Evidence map›Paper›PMID 40342213›Full record

ArticleJournal of cachexia, sarcopenia and muscle2025

A Longitudinal Study of the Bidirectional Temporal Dynamics Between Body Mass Index and Biological Aging.

Peggy Ler, Jonathan K L Mak, Chandra A Reynolds, Alexander Ploner, Nancy L Pedersen, Juulia Jylhävä, Anna K Dahl Aslan, Deborah Finkel, Ida K Karlsson

Abstract readTwin Study
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Peggy LerDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.ORCID 0000-0002-4845-1180
Jonathan K L MakDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
Chandra A ReynoldsInstitute for Behavioral Genetics and Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, Colorado, USA.
Alexander PlonerDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
Nancy L PedersenDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
Juulia JylhäväDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
Anna K Dahl AslanSchool of Health Sciences, University of Skövde, Skövde, Sweden.
Deborah FinkelCenter for Economic and Social Research, University of Southern California, Los Angeles, California, USA.
Ida K KarlssonDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.

Funding

Clarifying risk and protective factors for dementia with the Interplay of Genes and Environment in Multiple Studies (IGEMS) consortiumR01AG060470 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GATZ, MARGARET, PEDERSEN, NANCY L · 2018 to 2022
$3.6M
Differences in the association of education with ADRD across countries, historical eras, and men and women.R01AG081248 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DEBORAH G FINKEL, Brian K. Finch · 2024 to 2026
$3.6M
Gene-Environment Interplay of Social Contexts and Aging-Related OutcomesR01AG037985 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI PEDERSEN, NANCY L · 2010 to 2014
$3.2M
Gene-environment Interplay Among Modifiable Factors for AD/ADRD: Risk and Resilience Across the LifespanR01AG089666 · NIA · UNIVERSITY OF COLORADO · PI Jenae M. Neiderhiser, CHANDRA A REYNOLDS · 2024 to 2026
$2.3M
Axel and Margaret Ax:son Johnson's FoundationErik och Edith Fernströms stiftelse för medicinsk forskningFoundation for Geriatric Diseases at Karolinska Institutet 2022-01296Foundation for Geriatric Diseases at Karolinska Institutet 2023-01854Foundation for Geriatric Diseases at Karolinska Institutet 2024-02116Karolinska Institutet's Research Foundation 2022-01718Loo and Hans Osterman's Foundation 2022-01222Loo and Hans Osterman's Foundation 2023-01855Loo and Hans Osterman's Foundation 2024-02197MacArthur Foundation Research Network on Successful AgingNIA NIH HHS R01AG037985NIA NIH HHS R01 AG060470NIA NIH HHS R01 AG081248NIA NIH HHS R01AG081248NIA NIH HHS R01 AG089666NIA NIH HHS R01AG089666NIH HHS AG04563NIH HHS AG059329NIH HHS AG10175NIH HHS R01AG060470NIH HHS R01AG08861Strategic Research Program in Epidemiology (SFOepi) at Karolinska InstitutetSwedish Council for Social ResearchSwedish Foundation for Health Care Sciences and Allergy ResearchSwedish National Research School of Aging and Health (SWEAH)Swedish Research Council 2016-03081Swedish Research Council 825-2007-7460Swedish Research Council 825-2009-6141Swedish Research Council for Health, Working Life and Welfare 2022-00672Swedish Research Council for Working Life and Social Research 2009-0795Swedish Research Council for Working Life and Social Research 97:0147:1B
6 · The paper itself

Abstract

backgroundObesity and aging share biological processes, but their relationship remains unclear, especially in late life. Understanding how body mass index (BMI) and biological aging influence each other can guide strategies to reduce age- and obesity-related health risks. We examined the bidirectional, longitudinal association between changes in BMI and biological aging, measured by frailty index (FI) and functional aging index (FAI), across late life.

methodsThis longitudinal cohort study used data from the Swedish Twin Registry substudies, GENDER, OCTO-Twin and SATSA, collected via in-person assessments from 1986 to 2014 at 2- to 4-year intervals. We analysed 6216-6512 evaluations from 1902 to 1976 Swedish twins. Dual change score models were applied to assess the bidirectional, longitudinal association between BMI and FI or FAI from ages 60.0-91.9. FI measured physiological aging, while FAI assessed functional aging through a composite score of functional abilities.

resultsAt first measurement, mean age was 74 ± 8, and 41% were males. BMI-FI relationship was bidirectional (p value ≤ 0.001): Higher BMI predicted a greater increase in FI over time (coupling effect [γ] = 0.86, 95% confidence interval [CI] = 0.65-1.06, p value ≤ 0.001), and higher FI predicted steeper decline in BMI (γ = -0.04, 95% CI = -0.05 to -0.03, p value ≤ 0.001). When including coupling from FI, BMI showed a nonlinear trajectory with a mean intercept of 26.32 kg/m

conclusionsHigher BMI predicted a steeper increase in FI, substantiating the hypothesis that obesity accelerates biological aging. Higher biological aging, measured as FI and FAI, drove a steeper BMI decline in late life, signalling that late-life weight loss may result from accelerated aging. Higher BMI may accelerate aspects of the aging process, and the aging process, in turn, accelerates late-life BMI decline, necessitating an integrated approach to manage both obesity and unintentional weight loss among older adults.

Indexed as

AgingBody Mass IndexAgedAged, 80 and overFemaleHumansLongitudinal StudiesMaleMiddle AgedObesitySwedenbiological agingbody mass indexdual change scorefrailty indexobesitytrajectory

Identifiers

PMID40342213
PMCPMC12059470

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.