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Niacin
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In one pass Inside the cell, vitamin B3 is built into two molecules, NAD and NADP.
Educational content, not medical advice — consult a clinician.
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Chapter 1
Two electron-carrying molecules
Inside the cell, vitamin B3 is built into two molecules, and NADP. Their job is to catch electrons and hand them on. That is how cells pull energy out of food, and how they build things and fend off oxidation.
B3 in food and supplements comes in several forms: niacin, nicotinamide, and precursors such as nicotinamide riboside () and nicotinamide mononucleotide (). Once inside the cell, all of them feed the same NAD⁺ pool.
An analogy: NAD is like a power line that carries electrons from food to the generating station; NADP is like the point of use, spending electrons to build and to put out fires. The two cannot stand in for each other. The analogy ends there; they are not actual wires.
NAD (NAD⁺ when empty-handed, NADH once it holds electrons) leans toward breaking fuel down for energy. In the main energy loop, the tricarboxylic acid () cycle, it collects electrons and carries them into the mitochondria's power chain, which makes , the energy currency.NADP leans toward building and defense. Making fat, making cholesterol, and recycling glutathione for antioxidant defense all rely on (the loaded form of NADP, carrying electrons) to hand over electrons.
Cells keep NAD mostly empty-handed and NADP mostly loaded, so one system collects electrons while the other delivers them, without getting in each other's way.
B3 in food and supplements comes in several forms: niacin, nicotinamide, and precursors such as nicotinamide riboside () and nicotinamide mononucleotide (). Once inside the cell, all of them feed the same NAD⁺ pool.
An analogy: NAD is like a power line that carries electrons from food to the generating station; NADP is like the point of use, spending electrons to build and to put out fires. The two cannot stand in for each other. The analogy ends there; they are not actual wires.
NAD (NAD⁺ when empty-handed, NADH once it holds electrons) leans toward breaking fuel down for energy. In the main energy loop, the tricarboxylic acid () cycle, it collects electrons and carries them into the mitochondria's power chain, which makes , the energy currency.NADP leans toward building and defense. Making fat, making cholesterol, and recycling glutathione for antioxidant defense all rely on (the loaded form of NADP, carrying electrons) to hand over electrons.
Cells keep NAD mostly empty-handed and NADP mostly loaded, so one system collects electrons while the other delivers them, without getting in each other's way.
Mechanism · Enzymes that use NAD⁺ up
is more than an electron carrier. Several kinds of enzymes use it as a raw material, cutting it apart and never giving it back. These enzymes have mostly been studied in cells and animals; how much each one matters in the human body is, for the most part, not yet measured.PARP (poly-ADP-ribose polymerase) finds and repairs DNA damage. It cuts NAD⁺ into nicotinamide and ADP-ribose, then hangs the ADP-ribose on proteins around the damaged DNA to call repair proteins in. When DNA is damaged again and again (UV light, chemotherapy, aging), PARP stays switched on and the NAD⁺ pool is pulled down.
(SIRT1–7) are deacetylases, enzymes that strip acetyl groups off proteins, and they can only work by using NAD⁺. They help regulate metabolism and the stress response. SIRT1 is linked to insulin signaling and fat metabolism; SIRT3 sits in the mitochondria and tunes metabolic efficiency; SIRT6 has shown tumor-suppressing effects in animal experiments. Calorie restriction and regular exercise raise sirtuin activity in animals, which is one source of the sirtuin longevity hypothesis. The claim that resveratrol mimics calorie restriction rests partly on its ability to activate SIRT1, but the evidence is weak.
CD38 is an enzyme on the surface of immune cells (especially plasma cells and B cells) whose job is to cut NAD⁺ apart. In mice, CD38 rises with age and chronic inflammation and is the main reason NAD⁺ falls in old age (Camacho-Pereira 2016); in people, so far it has only been seen rising in fat tissue. That has made CD38 inhibitors (78c and apigenin) targets of anti-aging research in animals.
