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Is vitamin D status relevant to metabolic syndrome?

Review of the evidence on hypovitaminosis D as a risk factor for metabolic syndrome and its sequelae, T2DM and CVD, suggests long-term vitamin D repletion could reduce these risks. There is mechanistic evidence for protective effects for MetS and the balance of evidence, (cross-sectional and prospec...

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Detalles Bibliográficos
Autor principal: Boucher, Barbara J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427202/
https://www.ncbi.nlm.nih.gov/pubmed/22928079
http://dx.doi.org/10.4161/derm.20012
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author Boucher, Barbara J.
author_facet Boucher, Barbara J.
author_sort Boucher, Barbara J.
collection PubMed
description Review of the evidence on hypovitaminosis D as a risk factor for metabolic syndrome and its sequelae, T2DM and CVD, suggests long-term vitamin D repletion could reduce these risks. There is mechanistic evidence for protective effects for MetS and the balance of evidence, (cross-sectional and prospective), supports this postulate. Much of the data so far available from randomized controlled trials is weakened by inadequate power, low vitamin D dosages, starting supplementation too late in life or after MetS disorders have developed or, most importantly, by non-inclusion of many recognizable confounders. On balance, therefore, maintenance of US 2010 recommended intakes for bone protection has the potential to prove protective for MetS. Supplementation has been shown to increase survival in patients with cardiac disorders; whether higher doses would provide useful protection for apparently healthy people in the general population awaits the outcomes of ongoing randomized-controlled trials that, it is hoped, will prove or disprove causality for hypovitaminosis D in MetS and its long-term ill-effects.
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spelling pubmed-34272022012-08-27 Is vitamin D status relevant to metabolic syndrome? Boucher, Barbara J. Dermatoendocrinol Commentary Review of the evidence on hypovitaminosis D as a risk factor for metabolic syndrome and its sequelae, T2DM and CVD, suggests long-term vitamin D repletion could reduce these risks. There is mechanistic evidence for protective effects for MetS and the balance of evidence, (cross-sectional and prospective), supports this postulate. Much of the data so far available from randomized controlled trials is weakened by inadequate power, low vitamin D dosages, starting supplementation too late in life or after MetS disorders have developed or, most importantly, by non-inclusion of many recognizable confounders. On balance, therefore, maintenance of US 2010 recommended intakes for bone protection has the potential to prove protective for MetS. Supplementation has been shown to increase survival in patients with cardiac disorders; whether higher doses would provide useful protection for apparently healthy people in the general population awaits the outcomes of ongoing randomized-controlled trials that, it is hoped, will prove or disprove causality for hypovitaminosis D in MetS and its long-term ill-effects. Landes Bioscience 2012-04-01 /pmc/articles/PMC3427202/ /pubmed/22928079 http://dx.doi.org/10.4161/derm.20012 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Commentary
Boucher, Barbara J.
Is vitamin D status relevant to metabolic syndrome?
title Is vitamin D status relevant to metabolic syndrome?
title_full Is vitamin D status relevant to metabolic syndrome?
title_fullStr Is vitamin D status relevant to metabolic syndrome?
title_full_unstemmed Is vitamin D status relevant to metabolic syndrome?
title_short Is vitamin D status relevant to metabolic syndrome?
title_sort is vitamin d status relevant to metabolic syndrome?
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427202/
https://www.ncbi.nlm.nih.gov/pubmed/22928079
http://dx.doi.org/10.4161/derm.20012
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