Potential Impact of the Steroid Hormone, Vitamin D, on the Vasculature Vitamin D-hormones and cardiovascular disease

AbstractMost studies of severe/fatal COVID-19 risk have used routine/hospitalisation data without detailed pre-morbid characterisation. Using the community-based UK Biobank cohort, we investigate risk factors for COVID-19 mortality in comparison with non-COVID-19 mortality. We investigated demographic, social (education, income, housing, employment), lifestyle (smoking, drinking, body mass index), biological (lipids, cystatin C, vitamin D), medical (comorbidities, medications) and environmental (air pollution) data from UK Biobank (N = 473,550) in relation to 459 COVID-19 and 2626 non-COVID-19 deaths to 21 September 2020. We used univariate, multivariable and penalised regression models. Age (OR = 2.76 [2.18–3.49] per S.D. [8.1 years], p = 2.6 × 10–17), male sex (OR = 1.47 [1.26–1.73], p = 1.3 × 10–6) and Black versus White ethnicity (OR = 1.21 [1.12–1.29], p = 3.0 × 10–7) were independently associated with and jointly explanatory of (area under receiver operating characteristic curve, AUC = 0.79) increased risk of COVID-19 mortality. In multivariable regression, alongside demographic covariates, being a healthcare worker, current smoker, having cardiovascular disease, hypertension, diabetes, autoimmune disease, and oral steroid use at enrolment were independently associated with COVID-19 mortality. Penalised regression models selected income, cardiovascular disease, hypertension, diabetes, cystatin C, and oral steroid use as jointly contributing to COVID-19 mortality risk; Black ethnicity, hypertension and oral steroid use contributed to COVID-19 but not non-COVID-19 mortality. Age, male sex and Black ethnicity, as well as comorbidities and oral steroid use at enrolment were associated with increased risk of COVID-19 death. Our results suggest that previously reported associations of COVID-19 mortality with body mass index, low vitamin D, air pollutants, renin–angiotensin–aldosterone system inhibitors may be explained by the aforementioned factors.

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Vitamin D and Cardiovascular Disease: An Updated Narrative Review

International Journal of Molecular Sciences ◽

10.3390/ijms22062896 ◽

2021 ◽

Vol 22 (6) ◽

pp. 2896

Author(s):

Armin Zittermann ◽

Christian Trummer ◽

Verena Theiler-Schwetz ◽

Elisabeth Lerchbaum ◽

Winfried März ◽

...

Keyword(s):

Cardiovascular Disease ◽

Vitamin D ◽

High Risk ◽

General Population ◽

Vitamin D Deficiency ◽

Specific Gene ◽

Vitamin D Status ◽

Cvd Risk ◽

Severe Vitamin ◽

Increased Risk

During the last two decades, the potential impact of vitamin D on the risk of cardiovascular disease (CVD) has been rigorously studied. Data regarding the effect of vitamin D on CVD risk are puzzling: observational data indicate an inverse nonlinear association between vitamin D status and CVD events, with the highest CVD risk at severe vitamin D deficiency; however, preclinical data and randomized controlled trials (RCTs) show several beneficial effects of vitamin D on the surrogate parameters of vascular and cardiac function. By contrast, Mendelian randomization studies and large RCTs in the general population and in patients with chronic kidney disease, a high-risk group for CVD events, largely report no significant beneficial effect of vitamin D treatment on CVD events. In patients with rickets and osteomalacia, cardiovascular complications are infrequently reported, except for an increased risk of heart failure. In conclusion, there is no strong evidence for beneficial vitamin D effects on CVD risk, either in the general population or in high-risk groups. Whether some subgroups such as individuals with severe vitamin D deficiency or a combination of low vitamin D status with specific gene variants and/or certain nutrition/lifestyle factors would benefit from vitamin D (metabolite) administration, remains to be studied.

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Potential impact of a modest reduction in salt intake on blood pressure, cardiovascular disease burden and premature mortality: a modelling study

Open Heart ◽

10.1136/openhrt-2018-000943 ◽

2019 ◽

Vol 6 (1) ◽

pp. e000943 ◽

Cited By ~ 4

Author(s):

Leopold Ndemnge Aminde ◽

Linda J Cobiac ◽

J Lennert Veerman

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Heart Disease ◽

Salt Intake ◽

Sodium Intake ◽

Premature Mortality ◽

Relative Reduction ◽

Life Years ◽

Potential Impact ◽

The Impact

ObjectiveTo assess the potential impact of reduction in salt intake on the burden of cardiovascular disease (CVD) and premature mortality in Cameroon.MethodsUsing a multicohort proportional multistate life table model with Markov process, we modelled the impact of WHO’s recommended 30% relative reduction in population-wide sodium intake on the CVD burden for Cameroonian adults alive in 2016. Deterministic and probabilistic sensitivity analyses were conducted and used to quantify uncertainty.ResultsOver the lifetime, incidence is predicted to decrease by 5.2% (95% uncertainty interval (UI) 4.6 to 5.7) for ischaemic heart disease (IHD), 6.6% (95% UI 5.9 to 7.4) for haemorrhagic strokes, 4.8% (95% UI 4.2 to 5.4) for ischaemic strokes and 12.9% (95% UI 12.4 to 13.5) for hypertensive heart disease (HHD). Mortality over the lifetime is projected to reduce by 5.1% (95% UI 4.5 to 5.6) for IHD, by 6.9% (95% UI 6.1 to 7.7) for haemorrhagic stroke, by 4.5% (95% UI 4.0 to 5.1) for ischaemic stroke and by 13.3% (95% UI 12.9 to 13.7) for HHD. About 776 400 (95% UI 712 600 to 841 200) health-adjusted life years could be gained, and life expectancy might increase by 0.23 years and 0.20 years for men and women, respectively. A projected 16.8% change (reduction) between 2016 and 2030 in probability of premature mortality due to CVD would occur if population salt reduction recommended by WHO is attained.ConclusionAchieving the 30% reduction in sodium intake recommended by WHO could considerably decrease the burden of CVD. Targeting blood pressure via decreasing population salt intake could translate in significant reductions in premature CVD mortality in Cameroon by 2030.

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