenopausal women with prediabetes.[13] Oral NMN for six weeks improved ventilatory thresholds and skeletal muscle aerobic function in trained runners, supporting NAD+ repletion for mitochondrial endurance capacity.[14] Low-dose niacinamide for three weeks cut diet-induced obesity fat mass nearly in half, raised adipose NAD+ roughly thirtyfold, upregulated NAMPT and mitochondrial OXPHOS proteins, and improved glucose tolerance without reducing food intake.[15] Topical NMN promoted hair regrowth with magnitude similar to minoxidil by raising VEGF and beta-catenin while lowering DKK-1 and androgen-receptor expression in dermal papilla cells.[16] NLRC5 detects NAD+ depletion and nucleates a PANoptosome that executes PANoptosis, positioning cellular NAD+ status as a checkpoint for innate inflammatory cell death.[17] NAMPT-activating P7C3-A20 restored brain NAD+ and reversed advanced Alzheimer's pathology in mice.[18] Niacinamide supplementation in bioreactor culture raises NAD+, reverses aerobic glycolysis, and shifts CHO cells toward mitochondrial oxidative metabolism.[19]

Estrogen diverts tryptophan away from niacin synthesis, and niacinamide opposes some of these estrogen-driven metabolic shifts.[21]

Nicotinamide inhibits inducible nitric oxide synthase and cut endotoxin-induced TNF-alpha production in vitro and in vivo.[22]

Niacinamide has many effects, but the first one is inhibiting the lipase that liberates fats from your fat stores.

— Ray Peat[23]

Stored PUFA released by stress or hunger slow the metabolism; niacinamide lowers free fatty acids while good nutrition lets the liver detoxify the PUFA slowly.[24]

Niacinamide lowered serum phosphorus in hemodialysis patients,[25] and its antilipolytic action, which protects glucose use for energy, may be part of that phosphate-lowering effect.[26]

In rats, nicotinamide infused into the nucleus accumbens kept high-anxious animals from becoming socially subordinate; complex I and II inhibitors there did the opposite.[27] See Anxiety.

Niacin vs niacinamide

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Nicotinic acid at pharmaceutical doses is an established lipid-lowering drug (flushing via prostaglandins). Niacinamide does not lower cholesterol at ordinary doses and lacks that flush. Peat's preference is specifically for niacinamide, not megadose niacin.

Alzheimer's disease

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A completed human clinical trial tested nicotinamide as an early Alzheimer's disease treatment, with proof-of-concept results reported as beneficial, direct clinical support (not just animal-model evidence) for niacinamide/NAD+ repletion in early AD.[28]

Female reproductive aging

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Topical nicotinamide mononucleotide or nicotinamide riboside restores meibomian-gland 3β-HSD activity and androgen-driven lipid secretion in age-related dry eye, linking NAD+ cofactor availability to local steroidogenesis.[29] Low-dose NMN (0.5 g/L drinking water for four weeks) in 13-month-old mice improved time to first live birth and overall live-birth rates more than higher doses, via raised NAD⁺/NADH and improved oocyte quality.[30]

Peripheral artery disease

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Six months of oral nicotinamide riboside improved 6-minute walk distance by 17.6 meters versus placebo in peripheral artery disease (NICE trial, n=90); resveratrol added no benefit to NR alone.[31]

Muscle regeneration and sarcopenia

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In a US epidemiological cohort, dietary niacin intake correlated positively with appendicular lean mass, total lean mass, and bone mineral content, and negatively with total and trunk fat: roughly 60 g lean-mass gain and 60 g fat loss per 1 mg/kg/day niacin; associations were stronger with obesity, hypertension, and age 50–60 years (intake range up to ~238 mg/day).[32] Skeletal muscle wasting accompanied mitochondrial respiratory defects, supporting NAD-dependent oxidative metabolism as a determinant of lean-mass maintenance.[33] Vitamin D receptor deletion caused muscle glycogen trapping and wasting, highlighting steroid-hormone control of glycogen phosphorylase activity as a determinant of lean-mass maintenance.[34] Hepatocyte mitochondrial NAD+ pool size (via SLC25A51) limits liver regeneration after partial hepatectomy; boosting mitochondrial NAD+ matches high-dose precursor supplementation.[35] Nicotinamide and pyridoxine synergistically activate aged muscle stem cells and improve regenerative capacity in preclinical screening.[36]

