Vitamin D in healthy Tunisian population: Preliminary results

BackgroundVitamin D deficiency is one of the most common medical conditions worldwide. In Tunisia, several studies evaluated Vitamin D status, but this was concerning specific populations (pregnant women, obese or diabetic patients and children with asthma). The only study that evaluated Vitamin D status in a healthy Tunisian population was conducted by Meddeb and associeties in 2002. The update of data available, based on the currently recommended limits, is necessary. This study aimed to estimate the prevalence of hypovitaminosis D in a healthy Tunisian population, and correlate the values with potential risk factors.MethodsIt was conducted on 209 Tunisian healthy subjects. Data collected included clinical characteristics and dietary intakes. We measured 25-hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH), glycemia, creatinine, calcium, phosphorus, and alkaline phosphatase concentrations. Hypovitaminosis D was retained for 25(OH)D concentrations <75 nmol/L. Vitamin D deficiency was defined by 25(OH)D concentrations <25 nmol/L.ResultsThe prevalence of hypovitaminosis D and vitamin D deficiency were respectively 92.3% and 47.6%. The main factors that were significantly associated with low vitamin D levels in our multivariate analysis were veiling, living in rural areas and sunscreen use. However, sex, age, socioeconomic level, phototype, solar exposure score, smoking and bone mass index, were not statistically associated with hypovitaminosis D. The study of relationship between vitamin D status and serum PTH levels showed a significative and negative correlation (P < 0.005).ConclusionsGiven the high prevalence of vitamin D, an adapted health policy is essential. A widespread vitamin D supplementation and food fortification seems to be necessary in Tunisia.     

Impact of Vitamin D Replacement on Markers of Glucose Metabolism and Cardio-Metabolic Risk in Women with Former Gestational Diabetes—A Double-Blind,Randomized Controlled Trial

Gestational Diabetes Mellitus (GDM) and vitamin D deficiency are related to insulin resistance and impaired beta cell function, with heightened risk for future development of diabetes. We evaluated the impact of vitamin D supplementation on markers of glucose metabolism and cardio metabolic risk in Asian women with former GDM and hypovitaminosis D. In this double blind, randomized controlled trial, 26 participants were randomized to receive either daily 4000 IU vitamin D3 or placebo capsules. 75g Oral Glucose Tolerance Test (OGTT) and biochemistry profiles were performed at baseline and 6 month visits. Mathematical models, using serial glucose, insulin and C peptide measurements from OGTT, were employed to calculate insulin sensitivity and beta cell function. Thirty three (76%) women with former GDM screened had vitamin D level of <50 nmol/L at baseline. Supplementation, when compared with placebo, resulted in increased vitamin D level (+51.1 nmol/L vs 0.2 nmol/L, p<0.001) and increased fasting insulin (+20% vs 18%, p = 0.034). The vitamin D group also demonstrated a 30% improvement in disposition index and an absolute 0.2% (2 mmol/mol) reduction in HbA_1c. There was no clear change in insulin sensitivity or markers of cardio metabolic risk. This study highlighted high prevalence of vitamin D deficiency among Asian women with former GDM. Six months supplementation with 4000 IU of vitamin D3 safely restored the vitamin D level, improved basal pancreatic beta-cell function and ameliorated the metabolic state. There was no effect on markers of cardio metabolic risk. Further mechanistic studies exploring the role of vitamin D supplementation on glucose homeostasis among different ethnicities may be needed to better inform future recommendations for these women with former GDM at high risk of both hypovitaminosis D and future diabetes.     

Vitamin D and disease prevention with special reference to cardiovascular disease

