Hormones (2018) 17:321–331

https://doi.org/10.1007/s42000-018-0049-x

REVIEW ARTICLE

Sarcopenic obesity
Stergios A. Polyzos 1 & Andrew N. Margioris 2

Received: 11 December 2017 / Accepted: 23 May 2018 / Published online: 16 July 2018
# Hellenic Endocrine Society 2018

Abstract
Sarcopenic obesity, a chronic condition, is today a major public health problem with increasing prevalence worldwide, which is
due to progressively aging populations, the increasing prevalence of obesity, and the changes in lifestyle during the last several
decades. Patients usually present to healthcare facilities for obesity and related comorbidities (type 2 diabetes mellitus, non-
alcoholic fatty liver disease, dyslipidemia, hypertension, and cardiovascular disease) or for non-specific symptoms related to
sarcopenia per se (e.g., fatigue, weakness, and frailty). Because of the non-specificity of the symptoms, sarcopenic obesity remains
largely unsuspected and undiagnosed. The pathogenesis of sarcopenic obesity is multifactorial. There is interplay between aging,
sedentary lifestyle, and unhealthy dietary habits, and insulin resistance, inflammation, and oxidative stress, resulting in a quanti-
tative and qualitative decline in muscle mass and an increase in fat mass. Myokines, including myostatin and irisin, and adipokines
play a prominent role in the pathogenesis of sarcopenic obesity. It has been suggested that a number of disorders affecting
metabolism, physical capacity, and quality of life may be attributed to sarcopenic obesity, although it is not as yet established
whether sarcopenia and obesity act synergistically. There is to date no approved pharmacological treatment for sarcopenic obesity.
The cornerstones of its management are weight loss and adequate protein intake combined with exercise, the latter in order to
reduce the loss of muscle mass observed during weight loss following diet unpaired with exercise. A consensus on the definition of
sarcopenic obesity is considered essential to facilitate the performance of mechanistic studies and clinical trials aimed at deepening
our knowledge, thus enabling improved management of affected individuals in the near future.

Keywords Muscle . Muscle mass . Muscle strength . Obesity . Physical capacity . Sarcopenia . Sarcopenic obesity . Treatment

Introduction
The increase in lifespan has brought the scientific community
face to face with new medical challenges related to the aging
population, one of which is sarcopenic obesity. Sarcopenia, a
term derived from the Greek words “sarx” (meaning flesh) and
“penia” (meaning loss), which refers to the loss of skeletal
muscle mass, first appeared in the biomedical literature of
Medline in 1993 [1, 2]. Sarcopenia is the result of a reduction
in motor unit number together with atrophy of muscle fibers [3].
Although there is no consensus as to whether there is a selective
* Stergios A. Polyzos
spolyzos@auth.gr
loss of specific types of muscle fiber [4], it was proposed early
on that both type I and type II muscle fibers decrease in number,
while type II muscle fibers also reduce in size (atrophy) [2].
Sarcopenic obesity is defined as the coexistence of sarcopenia
and obesity, the latter being the result of an increase in fat mass.
It is a silent, progressive condition, tightly linked to aging.
Although sarcopenic obesity has been associated with deteriora-
tion in quality of life (QoL) [5] and all-cause mortality [6], it
remains largely undiagnosed, which can have negative conse-
quences for the affected individuals and for the healthcare
system.
The aim of this review is to provide a summary of current data
on sarcopenic obesity with regard to its definition, pathogenesis,
clinical consequences, prevention and/or treatment, as well as to
provide proposals for future developments in this area.

