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42
calorie requirements by multiplying the patient’s actual body weight (in kg) by
25–30kcal [33]. Ideal or adjusted body weight is used for estimating needs of obese
and emaciated adults.
Skeletal muscle mass is relatively constant during young- to middle-aged
adulthood, suggesting that there is an equilibrium between protein synthesis dur-
ing absorptive states (i.e., postprandial, following feeding) that is balanced by
the catabolism during fasting states. However, this equilibrium in healthy muscle
between protein synthesis and breakdown is getting progressively disrupted with
aging. In older people, synthesis rate of mixed muscle proteins including myo-
brillar and mitochondrial proteins decrease with 30% [34]. Muscle protein syn-
thesis is stimulated by dietary intake of both essential and nonessential amino
acids. There is a substantial body of research suggesting that over 80% of the
stimulatory effect on protein synthesis observed after a meal can be attributed to
amino acids [35]. In older people compared to younger individuals, this stimula-
tory effect is being blunted but not absent. It can be overruled by increasing the
amount of protein. In addition to their role in protein synthesis, amino acids also
play a role in the regulation of protein breakdown [36]. Nitrogen balance studies
in aging populations (56–80years of age) have indicated greater protein needs
for the elderly (1.14g/kg/day) relative to the young (0.8g/kg/day) [37]. This
provides critical information in terms of inadequate protein intake as a possible
mechanism underlying muscle loss and the development of sarcopenia, particu-
larly because protein intake has been reported as inversely proportional to age.
Randomized controlled trial data indicate that it is more important to ingest a
sufcient amount of high-quality protein (25–30g) with each meal rather than 1
large bolus because greater than 30g in a single meal may not further stimulate
muscle protein synthesis [38].
An average daily intake of 1.0–1.2g protein per kilogram of body weight per day
is recommended for older people to maintain and regain lean body mass and func-
tion. A higher protein intake (≥1.2g/kg body weight/day) is advised for those who
are exercising and otherwise active. Most older adults who have acute or chronic
diseases need even more dietary protein (1.2–1.5g/kg body weight/day) [
39, 40].
Next to the existence of protein-calorie malnutrition attention should be given to
specic and selective aspects of malnutrition such as vitamin and mineral decien-
cies. Vitamin D has recently received recognition as another potential intervention
strategy for sarcopenia. Although our understanding of the relationship between
vitamin D and muscle function has advanced over the past decade, a complete
understanding of the vitamin D action on muscle tissue and how this translates into
improvements in muscular performance are yet to be elucidated. Older adults, how-
ever, are at increased risk of developing vitamin D insufciency and supplementa-
tion may be indicated in those older people with low vitamin D levels to combat
sarcopenia, functional decline, and falls risk [41].
Overall, preference should be given to nutritional support by adapting a dietary
pattern that is adequate in quality in older age to ensure sufcient intakes of protein,
vitamin D, antioxidant nutrients, and long-chain polyunsaturated fatty acids. In par-
ticular, there is substantial evidence to support the roles of dietary protein and
M. Vandewoude and S. Perkisas
https://t.me/med1917
43
physical activity as key anabolic stimuli for muscle protein synthesis [42]. The addi-
tion of oral nutritional supplements or enteral and parenteral feeding might be sub-
sequent steps when calorie or protein requirements cannot be met.
