Longevity Supplements: What the Evidence Actually Supports

The longevity supplement market is growing faster than the research behind it. Type the phrase into a search bar and you get tens of thousands of results, each promising to slow aging, protect your cells, or add years. The bottle usually cites a study on the label, and the study usually measures something you cannot feel.

That is the pattern this article is built to expose. Almost every compound below reliably moves a number in your blood, and almost none of them move an outcome you would notice. Here is what the human trials actually found, including the ones that failed.

Table of Contents

• Why "Longevity Supplement" Is a Marketing Category, Not a Scientific One
• The Pattern You Will See in Every Study Below
• NAD+ Precursors (NMN and NR): What the Trials Found
• Telomerase Activators (TA-65 and Cycloastragenol)
• Senolytics (Fisetin and Quercetin): Mouse Data, Human Protocols
• Spermidine and Autophagy: The Best Human Data Is Not in a Capsule
• Taurine: How a Mouse Headline Became a Supplement Aisle
• Multivitamins: The 390,000-Person Null Result
• What Actually Has the Better Evidence
• How to Read a Longevity Claim Before You Buy
• What We Recommend
• Frequently Asked Questions
• References

Why "Longevity Supplement" Is a Marketing Category, Not a Scientific One

There is no scientific definition of a longevity supplement. Nobody regulates the term. Nobody agrees on which endpoint a product would have to hit to earn it.

In the United States, supplements are regulated as a category of food, not as drugs. A manufacturer does not have to prove that a product extends life, improves function, or does anything at all before selling it. The claim "supports longevity" sits in a structure and function space that requires no pre-market evidence.

So the category boundary is set by shelf positioning, not by mechanism. The word "anti-aging" aged badly, so the industry swapped in "longevity." Same aisle, same bottles, better vocabulary.

Here is the honest starting point, and it is the one the best reporting on this topic keeps landing on: no supplement has been shown to extend human lifespan in a large clinical trial. Not one. That is not cynicism. It is the current state of the evidence.

No supplement has been shown to extend human lifespan in a large clinical trial. Everything below is graded against that fact.

That does not make supplements worthless. It makes them a narrower tool than the marketing suggests, and it means the useful question is not "does this extend life" but "does this improve something measurable, in humans, at a dose I can actually take."

At Agape Nutrition we sell supplements. The reason we publish an article like this is that a customer who understands the evidence buys better, stays longer, and wastes less money.

The Pattern You Will See in Every Study Below

Every category in this article follows the same shape, so learn the shape once and you can grade any longevity product yourself.

A biomarker is a measurable proxy. NAD+ level. Telomere length. Inflammatory markers. A biomarker is cheap and fast to measure, so trials are usually built around it.

An outcome is what you actually care about. How you feel. How you function. Whether you get sick. Whether you die sooner.

Biomarkers move easily. Outcomes mostly do not. The gap between them is where nearly every disappointing longevity result lives.

The telomere-function disconnect

Telomere length is the cleanest example, because a 2025 meta-analysis gave it a name. Researchers pooled 8 randomized controlled trials of TA-65, a telomerase activator, covering 750 people with a mean age of 63.3 years.

The telomeres responded:

• Telomere elongation: standardized mean difference (SMD) 0.47 (95% CI 0.31 to 0.62, p<0.00001)
• Frailty: SMD 0.09 (p=0.15)
• Inflammation: SMD -0.11 (p=0.07)

The telomeres got longer. Frailty and inflammation did not budge. The study authors call this a "telomere-function disconnect" (1).

What an SMD number actually means

An SMD, or standardized mean difference, is a way of comparing groups on different scales. As a rough guide: 0.2 is a small effect, 0.5 is moderate, 0.8 is large, and anything under about 0.2 is basically noise.

So 0.47 is a real effect size on the biomarker. 0.09 on frailty is not small, it is nothing. Two of those numbers came from the same trials, in the same people, over the same period.

