Sarcopenia

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Sarcopenia

Sarcopenia

Sarcopenia is a condition characterized by loss of muscle mass, strength, and function in older adults and it can affect both under- and overweight adults 1, 2, 3, 4, 5. The term “sarcopenia” was introduced into the medical literature by Irv Rosenberg in 1995 6 . At that time “sarcopenia” was defined as an abnormal loss of muscle associated with aging and was validated in 2001 to predict functional decline 7. However, Manini and Clark in 2012  8 pointed out that it was muscle power and not muscle mass that was the predominant feature that led to loss of functional status. In 2010, the European Working Group on Sarcopenia defined sarcopenia as low muscle mass together with low muscle function (strength or performance) 9. Subsequently, other international groups developed similar definitions for sarcopenia focusing on walking speed or distance walked in 6 minute or grip strength in persons with lean muscle mass 10, 11, 12. A number of studies have confirmed the validity of these definitions and it was recently demonstrated that cutoffs for the definitions need to be ethnically sensitive 13, 14, 15, 16. Based on the available literature, it would appear that sarcopenia is present in 5 to 10% of persons 65 years of age or older 17, 18, 19. Today, the definition for “sarcopenia” lacks global and widely accepted definition that can be routinely used in clinical settings, even though an ICD10-CM (International Classification of Diseases, Tenth Revision, Clinical Modification) M62.84 code for sarcopenia exists 2, 20, 16. Although the ICD10-CM M62.84 code for sarcopenia is available in some countries such as Australia and the United States 21, the World Health Organization (WHO) has yet to include an ICD-10 code for sarcopenia in its version. A global definition of sarcopenia would ease the adoption of an ICD-10 code for sarcopenia by WHO, which, in turn, would increase clinical recognition of this condition worldwide.

The lack of a single, standard definition of sarcopenia has led to several issues, resulting in variable prevalence estimates and conflicting treatment decisions 22, 23, 2. First, research into the prevalence, incidence, and causes and consequences of sarcopenia is often difficult to harmonize, as disparate definitions can lead to widely different estimates of prevalence 24 or can identify different important consequences of sarcopenia. Second, the lack of a single definition has clinical implications because those seeing patients may be uncertain as to which measures or cut-off points to use when evaluating patients 2. Third, the lack of a unified definition for sarcopenia has impeded the development of clinical care pathways for sarcopenia 2. While there is evidence that, even in the oldest individual, non-pharmacological interventions such as resistance-based exercise can increase muscle strength 25, 26, 27 and multicomponent exercise interventions (aerobic, strength and balance/flexibility) can reduce the risk of mobility disability 28, 29, there are few specific exercise or dietary prescriptions in regular clinical use to treat sarcopenia. There is also a stymied development of pharmacological treatments for sarcopenia.

Sarcopenia is a part of normal aging, and occurs even in master athletes, although it is clearly accelerated by physical inactivity 30. Sarcopenia most commonly affects elderly and sedentary populations and in people who have comorbidities that affect the musculoskeletal system or impair physical activity 5. Sarcopenia is different from muscle loss (cachexia) caused by inflammatory disease, or from the weight loss and attendant muscle wasting caused by starva-tion or advanced disease 31. Sarcopenia is increasingly recognized as a correlate of ageing and is associated with increased likelihood of adverse outcomes including falls, fractures, frailty and mortality 32. Sarcopenia is universal with advanced age. That is, reduced muscle mass and strength are evident in all elderly persons compared to young, healthy, physically active young adults 30. If the sarcopenia progresses beyond a threshold of functional requirements, it leads to disability and frailty, and this can occur independently of any disease-induced frailty 33, 34. Sarcopenia is the most important cause of frailty in older persons 35, 36, 37, 38, 39. Superimposed illness will accelerate the loss of muscle mass, and thus increase the risk of disability, frailty, and death 30. In addition, there is a close association between sarcopenia and bone loss and hip fracture‐osteosarcopenia 40, 41. Sarcopenia has also been found to be a major reason for poor outcomes in persons with diabetes mellitus 42, 43.

Sarcopenia signs and symptoms include weakness, fatigue, loss of energy, balance problems, and trouble walking and standing. Muscle loss or weakness can lead to falls, broken bones, and other serious injuries and can affect a person’s ability to care for oneself. Older age, getting little or no exercise, and poor nutrition may increase the risk of sarcopenia. Sarcopenia may also occur in people with cancer.

The term, sarcopenia, was first coined in 1988 by Irwin Rosenberg at a meeting in Albuquerque, New Mexico, to refer to muscle wasting of the older people 44. Its etymological origins are two Greek words: sarx for flesh and penia for reduced or deficiency. Baumgartner et al. 45 proposed an operational definition of sarcopenia in 1998. Utilizing dual energy X‐ray absorptiometry (DXA) to measure lean soft tissue, the authors defined sarcopenia as being <2 standard deviations (SDs) of appendicular muscle mass (ASM, kg) per height squared (m²) below the mean of a young reference group. Using this criterion, Baumgartner et al. 45 showed that the prevalence and the severity of sarcopenia significantly increased with age and that it was associated with physical disability. In 2002, Janssen et al. 46, using bioelectrical impedance analysis (BIA), showed that in the Third National Health and Nutrition Examination Survey (NHANES III), functional impairment was three times as likely in persons with an estimated lean mass below 2 SDs of the mean. Baumgartner et al 47, found that in older persons with obesity, those who had lost muscle mass had worse outcomes than those who had maintained their muscle mass. They coined the term ‘sarcopenic obesity’ for this condition. By the early 2000s, it was recognized that there are numerous causes of age‐related sarcopenia, including malnutrition, loss of motor units innervating muscle (α-motor neuron input), systemic inflammation-driven erosion of muscle mass, oxidative stress, decline in anabolic hormones, increased body fat and the ‘anorexia of aging’ coupled with a decrease in physical activity and disease burden are likely to culminate in sarcopena (see Figure 4 below) 48. At this stage, it was recognized that there were both primary sarcopenia (age related) and secondary sarcopenia (disease related, as with diabetes mellitus, cancer, chronic obstructive pulmonary disease, or heart failure) 49.

