calcitriol and Cardiovascular-Diseases

Topics: Autoimmune Diseases; Cardiovascular Diseases; Diabetes Complications; Diabetes Mellitus; Humans; Incidence; Neurodegenerative Diseases; Osteoporosis; Racial Groups; Sarcopenia; Survival Analysis; Vitamin D; Vitamin D Deficiency

Topics: Calcium; Cardiovascular Diseases; Clinical Trials as Topic; Dietary Supplements; Humans; Renin-Angiotensin System; Risk Factors; Survival Analysis; Ultraviolet Rays; Vascular Calcification; Vitamin D; Vitamin D Deficiency

Vitamin D is best known for its influence on skeletal health. There is growing recognition, however, that vitamin D has nonskeletal actions, which could have important implications for understanding the consequences of vitamin D deficiency. In epidemiologic studies, vitamin D deficiency has been consistently associated with an increased risk for cardiovascular disease and hypertension. Disruption of vitamin D signaling in animal models promotes hypertension, cardiac hypertrophy, and atherosclerosis. This evidence has led to the initiation of prospective randomized trials of vitamin D supplementation in individuals at risk for cardiovascular disease. The results of these trials should help to guide strategies for screening and management of vitamin D deficiency in the clinic and at the population level.

Topics: Animals; Cardiovascular Diseases; Cholecalciferol; Dietary Supplements; Humans; Randomized Controlled Trials as Topic; Renin-Angiotensin System; Risk Factors; Vitamin D; Vitamin D Deficiency

Vitamin D is a secosteroid, in which the B ring of the steroid structure is ruptured. The active form of vitamin D, 1α, 25-dihydroxyvitamin D3 [1,25 (OH) 2D3], regulates numerous physiological and pharmacological processes, including bone and calcium homeostasis, cellular growth and differentiation, immunity, and cardiovascular function, through binding to the vitamin D receptor (VDR), a member of the nuclear receptor superfamily. VDR ligands are promising in the treatment of bone and mineral disorders, cancer, autoimmune disease, and cardiovascular disease. However, the calcemic effect of vitamin D derivatives has limited their clinical application. Recently, nonsecosteroidal VDR modulators (VDRMs) have been developed. Several VDRMs have better therapeutic efficacy when compared to 1,25 (OH) 2D3 in experimental models of cancer and osteoporosis with less induction of hypercalcemia. Analysis of crystal structures reveals that nonsecosteroidal VDRMs bind to VDR in a position similar to 1,25 (OH) 2D3 and that hydrogen bond interactions between ligands and VDR are important for VDR transactivation. Pharmacokinetics of nonsecosteroidal VDRMs may be related to their less calcemic effect. Nonsecosteroidal VDRMs can induce VDR conformation distinct from that by 1,25 (OH) 2D3, likely leading to selective gene expression. Although the potential risk of unexpected adverse effects needs be considered, further development of nonsecosteroidal VDRMs should expand the possibility of VDR-targeted approaches.

Topics: Animals; Bone and Bones; Cardiovascular Diseases; Humans; Neoplasms; Osteoporosis; Receptors, Calcitriol; Vitamin D

In recent years, it became increasingly clear that vitamin D exerts important pleiotropic effects, besides its well-known effects on extracellular calcium homeostasis and on bone metabolism. This article gives a comprehensive overview of studies on cardiovascular and all-cause mortality with a focus on the most recent data. 25-hydroxyvitamin D (25[OH]D) is the best indicator of vitamin D status. Low 25(OH)D levels are highly prevalent among general populations. Prospective cohort studies support the assumption that poor vitamin D status, e.g., 25(OH) D levels below 30 nmol/l, is independently associated with CVD mortality risk. However, support from randomized controlled trials for a beneficial vitamin D effect on CVD risk is still lacking. Meta-analyses of prospective cohort studies indicate beneficial vitamin D effects on overall mortality as well. There is also likely evidence from meta-analyses of randomized controlled trials that vitamin D may improve overall mortality in elderly people. Therefore, it is reasonable to supplement institutionalized individuals and other people with deficient 25(OH)D levels with daily vitamin D amounts of 20 microg. However, it is also noteworthy that prospective cohort studies provide evidence for an inverse J-shaped association between vitamin D status and overall mortality, indicating increased overall mortality risk not only at deficient 25(OH)D levels but also at 25(OH)D levels above 125 nmol/l. Although there is evidence that high 25(OH)D levels sometimes reflect low availability of the vitamin D hormone 1,25-dihydroxyvitamin D, future studies are still needed to clarify the association of high 25(OH)D levels with high mortality rates more detailed.

