VITAMIN A AND UROLITHIASIS—A Review

The early observations of Osborne, Mendel, and Ferry, and later of Higgins, showed that the incidence of urolithiasis was high in rats fed on diets deficient in fat soluble vitamins. Subsequently, the results of dark adaptation studies were interpreted as showing a relationship between vitamin A deficiency and calculous disease. However, a review of the literature including more recent data discloses that there is no evidence either clinical or experimental to support the claim that vitamin A deficiency is an etiologic factor in calculous disease in man in the United States.     

Vitamin E and neurologic function in man

Despite the well-known detrimental effect of vitamin E deficiency on the nervous system of many experimental animal models for decades, only over the past decade has vitamin E become recognized as essential for the maintenance of the structure and function of the human nervous system. This discovery of the neurologic role of vitamin E in man is due primarily to the identification of a degenerative neurologic syndrome in children and adults with chronic vitamin E deficiency caused by gastrointestinal diseases impairing fat and vitamin E absorption. A compelling body of clinical, neuropathologic, and therapeutic response evidence conclusively demonstrates that vitamin E deficiency is responsible for the neurologic disorder seen in such patients. In addition, an inborn error in vitamin E metabolism, the Isolated Vitamin E Deficiency Syndrome, causes vitamin E deficiency and similar neurologic degeneration in the absence of fat malabsorption. Guidelines for the evaluation and treatment of vitamin E deficiency in relevant clinical circumstances are provided. The possible role of vitamin E in treating other neurologic diseases is discussed.     

Contribution of vitamin A deficiency to calculogenic risk factors of urine: studies in children.

Studies in experimental animals showed that vitamin A deficiency enhanced the severity of urinary calculi disease. In India, children with low socioeconomic status are the major victims of bladder stone disease, and vitamin A deficiency is also more prevalent among these children. However, no systematic study is available to correlate the vitamin A-deficient status of children with their predisposition to urinary calculi disease. Vitamin A-deficient and normal boys were the subjects of this study. Twenty-four-hour samples of urine were collected from all the children at the beginning of the study and after normalizing the vitamin A status of the deficient children. Important risk factors were estimated in urine. Plasma vitamin A levels were also measured in these children. Among the deficient group, only children with plasma vitamin A levels of 15 micrograms and lower exhibited calcium oxalate crystalluria. Most importantly, abnormal crystalluria was observed in all children whose plasma vitamin A levels were 13 micrograms/dl or less. Compared to normal children the urine of vitamin A-deficient children showed the following changes: (a) reduced concentration of crystal growth inhibitors, namely citrate and glycosaminoglycans; (b) a decline in inhibitory activity toward calcium oxalate crystal growth; and (c) enhanced excretion of high risk factors, namely calcium and oxalate. Correction of vitamin A status normalized the above abnormal properties of urine. The results of this study strongly support the hypothesis that the vitamin A-deficient state is one of the factors that can enhance the risk of urolithiasis in susceptible populations.     

Protective and toxic effects of vitamin D on vascular calcification: clinical implications

The presence of vascular calcification (VC) is a predictor of poor survival in the general population. The development of VC is an active process that requires a pre-existing injury as an inducer and promoting factors such as hyperphosphatemia and hypercalcemia, as well as a deficiency in calcification repressor factors. Vascular smooth muscle cells possess an endogenous enzyme system for the biosynthesis of the vitamin D hormone calcitriol from its precursor 25-hydroxyvitamin D and also a cytosolic calcitriol receptor, indicating that the vasculature is an important target tissue for vitamin D. The toxic effects of supra-physiological vitamin D dosages on the vasculature have been known for several decades. Recent experimental data also demonstrate important physiological effects of vitamin D on factors that are protective for vascular health. This review article summarises the molecular basis of protective and toxic vitamin D actions on the vasculature. Chronic kidney disease can be considered as a human model of severe VC and poor survival. The disease is associated with calcitriol deficiency, hyperparathyroidism, and hyperphosphatemia. Evidence is increasing that phosphate overload plays a key role in the process of VC in chronic kidney disease. The first clinical studies indicate that vitamin D receptor activation can improve survival in these patients. Although less severe than in chronic kidney disease, vitamin D deficiency and secondary hyperparathyroidism are also frequent in the general population, especially in elderly and obese subjects. Future studies should focus on the impact of vitamin D deficiency on VC and clinical outcome in these groups.     