Circulating 25-hydroxyvitamin D [25(OH)D] is the hallmark for determining vitamin D status. Serum parathyroid hormone [PTH] increases progressively when 25(OH)D falls below 75 nmol/l. Concentrations of 25(OH)D below 50 nmol/l or even below 25 nmol/l are frequently observed in various population groups throughout the world. This paper highlights the relationship of vitamin D insufficiency with cardiovascular disease and non-insulin dependent diabetes mellitus, two diseases that account for up to 50% of all deaths in western countries. There is evidence from patients with end-stage renal disease that high PTH concentrations are causally related to cardiovascular morbidity and mortality. Activated vitamin D is able to increase survival in this patient group significantly. Moreover, already slightly enhanced PTH concentrations are associated with ventricular hypertrophy and coronary heart disease in the general population. Experimental studies have demonstrated that a lack of vitamin D action leads to hypertension in mice. Some intervention trials have also shown that vitamin D can reduce blood pressure in hypertensive patients. In young and elderly adults, serum 25(OH)D is inversely correlated with blood glucose concentrations and insulin resistance. Sun-deprived lifestyle, resulting in low cutaneous vitamin D synthesis, is the major factor for an insufficient vitamin D status. Unfortunately, vitamin D content of most foods is negligible. Moreover, fortified foods and over-the-counter supplements usually contain inadequate amounts of vitamin D to increase serum 25(OH)D to 75 nmol/l. As a consequence, legislation has to be changed to allow higher amounts of vitamin D in fortified foods and supplements.     

Vitamin D Deficiency in Unselected Patients from Swiss Primary Care: A Cross-Sectional Study in Two Seasons

Background

As published data on 25-hydroxy-cholecalciferol (25(OH)D) deficiency in primary care settings is scarce, we assessed the prevalence of hypovitaminosis D, potential associations with clinical symptoms, body mass index, age, Vitamin D intake, and skin type in unselected patients from primary care, and the extent of seasonal variations of serum 25(OH)D concentrations.

Methodology/Principal Findings

25(OH)D was measured at the end of summer and/or winter in 1682 consecutive patients from primary care using an enzyme-linked immunosorbant assay. Clinical symptoms were assessed by self-report (visual analogue scale 0 to 10), and vitamin D deficiency was defined as 25(OH)D concentrations < 50 nmol/l. 25(OH)D deficiency was present in 995 (59.2%) patients. 25(OH)D deficient patients reported more intense muscle weakness (visual analogue scale 2.7, 95% confidence interval 2.5 to 2.9) and had a higher body mass index (25.9kg/m², 25.5 to 26.2) than non-deficient patients (2.5, 2.3 to 2.7; and 24.2, 23.9 to 24.5, respectively). 25(OH)D concentrations also weakly correlated with muscle weakness (Spearman’s rho -0.059, 95% confidence interval -0.107 to -0.011) and body mass index (-0.156, -0.202 to -0.108). Self-reported musculoskeletal pain, fatigue, and age were not associated with deficiency, nor with concentrations. Mean 25(OH)D concentrations in patients with vitamin D containing medication were higher (60.6 ± 22.2 nmol/l) than in patients without medication (44.8 ± 19.2 nmol/l, p < 0.0001) but still below the targeted level of 75 nmol/l. Summer and winter 25(OH)D concentrations differed (53.4 ± 19.9 vs. 41.6 ± 19.3nmol/l, p < 0.0001), which was confirmed in a subgroup of 93 patients who were tested in both seasons (p = 0.01).

Conclusion/Significance

Nearly 60% of unselected patients from primary care met the criteria for 25(OH)D deficiency. Self-reported muscle weakness and high body mass index were associated with lower 25(OH)D levels. As expected 25(OH)D concentrations were lower in winter compared to summer.     

Low vitamin D in narcolepsy with cataplexy

Background

Narcolepsy with cataplexy (NC) is currently thought to be an autoimmune-mediated disorder in which environmental risk factors make a significant contribution to its development. It was proposed that vitamin D deficiency plays a role in autoimmune diseases. Here we investigated whether NC can be associated with 25-hydroxyvitamin D (25(OH)D) level deficiency in patients with NC compared with gender- and age-matched normal controls.

Methodology

Serum level of 25 (OH)D was determined in 51 European patients with typical NC compared to 55 age-, gender-, and ethnicity-matched healthy controls. Demographic and clinical data (age at onset, duration and severity of disease at baseline, and treatment intake at time of study) and season of blood sampling were collected to control for confounding variables.

