The DOI matches its Crossref record; 82 of the 83 references it cites were found in a registry or an index; 52 of the 74 sources its claims cite were checked for support.
Metformin as a Tool to Target Aging
Open accessAbstract
Aging has been targeted by genetic and dietary manipulation and by drugs in order to increase lifespan and health span in numerous models. Metformin, which has demonstrated protective effects against several age-related diseases in humans, will be tested in the TAME (Targeting Aging with Metformin) trial, as the initial step in the development of increasingly effective next-generation drugs.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This perspective argues that metformin engages multiple aging-related mechanisms and reviews evidence from model organisms and human studies to support testing it as an aging-targeted intervention. It describes the planned TAME trial, which would test metformin in older adults using a composite outcome of age-related diseases.
Key findings
- Metformin affects several pathways linked to aging, including reduced insulin/IGF-1 signaling, mTOR inhibition, mitochondrial complex I inhibition, AMPK activation, lower reactive oxygen species and DNA damage, and effects on inflammation, autophagy, and senescence. In C. elegans it extends lifespan partly by altering microbial folate and methionine metabolism, though the paper notes no human evidence for that mechanism.
- Animal lifespan results are mixed. Metformin increased mean lifespan by about 40% in female outbred mice, by 14% when started early (with weaker effects when started later), by 8% in a breast cancer model, by about 20% in a Huntington’s disease model only in males, and by 4%–6% across different mouse breeds; healthspan indices improved by about 30%. Some studies found no lifespan extension, including Drosophila at 1 mM and rats at a dose roughly 15 times the human dose, which the paper suggests may reflect toxicity.
- Human evidence includes a 31% reduction in type 2 diabetes incidence versus placebo over about 3 years in the Diabetes Prevention Program; in UKPDS, about 20% lower cardiovascular risk (p = 0.032) and 42% lower diabetes-related death (p = 0.017); in HOME, a 40% reduction in a cardiovascular composite over 4 years; a meta-analysis reporting 31% lower cancer incidence and 34% lower cancer mortality; a 51% lower risk of cognitive impairment in the Singapore Longitudinal Aging Study; and a 36% reduction in all-cause mortality in UKPDS long-term follow-up (p = 0.011). Negative trials included GIPS III and CAMERA.
- The proposed TAME trial would enroll 3,000 subjects aged 65–79 at about 14 U.S. centers and measure time to a composite outcome including cardiovascular events, cancer, dementia, and mortality, along with functional and geriatric endpoints.
Methods
- This is a narrative review/perspective that synthesizes evidence from model organisms, randomized clinical trials, and observational studies to justify metformin as an initial aging-targeted drug.
- It describes the design of the planned TAME randomized controlled trial: 3,000 participants, ages 65–79, approximately 14 centers, and a composite outcome of cardiovascular events, cancer, dementia, and mortality plus functional and geriatric endpoints.
- No primary data analysis, systematic search strategy, or meta-analytic method is reported in the paper.
Limitations
- The paper states that it remains unclear whether metformin acts through multiple pathways or whether its effects are downstream of a single primary mechanism; that not all animal studies show lifespan extension, with high doses possibly toxic; that human observational data cannot exclude residual bias and confounding; that no definitive trials have tested cognition; and that TAME has not yet been conducted.
- Evident from the text: as a review/perspective, the evidence is selected rather than systematically appraised, and the TAME design description lacks details on dosing, follow-up duration, and statistical analysis. Human benefits are drawn largely from diabetic or high-risk populations, which limits generalization to broader aging populations.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
52 of 74 cited sources checked · 41 supported · 1 flagged · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“inhibition of mitochondrial complex 1 in the electron transport chain and reduction of endogenous production of reactive oxygen species (ROS) (Batandier et al., 2006; Bridges et al., 2014; Zheng et al., 2012)”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Not checked — no full text of the sourcecites Batandier et al., 2006 source
- Disputedcites Bridges et al., 2014 sourceExperimental — accuracy not yet measured
The Results section (“Biguanide effects on the flavin site and H2O2 production”) says metformin increases ‘native’ H2O2 production, rather than reducing it. It distinguishes that effect from a decrease in paraquat-stimulated H2O2 production. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Supportedcites Zheng et al., 2012 source
The Results section reports that metformin decreased ROS generation in cells exposed to high glucose. It also reports that metformin reduced the increase in retinal ROS in diabetic rats, supporting the attributed reduction in ROS production. (LLM, conf=0.92)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“When rapamycin is administered late in life, it extends lifespan (Harrison et al., 2009; Miller et al., 2011), slows aging in a dose-dependent manner, shows differential effects by sex (Wilkinson et al., 2012), and is synergistic with metformin.”
