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Background The causal relationship between the level of serum 25-hydroxyvitamin D [25(OH)D] and the risk of erectile dysfunction (ED) is still unclear. Aim We tried to determine the causal relationship between the level of serum 25(OH)D and ED risk. Methods In this study, we used genome-wide association study data from the UK Biobank to analyse the relationship between serum 25(OH)D (as the exposure) and ED (as the outcome). Linkage disequilibrium score regression (LDSC) was used to assess the genetic correlation between 2 traits. The CAUSE (Causal Analysis using Summary Effect estimates) method and Mendelian randomization (MR) were employed to evaluate the bidirectional causal relationship. The MRlap method was utilized to assess the impact of sample overlap on the results. To assess potential heterogeneity and horizontal pleiotropy, we utilized methods such as MR-Egger, MR-PRESSO (Mendelian Randomization Pleiotropy Residual Sum and Outlier), weighted median, and others. Outcomes The primary outcome was defined as self or physician-reported ED, or using oral ED medication, or a history of surgery related to ED. Results The LDSC analysis did not reveal a significant genetic correlation between serum 25(OH)D and ED (rg = 0.2787, P =.3536). Additionally, the CAUSE (P value testing that the causal model is a better fit >.05) and MR analyses (odds ratio, 0.8951; 95% confidence interval, 0.7480-1.0710; P =.2260) did not support a causal relationship between 25(OH)D and ED, and our study did not detect any heterogeneity and pleiotropy. Clinical implications This study provides evidence on whether vitamin D needs to be ingested to prevent or treat ED. Strengths and limitations We used LDSC and MR to avoid bias. However, the population in this study was limited to European ancestry. Conclusion No causal relationship was found between 25(OH)D and ED. [ABSTRACT FROM AUTHOR]

Background The association between vitamin D and dementia risk in those with prediabetes remains uncertain. We aimed to evaluate the association of serum 25-hydroxyvitamin D (25OHD) with incident dementia among older adults with prediabetes, and examine whether apolipoprotein E (APOE) genotypes, vitamin D receptor (VDR), and vitamin-D-binding protein (VDBP) gene polymorphisms may modify this association. Methods A total of 34 237 participants aged ≥60 with prediabetes (HbA1c <6.5% and ≥5.7%) and without dementia at baseline were included from the UK Biobank. Serum 25-hydroxyvitamin D (25OHD) was measured using chemiluminescent immunoassay method. The primary outcome was incident all-cause dementia. Secondary outcomes included incident Alzheimer's disease (AD) and vascular dementia, respectively. The VDR and VDBP gene polymorphisms included single nucleotide polymorphisms of rs7975232, rs1544410, rs2228570, rs731236, and rs7041, rs4588, respectively. Results During a median follow-up of 11.8 years, 941 (2.7%) participants developed incident all-cause dementia. Overall, serum 25OHD was inversely associated with all-cause dementia (per standard deviation increment, adjusted hazard ratio: 0.82; 95% confidence interval: 0.75, 0.89). Similar trends were found for incident AD and vascular dementia. Furthermore, there was a stronger inverse relationship between serum 25OHD and all-cause dementia among VDR rs7975232 C allele noncarriers (p -interaction < 0.05). However, APOE Ɛ4, other VDR, and VDBP gene polymorphisms did not significantly modify the relation of serum 25OHD with incident all-cause dementia (all p -interactions >.05). Conclusions There was an inverse association between serum 25OHD and incident dementia among older adults with prediabetes, especially in VDR rs7975232 AA allele carriers. [ABSTRACT FROM AUTHOR]

