Vitamin D and Vascular Disease

2020 ◽  
Vol 19 (3) ◽  
pp. 250-268 ◽  
Author(s):  
Ioanna Gouni-Berthold ◽  
Heiner K. Berthold

: Cardiovascular disease (CVD) is a major cause of morbidity and mortality worldwide. Vitamin D deficiency has been identified as a potential risk factor for a number of diseases unrelated to the classical skeletal pathophysiology, such as cancer and CVD, but the effects of vitamin D supplementation are less clear. Purpose of this narrative review is to discuss the evidence suggesting an association between vitamin D status and CVD as well as the results of supplementation studies. Vitamin D deficiency has been associated with CVD risk factors such as hypertension, dyslipidemia and diabetes mellitus as well as with cardiovascular events such as myocardial infarction, stroke and heart failure. While vitamin D deficiency might contribute to the development of CVD through its association with risk factors, direct effects of vitamin D on the cardiovascular system may also be involved. Vitamin D receptors are expressed in a variety of tissues, including cardiomyocytes, vascular smooth muscle cells and endothelial cells. Moreover, vitamin D has been shown to affect inflammation, cell proliferation and differentiation. While observational studies support an association between low plasma vitamin D levels and increased risk of CVD, Mendelian randomization studies do not support a causal association between the two. At present, high quality randomized trials do not find evidence of significant effects on CVD endpoints and do not support supplementation of vitamin D to decrease CVD events.

2018 ◽  
Vol 12 (1) ◽  
pp. 226-247 ◽  
Author(s):  
Alessandra Nerviani ◽  
Daniele Mauro ◽  
Michele Gilio ◽  
Rosa Daniela Grembiale ◽  
Myles J. Lewis

Background: Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease characterised by abnormal activation of the immune system, chronic inflammation and organ damage. Lupus patients are more prone to be vitamin D deficient. However, current evidence is not conclusive with regards to the role played by vitamin D in SLE development, progression, and clinical manifestations. Objective: Here, we will summarise the current knowledge about vitamin D deficiency prevalence, risk factors, molecular effects, and potential pathogenic role in SLE. We will focus on the link between vitamin D deficiency and lupus clinical manifestations, and on the clinical trials assessing the effects of vitamin D supplementation in SLE. Method: A detailed literature search was performed exploiting the available databases, using “vitamin D and lupus/SLE” as keywords. The relevant interventional trials published over the last decade have been considered and the results are reported here. Conclusion: Several immune cells express vitamin D receptors. Thus, an immunomodulatory role for vitamin D in lupus is plausible. Numerous observational studies have investigated the relationship between vitamin D levels and clinical/serological manifestations of SLE with contrasting results. Negative correlations between vitamin D levels and disease activity, fatigue, renal and cardiovascular disease, and anti-dsDNA titres have been described but not conclusively accepted. In experimental models of lupus, vitamin D supplementation can improve the disease. Interventional trials have assessed the potential therapeutic value of vitamin D in SLE, but further larger studies are needed.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Chaoxun Wang

Vitamin D deficiency is a highly prevalent condition. Low vitamin D levels have long been associated with bone diseases, such as rickets in children and osteomalacia and osteoporosis in adults. However, it has become apparent in recent years that adequate vitamin D levels are also important for optimal functioning of many organs and tissues throughout the body, including the cardiovascular system. Evolving data indicate that vitamin D deficiency is associated with an increased risk of cardiovascular disease (CVD). Studies have shown that low vitamin D levels are associated with hypertension, diabetes, metabolic syndrome, left ventricular hypertrophy, and chronic vascular inflammation, all of which are risk factors for CVD. This paper reviews the definition and pathophysiology of vitamin D deficiency, clinical evidence linking vitamin D and CVD risk, diabetes and its complications, and metabolic syndrome.


Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1400
Author(s):  
Niv Ben-Shabat ◽  
Abdulla Watad ◽  
Aviv Shabat ◽  
Nicola Luigi Bragazzi ◽  
Doron Comaneshter ◽  
...  