§ Metformin as a Tool to Target Aging > Introduction > Interventions to Prolong Lifespan
What the sources say
- Partly supportedcites Wilkinson et al., 2012 sourceExperimental — accuracy not yet measured
The Liver degeneration Results report a dose-dependent decline in an age-related liver lesion in male mice, and the Adrenal tumors Results report a significant trend across doses. The Discussion concludes more broadly that rapamycin slows aspects of aging in mice, but does not establish that its overall effect on aging is dose-dependent. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“activation of AMP-activated kinase (AMPK) (Cho et al., 2015; Duca et al., 2015; Foretz et al., 2010; Lien et al., 2014; Lu et al., 2015; Zheng et al., 2012)”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Supportedcites Cho et al., 2015 source
The Results passage reports that metformin induced AMPK activation in rat pituitary adenoma cells, measured by phosphorylation. This directly supports the attributed claim. (LLM, conf=0.94)
- Supportedcites Duca et al., 2015 source
In the passage labeled Abstract (Fig. 1f), the paper reports that intraduodenal metformin increased phosphorylated AMPK relative to total AMPK in rat duodenal mucosa. It also describes this as activation of duodenal AMPK. (LLM, conf=0.94)
- Supportedcites Foretz et al., 2010 source
The Introduction states that metformin treatment activates AMPK and reports that this has been observed in human and rodent tissues. The Discussion further suggests that metformin indirectly stimulates AMPK by lowering ATP levels; its finding that gluconeogenesis inhibition is AMPK-independent does not contradict the activation claim. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Metformin favorably influences metabolic and cellular processes closely associated with the development of age-related conditions, such as inflammation (Saisho, 2015), autophagy (Song et al., 2015; Xie et al., 2011), and cellular senescence (Jadhav et al., 2013; Moiseeva et al., 2013).”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Not checked — no full text of the sourcecites Saisho, 2015 source
- Supportedcites Song et al., 2015 source
Song et al. is cited for the autophagy portion of the sentence, not for inflammation or cellular senescence. The Results section reports increased autophagic flux after metformin treatment in hepatocytes, and the Discussion reports induced liver autophagic flux in ob/ob mice. The Discussion also notes that autophagy function can decline with age; it does not establish a benefit for age-related conditions in humans. (LLM, conf=0.92)
- Supportedcites Xie et al., 2011 source
The Discussion reports that chronic metformin treatment enhanced cardiac autophagy in diabetic mice. Xie et al. is cited for the autophagy portion of the sentence, not for its separate claims about inflammation or cellular senescence. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesEvery source the paper cites for this claim was checked and supports it.
In the paper
“More importantly, these pathways have been evaluated in mammalian models, in which health span and lifespan have been extended by genetic manipulation or drugs (Johnson et al., 2013).”
§ Metformin as a Tool to Target Aging > Introduction > Targeting Health Span
What the sources say
- Supportedcites Johnson et al., 2013 source
The “mTOR in mammalian ageing and healthspan” section reports that rapamycin extends lifespan in mice and delays several age-related changes. It also reports increased lifespan after S6K1 gene knockout in female mice. The paper thus supports the claim about drug and genetic interventions in mammalian models, though the knockout lifespan benefit was sex-specific. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In C. elegans metformin extends lifespan by several possible mechanisms including the alteration of the microbiome, specifically by changing microbial folate and methionine metabolism (Cabreiro et al., 2013).”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Supportedcites Cabreiro et al., 2013 source
The Introduction states that metformin’s lifespan-extending effects in C. elegans are mediated by cocultured E. coli, in which it inhibits folate and methionine metabolism. The Discussion adds that the lifespan effect depends on the bacterial strain; the citing sentence presents this as one possible mechanism, not a universal effect. (LLM, conf=0.94)
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Studies have demonstrated that genetic pathways modulate healthy lifespan in diverse species across great evolutionary distance and established that aging-related pathways constitute a target for intervention (Barzilai et al., 2012; Longo et al., 2015).”
