Moderate Vitamin Research Articles

Vitamin C Deficiency in the Brain Impairs Cognition, Increases Amyloid Accumulation and Deposition, and Oxidative Stress in APP/PSEN1 and Normally Aging Mice

Subclinical vitamin C deficiency is widespread in many populations, but its role in both Alzheimer's disease and normal aging is understudied. In the present study, we decreased brain vitamin C in the APPSWE/PSEN1deltaE9 mouse model of Alzheimer's disease by crossing APP/PSEN1(+) bigenic mice with SVCT2(+/-) heterozygous knockout mice, which have lower numbers of the sodium-dependent vitamin C transporter required for neuronal vitamin C transport. SVCT2(+/-) mice performed less well on the rotarod task at both 5 and 12 months of age compared to littermates. SVCT2(+/-) and APP/PSEN1(+) mice and the combination genotype SVCT2(+/-)APP/PSEN1(+) were also impaired on multiple tests of cognitive ability (olfactory memory task, Y-maze alternation, conditioned fear, Morris water maze). In younger mice, both low vitamin C (SVCT2(+/-)) and APP/PSEN1 mutations increased brain cortex oxidative stress (malondialdehyde, protein carbonyls, F2-isoprostanes) and decreased total glutathione compared to wild-type controls. SVCT2(+/-) mice also had increased amounts of both soluble and insoluble Aβ1-42 and a higher Aβ1-42/1-40 ratio. By 14 months of age, oxidative stress levels were similar among groups, but there were more amyloid-β plaque deposits in both hippocampus and cortex of SVCT2(+/-)APP/PSEN1(+) mice compared to APP/PSEN1(+) mice with normal brain vitamin C. These data suggest that even moderate intracellular vitamin C deficiency plays an important role in accelerating amyloid pathogenesis, particularly during early stages of disease development, and that these effects are likely modulated by oxidative stress pathways.

Isolated Vitamin D Deficiency Is Not Associated with Nonthyroidal Illness Syndrome, but with Thyroid Autoimmunity

Aim. This study aimed to compare thyroid functions, thyroid autoantibodies, and the existence of nonthyroidal illness syndrome (NTIS) according to vitamin D level. Materials and Methods. The study included age- and BMI-matched healthy volunteers with and without vitamin D deficiency. In addition, the nonthyroidal illness syndrome status was evaluated. Results. Anti-TPO positivity was significantly more common in those with severe and moderate vitamin D deficiency, as compared to those with a normal 25(OH)D level. Furthermore, TSH levels were significantly lower in those with severe and moderate vitamin D deficiency than in those with a normal 25(OH)D level. In addition, there was a significant weak inverse correlation between anti-TPO positivity and the 25(OH)D level and a positive correlation between the TSH level and 25(OH)D level. Only 1 thyroid function test result was compatible with NTIS among the participants with moderate vitamin D deficiency; therefore the difference was not significant. Conclusions. The prevalence of thyroid autoantibody positivity was higher in those with severe and moderate vitamin D deficiency than in those with a normal 25(OH)D level. Additional large-scale studies must be conducted to determine if vitamin D deficiency plays a causal role in the pathogenesis of Hashimoto's thyroiditis and NTIS.

Low vitamin D, and bone mineral density with depressive symptoms burden in menopausal and postmenopausal women.