Osteoarthritis

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Vitamin B1 is depleted in osteoarthritis synovial fluid and oral supplementation reduced chemokine-driven joint inflammation in preclinical models.[37] Twelve weeks of niacinamide 3 g/day improved global arthritis impact (~29%), joint mobility, and ESR versus placebo in a 72-patient RCT, with modest GI side effects.[38]

Hepatic miR-93 drives metabolic dysfunction-associated steatotic liver disease; raising NAD+ via vitamin B3 pathways is proposed as a genomic-level intervention.[39]

Cancer cachexia

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SIRT1 overexpression maintained chronic myeloid leukemia stem-cell survival and drug resistance; SIRT1 deletion sensitized leukemic cells to tyrosine-kinase inhibitors. Niacinamide is a SIRT1 inhibitor.[40] Oral niacin reprogrammed glioma-associated myeloid cells and slowed glioblastoma growth in mice with better tolerability than temozolomide at tested doses.[41] Niacin 750–1000 mg/day for months raised blood NAD+ up to eightfold, restored muscle NAD+ in adult-onset mitochondrial myopathy, improved strength, and halved liver fat.[42] Raising NAD+ pools is proposed as a countermeasure to alcohol-driven NAD+ depletion and fatty liver, since binge drinking converts NAD+ to NADH and impairs NAD-dependent liver metabolism.[43] Mitochondrial SIRT3 supports lymphoma growth through amino-acid metabolism and ATF4; pharmacologic SIRT3 inhibition starved tumor cells and enhanced lymphoma cell killing.[44] Tuberculosis macrophage killing depends on TNF-driven mitochondrial reverse electron transport; restoring NAD+-dependent electron flow is a proposed host-directed therapy.[45] One week of nicotinamide plus D-ribose raised blood NAD+ and NADP+, improved insulin sensitivity and glucose tolerance, increased ATP/ADP, lowered salivary cortisol, and reduced fatigue scores versus placebo.[46] Loss of autophagy depleted neuronal NAD+ through SIRT and PARP overconsumption; nicotinamide and related precursors restored NAD+ and prevented neurodegeneration in vitro.[47] Hypertensive humans and mice show roughly 50% lower aortic NAD+; six weeks of nicotinamide mononucleotide supplementation restored NAD+, lowered systolic pressure, and improved arterial pulse-wave velocity.[48] Oral nicotinamide riboside 3000 mg daily for four weeks improved Parkinson motor and non-motor UPDRS scores while raising whole-blood NAD+ roughly fourfold without serious adverse events.[49] Inflammation-impaired mitochondrial function in sensory neurons sustains chronic pain after resolution of acute inflammation; nicotinamide riboside restored mitochondrial metabolism and reversed hyperalgesia.[50]

Post-orgasmic illness syndrome

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A case of post-orgasmic illness syndrome with flu-like symptoms after ejaculation improved with niacinamide therapy after conventional treatments failed.[51] Glioblastoma diverts nicotinamide through tumor-specific NNMT, consuming methionine-derived methyl groups; dexamethasone plus methionine restriction synergizes with this metabolic rewiring to slow tumor growth.[52] Cancer-cachexia muscle wasting correlates with mitochondrial OXPHOS downregulation and NAD+ depletion; restoring NAD+ metabolism rescues protein synthesis in tumour-bearing mice.[53] Niacin supplementation (~150 mg/kg in mice) restores skeletal-muscle NAD+, improves mitochondrial metabolism, and attenuates cancer-cachexia weight and grip-strength loss in colon-cancer xenograft models.[54]

Niacinamide was one co-intervention, with N-acetylcysteine, whole thyroid extract, and thymus protein, in a Padayatty NCI Best Case Series intravenous vitamin C renal-cell case whose pulmonary cannonball metastases cleared. The series does not attribute that outcome to niacinamide alone.[55]