1
First Department of Pharmacology, Medical School, Aristotle
University of Thessaloniki, 13 Simou Lianidi, 551 Definition
34 Thessaloniki, Greece
2
Laboratory of Clinical Chemistry and Biochemistry, School of There is at present no consensus on the definition of
Medicine, University of Crete, Heraklion, Greece sarcopenic obesity, but an appropriate definition would
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include the criteria for both sarcopenia and for obesity. The
diagnosis of sarcopenia alone is based on two or three of the
following parameters: (a) low muscle mass, (b) low muscle
strength, and (c) low physical performance. The recommend-
ed diagnostic methods for clinical practice are the following:
whole-body dual energy X-ray absorptiometry [DEXA], (b)
handgrip strength, (c) gait speed, short physical performance
battery, squad-jump (SJ), countermovement-jump (CMJ), 10-
and 20-m sprint performance [7, 8]. Based on these parame-
ters, the European Working Group of Sarcopenia in Older
People (EWGSOP) in 2010 [9] and the Asian Working
Group for Sarcopenia (AWGS) in 2014 [10] recommended
that the definition of sarcopenia should include (a) low muscle
mass and (b) low muscle strength or low physical perfor-
mance. The International Working Group on Sarcopenia
(IWGS) in 2011 recommended the combination of (a) low
muscle mass and (b) low muscle strength for the definition
of sarcopenia, without considering physical performance [4],
whereas the Foundation for NIH Sarcopenia Project
(FNIHSP) in 2014 suggested that the definition of sarcopenia
should include all three parameters [11]. With many different
recommendations, it is unsurprising that the perceived preva-
lence of sarcopenia varies: it is lower when the three criteria
are required (FNIHSP) [11] but higher when two criteria are
required [4, 9, 10], as shown in a comparative study [12].
Notably, all definitions concurred that the prevalence of
sarcopenia is higher in women than in men [12].
Most definitions for sarcopenic obesity, as reviewed else-
where [13], include low muscle mass and strength and high
body fat. Regarding muscle mass, total [14] or appendicular
skeletal muscle mass (ASM) [15–18] in weight (kg)/height2
(m2) of an individual is compared with those of a reference
population of the same gender; values below two standard de-
viations of the reference population are defined as sarcopenia.
Body fat over a cutoff compared with a reference population of
the same sex and similar age is defined as obesity in most
definitions of sarcopenic obesity [14, 16–18]. However, the
cutoff varies: body fat above the 60th percentile was initially
proposed [18], but it varies in different definitions [14, 16, 17].
An advantage of these definitions is that the only test re-
quired is a whole body DEXA to measure both muscle and fat
mass. The use of DEXA is regarded as the gold standard, since
it is superior to bioelectrical impedance analysis (BIA) [19],
also proposed by some authors as a method for measuring of
sarcopenic obesity [20]. Furthermore, the use of DEXA for the
estimation of obesity is more accurate than that of body mass
index (BMI) and waist circumference (also employed by some
authors [21]), which may not reflect the amount of body fat in
some cases. For example, sumo wrestling athletes exhibit high
BMI and waist circumference, which is due to a high percent-
age of muscle mass compared to their fat mass, which is low.
Indeed, a limitation of BMI is that it measures total body
weight which includes muscle mass. In addition, it does not
Hormones (2018) 17:321–331
provide an estimation of strength and physical performance. A
limitation of all the aforementioned definitions is that they do
not include muscle strength and physical performance together
with muscle mass as criteria for sarcopenia, although some
authors have proposed muscle strength (evaluated with hand
grip) without muscle mass for defining sarcopenia of
sarcopenic obesity [21]. Indeed, the use of fewer than three
criteria (i.e., muscle mass, muscle strength, and physical per-
formance) may overestimate the prevalence of sarcopenic obe-
sity, as previously shown for the prevalence of sarcopenia alone
(when fewer than three criteria were used, resulting in a higher
prevalence of sarcopenia) [12].
As mentioned, the diversity of existing criteria in diagnosing
sarcopenic obesity results in a great variation of its perceived
prevalence. For example, when eight different definitions were
applied for a given population (aged ≥ 60 years), the prevalence
of sarcopenic obesity ranged from 4.4 to 84.0% in men and from
3.6 to 94.0% in women [22]. Practically speaking, this variation
renders sarcopenic obesity an ill-defined disease, which results in
non-comparable data in diagnosis and management of this clin-
ical entity and great variation in the conduct of clinical trials.
Clinical presentation
Typically, patients with sarcopenic obesity are aged over
60 years with a sedentary lifestyle and unhealthy dietary
habits (e.g., high-fat and/or high-carbohydrate diet, cigarette
smoking, and/or alcohol consumption). Since the disease re-
mains largely unrecognized, the patients usually present in
healthcare facilities for obesity or related comorbidities (e.g.,
type 2 diabetes mellitus [T2DM], non-alcoholic fatty liver
disease [NAFLD], dyslipidemia, hypertension, and cardiovas-
cular disease [CVD]), or for non-specific symptoms related to
sarcopenia (e.g., fatigue, weakness, and frailty). The disease
usually remains undiagnosed. While obesity-related comor-
bidities are managed separately, sarcopenia-related symptoms
are not adequately addressed and are generally attributed to
advanced age or stress. From a clinical point of view, the
employment of a high degree of suspicion is required to set
the diagnosis of sarcopenic obesity, thereby eliminating any
unnecessary diagnostic tests.