Principal Findings

Serum 25(OH)D concentration was lower in NC compared to controls (median, 59.45 nmol/l [extreme values 24.05–124.03] vs. 74.73 nmol/l [26.88–167.48] p = 0.0039). Patients with NC had significantly greater vitamin D deficiency (<75 nmol/l) than controls (72.5% vs 50.9%, p = 0.0238). Division into quartiles of the whole sample revealed that the risk of being affected with NC increased with lower 25(OH)D level, with a 5.34 OR [1.65–17.27] for the lowest quartile (p = 0.0051). Further adjustment for BMI did not modify the strength of the association (OR: 3.63, 95% CI = 1.06–12.46, p = 0.0191). No between BMI and 25(OH)D interaction, and no correlation between 25(OH)D level and disease duration or severity or treatment intake were found in NC.

Conclusion

We found a higher frequency of vitamin D deficiency in NC. Further studies are needed to assess the contribution of hypovitaminosis D to the risk of developing narcolepsy, and to focus on the utility of assessing vitamin D status to correct potential deficiency.     

Abnormalities of Vitamin D and Calcium Metabolism after Surgical Treatment of Morbid Obesity: A Study of 136 Patients

ObjectiveTo assess the effect of bariatric surgical treatment of morbid obesity on bone mineral metabolism.MethodsWe analyzed pertinent vitamin D and calcium metabolic variables in 136 patients who had undergone a malabsorptive bariatric operation. Measurements of bone mineral density (BMD), serum 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D [1,25-(OH)₂D], parathyroid hormone (PTH), calcium, phosphorus, and alkaline phosphatase were performed. Statistical analyses assessed correlations among various factors.ResultsThe mean age (± SD) of the study group was 48.34 ± 10.28 years. Their mean weight loss was 114.55 ± 45.66 lb, and the mean duration since the bariatric surgical procedure was 54.02 ± 51.88 months. Seventeen patients (12.5%) had a T-score of -2.5 or less, and 54 patients (39.7%) had a T-score between –1.0 and –2.5. Of 119 patients in whom serum 25-OHD was measured, 40 (34%) had severe hypovitaminosis D (25-OHD < 8 ng/mL), and 50 patients (42%) had low hypovitaminosis D (serum 25-OHD 8 to 20 ng/mL). The magnitude of weight loss correlated negatively with serum 25-OHD, calcium, phosphorus, and calcium × phosphorus product values and positively with serum alkaline phosphatase level. Serum 25-OHD and calcium concentrations correlated positively with the BMD. PTH, serum 1,25-(OH)₂D, and alkaline phosphatase concentrations correlated negatively with the BMD, a reflection of the presence of secondary hyperparathyroidism, an accelerated conversion of 25-OHD to 1,25-(OH)₂D by the elevated PTH levels, and increased osteoblastic activity. The mean daily vitamin D supplementation was 6,472 ± 9,736 IU.ConclusionHypovitaminosis D and subsequent bone loss are common in patients who have undergone a bariatric surgical procedure for morbid obesity. These patients require rigorous vitamin D supplementation. (Endocr Pract. 2007;13:131-136)     

Outdoor exercise reduces the risk of hypovitaminosis D in the obese

Obesity is associated with lower levels of serum 25-hydroxyvitamin D (25(OH)D). Obese individuals might need higher doses of vitamin D supplementation than the general population. In this cross-sectional study, associations between 25(OH)D serum levels, body mass index (BMI), and outdoor exercise were assessed in a population of 291 ambulatory patients attending the Osteoporosis Center at the University of Miami, mean age 62 ± 13.48 years. Obesity was defined as BMI ≥ 30 kg/m² and hypovitaminosis D as 25(OH)D ≤ 30 ng/ml. Overall, prevalence of obesity was 14.1% and of hypovitaminosis D was 42.4%. Among Hispanics, there was a significantly higher prevalence of hypovitaminosis D in obese (63.2%) compared to non-obese individuals (35.8%). Outdoor exercise had a significant effect on the prevalence of hypovitaminosis D in Hispanics, with a lower prevalence in those performing outdoor exercise (24.1%) compared to those who did not (47.9%). After adjusting for age, gender, and ethnicity, those reporting outdoor exercise were 47% less likely to have hypovitaminosis D, while those with obesity had more than twice the risk. Since outdoor exercise may protect overweight individuals from hypovitaminosis D, prevention programs involving higher doses of vitamin D and/or outdoor exercise may result in additional metabolic and functional benefits in this population.     