Scleroderma and NAD+

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Long-term nicotinamide mononucleotide (NMN) reduced frailty in male and female mice and raised levels of a gut bacterium linked to lower inflammation in mice. It improved metabolic health in males only and raised median lifespan by 8.5% in females only, without increasing tumors.[56] Nicotinamide inhibited TGF-β–driven epithelial-to-mesenchymal transition in retinal pigment epithelium and slowed fibrotic membrane formation in vitro.[57] Bleomycin-induced skin fibrosis depletes NAD+ via CD38; nicotinamide riboside supplementation or CD38 inhibition restores NAD+ and prevents scarring in aged mice.[58]

Genetic disease rescue

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High-dose vitamin B3 (nicotinamide riboside) from birth rescues lethal NAXD knockout mice by restoring NADHX repair and brain NAD+, with dozens of other inborn errors nominally treatable by B2 or B3 in a Cell micronutrient screen.[59]

ALS and gut microbiome

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Motor neuron metabolism

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Controlled-release niacin (up to 2000 mg/d) added to first-line glioblastoma therapy showed improved six-month progression-free survival in an interim phase II analysis.[60] Niacinamide (0.5 mM) raises mitochondrial NAD+ in familial and sporadic ALS motor neurons, restoring respiration and ATP production and reversing the hyper-glycolytic, low-OXPHOS phenotype shared across ALS subtypes.[61] In an ALS mouse model, Akkermansia muciniphila (a nicotinamide-producing commensal) slows disease progression; nicotinamide supplementation improves symptoms though less than restoring the bacterium, and ALS patients show lower Akkermansia abundance with reduced nicotinamide in blood and CSF correlating with severity.[62]

Low renal NAD+ is a feature of human kidney disease; raising NAD+ with NR or NMN precursors protects tubular mitochondrial function in animal models.[63]

Bacterial infection and nicotinamidase

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NMN raised intracellular NAD+, suppressed HIV-1 p24 production, and reduced hyperactivated CD25+ CD4+ T cells in vitro and in cART-treated humanized mice.[64] Mammals store vitamin B3 primarily as niacinamide and do not express nicotinamidase; bacteria that secrete nicotinamidase convert niacinamide to nicotinic acid, so an elevated nicotinic-acid/niacinamide ratio in culture medium or biological samples can indicate live bacterial contamination with high specificity and faster turnaround than conventional sterility assays.[65] In macrophages, nicotinamide restricts replication of mycobacteria that depend on functional nicotinamidase, linking bacterial NAD metabolism to host resistance.[66]

Niacin, miR-93, and fatty liver disease

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The microRNA miR-93 is elevated in the liver in metabolic dysfunction-associated steatotic liver disease (MASLD) and suppresses SIRT1, impairing fat-burning pathways. Of 150 FDA-approved drugs screened, niacin (vitamin B3) was the most effective at lowering miR-93; in treated mice this restored SIRT1 activity, reduced fat accumulation, and improved insulin sensitivity.[67]