Topics: Aged; Calcium; Cardiovascular Diseases; Dietary Supplements; Homeostasis; Humans; Prevalence; Prospective Studies; Randomized Controlled Trials as Topic; Risk; Vitamin D

Fibroblast Growth Factor 23 (FGF-23) is a bone-derived hormone involved in the regulation of phosphate homeostasis. FGF-23 levels are extremely elevated in Chronic Kidney Disease (CKD) and there is evidence supporting the role of this hormone in the pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Furthermore, recent data associates FGF-23 with the pathogenesis of systemic complications of CKD-MBD. The increasing evidence that the consequences of abnormal mineral metabolism are not restricted to bone disease changed the approach to the pathophysiology and treatment of disturbed bone and mineral metabolism in CKD patients. FGF-23 has been proposed to be the initial adaptive response in early CKD to protect the organism from the adverse effects of phosphate retention. Increased levels of FGF-23 observed in CKD patients are associated with cardiovascular mortality risk and was shown to mediate direct, "off-target" toxicity to the heart. This report aims to review the relevant aspects of the physiology of FGF-23 in bone biology and mineral homeostasis and the role of FGF-23 in the pathophysiology of CKD-BMD and its clinical implications.

Topics: Animals; Bone and Bones; Calcium; Cardiovascular Diseases; Chronic Kidney Disease-Mineral and Bone Disorder; Disease Progression; Feedback, Physiological; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Homeostasis; Humans; Iron; Mice; Models, Biological; Osteocytes; Parathyroid Hormone; Phosphorus; Renal Insufficiency, Chronic; Treatment Outcome; Vitamin D

Reduction in serum 1,25 (OH) (2)D level plays an important role in the pathophysiology of altered bone and mineral metabolism among patients with advanced stages of CKD. The use of vitamin D receptor activators (VDRA) has brought great progress in medical management of CKD-MBD. A number of observational studies have shown that the nonuse of VDRA, and low serum concentrations of 1,25 (OH) (2)D or 25 (OH) D are the predictors of poor clinical outcomes in CKD patients including dialysis patients, raising a possibility that the pleiotropic actions of vitamin D may be systemically involved in the poor survival of patients with CKD-MBD. Randomized controlled trials are needed to clarify whether or not VDRA could be beneficial in the protection of the cardiovascular system and good longevity.

Topics: Bone Diseases, Metabolic; Cardiovascular Diseases; Cholecalciferol; Chronic Disease; Ergocalciferols; Humans; Kidney Diseases; Minerals; Randomized Controlled Trials as Topic; Receptors, Calcitriol; Risk; Vitamin D

