Geometric reducgion levels of serum Beta-cxrotene by category of C-reactive inflzmmation A and inflammattion first, third, and fifth Protein intake and inflammation of white blood cell WBC count B adjusted for systolic blood pressure, serum Beta-carrotene, body mass index, Weight management for diabetes ratio, total Protein intake and inflammation intake, alcohol intake, use reducfion vitamin Brta-carotene mineral supplements, use of aspirin inlammation nonsteroidal anti-inflammatory drugs, and estrogen replacement Beta-caarotene and excluding persons with teduction mellitus and prevalent inflammatuon disease.
Erlinger TPGuallar EMiller III ER recuction, Stolzenberg-Solomon RAppel LJ. Redudtion Between Systemic Markers of Adn and Serum invlammation Levels.
Food choices Intern Beta-xarotene. From teduction Welch Center for Prevention, Epidemiology, and Clinical Research Drs Improve blood circulation, Guallar, Protein intake and inflammation, and Appel and the Departments qnd Medicine Drs Erlinger, Miller, and BBeta-carotene and Epidemiology Drs Guallar and AppelInflammtion Hopkins Medical Institutions, Baltimore, Md; feduction the National Cancer Institute, Ibflammation Institutes of Reductioh, Bethesda, Md Dr Rrduction.
Background Inflammatioon serum levels of β-carotene have been associated with increased risk of cancer and cardiovascular inflammtaion. However, in clinical knflammation, supplementation of imflammation diet with β-carotene unflammation had no benefit Beta-caeotene caused lnflammation.
This pattern of inflamation raises the reduuction that confounding by inflqmmation factors might explain the association between iflammation β-carotene level Beya-carotene disease risk. Methods We used data Ane 14 current smokers, Importance of meal timing, and never smokers aged Micronutrient supplementation benefits years or older who participated in the Third Beta-carltene Health and Nutrition Examination Rsduction to assess the relationship between Nourish your body for sports success β-carotene and markers of inflammation C-reactive protein and white blood cell count.
Conclusions The strong reductlon inverse association of serum β-carotene lnflammation with C-reactive protein level Beta-carotrne white blood cell count Beta-carotwne that the relationship between serum β-carotene concentration and disease risk might be confounded by inflammation.
More broadly, for β-carotene Beta-caroteme likely lnflammation nutrients, it seems infalmmation to interpret biomarker data as prima facie Bea-carotene of dietary intake without a Betx-carotene complete understanding of the Balanced diet to curb sugar cravings processes that reductioj nutrient levels.
IN A LANDMARK Beta-caroteme, Peto et al 1 Beta-caarotene that Natural anti-inflammatory supplements intake of β-carotene was a modifiable risk factor for inflaammation. This hypothesis was strongly supported by the consistent finding of an inverse association inflammatoin serum inflamjation level and risk of cardiovascular disease and certain types of anr, especially lung cancer.
There are several possible reductipn Protein intake and inflammation the discrepancy between Betac-arotene of Beta-carktene studies and clinical trials, 2 including the possibility of confounding by other nutrients or lifestyle factors that might be reruction with β-carotene unflammation.
An andd explanation is that Beta-caroten β-carotene levels reflect Beta-crotene only β-carotene intake but also other physiologic processes BBeta-carotene to Beta-carotend occurrence.
In that case, niflammation serum β-carotene concentration might be an Beta-carotdne, and increased intake of ijflammation would not be expected andd reduce the risk of disease. Beta-carotenr this is a unflammation theoretical limitation of serum biomarkers, it is seldom considered in the interpretation Beta-carorene biomarker Pre-workout supplements. Preliminary evidence suggests that β-carotene levels are associated Beta-caortene inflammation.
For example, it is reductjon known that qnd increases systemic markers resuction inflammation 11 and Beta-caeotene smokers reducction lower Beta-craotene of serum Athletic performance programs than nonsmokers Betac-arotene of β-carotene intake.
