Metformin's Aging Trial Has Never Enrolled a Patient

TAME has no registration and has never begun. Its closest randomized test followed 3,234 adults without diabetes for 21 years and found no survival gain.

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The Trial Everyone Cites

Ask why metformin belongs in a conversation about living longer and you will hear about TAME. Targeting Aging with Metformin. Over 3,000 adults aged 65 to 79. Six years. 14 research institutions. It would be the first study designed to ask a regulator to treat aging itself as a condition a drug can act on (1).

We went looking for it in the public record on 18 September 2026.

It is not there. We queried the ClinicalTrials.gov registry six different ways (2). By the trial's name. By its lead investigator, by its sponsor, by drug and condition together, and by the named coordinating centre. No record matches a 3,000-person, six-year, 14-site metformin aging trial. There is no NCT number, because there is no registration.

The trial's own funder says the same thing in its own words. The American Federation for Aging Research still describes TAME in the future tense on a page carrying a 2026 copyright. Study design "has been expertly prepared." What is wanted now is "visionary donors to help launch the multi-year, multi-site TAME Trial" (1).

So the most-cited trial in the longevity conversation has never enrolled a patient.

Our own supplement landscape article describes TAME as a trial that "will enroll 3,000 non-diabetic adults." Read alongside the registry, that sentence promises something that has not started. We are correcting it.

What TAME Was Designed to Test

The design is real even if the trial is not. TAME would randomize adults aged 65 to 79 to metformin or placebo and follow them for six years, coordinated from Wake Forest University School of Medicine (1).

Its primary endpoint is a composite: death, major cardiovascular events, new cancers, and cognitive impairment, counted together as one outcome (3). Grouping them is the point. No regulator recognizes "aging" as a condition. So the design asks whether one drug delays several age-related diseases at once. That is the closest a trial can get to testing aging without naming it.

The money is the obstacle. According to reporting in 2022, the requirement is 30 to 50 million dollars, with about 9 million from the National Institutes of Health toward biomarker work (4). Those figures come from a news report rather than a funder's ledger, so read them as approximate.

Nir Barzilai, the researcher behind it, was blunt in that same report. "I'm on the record saying I'm pretty sure it will start this year, for the last seven years. I have no credibility anymore" (4).

He was also candid about what TAME is for. "There's nothing in that clinical trial that hasn't already been shown before with metformin. We are just trying to package it all up and call it aging so the FDA will approve this for aging" (4).

That is worth sitting with. TAME was conceived as a regulatory move first. Its purpose was to open a door for every drug that came after it, more than to discover something new about metformin.

The Evidence That Does Exist, and What It Says

While TAME waited, other trials ran. Several of them asked close cousins of its question, and they have reported.

The largest randomized test in people without diabetes found nothing

The Diabetes Prevention Program randomized 3,234 adults at high risk of type 2 diabetes to intensive lifestyle change, metformin at 850 mg twice daily, or placebo. None had diabetes at the start. Researchers followed them for a median of 21 years and adjudicated 453 deaths through the end of 2018 (5).

Outcome	Hazard ratio, metformin against placebo	95 percent CI
All-cause mortality	0.99	0.79 to 1.25
Cancer mortality	1.04	0.72 to 1.52
Cardiovascular mortality	1.08	0.70 to 1.66

A hazard ratio of 1.00 means no difference. All three intervals sit across it.

The authors put it plainly: "Although metformin and lifestyle modification prevented diabetes, neither strategy reduced all-cause, cancer, or cardiovascular mortality rates" (5).

Two honest caveats. Mortality was a long-term secondary question in this study, not its registered primary endpoint, which was incident diabetes. And metformin did prevent diabetes, which is a real benefit. What it did not do, over 21 years, is postpone death.

Two trials found metformin working against exercise

This is the finding most likely to change what someone does on a Tuesday.

The MASTERS trial randomized 94 healthy adults aged 65 and over to metformin at 1,700 mg a day or placebo. All of them then did 14 weeks of supervised resistance training. Its registered title reads "Novel Actions of Metformin to Augment Resistance Training Adaptations in Older Adults" (6). The researchers expected metformin to help.

Its registered primary endpoint was the change in type 2 muscle fibre cross-sectional area. That endpoint showed no difference, 18.5 percent against 14.5 percent, between groups P = 0.610 (6). By its own main question, the trial found nothing.

The differences turned up elsewhere.

