— May 14, 2026 · Blood NAD+ Does Not Fall With Age: Seven Human Cohorts in Nature Metabolism

Table of Contents

1. At a Glance
2. What Was Done
3. What Was Found, Number by Number
4. How NAD+ Works, in Plain Language
5. How It Fits With Earlier Research
6. What NR and NMN Trials Have Measured
7. What It Cannot Show
8. What the Authors and Other Scientists Said
9. Since Then: May to October 2026
10. Sources and Primary Documents
11. Key Research Papers
12. Connections
13. Featured Videos

At a Glance

• The paper — Trętowicz MM, Scantlebery AML, Schomakers BV, et al., Houtkooper RH. Human whole-blood NAD+ levels do not vary with age or lifestyle interventions. Nature Metabolism 8(6):1282–1290, published online May 14, 2026 (a Brief Communication).
• Who — 32 authors from Amsterdam UMC and other institutions in the Netherlands, Spain, Finland and Australia; corresponding authors Georges E. Janssens and Riekelt H. Houtkooper of Amsterdam UMC.
• Design — measurement of NAD+ in whole blood with ultra-high-performance liquid chromatography and high-resolution mass spectrometry, applied to samples from seven independent human cohorts. No new treatment was tested.
• Size — the group sizes in the figure legends add up to 303 people; coverage described the total as “more than 300.” The largest single cohort had 70 people and the smallest group 7.
• Main result — whole-blood NAD+ “remain[s] remarkably stable with age and across lifestyle interventions,” and rose with nicotinamide riboside supplementation, “as expected.”
• Sensitivity — with 20 people per group, the authors calculate that any true age difference larger than 7 nanomoles per millilitre would have been detected with 80% power.
• Sample handling — freezing, frozen storage and repeated freeze–thaw cycles were tested separately; coverage reported that they “could substantially reduce measured levels.”
• Interests — “The authors declare no competing interests.” Funding listed includes the European Union’s Horizon Europe NADIS project and national research grants for the individual cohorts; one cohort was also supported in part by a nutrition company.

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What Was Done

Step one was the measuring method. How a blood sample is handled can change its NAD+ reading, and different laboratories have used different tests, from enzyme “cycling” assays to mass spectrometry. The Amsterdam team used ultra-high-performance liquid chromatography (which separates the molecules in a sample) coupled with high-resolution mass spectrometry (which weighs and counts them), and describe it as “rigorously validated” and built to account for “real-world analytical variability.” The validation work, shown in the paper’s first figure and its Extended Data, included:

• measuring NAD+ in plasma (the liquid part of blood, without the cells) from 10 donors, five men and five women, alongside whole blood;
• comparing fresh whole blood with the same blood after two days at −20 °C or −80 °C;
• putting whole blood from six people through repeated freeze–thaw cycles;
• comparing 15 paired fresh and frozen samples, and tracking NADH, NADP+ and NADPH (NAD+’s chemical relatives) over 10 weeks of different storage and methanol-preservation conditions;
• a test in mouse blood, including NAD+ measured before and one hour after an injection of NMN at 100 mg per kilogram (four mice);
• a statistical calculation of how many people a study needs to detect a given NAD+ difference once biological, laboratory and freeze–thaw variation are all counted.

Step two was applying the method to seven cohorts. The groups, with the sizes given in the figure legends, were:

1. A cross-sectional ageing cohort — 20 younger adults (under 30) compared with 20 older adults (over 60).
2. CardioHT — 26 people from a cardiovascular-risk study in Murcia, Spain, with age analysed as a continuous number.
3. ELITE — 23 elite athletes, 12 younger adults (under 40) and 12 older adults (over 40), from an Amsterdam heart study of athletes.
4. The Leiden Longevity Study — 70 people from a Dutch study of families with long-lived members, again with age as a continuous number.
5. TEAMS — frail older adults in a resistance-training trial: 31 who exercised and 34 who exercised and also followed a protein-rich diet.
6. MEJNES2019 — frail older adults in Valencia, Spain: 7 controls, 9 who received nutritional supplementation and 15 in a multimodal (combined) lifestyle programme.
7. A Finnish twin study — 24 people sampled before and after five months of nicotinamide riboside, with the dose raised step by step from 250 mg a day to 1 g a day. This cohort came from an earlier trial in identical twins published in 2023.

