Sarcopenic Obesity

, Stefan A. Czerwinski3, Audry C. Choh3, Eleonora Poggiogalle2, Silvia Migliaccio4 and Andrea Lenzi1



(1)
Department of Experimental Medicine, Section of Medical Pathophysiology, Endocrinology and Nutrition, Sapienza University, Rome, Italy

(2)
Department of Experimental Medicine, Medical Physiopathology, Food Science and Endocrinology Section, Food Science and Human Nutrition Research Unit, Sapienza University of Rome, Ple Aldo Moro, 5, 00185 Rome, Italy

(3)
Division of Epidemiology, Lifespan Health Research Center, Department of Community Health, Boonshoft School of Medicine, Wright State University, 3171 Research Blvd., Dayton, OH 45420-4014, USA

(4)
Department of Movement, Human and Health Sciences, Unit of Endocrinology, Foro Italico University, Largo de Bosis 14, 00135 Rome, Italy

 




9.1 Introduction


Sarcopenic obesity is a condition that is characterized by age-related loss of muscle mass and function (i.e., sarcopenia) concomitant with increases in regional or total body adiposity (i.e., obesity). Sarcopenic obesity is a critical public health issue that underlies two important problems: the rising prevalence of obesity in Western and developing countries and the increasing life span of humans [14]. The changes in body composition that occur as a result of the aging process and with obesity represent a common ground where sarcopenic obesity develops [3]. Body composition progressively changes with age. These changes begin around the third decade of life and accelerate in later life. A number of studies have now demonstrated a progressive loss of lean body mass in the elderly that is simultaneously accompanied by an increase in fat mass. These changes typically occur while body weight and body mass index (BMI) remain relatively stable [510].

While sarcopenic obesity is often considered a condition of aging, there is substantial evidence now that suggests that this condition can manifest at earlier ages. One of the more significant findings emerging from the literature is that sarcopenia may be present in relatively young obese subjects [11]. In line with the hypothesis that obesity produces low-grade inflammation and hormonal changes affecting muscle function and metabolism, obese young people could have similar changes as the elderly and meet the criteria for the diagnosis of sarcopenic obesity [511]. Factors such as being sedentary and having an unhealthy diet may lead to the development of phenotypic aspects of sarcopenic obesity in these younger subjects [810]. Chronic inflammation induced by obesity is thought to be a pivotal element that may influence the additional depletion of muscle mass in the overweight/obese [3, 7].

Both sarcopenia and obesity are linked to functional impairment [12, 13]. Sarcopenia is independently associated with a reduction in muscle strength and impairment in physical performance [12, 14]. Likewise, a wealth of studies have also demonstrated that obesity detrimentally affects physical function and is connected with the onset of physical disabilities [5, 15]. When coupled with sarcopenia, the presence of obesity worsens functional status and exacerbates physical disability [5, 16]. Currently, although sarcopenic obesity represents a serious public health concern, evidence supporting effective strategies for its management is relatively scarce. Furthermore, a universal consensus for its diagnosis, as well as its treatment, does not yet exist [17, 18].


9.2 Definition of Sarcopenic Obesity


Diagnostic criteria for sarcopenic obesity are not universally established, and different definitions are currently available. Hence, the prevalence of sarcopenic obesity ranges from 2.75 % to over 20 %, depending on the criteria used for the diagnosis and the methods of body composition assessment used [9, 16].

In a recent systematic review summarizing the state of the science regarding the current literature about sarcopenic obesity [19], 26 studies examining more than 23,000 subjects were considered. In all of the studies examined, except one, the definition of sarcopenic obesity was based on the co-occurrence of obesity and sarcopenia. To define the obesity component, various obesity parameters were used including BMI, fat mass, and visceral fat area, either as single parameters or in association with other adiposity measures. To define sarcopenia, several different parameters were used including appendicular skeletal muscle mass standardized for height or weight, cross-sectional muscle area at the quadriceps level, muscle strength, and/or muscle/fat-free mass indices [13].

In our view, a definition of sarcopenia based on a reduction in muscle mass in “absolute” terms is limited in obese subjects and does not accurately describe the picture in terms of functional outcome. Initially, at least in younger obese subjects, increases in fat mass are accompanied by increases in muscle mass [2023]. These increases in mass enable the body to maintain, for a relatively long time, reasonable metabolic control and a satisfactory physical efficiency. The ratio between real lean body mass and ideal lean body mass may represent an even more useful indicator of sarcopenia. According to existing literature concerning body composition in adults and healthy humans, the percentage of body weight that consists of lean mass is, respectively, 85 % for men and 75 % for women. A number of studies have also suggested that in obese subjects, excess body weight is not only made of fat mass but includes a certain amount of muscle mass that approximately corresponds to 25 % of the excess body weight [2226]. In fact, a relative and not an absolute reduction of muscle mass is sufficient to trigger reduced functional performance.