Vitamin D in Overweight/Obese Women and Its Relationship With Dietetic and Anthropometric Variables

Overweight/obese persons usually have an inadequate vitamin D status, a situation commonly made worse by an inadequate intake of this vitamin. For this reason, the aim of this study was to analyze dietetic and anthropometric differences in a group of young, overweight/obese Spanish women with respect to their vitamin D status. The study subjects were 66 white Spanish women (aged 20–35 years) with a BMI of 24–35 kg/m². Dietetic, anthropometric, and biochemical data were collected. Women were divided into two groups depending on their serum vitamin D concentrations: LD (women with <90 nmol/l 25(OH)D) and HD (women with ≥90 nmol/l 25(OH)D). The intakes of vitamin D, calcium, and supplements were similar in both groups. The body weight, BMI, and waist circumference of the HD subjects were smaller than those recorded for the LD subjects (68.6 ± 4.2 kg, 26.0 ± 1.3 kg/m², and 79.4 ± 3.4 cm compared to 76.2 ± 9.8, 28.6 ± 3.2 kg/m², and 86.2 ± 9.3 cm, respectively; P < 0.05). The hip circumference and the waist/hip ratio were similar in both groups. A BMI of <27.7 kg/m² (P50) was associated with serum vitamin D concentrations of ≥90 nmol/l (odds ratio = 0.1313; confidence interval: 0.0149–1.1599; P < 0.05). Overweight/obese women are at higher risk of vitamin D deficiency, largely due to excess adiposity rather than inadequate intake.     

Effect of vitamin D3 administration on serum 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3 and osteocalcin in vitamin D-deficient elderly people

In elderly institutionalized people, confined to bedroom and receiving no vitamin D supplementation, the frequency of vitamin D deficiency is found very high. Systematic administration of vitamin D has, therefore, been proposed to correct vitamin D deficiency. Within this context, we studied 40 elderly institutionalized subjects (mean age 80.5 + 7.2 yr) with low 25(OH)D3 concentrations (4.4 + 1.8 micrograms/l). Sixteen of them (Group I) had low serum calcium concentrations (less than 2.3 mmol/l) and 24 (Group II) had normal serum calcium concentrations (from 2.3 to 2.6 mmol/l). As hypocalcemia has been shown to regulate 1,25(OH)D3 production independent of PTH in animals and in humans, we compared their respective responses to the administration of vitamin D3. Subjects received a total dose of 15 mg (600,000 IU) of vitamin D3 divided into 3 i.m. injections at one month intervals and were explored before therapy and one and 6 months after the last dose of vitamin D3. The treatment induced a similar marked rise in 25(OH)D3 levels (from 4.1 + 1.7 to 24.4 + 8.7 micrograms/l for group I and from 5.1 + 1.8 to 27.2 + 8.0 micrograms/l for group II) in both groups but increased the 1,25(OH)2D3 concentrations only in group I (from 22.9 + 6.9 to 32.6 + 11.3 ng/l). Meanwhile serum calcium concentrations rose in group I (to low normal range i.e. 2.31 + 0.07 mmol/l) and were unaffected in group II. These results suggest that hypocalcemia is a potent stimulator of renal 1-hydroxylase in elderly people. Furthermore, a transient significant (P less than 0.01) increase in serum osteocalcin (from 10.6 + 4.1 to 14.1 + 5.9 micrograms/l) could be observed in group I which demonstrates for the first time that the osteocalcin response of osteoblasts to stimulation by 1,25(OH)2D3 is retained in very old people.     

