VitD Supplementation Research Articles

Geometric, elastic and contractile-relaxation changes in coronary arterioles induced by Vitamin D deficiency in normal and hyperandrogenic female rats

Vitamin D (VitD) hypovitaminosis and androgen excess (AE) are both risk factors for cardiovascular diseases in fertile women. However, the possible early interaction between AE and VitD status is not clear. Our goal was to describe how VitD status influences early changes in the biomechanical reactivity of small coronary arterioles in adult female rats after transdermal testosterone treatment.Forty-six adolescent, 90–110-gram-weighed female Wistar rats were randomly grouped into 4 groups. Twenty-four animals received an optimal VitD-supplemented diet, from which 12 animals underwent transdermal testosterone treatment. Twenty-two animals received a VitD-deficient diet, from which 11 were treated with testosterone. At 8 weeks of treatment, invasive arterial blood pressure was registered after in vivo cannulation of carotid artery. Arteriolar end and side branches (200 μm diameter) of the left anterior descendent coronary artery (LAD) were obtained and examined with pressure arteriography in vitro. Similar segments were removed for histological examination. The inner and outer radii of the arterioles were measured using video-microscopy. Normal myogenic tone, maximal passive vasorelaxation and vasoconstriction of the arterioles were measured and statistically analyzed. The vessels' maximal smooth muscle relaxant potential, thromboxane-induced contraction capacity and normal myogenic tone were significantly influenced by actual VitD status. A lower relaxation capacity and increased wall thickness were observed in VitD-deficient groups, which could cause rigidity of the coronary arterioles and elevate cardiovascular risk. Supplementation of VitD could improve myogenic tone and relaxation and hold cardiovascular benefits.

Vitamin D3 as adjunctive therapy in the treatment of depression in tuberculosis patients: a short-term pilot randomized double-blind controlled study.

ObjectiveWe aimed to evaluate whether high-dose cholecalciferol has beneficial effects on depression in pulmonary tuberculosis (PTB) patients.MethodsThis pilot, randomized, and double-blind trial enrolled 123 recurrent PTB patients (aged ≥18 years) meeting Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) criteria of major depressive disorder from four hospitals in Southeast China. Patients were randomly assigned to 8-week oral treatment with 100,000 IU/week cholecalciferol (Vit D group) or a matching placebo (control group). The primary outcome was treatment response, defined as a 50% reduction in symptoms and change in scores of the Chinese version of Beck Depression Inventory (BDI) from baseline to 8 weeks. Relative risks of depression were estimated using multivariable logistic regression.ResultsFinally, 120 patients were enrolled, including 56 test patients and 64 controls. After 8 weeks, the treatment response or BDI scores did not differ significantly between groups. Multivariate logistic regression showed that BDI scores were not significantly improved in the Vit D group after adjustment for age, time to first negative smear, or 25-hydroxyvitamin D level.ConclusionThe use of high-dose Vit D3 supplementation may not be warranted for reducing depressive symptoms in the PTB population. Nevertheless, this finding should be validated by further large-scale studies according to different kinds of depression or Vit D receptor polymorphism genotype.

Characterization of vitamin D supplementation and clinical outcomes in a large cohort of early Parkinson\u2019s disease

BackgroundVitamin D (VitD) deficiency is common in Parkinson’s disease (PD) and has been raised as a possible PD risk factor. In the past decade, VitD supplementation for potential prevention of age related conditions has become more common. In this study, we sought to characterize VitD supplementation in early PD and determine as an exploratory analysis whether baseline characteristics or disease progression differed according to reported VitD use.MethodsWe analyzed data from the National Institutes of Health Exploratory Trials in Parkinson’s Disease (NET-PD) Long-term study (LS-1), a longitudinal study of 1741 participants. Subjects were divided into following supplement groups according to subject exposure (6 months prior to baseline and during the study): no VitD supplement, multivitamin (MVI), VitD ≥400 IU/day, and VitD + multivitamin (VitD+MVI). Clinical status was followed using the Unified Parkinson’s Disease Rating Scale, Symbol Digit Modalities Test, total daily levodopa equivalent dose, and Parkinson’s Disease Questionnaire.ResultsAbout 5% of subjects took VitD alone, 7% took VitD+MVI, 34% took MVI alone, while 54% took no supplement. Clinical outcomes at 3 years were similar across all groups.ConclusionThis study shows VitD supplementation ≥400 IU/day was not common in early PD and that its use was similar to that seen in the US population. At 3 years, there was no difference in disease progression according to vitamin D supplement use.