All the comparisons were made with linear regression adjusted for sex. Besides NAD+ itself, the team looked at NADP+, other NAD+-related molecules, two ratios known as the “niacin index” and “niacin number,” and how whole-blood NAD+ related to hematocrit (the share of blood made up of red cells).

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What Was Found, Number by Number

Age. In the paper’s words, “whole-blood NAD+ levels remain remarkably stable with age.” The second figure is titled “Whole-blood NAD+ levels remain unchanged across age and lifestyle interventions.” The figure covers the under-30 versus over-60 comparison, age as a continuous measure in CardioHT (26 people) and the Leiden Longevity Study (70 people), and the younger and older adults in ELITE.

How small a difference could have been seen. The authors worked out the statistical power of their comparison. With 20 people per group, the size of the cross-sectional ageing cohort, “any true difference greater than 7 nmol/mL would have been detected with 80% power.” (One nanomole per millilitre is the same as one micromole per litre.) For scale, two earlier whole-blood studies that used other methods reported average levels of 23.4 and 33.0 micromoles per litre, so a gap of 7 would be roughly a fifth to a third of a typical level. A smaller true difference could have been missed.

Exercise, fitness and diet. The ELITE cohort set 23 elite athletes beside younger and older non-athletes; that comparison is part of the same second figure, and its own numbers are not in the public parts of the paper. In frail older adults, neither resistance training alone (31 people) nor training plus a protein-rich diet (34 people) shifted whole-blood NAD+ in a major way, and the same held in the three small MEJNES2019 groups of 7, 9 and 15 people.

Nicotinamide riboside. In the 24 twin-study participants, whole-blood NAD+ changed after five months of nicotinamide riboside, which the abstract calls the expected response. This was the method’s positive control: it shows the test can see a real rise when one is there. The size of the rise is not stated in the parts of the paper that are publicly visible.

Sample handling. The first figure is titled “Validation of NAD+ quantification and effects of pre-analytical handling on whole-blood NAD+ and metabolome.” Fresh and frozen samples were compared against a band of ±1 standard deviation, 3.5 nmol/mL, from the median. Coverage of the paper reported that NAD+ readings “were highly sensitive to how blood samples were stored and handled, where freezing and repeated freeze-thaw cycles could substantially reduce measured levels.” A companion calculation shows how this kind of handling and laboratory variation “can substantially inflate sample size requirements”: the noisier the measurement, the more people a study needs to find a real difference.

Not reported here. The paper also presents results for NADP+, the niacin index, the niacin number and hematocrit, and plasma NAD+ in its 10 donors. Those numbers sit in the paywalled figures and are not repeated here.

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How NAD+ Works, in Plain Language

An electron carrier. NAD+ is a coenzyme, a helper molecule that enzymes need to do their job. Inside the mitochondria, the cell’s power plants, NAD+ picks up electrons stripped from food molecules and becomes NADH, which hands them on to make the cell’s energy currency. The balance between NAD+ and NADH, called the redox state, tells researchers a lot about how a cell is running.

A fuel that gets used up. NAD+ is also consumed by enzymes. A 2012 study describes it as “the sole substrate” for the DNA-repair enzyme PARP and for the sirtuin family of enzymes involved in gene regulation. A third enzyme, CD38, breaks NAD+ down. In mice, a 2016 study found that CD38 rises with age and that mice lacking CD38 kept their NAD+ steady as they aged; the same team found higher CD38 gene activity (messenger RNA) in fat tissue from older people than from younger people.

Where it comes from. The body builds NAD+ from forms of vitamin B3: nicotinic acid (niacin), nicotinamide and nicotinamide riboside. NMN (nicotinamide mononucleotide) is a step on the way; the FDA describes it as an intermediate in NAD+ production made from nicotinamide. The site’s page on NAD+ precursors compared sets out how these forms differ, and the vitamin B3 food sources page lists where B3 occurs in whole foods.

Blood is not muscle. Whole blood is a mix of red cells, white cells, platelets and plasma. A 2016 Japanese study described NAD+ and NADP+ as coenzymes “enriched in” red blood cells. Mature red cells have no nucleus and no mitochondria, so the NAD+ they carry is used differently from NAD+ in a working muscle or nerve cell. The Amsterdam authors propose that the body keeps blood NAD+ “within a narrow physiological range” and that it is “possibly buffered against variation,” and they note that it does “not reflect tissue-specific changes, such as those observed in aging muscle.” In other words, NAD+ could fall in some tissues with age while the level in blood stays steady.