SARM1 is an NAD⁺-consuming enzyme in nerve cells. It switches on after an axon (a nerve fiber) is injured, and too much of it makes the axon degenerate. Animal experiments link it to chemotherapy-induced peripheral neuropathy, and some research on amyotrophic lateral sclerosis (ALS) also points to it; cause and effect are not settled.
So NAD⁺ is better seen as a pool whose income and spending both change. Income comes from niacin, nicotinamide, , , and tryptophan, which are built into the pool. Spending is set jointly by PARP (DNA damage), CD38 (inflammation), SARM1 (nerve injury), and sirtuins (routine regulation).
With aging, at least in mice, spending (PARP, CD38, SARM1) grows while income does not keep up, and NAD⁺ falls with age in some tissues. In people, how far it falls varies widely by tissue and by method; it is not a whole-body drop by half at some round-number birthday.
This is where the anti-aging case for NMN and NR comes from: bring in more supply to offset the larger spending. By this mechanism, adding supply without cutting spending (chronic inflammation, UV exposure, and DNA damage carrying on as before) is like pouring water into a bucket with holes. That step has not been measured directly in people.
Chapter 2
Tryptophan route
Tryptophan (an essential amino acid, one you can only get from food) can be turned into niacin in the body. This is a backup source of B3, but a poor bargain: it takes about 60 parts of tryptophan to make 1 part of niacin, roughly 60:1, so relying on it alone is not dependable.
The route also needs help from B2, B6, and iron, and runs slower if any one of them is short. The tuberculosis drug isoniazid drains B6 and slows it as well.
What this means in practice: if you eat enough protein (especially tryptophan-rich meat, eggs, and dairy), you depend relatively less on niacin from the diet. As a direct source of dietary niacin, chicken is a good one (see Chicken). But counting on tryptophan alone is unreliable: the same tryptophan is also needed to build protein and make serotonin, so not much is left over for niacin.
Corn and pellagra: corn is low in tryptophan, and most of its niacin is in a bound form that is hard to absorb. In Mexico, corn is traditionally cooked in limewater (nixtamalization), which releases the bound niacin. When corn reached Europe, that step did not travel with it, and pellagra later swept through regions where corn was the staple.
The route also needs help from B2, B6, and iron, and runs slower if any one of them is short. The tuberculosis drug isoniazid drains B6 and slows it as well.
What this means in practice: if you eat enough protein (especially tryptophan-rich meat, eggs, and dairy), you depend relatively less on niacin from the diet. As a direct source of dietary niacin, chicken is a good one (see Chicken). But counting on tryptophan alone is unreliable: the same tryptophan is also needed to build protein and make serotonin, so not much is left over for niacin.
Corn and pellagra: corn is low in tryptophan, and most of its niacin is in a bound form that is hard to absorb. In Mexico, corn is traditionally cooked in limewater (nixtamalization), which releases the bound niacin. When corn reached Europe, that step did not travel with it, and pellagra later swept through regions where corn was the staple.
Mechanism · Where tryptophan goes
Tryptophan (Trp) is an essential amino acid with three main routes through the body; how much goes down each is set by the activity of a few enzymes.The first route is building protein. This is the default main line: tryptophan is written straight into new protein.
The second leads to serotonin () and melatonin. Tryptophan hydroxylase (TPH, which needs iron and the cofactor BH4) turns tryptophan into , which then becomes serotonin and melatonin. About 90% of the body's serotonin is made in enterochromaffin cells of the gut, with the brain making only a small share; only a small portion of tryptophan goes this way.
The third is the kynurenine pathway, and this is the one tied directly to B3. IDO (indoleamine 2,3-dioxygenase) and TDO in the liver turn tryptophan into kynurenine, which becomes quinolinic acid (QUIN) and finally . Most of the tryptophan that is not used for protein is broken down along this route. Inflammatory signals (IFN-γ and other cytokines) turn IDO up, and the stress hormone cortisol turns up TDO in the liver; both send more tryptophan this way.