The effects of vitamin D supplementation on healthy and hypercholesterolemic rabbits on levels of OSI and paraoxonase

Abstract Objective Conflicting data are available in literature regarding the effects of vitamin D (VitD) supplementation diet on lipid panel. Therefore, we had the purpose to evaluate the effects of VitD supplementation on lipid panel by a controlled experimental study, and those of VitD supplementation on oxidative stress index (OSI) and paraoxonase-1 (PON1) values in healthy and hypercholesterolemic male rabbits. Methods Thirty New Zealand rabbits were randomly separated into control, VD, HC+VD and HC groups. Control and VD groups were fed with standard chow, whereas HC+VD and HC groups were fed with 0.5% cholesterol chow a period of 8 weeks. During this period, VD and HC+VD groups were orally administered with 300 IU/kg/day VitD. Results The increase in serum total cholesterol (TC) and OSI level of HC group were significant compared to those in HC+VD group. Decreases in serum HDL-cholesterol (HDL-C) and TC levels of VD group were significant within the groups. Conclusion Without any doubt it is important that applied VitD level should be in the ideal range for healthy living. However, it is also necessary to increase the serum HDL-C level (and hence PON1), which is decreases as a result of VitD supplementation. Therefore, we believe that during VitD supplementation, regular physical activity should be performed to increases serum HDL-C.

Risk factors analysis and prevention of metabolic bone disease of prematurity.

The present study aims to analyze the risk factors for metabolic bone disease (MBD) of prematurity.A total of 238 preterm infants who were born at <34 weeks of gestation and were hospitalized for at least 6 weeks in the Department of Neonatology, Fujian Maternity and Children Hospital between January 1, 2011 and November 30, 2015 were enrolled in the study. Sixteen preterm infants diagnosed with MBD were selected as the case group, and 32 non-MBD preterm infants were matched 2:1 at admission into the study. The 2 groups were compared to examine the differences in maternal obstetric conditions, conditions during parturition, neonatal conditions, and neonatal diseases and treatments. The risk factors for MBD of prematurity were analyzed using t tests, χ2 tests, and a logistic regression model.The mean gestational age and birth weight of the case group were significantly lower (P < .05) than those of the control group. Compared with the control group, the case group had a significantly higher ratios of small-for-gestational-age infants, antenatal maternal corticosteroids use, sedative use, ventilator use, aminophylline use, diuretic use, liver function impairment, vitamin D (VitD) supplementation at more than 14 days of age, achievement of total enteral nutrition (TEN) beyond 28 days of age, and feeding intolerance.Logistic regression analysis showed that birth at <30 weeks of gestation, VitD supplementation at >14 days of age, and achievement of TEN beyond 28 days of age were independent risk factors for MBD (P < .05).Level of Evidence: IV

Extra-skeletal impact of vitamin D supplementation protocol in an adult population with cystic fibrosis

Due to lack of vitamin D absorption in patients with cystic fibrosis (CF), vitamin D supplementation becomes necessary. Our aim was to study the association between serum vitamin D levels and key clinical factors, such as nutritional status, pulmonary function and pulmonary exacerbations (PEx) frequency, in an adult CF population. Prospective analysis of a published vitamin D (VitD3) supplementation protocol (N=200 adult patients) over a follow-up period of 5 years. Data were collected from the medical files before (baseline) and after (follow-up) the implementation of the VitD3 supplementation protocol, between 2009 and 2014. Serum samples to measure vitamin D were also collected at baseline and follow-up. A positive relationship between serum vitamin D and lung function was observed at baseline (R=0.158, P=0.027), but it disappeared at follow-up (P=0.454). There was no association between serum vitamin D levels and body mass index. At follow-up, patients with significantly higher serum vitamin D levels were women, older in age, had CF-related diabetes or had a history of recurring PEx. No direct link was observed between heightened serum vitamin D and lung function or BMI in an adult CF population. We suggest that better compliance to treatments and closer follow-up from health professionals could partially explain why such patients reached higher vitamin D serum levels.

