Evidence map›Paper›PMID 29149257›Full record

ArticleAmerican journal of epidemiology2018

Eleven Telomere, Epigenetic Clock, and Biomarker-Composite Quantifications of Biological Aging: Do They Measure the Same Thing?

Daniel W Belsky, Terrie E Moffitt, Alan A Cohen, David L Corcoran, Morgan E Levine, Joseph A Prinz, Jonathan Schaefer, Karen Sugden, Benjamin Williams, Richie Poulton and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of epidemiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 295 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
295citing papers in PubMed, 1 pooled it
13.4field-weighted citation impact, top 1% of its field
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

295 citing papers in PubMed, 1 synthesis or guideline pooled it, 416 citations in OpenAlex.

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  17. Functional, molecular, and digital measurements of biological age.The Journal of clinical investigation · 2026
    Review
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235 more citing papers are in PubMed but not listed here.

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

11 authors at 6 institutions in 4 countries.

Daniel W BelskyDepartment of Population Health Sciences, Duke University School of Medicine, Durham, North Carolina.
Terrie E MoffittDepartment of Psychology and Neuroscience, Duke University, Durham, North Carolina.
Alan A CohenDepartment of Family Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, Canada.
David L CorcoranCenter for Genomic and Computational Biology, Duke University, Durham, North Carolina.
Morgan E LevineDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut.
Joseph A PrinzCenter for Genomic and Computational Biology, Duke University, Durham, North Carolina.
Jonathan SchaeferDepartment of Psychology and Neuroscience, Duke University, Durham, North Carolina.
Karen SugdenDepartment of Psychology and Neuroscience, Duke University, Durham, North Carolina.
Benjamin WilliamsDepartment of Psychology and Neuroscience, Duke University, Durham, North Carolina.
Richie PoultonDunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.
Avshalom CaspiDepartment of Psychology and Neuroscience, Duke University, Durham, North Carolina.
Duke University · USKing's College London · GBSocial Science Research Council · USUniversité de Sherbrooke · CAUniversity of Otago · NZYale University · US

Funding

Resource Core 3 - Metabolomics CoreP30AG028716 · NIA · DUKE UNIVERSITY · PI Virginia B Kraus · 2006 to 2026
$24.6M
STALLARD Admin Supp: Predicting Future Care Needs and Costs for Individual Medicare Enrollees with Incident Suspected Alzheimer's DiseaseP30AG034424 · NIA · DUKE UNIVERSITY · PI SCOTT M. LYNCH · 2009 to 2026
$12.2M
Quantifying Individual Differences in Midlife Structural Brain Integrity Associated with Later AD/ADRD RiskR01AG049789 · NIA · DUKE UNIVERSITY · PI AHMAD R. HARIRI, TERRIE E MOFFITT · 2015 to 2026
$10.6M
Is mental disorder a preventable cause of age-related disease? The Dunedin Study.R01AG032282 · NIA · DUKE UNIVERSITY · PI CASPI, AVSHALOM, MOFFITT, TERRIE E · 2009 to 2025
$9.5M
T32 Administrative Supplement for Increase in Postdoc StipendsT32AG000139 · NIA · DUKE UNIVERSITY · PI LYNCH, SCOTT M. · 1987 to 2017
$4.0M
Genetic analysis of the Dutch Hunger Winter Families Study to Boost Rigor and Robustness for Testing In-Utero Famine Effects on Aging-Related Health Conditions and Biological AgingR01AG066887 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BELSKY, DANIEL WALKER, LUMEY, L H · 2020 to 2024
$3.5M
Long-term multi-omics follow-up of the CALERIE Trial to generate new knowledge for geroscienceR01AG061378 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Daniel Walker Belsky · 2019 to 2026
$2.9M
Data commons for 'omic, microscopy and analysis core facilitiesS10OD018164 · OD · DUKE UNIVERSITY · PI WRAY, GREGORY A. · 2014 to 2014
$598k
A pilot study to advance translation of molecular signatures of biological agingR21AG054846 · NIA · DUKE UNIVERSITY · PI BELSKY, DANIEL WALKER · 2017 to 2018
$437k
Generating new knowledge to support reversibility interventionsR01AG048895 · NIA · DUKE UNIVERSITY · PI MOFFITT, TERRIE E · 2014 to 2015
$311k
Explanations of Racial Disparities in Active LifeR03HD050374 · NICHD · PRINCETON UNIVERSITY · PI LYNCH, SCOTT M · 2005 to 2006
$156k
CIHRMedical Research Council MR/P005918/1NIA NIH HHS P30 AG028716NIA NIH HHS P30 AG034424NIA NIH HHS R01 AG032282NIA NIH HHS R01 AG048895NIA NIH HHS R01 AG049789NIA NIH HHS R01 AG061378NIA NIH HHS R01 AG066887NIA NIH HHS R21 AG054846NIA NIH HHS T32 AG000139NICHD NIH HHS R03 HD050374NIH HHS S10 OD018164
6 · The paper itself

Abstract

The geroscience hypothesis posits that therapies to slow biological processes of aging can prevent disease and extend healthy years of life. To test such "geroprotective" therapies in humans, outcome measures are needed that can assess extension of disease-free life span. This need has spurred development of different methods to quantify biological aging. But different methods have not been systematically compared in the same humans. We implemented 7 methods to quantify biological aging using repeated-measures physiological and genomic data in 964 middle-aged humans in the Dunedin Study (New Zealand; persons born 1972-1973). We studied 11 measures in total: telomere-length and erosion, 3 epigenetic-clocks and their ticking rates, and 3 biomarker-composites. Contrary to expectation, we found low agreement between different measures of biological aging. We next compared associations between biological aging measures and outcomes that geroprotective therapies seek to modify: physical functioning, cognitive decline, and subjective signs of aging, including aged facial appearance. The 71-cytosine-phosphate-guanine epigenetic clock and biomarker composites were consistently related to these aging-related outcomes. However, effect sizes were modest. Results suggested that various proposed approaches to quantifying biological aging may not measure the same aspects of the aging process. Further systematic evaluation and refinement of measures of biological aging is needed to furnish outcomes for geroprotector trials.

Indexed as

Biological ClocksBiomarkersTelomere HomeostasisAgingCohort StudiesFemaleHumansMaleMiddle AgedBiomarkers

Identifiers

PMID29149257
PMCPMC6248475
OpenAlexW2952009394

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.