Background:The reported association between vitamin D level and loss of Bone mineral densitometry measurements (BMD) has been controversial.Objective:The objectıve of the current study was to determine whether low vitamin D level and BMD are associated with depresive symptoms as burden in Arab women during the menopausal and postmenopausal period.Design and Setting:A cross-sectional descriptive study design was used at the Primary Health Care (PHC) Centers in Qatar.Subjects:A multi-stage sampling design was used and a representative sample of 1436 women aged 45-65 years were included during July 2012 and November 2013 and 1106 women agreed to participate (77.2%) and responded to the study.Materials and Methods:BMD (g/m2) was assessed at the BMD unit using a Lunar Prodigy DXA system (Lunar Corp., Madison, WI). The antero-posterior lumbar spine (L2-L4) and the mean of the proximal right and left femur were be measured by two technician and then reviewed by one radiologist. Data on body mass index (BMI), clinical biochemistry variables including serum 25-hydroxyvitamin D were collected. The Beck Depression Inventory (BDI) was administered for depression purposes.Results:Of the 1436 women living in urban and rural areas, 1106 women agreed to participate (77.0%) and responded to the study. The mean age and standard deviation of the subjects was 53.8 ± 3.2. The median age of natural menopausal in the present study was 49 years (mean and standard deviation 49.5 ± 3.1 and postmenopausal was 58.1 ± 3.3). There were statistically significant differences between menopausal stages with regards to ethnicity, education level, systolic and dialostic blood pressure, parity, sheesha smoking and depressive symptoms. Overall 30.4% of women were affected with osteopenia/osteoporosis in premenopausal and postmenopausal (24.4% vs 35.7%; P = 0.0442). Osteopenia in premenopausal and postmenopausal (18.7% vs 29.3%; P = 0.030) and Osteoporosis (9.9% vs 15.9%; P = 0.049) were significantly higher in post-menopausal women than in premenopausal women (P = 0.046). Similarly, vitamin D deficiency was more prevalent among postmenopausal women than menopausal women. Overall, only 15.1% of women had optimum vitamin D level and 15.5% had severe, 33.2% had moderate vitamin D insufficiency and 36.3% had mild vitamin D insufficiency in menopausal and post menopausal women (P = 0.021). The study revealed that vitamin D level, hemoglobin level, serum iron fasting plasma glucose, calcium, triglycerides, high density lipid (HDL) cholesterol, low density lipid (LDL) Cholesterol, alkaline phosphate and magnesium were considerably lower in postmenopausal compared to menopausal women (P < 0.001).Conclusion:The current study revealed that there was a strong association between vitamin D level and BMD in Arab women during the menopausal and post-menopausal period.

Changing trends in management of gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is on the rise globally. In view of the increasing prevalence of GDM and fetal and neonatal complications associated with it, there is a splurge of research in this field and management of GDM is undergoing a sea change. Trends are changing in prevention, screening, diagnosis, treatment and future follow up. There is emerging evidence regarding use of moderate exercise, probiotics and vitamin D in the prevention of GDM. Regarding treatment, newer insulin analogs like aspart, lispro and detemir are associated with better glycemic control than older insulins. Continuous glucose monitoring systems and continuous subcutaneous insulin systems may play a role in those who require higher doses of insulin for sugar control. Evidence exists that favors metformin as a safer alternative to insulin in view of good glycemic control and better perinatal outcomes. As the risk of developing GDM in subsequent pregnancies and also the risk of overt diabetes in later life is high, regular assessment of these women is required in future. Lifestyle interventions or metformin should be offered to women with a history of GDM who develop pre-diabetes. Further studies are required in the field of prevention of GDM for optimizing obstetric outcome.

Effect of vitamin D supplementation on physical performance and activity in non-western immigrants.

Vitamin D deficiency is highly prevalent among non-western immigrants in The Netherlands and associated with poor physical performance. The aim of this study was to assess the effect of vitamin D supplementation on physical performance, exercise capacity, and daily physical activity in vitamin D-deficient, overweight non-western immigrants. A randomized double-blind, placebo-controlled trial was conducted to assess the effect of vitamin D on physical performance. A total of 130 participants were included. Eligibility criteria included overweight (BMI >27 kg/m2), 25-hydroxy vitamin D (25(OH)D) ≤50 nmol/l, and an age range of 20–65 years. The intervention group received 1200 IU vitamin D3 daily for 4 months; the control group received placebo. Both groups received 500 mg calcium daily. Outcome measures included physical performance (physical performance score), exercise capacity (a 6-min walk test (6-MWT)), and daily physical activity (questionnaire and accelerometer). There was no significant effect on physical performance, exercise capacity, or physical activity in the intention to treat analysis. In an explorative post hoc analysis restricted to participants reaching a serum 25(OH)D concentration of >60 nmol/l after intervention, there was an improvement of 19 m in the 6-MWT compared with the control group (P=0.053). Moderate dose vitamin D supplementation did not significantly improve physical performance, exercise capacity, or physical activity. However, when 25(OH)D concentrations reached >60 nmol/l after intervention, there was a borderline significant improvement in exercise capacity. Although the clinical relevance is not clear, this is a promising result, as all participants were overweight and did not improve their overall activity levels.