Isolated vitamin D supplementation improves the immune-inflammatory biomarkers in younger postmenopausal women: a randomized, double-blind, placebo-controlled trial.

The aim of this study was to evaluate the effect of vitamin D (VitD) supplementation on immune-inflammatory biomarkers in younger postmenopausal women. In this double-blind, placebo-controlled trial, 160 postmenopausal women aged 50 to 65 years with amenorrhea ≥12 months were randomized into two groups: VitD group, oral supplementation with 1000 IU VitD3/day (n = 80) or placebo group (n = 80). The intervention time was 9 months, and the women were assessed at baseline and endpoint. Serum levels of interleukins (ILs)-1β, IL-5, IL-6, IL-10, IL-12ρ70, IL-17α, tumor necrosis factor-alpha, and interferon-gamma were determined by immunoassay. Plasma concentrations of 25-hydroxyvitamin D [25(OH)D] were measured by high-performance liquid chromatography. Per-protocol analysis was adopted as the statistical method using a gamma distribution and repeated measures design, followed by Wald's multiple comparisons test. The two groups were similar at baseline in terms of clinical and laboratory parameters. After 9 months, there was a significant increase of 25(OH)D levels in the VitD group (+45.4%, P < 0.001) and a decrease (-18.5%, P = 0.049) in the placebo group. A significant decrease in IL-5, IL-12p70, IL-17α, tumor necrosis factor-alpha, and interferon-gamma levels was observed in the VitD group (P < 0.05). IL-5 and IL-6 levels were significantly lower in the VitD group compared to the placebo group (P < 0.05). There were no significant intervention effects on serum IL-1β or IL-10 levels in either group (P > 0.05). In younger postmenopausal women, isolated supplementation with 1000 IU of VitD3 for 9 months was associated with a reduction in proinflammatory biomarkers.

Sex-Specific Gene-by-Vitamin D Interactions Regulate Susceptibility to Central Nervous System Autoimmunity.

Vitamin D3 (VitD) insufficiency is postulated to represent a major modifiable risk factor for multiple sclerosis (MS). While low VitD levels strongly correlate with higher MS risk in white populations, this is not the case for other ethnic groups, suggesting the existence of a genetic component. Moreover, VitD supplementation studies in MS so far have not shown a consistent benefit. We sought to determine whether direct manipulation of VitD levels modulates central nervous system autoimmune disease in a sex-by-genotype-dependent manner. To this end, we used a dietary model of VitD modulation, together with the autoimmune animal model of MS, experimental autoimmune encephalomyelitis (EAE). To assess the impact of genotype-by-VitD interactions on EAE susceptibility, we utilized a chromosome substitution (consomic) mouse model that incorporates the genetic diversity of wild-derived PWD/PhJ mice. High VitD was protective in EAE in female, but not male C57BL/6J (B6) mice, and had no effect in EAE-resistant PWD/PhJ (PWD) mice. EAE protection was accompanied by sex- and genotype-specific suppression of proinflammatory transcriptional programs in CD4 T effector cells, but not CD4 regulatory T cells. Decreased expression of proinflammatory genes was observed with high VitD in female CD4 T effector cells, specifically implicating a key role of MHC class II genes, interferon gamma, and Th1 cell-mediated neuroinflammation. In consomic strains, effects of VitD on EAE were also sex- and genotype dependent, whereby high VitD: (1) was protective, (2) had no effect, and (3) unexpectedly had disease-exacerbating effects. Systemic levels of 25(OH)D differed across consomic strains, with higher levels associated with EAE protection only in females. Analysis of expression of key known VitD metabolism genes between B6 and PWD mice revealed that their expression is genetically determined and sex specific and implicated Cyp27b1 and Vdr as candidate genes responsible for differential EAE responses to VitD modulation. Taken together, our results support the observation that the association between VitD status and MS susceptibility is genotype dependent and suggest that the outcome of VitD status in MS is determined by gene-by-sex interactions.