The biomarker itself is cruder than the ads suggest

Telomere length is a widely used but unreliable marker of biological age. Two reviews make that point from different directions. One concludes that leukocyte telomere length is a putative but unreliable biomarker with open issues still unresolved (15).

Another, older but foundational, showed in mouse cells that the shortest telomere, not the average length, is what determines whether a cell survives (16).

That second finding matters more than it sounds. If a trial reports how average telomere length changed, it may have missed the thing that actually matters. Short-telomere percentage would be the more meaningful measure, and most trials do not report it.

Who paid for the study changes the study's answer

This is the finding that no competitor article reports, and it is worth the whole section.

In that same TA-65 meta-analysis, the researchers split the trials by funding source. Industry-funded trials reported an efficacy SMD of 0.63. Independently funded trials reported 0.40, and the difference was statistically significant (p=0.03) (1).

The same molecule, reviewed by the same authors, produced a 57 percent larger effect when the company selling it paid for the trial. Keep that number in your pocket the next time a brand cites "clinical studies" on a product page.

NAD+ Precursors (NMN and NR): What the Trials Found

NAD+ is a molecule your cells use to make energy and repair damage, and its levels decline with age. That part is not in dispute. Neither is the marketing that follows from it: raise NAD+, reverse the decline.

Two precursors dominate the market, nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR). Both are sold on the promise of raising NAD+. In human trials, that rise is well documented for NR. The NMN trials have focused mainly on safety and metabolic markers rather than on the NAD+ rise itself. Raising the number is where the good news ends.

NR raised NAD+ without moving a single symptom

A 2025 double-blind randomized controlled trial followed 58 adults for 24 weeks, giving 2,000 mg of NR per day. NAD+ rose 2.6 to 3.1 fold within 5 to 10 weeks, which is a large and consistent biomarker effect (9).

Now the outcomes. There were no significant differences between groups in cognition, fatigue (p=0.59), sleep quality (p=0.69), anxiety (p=0.84), or depression (p=0.20). The authors put it plainly: NR increased NAD+ within 5 weeks but did not significantly improve cognition, fatigue, sleep, or mood versus placebo.

NAD+ up 2.6 to 3.1 fold. Fatigue, sleep, cognition, and mood: all statistically indistinguishable from placebo.

One fair caveat. This trial ran in people recovering from long COVID, not in the general population, so it is not the final word on cognition in healthy adults. But the NAD+ rise was large, the trial was well controlled, and the symptom outcomes were flat.

A second caveat belongs here, because of the filter this article asks you to apply. That trial was supported by Niagen Bioscience, a maker of nicotinamide riboside. That does not make the result wrong, and the NAD+ finding is not in dispute. But run the funding question on the NAD+ category exactly as you would on a telomere product.

NMN across 15 trials: safe, and metabolically inert

A 2026 systematic review and meta-analysis pooled 15 trials of oral NMN, with 10 contributing to the safety analyses. Doses ranged from 250 to 2,000 mg per day, and durations from 14 days to 24 weeks (8).

The safety picture was good. No increase in overall, serious, withdrawal-related, or system-specific adverse events. No significant rise in liver enzymes ALT or AST.

The efficacy picture was empty. No significant effects on body weight, BMI, fasting glucose, HbA1c, lipid profiles, or systolic blood pressure. Diastolic blood pressure fell slightly, and HOMA-IR, a marker used to estimate insulin sensitivity, showed a non-significant downward trend. That is the entire yield from 15 trials.

You cannot even compare the two products

NMN and NR get argued about constantly. Which is better, which absorbs, which the body prefers. A 2026 preprint mapped the evidence gap and found it wider than the debate suggests.

Across 15 studies and 740 participants, NR was dosed 1.9 to 9.2 times higher than NMN on a molar basis, meaning the two are almost never compared at equivalent doses. No indirect comparison between them reached statistical significance, and every comparison was rated Very Low certainty (17). Note that this is a preprint, meaning it has not completed peer review.