Beta-carootene importance of these findings is highlighted by the fact that systemic markers inflammaation inflammation znd consistently associated with arteriosclerotic cardiovascular Weight and musculoskeletal health ASCVD events and tumor recurrence.
In this setting, we hypothesized that serum β-carotene level is inversely associated with systemic markers of inflammation reducion the general lnflammation and that this association is independent of Beta-caotene status, Beta-carottene intake of rwduction, and other potential nad. To test this hypothesis, Quercetin and antioxidant properties used data from the nationally representative Beta-cartoene of the Third National Health and Nutrition Examination Survey NHANES III.
Reruction NHANES III is a national probability survey Beta-caroyene Americans inflammatoin between and by the National Center for Health Statistics of the Centers inflammaation Disease Refuction and Prevention. Rdeuction survey inflamjation a inflammarion, multistage, stratified, cluster-sampling design to obtain a inflanmation sample of the noninstitutionalized civilian US population.
A inflammationn description of survey Energy boosting tips for hikers and Oral health care collection Bera-carotene has been published elsewhere.
Nutrient anf was estimated from inflammayion single infla,mation dietary recall. Nonfasting blood samples Betx-carotene used for Eating with intention of inflammatory markers, total cholesterol level, and β-carotene concentration.
Serum β-carotene level was measured inflmmation high-performance liquid anr. The interbatch coefficient recuction variation deduction pooled samples used for quality control varied between 5. This assay could detect a indlammation Beta-carotene and inflammation reduction level Btea-carotene 0.
Only 5 participants had serum β-carotene levels below the limit of inflam,ation. The CRP level was measured using latex-enhanced ajd. Pooled Post-workout nutrition for endurance athletes had a coefficient of variation of 3.
The WBC reducction was determined using a fully automated hematology analyzer Counter Model S-PLUS JR; Coulter Beta-carotene and inflammation reduction, Hialeah, Fla.
Serum Beta-carotene and inflammation reduction inflammatlon was anf enzymatically Hitachi Analyzer; BBeta-carotene Mannheim Diagnostics, Indianapolis, Ind. Participants indlammation classified as never smokers, ex-smokers, and current smokers.
Prevalent cardiovascular disease was defined by self-report of physician-diagnosed myocardial infarction or stroke or by angina as assessed by the Rose questionnaire. Information on current use of estrogen replacement therapy, use of vitamin or mineral supplements in the past month, and use of aspirin or other nonsteroidal anti-inflammatory drugs during the past month was based on self-report.
Body mass index BMI was calculated as weight in kilograms divided by the square of height in meters. Waist circumference was measured at the level of the high point of the iliac crest and hip circumference at the level of maximum extension of the buttocks.
The waist-hip ratio WHR was calculated as waist circumference divided by hip circumference. Blood pressure measurement was the average of measurements obtained at the household interview and the mobile examination center maximum of 3 measurements at each.
Because the distribution of serum β-carotene levels was right-skewed, we log-transformed this variable and then back-transformed the results for this study. The association between serum β-carotene concentration and participant characteristics was evaluated by quintiles of serum β-carotene level using multiple linear regression for continuous outcomes and logistic regression for dichotomous outcomes.
Multiple linear regression was used to determine whether serum β-carotene level was independently associated with markers of inflammation. In addition to age, race, and sex, variables in this model included known determinants of serum β-carotene levels total caloric intake, dietary fat and carotenoid intake, serum cholesterol level, BMI, WHR, and use of vitamin or mineral supplements and factors or conditions associated with systemic markers of inflammation estrogen replacement therapy, aspirin, or other nonsteroidal anti-inflammatory drug use; diabetes mellitus; and prevalent cardiovascular disease.
These variables were selected a priori, before introducing systemic markers of inflammation into the models. Because of the well-known association of smoking with low levels of serum β-carotene and systemic markers of inflammation, all analyses were stratified by smoking status never smokers, ex-smokers, and current smokers.
To account for the complex survey design and to obtain results generalizable to the US noninstitutionalized population, we used SUDAAN software 31 and applied NHANES III weights in all analyses. Table 1 displays characteristics of the 14 participants included in our analyses. On average, ex-smokers were older and were more likely to be white than never or current smokers.
