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Anti-ageing 'supermodel granny' drug extends life in animal tests (opens in a new tab)

bbc.com · 2024-07-17

Short answerEvidenceSource

Short answer

Mixed

Mixed.

The claims we could check match the study, but some claims were not covered by the evidence reviewed.

  • 3 supported
  • 3 not covered

Checked against the study summary. The full text wasn't available, so some details couldn't be settled either way.

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Follow the evidence trail
1
2

NewsLink checks it

Mixed

Every claim we could check holds up. Three of six claims match the study. This overall rating is based only on the claims we could check. Three claims the study doesn't address.

  • 3 supported
  • 3 not covered
Open claim evidence
3
Then inspect each claim

Evidence layer

Claim by claim

Each claim gets a verdict. Expand it to see the evidence directly below.

6 claims in this story

Showing all 6 claimsChoose a verdict to focus the list.

Claim 1 of 6Not coveredThe treated mice were described as "supermodel grannies" because of their youthful appearance, and they were healthier, stronger and developed fewer cancers than unmedicated peers.View evidenceHide evidence

As statedfewer cancers

Why this verdict

The abstract-level profile supports improved healthspan-related outcomes such as muscle function, frailty, metabolism, multimorbidity and biomarkers in aged mice. However, the specific colourful description of youthful appearance, 'supermodel grannies', healthier fur, and especially fewer cancers is not present in the supplied abstract profile, so those parts cannot be verified at this evidence depth.

1

Study evidence

Deletion of Il11 or Il11ra1 in mice protects against metabolic decline, multimorbidity and frailty in old age.

“Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age.”
2

Study evidence

Administration of anti-IL-11 from 75 weeks for 25 weeks improved metabolic measures in aged mice.

“Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes.”
Claim 2 of 6Not coveredThe results, published in Nature, showed lifespans increased by 20-25% depending on experiment and sex, with lower cancer levels, improved muscle function, leaner bodies, healthier fur and better frailty scores.View evidenceHide evidence

As stated20-25%

Why this verdict

The lifespan magnitude is supported: genetic Il11 deletion extended lifespan by 24.9% on average, and anti-IL-11 increased median lifespan by 22.5% in males and 25% in females. Improved muscle function and frailty are also supported. But lower cancer levels, leaner bodies and healthier fur are not in the supplied abstract profile, and the abstract profile does not provide the detailed outcome set needed to verify those specifics.

1

Study evidence

Deletion of Il11 or Il11ra1 in mice protects against metabolic decline, multimorbidity and frailty in old age.

“Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age.”
2

Study evidence

Administration of anti-IL-11 from 75 weeks for 25 weeks improved metabolic measures in aged mice.

“Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes.”
Claim 3 of 6Not coveredThe anti-interleukin-11 drug is already being trialled in patients with lung fibrosis, and the article says the trials had not been completed, though the data suggested it was safe to take.View evidenceHide evidence

Why this verdict

The profile supports that anti-IL-11 agents are in early-stage clinical trials for fibrotic lung disease. However, the supplied abstract profile does not verify that those trials were incomplete or that available human data suggested the drug was safe; it explicitly notes that adverse effects or tolerability were not reported in the abstract.

1

Study evidence

Administration of anti-IL-11 from 75 weeks for 25 weeks improved metabolic measures in aged mice.

“Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes.”
2

Study evidence

Anti-IL-11 treatment initiated at 75 weeks and continued until death increased median lifespan in mice: male +22.5%, female +25% (abstract).Median lifespan: males +22.5%; females +25%

“Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%.”
Claim 4 of 6SupportedA drug increased the lifespans of laboratory animals by nearly 25% in a discovery scientists hope could slow human ageing too.View evidenceHide evidence

As statednearly 25%

Why this verdict

The abstract-level profile reports that anti-IL-11 treatment begun at 75 weeks and continued until death extended median lifespan in mice by 22.5% in males and 25% in females. The headline's 'nearly 25%' is consistent with this. The human-ageing part is framed as scientists' hope rather than an observed human effect, and the story elsewhere notes human effects are unknown.