Vitamin D and vascular calcification

PURPOSE OF REVIEW: Vascular calcification is frequently found in patients with osteoporosis, atherosclerosis and chronic kidney disease, leading to high morbidity and mortality rates. The effects of vitamin D excess and deficiency on vascular calcification are reviewed in this article. RECENT FINDINGS: There is evidence from experimental studies that mediacalcinosis induced by vitamin D excess is an active and reversible process. Vitamin D excess, however, is rarely seen in the general human population. Experimental data also demonstrate that physiologic vitamin D actions include the inhibition of processes that are important for intimal and medial artery calcification such as pro-inflammatory cytokine release, adhesion molecule release, and proliferation and migration of vascular smooth muscle cells. In uremic rats, low levels of the vitamin D hormone calcitriol are associated with massive vascular and soft tissue calcifications. Whereas retrospective studies already indicate a beneficial effect of active vitamin D on mortality rates in chronic kidney disease, little is yet known about the effect of vitamin D deficiency on cardiovascular morbidity and mortality in the general population. SUMMARY: Available data indicate that vitamin D exerts a biphasic 'dose response' curve on vascular calcification with deleterious consequences not only of vitamin D excess but also of vitamin D deficiency.     

Vitamin D or hormone D deficiency in autoimmune rheumatic diseases,including undifferentiated connective tissue disease

Epidemiological evidence indicates a significant association between vitamin D deficiency and an increased incidence of autoimmune diseases. The presence of vitamin D receptors in the cells of the immune system and the fact that several of these cells produce the vitamin D hormone suggested that vitamin D could have immunoregulatory properties, and now potent immuno-mudulatory activities on dendritic cells, Th1 and Th17 cells, as well as B cells have been confirmed. Patients with undifferentiated connective tissue disease also show vitamin D deficiency and, interestingly, patients who progress into connective tissue diseases have lower vitamin D levels than those who remain in the undifferentiated connective tissue disease stage.     

The Importance of Vitamin D Level in Subacute Thyroiditis Disease and the Effect of Vitamin D on Disease Prognosis

Objective: Subacute thyroiditis (SAT) is an inflammatory thyroid disease that manifests with severe pain. The presence of the vitamin D receptor in immune system cells shows that vitamin D deficiency can trigger inflammatory diseases. The aim of the present study was to determine the prevalence of vitamin D deficiency in SAT patients, and the relationship between vitamin D level and permanent hypothyroidism and recurrence rate.Methods: In this retrospective study, 25-hydroxyvitamin D (25[OH]D) levels of 170 SAT patients and 86 control subjects were compared.Results: The 25(OH)D levels were significantly lower in the SAT patients, and there was no seasonal difference. A negative correlation was determined between the erythrocyte sedimentation rate and 25(OH)D, but no significant relationship was found between vitamin D level and prognosis.Conclusion: As a result of this study, it was shown that vitamin D levels in subacute thyroiditis patients were significantly lower than in the healthy control group. Although there is no relationship between vitamin D level and disease prognosis, vitamin D deficiency may increase the rate of respiratory tract infections (especially, influenza, coxsackievirus, measles, adenovirus, retroviruses) and eventually SAT development.     

Risk Factors for Vitamin D Deficiency among HIV-Infected and Uninfected Injection Drug Users

Introduction

Vitamin D deficiency is highly prevalent and is associated with bone disease, cardiovascular disease, metabolic syndrome and malignancy. Injection drug users (IDUs), with or without HIV infection, are at risk for these conditions; however, limited data on vitamin D deficiency exist in this population. We determined the prevalence and correlates of vitamin D deficiency among urban IDUs in the AIDS Linked to the IntraVenous Experience (ALIVE) Study cohort.