As mentioned above, both BMI and even waist circumfer-
ence, which is regarded as a better index of abdominal obesity,
are not the best tests to evaluate obesity of sarcopenic obesity.
The efficacy of BMI is further diminished with aging, since
height may be decreased owing to concomitant osteoporosis.
Body composition may also largely vary for a given BMI [23].
To cite one example, Asians typically have higher fat mass
than Caucasians with the same BMI. Apart from the charac-
teristic patients with sarcopenic obesity in whom high BMI or
increased waist circumference are mainly attributable to high
fat mass, there are individuals in whom high BMI or waist
Hormones (2018) 17:321–331
circumference are due mainly to high muscle mass rather than
fat mass (e.g., sumo athletes). Moreover, there are individuals
with normal BMI or waist circumference but high fat mass and,
thus low muscle mass, who are thus categorized as having
sarcopenic obesity. In this regard, sarcopenia may coexist with
obesity, though not all obese persons are sarcopenic nor all
sarcopenic are obese. Anthropometric and imaging findings
that can differentiate between sarcopenic obesity and
sarcopenia alone or obesity alone are presented in Table 1.
The table displays the general tendency; no cutoffs can current-
ly be provided, since head-to-head comparative studies are
scarce. Based on these considerations, it is not at present pos-
sible to differentiate between sarcopenic obesity and sarcopenia
alone or obesity alone based only on anthropometric findings.
Pathogenesis
The pathogenesis of sarcopenic obesity is multifactorial, with
an interplay between aging, sedentary lifestyle, unhealthy di-
etary habits, and insulin resistance (IR), systemic inflamma-
tion, and oxidative stress, resulting in quantitative and quali-
tative decline in muscle mass and function and a parallel in-
crease in fat mass [13]. In this regard, common etiologic fac-
tors may affect both muscle and fat mass.
Sarcopenic obesity is commonly, albeit not exclusively,
related to aging. Indeed, the amount of muscle mass increases
in adolescence and young adulthood. It has been estimated
that bone mass and muscle mass peak around the age of
30 years. In contrast, aging is accompanied by a gradual loss
of muscle mass [or fat-free mass (FFM)] and a parallel in-
crease in fat mass [19]. This is usually accompanied by an
increase in body weight, but may also occur without increase
in body weight, or more rarely, even with a minor decrease in
body weight [24]. Of note, the inevitable decline in total body
weight with aging may mask the diagnosis of sarcopenic obe-
sity. Therefore, sarcopenic obesity represents a relative in-
crease of fat mass in relation to muscle mass (or FFM). It
should be also noted that during aging, fat tends to be ectop-
ically redistributed, usually in the liver (NAFLD) [25] and,
most importantly, in the muscles [26] and in the pancreas
(non-alcoholic pancreas disease) [27].
Table 1 Anthropometric and
imaging findings for the Findings
differentiation between
sarcopenic obesity and sarcopenia Anthropometric
alone or obesity alone Weight, BMI, waist circumference
Imaging (DXA, BIA, CT, or MRI)
Fat mass
Muscle mass
BIA, bioelectrical impedance analysis; BMI, body mass index; CT, computed tomography; DXA, dual energy X-
ray absorptiometry; MRI, magnetic resonance imaging
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Age-associated sarcopenia and obesity [28] is usually due
to a progressive decrease in physical activity and in protein
intake. Sarcopenia-related muscle weakness results in a further
decline in physical activity (thus, in energy expenditure), but
also in IR increase, both of which negatively affect adipose
tissue; more specifically, adipocytes increase in size and num-
ber, causing a secondary infiltration of adipose tissue by im-
mune cells leading to inflammatory response. Specifically, ad-
ipocytes and immune cells produce adipokines (e.g., increase
in leptin, chemerin, resistin, but decrease in adiponectin) and
cytokines (e.g., increase in tumor necrosis factor [TNF]-α,
interleukins [ILs], interferon [INF]-γ), thereby creating a con-
dition of low-grade inflammation. The latter may be not con-
fined to adipose tissue but be generalized, since most
adipokines and cytokines are secreted into the circulation
[29]. This unfavorable adipokine/cytokine profile further in-
creases IR, which amplifies inflammation and oxidative stress,
but also contributes to ectopic fat disposition [29, 30]. It is thus
obvious that a vicious cycle is established between decline in
physical activity–sarcopenia–IR–inflammation–oxidative
stress–obesity, which results in the downward spiral of
sarcopenic obesity [28].
