The emerging role of vitamin C as a treatment for sepsis.

PMID: 

Nutrients. 2020 Jan 22 ;12(2). Epub 2020 Jan 22. PMID: 31978969

Abstract Title: 

The Emerging Role of Vitamin C as a Treatment for Sepsis.

Abstract: 

Sepsis, a life-threatening organ dysfunction due to a dysregulated host response to infection, is a leading cause of morbidity and mortality worldwide. Decades of research have failed to identify any specific therapeutic targets outside of antibiotics, infectious source elimination, and supportive care. More recently, vitamin C has emerged as a potential therapeutic agent to treat sepsis. Vitamin C has been shown to be deficient in septic patients and the administration of high dose intravenous as opposed to oral vitamin C leads to markedly improved and elevated serum levels. Its physiologic role in sepsis includes attenuating oxidative stress and inflammation, improving vasopressor synthesis, enhancing immune cell function, improving endovascular function, and epigenetic immunologic modifications. Multiple clinical trials have demonstrated the safety of vitamin C and two recent studies have shown promising data on mortality improvement. Currently, larger randomized controlled studies are underway to validate these findings. With further study, vitamin C may become standard of care for the treatment of sepsis, but given its safety profile, current treatment can be justified with compassionate use.

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Periodontitis is associated with a low concentration of vitamin C in plasma.

PMID: 

Clin Diagn Lab Immunol. 2003 Sep ;10(5):897-902. PMID: 12965924

Abstract Title: 

Periodontitis is associated with a low concentration of vitamin C in plasma.

Abstract: 

This study aimed to clarify how concentrations of vitamin C in plasma relate to the serology of periodontitis. The random sample used comprised 431 men, 194 from Finland and 237 from Russia. The plasma vitamin C concentration was determined by o-phtaldialdehyde-fluorometry, and serum immunoglobulin G antibodies to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were determined by a multiserotype enzyme-linked immunosorbent assay (ELISA). The mean plasma vitamin C concentration was higher (P

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Wild pistachio oil improve metabolic syndrome features in rats with high fructose ingestion.

PMID: 

Iran J Basic Med Sci. 2018 Dec ;21(12):1255-1261. PMID: 30627369

Abstract Title: 

Wild pistachio () oil improve metabolic syndrome features in rats with high fructose ingestion.

Abstract: 

Objectives: Metabolic syndrome is a multiplex risk factor for diabetes and cardiovascular disease. Since some dietary fats such as mono-unsaturated fatty acids (MUFA) modify metabolic syndrome components the aim of the present study was to evaluate the preventive effects of mixture, kernel and hull oils of wild pistachio (WP) () as good sources of MUFA on different features of this abnormality in rats under induction.Materials and Methods: In this study rats were randomly assigned to six groups with 12 animals per group. Metabolic syndrome was induced by fructose solution in groups 2, 3, 4, 5, and 6. Group 3 received sunflower oil and groups 4, 5, and 6 received mixture, hull and kernel oils of WP (2 ml/kg/day), respectively, for 10 weeks. Then, lipid profiles, glycemic indices, oxidative stress and inflammatory parameters were measured using standard laboratory tests.Results: Different forms of WP oil induced hypotriglyceridemia, but the hypocholesterolemia effect was seen only in the mixed and kernel oil groups. Kernel oil also significantly reduced LDL and HDL cholesterol (

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Chronic pistachio consumption reduces oxidative damage to DNA and increases the gene expression of some telomere-associated genes.

PMID: 

Am J Clin Nutr. 2019 06 1 ;109(6):1738-1745. PMID: 31051499

Abstract Title: 

Pistachio consumption modulates DNA oxidation and genes related to telomere maintenance: a crossover randomized clinical trial.