The honest summary: nobody has run the trial that would answer the question, so the NMN-versus-NR debate is a marketing argument, not a scientific one. If you want a longer look at what energy metabolism actually responds to, our Weight & Metabolism pillar page covers the levers with better evidence. For the cognitive side of the same question, see our Brain & Memory pillar page.

Telomerase Activators (TA-65 and Cycloastragenol)

TA-65 is the telomerase activator with the largest human trial record by a wide margin, and it is the most instructive. It is a purified extract of Astragalus membranaceus built around a compound called cycloastragenol, and the trials around it show the biomarker gap in high resolution.

The pooled result from 8 trials and 750 people is the telomere-function disconnect described above. Telomeres elongated (SMD 0.47), while frailty (SMD 0.09) and inflammation (SMD -0.11) did not (1).

Individual trials reinforce it. One 12-month study of 117 CMV-positive adults found telomeres in the 250-unit group lengthened by a median of 530 base pairs while the placebo group's telomeres shortened. The 1,000-unit dose showed a trend toward improvement that did not reach statistical significance (2). A 500-person, 9-month trial found changes in a type of aged immune cell, with the strongest signal again in participants who were CMV-positive (3).

A 12-month trial in 90 older adults who had recently had a heart attack, dosed at 250 units twice daily, found no significant effect on its primary immune-aging outcome, though lymphocyte counts rose and hsCRP fell 62 percent versus placebo (4). A 40-person crossover trial in metabolic syndrome reported improvements in several cardiovascular risk markers, including a modest rise in HDL cholesterol, but found no significant effect on glucose metabolism or telomere length (5, 6).

Dosing across these trials was typically 250 units once or twice daily (6). Reported side effects were mostly gastrointestinal, at 12.4 percent overall, with nausea at 7.1 percent and abdominal discomfort at 5.3 percent (1).

On safety framing, the independent assessment is specific and worth quoting precisely. Telomerase activation carries a theoretical cancer risk, but no clinical evidence of that risk has been observed with TA-65 to date, and long-term safety data is still needed (6).

The same assessment notes that meaningful effects on longevity have not been established, and that there is no direct evidence TA-65 extends lifespan in any animal model. The mouse study that started the category found telomere elongation and healthspan gains in adult and old mice without an increase in cancer incidence (14). That is a mouse result, and mouse results in this field have a poor record of transferring.

For the full trial-by-trial breakdown, including the immunosenescence data and the dose-response problems, see our telomere supplement guide.

Senolytics (Fisetin and Quercetin): Mouse Data, Human Protocols

Senescent cells are damaged cells that stop dividing but refuse to die. They accumulate with age and leak inflammatory signals. Clearing them extends healthspan in mice.

Fisetin and quercetin are the two flavonoids most often sold as senolytics. The mouse signal is real. The human question is wide open, and the honest answer is narrower than the marketing suggests. Fisetin has completed human trials, but they have measured inflammatory and metabolic markers in specific groups, often alongside an exercise program, rather than the senolytic endpoints the anti-aging pitch implies (20, 21). The trials designed to test it as a senolytic have not reported results yet.

• A 2026 randomized protocol investigates daily low-dose fisetin and chronic inflammation in people over 50, over 7 weeks (12).
• A second 2026 protocol, the REPROGRAM trial, tests geroprotectors and biological resilience in 60 people over age 70 across 21 days, with fisetin at 100 mg among the arms (13).

Neither has reported outcomes yet. Both exist because the human data on senolytic endpoints is scarce enough that researchers are still designing the first trials to test them. The protocol dose for fisetin is 100 mg.

So if a product claims senolytic benefits today, it is selling ahead of the evidence. That is not a scandal, since it is an early category and the trials to settle it are underway. You should just know that you are paying for a hypothesis rather than a result.