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How It Fits With Earlier Research

The “NAD+ declines with age” idea rests on a mix of animal work, human tissue studies and a smaller, less consistent set of human blood studies. In a 2025 review, the Amsterdam group itself wrote that an age-related decline in humans “has been consistently observed only in a limited number of studies.”

Human tissues: mostly a decline

• Skin (2012). In pelvic skin from 49 people aged 0 to 77, collected during unrelated operations, NAD+ fell with age in men (correlation r = −0.706) and women (r = −0.537).
• Brain (2015). A magnetic-resonance method that measures NAD+ inside the living brain found “age-dependent reductions in NAD+, total NAD contents, and NAD+/NADH redox potential” in healthy volunteers.
• Muscle (2022). In a study led by Georges Janssens, now a corresponding author of the May 2026 paper, NAD+ was one of the most prominent metabolites lower in older adults’ muscle, lower still in physically impaired older adults, and closer to young levels in exercise-trained older adults. It tracked daily step counts.

Human blood: mixed results

• Whole blood, 15 young vs 15 elderly (2016). NAD+ and NADP+ were less abundant in people averaging 81 years old than in people averaging 29.
• Plasma, ages 20 to 87 (2019). A study measuring plasma rather than whole blood reported a significant decline in plasma NAD+, NADP+ and a related molecule (NAAD) with age, and a rise in NADH.
• Whole blood, 151 blood donors aged 19 to 68 (2020). Average 23.4 micromoles per litre with no significant correlation with age or sex overall, though men showed a downward trend. Nineteen patients aged 75 to 101 hospitalised for heart failure had lower levels (20.7), a group that differs in illness as well as age.
• Whole blood, 1,518 adults in China (2022). Average 33.0 micromoles per litre, higher in men (34.5) than women (31.3). The study found a downward trend before age 50 that disappeared after 50, a significant drop only in men aged 60 and over, and no age difference in women.
• Fingerstick blood (2023). A rapid test on 5 microlitres of capillary blood found that men had higher NAD+ than women before age 50, that a person’s own level was stable over 100 days, and that aerobic sport and NMN raised whole-blood NAD+.

Set against this record, the May 2026 paper sides with the studies that found no clear blood decline, and it offers one reason the record is mixed: sample handling and laboratory variation can be large enough to create or hide differences. Its finding that exercise did not change whole-blood NAD+ differs from the 2023 fingerstick study, which used a different test and different people. The tissue findings are not contradicted, because the new study did not measure tissue.

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What NR and NMN Trials Have Measured

Blood NAD+ has served as the main yardstick in human trials of NAD+ precursors, because muscle biopsies and brain scans are harder to obtain. The published trials show a consistent pattern: the precursors raise NAD+-related molecules in blood, while, in the words of the Amsterdam group’s 2025 review, human clinical trials “have shown limited efficacy.”

• First human dosing (2016). Single doses of 100, 300 and 1,000 mg of nicotinamide riboside produced dose-dependent rises in the blood NAD+ metabolome; in a one-person pilot, blood NAD+ rose as much as 2.7-fold.
• Middle-aged and older adults (2018). A randomised, double-blind, placebo-controlled crossover trial (two six-week periods) found nicotinamide riboside well tolerated and found that it “effectively stimulates NAD+ metabolism”; the authors flagged blood pressure and arterial stiffness for future trials.
• Obese men (2018). Forty men aged 40 to 70 took 1,000 mg twice a day or placebo for 12 weeks. Insulin sensitivity and glucose metabolism did not improve; no serious adverse events were seen.
• Older men’s muscle (2019). Twelve men took 1 g a day for 21 days in a crossover trial. The muscle NAD+ metabolome rose and circulating inflammatory signalling proteins fell, but mitochondrial energy output did not change.
• Older men and NMN (2022). 250 mg of NMN a day for 6 or 12 weeks raised whole-blood NAD+; changes in walking speed and grip were only “nominally significant” and body composition did not change.
• Identical twins (2023). Twenty twin pairs took nicotinamide riboside rising from 250 to 1,000 mg a day for five months. Systemic NAD+ metabolism, muscle mitochondrial number and gut bacteria changed, but the treatment “did not ameliorate adiposity or metabolic health.” Samples from this trial form the seventh cohort of the May 2026 paper.