However, there is no absolute level of lean mass, body cell mass, or muscle mass at which one can definitely say that sarcopenia is present 30. Such a definition would be an important advance. In reaching such a definition, one should consider two important and generally agreed-upon concepts in relation to lean body mass. First, there is a direct structure ± function link between muscle mass and strength, in that more muscle generally equals greater strength and vice versa. However, the function defining the relationship between muscle loss and strength loss is not the same as that applying to muscle and strength gain 30.

Making the clinical diagnosis of sarcopenia is difficult for the following reasons. There is no absolute level of lean mass, body cell mass, or muscle mass for comparison. There is no generally accepted clinical test to diagnose sarcopenia. Finally, there is no accepted threshold of functional decline at which sarcopenia is implied. Dual-energy x-ray absorptiometry (DXA) is a well-established, low-radiation technique used to assess body composition and provides reproducible estimates of appendicular skeletal lean mass 50. It is acknowledged that the accuracy of DXA for assessing muscle mass in people of different ages and different pathological conditions may vary. Moreover, DXA (in contrast to CT-scan and MRI) cannot assess intra-muscular fat, which turns out to be of increasing importance in terms of the quality of muscle and associations with clinical outcomes. Bearing these limitations in mind, DXA is still considered as the procedure of choice for routine clinical assessment 32. Using DXA, appendicular skeletal lean mass (ASM) is measured as the sum of the non-bone and non-fat mass of the four limbs. To adjust for body size, a skeletal muscle index (SMI) is derived as ASM/height². Thresholds of skeletal muscle index (SMI) at two standard deviations (SDs) below the mean skeletal muscle index (SMI) of young male and female reference groups have been proposed as gender-specific cut-off points for sarcopenia. This results in two thresholds, proposed by the European Working Group on Sarcopenia (EWGSOP) 51, the first of 5.5 kg/m² for women and 7.26 kg/m² 52 for men and the second of 5.67 kg/m² for women and 7.25 kg/m² for men 53, depending on the reference group on which these cut-off have been established. Using a different approach, the Function NIH sarcopenia project 54 has also recently defined cut-offs for appendicular lean mass adjusted for body mass index (BMI), giving values of < 0.512 for women and < 0.789 for men. However, it should be pointed that these cut-offs might also be modified according to ethnicity 55.

Bio-electrical impedance analysis (BIA) is a method which estimates the volume of fat and lean body mass based on the relationship between the volume of a conductor and its electrical resistance. The method is not expensive, requires no specialized staff and is relatively easy to use in clinical practice, both on ambulatory subjects or on hospitalized patients. Moreover, reference values have been established for older individuals 51. Even if the method’s accuracy has been challenged and has been reported to overestimate muscle mass and underestimate fat mass 56, it is possible to use some adjustment equations to obtain valid measurements 57.

Possible therapeutic strategies include increased protein intake and aggressive resistance-based exercise programs, but long-term randomized controlled trials are needed to evaluate the efficacy of these modalities. Hormonal supplementation may help if levels are low. Countermeasures should have the goals of maintaining adequate total body mass and protein intake. Physical activity incorporating resistance training is probably the most effective countermeasure to sarcopenia.

Pharmacologic interventions such as growth hormone or testosterone, which increase lean mass (and evidently muscle mass as well) do not alter strength much, while progressive resistance training, which causes large increases in strength, can do so with little evident muscle hypertrophy, at least in the first few months of training 30. For example, the strength and vastus lateralis area (measured by CT scan) lost over a 12 years follow-up period in seven healthy men, and the amount gained during a 12 week period of intensive resistance training 58. It is clear that there is hysteresis in this system: the decline and the regain occur at vastly different rates. Thus, defining sarcopenia solely on compositional terms may be useful and attractive for research purposes, but it may be simplistic in explaining functional changes caused by treatment of sarcopenia 30.

Second, there is reasonable evidence that there is a limit on how much lean body mass can be lost before death supervenes. The available data, based on starvation 59, AIDS patients 60, and critical illness 61, suggest that loss of more than about 40% of baseline lean mass is fatal. `Baseline’ is a slippery concept here, because again absolute mass is not explanatory – basketball players do not necessarily outlive jockeys, but rather the amount of loss as a function of the baseline mass that the individual started with. Reference Man and Woman are one benchmark, based on a few cadaver studies in generally healthy persons 62. Kehayias et al 63 defined baseline as the mean for adults aged 20 ± 30 years; no healthy subjects were found below approximately 70% of that standard, and there was a steady decline in body cell mass for both men and women across age groups between 30 and 100 years (see Figure 2).