Measure, 14 weeks of training	Placebo	Metformin	P
Lean body mass	+1.95%	+0.41%	0.003
Thigh muscle mass	+3.90%	+0.45%	less than 0.001
Thigh muscle area, CT	+6.43%	+2.27%	0.005
Knee extension 1RM strength	+23.1%	+15.3%	0.055

Strength did not differ to a statistically significant degree on any measure. The three strength results were trends, at P = 0.055, 0.082 and 0.064, and the authors say so (6). Adverse events were more common with metformin, P = 0.002.

A second trial, in 53 adults averaging 62 years, put everyone through 12 weeks of aerobic training. Metformin blocked the improvement in whole-body insulin sensitivity, P = 0.02, and abolished the roughly 25 percent rise in muscle mitochondrial respiration that the placebo group got (7).

Be careful with the number this trial is famous for. Metformin cut the rise in VO2 max by about half, but that comparison came out at P = 0.08, which is not statistically significant (7). Anyone telling you metformin significantly blunts VO2 max gains is overstating the paper. What holds up is muscle mass, muscle area and mitochondrial respiration.

The honest summary is narrower than the headline and still uncomfortable. In healthy older adults, metformin appears to reduce some of what training builds. Exercise has the strongest evidence of anything in this field, which we cover in zone 2 training and VO2 max. A drug that subtracts from it has to earn its place back.

The first trial built around a biological age clock came back null

In 2026, METFORAGING reported. It randomized 40 non-diabetic adults aged 50 and over to metformin at 850 mg twice daily or placebo for 96 weeks. Its primary endpoint was prespecified: the between-group difference in PhenoAge epigenetic age acceleration at 96 weeks (8).

The result was a difference of minus 1.02 years, 95 percent CI minus 5.30 to 3.26, P = 0.627 (8). The interval spans zero comfortably.

Adherence was 97.5 percent by pill count. The drug was taken. The clock did not move. What epigenetic clocks can and cannot tell you is covered in biological age tests.

The trial closed enrolment at 40 against a protocol target of 60, because recruitment was slow (8). It is underpowered by its own design, so read it as one honest null rather than a settled answer.

A separate 2025 trial testing metformin against a different biological age measure, glycosylation patterns, also found no statistically significant change, while testosterone in the same trial did (9).

The one recent positive result splits down the middle

A 2026 trial in 145 older adults with glucose intolerance had two co-primary endpoints and reported opposite answers on them (10).

On a frailty index built from accumulated deficits, metformin did better, minus 0.006 per year against placebo, P = 0.0222. On the Fried frailty phenotype, metformin did worse in year one, plus 0.72 per year, P = 0.0011.

The authors explain the second result. Metformin caused more weight loss, 5.7 kg against 2.3 kg, P = 0.0002, and unintentional weight loss is one of the five Fried criteria. Remove that criterion and the difference disappears (10).

That explanation is reasonable. It also raises its own question, because 5.7 kg of unintended weight loss in people averaging 72 is not obviously a good thing. This trial is a preprint and has not been peer reviewed.

In frailer people still, a 2025 trial gave metformin to 72 adults averaging 80 years old for four months. Walking speed did not improve, 0.001 m/s, 95 percent CI minus 0.06 to 0.06, P = 0.96. Twelve of 35 on metformin were admitted to hospital, against 3 of 36 on placebo. The authors concluded that metformin "did not improve 4-m walk speed and was poorly tolerated in this population" (11).

The Animal Evidence Is Not What You Have Heard

The best mouse experiment was negative

The Interventions Testing Program is the most careful lifespan work in the field. Three independent sites, one protocol, genetically varied mice rather than a single inbred strain, both sexes, compounds nominated in advance. It exists because single-lab mouse lifespan results kept failing to replicate.

It tested metformin at 0.1 percent of the diet, started at 9 months (12).

Group	n	Median lifespan	Change	P
Male control	294	780 days
Male metformin	148	835 days	+7%	0.348
Female control	281	874 days
Female metformin	140	872 days	0%	0.791

The paper's own sentence: "Metformin alone, at a dose of 0.1 percent in the diet, did not significantly extend lifespan" (12). In males, lifespan at the 90th percentile went down 2 percent.

Metformin combined with rapamycin did extend lifespan, by 23 percent in both sexes. But that cohort had no rapamycin-only group running alongside it. The comparison was against rapamycin mice from earlier years, and it reached P = 0.12 by the program's standard method. The authors call the result "equivocal" in their own words (12). We cover rapamycin's own human evidence in rapamycin and mTOR.