Effect of dietary vitamin E on the growth performance and nonspecific immunity in sub-adult turbot (Scophthalmus maximus)

This study investigated the growth performance and non-specific immunity in sub-adult turbot fed with graded levels of vitamin E (0, 120, 240, 480 and 960 mg kg−1) for 15 weeks. Results showed that the final weight, specific growth rate, nitro blue tetrazolium positive leucocytes of head kidney, phagocytic index, serum lysozyme activity and superoxide dismutase activity significantly increased with increasing vitamin E levels. The highest values were recorded in the diet with 480 mg kg−1 vitamin E. However, no significant differences in the hepatosomatic index, viscerosomatic index and survival rate were found among all dietary treatment. Furthermore, the expression levels of complement component 3 (C3), tumor necrosis factor-α (TNF-α) and interleukine 1β (IL-1β) were significantly upregulated in the fish feed with the vitamin E-supplemented diets. Compared with the basal diet, the diet supplemented with 480 mg kg−1 vitamin E significantly augmented the mRNA expression of IL-1β, TNF-α in the spleen and head-kidney, C3 in the liver, respectively. In conclusion, the obtained results indicate the basal diet supplemented with moderate dietary vitamin E (480 mg kg−1) increased the growth, nonspecific immune responses, and expression levels of some immune-related genes in sub-adult turbot. These observations suggest that optimal dietary vitamin E can promote the growth, maintain the health and improve the broodstock management for turbot.

In vivo vitamin C deficiency in guinea pigs increases ascorbate transporters in liver but not kidney and brain

Moderate vitamin C (vitC) deficiency (plasma concentrations less than 23 μmol/L) affects as much as 10% of adults in the Western World and has been associated with an increased mortality in disease complexes such as cardiovascular disease and the metabolic syndrome. The distribution of vitC within the body is subjected to complex and nonlinear pharmacokinetics and largely depends on the sodium-dependent vitC-specific transporters, sodium-dependent vitamin C transporter 1 (SVCT1) and sodium-dependent vitamin C transporter 2 (SVCT2). Although currently not established, it is likely to expect that a state of deficiency may affect the expression of these transporters to preserve vitC concentrations in specific target tissues. We hypothesized that diet-induced states of vitC deficiency lead to alterations in the messenger RNA (mRNA) and/or protein expression of vitC transporters, thereby regulating vitC tissue distribution. Using guinea pigs as a validated model, this study investigated the effects of a diet-induced vitC deficiency (100 mg vitC/kg feed) or depletion (0 mg vitC/kg feed) on the expression of transporters SVCT1 and SVCT2 in selected tissues and the transport from plasma to cerebrospinal fluid (CSF). In deficient animals, SVCT1 was increased in the liver, whereas a decreased SVCT1 expression but increased SVCT2 mRNA in livers of depleted animals suggests a shift in transporter expression as response to the diet. In CSF, a constant plasma:CSF ratio shows unaltered vitC transport irrespective of dietary regime. The study adds novel information to the complex regulation maintaining vitC homeostasis in vivo during states of deficiency.