The authors’ conclusion that whole-blood NAD+ “cannot be used to track the aging process” bears on how such trials are read. A rise in blood NAD+ after supplementation shows that the compound is absorbed and converted, which one outside scientist quoted below calls target engagement; on its own it does not show a change in ageing. The May 2026 study did not test whether any precursor helps or harms. The regulatory status of NMN in the United States is covered on the site’s page on the FDA’s 2025 NMN decision, and the wider evidence on these compounds on the NAD boosters page.

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What It Cannot Show

• Blood only. No muscle, brain, liver or skin was measured. The study does not test, and cannot overturn, the tissue studies that found lower NAD+ with age.
• Small groups. The cohorts ranged from 7 to 70 people. With 20 per group, differences smaller than 7 nmol/mL could have been missed. Coverage reported that the authors acknowledged “the moderate cohort sizes” used.
• Mostly snapshots. As described in the figure legends, the age comparisons set different people of different ages side by side. Following the same people across decades is the most direct way to show whether a level changes with age, and coverage reported that the authors pointed to the need for larger longitudinal studies.
• Seven different studies. The cohorts were recruited in different countries, for different reasons, with different ages, health states and designs. Pooling them across one laboratory method is a strength for measurement, but the groups are not a random sample of the population.
• No health outcomes. Nothing in the paper tests whether NAD+ levels, or NAD+ precursors, affect disease, fitness or lifespan.
• Lifestyle programmes were not built to move NAD+. The exercise and diet interventions came from trials designed for other purposes in frail older adults; a different programme, or a different group of people, might behave differently.
• Full text not read for this report. The magnitude of the freeze–thaw effect, the plasma values, the hematocrit results and the size of the nicotinamide riboside rise are in parts of the paper that are not public, and are not reported here.

Questions that remain open after the paper include whether NAD+ in specific blood cells (white cells, for example) changes with age even if the whole-blood total does not; how blood and tissue NAD+ pools exchange; whether NAD+ in tissues such as muscle can be estimated from any blood measure; and whether the different blood results of earlier studies can be reproduced when samples are handled the way this paper describes.

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What the Authors and Other Scientists Said

The authors. In the research briefing published alongside the paper on May 14, as quoted by the trade publication NutraIngredients on June 2, 2026, first author Maria Trętowicz and senior author Riekelt Houtkooper wrote: “Our findings provide important clarity in a field marked by conflicting reports, hype and commercial promises.” They continued: “Pragmatically, they indicate that whole-blood NAD+ levels cannot be used to track the aging process in humans and also provide new insight into the regulation of systemic NAD+ pools, which seem to be maintained within a narrow physiological range and are possibly buffered against variation.” According to the same report, they added that the findings “do not imply that whole-blood NAD+ lacks biological relevance.”

A peer reviewer. Lindsay Wu, an associate professor at the University of New South Wales Sydney who is one of the three peer reviewers named on the paper’s page, was quoted from the briefing: “I applaud the authors for how they have drawn attention to small details in sample prep that may have a substantial impact on downstream measurements, which will be important to the field.” Wu also noted that “each of these studies is quite small in size” and that “these smaller cohort studies could obscure any real changes.”

An independent researcher. Mark Tarnopolsky, a professor at McMaster University who studies mitochondrial disorders and ageing, told NutraIngredients that many studies rely on blood, plasma or serum NAD+ because tissue measurements are hard to obtain in people. “That convenience has been overinterpreted,” he said, adding that the rise in circulating NAD+-related molecules seen in nicotinamide riboside and NMN trials amounts to “pharmacodynamic target engagement rather than evidence of improved mitochondrial function, biological age or healthspan.” He described the strongest human studies as showing “reliable biochemical engagement” but “little convincing evidence of reproducible, clinically meaningful functional benefit.”

A supplement-industry scientist. A senior scientific executive at a company that supplies nicotinamide riboside told the same publication that “the study conflicts with several other studies which did observe an inverse association between age and whole blood or blood cell NAD+ levels,” and that it “did also confirm that NR supplementation raises blood NAD+.” Several of the earlier studies listed above did report lower blood NAD+ at older ages, in some cases only in men.

