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      The effects of alpha-lipoic acid supplementation on inflammatory markers among patients with metabolic syndrome and related disorders: a systematic review and meta-analysis of randomized controlled trials

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          Abstract

          Objective

          This systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to determine the effect of alpha-lipoic acid (ALA) supplementation on the inflammatory markers among patients with metabolic syndrome (MetS) and related disorders.

          Methods

          We searched the following databases until November 2017: PubMed, MEDLINE, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials. Three reviewers independently assessed study eligibility, extracted data, and evaluated risk of bias of included primary studies. Statistical heterogeneity was assessed using Cochran’s Q test and I-square (I 2) statistic. Data were pooled by using the random-effect model and standardized mean difference (SMD) was considered as the summary effect size.

          Results

          Eighteen trials out of 912 potential citations were found to be eligible for our meta-analysis. The findings indicated that ALA supplementation significantly decreased C-reactive protein (CRP) (SMD = − 1.52; 95% CI, − 2.25, − 0.80; P < 0.001), interlokin-6 (IL-6) (SMD = − 1.96; 95% CI, − 2.60, − 1.32; P < 0.001), and tumor necrosis factor alpha levels (TNF-α) (SMD = − 2.62; 95% CI, − 3.70, − 1.55; P < 0.001) in patients diagnosed with metabolic diseases.

          Conclusion

          In summary, the current meta-analysis demonstrated the promising impact of ALA administration on decreasing inflammatory markers such as CRP, IL-6 and TNF-α among patients with MetS and related disorders.

          Electronic supplementary material

          The online version of this article (10.1186/s12986-018-0274-y) contains supplementary material, which is available to authorized users.

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          Most cited references 36

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          From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.

          Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.
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            Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

            Arterial stiffness predicts an increased risk of cardiovascular events. Inflammation plays a major role in large arteries stiffening, related to atherosclerosis, arteriosclerosis, endothelial dysfunction, smooth muscle cell migration, vascular calcification, increased activity of metalloproteinases, extracellular matrix degradation, oxidative stress, elastolysis, and degradation of collagen. The present paper reviews main mechanisms explaining the crosstalk between inflammation and arterial stiffness and the most common inflammatory markers associated with increased arterial stiffness, considering the most recent clinical and experimental studies. Diverse studies revealed significant correlations between the severity of arterial stiffness and inflammatory markers, such as white blood cell count, neutrophil/lymphocyte ratio, adhesion molecules, fibrinogen, C-reactive protein, cytokines, microRNAs, and cyclooxygenase-2, in patients with a broad variety of diseases, such as metabolic syndrome, diabetes, coronary heart disease, peripheral arterial disease, malignant and rheumatic disorders, polycystic kidney disease, renal transplant, familial Mediterranean fever, and oral infections, and in women with preeclampsia or after menopause. There is strong evidence that inflammation plays an important and, at least, partly reversible role in the development of arterial stiffness, and inflammatory markers may be useful additional tools in the assessment of the cardiovascular risk in clinical practice. Combined assessment of arterial stiffness and inflammatory markers may improve non-invasive assessment of cardiovascular risk, enabling selection of high-risk patients for prophylactic treatment or more regular medical examination. Development of future destiffening therapies may target pro-inflammatory mechanisms.
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              Tomato and lycopene supplementation and cardiovascular risk factors: A systematic review and meta-analysis.

              Epidemiological evidence suggests an association between consumption of tomato products or lycopene and lower risk for cardiovascular diseases (CVD). Our aim was to evaluate the state of the evidence from intervention trials on the effect of consuming tomato products and lycopene on markers of cardiovascular (CV) function. We undertook a systematic review and meta-analysis on the effect of supplementing tomato and lycopene on CV risk factors.
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                Author and article information

                Contributors
                m.akbari45@yahoo.com
                vrom.1993@gmail.com
                kmsrc89@gmail.com
                mobinimoein@outlook.com
                lankaran@sums.ac.ir
                Mmoosazadeh1351@mazums.ac.ir
                heidaryt@sums.ac.ir
                +98-31-55463378 , Maryam.chamani.k@gmail.com
                fariba.kolahdooz@ualberta.ca
                +98-31-55463378 , asemi_r@yahoo.com
                Journal
                Nutr Metab (Lond)
                Nutr Metab (Lond)
                Nutrition & Metabolism
                BioMed Central (London )
                1743-7075
                5 June 2018
                5 June 2018
                2018
                : 15
                Affiliations
                [1 ]ISNI 0000 0000 8819 4698, GRID grid.412571.4, Health Policy Research Center, Institute of Health, Student Research Committee, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [2 ]ISNI 0000 0004 0612 1049, GRID grid.444768.d, Research Center for Biochemistry and Nutrition in Metabolic Diseases, , Kashan University of Medical Sciences, ; Kashan, I.R Iran
                [3 ]ISNI 0000 0004 1936 7697, GRID grid.22072.35, Kinesiology Department, , University of Calgary, ; Calgary, AB Canada
                [4 ]ISNI 0000 0000 8819 4698, GRID grid.412571.4, Health Policy Research Center, Institute of Health, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [5 ]ISNI 0000 0001 2227 0923, GRID grid.411623.3, Health Science Research Center, Addiction Institute, , Mazandaran University of Medical Sciences, ; Sari, Iran
                [6 ]GRID grid.411746.1, Department of Gynecology and Obstetrics, School of Medicine, , Iran University of Medical Sciences, ; Tehran, Iran
                [7 ]GRID grid.17089.37, Indigenous and Global Health Research, Department of Medicine, , University of Alberta, ; Edmonton, Canada
                Article
                274
                10.1186/s12986-018-0274-y
                5989440
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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                Review
                Custom metadata
                © The Author(s) 2018

                Nutrition & Dietetics

                alpha-lipoic acid, inflammatory markers, meta-analysis

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