Spermidine and Autophagy: The Best Human Data Is Not in a Capsule

Autophagy is your cells' recycling and cleanup process. Spermidine, a compound found in wheat germ, aged cheese, mushrooms, soy, and legumes, induces it in laboratory models. The supplement aisle filled up on the strength of that mechanism.

Here is the striking part. Spermidine also has the best human mortality data of any compound in this article, and it does not come from a capsule.

A prospective population study followed 829 adults aged 45 to 84, collected 2,540 dietary assessments, and recorded 341 deaths between 1995 and 2015. All-cause mortality fell steadily across increasing thirds of spermidine intake: 40.5, then 23.7, then 15.1 deaths per 1,000 person-years.

The adjusted hazard ratio was 0.74 per 1-standard-deviation higher spermidine intake (95% CI 0.66 to 0.83, p<0.001), which means roughly 26 percent lower risk of death. An independent cohort, the SAPHIR study, reproduced the direction of the finding at HR 0.71 (95% CI 0.53 to 0.95) (7).

The strongest mortality signal in this entire article comes from food, not from a supplement bottle.

Two honest limits. First, this is dietary intake, not a supplement trial. It is observational, so it shows an association and cannot prove that spermidine caused the difference.

People who eat more spermidine also eat more whole foods, and the analysis cannot fully separate those. Second, no spermidine supplement trial has reproduced this mortality signal.

The practical takeaway is unusual for a supplement article: the behavior with the evidence is eating the foods, not buying the pill.

Taurine: How a Mouse Headline Became a Supplement Aisle

In 2023 a mouse study reported that taurine supplementation extended healthspan and lifespan in mice. The headlines were enormous. Within months, taurine was a supplement category.

Then the pushback arrived, and Nature documented it. Researchers challenged the interpretation of the mouse data and the strength of the anti-aging conclusion drawn from it (11). The mouse finding was real; the leap to a human recommendation was not.

What is actually true: taurine is an amino acid your body makes and uses, it matters for normal function, and blood taurine levels do decline with age. What is also true is that observing that people with lower taurine do worse is not the same as showing that taking taurine helps. That reversal is the single most common error in supplement marketing, and it applies to nearly every compound in this article.

No human trial has shown that a taurine supplement extends lifespan. If the heart and circulation angle is what interests you, our Heart & Circulation pillar page covers the nutrients with more settled evidence.

Multivitamins: The 390,000-Person Null Result

This is the largest and longest dataset in this article, and it is worth sitting with.

A 2024 study pooled three prospective US cohorts totaling roughly 390,000 participants, with follow-up of up to 27 years. The analysis adjusted for healthy-user bias and reverse causation, two of the standard ways observational nutrition data misleads (10).

The result: multivitamin use was not associated with a mortality benefit, with a multivariable-adjusted hazard ratio of 1.04. The finding held consistently across major causes of death.

Those two adjustments are the reason to take this seriously. Healthy-user bias is the tendency of people who take vitamins to also exercise, sleep well, and see doctors. Reverse causation is the possibility that people start taking vitamins because they are already getting sick.

Both make supplements look better than they are. This study corrected for both and still found nothing.

Roughly 390,000 people. Up to 27 years. Adjusted for the two biases that usually flatter supplements. No mortality benefit.

The honest caveat: this is observational, not randomized, and it does not mean a multivitamin is useless. If you have a documented deficiency, correcting it matters. What a multivitamin does not do is make you live longer.

What Actually Has the Better Evidence

Strip away the exotic compounds and a shorter list survives. None of it is exciting, and that is the point.