§ Metformin as a Tool to Target Aging > Introduction
What the sources say
- Supportedcites Barzilai et al., 2012 source
The section on attenuated mTOR signaling describes a highly conserved pathway whose genetic inhibition extends lifespan in yeast, nematodes and fruit flies. The section on exceptional human survival links FOXO3A to longevity and healthy aging, supporting the cross-species paraphrase. Page numbers are not available in our copy. (LLM, conf=0.88)
- Supportedcites Longo et al., 2015 source
In “Inhibitors of the TOR pathway,” the paper links mTOR signaling to lifespan and healthspan in several model species and reports that genetic or pharmacological reduction extends lifespan in yeast, worms, flies, and mice. It also identifies mTOR signaling as a candidate for targeted intervention. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“inhibition of mitochondrial complex 1 in the electron transport chain and reduction of endogenous production of reactive oxygen species (ROS) (Batandier et al., 2006; Bridges et al., 2014; Zheng et al., 2012)”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Not checked — no full text of the sourcecites Batandier et al., 2006 source
- Supportedcites Bridges et al., 2014 source
The Results section (‘Metformin and related compounds inhibit catalysis by isolated complex I’) reports that metformin inhibits complex I catalysis, although weakly and reversibly. This supports the attributed claim about complex I inhibition; the claim does not attribute the sentence’s separate ROS-reduction point to this source alone. (LLM, conf=0.94)
- Partly supportedcites Zheng et al., 2012 sourceExperimental — accuracy not yet measured
The Results section reports that metformin decreased ROS generation in retinal endothelial cells under high-glucose stress. The Discussion links this effect to the SIRT1/LKB1/AMPK pathway, but the paper does not say that metformin inhibits mitochondrial complex I of the electron transport chain. No page number is available in our copy. (LLM, conf=0.86)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A more recent study (Martin-Montalvo et al., 2013) demonstrated that metformin increased lifespan by 4%–6% in different mouse breeds.”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Partly supportedcites Martin-Montalvo et al., 2013 sourceExperimental — accuracy not yet measured
The Results (‘Metformin increases healthspan and longevity of mice’) report mean lifespan extensions of 5.83% in C57BL/6 mice and 4.15% in B6C3F1 mice at the 0.1% dose. The B6C3F1 result was not statistically significant, so saying the study ‘demonstrated’ an increase in both strains overstates the evidence. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Studies have demonstrated that genetic pathways modulate healthy lifespan in diverse species across great evolutionary distance and established that aging-related pathways constitute a target for intervention (Barzilai et al., 2012; Longo et al., 2015).”
§ Metformin as a Tool to Target Aging > Introduction
What the sources say
- Supportedcites Barzilai et al., 2012 source
The Conclusions and Future Directions section identifies metabolic signaling pathways as potential therapeutic targets for delaying aging and reports that rapamycin can extend mammalian life span. The section on attenuated mTOR signaling also describes genetic and pharmacological interventions in that aging-related pathway that extend life span in model organisms. (LLM, conf=0.93)
- Supportedcites Longo et al., 2015 source
The ‘Inhibitors of the TOR pathway’ section reports lifespan extension through genetic or pharmacological intervention in yeast, worms, flies, and mice, and identifies mTOR signaling as a target. The Conclusions likewise identify aging-related pathways and interventions to target them. Page numbers were not provided in our copy. (LLM, conf=0.93)
Load-bearingStrength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
- It may state two separate claims as one. 20
- Probably not a substantial claim. 7
Every source the paper cites for this claim was checked and supports it.
In the paper
“When started early in life, mean lifespan was increased by 14%, but with initiation at older ages, this effect declined (Anisimov et al., 2011).”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Supportedcites Anisimov et al., 2011 source
The Abstract reports a 14% increase in mean lifespan when metformin treatment began at 3 months in female SHR mice, compared with 6% when it began at 9 months and no increase at 15 months. The Results (Survival and longevity of female SHR mice) give the corresponding figures as 14.1% and 6.1% and note p>0.05. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Metformin delays the onset of carcinoma and extends lifespan by a mean of 8% in a breast cancer model (Anisimov et al., 2010)”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Supportedcites Anisimov et al., 2010 source
The Introduction reports that metformin increased mean lifespan by 8% and delayed mammary adenocarcinoma onset in HER-2/neu mice. The Discussion likewise says it slowed mammary tumor development in this breast-cancer model. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Beyond these cellular processes, there is a growing body of evidence that metformin can delay aging and increase healthy lifespan in vivo, specifically in nematodes and several rodent strains by adding metformin to the diet (Anisimov et al., 2008, 2011; Cabreiro et al., 2013; De Haes et al., 2014).”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Partly supportedcites Anisimov et al., 2008 sourceExperimental — accuracy not yet measured
The Abstract reports that metformin extended lifespan and slowed age-related loss of estrous function in female SHR mice; the Introduction also describes findings in another mouse strain. This paper does not report metformin extending lifespan in nematodes, and its own experiment administered metformin in drinking water, not in the diet. (LLM, conf=0.88)
- Partly supportedcites Anisimov et al., 2011 sourceExperimental — accuracy not yet measured
The Discussion reports increased lifespan, delayed tumors, and signs of delayed cellular senescence in female SHR mice treated with metformin, supporting the rodent portion of the claim. But Materials and Methods (Experimental design; page unavailable) specifies metformin was given in drinking water, not added to the diet. This paper does not provide the nematode evidence, which the citing sentence also attributes to other citations. (LLM, conf=0.89)
- Supportedcites Cabreiro et al., 2013 source
The Results section reports that metformin increased C. elegans lifespan and slowed its age-related rise in mortality. The Experimental Procedures describe metformin-supplemented culture medium. The Introduction also reports delayed aging in rodents as background, while the sentence provides separate citations for the rodent evidence. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“When rapamycin is administered late in life, it extends lifespan (Harrison et al., 2009; Miller et al., 2011), slows aging in a dose-dependent manner, shows differential effects by sex (Wilkinson et al., 2012), and is synergistic with metformin.”