See also

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References

[edit]
  1. ↑ Ray Peat, "One Radio Network: Dr. Peat Answers Questions Regarding Health, Diet and Nutrition Part 2", One Radio Network, 40:46
  2. ↑ Ray Peat, Niacin(amide) email Q&A, raypeatemails.com.
  3. ↑ Knip M, Douek IF, Moore WP, et al. "Safety of high-dose nicotinamide: a review," Diabetologia. 2000;43(11):1337-1345. doi:10.1007/s001250051536. PMID 11126400.
  4. ↑ Bissett DL, Oblong JE, Berge CA. "Niacinamide: A B vitamin that improves aging facial skin appearance," Dermatol Surg. 2005;31(7 Pt 2):860-5. PMID 16029679.
  5. ↑ Barrong H, et al. "Vinegar, depression, and niacin metabolism," Nutrients. 2024. doi:10.3390/nu16142305.
  6. ↑ Glycemia, starch, and sugar in context, raypeat.com
  7. ↑ Protecting and Restoring Nerves, Ray Peat newsletter
  8. ↑ Ray Peat, "Ask the Herb Doctor: Diabetes II and How to Restore and Protect Nerves", Ask the Herb Doctor, 21:29
  9. ↑ Smyrnias I, Gray SP, Okonko DO, et al. "Cardioprotective Effect of the Mitochondrial Unfolded Protein Response During Chronic Pressure Overload," J Am Coll Cardiol. 2019;73(14):1795-1806. doi:10.1016/j.jacc.2018.12.087. PMID 30975297.
  10. ↑ Müller KH, et al. "Poly(ADP-Ribose) Links the DNA Damage Response and Biomineralization," Cell Rep. 2019. PMID 31189100.
  11. ↑ Zhao J, Zhang Y, Liu Y, et al. "Antidepressant-like effects of 1-methylnicotinamide in a chronic unpredictable mild stress model of depression," Neurosci Lett. 2021;742:135535. doi:10.1016/j.neulet.2020.135535. PMID 33248165.
  12. ↑ Harder JM, Guymer C, Wood JPM, et al. "Disturbed glucose and pyruvate metabolism in glaucoma with neuroprotection by pyruvate or rapamycin," Proc Natl Acad Sci U S A. 2020;117(52):33619-33627. doi:10.1073/pnas.2014213117. PMID 33318177.
  13. ↑ Yoshino J, et al. "NMN increases muscle insulin sensitivity in prediabetes," Science. 2021. doi:10.1126/science.abe9985.
  14. ↑ Liao B, et al. "NMN supplementation and aerobic capacity in runners," J Int Soc Sports Nutr. 2021. doi:10.1186/s12970-021-00442-4.
  15. ↑ Luo C, et al. "Nicotinamide reprograms adipose cellular metabolism and increases mitochondrial biogenesis," J Nutr Biochem. 2022. doi:10.1016/j.jnutbio.2022.109056.
  16. ↑ Xu C, et al. "β-Nicotinamide Mononucleotide Promotes Cell Proliferation and Hair Growth by Reducing Oxidative Stress," Molecules. 2024. PMID 38398550.
  17. ↑ Sundaram B, et al. "NLRC5 senses NAD+ depletion and drives PANoptosis," Cell. 2024. doi:10.1016/j.cell.2024.05.034.
  18. ↑ Chaubey K, Vázquez-Rosa E, Tripathi SJ, et al. "Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain," Cell Rep Med. 2026;7(1):102535. doi:10.1016/j.xcrm.2025.102535. PMID 41435831.
  19. ↑ Morrissey J, et al. "Nicotinamide reverses the Warburg effect in CHO cells," Biotechnol Bioeng. 2026. doi:10.1002/bit.70224.
  20. ↑ "Leakiness, aging, and cancer," Ray Peat article
  21. ↑ Ray Peat, "Rosacea, inflammation, and aging," raypeat.com.
  22. ↑ Fukuzawa M, Satoh J, Muto G, et al. "Inhibitory effect of nicotinamide on in vitro and in vivo production of tumor necrosis factor-alpha," Immunol Lett. 1997;59(1):7-11. doi:10.1016/s0165-2478(97)00088-6. PMID 9334851.
  23. ↑ Ray Peat, "Ask the Herb Doctor: Diabetes II and How to Restore and Protect Nerves", Ask the Herb Doctor, 21:29
  24. ↑ Ray Peat, email, Weight Loss, raypeatemails.com.
  25. ↑ Cheng SC, Young DO, Huang Y, Delmez JA, Coyne DW. "A randomized, double-blind, placebo-controlled trial of niacinamide for reduction of phosphorus in hemodialysis patients," Clin J Am Soc Nephrol. 2008. PMID 18385391.