Methods

For this cross-sectional sub-study, vitamin D deficiency was defined as a serum 25(OH)-vitamin D level <20 ng/mL. Multivariable logistic regression was used to identify factors independently associated with vitamin D deficiency.

Results

Of 950 individuals analyzed, 29% were HIV-infected. The median age was 49 years; 65% were male, and 91% were black. The median vitamin D level was 13.5 ng/mL (IQR, 9.0–20.3); 74% were deficient (68% in HIV-infected vs. 76% in HIV-uninfected, p = 0.01). Non-black race, fall/winter season, multivitamin intake, higher serum albumin, HCV seropositivity and HIV-infection were associated with significantly lower odds of vitamin D deficiency.

Conclusions

Vitamin D deficiency is prevalent among IDUs. Notably, HIV-infected IDUs were less likely to be vitamin D deficient. Higher vitamin D levels were associated with multivitamin intake and with higher albumin levels, suggesting that nutritional status contributes substantially to deficiency. The association between HCV serostatus and vitamin D level remains unclear. Further investigation is needed to define the clinical implications of the heavy burden of vitamin D deficiency in this high-risk, aging population with significant co-morbidities.     

Dietary vitamins A and E influence retinyl ester composition and content of the retinal pigment epithelium

Experiments were conducted to determine the influence of dietary levels of vitamin A and alpha-tocopherol on the amounts and composition of retinyl esters in the retinal pigment epithelium of light-adapted albino rats. Groups of rats were fed diets containing alpha-tocopherol and either no retinyl palmitate, adequate retinyl palmitate, or excessive retinyl palmitate. Other groups of rats received diets lacking alpha-tocopherol and containing the same three levels of retinyl palmitate. Retinoic acid was added to diets lacking retinyl palmitate. After 27 weeks, the animals were light-adapted to achieve essentially total visual pigment bleaches, and the neural retinas and retinal pigment epithelium-eyecups were then dissected from each eye for vitamin A ester determinations. Almost all of the retinyl esters were found in the retinal pigment epithelium-eyecup portions of the eyes, mainly as retinyl palmitate and retinyl stearate. Maintaining rats on a vitamin A-deficient, retinoic acid-containing diet led to significant reductions in retinal pigment epithelial retinyl ester levels in rats fed both the vitamin E-supplemented and vitamin E-deficient diets; contrary to expectations, the effect of dietary vitamin A deficiency was more pronounced in the vitamin E-supplemented rats. Vitamin A deficiency in retinoic acid-maintained animals also led to significant reductions in retinyl palmitate-to-stearate ester ratios in the retinal pigment epithelia of both vitamin E-supplemented and vitamin E-deficient rats. Excessive dietary intake of vitamin A had little, if any, effect on retinal pigment epithelial retinyl ester content or composition. Vitamin E deficiency resulted in significant increases in retinal pigment epithelial retinyl palmitate content and in palmitate-to-stearate ester ratios in rats fed all three levels of vitamin A, but had little effect on retinal pigment epithelial retinyl stearate content. In other tissues, vitamin E deficiency has been shown to lower vitamin A levels, and it is widely accepted that this effect is due to autoxidative destruction of vitamin A. The increase in retinal pigment epithelial vitamin A ester levels in response to vitamin E deficiency indicates that vitamin E does not regulate vitamin A levels in this tissue primarily by acting as an antioxidant, but rather may act as an inhibitor of vitamin A uptake and/or storage. The effect of vitamin E on pigment epithelial vitamin A levels may be mediated by the vitamin E-induced change in retinyl palmitate-to-stearate ratios.     