Both low-grade generalized inflammation and intramuscular
fat disposition result in mitochondrial dysfunction and an im-
balance of myokines (e.g., myostatin, irisin, TNF-α, and ILs)
produced by the myocytes [31]. More specifically, mitochon-
drial β-oxidation is impaired, which leads to increased lipid
peroxidation. This in turn enhances the accumulation of lipid
intermediates and reactive oxygen metabolites (ROMs), which
augment IR, inflammation, oxidative stress, and lipotoxicity
within the myocyte [31], a condition that can result in dysfunc-
tion and apoptosis of the affected myocytes. Moreover,
myokines secreted by myocytes may exacerbate IR in adipose
tissue and other tissues, thus maintaining a negative cross-talk
between skeletal muscle and adipose tissue [28, 31].
Regarding dietary factors, inadequate protein intake [32,
33] and vitamin D [33, 34] have been shown to worsen
sarcopenic obesity. Sufficient protein intake is considered to
be essential in maintaining muscle mass and strength; howev-
er, among the aged, protein intake is usually decreased [35].
Furthermore, vitamin D levels decline with aging, partly ow-
ing to the decrease in outdoor activities and the declining
Obesity Sarcopenia Sarcopenic obesity
High Low or normal Normal or high
High Low or normal High
Normal or high Low Low
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ability of the skin to produce the precursors of vitamin D, even
when exposed to sufficient ultraviolet radiation [36].
Myokines, including myostatin and irisin, which are most-
ly though not exclusively produced by the skeletal muscle
[37], may participate in the pathogenesis of sarcopenic obesi-
ty. Indeed, several reports have suggested that myostatin
(which negatively regulates muscle mass) is upregulated
[38] and irisin (which is positively associated with muscle
mass) is downregulated [39] in sarcopenia. Since downregu-
lation of myostatin [40] and upregulation of irisin [41] have
also been proposed as promoting browning of white adipose
tissue, pathophysiological studies are required to investigate
whether myostatin and irisin are central players in the patho-
genesis of sarcopenic obesity, which may provide clues for
effective therapeutic intervention.
Although concrete evidence is currently limited, several
endocrine factors are thought to contribute to the pathogenesis
of sarcopenic obesity, some of which are herein noted. In
males, late-onset hypogonadism may negatively affect adi-
pose tissue dynamics and muscle cell function. In women,
the cessation of ovarian estrogen production in menopause
affects both adipocyte and muscle function. Other endocrine
diseases may also play a role in the pathogenesis of sarcopenia
and/or obesity, such as hypothyroidism, hyperthyroidism,
adult growth hormone deficiency, and Cushing’s syndrome.
It is obvious that further studies are needed to specifically
address the contribution of each one of these endocrine dis-
eases to the pathogenesis of sarcopenic obesity.
Consequences
As mentioned above, it has been suggested that sarcopenia
and obesity may affect synergistically the physiology of ener-
gy balance and muscular function/physical capacity [42]. It
should be noted however that existing studies are often low
on the pyramid of evidence-based medicine and have provid-
ed conflicting data. A few examples are the following.
Sarcopenic obesity has been independently associated with
multimorbidity in a large Korean study [43]. Similarly, a
dose-dependent association between sarcopenic obesity and
higher rates of chronic diseases has been observed in a
multi-continent study [44]. More importantly, sarcopenic obe-
sity was shown to increase all-cause mortality in a recent
meta-analysis of prospective cohort studies [6]. However, in
subgroup analysis, all-cause mortality was dependent on the
criteria in diagnosing sarcopenic obesity. More specifically,
all-cause mortality was higher when the diagnosis of
sarcopenic obesity was based on mid-arm muscle circumfer-
ence or muscle strength, but not on the skeletal muscle mass-
based definition [6]. These discrepancies highlight the need
for a consensus on the definition of sarcopenic obesity. For the
sake of clarity, we hereby divide the consequences of
Hormones (2018) 17:321–331
sarcopenic obesity into those related to metabolic diseases,
to physical capacity (including bone metabolism), and to
QoL. Potential consequences of sarcopenic obesity are sum-
marized in Table 2.