The latter point also raises the issue of the importance of sarcopenia as an indicator of reduced protein stores for times of stress 30. It is well accepted that during illness, gluconeogenesis increases in importance, while ketogenesis is relatively suppressed, so that protein is burned for energy in excess of the levels seen in starvation adaptation  30. Given the anorexia caused by acute illness, and by the iatrogenic limitation on dietary intake that often obtains in hospitals, endogenous protein stores are crucial in determining the availability of metabolic substrate to cope with the illness, and thus the ability to survive it. Therefore, it is no wonder that elderly, sarcopenic patients fare worse than young, healthy adults for almost all diseases. Tellado et al 61 have shown that measurement of body cell mass was the only independent determinant of survival in intensive care unit patients in multivariate analysis, removing the significance of univariate predictors such as albumin, age, and even diagnosis. Thus, the metabolic significance of sarcopenia in illness should be considered independently of its functional impact during times of better health, as both are important to the survival and well-being of elderly persons.

Figure 1. Sarcopenia definition (conceptual definition of sarcopenia)

Sarcopenia definition
[Source 2 ]

Figure 2. Lean body mass

Lean body mass

Footnote: Body cell mass or lean body mass, measured as total body potassium (TBK) per kg body weight, as a function of age in a cross-sectional study. Data are expressed as a percentage of the reference 20 ± 30-year-old groups for men (O) and women (x) separately.

[Source  63 ]

Primary sarcopenia (sarcopenia of aging)

In 2010, the European Working Group on Sarcopenia for Older Persons 64 recommended a new operational definition of sarcopenia of aging, i.e. the presence of low muscle mass together with low muscle function (strength or performance). Over the last decade, numerous other consensus groups have agreed to this revision to the meaning of sarcopenia of aging 65. However, these groups all used different cut‐offs to define sarcopenia of aging, highlighting the fact that different cut‐offs are necessary for different ethnic groups 66.

Towards the end of last year, two consensus articles on sarcopenia of aging were published. One was an update by the European Working Group on Sarcopenia (EWGSOP2) 67 and the other was on the management of sarcopenia of aging by the International Clinical Practice Guidelines for Sarcopenia (ICFSR) 68. The European Working Group on Sarcopenia (EWGSOP2) requires low muscle strength as a key characteristic of low muscle quality and the presence of low muscle quantity to confirm the diagnosis. If a person also has functional impairment, confirmed with a physical performance measure 69, this is characterized as severe sarcopenia. The authors recommended measuring muscle strength with either grip strength or the chair stand test. Muscle mass can be measured by DXA, magnetic resonance imaging, or computed tomography. Either gait speed, the Short Physical Performance Battery (SPPB), the Timed Up and Go test, or the 400‐m‐walk can be used for the assessment of physical performance. The Short Physical Performance Battery (SPPB) takes about 10 min to complete 70. Participants presenting a score ≤8 points have been described as having a poor physical performance 51.

Recognizing the limited time available during a typical visit to a health care professional, the European Working Group on Sarcopenia also suggested that case finding should be used to identify older persons at risk for sarcopenia. They recommended the use of clinical symptoms usually associated with sarcopenia or the SARC‐F (Figure 2), a questionnaire with five questions, which has high specificity, albeit low sensitivity, to identify persons with sarcopenia 71. The SARC‐F has been translated into multiple languages. The SARC‐F is also recommended by the International Clinical Practice Guidelines for Sarcopenia (ICFSR) for screening 68. The specificity of the SARC‐F can be improved by measuring calf circumference as well 72. The Ishii screening test (age, grip strength, and calf circumference) is recommended as an alternative screening test 73. However, this already includes grip strength, which is a core measure of sarcopenia.

While bioelectrical impedance analysis (BIA) was not strongly supported by the European Working Group on Sarcopenia, to measure muscle mass, they recognize that its portability, affordability, and availability make bioelectrical impedance analysis (BIA) a feasible tool to estimate muscle mass in many care settings. Ultrasound of muscle such as the quadriceps is emerging as a potential tool to measure muscle quantity and, because it excludes intermuscular adipose tissue from the measurement, also muscle quality 74; a protocol for using ultrasounds in sarcopenia has recently been proposed by the European Geriatric Medicine Society 75.

There is increasing evidence that creatine dilution, implemented by ingesting a dose of the deuterium labelled isotope, may also offer an accurate approach for measuring muscle mass 76. Studies so far suggest creatine dilution estimates of muscle mass may have good correlations with functional outcomes 77. Nonetheless, its relevance and practicality in clinical settings remain to be determined.

The International Clinical Practice Guidelines for Sarcopenia (ICFSR) consensus made similar conditional recommendations utilizing the strength, assistance with walking, rising from a chair, climbing stairs, and falls (SARC-F) questionnaire for screening and applying either the original European Working Group on Sarcopenia or Foundation for NIH diagnostic criteria 68.

Figure 3. Sarcopenia questionnaire (SARC‐F questionnaire includes scoring)

Sarcopenia questionnaire
[Source 49 ]

Secondary sarcopenia

Malignant disease has been the most studied secondary sarcopenia, and international consensus definitions specific to cancer sarcopenia 78 are predicated on disease specific outcomes: mortality, complications of cancer surgery, and chemotherapy toxicity. Whether this secondary sarcopenia should be considered early cachexia or sarcopenia remains controversial 79, but it is becoming clearer that sarcopenia is only one of the different features of muscle changes during cancer cachexia. Owing to the prevalent use of computed tomography imaging in cancer diagnosis and follow‐up, secondary analysis of oncologic imaging for skeletal muscle cross‐sectional areas or volumes is the current standard for the quantification of muscle mass in this domain.

