Evidence map›Paper›PMID 40275394›Full record

ArticleClinical epigenetics2025

Low blood levels of selenium, selenoprotein P and GPx3 are associated with accelerated biological aging: results from the Berlin Aging Study II (BASE-II).

Valentin Max Vetter, Kamil Demircan, Jan Homann, Thilo Samson Chillon, Michael Mülleder, Orr Shomroni, Elisabeth Steinhagen-Thiessen, Markus Ralser, Christina M Lill, Lars Bertram and 2 more

Abstract read
In one paragraph

Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Selenium status markers and their relationship with anthropometric, glycemic, and inflammatory variables in institutionalized older adults.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Article
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

12 authors.

Valentin Max Vetter *Department of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Lipid Clinic at the Interdisciplinary Metabolism Center, Biology of Aging Working Group, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany. valentin.vetter@charite.de.ORCID http://orcid.org/0000-0001-5003-7766
Kamil Demircan *Max Rubner Center (MRC) for Cardiovascular Metabolic Renal Research, Institute for Experimental Endocrinology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10115, Berlin, Germany.
Jan HomannInstitute of Epidemiology and Social Medicine, University of Münster, Münster, Germany.
Thilo Samson ChillonMax Rubner Center (MRC) for Cardiovascular Metabolic Renal Research, Institute for Experimental Endocrinology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10115, Berlin, Germany.
Michael MüllederCore Facility High Throughput Mass Spectrometry, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Orr ShomroniCore Facility High Throughput Mass Spectrometry, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Elisabeth Steinhagen-ThiessenDepartment of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Lipid Clinic at the Interdisciplinary Metabolism Center, Biology of Aging Working Group, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Markus RalserCore Facility High Throughput Mass Spectrometry, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Christina M LillInstitute of Epidemiology and Social Medicine, University of Münster, Münster, Germany.
Lars BertramLübeck Interdisciplinary Platform for Genome Analytics (LIGA), University of Lübeck, Lübeck, Germany.
Lutz Schomburg *Max Rubner Center (MRC) for Cardiovascular Metabolic Renal Research, Institute for Experimental Endocrinology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10115, Berlin, Germany.
Ilja Demuth *Department of Endocrinology and Metabolic Diseases (Including Division of Lipid Metabolism), Lipid Clinic at the Interdisciplinary Metabolism Center, Biology of Aging Working Group, 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 http://orcid.org/0000-0002-4340-2523

Funding

Berlin University Alliance BUA Link Lab, 501_Massenspektrometrie, 501_LinklabBundesministerium für Bildung und Forschung 01EP2201Bundesministerium für Bildung und Forschung #01UW0808; #16SV5536K, #16SV5537, #16SV5538, #16SV5837, #01GL1716A, and #01GL1716BBundesministerium für Bildung und Forschung 16LW0239KCure Alzheimer's Fund "CIR-CUITS" consortiumDeutsche Forschungsgemeinschaft 460683900Deutsche Forschungsgemeinschaft CRC/TR 296 "LocoTact"Deutsche Forschungsgemeinschaft LI 2654/4-1Deutschen Konsortium für Translationale Krebsforschung BE01 1020000483European Research Council Lifebrain
6 · The paper itself

Abstract

backgroundBiological age reflects inter-individual differences in biological function and capacity beyond chronological age. DNA methylation age (DNAmA) and its deviation from chronological age, DNAmA acceleration (DNAmAA), which was calculated as residuals of leukocyte cell count adjusted linear regression of DNAmA on chronological age, were used to estimate biological age in this study. Low levels of serum selenium, selenoprotein P (SELENOP), and the selenocysteine-containing glutathione peroxidase 3 (GPx3) are associated with adverse health outcomes and selenium supplementation is discussed as an anti-aging intervention.

methodsIn this study, we cross-sectionally analyzed 1568 older participants from the observational Berlin Aging Study II (mean age ± SD: 68.8 ± 3.7 years, 51% women). Serum selenium was measured by total reflection X-ray fluorescence (TXRF) spectroscopy and SELENOP was determined by sandwich ELISA. GPx3 was assessed as part of a proteomics dataset using liquid chromatography-mass spectrometry (LC-MS). The relationship between selenium biomarkers and epigenetic clock measures was analyzed using linear regression analyses. P values and 95% confidence intervals (not adjusted for multiple testing) are stated for each analysis.

resultsParticipants with deficient serum selenium levels (< 90 μg/L) had a higher rate of biological aging (DunedinPACE, β = - 0.02, SE = 0.01, 95% CI - 0.033 to - 0.004, p = 0.010, n = 865). This association remained statistically significant after adjustment for age, sex, BMI, smoking, and first four genetic principal components (β = - 0.02, SE = 0.01, 95% CI - 0.034 to - 0.004, p = 0.012, n = 757). Compared to the highest quartile, participants in the lowest quartile of SELENOP levels showed an accelerated biological aging rate (DunedinPACE, β = - 0.03, SE = 0.01, 95% CI - 0.051 to - 0.008, p = 0.007, n = 740, fully adjusted model). Similarly, after adjustment for confounders, accelerated biological age was found in participants within the lowest GPx3 quartile compared to participants in the fourth quartile (DunedinPACE, β = - 0.04, SE = 0.01, 95% CI - 0.06 to - 0.02, p = 0.001, n = 674 and GrimAge, β = - 0.98, SE = 0.32, 95% CI - 1.6 to - 0.4, p = 0.002, n = 608). Only the association with GPx3 remained statistically significant after multiple testing correction.

conclusionOur study suggests that low levels of selenium biomarkers are associated with accelerated biological aging measured through epigenetic clocks. This effect was not substantially changed after adjustment for known confounders.

Indexed as

AgingGlutathione PeroxidaseSeleniumSelenoprotein PAgedBiomarkersCross-Sectional StudiesDNA MethylationEpigenesis, GeneticFemaleHumansMaleMiddle AgedObservational Studies as TopicSecondary Data AnalysisBiomarkersGlutathione PeroxidaseGPX3 protein, humanSeleniumSelenoprotein P

Identifiers

PMID40275394
PMCPMC12023433

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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.