SUPPLEMENTATION OF VITAMIN D IN HYPERTENSIVE PATIENTS WITH CKD STAGE 3 AND VITAMIN D-DEFICIENCY DOES NOT IMPROVE ARTERIAL STIFFNESS

Objective: Elevated arterial stiffness has been described in hypertensive patients with CKD stage 3 and Vitamin D-deficiency in population-based cross-sectional studies. However, the role of supplementation in improving pulse wave velocity is controversial in most published series. Aim of this study is to analyze if the supplementation of VitD in never before treated hypertensive patients with CKD stage 3 and Vitamin D-deficiency modifies arterial stiffness. Design and method: Longitudinal study in the Hypertension Unit of a district hospital in 221 consecutive hypertensive patients with CKD stage 3 (CKD- EPI 30 – 60 ml/min), not treated before with VitD and with VitD-levels < 20 ng/ml. Arterial stiffness was measured as Pulse Wave Velocity (PWV, m/s) and Augmentation Index (%) in all the patients by brachial oscillometry (MOBIL-O-GRAPH®, IEM, Stolberg, Germany). Oral Calcifediol (266 mircrog/month) was prescribed to all the patients. A follow-up visit was performed after 12 months. Results: 126 (57%) patients were women, 95 men (43%). Mean age was 74.5 (SD ± 9.5), years, renal function measured by CKD-EPI was 49.3 ml/min (SD ± 7.2), BP averaged 130/66 mmHg, mean number of antihypertensive drugs was 3,5. Mean levels of baseline VitD were 15.6 ng/ml (SD ± 6.6), mean PWV was 11.0 m/s (SD ± 1.8). At follow-up after one year, mean levels of VitD in the whole group increased to 24.2 (DE ± 11.5), PWV was 11.1 m/s (DE ± 1.8). 63.8% of the patients were still under supplementation with VitD at follow-up while 36.2% had stopped the treatment. In the former, VitD increased to 29.0 ng/ml versus 15.3 ng/ml in the latter. Although the significant difference between those patients who kept the treatment and those who stopped were highly significant, no significant change of PWV was found between the two groups at follow-up. Conclusions: Correction of VitD-deficiency in hypertensive patients with CKD stage 3 and Vitamin D-deficiency is readily feasible, but in our study it did not translate into a significant change in vascular damage, measured as decrease of PWV, suggesting that the relationship between variables of arterial stiffness and VitD metabolism is not causal.

Vitamin D replacement ameliorates serum lipoprotein functions, adipokine profile and subclinical atherosclerosis in pre-menopausal women

Background and aimsLow vitamin D (vitD) has been linked to increased cardiovascular (CV) risk, but the effects of vitD supplementation are not clarified. We evaluated the impact of vitD normalization on HDL cholesterol efflux capacity (CEC), which inversely correlates with CV risk, the proatherogenic serum cholesterol loading capacity (CLC), adipokine profile and subclinical atherosclerosis. Methods and resultsHealthy premenopausal women with vitD deficiency (n = 31) underwent supplementation. Subclinical atherosclerosis was evaluated by flow-mediated dilation (FMD), pulse wave velocity (PWV) and augmentation index (AIx), measured with standard techniques. HDL CEC and serum CLC were measured by a radioisotopic and fluorimetric assay, respectively. Malondialdehyde (MDA) in HDL was quantified by the TBARS assay. Pre-β HDL was assessed by 2D-electrophoresis. Serum adipokines were measured by ELISA.VitD replacement restored normal levels of serum 25-hydroxyvitamin D (25OHD) and significantly improved FMD (+4%; p < 0.001), PWV (−4.1%: p < 0.001) and AIx (−16.1%; p < 0.001). Total CEC was significantly improved (+19.5%; p = 0.003), with a specific increase in the ABCA1-mediated CEC (+70.8%; p < 0.001). HDL-MDA slightly but significantly decreased (−9.6%; p = 0.027), while no difference was detected in pre-β HDL. No change was observed in aqueous diffusion nor in the ABCG1-mediated CEC. Serum CLC was significantly reduced (−13.3%; p = 0.026). Levels of adiponectin were increased (+50.6%; p < 0.0001) and resistin levels were decreased (−24.3%; p < 0.0001). After vitD replacement, an inverse relationship was found linking the ABCA1-mediated CEC with pre-β HDL (r2 = 0.346; p < 0.001) and resistin (r2 = 0.220; p = 0.009). ConclusionOur data support vitD supplementation for CV risk prevention.