There are several points of relevance regarding age‐related and disease‐related loss of muscle mass. Loss of muscle mass with age occurs in a continuous fashion after reaching peak muscle mass in young adulthood (at about 30 years of age). A variety of longitudinal observational studies provide information on the rate of muscle loss per decade. The percentage loss of appendicular muscle mass per 10 years is of the order of ~5% in men and is usually reported to be somewhat lower in women. Chronic illness‐related muscle loss is also progressive; however, these are non‐linear and of a considerably greater magnitude than the values seen in aging. For example, cancers of advanced stage induce muscle loss over time that take an exponential course 80 with increasing intensity according to the disease progression, varying from 2% per 100 days to 15% per 100 days. Total cumulative loss in 12 months in colon cancer patients was 15.6%, equivalent to circa 30 years of aging 80; this is partially disease‐related but also in part a consequence of cancer surgery or systemic antineoplastic therapies which induce punctate short‐term losses. Acute illness requiring hospitalization is associated with even higher intensity of muscle loss than in cancer. In elective hip replacement surgery during an average of 5.6 ± 0.3 days of hospitalization, associated with significant decline in quadriceps (−3.4 ± 1.0%) and thigh muscle cross‐sectional area (CSA) (−4.2 ± 1.1%) in the non‐operated leg aging 81. This could be in part due to bed rest as 5 days of one‐legged knee immobilization using a full leg cast resulted in decline of quadriceps muscle cross‐sectional area from baseline of 3.5 ± 0.5%. Acute sarcopenia secondary to hospitalization or chronic disease exacerbations may be partially recoverable or may lead to heightened risk of developing sarcopenia at a young age 82.

Sarcopenia causes

Causes of sarcopenia are generally attributable to the natural processes of aging, which are not entirely understood and are multifactorial 10. Factors contributing to the development of sarcopenia include decreased Type 2 Fast-Twitch muscle fiber size and number and a decline in satellite cells 83, inactivity, obesity, insulin resistance, reduced androgen and growth factor serum concentrations, inadequate protein intake, and a blunted muscle protein synthesis response to protein meals or resistance exercise 84, 85, 86, 87, 88, 89, 90. A major component of muscle loss with aging is due to a loss of motor units innervating muscle 91. Over the lifespan there is a loss of approximately 25% of motor neurons innervating Type 2 Fast-Twitch muscle fibers 92. Damage to motor units can be detected by measuring
circulating C-terminal agrin fragment (CAF) 93. The accelerated loss of muscle mass that occurs in persons with diabetes mellitus is due to the decreased muscle innervation coupled with decreased blood flow to muscle 42, 94, 95.

Additionally, sarcopenia is associated with and may, in part, be caused by several chronic diseases that negatively affect the musculoskeletal system and physical activity 10. These include chronic obstructive pulmonary disease (COPD), chronic heart failure (CHF), chronic kidney disease (CKD), diabetes mellitus (DM), human immunodeficiency virus (HIV), and cancer 96, 97, 98, 99, 100, 101. Theoretically, the role of these disease processes on sarcopenia may exert themselves primarily through direct effects on muscle function, or secondarily through retardation of physical activity or caloric restriction 102. It should be noted that in the context of cancer, cachexia is more commonly assessed as an indicator of tissue loss than is sarcopenia, though the clinical presentations of both diseases demonstrate significant overlap 103.

Figure 4. Sarcopenia causes

causes of Sarcopenia

Sarcopenia Pathophysiology

Generally, a significant decline of type 2 Fast-Twitch muscle fiber, but not type 1 Slow-Twitch muscle fibers are observed in sarcopenic patients 104. Muscles atrophy and are replaced by connective tissue, though the mechanism in sarcopenia may be different than that seen in other settings of “muscle atrophy”, since in younger individuals there is not an obvious problem with the satellite cells.

Several mechanisms of the underlying pathophysiology of sarcopenia have been described 5:

  • Age-related declines in anabolic hormone serum concentrations: Normal physiological serum levels of anabolic hormones such as testosterone, human growth hormone (hGH), and insulin-like growth factor-1 (IGF-1) have been demonstrated to function in the development, maintenance, or rejuvenation of muscle tissue 105, 106, 107, 108. Age-related declines of anabolic hormones are observed in patients with sarcopenia and thus, support this underlying pathophysiology of sarcopenia 109.
  • Insulin resistance with “sarcopenic obesity”: Aging patients often experience changes in body composition represented by increased fatty tissue alongside decreased muscle mass, coined as “sarcopenic obesity” 110. These changes are associated with metabolic dysfunction, including insulin resistance, leading to the accumulation of fat around internal organs 111. Additionally, insulin resistance is inversely associated with skeletal muscle mass 112. Such pathophysiology is likely mediated via dysfunction of insulin’s exerted effects on skeletal muscle – insulin resistance impairs the anti-proteolytic and muscle protein synthesis enhancing properties of the hormone on skeletal muscle tissue 113. Similarly, diminished lean body mass reduces uptake of glucose into skeletal muscle, further propagating insulin resistance 114, 115.
  • Age-related neurodegeneration: Progressive neurodegeneration is a commonly observed phenomenon in aging populations 116, 91. Aging is accompanied by a decline of alpha motor neurons in the spinal cord, loss of peripheral nerve fibers, and reduced number of neuromuscular junctions 109, 117. Considering the role of the neurological system in muscle fiber recruitment, current evidence supports neurodegeneration as underlying pathophysiology for reduced muscle strength and size in sarcopenia 117.
  • Age-related increase in inflammatory markers: Elevated levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF), interleukin (IL)-6, and IL-1 (IL1-Ra) are observed in elderly populations with significant sarcopenia 118. The catabolic effects that may be exerted by these cytokines on skeletal muscle are well documented and may present a mechanism in which sarcopenia develops with age 119, 120, 121.

Decreased protein intake in the elderly also plays a role: 1/3 of men over the age of 60 eat less than the recommended dietary allowance (RDA) of 0.8 g/kg. A decline in exercise, a potent stimulus to protein synthesis, also contributes.