Metabolic consequences
The aforementioned vicious cycle linking sarcopenia, obesity,
and IR implies that sarcopenic obesity may be implicated in the
metabolic syndrome (MetS) and related comorbidities, includ-
ing T2DM, NAFLD, dyslipidemia, hypertension, and CVD.
More specifically, IR and the risk of MetS were higher in pa-
tients with sarcopenic obesity than in those with sarcopenia
alone or obesity alone in the Korean Longitudinal Study on
Health and Aging (KLoSHA) [45]. Similarly, sarcopenic obesi-
ty was inversely associated with MetS in the Korean Sarcopenic
Obesity Study (KSOS) [46] and the Korean National Health and
Nutrition Examination Survey (KNHNES) [47], but also in
Caucasians [48]. In a retrospective cohort study, the 10-year risk
of MetS was higher in patients with sarcopenic obesity than
those with sarcopenia alone and non-sarcopenia/non-obesity,
but similar to those with obesity alone (approximately 52 vs.
16 vs. 17 vs. 47%, respectively) [49].
In the KSOS, sarcopenic obesity was also inversely associ-
ated with arterial stiffness, regarded as an index of early CVD
[46]. In the KNHNES, sarcopenic obesity was independently
inversely associated with dyslipidemia in men, but not in wom-
en [50]. More specifically, men with sarcopenic obesity had the
highest risk of hypercholesterolemia, hypertriglyceridemia, low
Table 2 Potential consequences of sarcopenic obesity
Metabolic consequences
Higher IR
Higher rates of MetS
Increased arterial stiffness
Higher rates of dyslipidemia
Higher rates of arterial hypertension
Positive association with GGT
Physical capacity
Lower levels of physical fitness
Impaired physical functioning
Worse balance
Worse aerobic capacity
Higher rates of frailty
Positive association with osteoporosis
Higher rates of falls and fractures
Quality of life
Inverse association with QoL (controversial)
Inverse association with perceived stress and suicidal ideation
GGT, gamma-glutamyl transferase; IR, insulin resistance; MetS, metabol-
ic syndrome; QoL, quality of life
Hormones (2018) 17:321–331
high-density lipoprotein cholesterol, and high low-density lipo-
protein cholesterol. Notably, a higher risk of dyslipidemia was
shown for sarcopenic obesity compared with either obesity
alone or sarcopenia alone [50]. In another study, sarcopenic
obesity was shown to be independently associated with hyper-
tension [51]. However, in the aforementioned retrospective co-
hort study, the 10-year risk of hypertension was higher in pa-
tients with sarcopenic obesity than in those with sarcopenia
alone or non-sarcopenia/non-obesity, but similar to those with
obesity alone (approximately 53 vs. 28 vs. 28 vs. 45%, respec-
tively) [49].
Regarding NAFLD, KNHNES showed that sarcopenic
obesity increased stepwise from the lowest (8%) to highest
(28%) quintile of serum gamma-glutamyl transferase activity
(GGT) in community-dwelling older adults. Those in the
highest GGT quintile had an independent 3.4-fold risk of
sarcopenic obesity compared with those in the lowest GGT
quintile [52]. Sarcopenic obesity was also highly prevalent
(42%) in patients with liver cirrhosis [53]. Importantly, non-
alcoholic steatohepatitis, regarded as an advanced stage of
NAFLD and the main pharmacological target [54], was an
independent predictor of sarcopenic obesity in patients with
liver cirrhosis [53].
The 10-year risk for T2DM was higher in patients with
sarcopenic obesity than in those with sarcopenia alone, non-
sarcopenia/non-obesity, or obesity alone (approximately 21
vs. 5 vs. 4 vs. 6%, respectively) [49]. Notably, the 10-year risk
of CVD was not statistically different between groups in this
study (approximately 6 vs. 5 vs. 4 vs. 3%, respectively) [49].
In contrast, other authors support the view that that sarcopenic
obesity is associated with an increased 10-year CVD risk,
estimated by the Framingham risk score [55]. Further well-
designed, prospective cohort studies are needed to elucidate
the impact of sarcopenic obesity on metabolic and cardiovas-
cular diseases.
