The Role of Vitamin D in atherosclerosis inflammation revisited. More bystander than player?

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• 作者：Harald MANGGE^a ; Daniel WEGHUBER^b ; ^{d.weghuber@salk.at" class="auth_mail} ; Ruth PRASSL^c ; Astrid HAARA^d ; Wolfgang SCHNEDL^e ; ^f ; Teodor T. POSTOLACHE^e ; ^f ; Katharina PAULMICHL^b ; Dietmar FUCHS^d
• 刊名：Appetite (APPET)
• 出版年：1 May, 2014
• 年：2014
• 卷：76
• 期：Complete
• 页码：215
• 全文大小：35 K

文摘

Levels of 25-Hydroxy Vitamin D [25(OH)D] were reported to be decreased in cardiovascular disease (CVD) and in other chronic immunopathologies. In multiple studies, 25(OH)D has been shown to be significantly linked to mortality. Supplementation with Vitamin D2 or D3 has been suggested to improve clinical outcomes. Nevertheless, supplementation may require high doses to achieve efficient blood levels of 25(OH)D. In contrast to this causal assumption, we hypothesize that decreased 25(OH)D levels are secondary phenomena to inflammation, and not as pathophysiologically relevant as suggested by the current hype. Under these conditions, low 25(OH)D levels might be caused by the oxidative stress that results from chronic inflammation encountered in patients with CVD. The oxidative environment most likely interferes with key enzymes, disturbing the biosynthesis as well as biodegradation of 1.25 (OH)D. There is no clear evidence of a beneficial effect of Vitamin D supplementation, except for treating Vitamin D deficiency (i.e. levels of <50 nmol/L) for improvement of skeletal health. Moreover, a prolonged and/or high dose Vitamin D supplementation may even become immunologically harmful by downregulating Th1 immune responses and indirectly upregulating Th2 immune activation with potential detrimental cardiovascular effects. Large randomized controlled studies of Vitamin D in relation to different outcomes are urgently needed.