§ Metformin as a Tool to Target Aging > Introduction > Interventions to Prolong Lifespan
What the sources say
- Supportedcites Wilkinson et al., 2012 source
The Discussion reports that rapamycin diminished the age-dependent decline in spontaneous activity, but the effective dose differed between males and females. The Results also describe age-related lesions affected by rapamycin in males, females, or both sexes. (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Surprisingly, metformin-treated diabetic patients had survival rates similar to (and, among those age > 70, even better than) their matched non-diabetic control group, despite the fact that the diabetic patients were more obese and had greater co-morbidities at baseline.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Association of Metformin with Decreased Mortality
What the sources say
- Partly supportedcites Bannister et al., 2014 sourceExperimental — accuracy not yet measured
The Metformin monotherapy compared with matched control group section reports higher BMI and greater baseline morbidity in the metformin group. The Unadjusted survival patterns section reports little overall survival difference and better survival with metformin among patients aged 71–75, but it does not establish that result for everyone over 70. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Feeding metformin to Drosophila resulted in a robust activation of AMPK and reduced lipid stores, but did not increase lifespan (Slack et al., 2012).”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Supportedcites Slack et al., 2012 source
The Abstract states that feeding metformin to adult Drosophila robustly activated AMPK, reduced lipid stores, and did not increase lifespan in either sex. The Results section, “Metformin Treatment does not Extend Lifespan in Drosophila,” likewise reports no survival benefit across the tested concentrations. (LLM, conf=0.95)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“One study suggested that T2DM patients treated with metformin had increased risk for poor cognitive performance (Moore et al., 2013); however, it had a number of methodological flaws (Alagiakrishnan et al., 2013) and has not been replicated.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Association of Metformin with Better Cognitive Function
What the sources say
- Supportedcites Moore et al., 2013 source
The Results section reports worse cognitive performance among participants with diabetes who were taking metformin (adjusted OR 2.23, 95% CI 1.05–4.75), and the Conclusions describe the finding as an association. The methodological-flaws clause cites a different source, while the replication statement is not attributed to Moore et al.; neither is part of this verdict. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Alagiakrishnan et al., 2013
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In non-diabetic subjects, the GIPS III study (Lexis et al., 2014) failed to demonstrate the benefit of short-term metformin treatment (4 months) on left ventricular ejection fraction, major adverse cardiovascular events, and mortality in post-myocardial infarction patients”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Clinical Trials
What the sources say
- Supportedcites Lexis et al., 2014 source
The Abstract reports that four months of metformin did not improve left ventricular ejection fraction compared with placebo in patients without diabetes after STEMI. Major adverse cardiac events were not significantly different between groups (P = .16), and all patients were alive at four months, so the trial demonstrated no benefit on mortality during that period. (LLM, conf=0.94)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“a more thorough analysis that included more data and accounted for heterogeneous comparators showed that overall cancer incidence was reduced by 31% and cancer mortality by 34% (Gandini et al., 2014).”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Observational Studies Suggest Metformin Decreases Cancer Incidence
What the sources say
- Supportedcites Gandini et al., 2014 source
The Results section, “Overall Cancer Incidence and Mortality – Effects of BMI and Study Type,” reports 31% lower overall cancer incidence and 34% lower cancer mortality among metformin users compared with users of other anti-diabetic compounds. These are the paper’s pooled estimates; the paper also cautions that the associations may not be causal and become smaller or nonsignificant in some bias-adjusted analyses. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“As expected in these studies, metformin also increased AMPK activity and increased antioxidant protection, resulting in reductions in both chronic inflammation and accumulation of oxidative damage (Martin-Montalvo et al., 2013)”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
What the sources say
- Supportedcites Martin-Montalvo et al., 2013 source
The Results section (page unavailable) reports increased phosphoactive AMPK in metformin-treated mice and increased antioxidant and stress-response proteins that contributed to reduced hepatic oxidative damage. It also reports reduced inflammatory signaling and increased expression of anti-inflammatory genes in their livers. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“After a single 1.5 g dose, the peak plasma concentration of 18 mM occurs in 3 hr, with a mean plasma half-life of about 20 hr (Foretz et al., 2014).”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Considerations in Designing Human Metformin Trials
What the sources say
- Partly supportedcites Foretz et al., 2014 sourceExperimental — accuracy not yet measured
The Pharmacokinetics of metformin section reports a peak at 3 hours after a 1.5 g dose and a mean plasma half-life of about 20 hours. It gives the peak concentration as about 18 µM, not 18 mM; the citing sentence overstates it by a factor of 1,000. (LLM, conf=0.95)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“While one meta-analysis (Stevens et al., 2012) did not show that metformin prevents cancer”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Observational Studies Suggest Metformin Decreases Cancer Incidence
What the sources say
- Supportedcites Stevens et al., 2012 source
The Discussion reports that the meta-analysis found no statistically significant beneficial effect of metformin on cancer outcomes. It also cautions that the broad confidence intervals do not rule out a smaller protective effect, which is consistent with saying the analysis did not show prevention rather than that it disproved it. (LLM, conf=0.94)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“To date, there is no evidence for such effects in humans.”
