Can sarcopenia be diagnosed without measurements?

Can sarcopenia be diagnosed without measurements?

European Geriatric Medicine 5 (2014) 291–293 Available online at ScienceDirect www.sciencedirect.com Editorial Can sarcopenia be diagnosed without...

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European Geriatric Medicine 5 (2014) 291–293

Available online at

ScienceDirect www.sciencedirect.com

Editorial

Can sarcopenia be diagnosed without measurements? MacDonald Critchley noted that with aging there was a visual loss of muscle in the hands and feet [1]. This loss of muscle was named sarcopenia by Irwing Rosenberg. Baumgartner provided an objective definition using appendicular muscle mass corrected for height [2]. Subsequently, numerous studies have shown that muscle wasting associated with old age leads to a decrease in function, fractures and an increase in mortality [3–6]. Sarcopenia is a major cause of frailty [7–11]. It has been suggested that sarcopenia should be screened for even in the absence of complaints [12], as sarcopenia is potentially reversible [13]. More recently it was recognized that muscle function was not necessarily related to muscle mass [14,15]. This is in part due to lipid infiltration with aging. It has been clearly demonstrated that obese persons with muscle wasting–‘‘Sarcopenic obesity’’–have poorer function than those who have sarcopenia alone [16,17]. With aging, there is not a direct correlation between muscle quality and muscle mass [18,19]. Further, an increase in muscle mass, produced by growth hormone does not lead to an increase in muscle strength [20]. This led to a number of organizations to redefine sarcopenia as being limited muscle function (walking speed or distance or grip strength) associated with a low muscle mass (Table 1) [21–25]. A number of studies have validated this definition, which appears to be more predictive of poor outcomes [26–30]. By coupling function with muscle mass, this excludes other causes of poor function such as arthritis, chronic obstructive pulmonary disease, congestive heart failure and anaemia [31]. There are many causes of sarcopenia. Approximately half of the persons with sarcopenia have degeneration of the motor end plates [32]. This leads to an increase in c-terminal agrin, which is an excellent biomarker for sarcopenia due to nerve damage [33]. Table 1 Comparison of sarcopenia definitions: while definitions include similar criteria, there is marked variation in cut-off values. Definition

Function

Muscle Mass

EWGSOP [21]

Gait speed Grip strength Gait speed

Low muscle mass

IANA Sarcopenia Task Force [22] Sarcopenia with Limited Mobility (SCWD) [23] Asian Working Group for Sarcopenia [25] FNIH Sarcopenia Project [24]

6 min walk or gait speed Grip strength Gait speed Grip strength Gait speed

Low appendicular lean mass/height2 Low appendicular lean mass/height2 Low appendicular lean mass/height2 Appendicular lean mass/BMI

EWGSOP: European Working Group on Sarcopenia in Older People; SCWD: Society on Sarcopenia, Cachexia and Wasting Diseases; IANA: International Academy on Nutrition and Aging; FNIH: Foundation for the National Institutes of Health. http://dx.doi.org/10.1016/j.eurger.2014.07.014 1878-7649/ß 2014 Published by Elsevier Masson SAS.