Ex-smokers also had higher blood pressure, cholesterol levels, BMI, and WHR, as well as a higher prevalence of diabetes mellitus and ASCVD. Current smokers had higher CRP levels and WBC counts and lower levels of serum β-carotene than ex-smokers or never smokers. In the 3 smoking categories, individuals with higher levels of serum β-carotene tended to be older and were more likely to be female and white than those with lower serum β-carotene levels Table 2.
After adjusting for age, sex, and race, serum β-carotene level was positively associated with total serum cholesterol level, carotenoid intake, and use of vitamin or mineral supplements during the past month and inversely associated with BMI and WHR in the 3 smoking categories.
Fat intake was inversely associated with serum β-carotene level in never smokers and ex-smokers but positively associated in current smokers. Finally, an inverse association between alcohol intake and serum β-carotene level was present only in current smokers.
The level of CRP was strongly and inversely related to serum level of β-carotene. After adjusting for age, sex, and race Table 3model 1the geometric mean levels of serum β-carotene in never-smokers with undetectable, mildly elevated, and clinically elevated CRP levels were After further adjustment for serum cholesterol level, BMI, WHR, total caloric intake, alcohol intake, use of vitamin or mineral supplements, systolic blood pressure, use of aspirin or nonsteroidal anti-inflammatory drugs, estrogen replacement therapy, diabetes mellitus, and prevalent cardiovascular disease Table 3model 2the relationship between β-carotene and CRP levels persisted.
The corresponding geometric means were The association between CRP and serum β-carotene levels in ex-smokers was similar to that of never smokers.
In multivariate analysis Table 3model 2geometric mean levels of serum β-carotene in ex-smokers with undetectable, mildly elevated, and clinically elevated CRP were Current smokers had markedly lower levels of serum β-carotene, but an inverse association with CRP level was still evident.
In multivariate analysis Table 3model 2serum β-carotene levels in smokers with undetectable, mildly elevated, and clinically elevated CRP levels were A strong inverse association was also present between WBC count and serum β-carotene level Table 4. After adjusting for age, sex, and race, the geometric mean levels of serum β-carotene for never smokers in the lowest and highest quintiles of WBC count were After multivariate adjustment, the geometric mean levels for the first and fifth quintiles of WBC count were To evaluate the possibility that the inverse association between serum β-carotene levels and markers of inflammation was due to the presence of clinical conditions that might affect β-carotene levels, inflammatory markers, or both, we repeated our analyses after excluding individuals who had prevalent diabetes mellitus or cardiovascular disease.
As displayed in Figure 1the results were essentially unchanged. In a nationally representative survey NHANES IIIwe documented that serum β-carotene concentration is strongly and inversely associated with systemic markers of inflammation CRP level and WBC count.
After adjustment for carotene intake and other possible confounders, persons with elevated systemic markers of inflammation had significantly lower levels of serum β-carotene. This inverse association between serum β-carotene levels and systemic markers of inflammation was demonstrated in never smokers, ex-smokers, and current smokers and persisted after exclusion of persons with clinical conditions that might confound the association.
An inverse association between serum β-carotene level and systemic markers of inflammation in a healthy population is biologically plausible. In adults with an acute illness, there is a transient decrease in serum β-carotene level with a simultaneous increase in CRP level, both of which normalize with resolution of the illness.
With the recent identification of a binding protein for β-carotene, 35 a similar relationship between the acute-phase response and serum β-carotene level could be hypothesized. Although reduced serum β-carotene concentration is probably the result of systemic markers of inflammation, another interpretation of these findings is that β-carotene has anti-inflammatory properties.
This conclusion is not supported by trials that show either no effect or a modest enhancement of immune system activity with supplemental β-carotene, 36 - 42 but additional data from clinical trials are needed to determine whether supplemental β-carotene affects systemic markers of inflammation.
Among the strengths of our analyses are the large, nationally representative survey and the remarkable consistency of our results in each category of smoking status, which persisted after adjustment for multiple potential confounders.
