Archive October 2015

Vitamin D for Crohn’s Disease!

Researchers conducted a double-blind randomized placebo-controlled study, assigning 27 Crohn’s disease (CD) patients in remission to 2000 IU/day of vitamin D3 or placebo for 3 months. They determined intestinal permeability (IP), plasma-cathelicidin (LL-37), human-beta-defensin-2 (hBD2), disease activity [Crohn’s Disease Activity Index (CDAI)], c-reactive protein (CRP), fecal calprotectin, Quality of Life (QoL) and serum vitamin d (25(OH)D) at 0 and 3 months. Results showed that at 3 months, 25(OH)D concentrations were significantly higher in the treated group, and intra-group analysis showed increased LL-37 [an antimicrobial peptide (AMP) of the innate immune system expressed by the gastrointestinal epithelium] concentrations, and maintenance of IP measures. In contrast, in the placebo group, the small bowel and gastro-duodenal permeability increased from baseline. At 3 months, patients with 25(HO)D levels ≥ 75 nmol/L had significantly lower CRP, higher QoL, higher LL-37 concentrations and lower CDAI scores compared to those with lower 25(OH)D levels.

T Raftery, et al. Effects of vitamin D supplementation on intestinal permeability, cathelicidin and disease markers in Crohn’s disease: Results from a randomized double-blind placebo-controlled study. United Euro Gastro Journal 2015, Vol. 3(3) 294-302


Melatonin Protects Neurons and Glia!

Melatonin is an uncommonly effective direct free radical scavenger and indirect antioxidant. It detoxifies both reactive oxygen species (ROS) and reactive nitrogen species (RNS), both of which are produced in the brain. Researchers from the Dept. of Cellular and Structural Biology, University of Texas Health Science Center in San Antonio, conducted and published a review of melatonin’s role in detoxifying and metabolizing ROS and RNS. Melatonin, from either the blood or the cerebrospinal fluid (CSF), readily enters the brain to protect neurons and glia from molecular damage induced by ROS and RNS. Melatonin’s efficacy in reducing molecular damage resulting from toxic oxygen and nitrogen derivatives in both the brain and spinal cord supports the concept that this non-toxic molecule may have utility in forestalling and/or delaying the development and progression of neurodegenerative diseases that have a massive free radical component. Disease models of interest and in which melatonin has been most thoroughly tested include Alzheimer disease, Parkinson disease, and to a lesser extent Huntington disease and amyotrophic lateral sclerosis. Their summarization of experimental findings clearly document that melatonin readily prevents oxidative damage to both neurons and glia, and in doing so, greatly reduces apoptosis of critical cells within the central nervous system.

RJ Reiter, et al. Melatonin Reduces Oxidative Catastrophe in Neurons and Glia. Act Nerv Super Rediviva 2010; 52(2): 93-103


Vitamin D and Lung Cancer!

! Mounting evidence supports a protective effect of high 25(OH)D, an indicator of vitamin D status, on risk of various cancers including lung cancer. Researchers carried out a dose-response meta-analysis to elucidate the 25(OH)D – lung cancer association. Eligible studies were identified by searching PubMed and EMBASE databases, and the summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated using the random-effects model. Thirteen reports from ten prospective studies were included, totaling 2,227 lung cancer events. Results of the meta-analysis showed a significant reduction in the risk of lung cancer for each 10 nmol/L increment in 25(OH)D concentrations. There was evidence of a nonlinear relationship between 24(OH)D and risk of lung cancer, with the greatest reductions in risk observed at 53 nmol/L, and remained protective until approximately 90 nmol/L. Higher levels showed no further significant association with cancer risk.

Guo-Chong Chen, et al. Circulating 25-hydroxyvitamin D and risk of lung cancer: a dose-response meta-analysis. Cancer Causes & Control Sept 2015. Doi:10.1007/s10552-015-0665-6


Zinc, Prenatal LPS and Autism:

In order to understand the causes of autistic-like behaviors, researchers from the University of Sao Paulo evaluated maternal serum metal concentrations involved in intra uterine development and infection/inflammation. They identified reduced maternal levels of zinc, magnesium, selenium and manganese after lipopolysaccharide (LPS) exposure in prenatal rats. They selected zinc as the prenatal treatment to prevent or ease the impairments induced by LPS, as cytokines produced after LPS exposure induce metallothionein, which sequesters zinc and induces maternal and fetal hypozincemia. They then treated the dams with zinc in an attempt to prevent or ease the impairments in the offspring, and evaluated the social and cognitive autistic-like behaviors and brain tissues of the offspring to identify the central mechanism that trigger the development of autism. LPS exposure impaired play behaviors and induced autistic-like behaviors. Prenatal LPS also decreased tyrosine hydroxylase levels and increased the levels of mammalian target of rapamycin (mTOR) in the striatum. Thus, striatal dopaminergic impairments may be related to autism. Excessive signaling through the mTOR pathway has been considered a biomarker of autism, corroborating their rat model of autism. Prenatal zinc treatment prevented these autistic-like behaviors and striatal dopaminergic and mTOR disturbances in the offspring induced by LPS exposure. Findings reveal a possible relation between maternal zinc deficiency during gestation and the onset of autism. In this study, prenatal zinc administration demonstrates a beneficial effect on the prevention of autism.

TB Kirsten, et al. Lipopolysaccharide Exposure Induces Maternal Hypozincemia, and Prenatal Zinc Treatment Prevents Autistic-Like Behaviors and Disturbances in the Striatal Dopaminergic and mTOR Systems of Offspring. PLOS.ONE DOI:10.1371/journal.pone.0134565 July, 28, 2015


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