1. Protein and resistance training for muscle. Muscle mass and strength are among the most meaningful healthspan markers there are, because they determine whether you can carry groceries, climb stairs, and recover from illness at 75. This is the intervention with the clearest human evidence behind it. A 2024 meta-analysis of 10 trials in 1,154 older adults diagnosed with sarcopenia found whey protein significantly increased appendicular skeletal muscle mass index and gait speed, and improved handgrip strength when combined with resistance training (18). Our guide to muscle mass as you age covers the practical detail.
2. Vitamin D, but only if you are actually low. Correcting a deficiency is a real intervention. Adding more on top of a normal level is not.
3. Omega-3 fats. These have one of the longest human trial records of any fat supplement, and the honest version of the story is instructive. In the VITAL trial, 25,871 adults took 1 gram per day of marine omega-3 for a median of 5.3 years. Both co-primary endpoints were null: major cardiovascular events came in at a hazard ratio of 0.92 (95% CI 0.80 to 1.06, p=0.24), and cancer incidence was unchanged (19). Total heart attacks did fall, at an HR of 0.72, while death from any cause was unchanged at HR 1.02. So even the best-evidenced fat supplement here missed its main endpoints and produced a mixed secondary picture. That is what "better evidence" actually looks like in this field: a modest signal, honestly reported, rather than a headline.
4. Magnesium. Widely under-consumed, involved in hundreds of enzymatic reactions, and cheap to correct.

Three things to be clear about. First, none of these four has been shown to extend human lifespan in a large clinical trial either. They win on function and on the quality of their evidence, not on a lifespan claim. Second, the reason they win is that they connect to outcomes, not biomarkers. Third, notice what just happened with omega-3: the best-supported supplement in the article still missed its primary endpoint. If that is the ceiling, treat every more exotic claim below it as marketing until the data says otherwise.

This is where the healthspan-versus-lifespan distinction earns its keep. Lifespan is how long you live. Healthspan is how long you live well, meaning how many of those years you spend functional, mobile, and cognitively intact.

No supplement in this article has a convincing lifespan result in humans. Several everyday interventions have a plausible healthspan case, which is a smaller and more honest claim.

How to Read a Longevity Claim Before You Buy

These filters work on any longevity product, in any category, at any price. Run them in order and most bottles eliminate themselves.

1. Find the outcome. Read past the mechanism and the biomarker. Does the cited study measure anything a person would notice, or does it measure a number?
2. Count the humans. Look for the sample size and the duration. A mouse study is not a human study. A 20-person, 8-week study is a signal, not a proof.
3. Look for the null. Ask what the trial failed to find. If a product page only reports the endpoints that moved, assume the rest did not. The TA-65 meta-analysis is the model here: it reported the telomere win and the frailty and inflammation failures in the same paper (1).
4. Check who paid. Industry-funded trials in that same meta-analysis reported a 57 percent larger effect than independent ones (1). Funding source is not proof of bias, but it is the single best predictor of a flattering result.
5. Check the comparator. Was the supplement tested against a placebo, against nothing, or against a healthy behavior it cannot beat? "Better than nothing" is a low bar.
6. Match the dose. Human trials used specific amounts: 250 to 2,000 mg per day for NMN (8), 2,000 mg per day for NR (9), 250 units once or twice daily for TA-65 (6), 100 mg for fisetin in the current protocols (13). If the bottle's dose is far below the trial's dose, the trial does not apply to that bottle.
7. Ask whether it is a result or a protocol. A registered trial design is not evidence of benefit (12, 13). Neither is a mechanism. Neither is a mouse.
8. Ask whether food or a behavior already does it. Spermidine's best data is dietary (7). Taurine's is a mouse (11). Sometimes the honest answer is a grocery list.

One more, and it is the most useful of the eight: ask what would change your mind. If no possible result would talk you out of the purchase, you are not evaluating, you are shopping.

What We Recommend

Every product below sits in the foundational cluster rather than the exotic one, and each connects to an outcome instead of a biomarker. These are general educational picks, not a personal protocol. If you take prescription medication or you are working with a health condition, run any addition past your practitioner first.