In this study, we aimed to examine the effect of vitamin D deficiency on all-cause mortality in ankylosing spondylitis (AS) patients and in the general population. This is a retrospective-cohort study based on the electronic database of the largest health-maintenance organization in Israel. AS patients who were first diagnosed between 2002–2007 were included. Controls were matched by age, gender and enrollment-time. Follow-up continued until death or end of study follow-up on 1 July 2019. Laboratory measures of serum 25-hydroxyvitamin-D levels during the entire follow-up period were obtained. A total of 919 AS patients and 4519 controls with a mean time of follow-up of 14.3 years were included. The mean age at the time of enrollment was 52 years, and 22% of them were females. AS was associated with a higher proportion of vitamin D deficiency (odds ratio 1.27 [95% confidence-interval (CI) 1.03–1.58]). In AS patients, insufficient levels of vitamin D (<30 ng/mL) were significantly associated with increased incidence of all-cause mortality (hazard ratio (HR) 1.59 [95% CI 1.02–2.50]). This association was more prominent with the decrease in vitamin D levels (< 20 ng/mL, HR 1.63 [95% CI 1.03–2.60]; <10 ng/mL, HR 1.79 [95% CI 1.01–3.20]) and among male patients (<30 ng/mL, HR 2.11 [95% CI 1.20–3.72]; <20 ng/mL, HR 2.12 [95% CI 1.19–3.80]; <10 ng/mL, HR 2.23 [95% CI 1.12–4.43]). However, inadequate levels of vitamin D among controls were not associated with an increased all-cause mortality. Our study has shown that vitamin D deficiency is more common in AS patients than controls and is linked to an increased risk for all-cause mortality. These results emphasize the need for randomized-controlled trials to evaluate the benefits of vitamin D supplementation as a secondary prevention of mortality in patients with chronic inflammatory rheumatic disease.


2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Letícia Veríssimo Dutra ◽  
Fernando Alves Affonso-Kaufman ◽  
Fernanda Ramires Cafeo ◽  
Milene Saori Kassai ◽  
Caio Parente Barbosa ◽  
...  

Abstract Background Premature birth is the main cause of mortality in children under 1 year, and vitamin D deficiency during gestation is associated with prematurity. The effects of vitamin D are mediated by its receptor, which is encoded by the VDR gene. VDR variants—such as single nucleotide variation (SNV)—are associated with increased risk of prematurity, but there are conflicting results. We evaluated serum vitamin D concentrations and the frequency of TaqI/A > G, BsmI/C > T, ApaI/C > A, and FokI/A > T VDR variants in mothers and preterm (PTN) and full-term (FTN) newborns. Methods We conducted a case-control study comprising 40 pairs of mothers and their PTNs (gestational age < 32 weeks and/or weight < 1500 g), and 92 pairs of mothers and FTNs as controls. Genotyping was performed by real-time PCR, and plasma vitamin D concentrations were measured by electrochemiluminescence. Results Vitamin D levels were significantly lower in PTN mothers. Genotypes TaqI/GG and BsmI/TT, and haplotypes AAG (TaqI/A-ApaI/A-FokI/G) and GCA (TaqI/G-ApaI/C-FokI/A) were significantly more frequent in PTN mothers, and genotypes TaqI/AG, ApaI/AA, and FokI/AG resulted in significantly lower vitamin D levels. Genotypes BsmI/TT and ApaI/AA were associated with vitamin D deficiency and 2.36 and 7.99 times greater likelihood of PTB, respectively. Vitamin D levels were also lower in PTNs, although it was not statistically significant. Genotypes BsmI/TT, ApaI/AA, and FokI/GG, and haplotype GAG (TaqI/G-ApaI/A-FokI/G) were significantly more frequent in PTNs. Those with FokI/GG genotypes had significantly lower vitamin D levels. Conclusions VDR variants contribute to variations in vitamin D concentrations and the increased risk of prematurity.


Author(s):  
Xiaoying Cui ◽  
John J. McGrath ◽  
Thomas H. J. Burne ◽  
Darryl W. Eyles

AbstractMany epidemiological studies have highlighted the link between vitamin D deficiency and schizophrenia. In particular, two prominent studies report an association between neonatal vitamin D deficiency and an increased risk of schizophrenia. In parallel, much has been learnt about the role of vitamin D in the developing central nervous system over the last two decades. Studies in rodent models of developmental vitamin D (DVD)-deficiency describe how brain development is altered leading to a range of neurobiological and behavioral phenotypes of interest to schizophrenia. While glutamate and gamma aminobutyric acid (GABA) systems have been little investigated in these models, alterations in developing dopamine systems are frequently reported. There have been far more studies reporting patients with schizophrenia have an increased risk of vitamin D deficiency compared to well controls. Here we have conducted a systematic review and meta-analysis that basically confirms this association and extends this to first-episode psychosis. However, patients with schizophrenia also have poorer general health, poorer diets, are frequently less active and also have an increased risk of other medical conditions, all factors which reduce circulating vitamin D levels. Therefore, we would urge caution in any causal interpretation of this association. We also summarize the inconsistent results from existing vitamin D supplementation trials in patients with schizophrenia. In respect to animal models of adult vitamin D deficiency, such exposures produce subtle neurochemical alterations and effects on cognition but do not appear to produce behavioral phenotypes of relevance to schizophrenia. We conclude, the hypothesis that vitamin D deficiency during early life may increase the risk of schizophrenia remains plausible and warrants ongoing research.


