Recent research has reported a possible link between calcium supplementation and increased risk of cardiovascular disease and its endpoints in healthy, older adults. To evaluate the current evidence regarding the impact of calcium supplementation on cardiovascular disease risk and to address research gaps, the present review was conducted. Systematic reviews and meta-analyses were included, when available, along with original articles. The articles included in the review were obtained from PubMed using the following search terms: calcium intake, calcium supplementation, cardiovascular disease, myocardial infarction, mortality, and vascular calcification. The majority of the studies reviewed demonstrated no statistically significant adverse or beneficial effect of calcium supplementation on cardiovascular disease or its endpoints. While some studies indicate a possible increased risk, there is a lack of consensus on these findings and a need exists to further elucidate a mechanism. More experimental data are necessary to understand the impact of calcium intake, both levels and sources, on vascular calcification and vascular disease. The use of (41) C kinetic modeling in the Ossabaw swine provides an approach for assessing soft tissue calcification in an atherosclerotic and normal state to address research gaps.
[Show abstract][Hide abstract] ABSTRACT: Growing evidence suggests that vitamin D deficiency Is associated with clinical coronary artery disease (CAD). The relationship between vitamin D deficiency and subclinical CAD in HIV-infected individuals is not well-characterized.
Computed tomographic (CT) coronary angiography was performed using contrast-enhanced 64-slice multidetector CT imaging, and vitamin D levels and the presence of traditional and novel risk factor for CAD were obtained in 674 HIV-infected African American (AA) participants aged 25-54 years in Baltimore, MD, without symptoms/clinical evidence of CAD.
The prevalence of vitamin D deficiency (25-hydroxy vitamin D <10 ng/mL) was 20.0% (95% confidence interval [CI], 16.9-23.1). Significant (≥50%) coronary stenosis was present in 64 (9.5%) of 674 participants. Multiple logistic regression analysis revealed that male gender (adjusted odds ratio [OR], 2.19; 95% CI, 1.17-4.10), diastolic BP ≥85 mmHg (adjusted OR: 1.94, 95% CI: 1.02 -3.68), low-density lipoprotein cholesterol ≥100 mg/dL (adjusted OR, 1.95; 95% CI, 1.13-3.36), cocaine use for ≥15 years (adjusted OR, 1.77; 95% CI, 1.01-3.10), use of antiretroviral therapies for ≥6 months (adjusted OR, 2.26; 95% CI, 1.17-4.36), year of enrollment after 2005 (adjusted ORs for 2006-2007, 2008-2009, and 2010 were 0.32 [95% CI, 0.13-0.76], 0.26 [95% CI, 0.12-0.56], and 0.32 (95% CI, 0.15-0.65], respectively), and vitamin D deficiency (adjusted OR, 2.28; 95% CI, 1.23-4.21) were independently associated with significant coronary stenosis.
Both vitamin D deficiency and silent CAD are prevalent in HIV-infected AAs. In addition to management of traditional CAD risk factors and substance abuse, vitamin D deficiency should be evaluated in HIV-infected AAs. These data support the conduct of a prospective trial of vitamin D in this high-risk patient population.
[Show abstract][Hide abstract] ABSTRACT: Purpose of review:
This review presents new evidence related to molecular mechanisms involved in the process of cardiovascular calcification, as well as to discuss new biomarkers and novel therapeutic strategies related to vascular calcification in chronic kidney disease (CKD) patients.
microRNAs have emerged as potential players in the genesis of osteo-chondrogenic transformation, depending on the stimulus and the localization of vascular calcification. The disturbances of the fibroblast growth factor-23 (FGF23)/alpha-Klotho (Klotho) axis observed in CKD appear to play an important role in CKD-associated vascular calcification. Numerous studies have identified circulating biomarkers potentially responsible for vascular calcification and have evaluated their link with this process. The respective role of these biomarkers is not yet elucidated. Beyond phosphate binders, modulation of calcium-sensing receptor and vitamin K supplementation come into sight as new potential strategies to prevent cardiovascular calcification.
A better understanding of the molecular mechanisms which are responsible for cardiovascular calcification have led to a better detection and more adequate follow-up of this pathologic process, as well as the identification of novel therapeutic targets. Whether these new insights will lead to improved care and better survival of CKD patients with cardiovascular calcification remains to be demonstrated.
Current Opinion in Nephrology and Hypertension 05/2013; 22(4). DOI:10.1097/MNH.0b013e328362155b · 3.86 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Typical clinical biomarker analyses on urine and plasma samples from human dietary interventions do not provide adequate information about diet-induced metabolic changes taking place in tissues. The aim of this study was to show how a large-scale non-targeted metabolomic approach can be used to reveal metabolite groups for generating new hypotheses of obesity-related metabolic disturbances produced in an animal model. A large spectrum of metabolites in the semi-polar region, including small water soluble molecules like betaine and dihydroxyindole, and a wide range of bile acids as well as various lipid species were detected. The high fat diet influenced metabolic homeostasis of Ossabaw pigs, especially the lipid metabolome, throughout all the analyzed sample types, including plasma, urine, bile, liver, pancreas, brain cortex, intestinal jejunum and proximal colon. However, even dramatic metabolic changes in tissues were not necessarily observed in plasma and urine. Metabolite profiling involving multiple sample types was shown to be a feasible method for the examination of a wide spectrum of metabolic species extending from small water soluble metabolites to an array of bile acids and lipids, thus pointing to the pathways of metabolism affected by the dietary treatment.
Journal of Proteome Research 06/2013; 12(9). DOI:10.1021/pr400257d · 4.25 Impact Factor
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