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      Physical Activity, Bone Health, and Obesity in Peri-/Pre- and Postmenopausal Women: Results from the EPIC-Potsdam Study

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          Abstract

          Physical activity (PA) is suggested to increase the peak bone mass and to minimize age-related bone loss, and thereby to reduce the risk of osteoporosis. However, the relation between PA and bone health considering the obesity status is unclear so far. The present study examines the association between PA levels and calcaneal broadband ultrasound attenuation (BUA), particularly under consideration of obesity. Data from a population-based sample of 6776 German women from the EPIC-Potsdam cohort were analyzed. Calibrated PA data were used. Statistical analyses were stratified by menopausal and obesity status. Multiple linear regression was used to model the relationship between PA and BUA levels after adjustment for age, body mass index (BMI), smoking status, education, alcohol and calcium intake, and hormone use. Peri-/premenopausal had higher BUA levels (112.39 ± 10.05 dB/MHz) compared to postmenopausal women (106.44 ± 9.95 dB/MHz). In both groups, BUA levels were higher in the fourth compared to the lowest quartile of PA ( p for trend < 0.05). In women with BMI < 30, but not BMI ≥ 30 kg/m 2, PA remained positively associated with BUA levels ( p for interaction = 0.03). However, when waist circumference higher than 88 cm or body fat percentage (BF %) measures above the median were used to define obesity, a significant positive relationship was also observed in women with BMI < 30 kg/m 2 but with higher waist circumference or BF %. In conclusion, our results strengthen the hypothesis that PA has a positive influence on BUA levels, though dependent on weight.

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          The online version of this article (doi:10.1007/s00223-015-0027-0) contains supplementary material, which is available to authorized users.

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          Most cited references 44

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          Diagnostic performance of body mass index to identify obesity as defined by body adiposity: a systematic review and meta-analysis.

          We performed a systematic review and meta-analysis of studies that assessed the performance of body mass index (BMI) to detect body adiposity. Data sources were MEDLINE, EMBASE, Cochrane, Database of Systematic Reviews, Cochrane CENTRAL, Web of Science, and SCOPUS. To be included, studies must have assessed the performance of BMI to measure body adiposity, provided standard values of diagnostic performance, and used a body composition technique as the reference standard for body fat percent (BF%) measurement. We obtained pooled summary statistics for sensitivity, specificity, positive and negative likelihood ratios (LRs), and diagnostic odds ratio (DOR). The inconsistency statistic (I2) assessed potential heterogeneity. The search strategy yielded 3341 potentially relevant abstracts, and 25 articles met our predefined inclusion criteria. These studies evaluated 32 different samples totaling 31 968 patients. Commonly used BMI cutoffs to diagnose obesity showed a pooled sensitivity to detect high adiposity of 0.50 (95% confidence interval (CI): 0.43-0.57) and a pooled specificity of 0.90 (CI: 0.86-0.94). Positive LR was 5.88 (CI: 4.24-8.15), I (2)=97.8%; the negative LR was 0.43 (CI: 0.37-0.50), I (2)=98.5%; and the DOR was 17.91 (CI: 12.56-25.53), I (2)=91.7%. Analysis of studies that used BMI cutoffs >or=30 had a pooled sensitivity of 0.42 (CI: 0.31-0.43) and a pooled specificity of 0.97 (CI: 0.96-0.97). Cutoff values and regional origin of the studies can only partially explain the heterogeneity seen in pooled DOR estimates. Commonly used BMI cutoff values to diagnose obesity have high specificity, but low sensitivity to identify adiposity, as they fail to identify half of the people with excess BF%.
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            Biomechanical and molecular regulation of bone remodeling.

            Bone is a dynamic tissue that is constantly renewed. The cell populations that participate in this process--the osteoblasts and osteoclasts--are derived from different progenitor pools that are under distinct molecular control mechanisms. Together, these cells form temporary anatomical structures, called basic multicellular units, that execute bone remodeling. A number of stimuli affect bone turnover, including hormones, cytokines, and mechanical stimuli. All of these factors affect the amount and quality of the tissue produced. Mechanical loading is a particularly potent stimulus for bone cells, which improves bone strength and inhibits bone loss with age. Like other materials, bone accumulates damage from loading, but, unlike engineering materials, bone is capable of self-repair. The molecular mechanisms by which bone adapts to loading and repairs damage are starting to become clear. Many of these processes have implications for bone health, disease, and the feasibility of living in weightless environments (e.g., spaceflight).
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              Effects of mechanical forces on maintenance and adaptation of form in trabecular bone.

              The architecture of trabecular bone, the porous bone found in the spine and at articulating joints, provides the requirements for optimal load transfer, by pairing suitable strength and stiffness to minimal weight according to rules of mathematical design. But, as it is unlikely that the architecture is fully pre-programmed in the genes, how are the bone cells informed about these rules, which so obviously dictate architecture? A relationship exists between bone architecture and mechanical usage--while strenuous exercise increases bone mass, disuse, as in microgravity and inactivity, reduces it. Bone resorption cells (osteoclasts) and bone formation cells (osteoblasts) normally balance bone mass in a coupled homeostatic process of remodelling, which renews some 25% of trabecular bone volume per year. Here we present a computational model of the metabolic process in bone that confirms that cell coupling is governed by feedback from mechanical load transfer. This model can explain the emergence and maintenance of trabecular architecture as an optimal mechanical structure, as well as its adaptation to alternative external loads.
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                Author and article information

                Contributors
                +49 33200 88 2718 , Juliane.Menzel@dife.de
                Journal
                Calcif Tissue Int
                Calcif. Tissue Int
                Calcified Tissue International
                Springer US (New York )
                0171-967X
                1432-0827
                25 June 2015
                25 June 2015
                2015
                : 97
                : 4
                : 376-384
                Affiliations
                [ ]Research Group Cardiovascular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
                [ ]Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
                [ ]Department of Nutritional, Food and Consumer Sciences, Fulda University of Applied Sciences, Fulda, Germany
                [ ]Institute for Social Medicine, Epidemiology and Health Economics, Charité University Medical Center, Berlin, Germany
                27
                10.1007/s00223-015-0027-0
                4564447
                26108649
                © The Author(s) 2015

                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.

                Categories
                Original Research
                Custom metadata
                © Springer Science+Business Media New York 2015

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