That has led to a hypothesis called inflammation steals tryptophan. Chronic inflammation (rheumatoid arthritis, inflammatory bowel disease, , aging) raises IDO, more tryptophan is diverted into the kynurenine pathway, and less raw material may be left for serotonin. Intermediates on this pathway (3-hydroxykynurenine, 3-HK, and quinolinic acid) are also neurotoxic in experiments. This is the kynurenine hypothesis of depression. It is a hypothesis still under study; cause and effect in people are not settled.
So under this hypothesis, depression is not simply too little serotonin; where tryptophan is routed may also play a part. Whether controlling inflammation matters more than taking tryptophan or 5-HTP for people with chronic inflammation has not been answered by any trial. The evidence that 5-HTP supplements improve mood is thin, and taking it with antidepressants carries a risk of serotonin syndrome, so ask a doctor before combining them.
In practice: turkey, eggs, cheese, nuts, and seeds are relatively rich in tryptophan (though the claim that turkey makes you sleepy does not hold up once you look at the blood concentrations it can reach). For most people, eating enough protein means tryptophan is not short, and there is no need to take extra.
Chapter 3
Severe deficiency: pellagra
Severe B3 deficiency causes pellagra. The classic picture is the four Ds:
Dermatitis: a symmetrical rash with sharp borders on skin exposed to the sunDiarrhea: damage to the gut liningDementia: confusion and changes in memory and thinkingDeath: without treatment, it kills
The rash is worst where the sun hits. One explanation: sunlight damages DNA, which switches on PARP, the DNA-repair enzyme, so is used up faster in that skin.
Today pellagra is seen mostly in people with severe alcohol use disorder, a long-term very poor diet, or poor absorption. If such a person develops a rash after sun exposure together with diarrhea and confusion, they should see a doctor promptly; with niacin given in time, the symptoms can improve.
Pellagra is a reminder that vitamin is not a wellness-marketing word. Without one, the most basic cell physiology breaks down. NAD⁺ takes part in a huge number of redox reactions, and without it, both energy metabolism and DNA repair fail.
Dermatitis: a symmetrical rash with sharp borders on skin exposed to the sunDiarrhea: damage to the gut liningDementia: confusion and changes in memory and thinkingDeath: without treatment, it kills
The rash is worst where the sun hits. One explanation: sunlight damages DNA, which switches on PARP, the DNA-repair enzyme, so is used up faster in that skin.
Today pellagra is seen mostly in people with severe alcohol use disorder, a long-term very poor diet, or poor absorption. If such a person develops a rash after sun exposure together with diarrhea and confusion, they should see a doctor promptly; with niacin given in time, the symptoms can improve.
Pellagra is a reminder that vitamin is not a wellness-marketing word. Without one, the most basic cell physiology breaks down. NAD⁺ takes part in a huge number of redox reactions, and without it, both energy metabolism and DNA repair fail.
Background · Pellagra in the American South
From the 1900s to the 1920s, pellagra was epidemic in the American South. Cases ran into the hundreds of thousands and many died, mostly among poor farmers, textile workers, and people in orphanages and prisons. Mainstream medicine at the time assumed it was an infectious disease, by analogy with leprosy.Joseph Goldberger, a US Public Health Service physician who studied the disease from 1914 to 1929, believed the cause was diet. He noticed two things. First, wealthy families almost never got it, while poor Southerners lived mainly on corn, molasses, and salt pork. Second, prisoners got it often, while guards eating what looked like the same food rarely did; the difference was that guards could also eat meat and milk.
Two sets of experiments settled it. In the 1915 Rankin prison experiment, 11 volunteer prisoners ate only the local poor people's diet for 6 months; 6 of them developed pellagra, and all recovered once their diet improved. In 1916 he and colleagues experimented on themselves, injecting patients' blood and applying patients' skin and nasal secretions; not one of them fell ill, which directly refuted the contagion theory.
This evidence was then sidelined for nearly 20 years, partly because of racial and class bias: accepting that poverty, a single-crop cotton economy, and farm policy caused the disease was harder than blaming it on Southerners being constitutionally weak.