Continued Interest and Controversy: Vitamin D in HIV

Vitamin D (VitD) deficiency is highly prevalent among HIV-infected individuals. Given the overlapping risk for several chronic disease and immunomodulatory outcomes from both long-standing HIV and VitD deficiency, there is great interest in clarifying the clinical role of VitD for this population. Recent studies have expanded our knowledge regarding the epidemiology and mechanisms of VitD deficiency-associated outcomes in the setting of HIV. Clinical trials focusing on VitD supplementation have demonstrated a positive impact on bone mineral density in subgroups of HIV-infected individuals initiating ART or on suppressive ART regimens; however, significant heterogeneity exists between studies and data are less consistent with other clinical outcomes. Further research is needed to clarify uncertainly in several domains, including identifying patients at greatest risk for poor outcomes from VitD deficiency, standardizing definitions and measurement techniques, and better quantifying the benefits and risks of VitD supplementation across different demographic strata for skeletal and extra-skeletal outcomes.

Maternal vitamin D deficiency increases the risk of adverse neonatal outcomes in the Chinese population: A prospective cohort study.

BackgroundAlthough vitamin D (vitD) deficiency is a common problem in pregnant women, in China, few studies have focused on the relationship between maternal vitD deficiency throughout the three trimesters and subsequent neonatal outcomes in China.MethodsBetween 2015 and 2016, maternal serum and neonate cord blood samples were collected from 1978 mother-neonate pairs from Liuzhou city.ResultsThe mean concentrations of 25-hydroxy vitD (25(OH)D) were 16.17±6.27 and 15.23±5.43 ng/ml in the mother and neonate groups, respectively, and the prevalence values of vitD deficiency in the two groups were 78.18% and 83.27%, respectively. Logistic regression showed that maternal vitD deficiency independently increased the risk of gestational diabetes mellitus (GDM) (adjust OR, aOR 1.08; P = 0.026). A relatively lower risk of vitD deficiency was observed in the third trimester than in the first and second trimester (aOR 0.80; P = 0.004). VitD-calcium cosupplementation during pregnancy improves the vitD deficiency in both the maternal and neonatal groups (aOR 0.56, 0.66; P<0.001 and 0.021, respectively). Maternal vitD deficiency significantly increased the risk of neonatal low birth weight (LBW) (aOR 2.83; P = 0.005) and small-for-gestational-age (SGA) (aOR 1.17; P = 0.015). There was a positive correlation between maternal and neonatal vitD deficiency (r = 0.879, P<0.001). VitD supplementation during pregnancy significantly reduced the risk of giving birth to LBW infants (OR = 0.47, 95%CI = 0.33–0.68, P<0.001).ConclusionsFurther research focusing on the consumption of vitD with calcium during pregnancy and the consequential clinical outcomes in Chinese pregnant women is warranted.

Epidemic Vitamin D Deficiency in Prisoners Compared to the German Population: An Analysis Based on Laboratory Results

Effects of long-term imprisonment on the vitamin D (vitD) status of prison inmates in Germany have not been systematically assessed so far. Special circumstances in prisons - little sunlight exposure combined with restricted outdoor activities - may lead to vitD deficiency among prisoners. The aim of this study was to assess the vitD status of prisoners and the general population in order to quantify the extent of vitD deficiency in both groups. VitD status (25(OH)D in blood serum samples) was assessed in female inmates of a prison in southern Germany between May 2012-June 2013. Suboptimal vitD status was defined as levels of 10-<20 µg/l, severe deficiency as<10 µg/l. A systematic literature search in PubMed was conducted in order to compare study results with vitD levels in the general population. Blood sera of 84 inmates (median age: 43 years; range: 19-75) were analyzed. Thirty women (36%) showed severe vitD deficiency, 47 (56%) suboptimal vitD levels. The literature search identified 10 studies which reported considerable vitD deficiency in the general population in Germany. VitD deficiency is very common in both prison inmates and the general population. Unlike prison inmates, the population is able to decide whether, when and how long they want to exposure to sunlight. Moreover, they can counteract deficiency via a nutrition rich in vitD. This is not possible for inmates. To prevent long-term effects of vitD deficiency, intake of vitD supplements during duration of imprisonment seems reasonable.

Comparison of Vitamin D Serum Values between Rheumatoid Arthritis and Lupus Populations: An Observational Study.

