Vitamin D<sub>3</sub>Supplementation Has No Effect on Conventional Cardiovascular Risk Factors: A Parallel-Group, Double-Blind, Placebo-Controlled RCT

Wood, Andy; Secombes, K R; Thiès, Frank; Aucott, Lorna; Black, Alison; Mavroeidi, Alexandra; Simpson, William G.; Fraser, William D.; Reid, David M.; Macdonald, Helen

doi:10.1210/jc.2012-2126

Cited by 168 publications

(127 citation statements)

References 39 publications

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“…One study recruited healthy post-menopausal women [39], and did not report significant improvements in both endothelial/inflammatory markers measured (Table 1). Four studies [40][41][42][43], recruited participants with other diseases such as cystic fibrosis, human immunodeficiency virus (HIV), polycystic ovary syndrome and non-alcoholic fatty liver disease.…”

Section: Studies In Participants With Other Conditionsmentioning

confidence: 99%

Impact of vitamin D supplementation on endothelial and inflammatory markers in adults: A systematic review

Agbalalah

Hughes

Freeborn

et al. 2017

The Journal of Steroid Biochemistry and Molecular Biology

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Highlights• Vitamin D deficiency has been identified as a potential risk factor for cardiovascular disease.• Review of RCTs of effects of vitamin D supplementation on endothelial function/inflammation.• 8/29 studies reported improvements in the endothelial/inflammatory parameters measured.• This review does not support use of vitamin D as a preventative measure for CVD. AbstractThis systematic review aims to evaluate randomised controlled trials (

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Section: Studies In Participants With Other Conditionsmentioning

confidence: 99%

Impact of vitamin D supplementation on endothelial and inflammatory markers in adults: A systematic review

Agbalalah

Hughes

Freeborn

et al. 2017

The Journal of Steroid Biochemistry and Molecular Biology

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“…A meta-analysis of four prospective and fourteen cross-sectional studies found a pooled OR of 0·73 (95 % CI 0·63, 0·84) for hypertension in participants in the highest 25(OH)D category compared with those in the lowest category (73) . A number of RCT have measured changes in BP (primarily clinic BP) in response to vitamin D supplementation and shown mixed results (74)(75)(76)(77)(78)(79)(80) .…”

Section: Blood Pressurementioning

confidence: 99%

“…Currently, the best available inflammatory biomarker is CRP, an acute phase reactant that is a reliable, independent predictor of the risk of myocardial infarction, stroke and cardiovascular death (111) . Clinical trials of vitamin D supplementation show inconsistent results regarding an effect on CRP concentrations: most report no effect (77,80,97,(112)(113)(114)(115)(116) , whereas some show reductions in CRP concentrations (74,117,118) . Some trials have measured highsensitivity CRP (hsCRP), which can detect low-grade inflammation.…”

Section: Inflammationmentioning

confidence: 99%

Vitamin D and risk of CVD: a review of the evidence

Fry

Sanders

2015

Proc. Nutr. Soc.

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This review summarises evidence for an association between vitamin D status and CVD and the mechanisms involved. Vitamin D 3 is predominantly provided by the action of UVB from sunlight on skin. Average UK diets supply 2-3 μg/d vitamin D but diets containing at least one portion of oily fish per week supply about 7 μg/d. Pharmacological doses of vitamin D 2 (bolus injection of 7500 μg or intakes >50 μg/d) result in a smaller increase in plasma 25 (OH)D than those of D 3 but physiological doses 5-25 μg/d seem equivalent. Plasma 25 (OH)D concentrations are also influenced by clothing, obesity and skin pigmentation. Up to 40 % of the population have plasma 25(OH)D concentrations <25 nmol/l in the winter compared with <10 % in the summer. The relative risk of CVD death is 1·41 (95 % CI 1·18, 1·68) greater in the lowest quintile of plasma 25(OH)D according to meta-analysis of prospective cohort studies. Acute deficiency may inhibit insulin secretion and promote inflammation thus increasing the risk of plaque rupture and arterial thrombosis. Chronic insufficiency may increase arterial stiffness. There is no evidence to support claims of reduced CVD from existing trials with bone-related health outcomes where vitamin D was usually co-administered with calcium. Although several trials with cardiovascular endpoints are in progress, these are using pharmacological doses. In view of the potential toxicity of pharmacological doses, there remains a need for long-term trials of physiological doses of D 2 and D 3 with CVD incidence as the primary outcome. Ergocalciferol: Cholecalciferol: Cardiovascular riskVitamin D deficiency causes rickets in children and osteomalacia in adults and may contribute to the causation of CVD. Cholecalciferol (vitamin D 3 ) is made by the action of UVB light on the skin but is also provided in the diet from foods of animal origin (eggs, oily fish and meat). Ergocalciferol (vitamin D 2 ) is present in fungi that have been exposed to UVB irradiation. Both forms of vitamin D undergo 25-hydroxylation in the liver to form 25(OH) metabolites, most of which circulate in plasma bound to the vitamin D binding protein (VDBP). In the kidney, 25 hydroxyvitamin D (25(OH)D) is converted to the biologically active metabolite 1,25 dihydroxyvitamin D (1,25 (OH) 2 D) by the action of 1α-hydroxylase (Fig. 1). This then binds to the vitamin D receptor, which is a highaffinity nuclear hormone receptor that regulates gene expression (1) . Measurement of serum 25(OH)D to assess vitamin D status has predominantly used immunoassays, which show lower sensitivity (about 30 %) to D 2 metabolites than gold-standard methods such as HPLC/tandem MS. Formerly, a lack of standardisation of methods and appropriate quality control made comparisons between studies difficult (2) . The situation has been remedied by the availability (3) of standard reference serum (SRM 972, National Institute of Standards and Technology) and a quality control programme in the UK organised by the Vitamin D External Quality Assessment Scheme (4) . It has...