The famous positive study is smaller and used a different test

The study people cite for metformin extending mouse life reported a 5.83 percent gain in mean lifespan. That was in male C57BL/6 mice, 64 treated against 83 controls, at P = 0.02 (13). It used the Gehan-Breslow test rather than the log-rank test the ITP uses. Its second mouse strain came in at P = 0.064, which the paper itself calls not significant.

The same study found that ten times the dose, 1 percent of the diet, shortened mean lifespan by 14.4 percent, P < 0.001, "likely due to renal failure" (13).

A rat study found nothing at any point in the lifespan distribution, P > 0.05, in an experiment where the calorie-restriction control arm worked (14).

The monkey study did not measure whether monkeys lived longer

A 2024 study reported that metformin turned back measured brain aging in monkeys by about six years. The number is real and so are its limits.

Six monkeys received metformin. The old control group was five to eight animals depending on which measurement you look at. All were male cynomolgus monkeys, 13 to 16 years old at the start, given 20 mg/kg in drinking water for 40 months, and assessed on 68 biological parameters (15).

The six years is a reading from a DNA methylation clock on frontal lobe tissue, not a test of what the monkeys could do. The authors are direct about this: "conclusive evidence of functional rejuvenation is sparse," and the study "omitted assessments of monkey mortality" (15).

Five authors are employees of Altos Labs, a longevity company. One of them invented the epigenetic clock the study measures with, founded the non-profit that licenses his patents on it, and distributes the methylation array the measurement runs on (15). The finding may still be right. The reader deserves to know who built the ruler.

In worms the effect belongs to the bacteria

Metformin extends life in C. elegans, which is often quoted as deep evolutionary support. The mechanism is not what it sounds like. It works by changing the metabolism of the E. coli the worms eat, and the same drug "increases or decreases worm lifespan, depending on E. coli strain metformin sensitivity and glucose concentration" (16).

A later study found that metformin given late in life shortens lifespan in worms and in aged human cells, through energy exhaustion. Its authors wrote that this "could bring into question its benefits for older individuals without diabetes" (17).

The Claim That Started All of This

One study, in 2014, made metformin a longevity drug in the public mind. It reported that people with type 2 diabetes taking metformin lived longer than matched people without diabetes. A drug so good it beat not having the disease.

It drew on 78,241 metformin patients and 90,463 matched controls from UK primary care data, with a median follow-up of 2.4 years (18). The raw rates were close: 14.4 deaths per 1,000 person-years on metformin, 15.2 in matched controls. The headline came from a model, which put controls' median survival 15 percent lower.

Three design choices in that paper are worth naming, all quoted from the paper itself.

It adjusted diabetes out of the illness score. "The Charlson index was therefore modified to subtract 1 unit from all patients with diabetes so that uncomplicated diabetes contributed nothing to the index" (18). The harm of the exposure was removed before the exposed group was compared.

It stopped counting metformin patients when their disease progressed. Follow-up ended 90 days after any change of regimen (18). A patient who needed a second drug left the analysis. Controls had no equivalent exit.

Its median survival was extrapolated, not observed. Median follow-up was 2.4 years and the figure came out of a model, because the data broke the assumption a simpler method needs (18).

The study was "supported by AstraZeneca/Bristol-Myers Squibb." Six of its eight authors have commercial ties, and one is an employee of a sponsor (18).

In 2022, a Danish team set out to reproduce it. They used national registries, up to 16 years of follow-up, and twin pairs where one twin had diabetes and one did not. Twins control for genetics and upbringing in a way matching cannot.

They found the opposite direction. Metformin initiators died at 1.52 times the rate of matched people without diabetes, 95 percent CI 1.37 to 1.68. Within discordant twin pairs the figure was 1.90, 95 percent CI 1.35 to 2.67. After adjustment, 1.32 and 1.64. Increased mortality showed up at every level of cumulative use (19).

Their conclusion was direct. Treatment with metformin "was not associated with survival equal or superior to that of the general population without diabetes." They added that "further research is necessary before interpreting this line of research as supporting evidence for the anti-ageing or geroprotective potential of metformin" (19).

That study was funded by a foundation. Its conflict of interest statement reads "None declared" (19).