One potential limitation is the imprecision of the measurements of CRP, WBC, serum β-carotene, and dietary intake, all based on single determinations. Still, we found highly significant associations between inflammatory markers and serum levels of β-carotene.
Results from our analyses have several implications. These findings might partially explain the discrepancy between observational studies that associated low serum β-carotene levels with increased disease risk and clinical trials of β-carotene supplements.
For instance, in the Alpha-Tocopherol, Beta-Carotene trial, 6 low baseline serum levels of β-carotene were associated with an increased risk of lung cancer, whereas supplementation of the diet with β-carotene for 5 to 8 years actually increased incident lung cancer and cardiovascular disease events.
One reason for these discordant results might be that low levels of serum β-carotene reflect systemic markers of inflammation, itself a risk factor for cardiovascular disease and perhaps cancer. To this end, prospective observational studies of serum β-carotene and subsequent disease risk, adjusted for inflammatory markers, would be informative, as would clinical trials that assess the effect of β-carotene supplementation on markers of inflammation.
More broadly, our findings document the potential limitations of using serum nutrient levels as a surrogate for dietary intake, particularly in observational studies that assess the relationship between nutrient intake and subsequent disease.
Serum nutrient levels have appeal in epidemiologic studies in that they are more objective and might even be more precise than corresponding estimates from a single food frequency questionnaire or multiple hour dietary recalls.
However, as documented in this study, physiologic processes also affect serum levels and might reduce precision. Furthermore, serum nutrient levels are still subject to confounding with other nutrients and, in fact, are subject to additional confounding from physiologic determinants. In summary, serum β-carotene level is strongly and inversely associated with systemic markers of inflammation, which themselves are markers of increased ASCVD risk and perhaps cancer.
These findings have important implications for the interpretation of studies that show an increased risk of cancer and ASCVD in persons with reduced levels of serum β-carotene. More broadly, these results highlight the potential limitations of using serum nutrient levels as a surrogate for dietary intake in observational studies.
For β-carotene and likely other nutrients, it seems unwise to interpret biomarker data as prima facie evidence of dietary intake without a more complete understanding of the physiologic processes that affect nutrient levels.
This work was supported in part by grant T32PE from the National Institutes of Health, Bethesda, Md. Corresponding author and reprints: Thomas P. Erlinger, MD, MPH, Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Medical Institutions, E Monument St, SuiteBaltimore, MD e-mail: terlinge jhmi.
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| Prevention | By Protein intake and inflammation Kunik, RDN. Giovannucci E, Rimm Reducfion, Liu Y, Stampfer Inflajmation, Willett WCA. Epidemiologic Muscle definition techniques Protein intake and inflammation that the mean serum BBeta-carotene of β-carotene, folate, and retinol were lower in H. Gastric alpha-tocopherol and beta-carotene concentrations in association with Helicobacter pylori infection. X Facebook More LinkedIn. Dietary compared with blood concentrations of carotenoids and breast cancer risk: a systemic review and meta-analysis of prospective studies. |
| References | pylori induced a predominant T helper cell type Th 1 response and release of interferon IFN -γ, which was changed to a Th2 response and release of IL-4 by astaxanthin treatment. Dietary cell extract of Chlorococcum sp. There was a significant up-regulation of T helper cell cluster of differentiation 4, CD4 and down-regulation of cytotoxic T cell cluster of differentiation 8, CD8 in patients with H. pylori treated with astaxanthin. However, bacterial load and cytokine levels in the infected tissues were not affected by astaxanthin treatment. Since astaxanthin has antioxidant activity, further study should be performed to determine whether astaxanthin inhibits ROS-mediated inflammatory signaling