Katherine Tucker, professor and chair of the Department of Health Sciences at Northeastern University, explained that individuals’ dietary needs change with aging 122. Older adults may require less energy, experience less efficient absorption and utilization of many nutrients, and have different nutrient requirements due to chronic conditions and medications. These changes result in older adults needing a nutrient-dense diet. Unfortunately, it can be challenging for this population to obtain such a nutrient-dense diet because it involves overcoming barriers such as loss of appetite, changes in taste and smell, oral health decline, mobility constraints, and lower incomes.

Tucker concluded her presentation by recommending some dietary changes based on the available data. Older adults should be encouraged to eat:

  • more fruits and vegetables, especially orange and dark green vegetables, to increase intakes of vitamin C, carotenoids, folate, vitamin B6, magnesium, potassium, and dietary fiber;
  • more low-fat dairy to improve intakes of magnesium, calcium, potassium, and vitamins B12 and D;
  • more whole grains, including more fortified breakfast cereals, to increase intakes of vitamin B6, crystalline vitamin B12, magnesium, and dietary fiber;
  • fewer foods high in sugar, solid fats, sodium; and
  • fewer refined grains.

Inadequate Intake

Data from the 2003–2004 the National Health and Nutrition Examination Survey (NHANES) were used by the Institute of Medicine Committee to Review Child and Adult Care Food Program Meal Requirements to identify the prevalence of inadequacy of protein and select nutrients among adults 60 years and older (see Table 1) 123. Using NHANES data for adults 70 years and older, Lichtenstein and colleagues 124 reported calcium, potassium, fiber, and vitamins D, E, and K as shortfall nutrients. In addition to those nutrients, Tucker emphasized the importance of adequate protein intake for prevention of sarcopenia and noted the controversy regarding the current recommendation for protein intake among older adults; should it be the same as the recommendation for younger adults or should it be higher?

Table 1. Estimated Prevalence of Inadequacy (%) of Protein and Selected Vitamins and Minerals Among Adults ≥ 60 Years Based on Usual Nutrient Intakes from NHANES 2003–2004

NutrientMalesFemales
Protein1220
Vitamin A5443
Vitamin C4940
Vitamin E9298
Thiamin612
Riboflavin2.83.7
Niacin1.84.6
Vitamin B61939
Folate1124
Vitamin B122.49
Phosphorus1.24.8
Magnesium7873
Iron11.5
Zinc2621

Footnote: All nutrients in this table have an Estimated Average Requirement (EAR).

[Source 123  ]

Tucker highlighted several nutrients of concern in the older adult population.

  • Protein. The current Estimated Average Requirement for protein for all adults 19 years and older is 0.66 g/kg/day; however, Tucker indicated that a moderately higher protein intake (1.0–1.3 g/kg/day) may be required for older adults to maintain nitrogen balance due to decreased efficiency of protein synthesis and impaired insulin action. Need for increased protein intake is further supported by the Health, Aging, and Body Composition Study, which found that older adults with the highest intake of protein lost less lean body mass than those with lower protein intakes 125. However, there is some concern that higher protein intake may increase risk of toxicity or impaired renal function 126.
  • Vitamin E. Vitamin E is important because of its role as an antioxidant and in immune function. There is some controversy over whether the current Recommended Daily Allowance (RDA), 15 mg of α-tocopherol, is too high, as very few individuals are able to meet this recommendation from diet alone. Vitamin E supplements increase α-tocopherol levels while reducing γ-tocopherol, so supplements may not be the healthiest option for increasing intake. Some literature suggests that other tocopherols (found in nuts, seeds, and plant oils) are also important 127; however, there are no current nutrient recommendations for other forms of vitamin E.
  • Vitamin B12. Although the daily intake of total vitamin B12 does not appear to be low for most older adults, dietary intake data may underestimate the number of people who are vitamin B12 deficient given that atrophic gastritis and loss of stomach acid prevent some older adults from absorbing it. As a result, the Institute of Medicine 123 recommended that older adults get their vitamin B12 in crystalline form such as from fortified foods or supplements. The Framingham Offspring Study found that nonsupplement users had a higher prevalence of low B12 (less than 250 μmol/L) than those who were taking a supplement containing vitamin B12 128. Vitamin B12 deficiency can lead to peripheral neuropathy, balance disturbances, cognitive disturbances, physical disability, and increased risk of heart disease from high homocysteine. Tucker stated, “It’s critical that more attention be given to this important nutrient as many of these symptoms are nonspecific and not always diagnosed correctly” 128.
  • Vitamin B6. Vitamin B6 is important for numerous metabolic reactions and health outcomes. Inadequacy may lead to high homocysteine and impaired immune function and has been associated with impaired cognitive function and depression. Data from the Massachusetts Hispanic Elders Study showed that 30 percent of Hispanics and 28 percent of non-Hispanic whites had plasma pyridoxal 5′-phosphate (the active form of vitamin B6 used as a biomarker for vitamin B6 status) concentrations less than 30 nmol/L (indicator of inadequate status), and 11 percent of Hispanics and 16 percent of nonwhite Hispanics had concentrations less than 20 nmol/L (clinical cutoff level indicating deficient concentrations). Furthermore, pyridoxal 5′-phosphate was associated with depressive symptomatology in this population-based study of older adults 129.
  • Omega-3 fatty acids. Among adults 60 years and older, the median intake of α-linolenic acid by women was above the Adequate Intake (AI), whereas the median intake by men was not 123. Omega-3 fatty acids are associated with protection against heart disease, diabetes, and cognitive decline. Low intake may be partially due to the limited sources in the diet (e.g., fatty fish, flax seeds, and walnuts).
  • Dietary fiber. Fiber is important for intestinal health and protection against heart disease and metabolic syndrome; however, the median intakes of neither men nor women 60 years and older meet the AI 123.
  • Vitamin D. Tucker reported that older adults’ poor vitamin D intake and status may be due to low intakes of fortified dairy foods and fatty fish, low sun exposure, reduced dermal synthesis of vitamin D3 130, and decreased capacity of kidneys to convert 25OHD into 1,25-OH2-D. A study of homebound older adults found that about 65 percent had suboptimal concentrations of 25OHD in their blood (less than 50 nmol/L) and 48 percent had intakes below 400 International Units 131. In addition to its importance to bone status, vitamin D deficiency has been associated with neurological conditions, diabetes, and other metabolic conditions. Increasingly, more nutritionists are recommending that older adults take a vitamin D supplement.