Nordic Naturals, ProDHA Eye 60 and 120 Softgels

A marine omega-3 from the fat supplement category with the longest and most consistent human trial record in this article. $53.25

Integrative Therapeutics, Magnesium Glycinate Plus 120 Tablets

Chelated magnesium, the cheapest correction on this list for a nutrient most people simply do not get enough of. $29.25

XYMOGEN, K2-D3 5000 | 120 Capsules

Vitamin D3 paired with K2, for the one case where this article says the evidence is clear: a blood test that shows your level is actually low. $64.99

Frequently Asked Questions

Do longevity supplements actually work?

Some move biomarkers reliably, and that is not the same thing. NR raises NAD+ substantially (9), and TA-65 lengthens telomeres (1, 2), but neither has produced a matching improvement in how people function. No supplement has been shown to extend human lifespan in a large clinical trial.

What are the most powerful longevity supplements?

By the strength of their human evidence, the strongest are unglamorous: protein and resistance training for muscle (18), vitamin D if you are deficient, omega-3 fats (19), and magnesium. Among the exotic compounds, spermidine has the best mortality data, and it comes from food rather than a capsule (7).

What supplements actually extend lifespan?

None have been proven to, in humans. The best-supported mortality finding in this article is dietary spermidine, an observational association rather than a supplement trial (7). The largest null result is multivitamins, across roughly 390,000 people and up to 27 years of follow-up (10).

Is NMN or NR better?

Nobody knows, and the comparison has essentially never been run fairly. A 2026 preprint found NR was dosed 1.9 to 9.2 times higher than NMN on a molar basis across 15 studies, with no significant indirect comparison and every comparison rated Very Low certainty (17). Treat the NMN-versus-NR debate as marketing until a head-to-head trial exists.

Are senolytics safe to take?

The safety picture is not the same as the marketing picture. Fisetin has completed human trials, but they measured inflammatory and metabolic markers in specific groups, often alongside an exercise program, not the senolytic endpoints the anti-aging marketing implies (20, 21). The trials testing it as a senolytic are still protocols with no published outcomes (12, 13). Early, low-dose work is the right place to be cautious, and "no results yet" is not the same as "shown safe."

Does TA-65 cause cancer?

The concern is theoretical. Telomerase activation could in principle encourage uncontrolled cell growth, and the independent assessment of TA-65 states that long-term safety data is still needed. That same assessment also states that no clinical evidence of this risk has been observed with TA-65 to date (6). It is a genuinely open question, not a known harm, and not a proven safety record either.

What is the difference between healthspan and lifespan?

Lifespan is how long you live. Healthspan is how long you live well, meaning the years you spend functional and independent. The confusion matters because most supplement marketing implies a lifespan claim while the supporting data, when it exists at all, is about healthspan metrics (6).

What is the single best thing to take for healthy aging?

Nothing in a capsule has beaten the basics. Muscle-preserving protein intake and resistance training (18), adequate vitamin D if you are low, omega-3 fats (19), and magnesium all have better evidence than any exotic longevity compound, and none of them requires a subscription. Keep the ceiling in mind, though: even omega-3 missed its primary endpoint in the largest trial of it (19).