In 1937 Elvehjem found that niacin cured black tongue in dogs, the canine form of pellagra. From 1942 the US enriched flour and added niacin to it; together with economic growth, pellagra had nearly vanished within 20 years. Goldberger did not live to see it.
What this history leaves is a pattern with a mechanism behind it: a single staple (corn, white rice, cassava) plus poverty leaves people short of both tryptophan and absorbable niacin. Public-health measures such as flour enrichment usually reach far more people than individual supplements do.
Pellagra still occurs today: in refugee camps that rely on corn, in some dry regions of India, with severe alcohol use disorder, in Hartnup disease (an inherited defect in tryptophan absorption), and with long-term isoniazid (a tuberculosis drug that drains B6 and so interferes with making niacin).
Chapter 4
NAD decline with age and supplements
In mice and in some human tissues, falls with age. It is one of the most closely watched findings in the biology of aging over the past decade.
Why it falls: PARP, the DNA-repair enzyme, burns through NAD⁺; aging cells make more CD38, an enzyme that cuts NAD⁺ apart (shown mainly in mice); and as mitochondria work less well, less NAD⁺ is regenerated.
Precursor supplements: nicotinamide mononucleotide () and nicotinamide riboside () are both precursors in the B3 family and can be turned into NAD⁺ in the body. In the US, NR has generally recognized as safe (GRAS) status.
Where the evidence stands: in mice, giving these precursors improved several measures, including muscle, cognition, and metabolism, with fairly consistent results. Randomized trials in people show that NR and NMN do raise NAD⁺ in the blood, but large trials looking at clinical endpoints such as lifespan, strength, and cognition have not been completed.
Conclusion: the mechanism makes sense, short-term safety over weeks to months looks good, and there is no evidence yet of clinical benefit. This is a research frontier, not something proven to work.
Why it falls: PARP, the DNA-repair enzyme, burns through NAD⁺; aging cells make more CD38, an enzyme that cuts NAD⁺ apart (shown mainly in mice); and as mitochondria work less well, less NAD⁺ is regenerated.
Precursor supplements: nicotinamide mononucleotide () and nicotinamide riboside () are both precursors in the B3 family and can be turned into NAD⁺ in the body. In the US, NR has generally recognized as safe (GRAS) status.
Where the evidence stands: in mice, giving these precursors improved several measures, including muscle, cognition, and metabolism, with fairly consistent results. Randomized trials in people show that NR and NMN do raise NAD⁺ in the blood, but large trials looking at clinical endpoints such as lifespan, strength, and cognition have not been completed.
Conclusion: the mechanism makes sense, short-term safety over weeks to months looks good, and there is no evidence yet of clinical benefit. This is a research frontier, not something proven to work.
Evidence · Human trials of NMN and NR
Should I buy or ? is the most common shopping question in anti-aging circles. Start with the evidence.Chemistry: NR (nicotinamide riboside) is nicotinamide plus a ribose sugar, the smaller molecule; NMN (nicotinamide mononucleotide) is NR with a phosphate group added. In the body the two are interconverted by NRK enzymes, and both pass through NMN on the way to . The body's main line for recycling nicotinamide runs through NAMPT, which turns it into NMN (NAMPT→NMN→NAD⁺).
Several randomized trials in people have been published (2018–2024), all of them small:
NR (Trammell 2016, Dollerup 2018, Martens 2018, Conze 2019, Remie 2020): doses mostly ranged from a few hundred up to 1000 mg a day. In Martens 2018, middle-aged and older adults took 1000 mg a day for 6 weeks, and NAD⁺ in peripheral blood mononuclear cells (a type of white blood cell) was about 60% higher than in the placebo period. In Conze 2019, people took 100, 300, or 1000 mg a day for 8 weeks, and whole-blood NAD⁺ rose by 22%, 51%, and 142% respectively within 2 weeks. On raising NAD⁺, the results agree. On clinical endpoints, Martens 2018 saw a trend toward lower blood pressure that was not significant after correcting for multiple comparisons; muscle strength, insulin sensitivity, and exercise performance mostly did not change or showed only weak signals.NMN (Yoshino 2021, postmenopausal women with prediabetes and overweight or obesity; Yamane 2023, older adults; Igarashi 2022, healthy men aged 65 or older): doses of 250–900 mg a day raised blood NAD⁺ about as much as NR did. In Yoshino 2021, muscle insulin sensitivity was about 25% higher than before NMN (a within-group comparison; the placebo group did not change), and other metabolic measures did not change. In Igarashi 2022, gait speed and grip strength improved only nominally, and the authors themselves say larger trials are needed to confirm it. The samples are all small, and some of the authors hold patents or industry interests.