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“…Thus, vitamin D-fortified foods need to be considered as a possible strategy to facilitate population intake of the RNI. Furthermore, a few recent studies have used higher doses of vitamin D in their intervention trials (33)(34)(35) , which also showed no associations of vitamin D intake with CVD risk. The strength of the CAPS is the long (over 20 years) follow-up period.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D intake and risk of CVD and all-cause mortality: evidence from the Caerphilly Prospective Cohort Study

Guo

Cockcroft

Elwood

et al. 2017

Public Health Nutr.

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Objective: Prospective data on the associations between vitamin D intake and risk of CVD and all-cause mortality are limited and inconclusive. The aim of the present study was to investigate the associations between vitamin D intake and CVD risk and all-cause mortality in the Caerphilly Prospective Cohort Study. Design: The associations of vitamin D intake with CVD risk markers were examined cross-sectionally at baseline and longitudinally at 5-year, 10-year and >20-year follow-ups. In addition, the predictive value of vitamin D intake for CVD events and all-cause mortality after >20 years of follow-up was examined. Logistic regression and general linear regression were used for data analysis. Setting: Participants in the UK. Subjects: Men (n 452) who were free from CVD and type 2 diabetes at recruitment. Results: Higher vitamin D intake was associated with increased HDL cholesterol (P = 0·003) and pulse pressure (P = 0·04) and decreased total cholesterol:HDL cholesterol (P = 0·008) cross-sectionally at baseline, but the associations were lost during follow-up. Furthermore, higher vitamin D intake was associated with decreased concentration of plasma TAG at baseline (P = 0·01) and at the 5-year (P = 0·01), but not the 10-year examination. After >20 years of follow-up, vitamin D was not associated with stroke (n 72), myocardial infarctions (n 142), heart failure (n 43) or all-cause mortality (n 281), but was positively associated with increased diastolic blood pressure (P = 0·03). Conclusions: The study supports associations of higher vitamin D intake with lower fasting plasma TAG and higher diastolic blood pressure. KeywordsVitamin D CVD All-cause mortality Caerphilly Prospective Cohort Study TAG Recently, the UK Scientific Advisory Committee on Nutrition (1) reported that 22-24 % of individuals aged 19-64 years and 17-24 % of those aged ≥65 years in the UK were vitamin D deficient (plasma 25-hydroxycholecalciferol <25 nmol/l).People generally obtain vitamin D from synthesis in the skin due to sunlight UV radiation and/or foods. However, a number of relatively recent lifestyle changes (increased working indoors, sunscreen use), personal characteristics (ageing, skin pigmentation) and geographic reasons (latitude) limit the ability to synthesise adequate vitamin D from sunlight (2) . As a result, vitamin D intake from foods has become more important than previously. This led the Scientific Advisory Committee on Nutrition to recommend a daily vitamin D intake of 10 µg for all adults within the UK (1) . CVD is one of the main causes of morbidity and mortality in the world and there is mounting evidence indicating an association between suboptimal vitamin D status and increased risk of CVD (3)(4)(5)(6) and all-cause mortality (7)(8)(9) . However, few prospective cohort studies have analysed the relationship between vitamin D intake and CVD risk and allcause mortality. In a 10-year cohort of 361 men and 394 women (10) , lower vitamin D intake was associated with an increased risk of stroke, but not myocardial...

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Vitamin D₃Supplementation Has No Effect on Conventional Cardiovascular Risk Factors: A Parallel-Group, Double-Blind, Placebo-Controlled RCT

Abstract: Improving vitamin D status through dietary supplementation is unlikely to reduce CVD risk factors. Confounding of seasonality should be recognized and addressed in future studies of vitamin D.

Cited by 168 publications

References 39 publications

Impact of vitamin D supplementation on endothelial and inflammatory markers in adults: A systematic review

Impact of vitamin D supplementation on endothelial and inflammatory markers in adults: A systematic review

Vitamin D and risk of CVD: a review of the evidence

Vitamin D intake and risk of CVD and all-cause mortality: evidence from the Caerphilly Prospective Cohort Study

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Vitamin D3Supplementation Has No Effect on Conventional Cardiovascular Risk Factors: A Parallel-Group, Double-Blind, Placebo-Controlled RCT

Abstract: Improving vitamin D status through dietary supplementation is unlikely to reduce CVD risk factors. Confounding of seasonality should be recognized and addressed in future studies of vitamin D.

Cited by 168 publications

References 39 publications

Impact of vitamin D supplementation on endothelial and inflammatory markers in adults: A systematic review

Impact of vitamin D supplementation on endothelial and inflammatory markers in adults: A systematic review

Vitamin D and risk of CVD: a review of the evidence

Vitamin D intake and risk of CVD and all-cause mortality: evidence from the Caerphilly Prospective Cohort Study

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Product

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Vitamin D₃Supplementation Has No Effect on Conventional Cardiovascular Risk Factors: A Parallel-Group, Double-Blind, Placebo-Controlled RCT