Physical capacity
Low levels of physical activity were observed in individuals
with sarcopenic obesity [44]. Lower levels of physical fitness
were shown in patients with sarcopenic obesity than in non-
sarcopenic/non-obese individuals [56]. By contrast, better bal-
ance and aerobic capacity were related to lower risk of
sarcopenic obesity [56]. In the Quebec longitudinal study,
patients with sarcopenic obesity showed lower physical ca-
pacity than non-sarcopenic/non-obese individuals, though it
was similar to those with obesity alone [17]. In another study,
physical functioning was also impaired in patients with
sarcopenic obesity compared with non-sarcopenic/non-obese
individuals, but was similar to those with obesity alone [15].
Notably, sarcopenic obesity was an independent risk factor for
impaired physical functioning in this study [15]. In a post hoc
analysis of a cohort study, higher adiposity-to-muscle ratio,
325
proposed as a measure of sarcopenic obesity, was able to pre-
dict a 4-year worsening in physical limitation [57].
Similarly to sarcopenia, sarcopenic obesity was, early on,
linked to frailty, defined as having some of the following
characteristics: weakness, poor endurance or exhaustion,
slowness, and low activity levels [58]. In a 5-year cohort
study, men with sarcopenic obesity, but not those with obesity
alone, had a higher risk of frailty, activities of daily living
(ADL) disability, and instrumental ADL disability as com-
pared with non-sarcopenic/non-obese men [59].
Furthermore, sarcopenic obesity has been linked to osteo-
porosis. In an initial cross-sectional study, higher rates of os-
teoporosis (assessed by femoral neck bone mineral density
[BMD]) were observed in sarcopenic obese than in obese
alone or non-sarcopenic/non-obese [60]. Recently, sarcopenic
obesity has been associated with the risk of falls and fractures
in men in a cohort study (the Concord Health and Ageing in
Men Project) [61]. Although sarcopenic obese men had sim-
ilar total hip BMD to non-sarcopenic/non-obese men, the 2-
year fall rates in men with sarcopenic obesity were higher than
in those with obesity alone, sarcopenia alone, or non-
sarcopenia/non-obesity. Notably, the 6-year fracture risk was
higher in men with sarcopenic obesity than in those with obe-
sity alone [61]. However, higher fall rates and fracture risk
were not evidenced with all definitions of sarcopenic obesity
[61]. In another cohort study with community-dwelling older
adults, lower BMD and higher fracture risk (self-reported)
were observed in individuals with sarcopenic obesity than
with obesity alone, despite notable differences between sexes
[62]. It is also of interest that higher ASM was shown to be
independently associated with parameters of bone mass and
strength in patients with sarcopenic obesity, implying that low
muscle mass may also compromise bone health and balance
[63]. Based on these observations, interventions that improve
muscle mass and composition may decrease fracture risk in
sarcopenic obesity and are therefore recommended. Owing to
the close cellular, hormonal, and clinical relationship between
muscle, fat, and bone, the term osteosarcopenic obesity has
been proposed [64]. Based on this consideration, osteoporosis
and sarcopenia was characterized as the “obesity” of bone and
muscle, respectively [64]. In this regard, low physical activity
seems to be involved in the pathogenesis and management of
both sarcopenic obesity and osteoporosis. Therefore, interven-
tional studies set up to elucidate the effect of physical activity
on the triad of sarcopenia, obesity, and osteoporosis would be
of great interest and clinical significance.
Quality of life
Based on the evidence that both obesity alone and sarcopenia
alone negatively impact QoL, it is speculated that sarcopenic
obesity will also adversely affect QoL. More specifically, a
meta-analysis showed that overweight and obese individuals
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have reduced physical QoL with a dose-response relationship
across all categories of BMI [65]. Another meta-analysis with
randomized controlled trials (RCTs) showed that combined
diet and exercise led to the greatest improvement in QoL while
mitigating reductions in muscle mass, which was observed in
diet-only study arms [66]. Likewise, QoL was reduced in most
studies with sarcopenia alone [67, 68].
However, the data so far are limited and conflicting. In the
KNHNES, sarcopenic obesity was inversely associated with
QoL [5], an association that was more robust in participants
under the age of 60. Of importance, in the same study,
sarcopenic obesity was shown to be independently associated
with psychological conditions, specifically the perceived stress
and suicidal ideation [5], which is thought to affect QoL but
also to be affected by it. In another study, better perceived
health was associated with superior physical fitness perfor-
mance in patients with sarcopenic obesity [56]. Conversely,
in two smaller studies, sarcopenic obesity was not significantly
associated with QoL [69, 70]. More studies are needed to
elucidate the effect of sarcopenic obesity on QoL.