A 2025 review found the same pattern across the wider literature. Its authors include one of the ITP's own investigators. Their summary: "metformin has so far not demonstrated its anticipated preventative or therapeutic effects in most, although not all, major clinical trials in nondiabetic or prediabetic populations conducted to date" (3).

What Is Actually Running

One large randomized trial is testing metformin in people without diabetes right now, and it is not TAME.

The VA-IMPACT trial enrolled its first participant in April 2023 and is recruiting toward 7,410 US veterans. Every participant has both prediabetes and established cardiovascular disease. Its primary endpoint is time to death, heart attack, stroke, hospitalization for unstable angina, or coronary revascularization. Primary completion is estimated for September 2029 (20).

It is not a healthy-aging trial. It tests a drug in sick people at high risk, which is a different question from the one TAME was written to ask. Do not read one as the other.

What This Means If You Are Considering Metformin

If you have type 2 diabetes or prediabetes, none of this applies to your treatment. Metformin has sixty years of evidence there and this article does not touch it. Keep taking what you have been prescribed and raise any question with your doctor.

If you are healthy and considering metformin to slow aging, the evidence as it stands says four things.

No randomized trial has shown it extends life in people without diabetes. The largest and longest, at 3,234 people over 21 years, found no difference (5).

It may cost you some of what exercise gives you. Two randomized trials in healthy older adults found reduced gains in lean mass and mitochondrial function (6, 7).

It has a real and measurable side effect over time. In the same 21-year study, 19.1 percent of metformin users had low or borderline-low vitamin B12 at five years. That is against 9.5 percent on placebo. Each additional year of use raised the odds by 13 percent. Neuropathy was more common among metformin users with low B12 (21). If you take it long-term, B12 is worth testing.

One fear is not supported by the data. Lactic acidosis, the complication metformin is best known for, did not occur once in 70,490 patient-years of metformin use across 347 studies. The statistical upper bound for metformin, 4.3 cases per 100,000 patient-years, is lower than the bound for the comparison group at 5.4 (22). That said, those trials excluded people with kidney impairment, who are the people at risk.

Frequently Asked Questions

Is the TAME trial happening?

Not as of 18 September 2026. It has no ClinicalTrials.gov registration, and its funder still describes it as a trial it is seeking donors to launch (1, 2). It has been described as imminent in press coverage since roughly 2015.

Does metformin extend lifespan in healthy people?

No randomized trial has shown that. The largest test, in 3,234 adults without diabetes followed a median of 21 years, found all-cause mortality identical to placebo, hazard ratio 0.99 (5).

Should I stop exercising if I take metformin?

No. Exercise has far stronger evidence than metformin does. The finding is the other way round: two randomized trials suggest metformin reduces some of what training builds, so exercise is the thing worth protecting (6, 7).

What about the monkey study that reversed six years of brain aging?

It measured a molecular clock on tissue in six treated monkeys, across 68 measured parameters. Its authors state that evidence of functional improvement is sparse and that the study did not measure whether the monkeys lived longer (15).

Is metformin safe to take if I do not have diabetes?

Short-term trials in older adults report it is tolerated by most people, though adverse events were more common on metformin in one of them, P = 0.002 (6). Long-term use lowers vitamin B12 in about one user in five by five years (21). In adults averaging 80, one trial found poor tolerance and more hospital admissions (11). This is a prescription medicine and the decision belongs with your doctor.