The Importance of Body Weight for the Dose Response Relationship of Oral Vitamin D Supplementation and Serum 25-Hydroxyvitamin D in Healthy Volunteers

Unlike vitamin D recommendations by the Institute of Medicine, the Clinical Practice Guidelines by the Endocrine Society acknowledge body weight differentials and recommend obese subjects be given two to three times more vitamin D to satisfy their body''s vitamin D requirement. However, the Endocrine Society also acknowledges that there are no good studies that clearly justify this. In this study we examined the combined effect of vitamin D supplementation and body weight on serum 25-hydroxyvitamin (25(OH)D) and serum calcium in healthy volunteers. We analyzed 22,214 recordings of vitamin D supplement use and serum 25(OH)D from 17,614 healthy adult volunteers participating in a preventive health program. This program encourages the use of vitamin D supplementation and monitors its use and serum 25(OH)D and serum calcium levels. Participants reported vitamin D supplementation ranging from 0 to 55,000 IU per day and had serum 25(OH)D levels ranging from 10.1 to 394 nmol/L. The dose response relationship between vitamin D supplementation and serum 25(OH)D followed an exponential curve. On average, serum 25(OH)D increased by 12.0 nmol/L per 1,000 IU in the supplementation interval of 0 to 1,000 IU per day and by 1.1 nmol/L per 1,000 IU in the supplementation interval of 15,000 to 20,000 IU per day. BMI, relative to absolute body weight, was found to be the better determinant of 25(OH)D. Relative to normal weight subjects, obese and overweight participants had serum 25(OH)D that were on average 19.8 nmol/L and 8.0 nmol/L lower, respectively (P<0.001). We did not observe any increase in the risk for hypercalcemia with increasing vitamin D supplementation. We recommend vitamin D supplementation be 2 to 3 times higher for obese subjects and 1.5 times higher for overweight subjects relative to normal weight subjects. This observational study provides body weight specific recommendations to achieve 25(OH)D targets.     

The involvement of intracellular calcium ion concentration and calmodulin in the 25-hydroxylation of cholecalciferol in ovine and rat liver

The effect of Ca2+ ion concentration on the 25 hydroxylation of tritiated cholecalciferol (3HD3) was investigated using homogenates of ovine liver from vitamin D replete sheep. A significant decrease in the production of 25 hydroxycholecalciferol (25OHD3) was observed when the concentration of Ca2+ in the homogenate was raised above 0.68 mmol/l by the addition of calcium gluconate. Similarly, a final concentration of 37 mumol EGTA/1 (equivalent to a Ca2+ concentration of 26.5 nmol/l) was associated with a 50% reduction of 25OHD3 production. That is, a broad bell-shaped relationship was observed between the production of 25OHD3 and the Ca2+ concentration in the homogenate. These changes in the rate of production of 25OHD3 were reproduced with hepatocytes from vitamin D replete rats, prepared by collagenase perfusion, using the drugs dantrolene sodium (DaNa) to reduce (ED50 = 57 mmol/l) and veratridine to increase (ED50 = 550 mmol/l) the intracellular Ca2+ concentration. Hepatocytes from vitamin D replete rats also showed a reduction in 25 hydroxylation of D3 (ED50 = 6 ng/ml) in response to the addition of 1-25 dihydroxycholecalciferol (1-25 (OH)2D3). The calmodulin antagonists; W7, compound 48/80, trifluoperazine (TFP) and calmidazolium (R24571) were all found to effect a dose response inhibition of the 25 hydroxylation of cholecalciferol by homogenates of ovine liver. R24571 had a similar inhibitory effect (ED50 = 70 mumol/l) upon the 25 hydroxylase enzyme of rat hepatocytes. It is concluded that the 25 hydroxylation of cholecalciferol in liver of vitamin D replete rats and sheep is calcium sensitive and is reduced in the presence of increased concentrations of 1,25(OH)2D3. Calmodulin may also be involved in the regulation of hepatocyte 25-hydroxylase activity by Ca2+.     

Determinants of Vitamin D Status in Fair-Skinned Women of Childbearing Age at Northern Latitudes

Background and Objective

Poor vitamin D status during pregnancy has been associated with unfavorable outcomes for mother and child. Thus, adequate vitamin D status in women of childbearing age may be important. The aim of this study is to investigate the determinants of 25-hydroxyvitamin D (25(OH)D) serum concentrations in women of childbearing age living in Sweden, at latitude 57–58° north.

Method

Eighty four non-pregnant, non-lactating, healthy, fair-skinned women aged between 25–40 years were included. All subjects provided blood samples, four day food records and answered questionnaires about sun exposure and lifestyle. Total serum 25(OH)D was analyzed using Roche Cobas® electrochemoluminiescent immunoassay.