§ Metformin as a Tool to Target Aging > Metformin Modulates the Biology of Aging and Health Span in Model Organisms
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Lifespan has been verifiably modulated by genetic, pharmacologic, and dietary interventions in multiple model systems.”
§ Metformin as a Tool to Target Aging > Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“In the Singapore Longitudinal Aging Study, metformin use was associated with a 51% reduced risk of cognitive impairment (defined by modified Mini-Mental Status Exam score % 23), which remained robust to adjustment for vascular and non-vascular risk factors.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Association of Metformin with Better Cognitive Function
What the sources say
- Not matchedcites Ng et al., 2014
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Data from several randomized clinical trials and multiple observational studies provide evidence for such an effect, which would not be expected from glucose lowering alone.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
In the paper
“Further, the risk of lactic acidosis appears to be related to renal function, not age per se, and is currently considered to be very low (Aroda et al., 2016).”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Considerations in Designing Human Metformin Trials
What the sources say
- Not checked — no full text of the sourcecites Aroda et al., 2016 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The majority of observational data support metformin benefit in CVD, but residual bias and confounding cannot be ruled out”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Observational Studies
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Vitamin B12 deficiency occurred in ~7% of metformin group versus 5% in placebo group after 13 years; risk of B12 deficiency increases with duration of use but was not greater in older compared with younger subjects in DPPOS (Lalau et al., 1990).”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Considerations in Designing Human Metformin Trials
What the sources say
- Not checked — no full text of the sourcecites Lalau et al., 1990
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If metformin can target and delay aging, its administration should be associated with fewer age-related diseases in general, rather than merely the decreased incidence of a single disease.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Studies on biodistribution of metformin in mice showed accumulation mainly in the gastrointestinal tract, kidney, and liver.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Considerations in Designing Human Metformin Trials
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Patients with T2DM allocated to metformin compared with conventional treatment had risk reduction of ~20% (p = 0.032) for CVD and 42% (p = 0.017) for diabetes-related death (UKPDS Group, 1998).”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Clinical Trials
What the sources say
- Not matchedcites UKPDS Group, 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The mechanisms proposed relate to reduced insulin levels, improved insulin action, decreased IGF-1 signaling, and activation of AMPK.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Observational Studies Suggest Metformin Decreases Cancer Incidence
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“While metformin can beprescribed at dosages of up to 2,250 mg/day, no further effects of decreasing glucose are noted after 1,600–1,700 mg/day.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Considerations in Designing Human Metformin Trials
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear? Based: unclearIt may state two separate claims as one.
In the paper
“the safety of met-formin use in DPP/DPPOS was reported on in 2012, when over 18,000 patients-years of follow-up had accrued, and by which time ~20% of the cohort was age 70 or older (mean age ~64). There were no cases of lactic acidosis or significant hypoglycemia (Diabetes Prevention Program Research Group, 2012).”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Considerations in Designing Human Metformin Trials
What the sources say
- Not matchedcites Diabetes Prevention Program Research Group, 2012
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
In the paper
“In one small clinical trial, T2DM patients with depression (n = 58) were treated with metformin or placebo for 24 weeks (Guo et al., 2014). The metformin group showed improved cognitive performance and reduced depressive symptoms, concurrent with improved glycemic control.”
§ Metformin as a Tool to Target Aging > Human Studies of Metformin that Target Age-Related Diseases > Association of Metformin with Better Cognitive Function
What the sources say
- Not checked — no full text of the sourcecites Guo et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
Metformin's aging-related mechanisms observed in model organisms are conserved in humans.
“Metformin is a drug approved to treat diabetes but appears to target a number of aging-related mechanisms.”
The paper relies on this without support.
A composite outcome of cardiovascular events, cancer, dementia, and mortality can serve as a measure of aging per se in TAME.
“Rather than study the effects of metformin on each separate condition, we will measure time to a new occurrence of a composite outcome that includes cardiovascular events, cancer, dementia, and mortality.”
The paper relies on this without support.
Age-related diseases share a common aging process such that a single drug can delay them together.
“If metformin can target and delay aging, its administration should be associated with fewer age-related diseases in general, rather than merely the decreased incidence of a single disease.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Metformin is a powerful calorie restriction mimetic in aging mice (Dhahbi, Mote, Fahy, & Spindler, 2005) and has been proposed as a candidate for slowing aging in humans (Barzilai, Crandall, Kritchevsky, & Espeland, 2016).”