Considering that the vitamin D receptor as well as the 1-α-hydroxylase enzyme that converts 25-hydroxyvitamin D (25(OH)D) to its active form 1,25-dihydroxyvitamin D have been found in tissues throughout the body, it is likely that vitamin D is important for more than the calcium balance. Accordingly, low serum levels of 25(OH)D have been associated with mortality, cardiovascular disease, type 2 diabetes, hypertension and obesity. Low serum levels of 25(OH)D have also been associated with an unfavourable lipid profile, which could possible explain the relation with cardiovascular disease and mortality. However, the relation between vitamin D and lipids have so far received little attention and is therefore the main focus of the present review. A PubMed search identified 22 cross-sectional studies where serum levels of 25(OH)D and lipids were related and that included a minimum of 500 subjects, and 10 placebo-controlled double-blind intervention studies with vitamin D where more than 50 subjects were included. In all the cross-sectional studies serum 25(OH)D was positively associated with high-density lipoprotein cholesterol (HDL-C) resulting in a favourable low-density lipoprotein cholesterol (LDL-C) (or total cholesterol) to HDL-C ratio. There was also a uniform agreement between studies on a negative relation between serum 25(OH)D and triglycerides (TG). On the other hand, the intervention studies gave divergent results, with some showing a positive and some a negative effect of vitamin D supplementation. However, none of the intervention studies were specifically designed for evaluating the relation between vitamin D and lipids, none had hyperlipemia as an inclusion criterion, and none were sufficiently powered. In only one study was a significant effect seen with an 8% (0.28 mmol/L) increase in serum LDL-C and a 16% (0.22 mmol/L) decrease in serum TG in those given vitamin D as compared to the placebo group. Accordingly, the effect of vitamin D supplementation on serum lipids is at present uncertain. Considering the numerous other promising vitamins and minerals that when properly tested have been disappointing, one should wait for the results of forthcoming vitamin D intervention studies before drawing conclusions on potential beneficial effects of vitamin D.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Double-Blind Method; Female; Humans; Hypertension; Male; Obesity; Randomized Controlled Trials as Topic; Triglycerides; Vitamin D; Vitamin D Deficiency

Chronic kidney disease-mineral bone disorder (CKD-MBD) is a multifaceted definition used to help describe the systemic derangement of mineral bone metabolism in renal disease. This was previously referred to, rather simplistically, as 'renal osteodystrophy' or 'renal bone disease'. In this review, we will try to show the evidence relating these factors to cardiovascular morbidity and mortality and give some evidence as to the mechanisms for this. The treatments used for this condition are also integral to the increased cardiovascular mortality seen in renal patients and a summary of these effects will also be covered.

Topics: Bone Remodeling; Calcinosis; Calcium; Cardiovascular Diseases; Chronic Kidney Disease-Mineral and Bone Disorder; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Renal Dialysis; Survival Rate; Vitamin D

A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1 alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) and extracellular Ca(2+) act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)(2)D(3)-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

Topics: Autoimmune Diseases; Calcium; Calcium, Dietary; Cardiovascular Diseases; Chronic Disease; Gene Expression Regulation; Humans; Metabolic Diseases; Neoplasms; S100 Calcium Binding Protein G; Vitamin D; Vitamin D Deficiency

Chronic kidney disease is associated with an increased risk of cardiovascular disease. Vitamin D deficiency is common in patients with chronic kidney disease. In epidemiological studies, vitamin D deficiency and absence of treatment with vitamin D is associated with increased cardiovascular mortality. Several possible mechanisms may explain how vitamin D can influence the development of cardiovascular disease. Clinical intervention studies are needed to clarify whether treatment with vitamin D decreases the risk of cardiovascular disease in chronic kidney disease.

Topics: Animals; Calcinosis; Cardiovascular Diseases; Heart Failure; Humans; Kidney Failure, Chronic; Renal Dialysis; Risk Factors; Vascular Diseases; Vitamin D; Vitamin D Deficiency

Vitamin D(3) needs to be activated into 1,25-dihydroxyvitamin D(3) in order to bind to vitamin D receptor (VDR) for functional responses. Studies in the past have focussed on the role of VDR in mineral homeostasis, with VDR activators used mainly to treat hyperparathyroidism secondary to chronic kidney disease. Chronic kidney disease patients encounter a higher risk of cardiovascular disease than the general public and experience an extremely high cardiovascular-related mortality rate. Recent clinical observations show that VDR therapy reduces mortality and morbidity in chronic kidney disease. Preclinical studies demonstrate that VDR is likely to be involved in the cardiovascular pathophysiology.