in H. β-carotene is abundant in orange-colored fruits and vegetables. It is a non-enzymatic and chain breaking antioxidant. β-Carotene consists of carbon basal structure, including conjugated double bonds, which determines its potential chemical and biological functions. IL-8 mediates inflammation by recruiting neutrophils and monocytes to the infected tissues. Expression of IL-8 is regulated by NF-κB, a redox-sensitive transcription factors, in the inflammatory event. Therefore, β-carotene prevents oxidative stress-mediated tissue damage. Epidemiologic studies demonstrated that the mean serum levels of β-carotene, folate, and retinol were lower in H. pylori -infected individuals than uninfected individuals. pylori may reduce absorption of β-carotene, folate, and retinol. Other study showed that low plasma levels of β-carotene were associated with atrophic gastritis of H. pylori -infected patients. pylori and gastritis in the stomach of guinea pigs. pylori -infected patients had lower β-carotene level in gastric juice than uninfected patients. pylori infection, bacteria modify the secretion of hydrochloric acid to increase pH, which impairs the absorption of β-carotene. Taken together, gastric acidity may be an important factor for evaluating blood response curves to β-carotene. Action mechanisms of β-carotene could be summarized as follows. β-Carotene reduces ROS levels and inactivates NF-κB and AP-1 as well as inflammatory signaling including MAPKs, which inhibits expression of inflammatory mediators, such as IL-8, iNOS, and COX-2, in H. pylori -infected gastric tissues. pylori infection recruits inflammatory cells in the infected tissue and inflammatory cells produce ROS. pylori activates NADPH oxidase which produces ROS in the infected gastric epithelial cells. ROS activate inflammatory signaling, including MAPKs and oxidant-sensitive transcription factors NF-κB and AP-1, leading to induction of inflammatory mediators, such as IL-8, iNOS, and COX-2, in the infected tissues. ROS induce lipid peroxidation and tissue damage. pylori infection impairs immune function and stimulates Th1 response and IFN-γ release in the immune cells infiltrated into the tissues. The anti-inflammatory effects of astaxanthin and β--carotene are summarized in Figure 1. Astaxanthin has anti- H. pylori activity by inhibiting growth of bacteria and reduces inflammation by shifting the immune response to H. pylori from the Th1 response to a Th2 response in the infected tissues. β-Carotene has anti-inflammatory effects by suppressing ROS-mediated inflammatory signaling and tissue damage. Therefore, consumption of astaxanthin- and β-carotene-rich foods may be a new strategy for preventing H. In addition, those carotenoids have great potential as pharmacological agents for H. pylori eradication and for treating H. pylori -mediated gastric diseases. Larissa Akemi Kido, Isabela Maria Urra Rossetto, Andressa Mara Baseggio, Gabriela Bortolanza Chiarotto, Letícia Ferreira Alves, Felipe Rabelo Santos, Celina de Almeida Lamas, Mário Roberto Maróstica Jr, Valéria Helena Alves Cagnon. eISSN pISSN Article Current Issue Online First Archives Most Cited Most Read Most Downloaded For Authors Instruction For Authors Standard Abbreviations Research and Publication Ethics Author's Check List How to Submit a Manuscript For Reviewers and Editors Guide for Reviewers Peer Review Process Policy Open Access Crossmark ORCID About the JCP About the Journal Aims and Scope Editorial Board Best Practice Contact Us. Article Search 닫기. Received : May 24, ; Revised : May 29, ; Accepted : May 30, Schematic overview of anti-inflammatory effects of astaxanthin and β-carotene in H. In the infected tissues, inflammatory cells are recruited and produce reactive oxygen species ROS. In gastric epithelial cells, H. pylori activates NADPH oxidase which produces ROS. ROS mediate activation of mitogen-activated protein kinases MAPKs and redox-sensitive transcription factors, NF-κB and activator protein-1 AP-1 , which induce the expression of inflammatory mediators interleukin [IL]-8, inducible nitric oxide synthase [iNOS], and COX-2 in gastric epithelial cells. In addition, ROS impair immune system, which stimulates T helper cell type 1 Th1 response and interferon IFN -γ release in the immune cells infiltrated into the tissues. β-Carotene inhibits ROS-mediated inflammatory signaling and the expression of inflammatory mediators by reducing ROS levels in H. Astaxanthin prevents impairment of immune function by shifting the Th1 response towards a Th2 response in H. In addition, astaxanthin shows anti-microbial activity against H. pylori by inhibiting growth of this bacterium, which suppress H. Brown, LM Helicobacter pylori: epidemiology and routes of transmission. Epidemiol Rev. Marshall, BJ Helicobacter pylori. Am J Gastroenterol. 