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Source study found

Story checked

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

BBC News · 2024-07-17

Short answerEvidenceSource

Short answer

Supported

Supported.

The story matches what the study reports.

  • 5 supported

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

Supported

Every claim holds up. All five claims match what the study reports.

  • 5 supported
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.

5 claims in this story

Showing all 5 claimsChoose a verdict to focus the list.

Claim 1 of 5SupportedA drug has increased the lifespans of laboratory animals by nearly 25%, in a discovery scientists hope can slow human ageing too.View evidenceHide evidence

As statednearly 25%

Why this verdict

The abstract supports late-life anti-IL-11 treatment extending median lifespan in mice by 22.5% in males and 25% in females, matching the story's 'nearly 25%' laboratory-animal claim. The human-ageing angle is framed as hope/unknown rather than proven, consistent with the paper's translational suggestion.

1

Study evidence

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% (abstract).Median lifespan +22.5% (males), +25% (females)

“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%.”
2

Study evidence

The authors propose anti-IL-11 therapy may be a translational opportunity to determine effects of IL-11 inhibition on ageing pathologies in older people, noting anti-IL-11 is in early-stage clinical trials for fibrotic lung disease.

“We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people.”
Claim 2 of 5SupportedThe treated mice were healthier, stronger and developed fewer cancers than their unmedicated peers.View evidenceHide evidence

Why this verdict

The abstract reports anti-IL-11 treatment improved metabolism and muscle function and reduced ageing biomarkers and frailty, and genetic loss protected against metabolic decline, multimorbidity and frailty. 'Developed fewer cancers' is not directly visible in the abstract profile, but the broader healthier/stronger comparison is supported; cancer-specific detail is not verifiable at abstract depth.

1

Study evidence

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.

“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

Genetic deletion of Il11 or Il11ra1 protects aged mice from metabolic decline, multimorbidity and frailty.

“Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age.”
Claim 3 of 5SupportedThe researchers performed two experiments: one genetically engineered mice unable to produce interleukin-11, and another that gave old mice a drug to purge interleukin-11 from their bodies.View evidenceHide evidence

Why this verdict

The abstract profile supports two broad experimental approaches: genetic deletion of Il11/Il11ra1 and pharmacologic anti-IL-11 treatment in old mice. The story's wording that old mice were given a drug to purge IL-11 is a lay rendering of anti-IL-11 administration; abstract details do not fully specify depletion/purging mechanics, but the experiment description is substantially aligned.

1

Study evidence

Genetic deletion of Il11 or Il11ra1 protects aged mice from metabolic decline, multimorbidity and frailty.

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

Study evidence

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.

“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 4 of 5SupportedThe results, published in Nature, showed lifespans were increased by 20-25% depending on the experiment and sex of the mice.View evidenceHide evidence

As stated20-25%

Why this verdict

The abstract reports lifespan extension by 24.9% on average with Il11 deletion and median lifespan extension of 22.5% in males and 25% in females with anti-IL-11 treatment. Thus the 20-25% range depending on experiment/sex is supported by the supplied profile.

1

Study evidence

Genetic deletion of Il11 extended the lives of mice of both sexes.24.9% average increase in lifespan

“In lifespan studies, genetic deletion of Il11 extended the lives of mice of both sexes, by 24.9% on average.”
2

Study evidence

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% (abstract).Median lifespan +22.5% (males), +25% (females)

“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 5SupportedThe drug is already being tested in people with lung fibrosis, but whether it would have the same anti-ageing effect is unknown.View evidenceHide evidence

Why this verdict

The abstract states anti-IL-11 therapy is currently in early-stage clinical trials for fibrotic lung disease and may provide a translational opportunity to determine effects on ageing pathologies in older people. The story's caveat that the same anti-ageing effect in people is unknown is consistent with the paper profile.

1

Study evidence

The authors propose anti-IL-11 therapy may be a translational opportunity to determine effects of IL-11 inhibition on ageing pathologies in older people, noting anti-IL-11 is in early-stage clinical trials for fibrotic lung disease.

“We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people.”
Then look for missing context

Context layer

What the story left out

Important study details the story did not include.

  • Mechanistic claim: IL-11 rises with age and regulates ERK–AMPK–mTORC1 signalling

    The paper profile includes a mechanistic pathway element, but the story presentation focuses on intervention, lifespan, healthspan and translation rather than the ERK–AMPK–mTORC1 mechanism.