Alterations of KCl- and ATP-induced increase in [Ca2+]i in cardiomyocytes from vitamin B6 deficient rats

Although vitamin B6 deficiency is related to coronary heart disease, no information regarding changes in myocardium due to vitamin B6 deficiency is available in the literature. In view of the critical role played by Ca2+ in cellular function, we investigated alterations in [Ca2+]i induced by KCI or ATP in vitamin B6 deficient and age-matched control rats. [Ca2+]i was measured in isolated cardiomyocytes by using the Fura-2 fluorescence technique. The KC1-induced increase in [Ca2+]i was augmented in vitamin B6 deficient cardiomyocytes, whereas the ATP-induced increase in [Ca2+]i was attenuated. The specific ATP binding to sarcolemma from hearts of vitamin B6 deficient rats was decreased. A single injection of vitamin B6 (10 mg/kg) to vitamin B6 deficient animals completely reversed the KC1- or ATP-induced changes in [Ca2+]i in cardiomyocytes as well as ATP binding with sarcolemma. These results regarding altered regulation of [Ca2+]i in cardiomyocytes and sarcolemmal ATP receptors indicate myocardial abnormalities due to vitamin B6 deficiency.     

维生素D缺乏和2型糖尿病视网膜病变风险度的相关性研究

摘要 目的：是探讨维生素D缺乏与2型糖尿病（T2DM）患者视网膜病变（DR）发生风险度的关系。方法：选取2020年12月至2022年8月在新疆医科大学第二附属医院内分泌科住院的2型糖尿病患者作为研究对象。将209名患者根据眼底检查分为DR组（n=50）和正常眼底（NDR）组（n=159）。比较各组患者一般资料、实验室检查指标;采用Spearman分析法分析病程、FBG、HbAlC、25(OH)D与DR的相关性,采用Pearson分析居住地（城镇）、与维生素D缺乏、SBP与DR的相关性,采用Logistics回归分析DR发生的影响因素,比较各组患者维生素D缺乏、病程、FBG、HbA1c及25(OH)D对DR的预测价值。结果：DR组的居住地（农村）、FBG、HbA1c、病程等均大于NDR组,25(OH)D水平低于NDR组,DR组维生素D缺乏率大于NDR组,差异有统计学意义（P＜0.05）。Pearson相关性分析结果表明DR与居住地（城镇）呈负相关（P＜0.05）,与SBP、维生素D缺乏呈正相关（P＜0.05）;Spearman相关分析表明DR与25(OH)D呈负相关（P＜0.05）,与病程、空腹血糖和糖化血红蛋白等呈正相关（P＜0.05）。Logistic回归分析结果显示,维生素D缺乏、病程、FBG、HbA1c为DR的独立危险因素（P＜0.05）,维生素D缺乏的T2DM患者DR发病风险是维生素D不缺乏者的22.019倍（OR=22.019,95%CL 2.119~228.771,P＜0.05）。受试者工作特征（ROC）曲线分析显示,病程、FBG、HbA1c、25(OH)D作为联合变量可有效预测DR,ROC曲线下面积为0.924。结论：25(OH)D与DR呈负相关,维生素D缺乏可能与T2DM患者DR的发生有关。     

RBP4 disrupts vitamin A uptake homeostasis in a STRA6-deficient animal model for Matthew-Wood syndrome

The cellular uptake of vitamin A from its RBP4-bound circulating form (holo-RBP4) is a homeostatic process that evidently depends on the multidomain membrane protein STRA6. In humans, mutations in STRA6 are associated with Matthew-Wood syndrome, manifested by multisystem developmental malformations. Here we addressed the metabolic basis of this inherited disease. STRA6-dependent transfer of retinol from RBP4 into cultured NIH 3T3 fibroblasts was enhanced by lecithin:retinol acyltransferase (LRAT). The retinol transfer was bidirectional, strongly suggesting that STRA6 acts as a retinol channel/transporter. Loss-of-function analysis in zebrafish embryos revealed that Stra6 deficiency caused vitamin A deprivation of the developing eyes. We provide evidence that, in the absence of Stra6, holo-Rbp4 provokes nonspecific vitamin A excess in several embryonic tissues, impairing retinoic acid receptor signaling and gene regulation. These fatal consequences of Stra6 deficiency, including craniofacial and cardiac defects and microphthalmia, were largely alleviated by reducing embryonic Rbp4 levels by morpholino oligonucleotide or pharmacological treatments.     