From Reversal of epigenetic aging and immunosenescent trends in humans. (2019) · cites this paper as Barzilai, Crandall, Kritchevsky, & Espeland, 2016
In the citing paper
“Metformin- a biguanide that combats age-related disorders and improves healthspan”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Barzilai et al. 2016
In the citing paper
“Association studies suggest a decrease in the incidence of most age-related cancers, Alzheimer’s Disease while clinical studies support metformin’s role in a decrease in cognitive decline and reduced mortality in diabetics taking metformin compared to non-diabetics”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Barzilai et al. 2016
In the citing paper
“One of the main actions of metformin is the inhibition of mitochondrial complex I (NADH:ubiquinone oxidoreductase), that leads to multiple downstream effects both on metabolic and non-metabolic pathways responsible in the aging process”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Barzilai et al. 2016
In the citing paper
“In humans, metformin has been in clinical use for over 60 years, studied extensively, has a high safety profile and is uniquely positioned to intervene several crucial pathways responsible for aging and age-related diseases”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Barzilai et al. 2016
In the citing paper
“Metformin, a widely prescribed antidiabetic drug, has been shown to alleviate aging in preclinical studies [177].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [177]
In the citing paper
“New insights may also come from the use of caloric restriction mimetics, such as metformin, an activator of 5′ AMP-activated protein kinase (AMPK).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [94]
In the citing paper
“The lifespan and healthspan of invertebrates are extended by mutations in pathways such as the DAF-2, a gene that encodes for the IGF-1 pathway in the nematode Caenorhabditis elegans (C. elegans), or the mTOR signaling pathways that are linked to accelerating the aging process (60, 62–65).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [60]
In the citing paper
“The same pathways studied in C. elegans have also been investigated in mammals, where lifespan and healthspan were prolonged through modifying the ‘aging’ pathways or through drugs, including metformin (60, 87).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [60]
In the citing paper
“Targeting Aging with Metformin (TAME) trial is a double-blinded, placebo-controlled, multicenter trial that is planned to involve 14 research centers in the USA, and subject to funding and approval, will enroll 3000 ethnically diverse, non-diabetic subjects aged 65–80 (60, 261).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [60]
In the citing paper
“It is argued that TAME trial outcomes will give more insight on whether metformin decreases the risk of developing age-dependent diseases, excluding diabetes, in non-diabetic individuals, and potentially provide a tool to target aging itself and not related diseases individually (60, 261).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [60]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Trial described as unpublished despite a published citation
MinorThe text calls the Luchsinger et al. trial unpublished, but its reference lists results of a randomized clinical trial published in the Journal of Alzheimer's Disease in 2016.
“In an unpublished trial, non-diabetic subjects (n = 80) with mild cognitive impairment showed significant improvements in some cognitive domains after 12 months of metformin treatment (Luchsinger et al., 2016).”
“51. Luchsinger JA Perez T Chang H Mehta P Steffener J Pradabhan G Ichise M Manly J Devanand DP Bagiella E 2016 Metformin in Amnestic Mild Cognitive Impairment: Results of a Pilot Randomized Placebo Controlled Clinical Trial J Alzheimers Dis 51 501 514”
Citations
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Items 701–800 of 1,150
Metformin Induces Lipogenesis and Apoptosis in H4IIE Hepatocellular Carcinoma Cells
Park, D., Lee, S.-Y., & Boo, H. (2023) · Development & Reproduction · doi:10.12717/dr.2023.27.2.77 · Cited by 7
“These include its anti-cancer (Zhang et al., 2013a), anti-inflammatory (Zhang et al., 2021), and anti-aging (Barzilai et al., 2016) effects.”
Exploring the potential of epigenetic clocks in aging research
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Ageotypes: Distinct Biomolecular Trajectories in Human Aging
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From bench to bedside: translational insights into aging research
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Metformin as an activator of AMP-activated protein kinase. Known and new mechanisms of action
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Potential Diets to Improve Mitochondrial Activity in Amyotrophic Lateral Sclerosis
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“Also, metformin can be used to treat a variety of aging-related metabolic disorders, like cardiovascular disease or cognitive decline [43].”
BackgroundGeroscience: just another name or is there more to it?
Okholm, S. (2024) · Biogerontology · doi:10.1007/s10522-024-10105-x · Cited by 7
“In brief, TAME is a clinical trial to determine if repurposing metformin for non-diabetic elderly can delay the time-to-event between acquiring the first and second late-life disease, taking the rate of multimorbidity as a proxy for aging’s rate (Barzilai et al. 2016).”
Insights into Dysregulated Neurological Biomarkers in Cancer
Duranti, E., & Villa, C. (2024) · Cancers · doi:10.3390/cancers16152680 · Cited by 7
“Metformin, a biguanide used to treat type 2 diabetes, was found to reduce the risk of dementia, cancer, and other age-related disorders [235,236] by reducing insulin and IGF-1 levels, inhibiting the mTOR pathway, blocking mitochondrial function, reducing oxidative damage, and activating the AMP…”
BackgroundUpdate on Therapy for Myotonic Dystrophy Type 1
Ivanović, V., Meola, G., Vukojević, Z., & Perić, S. (2023) · Current Treatment Options in Neurology · doi:10.1007/s11940-023-00760-9 · Cited by 7
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InfluentialPeng, L. C., Hsiao, F. S. H., & Chen, L. (2026) · Journal of the Chinese Medical Association · doi:10.1097/jcma.0000000000001374 · Cited by 6
“42,43 ) 29,30 MG2A (functional monitoring) 30 MG2A (primary diagnostic indication) 30,31 Fig.”
