Sarcopenia: An Undiagnosed Condition in Older Adults. Current Consensus Definition: Prevalence, Etiology, and Consequences. International Working Group on Sarcopenia

Nutrition, Exercise Physiology, and Sarcopenia Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Boston, MA 02111, USA.
Journal of the American Medical Directors Association (Impact Factor: 4.94). 05/2011; 12(4):249-56. DOI: 10.1016/j.jamda.2011.01.003
Source: PubMed


Sarcopenia, the age-associated loss of skeletal muscle mass and function, has considerable societal consequences for the development of frailty, disability, and health care planning. A group of geriatricians and scientists from academia and industry met in Rome, Italy, on November 18, 2009, to arrive at a consensus definition of sarcopenia. The current consensus definition was approved unanimously by the meeting participants and is as follows: Sarcopenia is defined as the age-associated loss of skeletal muscle mass and function. The causes of sarcopenia are multifactorial and can include disuse, altered endocrine function, chronic diseases, inflammation, insulin resistance, and nutritional deficiencies. Although cachexia may be a component of sarcopenia, the 2 conditions are not the same. The diagnosis of sarcopenia should be considered in all older patients who present with observed declines in physical function, strength, or overall health. Sarcopenia should specifically be considered in patients who are bedridden, cannot independently rise from a chair, or who have a measured gait speed less that 1 m/s(-1). Patients who meet these criteria should further undergo body composition assessment using dual energy x-ray absorptiometry with sarcopenia being defined using currently validated definitions. A diagnosis of sarcopenia is consistent with a gait speed of less than 1 m·s(-1) and an objectively measured low muscle mass (eg, appendicular mass relative to ht(2) that is ≤ 7.23 kg/m(2) in men and ≤ 5.67 kg/m(2) in women). Sarcopenia is a highly prevalent condition in older persons that leads to disability, hospitalization, and death.

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Available from: Aimo Kannt, Oct 09, 2015
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    • "There is also an agingassociated increase in collagen accumulation which can diminish force production (Ramaswamy et al., 2011). In humans, muscle mass is positively correlated with a greater longevity (Miller et al., 2002), and the rapid decrease in muscle mass and strength that occurs toward the end of the lifespan can lead to severe disability and reduced quality of life (Fielding et al., 2011). Myostatin is a negative regulator of skeletal muscle mass, with adult MSTN À/À mice displaying up to a twofold increase in muscle mass (Gumucio & Mendias, 2013). "
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    ABSTRACT: The molecular mechanisms behind aging-related declines in muscle function are not well understood, but the growth factor myostatin (MSTN) appears to play an important role in this process. Additionally, epidemiological studies have identified a positive correlation between skeletal muscle mass and longevity. Given the role of myostatin in regulating muscle size, and the correlation between muscle mass and longevity, we tested the hypotheses that the deficiency of myostatin would protect oldest-old mice (28-30 months old) from an aging-related loss in muscle size and contractility, and would extend the maximum lifespan of mice. We found that MSTN(+/-) and MSTN(-/-) mice were protected from aging-related declines in muscle mass and contractility. While no differences were detected between MSTN(+/+) and MSTN(-/-) mice, MSTN(+/-) mice had an approximately 15% increase in maximal lifespan. These results suggest that targeting myostatin may protect against aging-related changes in skeletal muscle and contribute to enhanced longevity. © 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
    Aging cell 03/2015; 14(4). DOI:10.1111/acel.12339 · 6.34 Impact Factor
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    • "Aging contributes to the structural and functional changes in skeletal muscle in a wide range of mammals [44]. Sod1−/− mice showed significant decreases in the whole hindlimb muscle mass compared with age-matched Sod1+/+ mice, and this occurred in an age-dependent manner [25]. "
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    ABSTRACT: Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1(-/-) ) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1(-/-) mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1(-/-) mice.
    BioMed Research International 09/2014; 2014:140165. DOI:10.1155/2014/140165 · 2.71 Impact Factor
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    • "There are three conventional methods to evaluate muscle mass; dual energy x-ray absorptiometry, bioelectric impedance measurement, and cross-sectional imaging such as CT scan and magnetic resonance image (28, 29). In the literature, the assessment of the psoas muscle mass was found very accessible and highly precise to quantify the skeletal muscle in the body (17, 18). "
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    ABSTRACT: This study aimed to assess and compare sarcopenia with other prognostic factors for predicting long-term mortality in cirrhotic patients with ascites. Clinical data of 65 among 89 patients with measurement of all parameters were consecutively collected. Sarcopenia was evaluated as right psoas muscle thickness measurement divided by height (PMTH) (mm/m). During a mean follow-up of 20 (range: 1-49) months, 19 (29.2%) of 65 patients died. The values of the area under the receiver operating characteristics curve (AUROC) of Child-Pugh score, Model for End-Stage Liver Disease (MELD) score, MELD-Na, and PMTH for predicting 1-yr mortality were 0.777 (95% CI, 0.635-0.883), 0.769 (95% CI, 0.627-0.877), 0.800 (95% CI, 0.661-0.900), and 0.833 (95% CI, 0.699-0.924), whereas hepatic venous pressure gradient was not significant (AUROC, 0.695; 95% CI. 0.547-0.818, P=0.053). The differences between PMTH and other prognostic variables were not significant (all P>0.05). The best cut-off value of PMTH to predict long-term mortality was 14 mm/m. The mortality rates at 1-yr and 2-yr with PMTH>14 mm/m vs. PMTH≤14 mm/m were 2.6% and 15.2% vs. 41.6% and 66.8%, respectively (P<0.001). The mortality in cirrhotic patients with PMTH≤14 mm/m was higher than those with PMTH>14 mm/m (HR, 5.398; 95% CI, 2.111-13.800, P<0.001). In conclusion, sarcopenia, evaluated by PMTH, is an independent useful predictor for long-term mortality in cirrhotic patients with ascites. Graphical Abstract
    Journal of Korean Medical Science 09/2014; 29(9):1253-9. DOI:10.3346/jkms.2014.29.9.1253 · 1.27 Impact Factor
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