Context Findings of previous observational studies that examined the association between circulating vitamin D levels and lipid profiles have been inconsistent. Objective A dose-response meta-analysis of epidemiologic studies was conducted to investigate the relationship between serum 25-hydroxyvitamin D levels and dyslipidemia in adults. Data Sources Electronic databases were searched systematically for articles published up to June 2021. Data Extraction Fifty-seven observational studies and 2 cohort studies that reported odds ratios (ORs) or relative risks (RRs) with 95%CIs for dyslipidemia in relation to serum 25-hydroxyvitamin D levels in adults were included. Data Analysis A high level, vs a low level, of serum 25-hydroxyvitamin D was related to a significant 19% decrease in the odds of hypertriglyceridemia (OR 0.81; 95%CI, 0.74–0.89), an 18% reduction in low high-density lipoprotein cholesterol (HDL-C) (OR 0.82; 95%CI, 0.76–0.89), and an 18% reduction in dyslipidemia (OR 0.82; 95%CI, 0.75–0.91). No significant association was found between a high vs a low level of serum 25-hydroxyvitamin D and risk of high low-density lipoprotein cholesterol (LDL-C) levels (OR 0.86; 95%CI, 0.62–1.19) or hypercholesterolemia (OR 1.03; 95%CI, 0.93–1.15). Dose-response analyses demonstrated that each 10 ng/mL increase in the serum 25-hydroxyvitamin D level was linked, respectively, to a 7% (OR 0.93;95%CI, 0.85–1.02), a 3% (OR 0.97; 95%CI, 0.90–1.05), and a 4% (OR 0.96; 95%CI, 0.92–1.00) marginally significant decrease in the odds of hypertriglyceridemia, low HDL-C, and dyslipidemia. Conclusion Higher serum 25-hydroxyvitamin D levels are associated with significant reductions in the odds of hypertriglyceridemia, low HDL-C, and dyslipidemia in a dose-response trend. Systematic Review Registration PROSPERO registration no. CRD42021219484. [ABSTRACT FROM AUTHOR]

Objectives: Studies in Canada have reported varying prevalences of low serum 25-hydroxyvitamin D (25(OH)D) levels, but none have been conducted in rural paediatric populations. The purpose of this study was to determine the prevalence and predictors of low vitamin D levels in rural communities. Methods: We conducted a cross-sectional study of children aged 3 to 15 living in Canadian Hutterite communities. Serum 25(OH)D levels were measured between October 2008 and April 2009 using a chemiluminescence assay. Predictors of vitamin D levels were evaluated using multivariable linear regression. A multilevel model was used to evaluate the impact of individual, household and colony factors on the variation in vitamin D levels. Results: Serum 25(OH)D levels were available on 743 children/adolescents. The median was 62.0 nmol/L (interquartile range 51.0, 74.0). Levels lower than 50 nmol/L and 75 nmol/L were found in 152 (20.5%) and 565 (76%) children, respectively. Adolescents were at highest risk for levels <75 nmol/L (odds ratio 3.38, 95% confidence interval 2.00, 5.80). Age and latitude were negatively correlated with serum 25(OH)D level. In the multilevel model, most of the variation in levels was associated with individual children. Conclusion: Low vitamin D levels are a significant problem in rural Hutterite communities in Canada. Adolescents were at greatest risk for low levels and represent an important target group for supplementation. Variation in serum 25(OH)D levels was explained mostly at the individual level. Additional studies are needed to explore factors associated with individuals (e.g., genetics) leading to lower 25(OH)D levels. [ABSTRACT FROM AUTHOR]

Respiratory tract infections (RTIs) are very common worldwide. We prospectively demonstrate an association between low serum 25-hydroxyvitamin D level and increased risk of laboratory-confirmed viral upper RTI in children. Future studies should evaluate the role of supplementation to reduce RTIs.Background. Vitamin D may be important for immune function. Studies to date have shown an inconsistent association between vitamin D and infection with respiratory viruses. The purpose of this study was to determine if serum 25-hydroxyvitamin D (25(OH)D) was associated with laboratory-confirmed viral respiratory tract infections (RTIs) in children.Methods. Serum 25(OH)D levels were measured at baseline and children from Canadian Hutterite communities were followed prospectively during the respiratory virus season. Nasopharyngeal specimens were obtained if symptoms developed and infections were confirmed using polymerase chain reaction. The association between serum 25(OH)D and time to laboratory-confirmed viral RTI was evaluated using a Cox proportional hazards model.Results. Seven hundred forty-three children aged 3–15 years were followed between 22 December 2008 and 23 June 2009. The median serum 25(OH)D level was 62.0 nmol/L (interquartile range, 51.0–74.0). A total of 229 participants (31%) developed at least 1 laboratory-confirmed viral RTI. Younger age and lower serum 25(OH)D levels were associated with increased risk of viral RTI. Serum 25(OH)D levels <75 nmol/L increased the risk of viral RTI by 50% (hazard ratio [HR], 1.51; 95% confidence interval [CI], 1.10–2.07, P = .011) and levels <50 nmol/L increased the risk by 70% (HR, 1.67; 95% CI, 1.16–2.40, P = .006).Conclusions. Lower serum 25(OH)D levels were associated with increased risk of laboratory-confirmed viral RTI in children from Canadian Hutterite communities. Interventional studies evaluating the role of vitamin D supplementation to reduce the burden of viral RTIs are warranted. [ABSTRACT FROM AUTHOR]