Transcranial Electromagnetic Wave Treatment: A Fountain of Healthy Longevity?
Arendash, G. W., & Cao, C. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24119652 · Cited by 6
“Methformin has a long record of clinical trials purporting to reduce cancer, cognitive impairment, and mortality [5], apparently indirectly through its antihyperglycemic and insulin-sensitizing effects [6].”
BackgroundExploring the Complexity and Promise of Tumor Immunotherapy in Drug Development
Feng, Y., He, C., Liu, C., Shao, B., Wang, D., & Wu, P. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25126444 · Cited by 6
“The findings of metformin, a widely used antidiabetic drug, suggest it may play a role in decelerating the aging process [173].”
BackgroundProtection of nuclear DNA by lifespan-extending compounds in the yeast Saccharomyces cerevisiae
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“One study has pointed out that the use of metformin is associated with a relatively low incidence of cancer in diabetic patients and is considered useful for cancer therapy in nondiabetic patients [10], and one other study has revealed that in breast cancer models, metformin can delay the onset of breast cancer and pr…”
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“Rapidly gaining momentum in the geroscience research community, metformin is the focus of ongoing clinical trials to confirm the safety and efficacy of its potential role in altering the pace of biological aging (5).”
BackgroundAn Incipient Revolution in the Testing of Anti-aging Strategies
Mitteldorf, J. (2018) · Biochemistry (Moscow) · doi:10.1134/s000629791812009x · Cited by 6
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Senotherapeutics for metabolic disease and diabetic complications
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“The proposed but not yet active TAME trial will investigate its potential to extend healthspan and delay age-related diseases beyond glycemic control [110].”
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“11”
Lifestyle and Metformin Interventions and Risk of Multimorbidity in Adults With Prediabetes
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“For instance, aspirin and statin are potentially bene fi cial for cancer (Zaleska et al., 2018; Ahmadi et al., 2020; Wang et al., 2021), or the pleiotropic effect of metformin in cancer, cardiovascular disease, and dementia in diabetic patients (Barzilai et al., 2016).”
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“Es destacable también su posible beneficio en términos de combatir el envejecimiento y las enfermedades neurodegenerativas incluso en los no diabéticos, hecho que está siendo evaluado actualmente en un ensayo clínico 10 .”
Obesity: The Crossroads of Opinion, Knowledge, and Opportunity
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Pioneers: Glucose Sensing and Control of Health-span and Lifespan
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“Studies such as Targeting Aging with Metformin (TAME) will help identify efficacy of metformin on healthspan and expanding use in older adults (Barzilai et al., 2016).”
BackgroundProspects of Pharmacological Interventions to Organismal Aging
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“…brain damage by inhibiting mitochondrial respiratory chain complex 1, [4] regulating mitochondrial function [5] and energy metabolism by activating AMP-activated protein kinase, [6,7] improving cell metabolism and cell senescence in age-related diseases, [8,9] and exerting anti-tumor effects.”
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In silico clinical trials for anti-aging therapies
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“Accordingly, a recent study has raised concerns about broad recommendations for the use of metformin as a potential healthspan extending treatment [10,41] in healthy individuals [42].”
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“Positive Biology” and Well-Ordered Science
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How should wetheorizeabout justice in the genomic era?
Farrelly, C. (2021) · Politics and the Life Sciences · doi:10.1017/pls.2021.3 · Cited by 5
“This novel strategy of preventive medicine, which targets the largest risk factor for chronic disease (i.e., aging), is already underway with the launch of TAME (Targeting Aging with Meformin) (Barzilai et al., 2016).”
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“Besides, metformin was shown to have a function in the regulation of the microbiome, which may be another way to affect aging [91].”
BackgroundPEN2: Metformin’s new partner at lysosome
Sakamoto, K., & Jessen, N. (2022) · Cell Research · doi:10.1038/s41422-022-00661-7 · Cited by 5
DNA damage-induced stalling of transcription drives aging through gene expression imbalance
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Liver enzyme trends in patients taking uninterrupted metformin before and after coronary surgery
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“These include a myriad of pathways leading to reduced insulin-like growth factor signaling; inhibition of the mechanistic target of rapamycin (mTOR); inhibition of mitochondrial complex-1, causing a reduced production of reactive oxygen species (ROS); and the activation of AMP-activated kinase, which inhibits gluconeo…”
BackgroundMetformin, the gut microbiome and neurogenesis: Lessons learned in rebirth of an old drug
Clarke, G. A. (2021) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2021.04.012 · Cited by 5
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“Epidemiological studies have shown that moderate doses of metformin and rapamycin can prevent the development of many cancers, prolong life expectancy, and reduce the incidence of neurodegenerative diseases (Barzilai et al. 2016).”