Excessive intakes

Excessive intake of some nutrients is also a concern among older adults as it is for the general population.

  • Sodium. The Tolerable Upper Intake Level for sodium is 2.3 g/day; however, the 2015 Dietary Guidelines Advisory Committee recommended it should be lowered to 1.5 g/day 132 to reduce the risk of hypertension and heart disease. Men and women over the age of 70 years are exceeding both recommendations; the usual daily mean intake for men and women is 3.0 and 2.4 g, respectively 133.
  • Saturated fat. The Dietary Guidelines for American’s recommendation for saturated fat intake is less than 10 percent of energy intake, with the goal of reducing that recommendation to 7 percent 132. However, most adults have intakes greater than 10 percent of their energy intake 134.
  • Folic acid. Whereas some adults do not meet the recommended intake levels of folic acid (400 μg), research shows that others are at risk of exceeding the upper level of 1,000 μg per day due to intake of fortified flour and breakfast cereals, and supplement use. More research is needed but high folic acid may contribute to the progression of neurological diseases associated with vitamin B12 deficiency 135 and lead to increased risk of some cancers 136.

Food intakes

In order to determine why older adults’ nutrient intakes are inadequate, one must review their food intake patterns. The 2011 IOM report Child and Adult Care Food Programs: Aligning Dietary Guidance for All presented the mean daily food group intakes by adults ages 60 years and older as compared to the 2,000-calorie MyPyramid food group pattern. It showed that older adults are not meeting any of the MyPyramid food group recommendations and are exceeding the recommendations for daily intake of solid fats and added sugar (see Table 2).

Table 2. 2,000-Calorie MyPyramid Food Group Pattern and Mean Daily Amounts Consumed by Adults ≥ 60 Years of Age

Food Group or Component≥ 19 Years≥ 60 Years
2,000-kcal Pattern 137Mean Intake 134
Total fruit (cup eq)21.1
Total vegetables (cup eq)2.51.7
Whole grains (oz eq)30.86
Total milk group (8 fl oz eq)31.3
SoFAS (kcal)267570

Abbreviations: eq = equivalent; fl = fluid; kcal = calories; oz = ounce; SoFAS = solid fats and and sugar.

[Source 123 ]

Sarcopenia prevention

Sarcopenia prevention include the following 20:

  • A healthy lifestyle, including balanced diet, adequate protein intake, and regular exercise should be encouraged in adults of all ages.
  • Person‐centred physical and dietary interventions, developed with an accredited healthcare professional, are recommended for adults with health conditions known as likely to increase the risk of sarcopenia, such as frailty. It is noteworthy that anterior thigh muscles undergo atrophy earlier with ageing, and this issue is paramount for the prevention of impairments and interventions 138, 139, 140, 141. Hence, in the earlier stages, the loss of anterior thigh muscle function (e.g. mobility, sitting to standing, climbing stairs) may precede those of the other sites. Furthermore, physical activity is a powerful factor in the prevention and treatment of many health conditions in older adults 142.

Sarcopenia signs and symptoms

Sarcopenia is characterized by decreased muscle mass, strength, and physical performance in older adults 5. People with sarcopenia are often elderly, sedentary, and may present with various comorbidities or disabilities, with a subsequent decrease in function and quality of life. A patient history consistent with sarcopenia includes progressive loss of muscle mass, strength, and function to the extent that daily activities become increasingly difficult to accomplish.

Sarcopenia complications

  • Fall, fracture, and nosocomial infection risk in the elderly: In a meta-analysis of 33 studies encompassing 45,926 patients, Yeung et al. 143 found that sarcopenia significantly increases both fall and fracture risk in the elderly. Additionally, sarcopenia increases the risk of nosocomial infection in elderly populations 144.
  • Sarcopenia complications in medicine: Sarcopenia is associated with increased mortality in patients with end-stage renal disease (chronic kidney disease), pancreatic cancer, and chronic heart failure 145, 146. Additionally, sarcopenia is associated with increased dose-limiting toxicities (DLT) in patients undergoing chemotherapy for kidney cancer (renal cell carcinoma), liver cancer (hepatocellular carcinoma) and breast cancer 147, 148, 149
  • Sarcopenia complications in surgery: Sarcopenia is associated with increased postoperative complication risk in patients undergoing general surgical procedures and liver transplant surgery 150, 151. Additionally, sarcopenia is associated with greater mortality in patients undergoing general surgical procedures and colorectal surgery 150, 152.

Sarcopenia diagnosis

Sarcopenia diagnosis includes several modalities and screening tools, some of which are more readily available and practical than others. Sarcopenia evaluation ranges from screening questionnaires to radiographic imaging to the assessment of muscle mass cross-sectional area (CSA) 4, 153. Additionally, the European working group on sarcopenia in older people 2 (EWGSOP2) describes an algorithm that presents as follows: “find-assess-confirm-severity” or F-A-C-S 4.

