Evidence map›Paper›PMID 30993509›Full record

ArticleEuropean journal of epidemiology2019

Quantification of biological age as a determinant of age-related diseases in the Rotterdam Study: a structural equation modeling approach.

Reem Waziry, Luuk Gras, Sanaz Sedaghat, Henning Tiemeier, Gerrit J Weverling, Mohsen Ghanbari, Jaco Klap, Frank de Wolf, Albert Hofman, M Arfan Ikram and 1 more

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Article in European journal of epidemiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

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  10. No winners or losers: clinical chemistry-based biological aging metrics perform similarly across cohorts and health outcomes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025
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  18. Beyond Chronological Age: A Multidimensional Approach to Survival Prediction in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023
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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

11 authors.

Reem WaziryDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA, 02115, USA. waziry@hsph.harvard.edu.
Luuk GrasJanssen Prevention Center, Janssen Pharmaceutical Companies of Johnson & Johnson, Leiden, The Netherlands.
Sanaz SedaghatDepartment of Epidemiology, Erasmus Medical Center, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
Henning TiemeierDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA, 02115, USA.
Gerrit J WeverlingJanssen Prevention Center, Janssen Pharmaceutical Companies of Johnson & Johnson, Leiden, The Netherlands.
Mohsen GhanbariDepartment of Epidemiology, Erasmus Medical Center, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
Jaco KlapJanssen Prevention Center, Janssen Pharmaceutical Companies of Johnson & Johnson, Leiden, The Netherlands.
Frank de WolfJanssen Prevention Center, Janssen Pharmaceutical Companies of Johnson & Johnson, Leiden, The Netherlands.
Albert HofmanDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA, 02115, USA.
M Arfan IkramDepartment of Epidemiology, Erasmus Medical Center, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
Jaap GoudsmitDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA, 02115, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronological age alone is not a sufficient measure of the true physiological state of the body. The aims of the present study were to: (1) quantify biological age based on a physiological biomarker composite model; (2) and evaluate its association with death and age-related disease onset in the setting of an elderly population. Using structural equation modeling we computed biological age for 1699 individuals recruited from the first and second waves of the Rotterdam study. The algorithm included nine physiological parameters (c-reactive protein, creatinine, albumin, total cholesterol, cytomegalovirus optical density, urea nitrogen, alkaline phosphatase, forced expiratory volume and systolic blood pressure). We assessed the association between biological age, all-cause mortality, all-cause morbidity and specific age-related diseases over a median follow-up of 11 years. Biological age, compared to chronological age or the traditional biomarkers of age-related diseases, showed a stronger association with all-cause mortality (HR 1.15 vs. 1.13 and 1.10), all-cause morbidity (HR 1.06 vs. 1.05 and 1.03), stroke (HR 1.17 vs. 1.08 and 1.04), cancer (HR 1.07 vs. 1.04 and 1.02) and diabetes mellitus (HR 1.12 vs. 1.01 and 0.98). Individuals who were biologically younger exhibited a healthier life-style as reflected in their lower BMI (P < 0.001) and lower incidence of stroke (P < 0.001), cancer (P < 0.01) and diabetes mellitus (P = 0.02). Collectively, our findings suggest that biological age based on the biomarker composite model of nine physiological parameters is a useful construct to assess individuals 65 years and older at increased risk for specific age-related diseases.

Indexed as

AdultAgedAge of OnsetAgingBiomarkersBlood PressureBody Mass IndexCardiovascular DiseasesCause of DeathCreatinineDiabetes MellitusFemaleHumansLongevityMaleMiddle AgedBiomarkersCreatinineBiological ageBiologically youngElderlyMorbidityMortality

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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.