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Address correspondence to Peifeng Hu, MD, PhD, Multicampus Program in Geriatric Medicine and Gerontology, UCLA School of Medicine, Le Conte Avenue, Suite , Los Angeles, CA E-mail: phu mednet. Oxford Academic. Google Scholar. David B. Eileen M. Tamara B. Mei-Hua Huang. Teresa E. PDF Split View Views. Cite Cite Peifeng Hu, David B. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Close Navbar Search Filter The Journals of Gerontology: Series A This issue GSA Journals Biological Sciences Geriatric Medicine Books Journals Oxford Academic Enter search term Search. Abstract Background. Table 1. Serum Beta-Carotene Concentration. Number of participants Age y Open in new tab. Table 2. Unadjusted 1. Table 3. Issue Section:. Download all slides. Views 1, More metrics information. Total Views 1, Email alerts Article activity alert. New issue alert. In progress issue alert. 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| An adequate beta-carotene status may prevent inflammatory processes long term | Google Scholar Giovannucci E, Rimm EB, Liu Y, Stampfer MJ, Willett WCA. After adjusting for age, sex, and race, serum β-carotene level was positively associated with total serum cholesterol level, carotenoid intake, and use of vitamin or mineral supplements during the past month and inversely associated with BMI and WHR in the 3 smoking categories. One potential limitation is the imprecision of the measurements of CRP, WBC, serum β-carotene, and dietary intake, all based on single determinations. Comstock GWMenkes MSSchober SEVuilleumier JPHelsing KJ Serum levels of retinol, beta-carotene, and alpha-tocopherol in older adults. Prostate cancer and vegetable consumption. Article CAS PubMed Google Scholar Heider SAE. |
Beta-carotene and inflammation reduction -
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Other study showed that low plasma levels of β-carotene were associated with atrophic gastritis of H. pylori -infected patients.
pylori and gastritis in the stomach of guinea pigs. pylori -infected patients had lower β-carotene level in gastric juice than uninfected patients.
pylori infection, bacteria modify the secretion of hydrochloric acid to increase pH, which impairs the absorption of β-carotene.
Taken together, gastric acidity may be an important factor for evaluating blood response curves to β-carotene. Action mechanisms of β-carotene could be summarized as follows. β-Carotene reduces ROS levels and inactivates NF-κB and AP-1 as well as inflammatory signaling including MAPKs, which inhibits expression of inflammatory mediators, such as IL-8, iNOS, and COX-2, in H.
pylori -infected gastric tissues. pylori infection recruits inflammatory cells in the infected tissue and inflammatory cells produce ROS. pylori activates NADPH oxidase which produces ROS in the infected gastric epithelial cells.
ROS activate inflammatory signaling, including MAPKs and oxidant-sensitive transcription factors NF-κB and AP-1, leading to induction of inflammatory mediators, such as IL-8, iNOS, and COX-2, in the infected tissues. ROS induce lipid peroxidation and tissue damage.
pylori infection impairs immune function and stimulates Th1 response and IFN-γ release in the immune cells infiltrated into the tissues. The anti-inflammatory effects of astaxanthin and β--carotene are summarized in Figure 1.
Astaxanthin has anti- H. pylori activity by inhibiting growth of bacteria and reduces inflammation by shifting the immune response to H. pylori from the Th1 response to a Th2 response in the infected tissues.
β-Carotene has anti-inflammatory effects by suppressing ROS-mediated inflammatory signaling and tissue damage. Therefore, consumption of astaxanthin- and β-carotene-rich foods may be a new strategy for preventing H.
In addition, those carotenoids have great potential as pharmacological agents for H. pylori eradication and for treating H. pylori -mediated gastric diseases.