Retinoic Acid Therapy Resistance Progresses from Unilineage to Bilineage in HL-60 Leukemic Blasts

Emergent resistance can be progressive and driven by global signaling aberrations. All-trans retinoic acid (RA) is the standard therapeutic agent for acute promyelocytic leukemia, but 10–20% of patients are not responsive, and initially responsive patients relapse and develop retinoic acid resistance. The patient-derived, lineage-bipotent acute myeloblastic leukemia (FAB M2) HL-60 cell line is a potent tool for characterizing differentiation-induction therapy responsiveness and resistance in t(15;17)-negative cells. Wild-type (WT) HL-60 cells undergo RA-induced granulocytic differentiation, or monocytic differentiation in response to 1,25-dihydroxyvitamin D3 (D3). Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Here, we show that the R38+ and R38- HL-60 cell lines display a progressive reduced response to D3-induced differentiation therapy. Exploiting the biphasic dynamic of induced HL-60 differentiation, we examined if resistance-related defects occurred during the first 24 h (the early or “precommitment” phase) or subsequently (the late or “lineage-commitment” phase). HL-60 were treated with RA or D3 for 24 h, washed and retreated with either the same, different, or no differentiation agent. Using flow cytometry, D3 was able to induce CD38, CD11b and CD14 expression, and G1/G0 arrest when present during the lineage-commitment stage in R38+ cells, and to a lesser degree in R38- cells. Clustering analysis of cytometry and quantified Western blot data indicated that WT, R38+ and R38- HL-60 cells exhibited decreasing correlation between phenotypic markers and signaling factor expression. Thus differentiation induction therapy resistance can develop in stages, with initial partial RA resistance and moderate vitamin D3 responsiveness (unilineage maturation block), followed by bilineage maturation block and progressive signaling defects, notably the reduced expression of Vav1, Fgr, and c-Raf.

AB0844 Detection of low Levels of Vitamin D or Free Testosterone in Patients Receiving Prednisone for A Rheumatic Disease

ObjectivesThe purpose of this cross-sectional study was to determine the prevalence of vitamin D insufficiency in males and females and testosterone deficiency in males, who have an increased risk for...

The combination of vitamin D deficiency and mild to moderate chronic kidney disease is associated with low bone mineral density and deteriorated femoral microarchitecture: results from the KNHANES 2008-2011.

Although mild to moderate chronic kidney disease (CKD) and vitamin D deficiency are prevalent in the elderly population worldwide and are associated with sarcopenia, their influence on bone mineral density (BMD) has not been determined. The objective of the study was to determine the combined effects of vitamin D deficiency and CKD on BMD in the elderly population and their relationships with sarcopenia and PTH levels. This was a cross-sectional study with nationally representative samples of 6949 subjects aged 55 years or older from the Korea National Health and Nutrition Examination Surveys conducted between 2008 and 2011. The study population was divided into four groups according to vitamin D and CKD status. The combined association of CKD and vitamin D deficiency [25(OH)D<20 ng/mL] with osteopenia or osteoporosis was assessed, and the status of PTH and the sarcopenic index (appendicular skeletal muscle mass as a percentage of body weight or appendicular skeletal muscle mass per weight) as a measure of sarcopenia were evaluated. BMD in the total hip and femoral neck as well as femoral bone geometry was markedly deteriorated in stage 3 and 4 CKD subjects with vitamin D deficiency compared with other groups. Regardless of gender, these subjects also had higher levels of PTH and increased prevalence of sarcopenia. Multivariable logistic regression analyses demonstrated that CKD subjects with vitamin D deficiency showed a significantly increased risk of osteoporosis or osteopenia [odds ratios 1.49 and 2.06 (1.81 and 2.65) at the femur neck and total hip, respectively, in women (men)], which was mainly associated with elevated levels of PTH and sarcopenia in these groups. The combination of mild to moderate CKD and vitamin D deficiency was significantly associated with low BMD in a geriatric population, linked with hyperparathyroidism and sarcopenia.

A double blind randomized controlled trial in neonates to determine the effect of vitamin A supplementation on immune responses: The Gambia protocol

