Evidence map›Paper›PMID 35562603›Full record

ArticleGeroScience2022

Vitamin D supplementation is associated with slower epigenetic aging.

Valentin Max Vetter, Yasmine Sommerer, Christian Humberto Kalies, Dominik Spira, Lars Bertram, Ilja Demuth

Abstract read
In one paragraph

Article in GeroScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
–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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  12. Vitamin D is glucoprotective in aging males but not females.The Journal of steroid biochemistry and molecular biology · 2026
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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

6 authors.

Valentin Max VetterBiology of Aging Working Group, Department of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Yasmine SommererLübeck Interdisciplinary Platform for Genome Analytics (LIGA), University of Lübeck, Lübeck, Germany.
Christian Humberto KaliesBiology of Aging Working Group, Department of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Dominik SpiraBiology of Aging Working Group, Department of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Lars BertramLübeck Interdisciplinary Platform for Genome Analytics (LIGA), University of Lübeck, Lübeck, Germany.
Ilja DemuthBiology of Aging Working Group, Department of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany. ilja.demuth@charite.de.ORCID 0000-0002-4340-2523

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adverse effects of low vitamin D level on mortality and morbidity are controversially discussed. Especially older people are at risk for vitamin D deficiency and therefore exposed to its potentially harmful consequences. A way of measuring differences in the biological age is through DNA methylation age (DNAm age) and its deviation from chronological age, DNAm age acceleration (DNAmAA). We previously reported on an association between vitamin D deficiency and higher 7-CpG DNAmAA in participants of the Berlin Aging Study II (BASE-II). In this study, we employ a quasi-interventional study design to assess the relationship between DNAmAA of five epigenetic clocks and vitamin D supplementation. Longitudinal data were available for 1,036 participants of BASE-II that were reexamined on average 7.4 years later in the GendAge study (mean age at follow-up: 75.6 years, SD = 3.8 years, age range: 64.9-94.1 years, 51.9% female). DNAmAA was estimated with the 7-CpG clock, Horvath's clock, Hannum's clock, PhenoAge, and GrimAge. Methylation data were obtained through methylation-sensitive single nucleotide primer extension (MS-SNuPE) or Illumina's Infinium "MethylationEPIC" array. Vitamin D-deficient participants who chose to start vitamin D supplementation after baseline examination showed a 2.6-year lower 7-CpG DNAmAA (p = 0.011) and 1.3-year lower Horvath DNAmAA (p = 0.042) compared to untreated and vitamin D-deficient participants. DNAmAA did not statistically differ between participants with successfully treated vitamin D deficiency and healthy controls (p > 0.16). Therefore, we conclude that intake of vitamin D supplement is associated with lower DNAmAA in participants with vitamin D deficiency.

Indexed as

Epigenesis, GeneticVitamin D DeficiencyAgedAged, 80 and overAgingDietary SupplementsFemaleHumansMaleMiddle AgedVitamin DVitamin DBASE-IIBiological ageDNA methylation ageEpigenetic clockGendAgeLongitudinalVitamin D supplementation

Identifiers

PMID35562603
PMCPMC9213628

What OpenQuestion holds

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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.