Figure 5. Sarcopenia diagnostic algorithm

Sarcopenia diagnostic algorithm

Abbreviations: BIA = bioelectrical impedance analysis; CT = computed tomography; DXA = dual energy X‐ray absorptiometry; MRI = magnetic resonance imaging; SPPB = Short Physical Performance Battery; TUG = Timed‐Up‐And‐Go test over 3 meters away.

Footnote: The recommendations for management of sarcopenia do not vary across sarcopenia categories (e.g., probable/confirmed/severe).

[Source 20 ]

Screening Tools to Identify Probable Sarcopenia

Strength, assistance with walking, rising from a chair, climbing stairs, and falls (SARC-F) questionnaire. The SARC-F (Strength, Assistance with walking, Rising from a chair, Climbing stairs, and Falls) questionnaire is a screening tool that can be rapidly implemented by clinicians to identify probable sarcopenic patients 49. The SARC-F (Strength, Assistance with walking, Rising from a chair, Climbing stairs, and Falls) questionnaire screens patients for self-reported signs suggestive of sarcopenia, which include deficiencies in strength, walking, rising from a chair, climbing stairs, and experiencing falls 154. Each of the self-reported parameters receives a minimum and maximum score of 0 and 2, respectively, with the greatest maximum SARC-F score being 10 155. Data suggests that a SARC-F score of ≥4 best predicts the need for further, more comprehensive evaluation 4, 49.

Sarcopenia questionnaire (SARC‐F questionnaire includes scoring)

Sarcopenia questionnaire
[Source 49 ]

Assessing sarcopenia muscle strength

  • Handgrip test: Generally, handgrip strength is one of the two methods utilized to quantify muscle strength in patients with suspected sarcopenia. Handgrip strength correlates with strength in other muscles and is therefore used as a surrogate to detect deficits in overall strength 156. Additionally, decreased handgrip strength predicts poor patient outcomes, including increased lengths of stay (LOS), functional deficits, and death 156, 157. Accurate grip strength measurement and interpretation of results rely on a calibrated dynamometer and relevant reference populations 158. The Martin Vigorimeter is a validated tool in measuring grip strength and may be used for this assessment 159. The suggested cutoff point for handgrip is <27 kg and <16 kg, for males and females, respectively 160.
  • Chair stand test: The chair stand test may be used as a proxy to gauge lower extremity strength, particularly the quadriceps muscles. The chair stand test measures the number of times a patient can stand and sit from a chair, without the use of their arms, over 30 seconds 161. The chair stand test has been established as a valid indicator of lower extremity strength in community-dwelling populations 162. The suggested cutoff point for the chair stand test is >15 seconds for five rises 161.

Confirming sarcopenia

To date, there is no consensus on the most effective method for confirming sarcopenia. Each comes with their strengths and weaknesses, and often, greater accuracy presents with the cost of inconvenience. Ultimately the goal of these modalities is to determine whether patients meet the requirement of sarcopenia through quantifying total body skeletal muscle mass (SMM), appendicular skeletal muscle mass (ASM), or the cross-sectional area (CSA) of a specific muscle. Because overall body mass is correlated with total body skeletal muscle mass (SMM), appendicular skeletal muscle mass (ASM), or the cross-sectional area (CSA), it may be adjusted for height or body mass index (BMI), yielding ratios in the format of (ASM/height²), (ASM/weight), or (ASM/BMI). The recommended cutoff for appendicular skeletal muscle mass (ASM) is <20 kg and <15 kg, for males and females, respectively 163. Similarly, the recommended cutoff for ASM/height² is <7.0 kg/m² and <5.5 kg/m² for males and females, respectively 164.

  • Magnetic resonance imaging (MRI): Magnetic resonance imaging (MRI) is considered a “gold standard” modality for confirming sarcopenia. MRI can provide highly accurate measurements of total body muscle mass 165, 166, 167. However, MRI requires highly trained technicians, lacks portability, presents little cost-effectiveness, and is therefore rarely used in the primary care setting 166, 168.
  • Computed tomography (CT): Computed tomography (CT) is also considered a “gold standard” for accurate lean muscle mass measurement. Computed tomography (CT) is rarely used in the primary care setting for similar reasons than MRI 166. However, settings in which CT is routinely performed, such as trauma or surgery, this modality presents greater value and practicability, as demonstrated in previous literature 169. More specifically, CT measured psoas cross-sectional area (PCSA) at the level of the 3rd lumbar vertebrae has consistently predicted outcomes among patient populations in the contexts of gastrointestinal cancer, heart valve surgery, orthopedic trauma, thoracolumbar surgery 170, 171, 172, 173.
  • Dual-energy X-ray absorptiometry (DEXA): Dual-energy X-ray absorptiometry (DEXA) is not as accurate as either CT or MRI. However, DEXA presents with greater convenience, and is, therefore, a more widely available and practical modality for confirmation of sarcopenia 4, 174.
  • Bioelectrical impedance analysis (BIA): Bioelectrical impedance analysis (BIA) is the most widely available and portable modality of muscle mass quantification. Bioelectrical impedance analysis (BIA) may also be used to confirm sarcopenia 4.

Sarcopenia severity

Once sarcopenia is confirmed through body composition assessment, the severity of the condition is determined by measuring physical performance. Suggested tests and their respective cutoff points for sarcopenia severity as recommended by the European Working Group on Sarcopenia in Older People 2 (EWGSOP2) 4 are listed below.