Results

Mean 25(OH)D was 65.8±19.9 nmol/l and 23% of the subjects had concentrations <50 nmol/l. Only 1% had concentrations <25 nmol/l. Determinants of 25(OH)D concentrations were recent sunbed use, recent travel to southern latitude, season, estrogen contraceptive use and use of supplementary vitamin D (R² = 0.27).

Conclusion

Every fifth woman had 25(OH)D concentrations <50 nmol/l. About 30% of the variation in vitamin D status was explained by sun exposure, use of vitamin D supplements and use of estrogen contraceptives. Cutaneous vitamin D synthesis seems to be a major contributor to vitamin D status, even at northern latitudes. Thus, recommendations on safe UV-B exposure could be beneficial for vitamin D status.     

Developmental vitamin D deficiency alters the expression of genes encoding mitochondrial, cytoskeletal and synaptic proteins in the adult rat brain

Epidemiology has highlighted the links between season of birth, latitude and the prevalence of brain disorders such as multiple sclerosis and schizophrenia. In line with these data, we have hypothesized that ‘imprinting’ with low prenatal vitamin D could contribute to the risk of these two brain disorders. Previously, we have shown that transient developmental hypovitaminosis D induces permanent changes in adult nervous system. The aim of this study was to examine the impact of prenatal hypovitaminosis D on gene expression in the adult rat brain. Vitamin D deficient female rats were mated with undeprived males and the offspring were fed with a control diet after birth. At Week 10, gene expression in the progeny's brain was compared with control animals using Affymetrix gene microarrays. Prenatal hypovitaminosis D causes a dramatic dysregulation of several biological pathways including oxidative phosphorylation, redox balance, cytoskeleton maintenance, calcium homeostasis, chaperoning, post-translational modifications, synaptic plasticity and neurotransmission. A computational analysis of these data suggests that impaired synaptic network may be a consequence of mitochondrial dysfunction. Since disruptions of mitochondrial metabolism have been associated with both multiple sclerosis and schizophrenia, developmental vitamin D deficiency may be a heuristic animal model for the study of these two brain diseases.     

Vitamin D deficiency in adult British Hindu Asians: a family disorder.

The vitamin D state of 60 apparently healthy adult Hindu Asian couples living in Britain was studied on a community basis. Twenty six (22%) of the Asian subjects had pronounced vitamin D deficiency, defined as 25-hydroxycholecalciferol concentrations below 10 nmol/l (4 ng/ml), while none of the white controls had such low concentrations. Asian men and women were equally affected, and plasma concentrations were similar in husbands and wives. Vitamin supplements were being taken by only 31 (26%) subjects, most of whom were women. It is suggested that the spouses of patients with osteomalacia should be screened for vitamin D deficiency.     

Vitamin D Deficiency and Insufficiency in Hospitalized COPD Patients

Introduction

31–77% of patients with COPD have vitamin D deficiency and insufficiency, with results being highly variable between studies. Vitamin D may also correlate with disease characteristics.

Aim

To find out the prevalence of vitamin D deficiency and insufficiency in patients with COPD admitted for exacerbation and a risk factors for lower vitamin D levels among comorbidities and COPD characteristics.

Methods

152 patients were studied for vitamin D serum levels (25(OH)D). All of them were also assessed for diabetes mellitus (DM) and metabolic syndrome (MS). Data were gathered also for smoking status and exacerbations in last year. All patients completed CAT and mMRC questionnaires and underwent spirometry.

Results

A total of 83,6% of patients have reduced levels of vitamin D. 42,8% (65/152) have vitamin D insufficiency (defined as 25–50 nmol/L) and 40,8% (62/152) have vitamin D deficiency (<25 nmol/L). The mean level of 25(OH)D for all patients is 31,97 nmol/L (95%CI 29,12–34,68). Vitamin D deficiency and insufficiency are more prevalent in females vs. males (97,7 vs 77,8%; p = 0.003). The prevalence and severity of vitamin D deficiency and insufficiency in this study is significantly higher when compared to an unselected Bulgarian population (prevalence 75,8%; mean level 38,75 nmol/L). Vitamin D levels correlate with quality of life (measured by the mMRC scale) and lung function (FVC, FEV1, FEV6, FEF2575, FEV3, but not with FEV1/FVC ratio and PEF), it does not correlate with the presence of arterial hypertension, DM, MS and number of moderate, severe and total exacerbations. Vitamin D deficiency is a risk factor for longer hospital stay.