The methods and tools used for the assessment of body composition, as well as the choice of functional indicators, represent another important issue in the identification of sarcopenic obese subjects. In research settings, computed tomography (CT scan) and magnetic resonance imaging (MRI) have been used for estimating muscle mass or fat mass. These techniques, and to a lesser extent, dual-energy X-ray absorptiometry (DXA), are considered to be very precise imaging systems able to separate fat from other soft tissues in the body. However, high cost and limited access to equipment in some facilities and concerns about radiation exposure limit the use of these whole-body imaging methods for routine clinical practice. Bioimpedance analysis (BIA) may represent a valid alternative to these methods in clinical practice as it is inexpensive, easy to use, and readily reproducible. BIA results, obtained under standard conditions, have been found to correlate well with gold standard techniques [27].

The choice of threshold values is also critical in properly identifying sarcopenic obese subjects. Cutoff points depend on the measurement technique chosen and on the availability of reference studies. Similarly to what happens for bone mineral density, a normative population (healthy young adults) needs to be used, with cutoff points at two standard deviations below the mean reference value. In the literature, the diverse threshold values and methods adopted by different authors makes it difficult to compare studies. This represents a significant limitation, given that different intervention procedures need to be compared in research fieldwork, as well as in clinical practice. Thus, it is important to verify the outcomes of these different intervention procedures. Further epidemiological data are needed in order to obtain good reference values for populations in different countries and for different ethnicities.

A final major obstacle in the creation of a reasonable definition for sarcopenic obesity is whether the definition of sarcopenic obesity should be based only on a criterion of body composition (i.e., reduced muscle mass or lean body mass and increased fat mass) or one that also includes functional criteria. Normally, obesity (one aspect of sarcopenic obesity) is defined using only fat mass or BMI. However, reduced fat-free mass along with muscle strength and functional impairment are used to define sarcopenia. In the case of sarcopenia, functional measurements are required for diagnosis. In the consensus by Cruz-Jentoft et al., the European Working Group on Sarcopenia in Older People (EWGSOP) [28] recommends considering the presence of both low muscle mass and low muscle function (strength or performance). Using this method, EWGSOP further classifies conceptual stages as “pre-sarcopenia,” “sarcopenia,” and “severe sarcopenia.” In the case of sarcopenic obesity, it is likely that the same logical pathway should be followed, even if no study presently hypothesizes a diagnosis of sarcopenic obesity in this manner. So far, only a simple evaluation of body composition has been used to define sarcopenic obesity. An implementation of this definition with muscle strength and functional parameters will probably be more useful in clinical practice. A wide range of tests is available for physical performance evaluation, particularly in the elderly population, including the Short Physical Performance Battery (SPPB), gait speed, the 6-min walk test, and the stair climb power test [29]. By including functional information, this definition will be more responsive to the patient’s clinical status and to the severity of the disease. This is important as an increase in fat mass together with the deterioration of lean body mass (with possible fatty infiltration) may lead to a progressive worsening of functional parameters, such as aerobic capacity, muscle strength, walking speed, and ability to maintain balance. Moreover, using this definition will also make it easier to track the course of the nutritional and rehabilitation treatment and to identify outcomes to be achieved.


9.3 Biology of Sarcopenic Obesity


In the case of sarcopenic obesity, the augmentation of lean body mass in parallel with fat mass represents a protective mechanism allowing the obese individual to sustain increased fat mass. This avoids, at least in the early phases of the process, the onset of metabolic and functional impairment during fat accumulation and a reduction in lean body mass (due to the aging process, inflammation, poor diet leading to rapid weight loss, or inactivity) that may cause a precocious onset of disability in obese subjects [8, 9]. In obese adults, an imbalance between lean mass, excess body fat, and total body size occurs earlier than in normal-weight individuals [8, 9]. This imbalance results in disproportionate ratios between the remaining conserved lean mass and excess fat mass, thereby creating a situation where body weight exceeds that which the lean mass can support. The pathogenetic and functional role of sarcopenia in obese elderly subjects, as well as in younger obese adults, still remains to be fully clarified [11].

Weight cycling is also known to exert deleterious effects on body composition and sarcopenic obesity, particularly among elderly subjects. Weight cycling can result in a greater loss of lean body mass during the weight-loss phase. Often when weight is regained lean mass is not conserved [6]. Hunter et al. [30] found that after dieting and weight loss, premenopausal women regained limb body mass, while trunk lean mass was not restored. The researchers hypothesized that the mechanism explaining the reduction of resting energy expenditure, the basis of the potential adipose tissue increase after dieting, was a consequence of the mass depletion from highly metabolically active tissue. On the other hand, in a more recent paper [13], young overweight and obese men and women who regained weight did not see negative effects in terms of body fat distribution and composition of lean body mass. It is clear from the literature that further research is needed examining weight cycling and its effect on body composition, especially in younger obese subjects.