Background:In recent years, the role of Vitamin D (VitD), as an immunomedulator in autoimmune diseases, has been evaluated in basic science and practice. There is a considerable volume of data on the effect of VitD position in lupus and rheumatoid arthritis exacerbation.Objective:This study aims to compare VitD serum values in lupus (SLE) and Rheumatoid Arthritis (RA) in the geographical region of northeastern Iran.Methods:Lupus and RA Patients were selected with various disease activity levels. All the patients received an equal amount of VitD supplementation and were selected by the same inclusion and exclusion criteria. VitD serum values were measured by a commercial ELISA kit. Data were analyzed in SPSS-15.Results:A total of 148 SLE and 156 RA patients were studied. VitD serum levels were 66.54±41.2 nmol/l in the SLE group and 83.74±46.45 nmol/l in the RA group. Statistical analysis showed that VitD serum levels were lower in lupus patients than RA ones (p=0.006).Conclusion: Since VitD deficiency is very common in Iran, physiologic doses of VitD supplementation in patients lead to higher serum levels of VitD. Lower VitD values in lupus patients compared with RA ones may stem from intestinal malabsorption, higher doses of corticosteroid therapy, renal involvement and proteinuria, different polymorphisms of VitD receptors, and more sun protection strategies in lupus patients.

Treatment of vitamin D deficiency in Chinese inflammatory bowel disease patients: A prospective, randomized, open-label, pilot study.

To assess the necessity and efficacy of vitamin D (VitD) supplementation in Chinese ulcerative colitis (UC) and Crohn's disease (CD) patients with vitamin D insufficiency/deficiency. UC and CD patients were randomly assigned into one of the three arms for 12 months: arm A (VitD3 150 000 IU once per 3 months plus elemental calcium 200 mg thrice daily), arm B (elemental calcium 200 mg thrice daily) and arm C (vehicle control group), in addition to conventional treatment. Improvement in 25-hydroxyvitamin D [25(OH)D] level was the primary outcome of the study. Secondary outcomes were changes in bone mineral density (BMD) and disease activity. Sixty-five UC and 59 CD patients completed the study. The difference in the pre-and post-treatment 25(OH)D [Δ25(OH)D] of arm A was significantly higher than in arm B or C (UC: 17.47 ± 13.01 ng/mL vs 5.30 ± 6.28 ng/mL or 2.02 ± 6.19 ng/mL, P < 0.001; CD: 12.47 ± 9.15 ng/mL vs 4.73 ± 6.97 ng/mL or 1.36 ± 4.75 ng/mL, P < 0.01). There was no significant difference between pre- and post-treatment BMD and disease activity in arm A compared to those in arms B and C (P > 0.05). Although the Mayo score and Crohn's disease activity index decreased by conventional treatment, serum 25(OH)D did not improve in arm C without vitamin D supplementation (P > 0.05). VitD supplementation is necessary to treat hypovitaminosis D in UC and CD patients, even with background amelioration of disease activity.

OP-374 - Preventive Effect of Preoperative Vitamin D Supplementation on Postoperative Atrial Fibrillation

Objective: The effect of preoperative vitamin D (vitD) supplementation on postoperative atrial fibrillation has not been evaluated. Therefore, we assessed the relationship between the preoperative vitD supplementation and development of atrial fibrillation after CABG (POAF).

Vitamin D in Human Immunodeficiency Virus Infection: Influence on Immunity and Disease.

People living with human immunodeficiency virus (HIV) infection typically have hypovitaminosis D, which is linked to a large number of pathologies, including immune disorders and infectious diseases. Vitamin D (VitD) is a key regulator of host defense against infections by activating genes and pathways that enhance innate and adaptive immunity. VitD mediates its biological effects by binding to the Vitamin D receptor (VDR), and activating and regulating multiple cellular pathways. Single nucleotide polymorphisms in genes from those pathways have been associated with protection from HIV-1 infection. High levels of VitD and VDR expression are also associated with natural resistance to HIV-1 infection. Conversely, VitD deficiency is linked to more inflammation and immune activation, low peripheral blood CD4+ T-cells, faster progression of HIV disease, and shorter survival time in HIV-infected patients. VitD supplementation and restoration to normal values in HIV-infected patients may improve immunologic recovery during combination antiretroviral therapy, reduce levels of inflammation and immune activation, and increase immunity against pathogens. Additionally, VitD may protect against the development of immune reconstitution inflammatory syndrome events, pulmonary tuberculosis, and mortality among HIV-infected patients. In summary, this review suggests that VitD deficiency may contribute to the pathogenesis of HIV infection. Also, VitD supplementation seems to reverse some alterations of the immune system, supporting the use of VitD supplementation as prophylaxis, especially in individuals with more severe VitD deficiency.