Conclusions

The patients with COPD admitted for exacerbation are a risk group for vitamin D deficiency and insufficiency, which is associated with worse disease characteristics.     

Vitamin D status and determinants of deficiency in non-supplemented athletes during the winter months in Tunisia

Recent reports suggest that hypovitaminosis D in athletes is as common as in the general population. This study was devised to examine vitamin D status and determinants of deficiency in athletes living in a sunny country (Tunisia). One hundred and fifty national elite athletes, training outdoors (n = 83) or indoors (n = 67), were enrolled from January to February 2012. Plasma 25-hydroxyvitamin D was measured by radioimmunoassay. Concentrations were between 50 and 75 nmol · l^-1 in 21.3% of participants, between 25 and 50 nmol · l^-1 in 55.3% of participants and <25 nmol · l^-1 in 14.7% of participants. The concentrations were significantly lower in indoor athletes than outdoor athletes (36.2±19.0 nmol · l^-1 vs. 49.1±19.2 nmol · l^-1; p < 0.001). In multivariate analysis, vitamin D deficiency (25-hydroxyvitamin D <50 nmol · l^-1) was associated with indoor sports [multi-adjusted odds ratio (95% confidence interval), 5.03 (1.64-15.4); p = 0.005], female gender [3.72 (1.44-9.65); p = 0.007] and age < 18 years [2.40 (1.01-5.85); p = 0.05]. Athletes living in sun-rich environments are exposed to a high risk of vitamin D inadequacy. Given the importance of vitamin D in health and athletic ability, targeting sufficient levels of plasma 25-hydroxyvitamin D in athletes is well justified.     

Vitamin D and the Risk of Atrial Fibrillation - The Rotterdam Study

Atrial fibrillation (AF) is the most common chronic arrhythmia and it increases the risk of cardiovascular morbidity and mortality. Still there is not a complete understanding of its etiology and underlying pathways. Vitamin D might regulate renin-angiotensin-aldosterone system and might be involved in inflammation, both implicated in the pathophysiology of AF. The objective of this work was to investigate the association between vitamin D status with the risk of AF in the elderly. This study was conducted within the Rotterdam Study, a community-based cohort of middle-aged and elderly participants in Rotterdam, The Netherlands. We had 3,395 participants who were free of AF diagnosis at the start of our study and who had vitamin D data available. We analyzed the association between serum 25-hydroxivitamin D (25(OH)D) and incidence of AF using Cox regression models. Vitamin D deficiency was defined as serum 25(OH)D concentrations <50nmol/l, insufficiency between 50nmol/l and 75nmol/l, while serum 25(OH)D concentrations equal to and above 75nmol/l were considered as adequate. After mean follow-up of 12.0 years 263 (7.7%) participants were diagnosed with incident AF. Vitamin D status was not associated with AF in any of the 3 multivariate models tested (model adjusted for socio-demographic factors and life-style factors: HR per 10 unit increment in serum 25(OH)D 0.96, 95% CI: 0.91-1.02; HR for insufficiency: 0.82, 95%CI: 0.60-1.11,and HR for adequate status: 0.76, 95%CI: 0.52-1.12 compared to deficiency). This prospective cohort study does not support the hypothesis that vitamin D status is associated with AF.     