Sources

1. American Federation for Aging Research. "TAME: Targeting Aging with Metformin." Accessed 18 September 2026. afar.org/tame-trial
2. ClinicalTrials.gov REST API v2. Six queries run 18 September 2026 on trial name, investigator, sponsor, drug and condition, and coordinating centre. No matching record returned. clinicaltrials.gov
3. Keys MT, Hallas J, Miller RA, Suissa S, Christensen K. Emerging uncertainty on the anti-aging potential of metformin. Ageing Res Rev. 2025;111:102817. PMID: 40582648. DOI: 10.1016/j.arr.2025.102817
4. Molteni M. "Anti-aging projects are drawing millions. A much-discussed trial is being overlooked." STAT News. 9 August 2022. statnews.com
5. Lee CG, Heckman-Stoddard B, Dabelea D, et al. Effect of Metformin and Lifestyle Interventions on Mortality in the Diabetes Prevention Program and Diabetes Prevention Program Outcomes Study. Diabetes Care. 2021;44(12):2775-2782. PMID: 34697033. DOI: 10.2337/dc21-1046
6. Walton RG, Dungan CM, Long DE, et al. Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults: the MASTERS trial. Aging Cell. 2019;18(6):e13039. PMID: 31557380. DOI: 10.1111/acel.13039. NCT02308228
7. Konopka AR, Laurin JL, Schoenberg HM, et al. Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults. Aging Cell. 2019;18(1):e12880. PMID: 30548390. DOI: 10.1111/acel.12880. NCT02552355
8. Marcelo-Calvo C, Esteban-Cantos A, Jurado F, et al. Metformin and epigenetic age in non-diabetic older people with HIV in Madrid (METFORAGING): a double-blind, randomised, placebo-controlled, pilot trial. EClinicalMedicine. 2026. PMID: 42023167. DOI: 10.1016/j.eclinm.2026.103874
9. Vinicki M, Pribić T, et al. Effects of testosterone and metformin on IgG and total plasma glycosylation. GeroScience. 2025. PMID: 39363095. DOI: 10.1007/s11357-024-01349-z. NCT02514629
10. Musi N, Wang CP, MacCarthy D, et al. A Randomized Clinical Trial of Metformin to Reduce Frailty in Older Adults with Glucose Intolerance. medRxiv. 28 July 2026. Preprint, not peer reviewed. PMID: 42620010. NCT02570672
11. Witham MD, McDonald C, Wilson N, et al. Metformin to treat sarcopenia and frailty (MET-PREVENT): a randomised controlled trial. Lancet Healthy Longev. 2025;6:100695. PMID: 40147475. DOI: 10.1016/j.lanhl.2025.100695. ISRCTN29932357
12. Strong R, Miller RA, Antebi A, et al. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an alpha-glucosidase inhibitor or a Nrf2-inducer. Aging Cell. 2016;15(5):872-884. PMID: 27312235. DOI: 10.1111/acel.12496
13. Martin-Montalvo A, Mercken EM, Mitchell SJ, et al. Metformin improves healthspan and lifespan in mice. Nat Commun. 2013;4:2192. PMID: 23900241. DOI: 10.1038/ncomms3192
14. Smith DL Jr, Elam CF Jr, Mattison JA, et al. Metformin supplementation and life span in Fischer-344 rats. J Gerontol A Biol Sci Med Sci. 2010;65(5):468-474. PMID: 20304770. DOI: 10.1093/gerona/glq033
15. Yang Y, Lu X, Liu N, et al. Metformin decelerates aging clock in male monkeys. Cell. 2024;187(22):6358-6378.e29. PMID: 39270656. DOI: 10.1016/j.cell.2024.08.021
16. Cabreiro F, Au C, Leung KY, et al. Metformin retards aging in C. elegans by altering microbial folate and methionine metabolism. Cell. 2013;153(1):228-239. PMID: 23540700. DOI: 10.1016/j.cell.2013.02.035
17. Espada L, Dakhovnik A, Chaudhari P, et al. Loss of metabolic plasticity underlies metformin toxicity in aged Caenorhabditis elegans. Nat Metab. 2020;2(11):1316-1331. PMID: 33139960. DOI: 10.1038/s42255-020-00307-1
18. Bannister CA, Holden SE, Jenkins-Jones S, et al. Can people with type 2 diabetes live longer than those without? Diabetes Obes Metab. 2014;16(11):1165-1173. PMID: 25041462. DOI: 10.1111/dom.12354
19. Keys MT, Thinggaard M, Larsen LA, Pedersen DA, Hallas J, Christensen K. Reassessing the evidence of a survival advantage in Type 2 diabetes treated with metformin compared with controls without diabetes: a retrospective cohort study. Int J Epidemiol. 2022;51(6):1886-1898. DOI: 10.1093/ije/dyac200
20. US Department of Veterans Affairs. Investigation of Metformin in Pre-Diabetes on Atherosclerotic Cardiovascular Outcomes (VA-IMPACT), CSP #2002. Recruiting as of last update 17 December 2025. NCT02915198
21. Aroda VR, Edelstein SL, Goldberg RB, et al. Long-term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study. J Clin Endocrinol Metab. 2016;101(4):1754-1761. PMID: 26900641. DOI: 10.1210/jc.2015-3754
22. Salpeter SR, Greyber E, Pasternak GA, Salpeter EE. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;(4):CD002967. PMID: 20393934. DOI: 10.1002/14651858.CD002967.pub4

Funding Transparency

LSD is editorially independent. We receive no funding from pharmaceutical, supplement or longevity companies. These are the funding ties behind each study above, taken from each paper's own funding and conflict statements.