ACUTE EFFECTS OF CARDIAC SURGERY ON 25 (OH) VITAMIN D (VITD) LEVELS AND RESPONSE TO VITD SUPPLEMENTATION: PRIMARY RESULTS OF THE ASSESS-D STUDY

Acute myocardial infarction (AMI) pts have significantly lower blood levels of vitamin D (VitD) than controls. Whether low VitD levels contribute to causing or exacerbating AMI or are simply a result of the acute AMI response, and how effective preemptive VitD supplementation (VitD-S) is on

A profile of body composition, omega-3 and vitamin D in National Football League players.

Body composition (percent body fat [%BF]), omega-3 fatty acids, and vitamin D (VitD) status are important components of an athlete's individual physiological profile, as each measure has potential to influence performance, inflammation, and injury recovery. The purpose of this study was to characterize %BF, omega-3, and VitD in a subset of professional football athletes. Secondary analyses investigated changes in %BF, omega-3, and VitD, throughout a competitive season, and evaluated the relationship between physiological variables, race, and injury prevalence. Forty-two professional football players (age: 24.0±2.4 years; height: 186.8±5.9 cm; weight: 108.8±19.4 kg) volunteered to participate. A-mode ultrasonography measured %BF and the percentage of highly unsaturated fatty acid content comprised of omega-3s was determined by an omega-3 bloodspot test. VitD levels and injury prevalence were obtained from the team athletic trainer. Omega-3 was moderately correlated with VitD (R=0.397, P=0.030). Throughout the season there was a significant decrease in omega-3 percentage (∆=-2.47±5.48%, P=0.030), no change in body composition (∆=0.26±1.97%, P=0.482) and a significant increase in VitD (∆=9.03±19.46 ng/mL, P=0.015). VitD was significantly higher in white athletes (48.00±13.73 ng/mL) than black athletes (27.09±9.28 ng/mL; P<0.001) and athletes of other races (23.33±4.73 ng/mL; P=0.004). Throughout the season, %BF was maintained, VitD levels increased, and omega-3 decreased. White athletes had significantly higher VitD levels than athletes of all other races. There were no differences in the physiological variables between injury severity categories. The results from the current study provides support for the potential importance of VitD and omega-3 supplementation for professional football athletes.

Vitamin D Enhances Alveolar Development in Antenatal Lipopolysaccharide-Treated Rats through the Suppression of Interferon-γ Production.

Bronchopulmonary dysplasia (BPD) is characterized by the premature arrest of alveolar development. Antenatal exposure to inflammation inhibits lung morphogenesis, thereby increasing the risk for the development of BPD. Here, we investigated whether vitamin D (VitD) enhances alveolar development in antenatal lipopolysaccharide (LPS)-treated rats, which is a model for BPD. We used an established animal model of BPD, and random assignment to the control group, LPS group, or LPS with VitD group. Levels of interferon (IFN)-γ and interleukin-4 were detected by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay. IFN-γ producing CD8+ T cells were assessed by flow cytometry, and the methylation status of the VitD-response element (VDRE) was analyzed by bisulfite sequencing PCR. 25-hydroxyvitamin D levels were measured by liquid chromatography tandem mass spectrometry in maternal serum samples collected from 86 pregnant women in a prospective birth cohort enrolled from 2012 to 2013. Our results showed that VitD effectively alleviated the simplification of the lung alveolar structure in BPD rats and suppressed LPS-induced IFN-γ expression in the lung and spleen tissues. Further investigation revealed that VitD suppressed IFN-γ production in CD8+ T cells. Specifically, VitD increased the methylation percentage of the VDRE in the IFN-γ-promoter region and suppressed LPS-induced expression of IFN-γ. Additionally, we observed an association between maternal VitD exposure during pregnancy and neonatal IFN-γ levels in a prospective birth cohort, with a trend similar to that observed in the animal model. Our data suggested that supplementation of VitD could suppress IFN-γ production, resulting in improved alveolar development in an LPS-induced BPD rat model.