Conclusion
When people grow older, they lose the capacity of adapting well to changes in
their environment. This loss of homeostasis in the broad sense leads to an
increased vulnerability, called frailty. Although no universal denition has been
dened, frailty could be described as an unstable equilibrium carrying a high
risk for functional loss. It is a clinical state in which there is an increase in an
individual’s vulnerability for developing increased dependency and/or mortality
when exposed to a stressor [1]. Losing weight with the emergence of malnutri-
tion is part of it. The decline in nutritional status in the geriatric patient is the
result of the effects of lower dietary intake (starvation), the effects of aging
(sarcopenia), and the effects of acute and chronic inammatory conditions
(cachexia). This results in a complex malnutrition syndrome with a major
impact on prognosis and benecial effects of intended treatment. The screening
for comorbidity in older people is essential and nutritional assessment is a major
issue in this regard. Difference should be made between assessment of risk and
actual nutritional status, which should be assessed with specic malnutrition
indices. Body weight assessment with specic attention to unintended weight
loss is essential in this evaluation. We should recognize the fact that BMI should
be interpreted with caution, but that a low value for BMI still heralds an
increased malnutrition risk. Weight loss alone, however, does not identify the
full effect of cachexia on physical function. It can be helpful to add to the item
of weight loss an estimate of reduction in food intake and systemic inamma-
tion. This would help to identify patients with both adverse function and prog-
nosis. This increased alertness based on a relative subjective global assessment
has a lot to offer in the willingness for early intervention. The nutritional assess-
ment must be framed in a larger CGA (comprehensive geriatric assessment)
addressing several functional domains. Early intervention with an adequate
amount of macronutrients (protein, calories) and micronutrients (vitamins, anti-
oxidants, minerals) offered through a balanced dietary pattern is key in this
approach. This may lead to an optimalization of the strategy for the prevention
and management of problems in older people.
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nutrition: a proposal for etiology-based diagnosis in the clinical practice setting from the
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Ageing 39:412–423
11. Perkisas S, De Cock A, Verhoeven V, Vandewoude M (2016) Physiological and architectural
changes in the ageing muscle and their relation to strength and function in sarcopenia. Eur
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12. Evans WJ, Morley JE, Argiles J etal (2008) Cachexia: a new denition. Clin Nutr 27:793–799
13. Vandewoude MF, Alish CJ, Sauer AC etal (2012) Malnutrition-sarcopenia syndrome: is this
the future of nutrition screening and assessment for older adults? J Aging Res 2012:651570
14. Vandewoude M, Hoeck S, Geerts J etal (2008) Mobility and frailty in community-dwelling
older people: the effect of weight loss. J Nutr Health Aging 12:573
15. Flegal KM, Graubard BI, Williamson DF etal (2005) Excess deaths associated with under-
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39. Bauer J, Biolo G, Cederholm T etal (2013) Evidence-based recommendations for optimal
dietary protein intake in older people: a position paper from the PROT-AGE Study Group. JAm
Med Dir Assoc 14:542–559
40. Deutz NE, Bauer JM, Barazzoni R etal (2014) Protein intake and exercise for optimal muscle
function with aging: recommendations from the ESPEN Expert Group. Clin Nutr 33:929–936
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4 Malnutrition Unrecognized andUntreated
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© Springer International Publishing AG, part of Springer Nature 2019
J.-P. Michel (ed.), Prevention of Chronic Diseases and Age-Related Disability,
Practical Issues in Geriatrics, https://doi.org/10.1007/978-3-319-96529-1_5
A. J. Cruz-Jentoft
Hospital Universitario Ramón y Cajal (IRYCS), Madrid, Spain
e-mail: alfonsojose.cruz@salud.madrid.org
5
Sarcopenia: Preventable andReversible
AlfonsoJ.Cruz-Jentoft
Key Messages
• Sarcopenia is associated with many undesirable outcomes: mortality, functional
decline, falls and fractures, hospital admission and reduced quality of life.
• It is more frequent with increasing age, female gender, low protein intake, low
levels of physical activity, not engaging in regular exercise and other habits.
• Adding resistance exercise to usual aerobic exercise is key in preventing sarco-
penia. Comprehensive resistance exercise programs are needed to treat this con-
dition, when present.
• A healthy diet that increases the amount of proteins is also important to prevent
sarcopenia from a lifelong perspective. When sarcopenia is present, proper nutri-
tional intervention—frequently with the use of oral nutrition supplements—is
needed to improve muscle function.
5.1 What Is Sarcopenia?
Sarcopenia is a progressive and generalized loss of skeletal muscle mass and func-
tion that increases the risk of adverse outcomes in old age [1].
The term sarcopenia is quite recent in the medical literature. It was proposed in
1998, and derives from two Greek words: sarx for esh and penia for loss to describe
a well-known long-standing observation: the progressive muscle wasting that many
individuals show when aging, that is commonly associated with reduced muscle
strength and power, and affects mobility and functional independence [2].