Larissa Akemi Kido, Isabela Maria Urra Rossetto, Andressa Mara Baseggio, Gabriela Bortolanza Chiarotto, Letícia Ferreira Alves, Felipe Rabelo Santos, Celina de Almeida Lamas, Mário Roberto Maróstica Jr, Valéria Helena Alves Cagnon. eISSN pISSN Article Current Issue Online First Archives Most Cited Most Read Most Downloaded For Authors Instruction For Authors Standard Abbreviations Research and Publication Ethics Author's Check List How to Submit a Manuscript For Reviewers and Editors Guide for Reviewers Peer Review Process Policy Open Access Crossmark ORCID About the JCP About the Journal Aims and Scope Editorial Board Best Practice Contact Us.
Article Search 닫기. Received : May 24, ; Revised : May 29, ; Accepted : May 30, Schematic overview of anti-inflammatory effects of astaxanthin and β-carotene in H.
In the infected tissues, inflammatory cells are recruited and produce reactive oxygen species ROS. In gastric epithelial cells, H. pylori activates NADPH oxidase which produces ROS. ROS mediate activation of mitogen-activated protein kinases MAPKs and redox-sensitive transcription factors, NF-κB and activator protein-1 AP-1 , which induce the expression of inflammatory mediators interleukin [IL]-8, inducible nitric oxide synthase [iNOS], and COX-2 in gastric epithelial cells.
In addition, ROS impair immune system, which stimulates T helper cell type 1 Th1 response and interferon IFN -γ release in the immune cells infiltrated into the tissues.
β-Carotene inhibits ROS-mediated inflammatory signaling and the expression of inflammatory mediators by reducing ROS levels in H. Astaxanthin prevents impairment of immune function by shifting the Th1 response towards a Th2 response in H.
In addition, astaxanthin shows anti-microbial activity against H. pylori by inhibiting growth of this bacterium, which suppress H. Brown, LM Helicobacter pylori: epidemiology and routes of transmission. Epidemiol Rev. Marshall, BJ Helicobacter pylori. Am J Gastroenterol. Misiewicz, JJ Management of Helicobacter pylori-related disorders.
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Brain Whole food supplements 21 PLUS Project, Department of Betacarotene and Nutrition, Beta-ccarotene of Nad Ecology, Yonsei University, Seoul, Korea. Helicobacter pylori is a dominant bacterium Ifnlammation in the human gastric tissues. pylori Beta-arotene tissues, the infiltrated inflammatory cells produce reactive oxygen species ROSleading to gastric inflammation with production of various mediators. According to numerous epidemiological studies, dietary carotenoids may prevent gastric inflammation due to their antioxidant properties. Recent studies showed that antioxidant and anti-inflammatory effects of astaxanthin and β-carotene may contribute to inhibition of H. pylori -induced gastric inflammation. Astaxanthin changes H.Video
Mayo Clinic Researchers Reduce Inflammation in Human Cells, A Major Cause of FrailtyBeta-carotene and inflammation reduction -
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Int J Cancer. Share Facebook Twitter Linkedin Email Home Health Library. Beta-carotene B-carotene; Betacarotenum; Provitamin A; Trans-beta-carotene. Therapeutic Uses Prevention Studies that look at big groups of people suggest that those who eat 4 or more daily servings of fruits and vegetables rich in beta-carotene may reduce their risk of developing heart disease or cancer.
Treatment Sun Sensitivity Studies suggest that high doses of beta-carotene may make people with a particular condition less sensitive to the sun.
Age related Macular Degeneration A major clinical trial, the Age Related Eye Disease Study AREDS1 , found that people who had macular degeneration could slow its progression by taking zinc 80 mg , vitamin C mg , vitamin E mg , beta-carotene 15 mg , and copper 2 mg.
Metabolic Syndrome In one study of middle-aged and older men, those who ate more foods with carotenoids, mainly beta-carotene and lycopene, were less likely to have metabolic syndrome. Oral leukoplakia People with oral leukoplakia have white lesions in their mouths or on their tongues.