Bacterial population and innate immunity-related genes in rat gastrointestinal tract are altered by vitamin A-deficient diet

Vitamin A and its derivatives have been shown to regulate the growth and differentiation of gastrointestinal epithelial cells; in addition, vitamin A deficiency has been convincingly shown to be associated with increased susceptibility to infection. The gastrointestinal mucosal barrier, which is a component of the innate immune system, is considered the first line of defense, as it provides a barrier between the external environment and the internal milieu. A disturbance in the integrity of the intestinal epithelium is one of the main factors involved in increased incidence of infections during vitamin A deficiency. In this study, the effects of vitamin A deficiency on microbial ecology and the expression of genes related to the intestinal mucosa's innate immunity were examined in a rat model. Using the 16s rDNA method, we demonstrate that a vitamin A-deficient (VAD) diet increases the total amount of bacteria in the gastrointestinal tract and alters the intestinal microflora. Results show a decrease in the relative proportion of Lactobacillus spp. and the simultaneous appearance of Escherichia coli strains. Lack of vitamin A significantly changed mucin (MUC) dynamics, as reflected by the enlarged goblet-cell "cup" area relative to controls; decreased MUC2 mRNA expression in the jejunum, ileum and colon of VAD rats and increased MUC3 mRNA expression in the ileum and colon of these rats. In addition, vitamin A deficiency down-regulated defensin 6 mRNA expression while up-regulating toll-like receptors 2 and 5 mRNA expressions. The current study indicates that vitamin A deficiency interferes with the integrity of the gastrointestinal mucosal barrier.     

Prevalence of Vitamin D Deficiency in Sickle Cell Disease: A Systematic Review

Vitamin D deficiency has emerged as a public health focus in recent years and patients with sickle cell disease (SCD) reportedly have a high prevalence of the condition. Our objectives were to summarize definitions of vitamin D deficiency and insufficiency used in the literature, and to determine the prevalence and magnitude of each in patients with SCD through a systematic review conducted according to PRISMA guidelines. From a PubMed search, 34 potential articles were identified and 15 met eligibility criteria for inclusion. Definitions of deficiency and insufficiency varied greatly across studies making direct comparisons difficult. This review provides evidence to suggest that suboptimal vitamin D levels are highly prevalent among those with SCD, far more so than in comparable non-SCD patients or matched control populations. Defining deficiency as vitamin D <20ng/mL, prevalence estimates in SCD populations range from 56.4% to 96.4%. When compared with results from the population-based National Health and Nutrition Examination Survey, however, the general African American population appeared to have a similarly high prevalence of vitamin D deficiency. African American patients with and without SCD were both substantially higher than that of Caucasians. What remains to be determined is whether there are adverse health effects for patients with SCD because of concurrent vitamin D deficiency.     

Sequential Evaluation of Plasma Retinol-Binding Protein Response to Vitamin A Administration in Very-Low-Birth-Weight Neonates

Vitamin A (retinol) deficiency is associated with impaired healing from lung injury in very-low-birth-weight (VLBW) neonates susceptible to bronchopulmonary dysplasia (BPD). Vitamin A supplementation from birth may ameliorate this adverse outcome. We hypothesized that plasma retinol-binding protein (REP) response to vitamin A administration, which provides a dynamic measure of vitamin A status, might be useful for early recognition of vitamin A deficiency in VLBW neonates at risk for BPD. We prospectively studied 20 VLBW neonates (inclusion criteria: birth weight <1300 g, gestational age <30 weeks, need for supplemental oxygen and mechanical ventilation for >24 h after birth) who were eligible to receive vitamin A supplementation. In addition to sequential assessment of vitamin A status, we measured plasma RBP just before and 3 and 6 h after an intramuscular injection of vitamin A (2000 IU/kg retinyl palmitate) on Postnatal Days 1, 7, 15, 21, 29, and 43. The percentage increase in plasma RBP (Δ-RBP) was calculated. A high plasma Δ-RBP value (>8%) is indicative of vitamin A deficiency. Based on pulmonary outcome, the infants were divided into two groups: BPD (n = 12) and No BPD (n = 8). Mean vitamin A intake ranged from 1414 to 2114 IU/kg/day and did not differ between infant groups. Mean plasma vitamin A concentration increased from baseline levels on Postnatal Day 1 to levels within the desired range of 1.05-2.10 μmol/liter (30.0-60.0 μg/dl) during supplementation period in both infant groups. Infants with BPD, in contrast to those without BPD, had worsening plasma Δ-RBP values from Postnatal Day 15, indicative of persistence of vitamin A deficiency despite supplementation and normalization of plasma vitamin A concentration. We conclude that plasma RBP response to vitamin A administration is useful for early recognition of vitamin A deficiency in VLBW neonates at risk for BPD.     