Topics: Cardiovascular Diseases; Humans; Kidney Failure, Chronic; Receptors, Calcitriol; Vitamin D

Vitamin D deficiency, low levels of fetuin-A, and fibroblast growth factor 23 (FGF-23) are related to vascular calcification, which is associated with cardiovascular disease. We hypothesized that omega-3 fatty acid (FA), which has cardioprotective properties, modifies vitamin D status, fetuin-A, and FGF-23 levels in dialysis patients. In a randomized, open-label, controlled study, a total of 47 patients treated with dialysis for at least 1 year were randomized to treatment for 6 months with omega-3 FAs (Omacor, 3 g/d; Pronova, Sandefjord, Norway) or a control group. Levels of fetuin-A and FGF-23 were measured by enzyme-linked immunoassay, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured by radioimmunoassay. The mean age of the enrolled patients was 57.4 ± 10.4 years, and mean dialysis duration was 46.5 ± 28.1 months. Twenty-seven hemodialysis patients and 16 peritoneal dialysis patients finished this trial. After 6 months, the levels of 1,25-dihydroxyvitamin D and fetuin-A were significantly increased in the group taking the omega-3 FA supplement compared with baseline. Levels of calcium, phosphorous, parathyroid hormone, 25-hydroxyvitamin D, FGF-23, and lipid profiles were not significantly changed in the omega-3 FA-supplemented group after 6 months compared with baseline. The erythrocyte membrane contents of eicosapentaenoic acid and docosahexaenoic acid were significantly increased, and oleic acid content was significantly decreased in the omega-3 FA-supplemented group after 6 months compared with baseline. Regarding vascular calcification and cardiovascular disease, omega-3 FA supplementation may have a clinical benefit caused by activating vitamin D, increasing fetuin-A levels, and modifying erythrocyte membrane FA contents in dialysis patients.

Topics: Adult; Aged; Aged, 80 and over; alpha-2-HS-Glycoprotein; Calcium; Cardiovascular Diseases; Diet; Dietary Supplements; Docosahexaenoic Acids; Drug Combinations; Eicosapentaenoic Acid; Energy Intake; Erythrocyte Membrane; Fatty Acids, Omega-3; Female; Fibroblast Growth Factor-23; Humans; Male; Middle Aged; Oleic Acid; Parathyroid Hormone; Peritoneal Dialysis; Phosphorus; Radioimmunoassay; Renal Dialysis; Vascular Calcification; Vitamin D

A growing body of scientific works investigating the physio-pathological mechanisms behind cardiovascular disease has suggested that vitamin D deficiency could play a key role on its development. However, it remains unclear whether its active form (1,25-dihydroxyvitamin D [1,25(OH). A total of 73 adults (~53% women; 54 ± 5 years old) were included in the current cross-sectional study. A sex-specific cardiometabolic risk score (MetScore) was calculated for each subject based on clinical parameters (i.e., waist circumference, systolic and diastolic blood pressure, plasma glucose, high-density lipoprotein cholesterol, and triglycerides) according to the International Diabetes Federation's clinical criteria. Plasma levels of 1,25(OH). No significant association was detected between 1,25(OH). In summary, the present results suggest that 1,25(OH)

Topics: Adult; Blood Pressure; Body Mass Index; Cardiovascular Diseases; Cross-Sectional Studies; Female; Humans; Male; Middle Aged; Risk Factors; Vitamin D; Vitamin D Deficiency; Waist Circumference