BackgroundVitamin A supplementation significantly reduces all-cause mortality when given between 6–59 months of age, but has a null or detrimental effect when given between 1–5 months. Studies of neonatal vitamin A supplementation conducted across Africa and South Asia have produced conflicting findings. These age-pattern variations might result from immunological interactions between vitamin A supplementation and vaccines. Knowledge on the potential immunological sequelae of human neonatal vitamin A supplementation is so scarce that the foremost aim of this study is to seek indicative data on aspects of immunity likely to be affected by neonatal vitamin A supplementation. The objective of this trial is to test whether human neonatal vitamin A supplementation modulates immune function including improved thymic maturation in infancy and improved systemic immune responses to routine immunization.Methods/designIn an area of moderate vitamin A deficiency in a peri-urban area of The Gambia, 200 mother–infant pairs were enrolled in a double-blind randomised controlled trial. Within 48 hours of birth, neonates were randomised with stratification by birth weight and sex to receive either an oral dose of 50,000 IU vitamin A or placebo. Expanded Programme of Immunisation birth vaccinations were administered after supplementation, with subsequent vaccinations administered at 8, 12 and 16 weeks of age. A range of immunological outcomes were examined up to 17 weeks of age, with additional morbidity and anthropometry follow-up carried out throughout the first year of life. The primary endpoint of this trial is the frequency of circulating T regulatory (Treg) cells expressing gut homing receptors in infants at 17 week post-supplementation, with secondary outcomes including thymus maturation and B cell immune responses.DiscussionIndicative immunological data from this trial (and its Bangladeshi counterpart), will complement the larger randomised controlled trials (conducted in India, Tanzania and Ghana), on the effectiveness and safety of neonatal vitamin A supplementation in improving infant survival. Combined these trials, in addition to the existing trials, will inform policy.Trial registrationclinicaltrials.gov NCT01476358

Vitamin C supplementation (1000 mg/d) increased physical activity and reduced cold symptoms in young men with adequate‐to‐low vitamin C status (828.3)

Nearly 25% of US adults have below adequate vitamin C status (plasma concentrations &lt;28 µmol/L), and 6% of the adult population is classified as deficient (&lt;11 µmol/L). Poor vitamin C status is underdiagnosed as early indications are unremarkable (fatigue, malaise, depression). Such feelings may manifest as a reduced desire to be physically active; moreover, hypovitaminosis C may be associated with increased cold duration and severity. This double‐blind, placebo‐controlled, randomized study examined the impact of vitamin C (1000 mg daily) on physical activity (PA) and symptoms of upper respiratory tract infections in men during the peak of the cold season. Consenting adults (23.2±3.6 y; 25.1±3.9 kg/m2; 29.5±8.7 μmol/L) completed the Wisconsin Upper Respiratory Symptom Survey‐21 daily and the Godin Leisure‐Time Exercise Questionnaire weekly. PA was lower in controls (n=14) over the course of the 8‐week trial in comparison to the vitamin C group (n=15) (METs: +5.9±3.2 and +18.2±5.9 kcal· kg‐1· wk‐1; p=0.046). The overall cold symptom severity score was 4‐fold higher for controls versus the vitamin C group (2.4±0.7 and 0.6±0.1; p=0.010). The incidence of colds was also higher in controls as compared to the vitamin C group (2.2±0.7 and 0.3±0.1 colds; p=0.008). These data suggest measurable health advantages associated with moderate vitamin C supplementation in a population with adequate‐to‐low vitamin C status.

Moderate vitamin D deficiency and inflammation related markers in overweight/obese schoolchildren.

Obesity has been associated with vitamin D deficiency and increased oxidative stress, which can lead to the dysregulation of adipokines and inflammation. The aim of the present work was to examine the association of vitamin D status [25(OH)D] on inflammatory related markers in overweight/obese children. A total of 137 Spanish schoolchildren between 9 and 12 years of age (31.4% with overweight/obesity) were studied. Being overweight was defined as BMI≥85th percentile and obesity as BMI≥97th percentile using the reference tables of Hernández. Serum 25(OH)D concentrations were measured by chemiluminescent assay. Plasma tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) were measured by immunoenzyme assay. Serum adiponectin was determined using an ELISA kit. Serum high-sensitivity C-reactive protein (hs-PCR) was tested by immunonephelometry. IL-6 concentrations were higher in the overweight/obese children with deficient serum 25(OH)D (<20 ng/mL) than in those in this group but whose serum 25(OH)D concentrations were adequate (≥20 ng/mL). Serum 25(OH)D was inversely associated with IL-6 concentrations in the overweight/obese subjects taking into account different covariates; thus, for every 1 ng/mL rise in the former, the latter fell by 0.160 pg/mL (β=-0.160±0.068; R2=0.131; p=0.023). The obese subjects with concentrations of ≥25 ng/mL had lower hs-CRP values compared to those with concentrations of <25 ng/mL (0.053±0.035 vs. 0.356±0.613 mg/dL; p=0.035). Low serum 25(OH)D was significantly associated high serum IL-6 in overweight/obese children, and with increased hs-CRP in obese children.