Management
Though novel drugs are under investigation, there is at present
no approved pharmacological treatment for sarcopenic obesi-
ty. Accordingly, the management of sarcopenic obesity is cur-
rently based on weight loss together with increase in physical
activity. Below, data are presented, primarily from RCTs and
systematic reviews/meta-analyses with the aim of selecting
the best available evidence. Management of sarcopenic obe-
sity based on the existing data is summarized in Table 3.
Diet and exercise
Although there are only limited data from well-designed RCTs
in individuals with sarcopenic obesity, it seems that weight loss
without exercise, while reducing fat mass, also inevitably
Table 3 Management guidance for sarcopenic obesity
Diet
Mild energy restriction with the aim of slowing weight loss
Avoidance of rapid weight loss (severe energy restriction or
bariatric surgery)
Adequate protein intake (diet and/or supplementation)
Exercise
Combination (aerobic plus resistance) or resistance exercise
Avoidance of energy restriction without exercise
Pharmacological treatment
No approved pharmacological treatment
Promising results from myostatin inhibitors
Hormones (2018) 17:321–331
decreases lean mass, thus worsening sarcopenia. In a systematic
review, it was reported that while the addition of exercise to
energy restriction does not appear to have a significant additive
effect on weight loss, it can attenuate the loss of lean mass [71],
considered to be essential, especially in patients with sarcopenic
obesity. Notably, more than 15% of lean mass loss was ob-
served in approximately 80 vs. 40% of overweight/obese indi-
viduals following energy restriction alone vs. energy restriction
combined with exercise, respectively [71]. In another system-
atic review, diet and exercise were reported as the best strategy
for obese older individuals, improving metabolic and functional
consequences related to excess fat and low muscle mass, while
as mentioned above, the addition of exercise to a well-balanced
diet seems to protect against lean mass loss [72].
The best type of exercise has not as yet been determined, but
the available data suggest that resistance exercise, or the com-
bination of aerobic plus resistance exercise, is the best choice.
Resistance training may be more useful to counteract sarcopenia
and aerobic training more useful to counteract obesity; based on
this rationale, their combination most likely provides the best
results in patients with sarcopenic obesity, although this remains
to be confirmed. In a recent 6-month RCT in obese older adults,
the physical performance test improved more in the combina-
tion exercise group than in the resistance-only or aerobic-only
groups (increased by 29, 14, and 14%, respectively) [73]. The
QoL (assessed by the SF-36 questionnaire) also improved more
in the combination than in the resistance or aerobic groups
(improvement by 24, 17, and 14%, respectively). Strength in-
creased more in the combination and resistance than in the
aerobic group (by 18, 19, and 4%, respectively). Lean mass
decreased less in the combination and resistance than in the
aerobic group (by 3, 2, and 5%, respectively). Notably, body
weight decreased by 9% in all groups and fat mass decreased
similarly in all groups (by 17, 17, and 16%, respectively) [73].
Likewise, in another 3-month RCT in older adults with
sarcopenic obesity, body weight and fat mass decreased slightly
and similarly in the combination, resistance, and aerobic groups.
However, strength increased more in the resistance group than
in the aerobic or combination groups [74].
There are also a few trials comparing resistance exercise
with no exercise (control). Resistance exercise increased lean
mass and physical capacity in older women with sarcopenic
obesity in a 3-month RCT [75] and in a 6-month RCT [76]. By
contrast, resistance exercise did not improve physical capacity
in older women with sarcopenic obesity in another 10-week
RCT [77]. However, the sample study was small (n = 26) and
the control group was followed up through telephone calls.
Limited data on other types of exercise, including whole-body
electrostimulation [78], vibration, yoga, tai-chi, and Pilates
[79], report that they may be effective in patients with
sarcopenic obesity and should be considered as alternatives
to other types of exercise, especially in physically disabled or
bedridden handicapped patients.