Topics: Animals; Antioxidants; Calcitriol; Cardiovascular Diseases; Cell Survival; Energy Metabolism; Heart; Homocysteine; Lipid Peroxidation; Male; Mitochondria; Oxidation-Reduction; Oxidative Stress; Protein Carbonylation; Rats, Wistar; Reactive Oxygen Species; Receptors, Calcitriol; Vitamin D

vitamin D deficiency has been associated with an increased risk of mortality, but whether this relationship is causal or linked to co-existent comorbidity and adverse life factors remains uncertain. Our objective was to determine whether endogenous 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D) and parathyroid hormone (PTH) levels predicted all-cause, cardiovascular and cancer mortality independently of health and lifestyle factors.. : prospective cohort analysis within the European Male Ageing Study.. : 2,816 community-dwelling men aged 40-79 years at baseline.. : Cox regression was used to examine the association of all-cause mortality with 25(OH)D, 1,25(OH)2D and PTH; cardiovascular and cancer mortality were modelled using competing-risks regression. Results were expressed as hazard ratios (HR) and 95% confidence intervals (CIs) for Cox models; sub-hazard ratios (SHR) and 95% CIs for competing-risks models.. : a total of 187 men died during a median of 4.3 years of follow-up. Serum levels of 25(OH)D (per 1 SD decrease: HR = 1.45; 95% CI = 1.16, 1.81) and 1,25(OH)2D (per 1 SD decrease: HR = 1.20; 95% CI = 1.00, 1.44) were associated with an increased risk of all-cause mortality after adjusting for age, centre, smoking, self-reported morbidities, physical activity and functional performance. Only levels of 25(OH)D <25 nmol/l predicted cancer mortality (SHR = 3.33; 95% CI = 1.38, 8.04).. : lower 25(OH)D and 1,25(OH)2D levels independently predicted all-cause mortality in middle-aged and older European men. Associations with cancer mortality were only observed among men with very low levels of 25(OH)D. These associations were only partially explained by the range of adverse health and lifestyle factors measured here.

Topics: Adult; Aged; Aging; Biomarkers; Cardiovascular Diseases; Cohort Studies; Europe; Follow-Up Studies; Humans; Life Style; Male; Middle Aged; Neoplasms; Parathyroid Hormone; Prospective Studies; Regression Analysis; Risk Factors; Surveys and Questionnaires; Survival Rate; Vitamin D

Vitamin D, estimated glomerular filtration rate (eGFR) and parathyroid hormone (PTH) are related to cardiovascular disease risk. We examined the associations between the levels of 25-hydroxyvitamin D (25-D) and 1,25-dihydroxyvitamin D (1,25-D) and both eGFR and PTH.. Cross-sectional population-based study in Kuopio, Eastern Finland.. A total of 909 men without known chronic kidney disease (CKD) and not receiving antidiabetic medication, aged from 45 to 73 years, were included in the study. Main outcome measures. Fasting levels of 25-D, 1,25-D, creatinine and PTH were measured, and an oral glucose tolerance test (OGTT) was performed.. High levels of 25-D were associated with low levels of eGFR and PTH (β = -0.17, P = 9 × 10(-7) and β = -0.28, P = 6 × 10(-17) , respectively, adjusted for age, body mass index and levels of calcium, phosphorus and glucose in a 2-h OGTT, and also for either eGFR or PTH). By contrast, high 1,25-D levels were associated with high levels of eGFR and PTH (β = 0.17, P = 2 × 10(-6) and β = 0.19, P = 5 × 10(-8) , respectively, adjusted as mentioned earlier and additionally for 25-D). Eighteen per cent of men in the highest 25-D quartile were in the lowest 1,25-D quartile and also had a lower eGFR than men with high levels of both 25-D and 1,25-D (P = 4 × 10(-5) ). Finally, 15% of men in the lowest 25-D quartile were in the highest 1,25-D quartile and also had higher PTH levels than men with low levels of both 25-D and 1,25-D (P = 2 × 10(-3) ).. Our findings suggest that both eGFR and PTH are significantly associated with vitamin D metabolism in men without known CKD.