1

Study evidence

Anti-IL-11 treatment initiated at 75 weeks and continued until death increased median lifespan in mice: male +22.5%, female +25% (abstract).Median lifespan: males +22.5%; females +25%

“Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%.”
Claim 5 of 6SupportedResearchers at the MRC Laboratory of Medical Science, Imperial College London and Duke-NUS Medical School were investigating interleukin-11, which they say increases with age and drives inflammation and ageing-related biology.View evidenceHide evidence

Why this verdict

The paper profile states that IL-11 is upregulated with ageing across tissues/cell types, is a pro-inflammatory cytokine, and regulates an ERK–AMPK–mTORC1 axis implicated in ageing-related decline. The institutional affiliations are not independently evidenced in the supplied profile, but the scientific substance of the claim is supported at abstract level.

1

Study evidence

The authors report that IL-11/Il11 expression increases with age across multiple cell types and tissues in mice, and that IL-11 is associated with regulation of an ERK–AMPK–mTORC1 signalling axis.

“As mice age, IL-11 is upregulated across cell types and tissues to regulate an ERK-AMPK-mTORC1 axis”
Claim 6 of 6SupportedThe team reported two mouse experiments: one genetically engineered mice unable to produce interleukin-11, and another gave older mice a drug that removes interleukin-11 from the body.View evidenceHide evidence

Why this verdict

The profile reports genetic loss/deletion of Il11 or Il11ra1 in mice and pharmacologic anti-IL-11 treatment started in older mice. The story simplifies multiple related genetic, healthspan, and lifespan studies into two experiment types, but those intervention categories are supported by the abstract-level profile.

1

Study evidence

Deletion of Il11 or Il11ra1 in mice protects against metabolic decline, multimorbidity and frailty in old age.

“Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age.”
2

Study evidence

Administration of anti-IL-11 from 75 weeks for 25 weeks improved metabolic measures in aged mice.

“Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes.”
Then look for missing context

Context layer

What the story left out

Important study details the story did not include.

  • Cancer outcomes, fur/appearance outcomes and exact body-composition descriptions are not present in the supplied abstract profile.

    The story presents fewer cancers, youthful appearance, healthier fur and leanness as findings, but these specifics cannot be checked from the supplied abstract-level paper profile.

8 things the story did carry across
  • IL-11 is upregulated with ageing across tissues/cell types and is linked to an ERK–AMPK–mTORC1 signalling axis.
  • Genetic loss of Il11 or Il11ra1 protects aged mice from metabolic decline, multimorbidity and frailty.
  • Late-life anti-IL-11 treatment improves healthspan metrics in aged mice, including metabolism, muscle function, ageing biomarkers and frailty, across sexes.
  • Genetic deletion of Il11 extends mouse lifespan by 24.9% on average in both sexes.
  • Anti-IL-11 treatment from 75 weeks of age until death extends median lifespan by 22.5% in male mice and 25% in female mice.
  • Anti-IL-11 agents are in early-stage clinical trials for fibrotic lung disease, not established as anti-ageing treatment in humans.
  • The findings are from mouse models and may not generalize to humans.
  • The abstract does not report adverse effects or tolerability of anti-IL-11 treatment.
Then read the study layer

Study layer

Study at a glance

Scan the study first. Expand only the parts you want to inspect.

Pieces of work

5

Evidence read

study summary

Lead result

in vivo animal

1Lead resultin vivo animalPharmacologic inhibition of IL-11 starting late in life (anti-IL-11) improves healthspan metrics (metabolism, muscle function, frailty biomarkers) in aged mice.late-life therapeutic antibody intervention in aged miceExpand

In plain English

Late-life treatment with an anti-IL-11 antibody, begun at 75 weeks of age and continued for 25 weeks, is reported to improve metabolic measures, enhance muscle function, and reduce ageing biomarkers and frailty in aged mice of both sexes.

Key findings

  • Administration of anti-IL-11 from 75 weeks for 25 weeks improved metabolic measures in aged mice.
  • Late-life anti-IL-11 treatment enhanced muscle function in aged mice.
“Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes.”
What this piece can’t prove
  • The abstract does not report potential adverse effects or tolerability of the antibody treatment.