No role for vitamin D or a moderate fat diet in aging induced cognitive decline and emotional reactivity in C57BL/6 mice

Epidemiological studies have shown associations between vitamin D, mental health and glucose homeostasis in the elderly. Causal evidence, however, is still lacking. The objective of this study was to investigate the importance of vitamin D in the prevention of emotional disturbances and cognitive decline in aging C57BL/6 mice, with pre-diabetes type II as potential effect modifier. Mice were exposed to one of four diets from 10 months till 24 months of age: low fat vitamin D adequate (LFD), LF vitamin D deficient (LF), moderate fat vitamin D adequate (MFD), and MF vitamin D deficient (MF). The MFD/MF diet was applied to induce a condition resembling pre-diabetes type II. Behavior was assessed twice in the same group of mice at 6-8 and at 22-23 months of age using the Open Field Test (OFT), Elevated Plus Maze (EPM), Object Recognition Test (ORT) and the Morris Water Maze (MWM). We successfully induced vitamin D deficiency in the LF/MF mice. Moreover, fasting glucose and fasting insulin levels were significantly higher in MFD/MF mice than in LFD/LF mice. A significant aging effect was observed for most behavioral parameters. A MF(D) diet was shown to delay or prevent the age-related increase in emotional reactivity in the EPM. No effect of vitamin D or vitamin D*fat on behavioral outcomes was measured. Aging significantly affected emotional reactivity and cognitive performance. Although other studies have shown effects of vitamin D on emotional reactivity and cognitive performance in mice, these findings could not be confirmed in aged C57BL/6 mice in this study.

Vitamin D Deficiency and Exogenous Vitamin D Excess Similarly Increase Diffuse Atherosclerotic Calcification in Apolipoprotein E Knockout Mice

BackgroundObservational data associate lower levels of serum vitamin D with coronary artery calcification, cardiovascular events and mortality. However, there is little interventional evidence demonstrating that moderate vitamin D deficiency plays a causative role in cardiovascular disease. This study examined the cardiovascular effects of dietary vitamin D deficiency and of vitamin D receptor agonist (paricalcitol) administration in apolipoprotein E knockout mice.MethodsMice were fed atherogenic diets with normal vitamin D content (1.5IU/kg) or without vitamin D. Paricalcitol, or matched vehicle, was administered 3× weekly by intraperitoneal injection. Following 20 weeks of these interventions cardiovascular phenotype was characterized by histological assessment of aortic sinus atheroma, soluble markers, blood pressure and echocardiography. To place the cardiovascular assessments in the context of intervention effects on bone, structural changes at the tibia were assessed by microtomography.ResultsVitamin D deficient diet induced significant reductions in plasma vitamin D (p<0.001), trabecular bone volume (p<0.01) and bone mineral density (p<0.005). These changes were accompanied by an increase in calcification density (number of calcifications per mm2) of von Kossa-stained aortic sinus atheroma (461 versus 200, p<0.01). Paricalcitol administration suppressed parathyroid hormone (p<0.001), elevated plasma calcium phosphate product (p<0.005) and induced an increase in calcification density (472 versus 200, p<0.005) similar to that seen with vitamin D deficiency. Atheroma burden, blood pressure, metabolic profile and measures of left ventricular hypertrophy were unaffected by the interventions.ConclusionVitamin D deficiency, as well as excess, increases atherosclerotic calcification. This phenotype is induced before other measures of cardiovascular pathology associated clinically with vitamin D deficiency. Thus, maintenance of an optimal range of vitamin D signalling may be important for prevention of atherosclerotic calcification.