  26. ↑ Ray Peat, "Phosphate, activation, and aging," raypeat.com.
  27. ↑ Hollis F, van der Kooij MA, Zanoletti O, Lozano L, Cantó C, Sandi C. "Mitochondrial function in the brain links anxiety with social subordination," Proc Natl Acad Sci U S A. 2015;112(50):15486-91. doi:10.1073/pnas.1512653112. PMID 26621716.
  28. ↑ "Nicotinamide as an Early Alzheimer's Disease Treatment," ClinicalTrials.gov NCT03061474. Completed.
  29. ↑ Sasaki L, Hamada Y, Yarimizu D, et al. "Intracrine activity involving NAD-dependent circadian steroidogenic activity governs age-associated meibomian gland dysfunction," Nat Aging. 2022;2(2):105-114. doi:10.1038/s43587-021-00167-8. PMID 37117756.
  30. ↑ Bertoldo MJ, Listijono DR, Ho WJ, et al. "NAD+ Repletion Rescues Female Fertility during Reproductive Aging," Cell Rep. 2020;30(6):1670-1681.e7. doi:10.1016/j.celrep.2020.01.058. PMID 32049001.
  31. ↑ McDermott MM, et al. "Nicotinamide riboside for peripheral artery disease," Nat Commun. 2024. doi:10.1038/s41467-024-49092-5.
  32. ↑ Xiang L, et al. "Dietary niacin intake and body composition," J Nutr Health Aging. 2023. doi:10.1007/s12603-023-1967-0.
  33. ↑ Peng M, et al. "Mitochondrial dysfunction and muscle atrophy," Skelet Muscle. 2021. doi:10.1186/s13395-021-00263-8.
  34. ↑ Das A, et al. "Systemic ablation of vitamin D receptor leads to skeletal muscle glycogen storage but energy deficiency," J Cachexia Sarcopenia Muscle. 2022. doi:10.1002/jcsm.12841.
  35. ↑ Mukherjee S, Baur JA, et al. "Mitochondrial NAD+ limits liver regeneration," Nat Metab. 2025. doi:10.1038/s42255-025-01408-5.
  36. ↑ Ancel D, Stuelsatz P, et al. "Bioactive nutrients and muscle stem cells," J Clin Invest. 2024. doi:10.1172/jci163648.
  37. ↑ Shen S, Liang Y, Zhao Y, et al. "Dietary supplementation of vitamin B1 prevents the pathogenesis of osteoarthritis," Proc Natl Acad Sci U S A. 2024;121(30):e2408160121. doi:10.1073/pnas.2408160121. PMID 39024114.
  38. ↑ Jonas WB, et al. "The effect of niacinamide on osteoarthritis: a pilot study," Inflamm Res. 1996;45(7):330-334. PMID 8841834.
  39. ↑ Lee S, et al. "Hepatic miR-93 in MASLD," Metabolism. 2025. doi:10.1016/j.metabol.2025.156266.
  40. ↑ Abraham AJ, Bhatia R, et al. "SIRT1 in CML leukemic stem cells," J Clin Invest. 2019. doi:10.1172/jci127080.
  41. ↑ Sarkar S, Yang R, Mirzaei R, et al. "Control of brain tumor growth by reactivating myeloid cells with niacin," Sci Transl Med. 2020;12(537):eaay9924. doi:10.1126/scitranslmed.aay9924. PMID 32238578.
  42. ↑ Pirinen E, Auranen M, Khan NA, et al. "Niacin Cures Systemic NAD+ Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy," Cell Metab. 2020;31(6):1078-1090.e5. doi:10.1016/j.cmet.2020.04.008. PMID 32386566.
  43. ↑ French SW. "Chronic alcohol binging injures the liver and other organs by reducing NAD⁺ levels required for sirtuin's deacetylase activity," Exp Mol Pathol. 2016. PMID 26896648. doi:10.1016/j.yexmp.2016.02.004.
  44. ↑ Li H, et al. "SIRT3 inhibition and ATF4 in lymphoma," Blood Cancer Discov. 2022. doi:10.1158/2643-3230.BCD-20-0183.
  45. ↑ Roca FJ, Ramakrishnan L, et al. "TNF and reverse electron transport in tuberculosis," Science. 2022. doi:10.1126/science.abh2841.
  46. ↑ Xue Y, et al. "Nicotinamide and D-ribose increase NAD+ metabolome," Nutrients. 2022. doi:10.3390/nu14112219.
  47. ↑ Sun Y, et al. "NAD depletion in autophagy-deficient neurons," Cell Rep. 2023. doi:10.1016/j.celrep.2023.112372.