Regulation (as of 2025): in the US, NR has generally recognized as safe (GRAS) status and has been notified to the FDA as a new dietary ingredient; the brand is Niagen (Tru Niagen). In 2022 the FDA said NMN no longer fits the definition of a dietary supplement because it first entered research as a drug; that position was later revisited, the product keeps circulating, and regulation sits in a gray zone. The EU treats these ingredients as novel foods, which need separate approval before sale. Rules differ by place, so the current documents of your local regulator are what count.
Three practical options:
If you want the safer bet: NR, with a clear regulatory status and relatively more human data, at a higher priceIf you want the frontier: NMN has come down in price, but product quality is uneven. Sandalova 2024 tested NMN and urolithin A supplements easily bought online or in pharmacies and found the measured content far from the label, from nearly 30% above the label down to none detectedIf you do not want to spend: nicotinamide (the most ordinary form of B3) also raises NAD⁺ and is very cheap, but in cell experiments it inhibits , so it is not fully equivalent to NR or NMN
The honest conclusion: large, long-term trials on endpoints such as lifespan, falls, and dementia have not been completed. The existing data show a mechanism that makes sense and good short-term safety, but weak effects on clinical endpoints. If you cannot wait and want to try, you can look to the doses used in trials (for example the 300 mg/day arm of Conze 2019), but know that you are betting on the frontier, not taking something already proven to work. The better-supported options are plain: regular strength training plus aerobic exercise, a Mediterranean-style diet, 7–9 h of sleep a night, staying socially connected, and managing stress. In large studies these are associated with less chronic disease, and they cost next to 0.
Chapter 5
High-dose flush and risks
Niacin (nicotinic acid) at drug doses, usually 1–3 g a day to treat high blood lipids, causes the typical niacin flush: the skin turns red, hot, and itchy. It comes from prostaglandin D2 released in the skin and lasts about 30 minutes.
Doses this large carry other risks as well: liver damage (especially with sustained-release forms), higher blood glucose (worsening insulin resistance), and higher uric acid (which can set off gout). Taken together with a statin, it also raises the risk of muscle damage (myopathy). If your skin or the whites of your eyes turn yellow or your urine darkens while you are on high-dose niacin, see a doctor promptly.
and enter metabolism through the nicotinamide branch and do not go down the nicotinic-acid route that causes flushing. In trials they did not cause flushing (Conze 2019), but data on long-term safety are still missing.
So keep three things apart: B3 from food, NMN and NR supplements, and niacin at drug doses. A conclusion drawn in one of these settings cannot be carried over to another.
Doses this large carry other risks as well: liver damage (especially with sustained-release forms), higher blood glucose (worsening insulin resistance), and higher uric acid (which can set off gout). Taken together with a statin, it also raises the risk of muscle damage (myopathy). If your skin or the whites of your eyes turn yellow or your urine darkens while you are on high-dose niacin, see a doctor promptly.
and enter metabolism through the nicotinamide branch and do not go down the nicotinic-acid route that causes flushing. In trials they did not cause flushing (Conze 2019), but data on long-term safety are still missing.
So keep three things apart: B3 from food, NMN and NR supplements, and niacin at drug doses. A conclusion drawn in one of these settings cannot be carried over to another.
