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Earlier menopause linked to faster biological aging, study finds (opens in a new tab)

medicalxpress.com · 2026-10-13

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Mixed

Mixed.

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

  • 5 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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Mixed

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

  • 5 supported
  • 3 not covered
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8 claims in this story

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What the story carried across

Nothing material from the study was dropped.

8 things the story did carry across
  • The paper is a systematic review and meta-analysis of 29 studies including 550,550 female participants assessing reproductive-history exposures and DNAm clock-derived EAA.
  • Meta-analysis of cross-sectional studies found earlier age at menopause associated with higher EAA, strongest for GrimAge, β = -0.08 years per one-year earlier menopause.
  • Parity/delivery was associated with higher PhenoAge EAA, β = 0.13 years per delivery.
  • Age at menarche showed no relationship with EAA across DNAm clocks.
  • Across studies, preterm birth was consistently associated with higher EAA, but the abstract profile does not provide pooled effect sizes or detailed directionality for pregnancy-time EAA prediction.
  • Findings for pregnancy complications and adverse birth outcomes were mixed across studies.
  • Associations were particularly apparent using second-generation DNAm clocks, especially PhenoAge and GrimAge.
  • Most reported associations are cross-sectional, limiting causal inference.
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Pieces of work

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study summary

Lead result

secondary data

1Lead resultsecondary dataQuantitatively pool (meta-analyze) effect estimates for selected reproductive-history exposures and DNAm clock outcomes (e.g., age at menopause with GrimAge EAA; parity with PhenoAge EAA; menarche with EAA).Meta-analysis of cross-sectional studiesExpand

In plain English

Meta-analysis of cross-sectional studies pooled effect estimates linking reproductive-history exposures (age at menopause, age at menarche, parity) with DNA methylation clock–derived epigenetic age acceleration (EAA). The pooled results reported: each one-year earlier age at menopause was associated with higher EAA (strongest for GrimAge, n=5,920, β = -0.08 years per year earlier, 95% CI -0.11 to -0.05); no relationship was found between age at menarche and EAA across clocks; and parity was positively associated with PhenoAge EAA (n=4,508, β = 0.13 years per delivery, 95% CI 0.04 to 0.21).

Key findings

  • Earlier age at menopause is associated with higher epigenetic age acceleration (EAA); association strongest for GrimAge in pooled cross-sectional studies.GrimAge: β = -0.08 years per one-year earlier menopause (95% CI -0.11 to -0.05); pooled n = 5,920
  • Age at menarche showed no relationship with epigenetic age acceleration across DNAm clocks in pooled analyses.
“Meta-analysis of cross-sectional studies showed each one-year earlier age at menopause was significantly associated with higher EAA, strongest in GrimAge (n = 5920, β=-0.08 years, 95% CI: -0.11, -0.05).”
What this piece can’t prove
  • Pooled analyses are restricted to cross-sectional studies, limiting causal interpretation.
  • Abstract does not report how many studies contributed to each pooled estimate or their study-level characteristics (age distributions, geographic settings, covariate adjustment).

2 further details could not be confirmed from the summary.

2secondary dataSynthesize evidence on associations between reproductive history exposures (e.g., age at menopause/menarche, parity, preterm birth, pregnancy complications) and epigenetic age acceleration (EAA) measured by DNA methylation clocks.Systematic review and meta-analysisExpand

In plain English

Systematic review and meta-analysis of 29 studies (total n=550,550; reported median mean age 35.4 years, 100% female) evaluating associations between reproductive history exposures (age at menopause, age at menarche, parity, preterm birth, pregnancy complications, adverse birth outcomes) and DNA methylation clock–derived epigenetic age acceleration (EAA). Across included studies, preterm birth and earlier age at menopause were consistently associated with higher EAA, while findings for age at menarche, pregnancy complications, and adverse birth outcomes were mixed. Meta-analyses of cross-sectional studies identified (1) each one-year earlier age at menopause associated with higher EAA (strongest for GrimAge: β = -0.08 years per year earlier, 95% CI -0.11 to -0.05; n = 5,920) and (2) parity associated with higher EAA using PhenoAge (β = 0.13 years per delivery, 95% CI 0.04 to 0.21; n = 4,508). No relationship was found between age at menarche and EAA in any DNAm clocks. The authors note associations were particularly evident using second-generation DNAm clocks (PhenoAge, GrimAge).

Key findings

  • Each one-year earlier age at menopause was associated with higher epigenetic age acceleration; meta-analysis strongest in GrimAge.GrimAge: β = -0.08 years per year earlier (95% CI -0.11 to -0.05); n = 5,920
  • Parity was associated with higher epigenetic age acceleration when measured with PhenoAge.PhenoAge: β = 0.13 years per delivery (95% CI 0.04 to 0.21); n = 4,508
“Biological age measured by DNA methylation clocks and reproductive history: Systematic review and meta-analysis”
What this piece can’t prove
  • Most reported associations are cross-sectional (review/meta-analysis reports cross-sectional associations).
  • Abstract does not report detailed risk-of-bias assessments, heterogeneity metrics, or study selection/search strategy details.
3secondary dataCompare patterns/consistency of associations across different DNAm clocks (including emphasis on 2nd-generation clocks such as PhenoAge and GrimAge) and study designs (notably cross-sectional).secondary data comparative synthesisExpand

In plain English

Secondary synthesis of 29 studies (550,550 participants, all female) indicates that certain aspects of reproductive history are cross-sectionally associated with epigenetic age acceleration (EAA). Earlier age at menopause and preterm birth showed more consistent associations with higher EAA. Meta-analyses reported that each one-year earlier age at menopause was significantly associated with higher EAA, with the strongest signal observed using the GrimAge clock (n = 5,920; reported β = -0.08 years, 95% CI -0.11 to -0.05). Parity was associated with higher EAA when measured by PhenoAge (n = 4,508; reported β = 0.13 years per delivery, 95% CI 0.04 to 0.21). No relationship was found between age at menarche and EAA; findings for pregnancy complications and adverse birth outcomes were mixed. The authors emphasize that associations were detected particularly with 2nd-generation DNAm clocks (PhenoAge, GrimAge), an interpretive cross-clock comparison derived from the compiled results.

Key findings

  • The authors report that associations between aspects of reproductive history and higher epigenetic age acceleration were detected particularly with 2nd-generation DNAm clocks (PhenoAge, GrimAge) based on cross-study synthesis.
  • Meta-analysis of cross-sectional studies found that each one-year earlier age at menopause was significantly associated with higher EAA, with the strongest pooled association observed using the GrimAge clock.GrimAge: β = -0.08 years per year earlier (95% CI: -0.11, -0.05); n = 5,920
“These findings highlight that aspects of reproductive history are cross-sectionally associated with higher EAA, particularly measured with 2nd generation DNAm clocks (PhenoAge, GrimAge).”
What this piece can’t prove
  • The unit represents an interpretive, cross-clock comparison synthesized from the included studies rather than a distinct primary analysis; the abstract provides limited clock-specific detail for all exposures.
  • Most reported associations are cross-sectional; causal interpretation is limited.
  • Abstract lacks full reporting of adjustment covariates, heterogeneity statistics, and study-level contributors for many of the reported associations.
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