No statement on the paper from a regulator or a medical guideline body was found for this report.

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Since Then: May to October 2026

Two later trials, both published after this paper, measured blood NAD+ alongside health outcomes.

• September 25, 2026 — high-dose NMN in older adults. A Japanese randomised, double-blind, placebo-controlled trial in npj Aging gave adults aged 65 and over 1,250 mg of NMN a day for 24 weeks. Whole-blood NAD+ and related molecules rose significantly. The authors report “no significant improvement” in the primary end point, hearing function, or in physical performance, and write that “evidence for broader physiological benefit remains limited.”
• October 8, 2026 — nicotinamide riboside in Parkinson’s disease. The NOPARK phase 3 trial in JAMA randomised 410 people with early Parkinson’s disease at 11 Norwegian hospitals to 500 mg of nicotinamide riboside twice a day or placebo for 52 weeks. Symptoms on the main rating scale worsened slightly more with nicotinamide riboside, a difference of 2.72 points favouring placebo (95% confidence interval 0.47 to 4.98). The site’s report is Nicotinamide Riboside Fails in Parkinson’s Phase 3 Trial.

Both trials are consistent with the pattern described above: NAD+ precursors raise blood NAD+, and that rise has not, in these trials, come with the clinical benefit that was tested.

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Sources and Primary Documents

The paper’s identifiers were checked against PubMed and Crossref. Its abstract, figure titles, Extended Data legends, acknowledgements and declarations were read on the journal’s page; the main text and main figures are paywalled and were not read.

1. Trętowicz MM, Scantlebery AML, Schomakers BV, Eroğlu KD, van Weeghel M, Spek V, et al., Janssens GE, Houtkooper RH (2026). Human whole-blood NAD+ levels do not vary with age or lifestyle interventions. Nature Metabolism 8(6):1282-1290. Published online May 14, 2026. — doi:10.1038/s42255-026-01537-5 · PubMed PMID: 42135539
2. Whole-blood NAD+ levels do not reflect healthy ageing (Research Briefing, 2026). Nature Metabolism 8:1260-1261. Published May 14, 2026. — doi:10.1038/s42255-026-01540-w
3. Lapatto HAK, Kuusela M, Heikkinen A, Muniandy M, van der Kolk BW, Gopalakrishnan S, et al. (2023). Nicotinamide riboside improves muscle mitochondrial biogenesis, satellite cell differentiation, and gut microbiota in a twin study. Science Advances 9(2):eadd5163. The trial that supplied the paper’s seventh cohort. — PubMed PMID: 36638183
4. Igarashi M, Naruse K, Takaoka Y, Miura M, Kashiwabara K, Sawada M, et al. (2026). Sustained NAD+ augmentation by high-dose nicotinamide mononucleotide supplementation in older adults: a 24-week randomized, double-blind, placebo-controlled trial. npj Aging, published September 25, 2026. — doi:10.1038/s41514-026-00482-7
5. Brakedal B, Skeie GO, Derad C, Alstadhaug KB, Anundskås I, Berven H, et al. (2026). Nicotinamide Riboside for Patients With Early-Stage Parkinson Disease: The NOPARK Randomized Clinical Trial. JAMA, published online October 8, 2026:e2618828. — doi:10.1001/jama.2026.18828 · PubMed PMID: 42848371

Coverage: NutraIngredients, June 2, 2026, “Blood NAD+ may not be a useful biomarker of aging after all”, the source of the quotations from the research briefing and of the comments by the outside scientists.

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Key Research Papers

Background papers on NAD+ and ageing and on NAD+ precursor trials, in the order they appear above. Each entry was checked against PubMed and Crossref before it was written down.