Initially, sarcopenia was approached by focusing on the loss of muscle mass that
starts in adult age, but increasing evidence showed that measured muscle mass was
https://t.me/med1917
48
only weakly associated with mobility problems and disability, so interest gradually
switched to muscle function. In 2010, several international groups proposed con-
sensus denitions that incorporated muscle strength and physical performance to
the concept of sarcopenia [3]. The most widely used is the denition of the
European Working Group for Sarcopenia in Older People (EWGSOP), that denes
sarcopenia as the association of a reduced muscle mass with a reduced muscle
strength or physical performance (or both) [1]. Only in 2016, the US version of the
International Classication of Diseases (ICD-10) coded sarcopenia as a specic
disease.
Sarcopenia can be best understood as an organ failure (skeletal muscle insuf-
ciency), contrasting with frailty, that is considered a whole-body issue (see next
chapter) [4]. Sarcopenia usually presents as a slowly progressive, age-associated
chronic disorder, but can also develop acutely (i.e., during hospital admission or
acute immobility), so considering sarcopenia as a chronic or acute skeletal muscle
insufciency may be an accurate clinical paradigm, already in use for other organs
or systems (i.e., renal or cardiac insufciency).
5.2 Why Is Sarcopenia aProblem?
Epidemiological studies have shown that sarcopenia is common in old age, it’s prev-
alence rising with increasing age. However, published prevalence and incidence
rates are quite variable, depending on the population age, gender, and characteris-
tics, the use of different measures of muscle mass and function, and the choice of
cutoff points [5]. Reported prevalence in community dwelling older people ranges
from 1 to 33%, most recent epidemiological reports seem to be in the 15–20%
range. Prevalence is higher in nursing homes or long-term care settings, and also in
older people admitted to the hospital. This means that at least one in ve older indi-
viduals may suffer from sarcopenia.
Sarcopenia is associated with many undesirable outcomes. Sarcopenic individu-
als have a higher mortality (at least threefold), high risk of functional decline and
fall more frequently. It also seems to be associated with a higher risk of hospital
admission and may be linked to longer stays and a higher risk of fractures [6]. It also
carries a reduced quality of life that has prompted the development of specic
instruments [7]. Moreover, sarcopenia is a real public health burden [8], and recent
evidence links sarcopenia with increased health care costs [9]. Costs associated with
increased disability have not been properly studied.
5.3 Life Course Perspective andDeterminants
ofSarcopenia
Sarcopenia does not come from clear sky, it develops along the lifetime of an indi-
vidual, starting very early in life. Weight at birth has been shown to be a determinant
of sarcopenia, probably through its inuence on peak muscle mass and strength in
A. J. Cruz-Jentoft
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49
early adulthood [10]. Little is known about how very early interventions may have
an impact in late life sarcopenia.
Recent research has focused on the determinants of sarcopenia in adulthood.
Some of them are well established: increasing age, female gender, body frame, eth-
nicity, and heritability have been conrmed in different studies. However, these
determinants cannot be changed. More important from a preventive point of view,
lower food intake, reduced protein intake, malnutrition, low levels of physical activ-
ity, and not engaging in regular exercise are all risk factors of sarcopenia, while
healthy food patterns and having appropriate levels of vitamin D seem to be protec-
tive [11]. Some diseases (diabetes mellitus, osteoporosis, osteoarthritis, and a num-
ber of other comorbid diseases) and multimorbidity by itself also increase the risk
of sarcopenia. New risk factors, as poor sleep or pain, may also have a role. All these
risk factors seem to be cumulative.
Individuals who become sarcopenic and have a negative lifestyle or some comor-
bid diseases may have an accelerated course of the disease. Sarcopenia reduces
physical activity—by reducing mobility—, increases nutrient needs, and may have
an impact on comorbid diseases (for instance, modifying the effect of drugs through
changes in body composition). Thus, when managing sarcopenic individuals, ter-
tiary prevention of existing risk factors is still needed.
5.4 Preventing Sarcopenia
Being sarcopenia a recently identied clinical problem, no long-term prevention
trials in large populations have been yet performed. However, epidemiological
studies and some small prevention studies may offer some guidelines.