6-Fluoro-vitamin D3: a new antagonist of the biological actions of vitamin D3 and its metabolites which interacts with the intestinal receptor for 1 alpha,25(OH)2-vitamin D3

The biological activity and the binding affinity for the 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] intestinal receptor of a new fluorine-containing vitamin D compound, namely 6-fluoro-vitamin D3 (6-F-D3), is reported. A significant interaction of 6-F-D3 with the 1,25(OH)2D3 receptor was found, with a relative competitive index (RCI) of 0.26 +/- 0.04, which is intermediate between 25-hydroxyvitamin D3 (0.14 +/- 0.01) and 1 alpha-hydroxyvitamin D3 (0.46 +/- 0.08), where the RCI of 1,25(OH)2D3 is defined to be 100. In contrast, vitamin D3 was unable to interact with the 1,25(OH)2D3 receptor. Also, the biological activity of 6-F-D3 was assessed in vivo in the vitamin D-deficient chick. 6-F-D3 at doses up to 130 nmol displayed no biological action on either intestinal calcium absorption (ICA) or bone calcium mobilization (BCM) over the time interval of 14-48 h after dosing. However, when 130 nmol 6-F-D3 was given 2 h before and 6 h after vitamin D3 (1.62 nmol), a significant inhibition of vitamin D-mediated ICA was noted. Also, a dose of 130 nmol 6-F-D3 given 2 h before and 6 h after 1,25(OH)2D3 (0.26 nmol) significantly inhibited ICA, as measured at 12 h. 6-F-D3 is the first vitamin D analog found which has an ability to both bind to the 1,25(OH)2D3 receptor and to antagonize the production of biological responses by 1,25(OH)2D3.     

Developmental vitamin D deficiency alters brain protein expression in the adult rat: implications for neuropsychiatric disorders

An increased risk for multiple sclerosis and schizophrenia is observed at increasing latitude and in patients born in winter or spring. To explore a possible link between maternal vitamin D deficiency and these brain disorders, we examined the impact of prenatal hypovitaminosis D on protein expression in the adult rat brain. Vitamin D-deficient female rats were mated with vitamin D normal males. Pregnant females were kept vitamin D-deficient until birth whereupon they were returned to a control diet. At week 10, protein expression in the progeny's prefrontal cortex and hippocampus was compared with control animals using silver staining 2-D gels associated with MS and newly devised data mining software. Developmental vitamin D (DVD) deficiency caused a dysregulation of 36 brain proteins involved in several biological pathways including oxidative phosphorylation, redox balance, cytoskeleton maintenance, calcium homeostasis, chaperoning, PTMs, synaptic plasticity and neurotransmission. A computational analysis of these data revealed that (i) nearly half of the molecules dysregulated in our animal model have also been shown to be misexpressed in either schizophrenia and/or multiple sclerosis and (ii) an impaired synaptic network may be a consequence of mitochondrial dysfunction.     

Vitamin D Status during Pregnancy and the Risk of Subsequent Postpartum Depression: A Case-Control Study

Epidemiological studies have provided evidence of an association between vitamin D insufficiency and depression and other mood disorders, and a role for vitamin D in various brain functions has been suggested. We hypothesized that low vitamin D status during pregnancy might increase the risk of postpartum depression (PPD). The objective of the study was thus to determine whether low vitamin D status during pregnancy was associated with postpartum depression. In a case-control study nested in the Danish National Birth Cohort, we measured late pregnancy serum concentrations of 25[OH]D3 in 605 women with PPD and 875 controls. Odds ratios [OR) for PPD were calculated for six levels of 25[OH]D3. Overall, we found no association between vitamin D concentrations and risk of PPD (p = 0.08). Compared with women with vitamin D concentrations between 50 and 79 nmol/L, the adjusted odds ratios for PPD were 1.35 (95% CI: 0.64; 2.85), 0.83 (CI: 0.50; 1.39) and 1.13 (CI: 0.84; 1.51) among women with vitamin D concentrations < 15 nmol/L, 15–24 nmol/L and 25–49 nmol/L, respectively, and 1.53 (CI: 1.04; 2.26) and 1.89 (CI: 1.06; 3.37) among women with vitamin D concentrations of 80–99 nmol/L and ≥ 100 nmol/L, respectively. In an additional analysis among women with sufficient vitamin D (≥ 50 nmol/L), we observed a significant positive association between vitamin D concentrations and PPD. Our results did not support an association between low maternal vitamin D concentrations during pregnancy and risk of PPD. Instead, an increased risk of PPD was found among women with the highest vitamin D concentrations.