1. Massudi H, Grant R, Braidy N, Guest J, Farnsworth B, Guillemin GJ (2012). Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLoS One 7(7):e42357. — PubMed PMID: 22848760
2. Camacho-Pereira J, Tarragó MG, Chini CCS, Nin V, Escande C, Warner GM, et al. (2016). CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metabolism 23(6):1127-1139. — PubMed PMID: 27304511
3. Vinten KT, Trętowicz MM, Coskun E, van Weeghel M, Cantó C, Zapata-Pérez R, Janssens GE, Houtkooper RH (2025). NAD+ precursor supplementation in human ageing: clinical evidence and challenges. Nature Metabolism 7(10):1974-1990. — PubMed PMID: 41083806
4. Zhu XH, Lu M, Lee BY, Ugurbil K, Chen W (2015). In vivo NAD assay reveals the intracellular NAD contents and redox state in healthy human brain and their age dependences. Proceedings of the National Academy of Sciences of the USA 112(9):2876-2881. — PubMed PMID: 25730862
5. Janssens GE, Grevendonk L, Perez RZ, Schomakers BV, de Vogel-van den Bosch J, Geurts JMW, et al. (2022). Healthy aging and muscle function are positively associated with NAD+ abundance in humans. Nature Aging 2(3):254-263. — PubMed PMID: 37118369
6. Chaleckis R, Murakami I, Takada J, Kondoh H, Yanagida M (2016). Individual variability in human blood metabolites identifies age-related differences. Proceedings of the National Academy of Sciences of the USA 113(16):4252-4259. — PubMed PMID: 27036001
7. Clement J, Wong M, Poljak A, Sachdev P, Braidy N (2019). The plasma NAD+ metabolome is dysregulated in “normal” aging. Rejuvenation Research 22(2):121-130. — PubMed PMID: 30124109
8. Breton M, Costemale-Lacoste JF, Li Z, Lafuente-Lafuente C, Belmin J, Mericskay M (2020). Blood NAD levels are reduced in very old patients hospitalized for heart failure. Experimental Gerontology 139:111051. — PubMed PMID: 32783906
9. Yang F, Deng X, Yu Y, Luo L, Chen X, Zheng J, et al. (2022). Association of human whole blood NAD+ contents with aging. Frontiers in Endocrinology 13:829658. — PubMed PMID: 35388296
10. Wang P, Chen M, Hou Y, Luan J, Liu R, Chen L, et al. (2023). Fingerstick blood assay maps real-world NAD+ disparity across gender and age. Aging Cell 22(10):e13965. — PubMed PMID: 37641521
11. Trammell SA, Schmidt MS, Weidemann BJ, Redpath P, Jaksch F, Dellinger RW, et al. (2016). Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications 7:12948. — PubMed PMID: 27721479
12. Martens CR, Denman BA, Mazzo MR, Armstrong ML, Reisdorph N, McQueen MB, 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. — PubMed PMID: 29599478
13. Dollerup OL, Christensen B, Svart M, Schmidt MS, Sulek K, Ringgaard S, et al. (2018). A randomized placebo-controlled clinical trial of nicotinamide riboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects. American Journal of Clinical Nutrition 108(2):343-353. — PubMed PMID: 29992272
14. Elhassan YS, Kluckova K, Fletcher RS, Schmidt MS, Garten A, Doig CL, et al. (2019). Nicotinamide riboside augments the aged human skeletal muscle NAD+ metabolome and induces transcriptomic and anti-inflammatory signatures. Cell Reports 28(7):1717-1728.e6. — PubMed PMID: 31412242
15. 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. — PubMed PMID: 35927255

PubMed Topic Searches

1. PubMed: Whole-blood NAD+ and ageing
2. PubMed: NAD+ decline in ageing human tissue
3. PubMed: Measuring NAD+ in blood by mass spectrometry
4. PubMed: Nicotinamide riboside randomised trials
5. PubMed: NMN randomised trials

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Connections

• News Archive
• NAD+ and NMN — the molecule, its chemistry and the ageing research
• NAD+ Precursors Compared — niacin, niacinamide, NR and NMN side by side
• NAD+ and Sirtuins — the longevity hypothesis and its evidence
• NAD+ and Mitochondria — energy metabolism research
• NAD+ History — from its discovery to the precursor era
• NAD Boosters — NMN and NR in longevity protocols
• Vitamin B3 — the vitamin family that supplies NAD+
• Vitamin B3 as an NAD+ Precursor — how each form becomes NAD+
• Vitamin B3 Food Sources — where niacin occurs in whole foods
• FDA NMN Decision 2025 — NMN’s legal status as a supplement
• NR in Parkinson’s: NOPARK — the October 2026 phase 3 trial
• Mitochondria — animation of how cells make energy
• Longevity & Healthy Aging — the site’s longevity section
• Longevity Molecules — compounds studied for ageing
• The Honest Picture — what longevity research does and does not show

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