• Source 1 (AFAR): AFAR is TAME's organiser and is soliciting funding for it. Its page is a fundraising page, and we read it as one.
• Source 3 (Keys 2025 review): Authors include Richard A. Miller, a principal investigator of the NIA Interventions Testing Program, and Samy Suissa, the pharmacoepidemiologist who identified the bias pattern the review describes. Both are established critics of this literature and that context belongs with the citation.
• Source 4 (STAT, 2022): Independent news reporting. The dollar figures are journalism rather than a funder's ledger. The quotations are direct.
• Source 5 (DPPOS mortality, 2021): NIDDK of the NIH under 22 named awards, with the National Institute on Aging, NCI, NHLBI and others. Merck KGaA provided medication for the follow-up study. Concomitant materials were donated by a list of companies including Bristol-Myers Squibb and Parke-Davis.
• Source 6 (MASTERS, 2019): National Institute on Aging grant R01AG046920 and NCATS. The authors declare no conflicts. No commercial drug supplier is named.
• Source 7 (Konopka, 2019): Dairy Management Inc, a dairy industry marketing body, and Dexcom Inc, which sells the continuous glucose monitors used in the study, plus NIH/NCATS. The authors declare no conflicts. We report the two commercial funders because the reader deserves to see them.
• Source 8 (METFORAGING, 2026): Funding is not stated in the abstract and the full text was unavailable to us.
• Source 10 (frailty, 2026): University of Texas Health Science Center at San Antonio, with the National Institute on Aging. A preprint.
• Source 11 (MET-PREVENT, 2025): NIHR Newcastle Biomedical Research Centre.
• Source 12 (ITP, 2016): National Institute on Aging grants and a Department of Veterans Affairs award. The institution holds a patent application on the encapsulated rapamycin used in the study, with royalty entitlements. That interest attaches to the rapamycin arm, which worked, and not to metformin, which did not.
• Source 13 (Martin-Montalvo, 2013): NIA Intramural Research Program, with parts done under a research agreement with Sirtris, a GlaxoSmithKline company. Metformin was donated by Farmhispania SA. The paper declares no competing financial interests. Both statements are reported here together.
• Source 14 (Smith, 2010): NHLBI and NIDDK. No conflicts listed.
• Source 15 (monkeys, 2024): Chinese national and academy research programmes and the XPLORER PRIZE. No pharmaceutical funding is declared. Five authors are Altos Labs employees. One founded the non-profit that licenses his epigenetic clock patents and distributes the methylation array the study measures with.
• Sources 16 and 17 (worms): Wellcome Trust, the UK Medical Research Council and BBSRC (16). No conflicts listed on either.
• Source 18 (Bannister, 2014): "Supported by AstraZeneca/Bristol-Myers Squibb." One author is an employee of Bristol-Myers Squibb. Four others are employees, contractors or a director of a research consultancy funded by pharmaceutical companies. The senior author reports grants from several manufacturers.
• Source 19 (Keys, 2022): The Velux Foundation, grant Velux 31205. Conflict of interest: none declared.
• Source 20 (VA-IMPACT): VA Office of Research and Development, Cooperative Studies Program. No industry collaborators listed.
• Source 21 (B12, 2016): NIDDK. Conflicts: none.
• Source 22 (Cochrane, 2010): No funding listed. Conflicts: none known.

Related Reading

• The Supplement Landscape, which compounds have human evidence behind them at all
• What 18 Trials of NMN, NR, Urolithin A and Spermidine Were Built to Test, the same question asked of four supplements
• Rapamycin's First Longevity Trial Missed Its Primary Endpoint, the drug metformin was paired with in the mouse study
• Rapamycin and mTOR Inhibition, the mechanism behind that pairing
• Epigenetic Clocks and Biological Age Tests, what a clock reading does and does not tell you
• Metabolic Health Fundamentals, the biology metformin acts on
• Zone 2 Training, the intervention metformin appears to work against

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A trial that has not started cannot have found anything. Check the registration before the headline.

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Written with the help of AI tools, shaped and verified by humans. Every result in this article was checked against the study's own paper, abstract or registration.

This article is for information only and is not medical advice. Do not start or stop a prescription medicine on the basis of an article.