Indicators of erythrocyte formation and degradation in rats with either vitamin A or iron deficiency

Vitamin A deficiency produces anemia and altered iron status. In this study with rats we tested two hypotheses regarding vitamin A deficiency: (1) that it impairs erythropoiesis, leading to an increased red cell turnover, and (2) that it inhibits the glycosylation of transferrin. Erythropoietic activity was assessed indirectly by determining the myeloid:erythroid ratio in bone marrow smears, the number of erythroid colonies in the red pulp of spleen, the blood reticulocyte index, and zinc protoporphyrin and plasma transferrin receptor concentrations. Transferrin glycosylation was assessed by measuring the sialic acid content of transferrin. The effects of vitamin A deficiency were compared with those of iron deficiency. Iron deficiency produced anemia and low iron levels in organs. Vitamin A deficiency produced low levels of plasma and hepatic retinol, and it induced decreased plasma total iron-binding capacity and raised iron levels in tibia and spleen. Short- but not long-term iron deficiency reduced the number of erythroid colonies in spleen; vitamin A deficiency had no influence. Neither iron nor vitamin A deficiency influenced the myeloid:erythroid ratio in bone marrow smears and the blood reticulocyte production. Plasma transferrin receptor and erythrocyte zinc protoporphyrin concentrations were not affected by vitamin A deficiency but increased with iron deficiency. Vitamin A deficiency did not stimulate erythrocyte breakdown, as indicated by unaltered plasma lactate dehydrogenase activity and reduced plasma total bilirubin levels. Both vitamin A and iron deficiencies raised the proportion of multiple sialylated transferrins in plasma. Thus, we have not found evidence that vitamin A deficiency affects erythropoiesis and erythrocyte turnover. The iron accumulation in spleen and bone marrow may be related to reduced iron transport due to inhibition of transferrin synthesis rather than inhibition of transferrin sialylation.     

Vitamin A deficiency reduces uptake of beta-carotene by brush border membrane vesicles but does not alter intestinal retinyl ester hydrolase activity in the rat

Vitamin A deficiency has been reported to result in mild structural and functional changes within the small intestine. The objective of this study was to measure the impact of vitamin A deficiency in the rat on several functional aspects of beta-carotene uptake and intestinal retinyl ester hydrolysis. These included uptake of (14)C-beta-carotene by brush border membrane vesicles (BBMV) and in vitro activity of intrinsic retinyl ester hydrolase (REH). Rats (n = 33) were randomly assigned to receive one of three dietary treatments: vitamin A deficient (-VA), vitamin A sufficient pair-fed (PF), or vitamin A sufficient free access-fed (FA). Liver, serum retinol, and growth data were used to verify clinical vitamin A deficiency. Rats in the -VA group were clinically vitamin A deficient by Day 56 on a vitamin A-free diet and, at that point, all rats were randomly assigned to one of two experimental treatments: BBMV studies or REH activity assays. Uptake of (14)C-beta-carotene by BBMV was significantly suppressed (P < 0.05) in -VA rats when compared to both PF and FA control rats during early passive uptake equilibration (10-20 sec). Uptake was also significantly decreased by BBMV isolated from -VA rats compared to PF controls, but not FA controls, after a 10-min incubation (P < 0.05). In vitro activity of REH was not impacted by vitamin A deficiency in rats, although a trend for greater activity from -VA rats was noted. These data suggest that vitamin A deficiency impairs enterocyte membrane uptake of beta-carotene without altering the enzymatic activity of intrinsic REH.     