Topics: 25-Hydroxyvitamin D 2; Aged; Algorithms; Analysis of Variance; Biomarkers; Cardiovascular Diseases; Creatinine; Cross-Sectional Studies; Finland; Glomerular Filtration Rate; Glucose Tolerance Test; Humans; Kidney Failure, Chronic; Male; Middle Aged; Multivariate Analysis; Parathyroid Hormone; Regression Analysis; Risk Factors; Sampling Studies; Surveys and Questionnaires; Vitamin D; Vitamins

Topics: 25-Hydroxyvitamin D 2; Cardiovascular Diseases; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Parathyroid Hormone; Vitamin D; Vitamins

Low vitamin D concentrations are detected in patients suffering from various clinical conditions which are characterized also by inflammation and immune activation.We investigated whether vitamin D levels in patients with coronary artery disease (CAD) are related to markers of immune activation.. Serum concentrations of 25-hydroxyvitamin D[25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH) 2 D] and the immune activation markers neopterin and high sensitivity C-reactive protein (hsCRP) were measured in 2015 patients derived from the LUdwigshafen RIsk and Cardiovascular Health (LURIC) study, a cohort study among patients referred for coronary angiography.. Serum concentrations of 25(OH)D and 1,25(OH) 2 D did not differ between patients with CAD [mean } SD:25(OH)D: 17.4 } 9.4 μ g/L; 1,25(OH) 2 D: 34.4 } 13.3 ng/L] and controls [25(OH)D: 18.4 } 11.7 μ g/L; 1,25(OH) 2 D: 35.3 } 12.7ng/L; Welch ’ s t-test: p = n.s.] but CAD patients had higher neopterin (8.6 } 7.4 nmol/L) and hsCRP (9.6 } 19.6 mg/L) concentrations compared to controls (neopterin: 7.5 } 4.8 nmol/L;p = 0.0004; hsCRP: 5.4 } 10.0 mg/L; p < 0.0001). There was an inverse correlation between serum 25(OH)D or 1,25(OH) 2 D concentrations and serum neopterin [Spearman ’ s rank correlation:25(OH)D: r s = – 0.183; 1,25(OH)2D: r s = – 0.230] and hsCRP [25(OH)D: r s = – 0.142; 1,25(OH) 2 D: r s = – 0.130; allp < 0.0001] concentrations.. Our results indicate increased inflammatory processes in patients with low vitamin D status. Further studies should clarify the underlying mechanisms for the observed associations of vitamin D status and inflammatory parameters.

Topics: Aged; C-Reactive Protein; Cardiovascular Diseases; Cohort Studies; Humans; Immune System; Inflammation; Middle Aged; Vitamin D; Vitamin D Deficiency

Globally, cardiovascular disease (CVD) is the number one cause of death, being responsible for approximately 30% of deaths worldwide. Urbanization and a westernized lifestyle are thought to play a major role in the development of CVD. There is accumulating evidence that vitamin D is a nonclassical risk factor for CVD. The active vitamin D metabolite, 1,25-dihydroxyvitamin D, which is synthesized from its precursor 25-hydroxyvitamin D (25[OH]D), down-regulates several negative and up-regulates various protective pathways in the heart and vasculature. First randomized trials demonstrate that vitamin D supplementation leads to vasodilatation and suppresses cardiovascular risk markers such as triglycerides and the inflammation marker tumor necrosis factor-α. Solar UV-B radiation is the major source of vitamin D for humans. Consequently, the vitamin D status is largely influenced by season, geographic latitude, daily outdoor activities, and the percentage of body surface exposed to solar UV-B. A significant proportion of individuals in Europe and North America have vitamin D concentrations in the deficiency range (25[OH]D<25 nmol/l). Available data indicate that low solar UV-B exposure and/or low 25(OH)D concentrations are associated with an increased risk of CVD. Large nonrandomized studies indicate that CVD mortality is more than twice as high in older individuals with deficient 25(OH)D concentrations compared with those individuals who have adequate 25(OH)D concentrations (>75 nmol/l). Together, experimental and epidemiological evidence does support a plausible role for improving vitamin D status in CVD prevention in the population at large. Nevertheless, future randomised clinical trials are needed to evaluate whether vitamin D is effective with respect to primary, secondary, and/or tertiary prevention of CVD.