Persons with diabetes mellitus have accelerated muscle loss associated with their peripheral neuropathy and decreased blood flow to the muscles [34,35]. In addition, insulin resistance leads to mitochondrial dysfunction resulting in oxidative damage. Another major cause of sarcopenia is the age related decline of anabolic hormones, i.e., testosterone, insulin growth factor and DHEA [36]. Testosterone stimulates beta-catenin leading to an increase in satellite cells as well as an increase in protein synthesis [37]. In parabiosis experiments, testosterone has been shown to have a necessary permissive effect to allow GDF-13 to reverse the atrophy of aging muscles [38]. An excess of inflammatory cytokines has been demonstrated to cause age-associated muscle loss [39]. The anorexia of aging results in a decrease in protein to maintain muscle mass [40]. Older persons tend to have a decrease in physical activity, which adds to muscle loss. Finally, a variety of genetic factors such as alterations in myostatin and angiotensin converting enzymes, as well as mitochondrial deficits, further decrease muscle mass and function. The factors causing sarcopenia are summarized in Fig. 1. It has been recognized that bone strength does not directly correlate with bone mineral density. This lead researchers to query whether the questions associated with the FRAX (www.shef.ac.uk.FRAX/) would be sufficient to identify the persons at highest risk for fractures. Recently, studies have shown that the FRAX questions alone are capable of identifying those at highest risk for fractures [41]. As muscle function is more observable than bone function, it was suggested that it should be feasible to develop a simple questionnaire to identify persons with sarcopenia. Our group developed such a questionnaire–the SARC-F (Table 2) [42]. A number of studies have provided a robust validation for the SARCF. Woo et al. [43] showed that the SARC-F performed at a similar level to the European Working Group on Sarcopenia in Older People [21] and the Asian Working Group for Sarcopenia [25] at identifying persons with sarcopenia. Similarly, a group in China demonstrated that the SARC-F was highly predictive of muscle function [44]. Further validations of the SARC-F exist in the St. Louis African American Health Study, the National Health and Nutrition Examination Survey (NHANES), and the Baltimore Longitudinal Study of Aging. Evans et al. [45] have developed a more complex sarcopenia questionnaire, but at present it lacks an in-depth validation. These studies certainly suggest that sarcopenia can be screened for without a necessity to measure muscle mass or to directly measure muscle function. Sarcopenia is a treatable malady of aging. It is clear that both aerobic and resistance exercise can improve muscle function [46–50]. Further, there is increasing evidence that high quality protein supplementation can enhance muscle mass and function

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Editorial / European Geriatric Medicine 5 (2014) 291–293

Fig. 1. Factors causing sarcopenia and outcomes in persons with sarcopenia. DHEAS: dehydroepiandrosterone sulfate; TNFa: tumor necrosis factor alpha; IL6: interleukin 6; CNTF: ciliary neurotrophic factor.

Table 2 The SARC-F Scale: A rapid, validated scale for the detection of sarcopenia. Scores of 4 or more–sarcopenia. Item

Scoring

Strength

Difficulty lifting and carrying 10 pounds

None = 0 Some = 1 A lot or unable = 2

Assistance in walking

Difficulty walking across a room

None = 0 Some = 1 A lot, use aids, or unable = 2

Rise from a chair

Difficulty transferring from a chair or bed

None = 0 Some = 1 A lot or unable without help = 2

Climb stairs

Difficulty climbing a flight of ten stairs

None = 0 Some = 1 A lot or unable = 2

Falls

Number of falls in the past year

None = 0 1–3 falls = 1 4 or more falls = 2

[51–56]. Vitamin D replacement in persons with low vitamin D also can improve muscle function [57]. At present, the role of testosterone is controversial [58]. Other drugs such as selective androgen receptor molecules and myostatin and activin receptor molecules are under development [59]. The availability of a simple questionnaire to identify persons at risk for sarcopenia becomes a powerful tool for general practitioners. Once identified simple interventions, viz. exercise, protein supplementation and vitamin D, can be utilized to improve health outcomes in older persons. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. Acknowledgements No outside funding was received by either of the authors (JEM, TKM) for the writing of this article.

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J.E. Morley MB, BCh* Divisions of Geriatric Medicine and Endocrinology, Saint Louis University School of Medicine, 1402, S. Grand Blvd., M238, Saint Louis, MO 63104, USA T.K. Malmstrom PhD Department of Neurology and Psychiatry and Division of Geriatric Medicine, Saint Louis University School of Medicine, Saint Louis, MO, USA *Corresponding author E-mail address: [email protected] (J.E. Morley)

Received 28 July 2014 Accepted 31 July 2014 Available online 17 September 2014