Evidence · Why niacin fell out of lipid care
The history of niacin (nicotinic acid) in lipid treatment is a textbook case of a drug being phased out by newer drugs and large trials.From 1955 through the 2000s were its golden years. In 1955 Altschul found by chance that high-dose niacin lowers cholesterol, and later studies showed that 1–3 g a day can lower (low-density lipoprotein cholesterol, often called bad cholesterol) by 10–25%, raise (high-density lipoprotein cholesterol) by 15–35%, lower (TG) by 20–50%, and lower lipoprotein(a) [, a lipoprotein largely set by genes and linked to atherosclerosis] by 20–30%. The Coronary Drug Project (in men who had had a heart attack; the 15-year follow-up was published in 1986) found long-term mortality about 11% lower in the niacin group than on placebo. That difference appeared in follow-up years after the drug was stopped; while the trial was running, niacin did not lower total mortality. At the time, it was one of the few drugs that could clearly raise HDL and also lower Lp(a).
In the 2000s, once it was being combined with statins, its standing began to slip. Statins took over the main job of lowering LDL, and niacin fell back to being an add-on when a statin is not enough. Then two large trials gave the answer:
AIM-HIGH (NEJM 2011): 3414 patients who already had atherosclerosis and whose LDL was already very low on a statin had niacin added on top. The trial was stopped early for lack of benefit after an average of 3 years; major cardiovascular events occurred in 16.4% vs 16.2%, with no added benefit.HPS2-THRIVE (NEJM 2014, n=25,673): extended-release niacin was added on top of a statin. Over a median of 3.9 years, major vascular events were 13.2% vs 13.7%, not a significant reduction, while serious loss of blood-glucose control, new diabetes, bleeding, and infections all went up.
In both trials HDL went up, yet cardiovascular events did not go down: a better number on the lab sheet is not the same as less heart disease. These two large negative trials largely ended niacin's role as a routine lipid drug.
There are roughly three reasons. On top of a statin, the added value is small. Flushing, liver damage, and higher blood glucose mean many people cannot stay on it. And ezetimibe and PCSK9 inhibitors offer safer ways to lower LDL.
The 2025 picture: it is now rarely used. A few doctors consider it when a patient cannot tolerate statins but still needs lower LDL. It lowers Lp(a) modestly, but whether lowering Lp(a) reduces cardiovascular events has not been shown in trials.
For ordinary shoppers there is one more trap: no-flush niacin supplements. Their ingredient is actually nicotinamide or inositol hexanicotinate, sold as the benefits of niacin without the flush. But nicotinamide has no lipid-lowering effect, and inositol hexanicotinate releases very little free niacin in the body and shows no reliable lipid-lowering effect either. So no-flush niacin lowers cholesterol is a marketing line that does not hold up.
What you can judge at home: buying niacin yourself to lower cholesterol has no evidence behind it and carries real side-effect risks. If your blood lipids really are high, you need a doctor's assessment (usually cardiology), and the first choice is drugs that large trials have shown reduce cardiovascular events (a statin, with ezetimibe or a PCSK9 inhibitor added when needed). This is not something a nutritional supplement can handle.