Association of homocysteine with global DNA methylation in vegetarian Indian pregnant women and neonatal birth anthropometrics

Objective: The present study was designed to evaluate if plasma maternal folate, vitamin B-12 and homocysteine levels had an effect on maternal global DNA methylation and neonatal anthropometrics in Indian pregnant women.Methods: A total of 49 participants having completed ≥36 weeks of pregnancy were enrolled in the study. Estimation of folate was by Ion capture assay, vitamin B-12 by microparticle enzyme immunoassay, total homocysteine by fluorescence polarization immunoassay and global DNA methylation using Cayman’s DNA methylation enzyme immunoassay (EIA) kit.Results: Folate and vitamin B-12 were inversely correlated to homocysteine in pregnant women consuming vegetarian and non-vegetarian diet. No difference in global DNA methylation was found between the vegetarian and non-vegetarian pregnant women. Folate and vitamin B-12 did not show association with global DNA methylation, however plasma total homocysteine of the vegetarian group showed significant correlation to global DNA methylation (r2 = 0.49, p = 0.011). Plasma total homocysteine was inversely related to tricep skinfold (r2 = −0.484, p = 0.01) and chest circumference (r2 = −0.104, p = 0.04) of neonates in vegetarian group.Conclusion: Moderate vitamin B-12 deficiency in vegetarian pregnant women might be the cause of hyperhomocystinemia, hypermethylation when compared to vitamin B-12 sufficient non-vegetarian group.

Levels of Serum 25-Hydroxy-Vitamin D in Benign and Malignant Breast Masses

The true association between breast cancer and vitamin D is currently under investigation. We compared serum 25-hydroxy-vitamin D levels in women with benign and malignant breast masses and controls. Levels of vitamin D were measured by electrochemiluminescense. Serum levels >35 ng/ml, 25-35 ng/ml, 12.5-25 ng/ml and <12.5 ng/ml were considered as normal, mild, moderate and severe vitamin D deficiency, respectively. Overall, 364 women were included in the control, 172 in the benign and 136 in the malignant groups. The median serum vitamin D level was significantly lower in breast cancers than controls. Levels were also lower in malignant than benign cases and in benign cases than controls although statistically non-significant. Multinomial logistic regression analysis showed that severe vitamin D deficiency causes a three-fold increase in the risk of breast cancer while this was not the case for moderate and mild deficiency.

Folic acid supplementation with and without vitamin B6 and revascularization risk: A meta-analysis of randomized controlled trials

There is a growing amount of data and a continuing controversy over the effect of folic acid supplementation with and without vitamin B6 on revascularization risk. We conducted a meta-analysis based on up-to-date published relevant randomized trials to further examine this issue. Relative risk (RR) was used to measure the effect of folic acid supplementation on risk of revascularization using a random-effects model. Total revascularization was defined as any arterial revascularization. Restenosis was defined as stenosis of more than 50 percent of the luminal diameter. Overall, folic acid supplementation had no significant effect on coronary revascularization (9 trials, n = 27,418, RR = 0.99; 95%CI:0.88-1.11, P = 0.88), coronary artery bypass grafting (CABG) (5 trials, n = 10,703, 0.90; 0.79-1.03, P = 0.11), percutaneous coronary intervention (PCI) (5 trials, n = 10,703, 1.05; 0.89-1.23, P = 0.59), coronary restenosis (3 trials, n = 926, 1.05; 0.89-1.23, P = 0.59) or total revascularization (7 trials, n = 29,314, 1.06; 95%CI: 0.99-1.13, P = 0.10). However, a greater beneficial effect was observed for coronary revascularization among those trials with a moderate dose of vitamin B6 (5-10 mg/d; RR: 0.47; 95%CI: 0.28-0.80, P = 0.005), but not in trials without vitamin B6 or with a high dose of vitamin B6. And a non-significant greater total revascularization risk was observed in trials with a higher folic acid dose (>2 mg/d, RR = 1.11; 95%CI: 0.98-1.25, P = 0.09; ≥5 mg/d, RR = 1.98; 95%CI: 0.93-4.20, P = 0.08). Our analyses indicate that folic acid supplementation has no significant effect on coronary revascularization, CABG, PCI, coronary restenosis or total revascularization. However, a combination of folic acid and moderate vitamin B6 may be beneficial in reducing coronary revascularization risk.