3 further details could not be confirmed from the summary.

2in vivo animalIL-11 signalling promotes age-associated decline via an ERK–AMPK–mTORC1 axis, and IL-11 is upregulated with ageing across tissues/cell types.in vivo animal cross-sectionalExpand

In plain English

In aged mice, IL-11 expression is increased across multiple cell types and tissues, and IL-11 signalling is reported to regulate an ERK–AMPK–mTORC1 signalling axis that is implicated in ageing-related cellular and tissue changes.

Key findings

  • The authors report that IL-11/Il11 expression increases with age across multiple cell types and tissues in mice, and that IL-11 is associated with regulation of an ERK–AMPK–mTORC1 signalling axis.
“As mice age, IL-11 is upregulated across cell types and tissues to regulate an ERK-AMPK-mTORC1 axis”
What this piece can’t prove
  • Findings are reported in mice and may not directly generalize to other species.

2 further details could not be confirmed from the summary.

3in vivo animalGenetic loss of Il11 or Il11ra1 protects aged mice from metabolic decline, multimorbidity and frailty (healthspan benefit).genetic knockout mouse ageing phenotypingExpand

In plain English

In aged mice, genetic deletion of Il11 or Il11ra1 is reported to protect against age-associated metabolic decline, multimorbidity and frailty based on comparative phenotyping of knockout animals versus controls.

Key findings

  • Deletion of Il11 or Il11ra1 in mice protects against metabolic decline, multimorbidity and frailty in old age.
“Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age.”
What this piece can’t prove
  • Summary is based on abstract information only; primary manuscript text, figures and supplementary data are needed to evaluate experimental design, sample sizes, statistical analyses and effect magnitude.

2 further details could not be confirmed from the summary.

4in vivo animalIL-11 inhibition extends lifespan in mice (genetic deletion; late-life anti-IL-11 treatment until death).mouse lifespan study (Il11−/− vs controls)Expand

In plain English

Abstract reports that genetic deletion of Il11 extended the lives of mice of both sexes by 24.9% on average in a survival-to-death lifespan study comparing Il11−/− animals with controls.

Key findings

  • Genetic deletion of Il11 extended lifespan in mice of both sexes by 24.9% on average (abstract statement).24.9% average lifespan extension (abstract-reported)
“In lifespan studies, genetic deletion of Il11 extended the lives of mice of both sexes, by 24.9% on average.”
What this piece can’t prove
  • Summary is based solely on the article abstract; full-method and full-results details (sample sizes, Kaplan–Meier curves, log-rank/Cox model outputs, exact statistical significance) are not available in the extracted text.
  • Unclear whether lifespan extension figure is averaged across sexes or computed from pooled data versus reported separately; abstract gives an average but lacks detailed breakdown.

1 further detail could not be confirmed from the summary.

5in vivo animalIL-11 inhibition extends lifespan in mice (genetic deletion; late-life anti-IL-11 treatment until death).therapeutic intervention survival study in aged mice (anti-IL-11 treatment started at 75 weeks until death)Expand

In plain English

In aged mice, administration of an anti-IL-11 antibody beginning at 75 weeks of age and continued until death increased median lifespan by ~22.5% in males and ~25% in females (reported in abstract).

Key findings

  • Anti-IL-11 treatment initiated at 75 weeks and continued until death increased median lifespan in mice: male +22.5%, female +25% (abstract).Median lifespan: males +22.5%; females +25%
“Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%.”
What this piece can’t prove
  • Uncertainty whether the described survival experiment used independent cohorts from the 25-week healthspan treatment study or the same animals followed to death.

1 further detail could not be confirmed from the summary.

Finally, the search trail

Method layer

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NewsLink checks the story. Tessa is where you inspect the paper, authors, evidence, and research context.

Papers considered

The selected paper, plus nearby candidates.

PubMed, Crossref, Europe PMC · 15 candidate papers

Candidate

Faculty Opinions recommendation of Interleukin-1 deficiency prolongs ovarian lifespan in mice.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2014 · Crossref

Source (opens in a new tab)

And 9 more candidates considered.