Abstract: 

BACKGROUND: Telomere attrition may play an important role in the pathogenesis and severity of type 2 diabetes (T2D), increasing the probability ofβ cell senescence and leading to reduced cell mass and decreased insulin secretion. Nutrition and lifestyle are known factors modulating the aging process and insulin resistance/secretion, determining the risk of T2D.OBJECTIVES: The aim of this study was to evaluate the effects of pistachio intake on telomere length and other cellular aging-related parameters of glucose and insulin metabolism.METHODS: Forty-nine prediabetic subjects were included in a randomized crossover clinical trial. Subjects consumed a pistachio-supplemented diet (PD, 50 E% [energy percentage] carbohydrates and 33 E% fat, including 57 g pistachios/d) and an isocaloric control diet (CD, 55 E% carbohydrates and 30 E% fat) for 4 mo each, separated by a 2-wk washout period. DNA oxidation was evaluated by DNA damage (via 8-hydroxydeoxyguanosine). Leucocyte telomere length and gene expression related to either oxidation, telomere maintenance or glucose, and insulin metabolism were analyzed by multiplexed quantitative reverse transcriptase-polymerase chain reaction after the dietary intervention.RESULTS: Compared with the CD, the PD reduced oxidative damage to DNA (mean: -3.5%; 95% CI: -8.07%, 1.05%; P = 0.009). Gene expression of 2 telomere-related genes (TERT and WRAP53) was significantly upregulated (164% and 53%) after the PD compared with the CD (P = 0.043 and P = 0.001, respectively). Interestingly, changes in TERT expression were negatively correlated to changes in fasting plasma glucose concentrations and in the homeostatic model assessment of insulin resistance.CONCLUSIONS: Chronic pistachio consumption reduces oxidative damage to DNA and increases the gene expression of some telomere-associated genes. Lessening oxidative damage to DNA and telomerase expression through diet may represent an intriguing way to promote healthspan in humans, reversing certain deleterious metabolic consequences of prediabetes. This study was registered at clinicaltrials.gov as NCT01441921.

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Pistachio consumption alleviates inflammation and improves gut microbiota composition in mice fed a high-fat diet.

PMID: 

Int J Mol Sci. 2020 Jan 6 ;21(1). Epub 2020 Jan 6. PMID: 31935892

Abstract Title: 

Pistachio Consumption Alleviates Inflammation and Improves Gut Microbiota Composition in Mice Fed a High-Fat Diet.

Abstract: 

High-fat diet (HFD) induces inflammation and microbial dysbiosis, which are components of the metabolic syndrome. Nutritional strategies can be a valid tool to prevent metabolic and inflammatory diseases. The aim of the present study was to evaluate if the chronic intake of pistachio prevents obesity-associated inflammation and dysbiosis in HFD-fed mice. Three groups of male mice (four weeks old;= 8 per group) were fed for 16 weeks with a standard diet (STD), HFD, or HFD supplemented with pistachios (HFD-P; 180 g/kg of HFD). Serum, hepatic and adipose tissue inflammation markers were analyzed in HFD-P animals and compared to HFD and STD groups. Measures of inflammation, obesity, and intestinal integrity were assessed. Fecal samples were collected for gut microbiota analysis. Serum TNF-α and IL-1β levels were significantly reduced in HFD-P compared to HFD. Number and area of adipocytes, crown-like structure density, IL-1β, TNF-α, F4-80, and CCL-2 mRNA expression levels were significantly reduced in HFD-P subcutaneous and visceral adipose tissues, compared to HFD. A significantreduction in the number of inflammatory foci and IL-1β and CCL-2 gene expression was observed in the liver of HFD-P mice compared with HFD./ratio was reduced in HFD-P mice in comparison to the HFD group. A pistachio diet significantly increased abundance of healthy bacteria genera such as,,,,, and, and greatly reduced bacteria associated with inflammation, such as,,, and. The intestinal conductance was lower in HFD-P mice than in the HFD mice, suggesting an improvement in the gut barrier function. The results of the present study showed that regular pistachio consumption improved inflammation in obese mice. The positive effects could be related to positive modulation of the microbiota composition.

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Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22-dependent manner.

PMID: 

JCI Insight. 2020 01 16 ;5(1). Epub 2020 Jan 16. PMID: 31941837

Abstract Title: 

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22-dependent manner.

