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      Association between Leukocyte Counts and Physical Fitness in Male Military Members: The CHIEF Study

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          Abstract

          Low-grade inflammation, which is related to obesity and toxic substance use in young adults, may be associated with poor physical fitness. We investigated the association between total leukocyte count and physical fitness in a military cohort of 3,453 healthy young Taiwanese males aged 20–50 years in a cross-sectional study in 2014. Low-grade inflammation was defined according to equally sized quartiles of total leukocyte counts within the suggested normal limits (4.00–9.99 × 10 3/mm 3). Aerobic fitness was assessed by the time for a 3-kilometer run test, and anaerobic fitness was evaluated by the numbers of sit-ups and push-ups performed in 2 minutes. Automatic monitoring systems were used to verify the scores for all procedures. Multiple linear regression was utilized to identify the associations among variables. When compared with the lowest counts (4.00–5.49 × 10 3/mm 3), the second highest (6.50–7.49 × 10 3/mm 3) and highest normal leukocyte counts (7.50–9.99 × 10 3/mm 3) were correlated with longer times for a 3-kilometer run (β and 95% confidence intervals =4.93 (1.61, 8.25) and 4.65 (2.20, 7.10), respectively) and fewer numbers of push-ups performed in 2 minutes (β = −0.59 (−1.15, −0.03) and −0.56 (−0.96, −0.17), respectively), after adjustments for age, service specialty, waist circumference, body mass index, alcohol consumption, tobacco smoking, and physical activity. However, the association with 2-minute sit-ups was null. Our study suggested an inverse association between total leukocyte count and not only aerobic fitness but also parts of anaerobic fitness in young males. The temporal association needs confirmation in longitudinal studies.

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          Low-grade inflammation, diet composition and health: current research evidence and its translation

          The importance of chronic low-grade inflammation in the pathology of numerous age-related chronic conditions is now clear. An unresolved inflammatory response is likely to be involved from the early stages of disease development. The present position paper is the most recent in a series produced by the International Life Sciences Institute's European Branch (ILSI Europe). It is co-authored by the speakers from a 2013 workshop led by the Obesity and Diabetes Task Force entitled ‘Low-grade inflammation, a high-grade challenge: biomarkers and modulation by dietary strategies’. The latest research in the areas of acute and chronic inflammation and cardiometabolic, gut and cognitive health is presented along with the cellular and molecular mechanisms underlying inflammation–health/disease associations. The evidence relating diet composition and early-life nutrition to inflammatory status is reviewed. Human epidemiological and intervention data are thus far heavily reliant on the measurement of inflammatory markers in the circulation, and in particular cytokines in the fasting state, which are recognised as an insensitive and highly variable index of tissue inflammation. Potential novel kinetic and integrated approaches to capture inflammatory status in humans are discussed. Such approaches are likely to provide a more discriminating means of quantifying inflammation–health/disease associations, and the ability of diet to positively modulate inflammation and provide the much needed evidence to develop research portfolios that will inform new product development and associated health claims.
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            The perfect storm: obesity, adipocyte dysfunction, and metabolic consequences.

            As the prevalence of adiposity soars in both developed and developing nations, appreciation of the close links between obesity and disease increases. The strong relationships between excess adipose tissue and poor health outcomes, including cardiovascular disease, diabetes, and cancer, mandate elucidation of the complex cellular, hormonal, and molecular pathophysiology whereby adiposity initiates and maintains adverse health effects. In this report we review adipocyte metabolism and function in the context of energy imbalance and postprandial nutrient excess, including adipocyte hypertrophy and hyperplasia, adipocyte dysfunction, and other systemic consequences. We also discuss implications for laboratory evaluation and clinical care, including the role of lifestyle modifications. Chronic energy imbalance produces adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These processes lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic beta-cells, and skeletal muscle as well as the heart and vascular beds. Several specialized laboratory tests can quantify these processes and predict clinical risk, but translation to the clinical setting is premature. Current and future pharmacologic interventions may target these pathways; modest changes in diet, physical activity, weight, and smoking are likely to have the greatest impact. Adipocyte endoplasmic reticulum and mitochondrial stress, and associated changes in circulating adipokines, free fatty acids, and inflammatory mediators, are central to adverse health effects of adiposity. Future investigation should focus on these pathways and on reversing the adverse lifestyle behaviors that are the fundamental causes of adiposity.
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              Inflammatory disease processes and interactions with nutrition.

              Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing as well as tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Various dietary components including long chain omega-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy. These components act through a variety of mechanisms including decreasing inflammatory mediator production through effects on cell signaling and gene expression (omega-3 fatty acids, vitamin E, plant flavonoids), reducing the production of damaging oxidants (vitamin E and other antioxidants), and promoting gut barrier function and anti-inflammatory responses (prebiotics and probiotics). However, in general really strong evidence of benefit to human health through anti-inflammatory actions is lacking for most of these dietary components. Thus, further studies addressing efficacy in humans linked to studies providing greater understanding of the mechanisms of action involved are required.
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                Author and article information

                Contributors
                farmer507@yahoo.com.tw
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                8 April 2020
                8 April 2020
                2020
                : 10
                : 6082
                Affiliations
                [1 ]ISNI 0000 0004 1797 2578, GRID grid.413601.1, Department of Medicine, Hualien Armed Forces General Hospital, ; Hualien, Taiwan
                [2 ]Department of Critical Care Medicine, Taipei Tzu-Chi Hospital, New Taipei, Taiwan
                [3 ]Departments of Neurology and Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
                [4 ]Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
                [5 ]ISNI 0000 0001 2299 3507, GRID grid.16753.36, Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, ; Chicago, IL 60611 USA
                Article
                63147
                10.1038/s41598-020-63147-9
                7142135
                32269281
                c7a5d01f-779e-443a-a557-c2b18c011948
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 27 December 2019
                : 21 March 2020
                Funding
                Funded by: Hualien Armed Forces General Hospital (805C-108-19 and 805-C109-05)
                Categories
                Article
                Custom metadata
                © The Author(s) 2020

                Uncategorized
                risk factors,chronic inflammation
                Uncategorized
                risk factors, chronic inflammation

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