From the Bloggers

Magnesium for Lower Fasting Glucose and Insulin?

Researchers examined cross-sectional associations of dietary magnesium intake with fasting glucose (FG) and fasting insulin (FI), associations of magnesium-related SNPs with FG and FI, and interactions between dietary magnesium (Mg) intake and both Mg-related and glycemia-related SNPs on FG and FI in meta-analysis of 15 cohort studies including more than 50,000 participants (Cohorts for Heart and Aging Research in Genomic Epidemiology). After adjustments for age, sex, energy intake, BMI, and behavioral risk factors, researchers found that Mg was inversely associated with FG and FI, and that no Mg-related SNP or interaction between any SNP and Mg reached significance after correction for multiple testing. Their findings support those of other recent met-analysis of studies on Mg and incident type 2 diabetes, which estimated a 14% reduced risk of disease per daily 100 mg increment in Mg intake.

A Hruby, et al. Higher Magnesium Intake Is Associated with Lower Fasting Glucose and Insulin, with No Evidence of Interaction with Select Genetic Loci, in a Meta-Analysis of 15 CHARGE consortium Studies1,2,3,4. J.Nutr. March 1, 2013 Vol 143, No. 3, 345-353

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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

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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

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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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Zinc, Hedgehog Autoprocesssing, and Chronic Disease!

Zinc is an essential trace mineral with a wide range of biological functions. Hedgehog (Hh) pathway is a key regulator of cell growth and development that helps to establish the body plan of all animals with bilateral symmetry. In many diseases, zinc deficiency and elevated level of Hh ligand co-exist, including prostate cancer, lung cancer, ovarian cancer, and autism. In this study, researchers demonstrate that there is a link between zinc and Hh signaling. The Hh ligand, which is the upstream activator of Hh signaling, originates from Hh autoprocessing. In an in vitro Hh autoprocessing assay, researchers showed that zinc inhibits Hh autoprocessing. They then demonstated that zinc inhibits Hh autoprocessing in a cellular environment. They found that zinc binds the active site residues of the Hh autoprocessing domain to inhibit autopreocessing. In normal physiology, zinc likely acts as a negative regulator of Hh autoprocessing and inhibits the generation of Hh ligand and Hh signaling. According to corresponding author Chunyu Wang, under normal conditions “zinc will inhibit the production of the Hh ligand, and therefore inhibit the Hh pathway, but if there is a zinc deficiency, the pathway can be activated due to enhanced production the Hh ligand.’ Their data suggest a causal relationship between zinc deficiency and the overproduction of Hh ligand.

J Xie, et al. Zinc Inhibits Hedgehog Autoprocessing: Liking Zinc Deficiency with Hedgehog Activation. Journal of Biological Chemistry, 2015; jbc.M114.623264 DOI: 10.1074/jbc.M114.623264

ML Martialay. Zinc Deficiency Linked to Activation of Hedgehog Signaling Pathway. RPI News. Apr 16, 2015

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Zinc deficiency linked to systemic inflammation and chronic disease!

A recent study helps explain how zinc deficiency impacts chronic diseases including cardiovascular disease, diabetes, autism and cancers including prostate, lung, ovarian and breast cancer. Zinc status is especially important for seniors, 40% of whom do not consume enough zinc, and their bodies do not appear to use or absorb zinc efficiently. In one study researchers showed that zinc deficiency induced an increase in inflammatory response in cells, and showed that reducing zinc caused improper immune cell activation and dysregulation of IL-6 cytokine, a protein that affects inflammation in the cell. In an animal model they found that older mice had low zinc levels that corresponded with increased chronic inflammation and decreased IL-6 methylation, an epigenetic mechanism used to control gene expression. They found the same decrease in IL-6 methylation in human immune cells from elderly people. Because the body doesn’t store zinc, adequate intake is crucial. Professor Ho, the lead investigator stated “zinc deficiency is probably a bigger problem that most people realize” and “Preventing that deficiency is important.”

CP Wong,NA rinaldi, E Ho. Zinc deficiency enhanced inflammatory response by increasing immune cell activation and inducing IL6 promoter demethylation. Molecular Nutrition and Food Research, 2015; DOI: 10.1002/mnfr.201400761

Oregon State U. “Zinc deficiency linked to immune system response, particularly in older adults”. ScienceDaily, 23 March 2015

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Vitamin D for chronic inflammatory rheumatic diseases (CIRD)?

Researchers studied a cross-section from the baseline visit of the CARMA (cardiovascular in rheumatology) project, a 10 year prospective study evaluating the risk of cardiovascular events in rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) patients, and non-CIRD patients who attended rheumatology outpatient clinics from 67 hospitals in Spain. 2,234 patients were assessed. Non-CIRD group was frequency matched by age with the joint distribution of the three CIRD groups included in the study. The aim was to evaluate the association between vitamin D status (25(OH)D) and the clinical characteristics of patients with CIRD. Deficiency was defined as 25(OH)D levels <20 ng/ml. Patients with CIRD had lower 25(OH)D levels than those form the non-CIRD controls. Globally, vitamin D deficiency was detected in 40.5% of patients with RA, 39.7 % of patients with AS, 40.9 % of patients with PsA, and 26.7% of those with non-CIRD. Overall, researchers found that RA patients have a high risk of vitamin D deficiency, in spite of presenting low-to-moderate disease activity. They concluded that clinicians must monitor the levels of vitamin D at baseline and during follow-up and supplement vitamin D if any deficiency is detected.

A. Urruticoechea-Arana, et al. Vitamin D deficiency in chronic inflammatory rheumatic diseases: results of the cardiovascular in rheumatology [CARMA] study. Arthritis Research & Therapy Aug 15, 2015

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