Topics: Animals; Cardiovascular Diseases; Clinical Trials as Topic; Humans; Mice; Risk Factors; Seasons; Sunlight; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency

recent systematic reviews have cast doubt on the association between vitamin D and cardiovascular disease. No prior studies have investigated the association between 25-hydroxyvitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH](2)D), or intact parathyroid hormone and cardiovascular mortality in a temperate climate.. a total of 1073 community-dwelling older adults were evaluated in 1997-1999; serum levels of 25(OH)D (mean 42 ng/mL), 1,25(OH)(2)D (median 29 pg/mL), and intact parathyroid hormone (median 46 pg/mL) were measured; mean estimated glomerular filtration rate was 74 mL/min/1.73 m(2). Participants were followed up to 10.4 (mean 6.4) years with 111 cardiovascular deaths.. in unadjusted Cox proportional hazards models, higher levels of 1,25(OH)(2)D were protective against cardiovascular mortality, whereas higher levels of intact parathyroid hormone predicted increased risk of cardiovascular death. After adjusting for age alone or multiple covariates, there was no significant association between 25(OH)D, 1,25(OH)(2)D, or intact parathyroid hormone and cardiovascular mortality; results did not differ by an estimated glomerular filtration rate ≥ 60 mL/min/1.73 m(2) or<60 mL/min/1.73 m(2).. in this prospective study of Caucasian, middle-income, community-dwelling older adults living in sunny southern California, serum levels of 25(OH)D, 1,25(OH)(2)D, and intact parathyroid hormone were not independently associated with cardiovascular mortality.

Topics: Age Factors; Aged; Aged, 80 and over; Biomarkers; California; Cardiovascular Diseases; Confounding Factors, Epidemiologic; Female; Glomerular Filtration Rate; Humans; Male; Multivariate Analysis; Odds Ratio; Parathyroid Hormone; Proportional Hazards Models; Prospective Studies; Renal Insufficiency, Chronic; Sunlight; Vitamin D; White People

It is known that vitamin D has many functions besides involvement in calcium metabolism. It has recently been recognized that vitamin D deficiency is associated with mortality, especially in cardiovascular disease (CVD). Vitamin D deficiency is common in end-stage renal disease, but develops from the early stage of chronic kidney disease (CKD). So we investigated whether the serum level of the activated form of vitamin D (1,25-dihydroxyvitamin D) affected mortality in patients with CKD stages 3 and 4.. Between January 1, 1995, and June 30, 2006 we measured serum 1,25-dihydroxyvitamin D In 226 patients with CKD stages 3 and 4 and classified the results into two groups depending on whether the level was below (group I) or above (group II) 20 pg/ml. We ended the follow-up period on December 31, 2006. We compared all-cause and cardiovascular mortality between the two groups. We also examined predictors of mortality by using Cox proportional regression analysis.. Two-hundred and twenty-six patients (67 men and 159 women, mean age 67.0) were registered in this study, and groups 1 and 2 comprised 84 and 142 patients, respectively. During the follow-up period 43 patients died. CVD was the major cause of death, followed by infectious disease. The Kaplan-Meier survival curve revealed that all-cause mortality was significantly higher in group I, but a significant difference between CVD mortality in the two groups was not demonstrated. By Cox proportional regression analysis, group I was related to all-cause mortality, but this was not proved to be an independent predictor.. The results suggested that serum level of 1,25-dihydroxyvitamin D was associated with all-cause mortality in patients with CKD stages 3 and 4.

Topics: Aged; Biomarkers; Cardiovascular Diseases; Communicable Diseases; Disease Progression; Female; Follow-Up Studies; Humans; Kaplan-Meier Estimate; Male; Middle Aged; Prognosis; Proportional Hazards Models; Renal Insufficiency, Chronic; Risk Assessment; Severity of Illness Index; Time Factors; Vitamin D; Vitamin D Deficiency