The effects of vitamin D and parathyroid hormone (PTH) levels on incident fracture remain uncertain. To test the hypothesis that increasing serum 25-hydroxyvitamin D [25(OH)D] and decreasing PTH levels are associated with decreased risk of hip and any nonspine fracture, we conducted a prospective cohort study among 2614 community-dwelling white and black participants, aged ≥70 years, from the Health, Aging and Body Composition (Health ABC) Study. Serum and plasma samples were drawn at year 2, which formed the baseline for this analysis. Serum 25(OH)D and intact PTH (1-84) were measured using radioimmunoassay with DiaSorin reagents and EDTA plasma with a two-site immunoradiometric assay kit, respectively. Incident fractures (hip and any nonspine) were assessed after year 2, every 6 months, by self-report and validated by radiology reports. The median (interquartile range) follow-up times for hip and any nonspine fractures were 6.4 (6.1-6.5) and 6.4 (5.5-6.5) years, respectively. Cox proportional hazards regression was used to estimate the hazard ratios (HR) with 95% confidence intervals (CI) for fracture. There were 84 hip and 247 nonspine fractures that occurred over the follow-up period. The multivariable adjusted HRs (95% CIs) of hip fracture for participants in the lowest (≤17.78 ng/mL), second (17.79 to 24.36 ng/mL), and third quartiles (24.37 to 31.94 ng/mL) of 25(OH)D were 1.92 (0.97 to 3.83), 0.75 (0.32 to 1.72) and 1.86 (1.00 to 3.45), respectively, compared with participants in the highest 25(OH)D quartile (>31.94 ng/mL) ( p trend = 0.217). Additional adjustment for IL-6 ( p = 0.107), PTH ( p = 0.124), and hip areal bone mineral density ( p = 0.137) attenuated HRs of hip fracture in the lowest quartile by 16.3%, 17.4%, and 26.1%, respectively. There was no evidence of an association between 25(OH)D and any nonspine fractures, or between PTH and hip or any nonspine fractures. We found limited evidence to support an association between calciotropic hormones and hip and nonspine fractures in older men and women. © 2012 American Society for Bone and Mineral Research. [ABSTRACT FROM AUTHOR]

Background. Recent European studies suggest that vitamin D deficiency may be associated with increased odds of cognitive impairment in older persons, although findings from the United States are equivocal. Our objective was to investigate the association between vitamin D deficiency and cognitive impairment in the elderly U.S. population. Methods. Three thousand and three hundred twenty-five adults aged 65 years or more completed cognitive assessments, medical examinations, and physical performance measures and provided blood samples in the Third National Health and Nutrition Examination Survey, a nationally representative cross-sectional study of the U.S. noninstitutionalized population. We determined whether low levels of serum 25-hydroxyvitamin D (25(OH)D) were associated with increased odds of cognitive impairment using logistic regression models. Cognitive impairment was assessed using measures of immediate and delayed verbal memory, orientation, and attention (impairment was defined as the worst 10% of the distribution of combined scores). Results. The multivariate adjusted odds ratios (95% confidence interval) of cognitive impairment in participants who were 25(OH)D insufficient (≥50 < 75 nmol/L), deficient (≥25 < 50 nmol/L), and severely deficient (<25 nmol/L) in comparison with those sufficient (≥75 nmol/L) were 0.9 (0.6–1.3), 1.4 (1.0–2.1), and 3.9 (1.5–10.4), respectively (p for linear trend = .02). Log-transformed levels of 25(OH)D were also significantly associated with the odds of cognitive impairment (p = .02). Conclusions. These findings suggest that vitamin D deficiency is associated with increased odds of cognitive impairment in the elderly U.S. population. Further exploration of a possible causal relationship between vitamin D deficiency and cognitive impairment is warranted. [ABSTRACT FROM PUBLISHER]