Inadequate dietary protein intake may also influence sarcopenic obesity. Current recommendations for protein intake [31] were determined based on studies performed in healthy individuals. These requirements may not be adequate when considering a complex condition such as sarcopenic obesity. Studies have shown that protein requirements in the elderly may not be adequate to maintain or prevent muscle loss [32]. Future studies are needed to address the question of what is a reasonable dietary protein intake to satisfy the nutritional requirements for sarcopenic obese subjects. Careful consideration should be made to increase protein intake while maintaining or reducing total calorie intake.


9.4 Sarcopenic Obesity, Physical Performance, Disability, and Quality of Life


Using a recently developed tool (TSD-OC) specifically designed to assess disability level in obese subjects [33], we investigated the relationship between sarcopenic obesity and performance. The TSD-OC test is composed of 36 items divided into seven sections (pain, stiffness, activities of daily living and indoor mobility, housework, outdoor activities, occupational activities, and social life), and in the validation study, the TSD-OC test was found to be significantly correlated to functional assessment (6MWT), handgrip strength and quality of life parameters (SF-36 questionnaire). Our results (not yet published) highlight that the presence of sarcopenia in obese subjects was associated with a worse TSD-OC test score. This finding is consistent with data presented in a recent study by Baumgartner, pointing out the coexistence of low physical capacity and sarcopenic obesity [5].

While evidence supports the synergistic pathological action exerted by obesity and sarcopenia, it is still a matter of debate which of the two components (increased fat mass or reduced lean body mass) in sarcopenic obesity is better correlated with disability. Some studies have concluded that excess body fat was a stronger contributor to physical function impairment than sarcopenia [30, 34]. However, Davison et al. [14] did not demonstrate any association between sarcopenia and functional limitations; instead, mobility impairment was related to percentage of body fat and BMI. Similarly, Cawthon et al. [35] found that adipose tissue and performance status were more closely related to disability than lean body mass. Some of this debate is depicted in the U-shaped relationship between BMI and physical limitations [36]. Our data suggest that the correlation is stronger for lean body mass and especially for the real lean body mass/ideal lean body mass ratio. In a recent paper [18], the authors hypothesized that disability caused by sarcopenia and sarcopenic obesity was related to the amount of adiposity or body weight bearing per unit of muscle mass (total body fat to lower limb muscle mass ratio). Our finding of increased disability in obese subjects with sarcopenia confirms that the sarcopenia, in the context of obesity, may be better defined as a “relative” sarcopenia. Despite the appearance that muscle mass is conserved, it probably is not enough in proportion to the total body mass to prevent the onset of functional impairment and disability. Moreover, fat infiltration of muscles, known as “myosteatosis” [11], could also be responsible for deteriorated muscle function in obese individuals.


9.5 Treatment of Sarcopenic Obesity


There are numerous potential approaches to consider in terms of treatment for sarcopenic obesity. Even though weight loss is beneficial in obese subjects in terms of reducing metabolic and cardiovascular risk [37], the concomitant changes in body composition that occur during caloric restriction create additional concerns for the maintenance of good functional status and physical performance. Especially in obese older adults, obesity-related disability tends to worsen because of the decline of lean mass with aging [5]. Even in younger subjects, a reduction in body weight consists of loss of both fat mass and lean body mass. The literature suggests that a decrease in lean body mass can range from 15 % of total body weight in the case of a mild energy restriction to as much as 50–70 % during semi-starvation [38]. Despite a reduction of body weight, diet combined with exercise has been shown to result in a minor decrease of fat-free mass when compared to diet alone. Intentional weight loss through diet alone was shown to deteriorate muscle mass particularly among the elderly [39, 40]. A number of other studies have shown that exercise has additional benefits in preserving or minimizing loss of lean mass during diet-induced weight loss [34]. In these studies, both aerobic and resistance activities, or their combination, appear to be effective in limiting muscle loss during dieting and preserving physical function. However, contrary to these findings, Hunter et al. demonstrated that resistance training, but not aerobic exercise, was able to conserve lean body mass and strength following weight loss [30]. Also, in a study by Hays et al. on sedentary older obese subjects [41], a dietary intervention based on fat restriction but not energy deficit resulted in beneficial effects on body weight and fat mass reduction that were greater than an ad libitum diet combined with exercise.

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Jul 5, 2017 | Posted by in UROLOGY | Comments Off on Sarcopenic Obesity

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