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References · 11
- National Institutes of Health, Office of Dietary Supplements. (2022). Niacin — Fact Sheet for Health Professionals. ods.od.nih.gov/factsheets/Niacin-HealthProfessional
- Camacho-Pereira, J., Tarragó, M. G., Chini, C. C. S., et al. (2016). CD38 dictates age-related NAD decline and mitochondrial dysfunction through a SIRT3-dependent mechanism. Cell Metabolism, 23(6), 1127-1139. 10.1016/j.cmet.2016.05.006
- National Institutes of Health, Office of Dietary Supplements. (2022). Riboflavin — Fact Sheet for Health Professionals. ods.od.nih.gov/factsheets/Riboflavin-HealthProfessional
- National Institutes of Health, Office of Dietary Supplements. (2022). Vitamin B6 — Fact Sheet for Health Professionals. Fact sheet (updated June 16, 2023; Wayback snapshot 17 September 2026): plasma PLP is the most common status measure; PLP above 30 nmol/L has been the traditional adequacy indicator in adults, but the FNB used 20 nmol/L as the major indicator when it calculated the adult RDAs; the FNB halved the dose used in the underlying studies to set an adult UL of 100 mg/day (fact sheet). ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional
- Martens, C. R., Denman, B. A., Mazzo, M. R., et al. (2018). Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications, 9(1), 1286. Randomized, double-blind, placebo-controlled crossover, 2 x 6 weeks of nicotinamide riboside 500 mg twice daily: 30 healthy adults randomized, 24 completed (mean age 65). NR raised PBMC NAD+ by about 60% vs placebo. Blood pressure fell but not significantly after correction for multiple comparisons (systolic -3.9, diastolic -2.0 mmHg); in a post hoc subgroup with baseline systolic 120-139 mmHg (n = 13) systolic was about 9 mmHg lower on NR, an exploratory analysis from which, the authors say, no statistical inferences can be made (full text, PMC5876407; abstract, PMID 29599478). 10.1038/s41467-018-03421-7
- Yoshino, M., Yoshino, J., Kayser, B. D., et al. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science, 372(6547), 1224-1229. 10-week randomized, placebo-controlled, double-blind trial in 25 postmenopausal women with prediabetes and overweight or obesity (NMN 250 mg/day n = 13, placebo n = 12). Muscle insulin sensitivity (clamp glucose disposal per kg fat-free mass) was 25 ± 7% higher after than before NMN (p < 0.01), a within-group change, and unchanged on placebo; body composition, blood pressure, fasting glucose and insulin, lipids, liver and adipose insulin sensitivity and muscle mitochondrial capacity did not change. Two authors disclosed NMN patent interests (full text, PMC8550608; abstract, PMID 33888596). 10.1126/science.abe9985
- Conze, D., Brenner, C., & Kruger, C. L. (2019). Safety and metabolism of long-term administration of NIAGEN (nicotinamide riboside chloride) in a randomized, double-blind, placebo-controlled clinical trial of healthy overweight adults. Scientific Reports, 9, 9772. 8-week randomized, double-blind, placebo-controlled trial in overweight healthy adults: NR 100, 300 or 1000 mg/day raised whole-blood NAD+ by 22%, 51% and 142% within 2 weeks; no flushing and no difference in adverse events vs placebo; LDL and 1-carbon metabolism unchanged. Funded by ChromaDex; two authors are ChromaDex employees and the third is inventor of intellectual property licensed by ChromaDex and its chief scientific adviser (abstract and COI, PMID 31278280). 10.1038/s41598-019-46120-z
- Igarashi, M., Nakagawa-Nagahama, Y., Miura, M., Kashiwabara, K., Yaku, K., Sawada, M., et al. (2022). Chronic nicotinamide mononucleotide supplementation elevates blood nicotinamide adenine dinucleotide levels and alters muscle function in healthy older men. npj Aging, 8(1), 5. Placebo-controlled, randomized, double-blind, parallel-group trial: 42 healthy men aged 65 or older (65 screened), NMN 250 mg/day or placebo for 12 weeks. NMN was well tolerated and raised whole-blood NAD+ and its metabolites; gait speed and left grip performance improved only nominally, which the authors say needs validation in larger studies; body composition did not change. Three authors are employees of Mitsubishi Corporation Life Sciences (abstract and full text, PMID 35927255, PMC9158788). 10.1038/s41514-022-00084-z
- Sandalova, E., Li, H., Guan, L., Raj, S. D., Lim, T. G., Tian, E., Kennedy, B. K., & Maier, A. B. (2024). Testing the amount of nicotinamide mononucleotide and urolithin A as compared to the label claim. GeroScience, 46(5), 5075-5083. 10.1007/s11357-024-01257-2
- AIM-HIGH Investigators. (2011). Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. NEJM, 365(24), 2255–2267. 10.1056/NEJMoa1107579
- HPS2-THRIVE Collaborative Group. (2014). Effects of extended-release niacin with laropiprant in high-risk patients. NEJM, 371(3), 203–212. 10.1056/NEJMoa1300955