Resistance exercise seems to be a key in preventing sarcopenia. It is quite clear
that physical exercise has a positive impact on muscle mass and muscle function in
healthy subjects aged 60years and older [12]. Exercise improves physical perfor-
mance (chair rising, gait speed, balance), even when no changes in muscle mass are
shown. Thus, adding resistance exercise to the usual recommendation to do aerobic
exercise may have a role in preventing sarcopenia. This should start early in life, as
muscle mass and function loss starts early in adulthood and is more prominent after
50 years old. The role of aerobic or balance exercise in preventing sarcopenia.
Increasing daily physical activity seems also advisable although the effect or size of
such increase is yet undetermined.
The other cornerstone of sarcopenia prevention is diet. Healthier dietary habits,
especially those that ensure an appropriate amount of proteins and avoid vitamin D
deciencies, will probably prevent sarcopenia—and other chronic diseases [13, 14].
Protein intake seems to be particularly important. In fact, the former recommendation
of a minimum intake of 0.8g of protein per kg of body weight and day for adults has
recently been increased by some international organizations to a minimum of 1.0–1.2g
for older adults to prevent sarcopenia and frailty [15, 16]. Thus, a recommendation to
increase protein intake seems sound advice to prevent sarcopenia. Some data also sug-
gest that the combination of exercise and diet may have a synergistic effect [17].
5 Sarcopenia: Preventable andReversible
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50
Of course, preventive measures that need changes in lifestyle that have been
present for 40–50 years are specially challenging, and many barriers have been
found (education, poverty, costs and availability of exercise programs, psychologi-
cal barriers, and others), but prevention of sarcopenia is key in the societies’ quest
to prevent physical disability in old age.
Although some persons may consider the use of botanicals or alternative medi-
cine approaches to prevent sarcopenia, there is no evidence to date that this approach
has any signicant effect [18].
5.5 Reversing Sarcopenia
More information is available on the treatment of sarcopenia. It is now clear that
sarcopenia is not a permanent state, and it can be reversed, either spontaneously
(i.e., acute sarcopenia after an acute condition is cured) or by interventions.
Management of sarcopenia starts with the identication and management of any
underlying cause found by a comprehensive geriatric assessment. Nutrition and
physical exercise are the cornerstones of treatment [12]. No drug has yet been
approved for this condition although many are in development [19], some even in
phase 2 trials [20].
Again, resistance exercise is the rst and most important treatment to reverse
sarcopenia. It has to be prescribed properly and adapted to the needs of each indi-
vidual. Total body exercise routines that include routines for major muscle groups,
for 30–60min three to four times a week, using multi-joint approaches with exer-
cise machines at an intensity of 65–75% of the maximum have the best evidence
[21]. Adding aerobic exercise training may also benet skeletal muscle and improve
insulin sensitivity. Exercise has to be properly prescribed by a physician or physical
therapist and is most probably benecial when properly supervised and sustained a
long time.
Correction of nutritional decits is also needed in sarcopenic patients [22].
Caloric intake should be increased to cover increased demands posed by exercise.
Protein requirements may be increased, when sarcopenia is present, to the range of
1.2–1.5g of protein per kilogram of body weight and day, with the only exception
of subjects with stage 4 or 5 renal failure [15]. Essential amino acids (EAA) supple-
ments including around 2.5g of leucine and β-hydroxy β-methylbutyric acid (HMB)
supplements may also help to improve muscle mass and function parameters [5].
Correction of vitamin D deciencies is needed for proper muscle function, but the
role of vitamin D when blood levels are normal it is yet to be determined. When
requirements cannot be reached by modifying usual diet, oral nutritional supple-
ments are needed to meet these needs. Supplements should be used for at least
3months to be most effective.
A. J. Cruz-Jentoft
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51
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from the PROT-AGE Study Group. J Am Med Dir Assoc 14(8):542–559
16. Deutz NEP, Bauer JM, Barazzoni R, Biolo G, Boirie Y, Bosy-Westphal A etal (2014) Protein
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