  48. ↑ Qiu Y, Xu S, Chen X, et al. "NAD+ exhaustion by CD38 upregulation contributes to blood pressure elevation and vascular damage in hypertension," Signal Transduct Target Ther. 2023;8(1):353. doi:10.1038/s41392-023-01577-3. PMID 37718359.
  49. ↑ Berven H, Kverneng S, Sheard E, et al. "NR-SAFE: a randomized, double-blind safety trial of high dose nicotinamide riboside in Parkinson's disease," Nat Commun. 2023;14(1):7793. doi:10.1038/s41467-023-43514-6. PMID 38016950.
  50. ↑ Willemen HLDM, et al. "Nicotinamide riboside and chronic pain," Cell Rep Med. 2023. doi:10.1016/j.xcrm.2023.101265.
  51. ↑ Alanazi FK, et al. "Post-orgasmic Illness Syndrome: A Case Report," Cureus. 2024. PMID 38952608.
  52. ↑ Allega MF, Deshmukh R, Hillinger T, et al. "Steroid-dependent metabolic rewiring reveals novel therapeutic and imaging approaches for glioblastoma," Sci Adv. 2026;12(4):eadx6539. doi:10.1126/sciadv.adx6539. PMID 41576167.
  53. ↑ Hulmi JJ, Penna F, Pöllänen N, et al. "Muscle NAD+ depletion and Serpina3n as molecular determinants of murine cancer cachexia-the effects of blocking myostatin and activins," Mol Metab. 2020;41:101046. doi:10.1016/j.molmet.2020.101046. PMID 32599075.
  54. ↑ Beltrà M, Pöllänen N, Fornelli C, et al. "NAD+ repletion with niacin counteracts cancer cachexia," Nat Commun. 2023;14(1):1849. doi:10.1038/s41467-023-37595-6. PMID 37012289.
  55. ↑ Padayatty SJ, Riordan HD, Hewitt SM, et al. "Intravenously administered vitamin C as cancer therapy: three cases," CMAJ. 2006;174(7):937-942. PMID 16567755.
  56. ↑ Kane AE, et al. "Long-term NMN treatment increases lifespan and healthspan in mice in a sex dependent manner," bioRxiv. 2024. PMID 38979132.
  57. ↑ Blenkinsop TA, et al. "Nicotinamide and retinal fibrosis," Stem Cell Reports. 2020. doi:10.1016/j.stemcr.2020.02.009.
  58. ↑ Shi B, Wang W, Korman B, et al. "Targeting CD38-dependent NAD+ metabolism to mitigate multiple organ fibrosis," iScience. 2021;24(1):101902. doi:10.1016/j.isci.2020.101902. PMID 33385109.
  59. ↑ Garg A, Blume SY, Huynh H, et al. "Vitamin B2 and B3 nutrigenomics reveals a therapy for NAXD disease," Cell. 2026;189(9):2648-2662.e19. doi:10.1016/j.cell.2026.01.022. PMID 41747729.
  60. ↑ Roldan Urgoiti G, et al. "Niacin in newly diagnosed glioblastoma," J Neurooncol. 2025. doi:10.1007/s11060-025-05351-z.
  61. ↑ Hor JH, Santosa MM, Lim VJW, et al. "ALS motor neurons exhibit hallmark metabolic defects that are rescued by SIRT3 activation," Cell Death Differ. 2021;28(4):1379-1397. doi:10.1038/s41418-020-00664-0. PMID 33184465.
  62. ↑ Blacher E, et al. "Potential roles of gut microbiome and metabolites in modulating ALS in mice," Nature. 2019;572(7770):474-480. doi:10.1038/s41586-019-1443-5.
  63. ↑ Zhao Y, et al. "NAD(+) and mtRNA sensing drive human kidney diseases," Nat Metab. 2023. PMID 36914910.
  64. ↑ Mo W, et al. "NMN modulates HIV-1 infection," eBioMedicine. 2023. doi:10.1016/j.ebiom.2023.104877.
  65. ↑ Huang J, et al. "The ratio of nicotinic acid to nicotinamide as a microbial biomarker for assessing cell therapy product sterility," Mol Ther Methods Clin Dev. 2022;25:248-261. PMID 35573051.
  66. ↑ Simmons JD, et al. "Nicotinamide Limits Replication of Mycobacterium tuberculosis and Bacille Calmette-Guérin Within Macrophages," J Infect Dis. 2020;221(6):989-999. PMID 31665359.
  67. ↑ Lee YH, Lee J, Jeong J, et al. "Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1," Metabolism. 2025;169:156266. doi:10.1016/j.metabol.2025.156266. PMID 40228656.