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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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          Most cited references40

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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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              Relationship of obesity with osteoporosis.

              The relationship between obesity and osteoporosis has been widely studied, and epidemiological evidence shows that obesity is correlated with increased bone mass. Previous analyses, however, did not control for the mechanical loading effects of total body weight on bone mass and may have generated a confounded or even biased relationship between obesity and osteoporosis. The objective of this study was to reevaluate the relationship between obesity and osteoporosis by accounting for the mechanical loading effects of total body weight on bone mass. We measured whole body fat mass, lean mass, percentage fat mass, body mass index, and bone mass in two large samples of different ethnicity: 1988 unrelated Chinese subjects and 4489 Caucasian subjects from 512 pedigrees. We first evaluated the Pearson correlations among different phenotypes. We then dissected the phenotypic correlations into genetic and environmental components with bone mass unadjusted or adjusted for body weight. This allowed us to compare the results with and without controlling for mechanical loading effects of body weight on bone mass. In both Chinese and Caucasian subjects, when the mechanical loading effect of body weight on bone mass was adjusted for, the phenotypic correlation (including its genetic and environmental components) between fat mass (or percentage fat mass) and bone mass was negative. Further multivariate analyses in subjects stratified by body weight confirmed the inverse relationship between bone mass and fat mass, after mechanical loading effects due to total body weight were controlled. Increasing fat mass may not have a beneficial effect on bone mass.
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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
                Article
                27
                10.1007/s00223-015-0027-0
                4564447
                26108649
                a07eca91-ba3b-434b-80b6-05c3255db651
                © 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.

                History
                : 18 March 2015
                : 17 June 2015
                Categories
                Original Research
                Custom metadata
                © Springer Science+Business Media New York 2015

                Human biology
                bone mineral density,physical activity,broadband ultrasound attenuation,bone loss,obesity

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