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Effect of selenium supplementation on biomarkers of bone turnover

Published online by Cambridge University Press:  17 August 2021

G. Perri
Affiliation:
Human Nutrition Research Centre, Centre for Healthier Lives, Population Health Sciences Institute, Newcastle University, Newcastle upon Tyne, UK
T. Hill
Affiliation:
Human Nutrition Research Centre, Centre for Healthier Lives, Population Health Sciences Institute, Newcastle University, Newcastle upon Tyne, UK
J.C. Mathers
Affiliation:
Human Nutrition Research Centre, Centre for Healthier Lives, Population Health Sciences Institute, Newcastle University, Newcastle upon Tyne, UK
J. Walsh
Affiliation:
Sheffield University, Department of Oncology and Metabolism, Metabolic Bone Centre, Sorby Wing, Northern General Hospital, Sheffield, UK
F. Gossiel
Affiliation:
Sheffield University, Department of Oncology and Metabolism, Metabolic Bone Centre, Sorby Wing, Northern General Hospital, Sheffield, UK
K. Winther
Affiliation:
Department of Endocrinology, Odense University Hospital, Odense, Denmark Centre for Diabetes, Academic Specialist Centre, Stockholm, Sweden Department of Molecular Medicine and Surgery, Karolinska Institute, Solna, Sweden
J. Frölich
Affiliation:
Department of Endocrinology, Odense University Hospital, Odense, Denmark
L. Folkestad
Affiliation:
Department of Endocrinology, Odense University Hospital, Odense, Denmark Department of Clinical Research, University of Southern Denmark, Odense, Denmark
S. Cold
Affiliation:
Department of Oncology, Odense University Hospital, Odense, Denmark
R. Eastell
Affiliation:
Sheffield University, Department of Oncology and Metabolism, Metabolic Bone Centre, Sorby Wing, Northern General Hospital, Sheffield, UK
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Abstract

Type
Abstract
Copyright
Copyright © The Authors 2021

Selenium is an essential trace element with roles in musculoskeletal health(Reference Moreno-Reyes1,Reference Zhang2) . Osteoclast inactivation is associated with selenium supplementation in vitro and selenium status is correlated negatively with markers of bone health(Reference Hoeg3,Reference Beukhof4) . However, the impact of selenium supplementation on bone turnover markers (BTM) has not been studied. This study investigated the effects of selenium supplementation for up to 5 years in older people on BTM including osteocalcin, procollagen type 1 N-terminal propeptide (P1NP), carboxy-terminal collagen crosslinks and bone alkaline phosphatase.

490 Danish men and women (60–74 y) were randomised to receive 0, 100, 200 or 300 μg of selenium daily as selenium-enriched yeast. Plasma selenium concentration was measured using inductively-coupled-plasma mass spectrometry and BTMs were measured using an autoanalyser at baseline, 6 months and 5 years in non-fasted samples. Data were analysed by ANCOVA with polynomial contrasts to investigate the shape of the dose-response relationships. Covariates included: age, body mass index, baseline plasma selenium concentration, baseline BTM, smoking, alcohol, supplement use and medication.

Plasma selenium concentration increased significantly with increasing selenium supplementation at 6 months (84.1, 155.2, 212.3, 258.3 ng/ml for placebo, 100, 200 and 300 μg selenium, respectively) (P < 0.001) and remained elevated at 5 years (88.2, 156.4, 223.8 and 270.9 respectively) (P < 0.001). At 6 months, there was a significant linear decrease in P1NP (P = 0.036, η2 = 0.019) with increasing selenium supplementation but this effect was not apparent at 5 years. There was no significant effect of selenium supplementation on any other BTM.

Selenium supplementation reduced P1NP at 6 months but there were no significant effects on other BTM or after 5 years. Since P1NP is a marker of osteoblast function, the fall in PINP with increasing selenium supplementation suggests a reduction in new bone formation 5. The impact of this change in bone turnover on bone health remains to be determined.

References

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Zhang, Z, et al. (2014) Biophys Acta 1840, 32463256.10.1016/j.bbagen.2014.08.001CrossRefGoogle Scholar
Hoeg, A, et al. (2012) J Clin Endocrinol Metab 97, 4061–70.10.1210/jc.2012-2121CrossRefGoogle Scholar
Beukhof, CM et al. (2016) PLoS ONE 11, e0152748.10.1371/journal.pone.0152748CrossRefGoogle Scholar
Kuo, T & Chen, CH (2017) Biomark Res 5, 18CrossRefGoogle Scholar