Abstract
Levels of 25-hydroxy vitamin D [25(OH)D] are reported to be decreased in cardiovascular disease (CVD) and in other chronic immunopathologies. Vitamin D (vitD) has been shown to be significantly linked to mortality, and is thought to be a predictor of survival. Therefore, supplementation with vitD has been suggested as an option to improve clinical outcomes.
In contrast to the causal assumption, we hypothesize that the decreased vitD levels, seen in patients with CVD and chronic immunopathologies is secondary to inflammation and not as pathophysiologically relevant as currently suggested. Under these conditions, low vitD might be mainly caused by oxidative stress that results from chronic, immune-mediated vascular and systemic inflammation seen in patients with CVD. The oxidative environment most likely causes biodegradation of vitD and interferes with key enzymes, disturbing the biosynthesis of 25(OH)D and 1,25(OH)D. Thus far, no clear evidence of a beneficial effect of vitD supplements exists, beyond treating vitD deficiency to improve skeletal health. Moreover, a prolonged and/or high dose vitD supplementation, unless needed to correct actual vitD deficiency [levels of 25(OH)D<20 ng/ml)] may even be immunologically harmful by downregulating Th1 immune responses and indirectly upregulating Th2 immune activation with potential detrimental metabolic and cardiovascular effects. Large randomized controlled studies of vitD with multiple outcomes (skeletal, metabolic, cardiovascular and mental) are urgently needed.
Keywords: Atherosclerosis, cardiovascular disease, immune-mediated inflammation, therapeutic potential, vitamin-D.
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Current Vascular Pharmacology
Title:The Role of Vitamin D in Atherosclerosis Inflammation Revisited: More a Bystander than a Player?
Volume: 13 Issue: 3
Author(s): Harald Mangge, Daniel Weghuber, Ruth Prassl, Astrid Haara, Wolfgang Schnedl, Teodor T. Postolache and Dietmar Fuchs
Affiliation:
Keywords: Atherosclerosis, cardiovascular disease, immune-mediated inflammation, therapeutic potential, vitamin-D.
Abstract: Levels of 25-hydroxy vitamin D [25(OH)D] are reported to be decreased in cardiovascular disease (CVD) and in other chronic immunopathologies. Vitamin D (vitD) has been shown to be significantly linked to mortality, and is thought to be a predictor of survival. Therefore, supplementation with vitD has been suggested as an option to improve clinical outcomes.
In contrast to the causal assumption, we hypothesize that the decreased vitD levels, seen in patients with CVD and chronic immunopathologies is secondary to inflammation and not as pathophysiologically relevant as currently suggested. Under these conditions, low vitD might be mainly caused by oxidative stress that results from chronic, immune-mediated vascular and systemic inflammation seen in patients with CVD. The oxidative environment most likely causes biodegradation of vitD and interferes with key enzymes, disturbing the biosynthesis of 25(OH)D and 1,25(OH)D. Thus far, no clear evidence of a beneficial effect of vitD supplements exists, beyond treating vitD deficiency to improve skeletal health. Moreover, a prolonged and/or high dose vitD supplementation, unless needed to correct actual vitD deficiency [levels of 25(OH)D<20 ng/ml)] may even be immunologically harmful by downregulating Th1 immune responses and indirectly upregulating Th2 immune activation with potential detrimental metabolic and cardiovascular effects. Large randomized controlled studies of vitD with multiple outcomes (skeletal, metabolic, cardiovascular and mental) are urgently needed.
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Cite this article as:
Mangge Harald, Weghuber Daniel, Prassl Ruth, Haara Astrid, Schnedl Wolfgang, Postolache T. Teodor and Fuchs Dietmar, The Role of Vitamin D in Atherosclerosis Inflammation Revisited: More a Bystander than a Player?, Current Vascular Pharmacology 2015; 13 (3) . https://dx.doi.org/10.2174/1570161111666131209125454
DOI https://dx.doi.org/10.2174/1570161111666131209125454 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |

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