Failure of a dietary model to affect markers of inflammation in domestic cats.

BackgroundOxidative stress and inflammation can be altered by dietary factors in various species. However, little data are available in true carnivorous species such as domestic cats. As numerous anti-inflammatory and anti-oxidative additives become available and might be of use in cats with chronic low-grade inflammatory diseases, the current study aimed to develop a model of diet-induced inflammation by use of two opposite diets. It was hypothesized that a high fat diet enhanced in n-6 PUFA and with lower concentrations of antioxidants would evoke inflammation and oxidative stress in domestic cats.ResultsSixteen healthy adult cats were allocated to two groups. One group received a moderate fat diet, containing pork lard and salmon oil (AA:(EPA + DHA) ratio 0.19) (MFn-3), while the other group was fed a high fat diet, containing pork lard and chicken fat (AA:(EPA + DHA) ratio 2.06) (HFn-6) for 12 weeks. Prior to and 2, 4, 6, 8, 10 and 12 weeks after starting the testing period, blood samples were collected. Erythrocytic fatty acid profile showed clear alterations in accordance to the dietary fatty acid profile. Serum thiobarbituric acid reactive substances was higher when fed MFn-3 compared to the HFn-6, suggesting augmented oxidative stress. This was associated with a reduced serum vitamin E status, as serum α-tocopherol concentrations were lower with MFn-3, even with higher dietary levels of vitamin E. Serum cytokine and serum amyloid A concentrations were not influenced by diet.ConclusionThese results point towards a resistance of cats to develop dietary fat-induced inflammation, but also suggest a high susceptibility to oxidative stress when fed a fish oil-supplemented diet even with moderate fat level and additional vitamin E.

Vitamin B12 Deficiency In Patients With Normal Blood Count

BackgroundVitamin B12 (Cobalamine) is essential for protein synthesis, cell proliferation and optimal systemic function, particularly for nervous system and blood. Moderate vitamin B12 deficiency is common even with normal hematological parameters. Diagnosis and treatment are delayed because of non-specific symptoms, normal blood count and lack of awareness. ObjectivesTo find out the prevalence of hidden vitamin B12 deficiency in patients with normal blood count. Materials and MethodsWe reviewed the results of vitamin B12 tests which were ordered for patients at King Khalid University Hospital, King Saud University between 1st of January- 30thof December 2012. Those with low vitamin B12 and normal blood count were contacted and interviewed and were asked for consent to participate in this retrospective study and to answer detailed medical history questions on dietary habits, medical illnesses, gastro-intestinal surgical procedures, and long term medications. ResultsOut of 3045 patients, there were 415 (155 males and 260 females, aged 36 +/- 18 years) with normal blood count, but low vitamin B12 level, which was between 40-140 pmol/l ( normal 145-637). 350 patients agreed (81 males and 170 females), but complete information was obtained only from 251 patients (71.71%). Symptoms included fatigue, tingling and numbness, impaired short-term memory, insomnia and impaired concentration. Identified causes of Vitamin B12 deficiency were as follows: 65 patients (26%) had partial gastrectomy, 12 (5%) had resection of the terminal ileum, 16 (6%) had gastric atrophy, 18 (7%) had celiac disease, 36 (14%) were vegetarians, 49 (20%) were diabetic on metformin, 47 (19%) were on proton pump inhibitors, and in 8 (3%) the cause could not be identified. ConclusionVitamin B12 deficiency is common even in patients with normal hematological values. There is a need for continuous awareness program for physicians, dietitians, and general population to identify risk factors, and to implement guidelines for prevention, early detection and treatment of hidden Vitamin B12 deficiency. Disclosures:No relevant conflicts of interest to declare.