2021 ◽  
Author(s):  
Rai-Hua Lai ◽  
Yueh-Ying Hsu ◽  
Feng-Shiun Shie ◽  
Mei-Hsin Chen ◽  
Jyh-Lyh Juang

Vitamin D is an important hormonal molecule, which exerts genomic and non-genomic actions in maintaining brain development and adult brain health. Many epidemiological studies have associated vitamin D deficiency with Alzheimer's disease (AD). Nevertheless, the underlying signaling pathway through which this occurs remains to be characterized. We were intrigued to find that although vitamin D levels are significantly low in AD patients, their hippocampal vitamin D receptor (VDR) levels are inversely increased in the cytosol of the brain cells, and colocalized with Aβ plaques, gliosis and autophagosomes, suggesting that a non-genomic form of VDR is implicated in AD. Mechanistically, Aβ induces the conversion of nuclear heterodimer of VDR/RXR heterodimer into a cytoplasmic VDR/p53 heterodimer. The cytosolic VDR/p53 complex mediates the Aβ induced autophagic apoptosis. Reduction of p53 activity in AD mice reverses the VDR/RXR formation and rescues AD brain pathologies and cognitive impairment. In line with the impaired genomic VDR pathway, the transgenic AD mice fed a vitamin D sufficient diet exhibit lower plasma vitamin D levels since early disease phases, raising the possibility that vitamin D deficiency may actually be an early manifestation of AD. Despite the deficiency of vitamin D in AD mice, vitamin D supplementation not only has no benefit but lead to exacerbated Aβ depositions and cognitive impairment. Together, these data indicate that the impaired genomic vitamin D pathway links Aβ to induce autophagic apoptosis, and suggest that VDR/p53 pathway could be targeted for the treatment of AD.


Author(s):  
Munmun Yadav ◽  
Mahendra Kumar Verma ◽  
Mohan Bairwa ◽  
Govardhan Meena ◽  
Lata Rajoria

Background: Vitamin D deficiency is widely prevalent throughout the world. Pregnant women, neonates and infants form most vulnerable groups for vitamin D deficiency. Hypovitaminosis D in pregnancy has been reported to cause various fetomaternal effect, i.e. increased risk of preeclampsia (PE), gestational diabetes mellitus (GDM), caesarean section, hypocalcemia, subclinical myopathy, neonatal tetany, hyperbilirubinemia congenital rickets and infantile rickets, etc. Only few Indian studies are available in this regard. The objectives are to find prevalence of vitamin D deficiency in pregnant women and to evaluate the effect of supplementation with cholecalciferol in improving vitamin D levels in pregnant women and evaluate its correlation with feto-maternal outcome.Methods: A prospective observational was conducted on 120 Pregnant women on their first visit to hospital irrespective of gestational age were offered the test and on the basis of inclusion and exclusion criteria are included in study and vitamin D level was done to know the prevalence of vitamin D deficiency. Apart from routine obstetrical investigation, serum vitamin D (total) level was estimated. All results were recorded and analyzed statically.Results: Out of 120 patients 101 (84.1%) were found to be vitamin D deficient. Mean age of vitamin D deficient group was 28.31±3.86 and sufficient group was 26.37±2.83.81 (67.5%) were vegetarian and 39 (32.5%) were nonvegetarian.75 (92.59%) vegetarian and 26 (66.66%) non-vegetarian found to be vitamin D deficient. (p<0.05). Vitamin D supplementation has been observed to reduce risk of preeclampsia. (p<0.05) and vitamin D sufficiency associated with reduced risk of low birth weight babies.Conclusions: Vitamin D supplementation reduces risk of maternal comorbidities and helps improve neonatal outcomes.


Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2861 ◽  
Author(s):  
Francesca Remelli ◽  
Aurora Vitali ◽  
Amedeo Zurlo ◽  
Stefano Volpato

Vitamin D deficiency is a common health problem worldwide, in particular among older people. Vitamin D regulates and modulates the physiology and function of multiple human systems, including the skeletal muscle. The effect of vitamin D on the muscle has been widely investigated, suggesting that this hormone can stimulate the proliferation and differentiation of skeletal muscle fibers, maintaining and improving muscle strength and physical performance. Older persons have a higher prevalence of low Vitamin D levels as a consequence of low dietary intake and reduced ultraviolet irradiation of the skin. Therefore, older people with vitamin D deficiency might be at risk of sarcopenia, a geriatric syndrome characterized by the progressive loss of skeletal muscle mass and strength often complicated by adverse events, such as falls, disability hospitalization and death. Several randomized clinical trials have been conducted to investigate the effect of oral vitamin D supplementation in older patients to prevent or treat sarcopenia, but results are still controversial. In this narrative review we summarize the biological, clinical and epidemiological evidence supporting the hypothesis of a causal association between Vitamin D deficiency and an increased risk of sarcopenia in older people.


2020 ◽  
Vol 41 (Supplement_1) ◽  
pp. S178-S179
Author(s):  
Sara Calder ◽  
Asia N Quan ◽  
Suzanne Osborn ◽  
Virginia Nisbet ◽  
Karen J Richey ◽  
...  

Abstract Introduction The potential consequences of vitamin D insufficiency/deficiency (I/D) in critically ill patients include: increased ICU length of stay, organ dysfunction, infectious complications, and mortality. Burn patients, in particular, may be at increased risk of vitamin D I/D due to bleeding, systemic inflammatory response syndrome, increased utilization of vitamin D by injured tissues, compromised vascular integrity, fluid shifts, and leakage of vitamin D binding protein (VDBP) and albumin. The purpose of this study is to determine the incidence of vitamin D I/D and evaluate the institutional vitamin D dosing regimen. Methods A retrospective chart review was performed on all adult patients from January 1, 2018 through December 31, 2019 who received cholecalciferol and had at least one 25-hydroxy vitamin D level during their hospitalization. Vitamin D level was drawn on admission, then weekly thereafter. Patients found to be I/D were initiated on high dose vitamin D supplementation and then adjusted based on the weekly levels. The therapeutic goal for vitamin D supplementation was set at 50 ng/ml. Results Three hundred and sixteen patients met criteria for review. Of those patients, 293 patients (93%) were vitamin D I/D. The magnitude of vitamin D deficiency was strongly negatively correlated with increasing % total body surface area (TBSA) burn size (p&lt; 0.001). Mean time to reach therapeutic vitamin D levels following initiation of supplementation was 19 days, requiring an average of 116,125 units cholecalciferol weekly. Time to reach therapeutic levels was also positively correlated with increasing burn size (p&lt; 0.05). Many patients, however, were discharged prior to reaching therapeutic levels. Conclusions Vitamin D I/D is present in over 90% of burn center patients and the degree of I/D was profound. Additionally, vitamin D I/D was not easily corrected, taking almost 3 weeks to reach therapeutic levels using an aggressive supplementation regimen. Further studies documenting the consequences of vitamin D I/D and development of evidence-based supplementation dosing regimens are warranted. Applicability of Research to Practice This study documents common and severe vitamin D deficiency in burn patients, and difficulty in correcting this deficiency.


Author(s):  
Aya Hallak ◽  
Mahmoud Malhis ◽  
Mohammad Yaser Abajy

Objective: This study aimed to investigate the relation between vitamin D plasma concentrations and prevalence of prespecified coronary risk factors, and to assess the role of vitamin D deficiency as an independent risk factor for the acute coronary syndrome (ACS).Methods: In this study, plasma 25-hydroxyvitamin D [25(OH)D] levels were measured in 60 consecutive ACS patients at hospital presentation, and patient data including socio-demographics and clinical variables were recorded at the time of admission. We used the Independent samples T-test and the chi-square test to compare differences in the continuous and categorical variables, respectively. The partial correlation coefficient was used to measure association between plasma vitamin D levels and acute coronary syndrome while controlling for traditional cardiovascular risk factors.Results: This study found significant associations between low plasma vitamin D levels and prevalence of hypertension and smoking. Whereas, no significant association between low plasma vitamin D levels and prevalence of diabetes mellitus (DM) was found. There was a statistically significant correlation between vitamin D deficiency and acute coronary syndrome, even after controlling for traditional cardiovascular risk factors (P = 0.028).Conclusion: Vitamin D deficiency is independently associated with acute coronary syndromes, and could be an independent risk factor for the acute coronary syndrome (ACS).


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