  • Gait speed test: Gait speed tests are simple to use in practice and predict adverse effects associated with sarcopenia 175. The “4-meter usual walking speed test” is practical and can be used to assess sarcopenia severity 176, 177. The 4-meter usual walking speed test measures time taken for a patient to travel 4 meters at their usual walking pace. A speed of ≤0.8 m/second may be indicative of severe sarcopenia 9.
  • Short physical performance battery (SPPB): The short physical performance battery (SPPB) test is composed of 3 timed tasks: chair stand tests, standing balance, and walking speed. The minimal and maximal achievable scores are 0 (low performance) and 12 (high performance), respectively. A score of ≤8 is an indicator of poor physical performance and may be indicative of greater sarcopenia severity 4, 178.
  • Timed-up and go test (TUG): The timed-up and go test (TUG) test observes the time taken for a patient to rise from a chair, walk 3 meters away from, and 3 meters back to the chair, terminating the test in a sitting position. Time ≥20 seconds is indicative of physical deficits, though the study used to support this recommendation failed to assess male populations and therefore, may only apply to elderly female populations 179
  • The 400-meter walk test: In the 400-meter walk test, a patient attempts to walk in a series of 20, 20-meter laps as quickly as possible, with a maximum of 2 minutes rest between each lap. The inability to complete or requiring ≥6 min to complete the entire 400-meters is concerning and may suggest greater sarcopenia severity 4, 180.

Sarcopenia differential diagnosis

Considering the high probability that sarcopenia may co-exist with the below conditions and considering the overlap between these conditions, an accurate differential diagnosis may be difficult.

  • Frailty: While sarcopenia and frailty present with significant overlap of symptoms, they remain indistinguishable. Frailty is defined as multi-system impairment and encompasses a broader range of dysfunction than sarcopenia, whereas sarcopenia mainly includes the musculoskeletal system. One condition may contribute directly to the other, as they often co-exist in elderly patients 181, 182.
  • Malnutrition: Both malnutrition and sarcopenia can present with low muscle mass, though sarcopenia more often presents with the additional loss of function. Additionally, as a function of caloric restriction, reduced fat mass is observed in patients with malnutrition – this is often not the case with sarcopenia. Functional tests for strength and performance may be administered to rule out malnutrition 4.
  • Cachexia: Cachexia is thought to have a more complex cause than sarcopenia. Cachexia is described as severe weight loss and muscle-wasting associated with conditions such as HIV, cancer, and end-stage organ failure. While cachexia and sarcopenia may co-exist, a patient with severe muscle wasting diseases such as HIV or cancer is more likely to have cachexia 183. Additionally, the Glasgow Prognostic Score can be utilized to distinguish the two conditions 184.
  • Osteoarthritis of the hand: Patients with osteoarthritis of the hand may elicit a false positive test when performing the handgrip strength test. In cases where severe osteoarthritis is suspected, patients may perform methods to measure isometric torque of the lower limb to more accurately assess or rule out sarcopenia 4, 185.

Sarcopenia treatment

For the management of sarcopenia, there is a strong recommendation that individuals with sarcopenia should be enrolled in a resistance training programme 186, 187, 49. There is a reasonable amount of evidence that resistance exercise will increase both muscle mass and strength 188. The prescription of exercise should be considered, discussed, and prescribed, with progress monitored like any other medical treatment. This may be best achieved by referral to an Accredited Exercise Physiologist or similarly qualified health professional.

Additionally, increasing total protein intake through supplementation or food sources can help prevent and manage sarcopenia. The use of a protein rich diet (1 to 1.5 g/kg body weight per day) or protein supplementation received a conditional recommendation based on a small amount of evidence and a previous consensus conference 189. Specifically, consuming 20 to 35 grams of protein per meal is advised, as such amounts provide sufficient amino acid content to maximize muscle protein synthesis, thus minimizing age-related muscle loss 190. Additionally, people with sarcopenia are recommended to consume 1 to 1.2 g/kg body weight per day 191. Higher doses of protein (up to 2 g/kg body weight per day) may be appropriate in persons with severe illness or injury or when there is evidence of a pro‐inflammatory/catabolic state 192. Furthermore, the greatest effects are observed when resistance training and high protein diets are combined and appear to act synergistically 193.

Beta-hydroxy-beta-methylbutyrate (HMB) has been shown to improve muscle mass and to preserve muscle strength and function in older people with sarcopenia or frailty 194. Vitamin D supplementation specifically for sarcopenia was found to have insufficient evidence, though there is evidence that persons with low vitamin D levels may improve their strength with vitamin D supplementation 195. Similarly, while testosterone can increase muscle mass and strength in older individuals and a meta‐analysis has confirmed its safety 196, the lack of evidence in persons with sarcopenia did not lead to its integration into these recommendations. Preliminary data with anamorelin, a growth hormone secretagogue receptor type 1 (ghrelin receptor) agonist that increases muscle mass but not strength 197 and anti‐myostatin antibodies 198 were considered insufficient to make recommendations in favour of their use.

Sarcopenia prognosis

The prognosis of sarcopenia largely depends on your age, comorbidities, falls, and fractures 199. Additionally, people who have sarcopenia undergoing surgical procedures have less favorable outcomes than those without sarcopenia. These include an increased risk of postoperative complications, falls, lengths of stay in the hospital, fractures, and greater morbidity and mortality. Ultimately, the prognosis of sarcopenia alone is uncertain and not well studied, though consistent evidence demonstrates sarcopenia as an indicator of poor prognosis in several medical conditions and surgical procedures 199.

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