Effect of vitamin A deficiency on pulmonary and hepatic in vitro metabolism of benzo(a)pyrene in rat

The metabolism of (3H)-benzo(a)pyrene and the activities of enzymes involved in its metabolism were studied in rat lung and liver in vitamin A deficiency. Deficiency of vitamin A resulted a significant decrease in the overall metabolism of benzo(a)pyrene in the liver in vitro, whereas no significant difference was evident in the lung. The ethyl acetate-soluble metabolites of benzo(a)pyrene formed by lung and liver preparations were unaltered qualitatively by vitamin A deficiency. However, quantitative analysis revealed that vitamin A deficiency decreased the yield of dihydrodiols, quinones and phenols in liver, and dihydrodiols in lung. The hepatic cytochrome P-450 content, arylhydrocarbon hydroxylase and uridine diphosphate-glucuronosyl transferase activities were reduced, whereas glutathione S-transferase activity was increased in the vitamin A deficient animals. Contrary to this, pulmonary cytochrome P-450 content was above the control values (p less than 0.01) and no alteration in pulmonary arylhydrocarbon hydroxylase activity was observed in vitamin A deficient rats. Uridine diphosphate-glucuronosyltransferase and glutathione S-transferase activities were impaired in lung by inducing vitamin A deficiency. However, no significant difference was evident in the overall metabolism of benzo(a)pyrene by lung supernatants from the two groups.     

Vitamin E and neurodegenerative diseases

Vitamin E is essential for neurological function. This fact, together with a growing body of evidence indicating that neurodegenerative processes are associated with oxidative stress, lead to the convincing idea that several neurological disorders may be prevented and/or cured by the antioxidant properties of vitamin E.

In this review, some aspects related to the role of vitamin E against Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and ataxia with vitamin E deficiency will be presented.     

The challenge resulting from positive and negative effects of sunlight: how much solar UV exposure is appropriate to balance between risks of vitamin D deficiency and skin cancer?

There is no doubt that solar ultraviolet (UV) exposure is the most important environmental risk factor for the development of non-melanoma skin cancer. Therefore, sun protection is of particular importance to prevent these malignancies, especially in risk groups. However, 90% of all requisite vitamin D has to be formed in the skin through the action of the sun-a serious problem, for a connection between vitamin D deficiency and a broad variety of independent diseases including various types of cancer, bone diseases, autoimmune diseases, hypertension and cardiovascular disease has now been clearly indicated in a large number of epidemiologic and laboratory studies. An important link that improved our understanding of these new findings was the discovery that the biologically active vitamin D metabolite 1,25(OH)(2)D is not exclusively produced in the kidney, but in many other tissues such as prostate, colon, skin and osteoblasts. Extra-renally produced 1,25(OH)(2)D is now considered to be an autocrine or paracrine hormone, regulating various cellular functions including cell growth. We and others have shown that strict sun protection causes vitamin D deficiency in risk groups. In the light of new scientific findings that convincingly demonstrate an association of vitamin D deficiency with a variety of severe diseases including various cancers, the detection and treatment of vitamin D deficiency in sun-deprived risk groups is of high importance. It has to be emphasized that in groups that are at high risk of developing vitamin D deficiency (e.g., nursing home residents or patients under immunosuppressive therapy), vitamin D status has to be monitored. Vitamin D deficiency should be treated, e.g., by giving vitamin D orally. Dermatologists and other clinicians have to recognize that there is convincing evidence that the protective effect of less intense solar UV radiation outweighs its mutagenic effects. Although further work is necessary to define an adequate vitamin D status and adequate guidelines for solar UV exposure, it is at present mandatory that public health campaigns and recommendations of dermatologists on sun protection consider these facts. Well-balanced recommendations on sun protection have to ensure an adequate vitamin D status, thereby protecting people against adverse effects of strict sun protection without significantly increasing the risk of developing UV-induced skin cancer.