References

1. Su X, Wang C, Gou Z, Qu Y. Effects of TA-65 on telomere length, functional outcomes, and inflammation: a systematic review and meta-analysis. Cell Biology and Toxicology. 2025. PMID 41286474.
2. Salvador L, Singaravelu G, Harley CB, Flom P, Suram A, Raffaele JM. A Natural Product Telomerase Activator Lengthens Telomeres in Humans: A Randomized, Double Blind, and Placebo Controlled Study. Rejuvenation Research. 2016;19:478-484. PMC5178008.
3. Singaravelu G, Harley CB, Raffaele JM, et al. Double-Blind, Placebo-Controlled, Randomized Clinical Trial Demonstrates Telomerase Activator TA-65 Decreases Immunosenescent CD8+CD28- T Cells in Humans. OBM Geriatrics. 2021;5:168.
4. Bawamia B, Spray L, Wangsaputra VK, et al. Activation of telomerase by TA-65 enhances immunity and reduces inflammation post myocardial infarction. GeroScience. 2023;45:2689-2705. PMC10122201.
5. Fernandez ML, Thomas MS, Lemos BS, et al. TA-65, A Telomerase Activator improves Cardiovascular Markers in Patients with Metabolic Syndrome. Current Pharmaceutical Design. 2018;24:1905-1911. PMID 29546832.
6. Alzheimer's Drug Discovery Foundation. Cognitive Vitality Report: TA-65. Last updated 2025-11-24.
7. Kiechl S, Pechlaner R, Willeit P, et al. Higher spermidine intake is linked to lower mortality: a prospective population-based study. American Journal of Clinical Nutrition. 2018;108(2):371-380. PMID 29955838.
8. Yang W, Huang J, Tang Z, Chen C, Sun Y. Safety and Metabolism-Related Outcomes of Oral Nicotinamide Mononucleotide Supplementation in Adults: A Systematic Review and Meta-Analysis. Nutrients. 2026. PMID 42514320.
9. Wu CY, Reynolds WC, Abril I, et al. Effects of nicotinamide riboside on NAD+ levels, cognition, and symptom recovery in long-COVID: a randomized controlled trial. EClinicalMedicine. 2025. PMID 41357333.
10. Loftfield E, O'Connell CP, Abnet CC, et al. Multivitamin Use and Mortality Risk in 3 Prospective US Cohorts. JAMA Network Open. 2024. PMID 38922615.
11. Basilio H. Anti-ageing effects of popular supplement taurine challenged. Nature. 2025. PMID 40481202.
12. Tavenier et al. A randomized protocol investigating daily low-dose fisetin and chronic inflammation in older individuals. Basic and Clinical Pharmacology and Toxicology. 2026. PMID 42633989.
13. Wilson et al. The REPROGRAM trial protocol assessing geroprotectors and biological resilience in seniors. PLoS One. 2026. PMID 42308222.
14. Bernardes de Jesus B, Schneeberger K, Vera E, et al. The telomerase activator TA-65 elongates short telomeres and increases health span of adult/old mice without increasing cancer incidence. Aging Cell. 2011;10:604-621. PMC3627294.
15. Vaiserman A, Krasnienkov D. Telomere Length as a Marker of Biological Age: State-of-the-Art, Open Issues, and Future Perspectives. Frontiers in Genetics. 2021;11:630186.
16. Hemann MT, Strong MA, Hao LY, et al. The shortest telomere, not average telomere length, is critical for cell viability and chromosome stability. Cell. 2001;107:67-77. PMID 11595186.
17. Nguyen AT, Nguyen B. Mapping Evidence Gap Between NMN and NR for Metabolic Outcomes. bioRxiv preprint, 2026.
18. Li ML, Zhang F, Luo HY, Quan ZW, Wang YF, Huang LT, Wang JH. Improving sarcopenia in older adults: a systematic review and meta-analysis of randomized controlled trials of whey protein supplementation with or without resistance training. The Journal of Nutrition, Health and Aging. 2024;28(4):100184. PMID 38350303.
19. Manson JE, Cook NR, Lee IM, Christen W, Bassuk SS, Mora S, et al. Marine n-3 Fatty Acids and Prevention of Cardiovascular Disease and Cancer. New England Journal of Medicine. 2019;380:23-32. PMID 30415637.
20. Alipour M, Saeidi A, Hejazi K, Laher I, Zouhal H. 12-weeks fisetin supplementation and interval resistance with aerobic training: changes in Maresin-1 and inflammatory markers in men with obesity: a randomized controlled trial. Journal of the International Society of Sports Nutrition. 2026. PMID 42218768.
21. Alipour M, Saeidi A, Hejazi K, Supriya R, Zouhal H. The Effects of Interval Resistance-Aerobic Training and Fisetin Supplementation on Asprosin and Selected Adipokines in Obese Men: A Double-Blind Randomized Control Trial. Nutrients. 2026. PMID 41683255.

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.