    From in vivo animal

4 things the story did carry across
  • Mouse/preclinical evidence, not demonstrated human anti-ageing efficacy
  • Magnitude of mouse lifespan extension from genetic deletion and anti-IL-11 antibody treatment
  • Healthspan improvements in aged mice with IL-11 inhibition
  • Translational positioning: anti-IL-11 is in early-stage trials for fibrotic lung disease, not ageing, with no human outcome data reported here
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

6

Evidence read

study summary

Lead result

in vivo animal

1Lead resultin vivo animalTherapeutic anti-IL-11 administered late-life improves metabolism, muscle function, ageing biomarkers and frailty in old mice (healthspan intervention).aged mouse therapeutic antibody interventionExpand

In plain English

Late-life therapeutic administration of an anti-IL-11 antibody to 75-week-old mice for 25 weeks was reported to improve metabolism and muscle function and to reduce ageing biomarkers and frailty in both sexes.

Key findings

  • 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.
“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
  • No information in abstract on sample size, statistical significance, dose, route, frequency, randomization, or blinding.

2 further details could not be confirmed from the summary.

2in vivo animalIL-11 increases with age and drives ageing pathologies by regulating an ERK–AMPK–mTORC1 signalling axis across tissues/cell types.Expand

In plain English

In ageing mice, IL-11 expression is reported to increase across cell types and tissues and to regulate an ERK–AMPK–mTORC1 signalling axis that modulates cellular, tissue- and organismal-level ageing pathologies.

Key findings

  • IL-11 expression is reported to increase with age across cell types and tissues in mice.
  • IL-11 is reported to regulate an ERK–AMPK–mTORC1 signalling axis that modulates cellular, tissue- and organismal-level ageing pathologies.
“As mice age, IL-11 is upregulated across cell types and tissues to regulate an ERK–AMPK–mTORC1 axis to modulate cellular, tissue- and organismal-level ageing pathologies.”
What this piece can’t prove

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 benefits).in vivo genetic deletion (Il11 and/or Il11ra1) with ageing/healthspan phenotypingExpand

In plain English

Abstract reports that genetic deletion of Il11 or Il11ra1 in mice protects aged animals from metabolic decline, multimorbidity and frailty, indicating healthspan benefits of loss of IL-11 signalling.

Key findings

  • Genetic deletion of Il11 or Il11ra1 protects aged mice from metabolic decline, multimorbidity and frailty.
“Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age.”
What this piece can’t prove
  • Summary based solely on abstract text; full methods, quantitative results, and statistical details are not available in the provided excerpt.
4in vivo animalIL-11 inhibition extends lifespan in mice (genetic deletion and late-life antibody treatment).in vivo genetic knockout lifespan studyExpand

In plain English

Lifespan experiment reporting that genetic deletion of Il11 extends survival in male and female mice, quantified as a 24.9% average increase in lifespan (abstract).

Key findings

  • Genetic deletion of Il11 extended the lives of mice of both sexes.24.9% average increase in lifespan
“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

2 further details could not be confirmed from the summary.

5in vivo animalIL-11 inhibition extends lifespan in mice (genetic deletion and late-life antibody treatment).late-life anti-IL-11 antibody treatment until death (mouse lifespan study)Expand

In plain English

Abstract reports that administering an anti-IL-11 antibody from 75 weeks of age until death extends median lifespan in mice (male +22.5%, female +25%).

Key findings

  • 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% (abstract).Median lifespan +22.5% (males), +25% (females)
“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

1 further detail could not be confirmed from the summary.

6otherAnti-IL-11 therapy is positioned as a translational opportunity for ageing pathologies in older people (contextual interpretation).Narrative interpretation / translational positioningExpand

In plain English

The paper's authors suggest that anti-IL-11 therapy, which is reported to be in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to evaluate the effects of IL-11 inhibition on ageing-related pathologies in older people; this is presented as a forward-looking, interpretive claim grounded in the paper's preclinical (mouse) results rather than new human trial data.

Key findings

  • The authors propose anti-IL-11 therapy may be a translational opportunity to determine effects of IL-11 inhibition on ageing pathologies in older people, noting anti-IL-11 is in early-stage clinical trials for fibrotic lung disease.
“We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people.”
What this piece can’t prove
  • No new human trial data presented in the paper/excerpt to support the translational claim.
  • The cited ongoing clinical trials are for fibrotic lung disease; relevance to ageing pathologies is proposed but unproven.
  • Speculative forward-looking interpretation based on preclinical (mouse) evidence; human translational validity is uncertain.
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Method layer

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Papers considered

The selected paper, plus nearby candidates.

Crossref, PubMed, Europe PMC · 16 candidate papers

Candidate

Decision letter: Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice

2016 · Crossref

Source (opens in a new tab)

And 10 more candidates considered.