Romero, M., Gelsomini, A., Miller, K., Suresh, D., Thaller, S. R., & Frasca, D. (2024) · Journal of Nutrition · doi:10.1016/j.tjnut.2024.10.013 · Cited by 5
A CellAgeClock for expedited discovery of anti-ageing compoundsPreprint
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“The first study to test broad-spectrum protection capacity of 333 metformin, the TAME study, is underway (Barzilai et al. 2016).”
BackgroundMetformin: An Old Drug with New Tricks—Promising Role in Vascular Aging and Cardioprotection
Sivakumar, R., Senghor, K. A. A., Vinodhini, V. M., & Kumar, J. S. (2025) · Drugs & Aging · doi:10.1007/s40266-025-01215-3 · Cited by 5
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Anti-aging properties of the aminosterols of the dogfish shark
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“A second compound, metformin, widely used as a fi rst-line treatment for Type 2 diabetes, is currently in Phase 3 clinical trials of life extension based on the results of longevity studies in rodents conducted in several laboratories 18 .”
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“Epidemiological studies suggest that metformin use might reduce the incidence of cancer and neurodegenerative disease 45 .”
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“A well-known illustration of this is TAME (Targeting Aging with Metformin) [22].”
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Precision geromedicine: Science meets clinical practice
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“Metformin, a first-line insulin sensitizer, has been shown in animal models to enhance hippocampal insulin signaling (pAkt/Akt ratio) under conditions of diet-induced IR (Barzilai et al., 2016).”
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Low-grade inflammation in the post-COVID period as a strategic goal of treatment and rehabilitation
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“…USA, a multicenter project evaluating interventions that enhance lifespan and delay the development of illness and dysfunction in mice (Miller et al. 2007), has developed rapamycin and metformin as effective FDA-approved therapies (Barzilai et al. 2016; Johnson et al. 2013; Mannick et al. 2014).”
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Mitochondria and Brain Disorders
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Inflammation and osteosarcopenia
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Werner Syndrome as a Model of Human Aging
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New use for an old drug: Metformin and atrial fibrillation
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Metformin-Induced Receptor Turnover Alters Antibody Accumulation in HER-Expressing Tumors
Panikar, S. S., Keltee, N., Berry, N.-K., Shmuel, S., Fisher, Z. T., Brown, E. L., Zidel, A., Mabry, A., & Pereira, P. M. R. (2023) · Journal of Nuclear Medicine · doi:10.2967/jnumed.122.265248 · Cited by 4
Biomedicines in Longevity and Aging The Quest to Resist Biological Decline
Raymond, R. D. D. (2024) · Biomedicine · doi:10.37796/2211-8039.1433 · Cited by 4
“Rapamycin will prevent further signalling, which then prevents further cell division, which in turn may prolong the time for healthy cells to reach their divisional limit [73].”
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Selecting Appropriate Clinical Trial Endpoints for Geroscience Trials: A Path Towards ConsensusPreprint
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Pharmacology of Aging: Drosophila as a Tool to Validate Drug Targets for Healthy Lifespan
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“A series of clinical trials are planned to assess if metformin also prevents the incidence of age-related diseases in humans 103 .”
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“Metformin, the usual first-line drug used to treat type 2 diabetes mellitus (T2DM), has other beneficial effects, such as anticancer effects, reduced body weight, and increased hepatic fat content (Barzilai et al. 2016; Foretz et al. 2019; Galal et al. 2024; Rena et al. 2017).”
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Metadata
- Authors
- Barzilai, N., Crandall, J. P., Kritchevsky, S. B., & Espeland, M. A.
- Affiliations
- Albert Einstein College of Medicine (US)
- Wake Forest University Health Sciences (US)
- Corresponding author
- Barzilai, Nir
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 23
- Issue
- 6
- Pages
- 1060-1065
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC5943638
- OpenAlex
- W2422981416
- Cited by
- 1,096
- References
- 83
- Citations by year
- 2026: 129 · 2025: 117 · 2024: 101 · 2023: 108 · 2022: 105 · 2021: 131 · 2020: 127 · 2019: 110 · 2018: 97 · 2017: 59 · 2016: 11
- FWCI
- 8.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P01AG021654, R24AG044396, P01AG027734, P30AG038072, R37AG018381, R01AG046949, P30AG021332)
- National Institute of Diabetes and Digestive and Kidney Diseases (U01DK048349)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- metformin, aging, lifespan extension, healthspan, age-related diseases, anti-aging drugs, drug repurposing
- MeSH terms
- Aging, Animals, Clinical Trials as Topic, Humans, Longevity, Metformin, Models, Biological, Models, Animal
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