Abstract: 

Colitis, an inflammatory bowel disease, is caused by a variety of factors, but luminal microbiota are thought to play crucial roles in disease development and progression. Indole is produced by gut microbiota and is believed to protect the colon from inflammatory damage. In the current study, we investigated whether indole-3-carbinol (I3C), a naturally occurring plant product found in numerous cruciferous vegetables, can prevent colitis-associated microbial dysbiosis and attempted to identify the mechanisms. Treatment with I3C led to repressed colonic inflammation and prevention of microbial dysbiosis caused by colitis, increasing a subset of gram-positive bacteria known to produce butyrate. I3C was shown to increase production of butyrate, and when mice with colitis were treated with butyrate, there was reduced colonic inflammation accompanied by suppression of Th17 and induction of Tregs, protection of the mucus layer, and upregulation in Pparg expression. Additionally, IL-22 was increased only after I3C but not butyrate administration, and neutralization of IL-22 prevented the beneficial effects of I3C against colitis, as well as blocked I3C-mediated dysbiosis and butyrate induction. This study suggests that I3C attenuates colitis primarily through induction of IL-22, which leads to modulation of gut microbiota that promote antiinflammatory butyrate.

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Probiotics prevent dysbiosis and the raise in blood pressure in genetic hypertension.

PMID: 

Mol Nutr Food Res. 2020 Jan 18:e1900616. Epub 2020 Jan 18. PMID: 31953983

Abstract Title: 

Probiotics Prevent Dysbiosis and the Raise in Blood Pressure in Genetic Hypertension: Role of Short-chain Fatty Acids.

Abstract: 

SCOPE: The objective of this study was to determine the cardiovascular effects of the probiotics Bifidobacterium breve CECT7263 (BFM) and Lactobacillus fermentum CECT5716 (LC40), and the short chain fatty acids butyrate and acetate in spontaneously hypertensive rats (SHR).METHODS AND RESULTS: Ten five-weeks old Wistar Kyoto rats (WKY) and fifty aged-matched SHR were randomly distributed into six groups: control WKY, control SHR, treated SHR-LC40, treated SHR-BMF, treated SHR-butyrate, and treated SHR-acetate. Chronic treatments with LC40 or BFM increased butyrate-producing bacteria and prevented the blood pressure increase in SHR. Oral treatment with butyrate or acetate also prevented the increase in both blood pressure and Firmicutes/Bacteroidetes ratio. All treatments restored the Th17/Treg balance in mesenteric lymph nodes, normalized endotoxemia, and prevented the impairment of endothelium-dependent relaxation to acetylcholine, as a result of reduced NADPH oxidase-driven reactive oxygen species production. These protective effects might be mediated by both the reduction in vascular lipopolysaccharide/toll-like receptor 4 pathway and the increase in Treg infiltration in the vasculature.CONCLUSION: The probiotics LC40 and BFM prevent dysbiosis and the development of endothelial dysfunction and high blood pressure in genetic hypertension. These effects seems to be related to endotoxemia reduction and to increase Treg accumulation in the vasculature. This article is protected by copyright. All rights reserved.

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Dysbiosis in Parkinson’s disease might be triggered by certain antibiotics.

PMID: 

Med Hypotheses. 2020 Jan 9 ;137:109564. Epub 2020 Jan 9. PMID: 31954994

Abstract Title: 

Dysbiosis in Parkinson's disease might be triggered by certain antibiotics.

Abstract: 

Parkinson's disease (PD) is a neurodegenerative amyloid disorder with debilitating motor symptoms due to the loss of dopamine-synthesizing, basal ganglia-projecting neurons in the substantia nigra. An interesting feature of the disease is that most of PD patients have gastrointestinal problems and bacterial dysbiosis, years before the full expression of motor symptoms. We hypothesized that antibiotic consumption might be a contributing factor of gut microbiome dysbiosis in PD, favoring curli-producing Enterobacteria. Curli is a bacterialα-synuclein (αSyn) which is deposited first in the enteric nervous system and amyloid deposits are propagated in a prion like manner to the central nervous system. In addition, antibiotics result in a low-grade systemic inflammation, which also contributes to damage of neurons in enteric- and central nervous system. To support our hypothesis, by comparing PD prevalence change with antibiotic consumption data in EU countries, we found significant positive correlation between use narrow spectrum penicillin + penicillinase resistant penicillin and increased prevalence of the disease.

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