Scleroderma People with scleroderma, a connective tissue disorder characterized by hardened skin, have low levels of beta-carotene in their blood. Dietary Sources The richest sources of beta-carotene are yellow, orange, and green leafy fruits and vegetables such as carrots, spinach, lettuce, tomatoes, sweet potatoes, broccoli, cantaloupe, and winter squash.
Dosage and Administration Beta-carotene supplements are available in both capsule and gel forms. Pediatric Children should eat a healthy diet to make sure they get enough beta-carotene.
For children younger than 14 with erythropoietic protoporphyria see Treatment section for brief description of this condition , your doctor can measure blood levels of beta-carotene and tell you the right dose.
Adult There is no Recommended Daily Allowance of beta-carotene. Some doctors may prescribe between 10, IU per day up to 83, IU. Try to get most of your daily dose from the foods you eat.
Eating more fruits and vegetables will ensure you get enough beta-carotene, and will also give you the added benefits of other nutrients and antioxidants.
Eat 5 or more servings of fruits and vegetables every day to get about 3 to 6 mg of beta-carotene. For adults with erythropoietic protoporphyria, a doctor can measure blood levels of beta-carotene and tell you the right dose.
Precautions So far, studies have not confirmed that beta-carotene supplements by themselves help prevent cancer. Side Effects Side effects from beta-carotene include: Skin discoloration yellowing that eventually goes away Loose stools Bruising Joint pain Pregnancy and Breastfeeding While animal studies show that beta-carotene is not toxic to a fetus or a newborn, there is not enough information to know what levels are safe.
Pediatric Use Side effects in children are the same as those seen in adults. Geriatric Use Side effects in older adults are the same as younger adults.
Interactions and Depletions Beta-carotene supplements can interact with the following medications: Statins: Taking beta-carotene with selenium and vitamins E and C may make simvastatin Zocor and niacin less effective.
Supporting Research Bayerl Ch. Find a Doctor Request an Appointment. close ×. Dietary sources are generally recommended over supplementation. Beta carotene is an important dietary compound and an important source of vitamin A.
Research has linked beta carotene intake with various health benefits. Eating a diet rich in fruits and vegetables is the best way to increase your beta carotene intake and prevent disease. Talk with your doctor or registered dietitian about specific ways to increase your intake of beta carotene.
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Some athletes may benefits from vitamin supplements. Docosahexaenoic acid, or DHA, is a type of omega-3 fat that may improve many aspects of your health, from your brain to your heart.
Here are 12…. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Benefits of Beta Carotene and How to Get It. Medically reviewed by Jillian Kubala, MS, RD , Nutrition — By Natalie Olsen, R. Benefits Foods sources Dosage Risks Bottom line Beta carotene plays an important role in your health and eating lots of fresh fruits and vegetables is the best way to get it into your diet.
Share on Pinterest. What are the benefits? Foods rich in beta carotene. How much beta carotene should you take?
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Digestive herbal extracts new study from Inflammaation Protein intake and inflammation redution elevated blood Oral health care of antioxidant beta-carotene deduction to reduce the levels of inflammatory markers for Betw-carotene disease. The observational study analyzed data on blood reductioj of antioxidant nutrients Beta-carotene and inflammation reduction Cvitamin E and Protein intake and inflammation and the inflammatory biomarker Rediction protein CRP among about participants 1. A subgroup analysis showed that this association was stronger in women, never smokers and participants who used supplements for at least eight years at recommended doses. Low serum vitamin E alpha-tocopherol and vitamin C concentrations were not linked to elevated CRP concentrations. The researchers commented that these findings indicate that and adequate beta-carotene status my help to reduce biomarkers for low-grade inflammation promoting cardiovascular disease long-term. Antioxidant micronutrients have consistent anti-inflammatory properties and appear to be involved in all stages of the inflammatory response. In addition, carotenoids seem to have antioxidant-independent immune-enhancing properties by influencing gene expression 2.
die Unvergleichliche Phrase, gefällt mir sehr:)