Hormones (2018) 17:321–331
Sufficient protein intake is also considered important in
individuals with sarcopenic obesity. In a meta-analysis of
17 RCTs comparing the effect of resistance exercise alone
vs. the combination of resistance exercise plus protein sup-
plementation in overweight/obese older individuals, it was
shown that the addition of protein supplementation to re-
sistance exercise decreased fat mass and increased lean
mass, upper body strength, and leg strength more than re-
sistance exercise alone [80]. However, optimal quantitative
and qualitative protein supplementation has not as yet been
identified specifically for patients with sarcopenic obesity,
although some authors sensibly proposed that supplemen-
tation with the essential amino-acids (e.g., leucine, argi-
nine, and cysteine) is the most important [13]. Regarding
the quantity of protein supplementation, 1.2–1.6 g/kg/d
have been proposed [13], though importantly, renal impair-
ment in older individuals should be carefully considered on
an individual basis.
As far as vitamin D supplementation is concerned, limited
data from interventional studies suggest that vitamin D to-
gether with amino-acid supplementation, tea catechins, and
combination exercise (aerobic plus resistance) for 3 months
improved body fat mass and physical function, but not mus-
cle mass, in elderly women with sarcopenic obesity [81].
However, the duration of this RCT may be too short to show
improvement in muscle mass. To date, no study has evaluated
vitamin D monotherapy in patients with sarcopenic obesity,
which, however, in our opinion, may not improve all the
different parameters of sarcopenic obesity due to the multi-
factorial pathogenesis of the disease.
To summarize, weight loss via energy restriction alone
should be avoided in patients with sarcopenic obesity because
of the simultaneous loss of muscle mass. The addition of ex-
ercise to diet is considered of importance, since it can prevent
excessive muscle loss. Concerning exercise, resistance or
combination exercise rather than aerobic exercise appears to
result in less muscle loss and in increasing strength.
Combination exercise seems to be the most effective strategy
for improving physical capacity, although further research is
required. Protein supplementation may also be important, al-
though more data are needed for its optimal quantitative and
qualitative synthesis.
Of note, calorie restriction may be important for the man-
agement of sarcopenic obesity as a non-genetic intervention
with anti-aging and anti-inflammatory effect [82]. More spe-
cifically, calorie restriction prevents age-associated diseases
and extends longevity in most animal models, mainly by mod-
ulating mitochondrial activity and decreasing oxidative stress
[82], both of which contribute to aging, inflammation, and the
pathogenesis of sarcopenic obesity. This is a concept that ap-
pears to offer deeper insight into the pathogenesis and man-
agement of sarcopenic obesity, though it needs further
investigation.
327
Pharmacologic management
Since to date there are no available data as to what effect
current anti-obesity medications, including orlistat, phen-
termine, phentermine/topiramate, lorcaserin, naltrexone/
bupropion, and liraglutide, may have on sarcopenic obesity,
it is not possible to recommend either for or against their
use for this condition. A point that needs careful consider-
ation is the speed of weight loss, which is usually faster
following anti-obesity medications than with diet and exer-
cise. In our opinion, weight loss should not be very rapid, to
avoid the rapid simultaneous loss of muscle mass, although
this also remains to be confirmed specifically in sarcopenic
obesity.
Though there are some emerging medications that have
been tested or which are presently under investigation for
sarcopenia or related disorders, including cachexia and frailty,
as summarized elsewhere [83], there are only limited data on
them for sarcopenic obesity. In a well-designed, 6-month
RCT, a myostatin antibody (LY2495655) decreased body
fat, increased skeletal mass, and improved physical capacity
in older individuals with frequent falls [84]. While growth
hormone also appeared to represent a candidate treatment for
sarcopenic obesity, due to its anabolic and lipolytic actions, its
adverse effects were not acceptable when it was administered
in healthy older individuals [85]. In contrast, tesamorelin, a
growth hormone-releasing hormone analog, shows promise of
having a beneficial effect on sarcopenic obesity, since it re-
duced fat mass and increased lean mass without affecting glu-
cose homeostasis when administered in young obese [86].
Other medications with a potential positive effect on
sarcopenic obesity include other myostatin antibodies (e.g.,
bimagrumab, REGN1033, PINTA-745, PF-06252616, and
BMS-986089), β-blockers (e.g., espindolol), hormonal re-
placement treatment for postmenopausal women, and andro-
gen receptor agonists (e.g., nandrolone, enobosarm, MT-102,
and MK-0773) for aging men, on careful consideration [83].
Recombinant irisin might also be available in the near future
and could be a candidate for the treatment of sarcopenic obe-
sity [87]. Other candidates for clinical trials for patients with
sarcopenic obesity may be androgens (especially for patients
with late-onset hypogonadism), angiotensin-converting en-
zyme inhibitors, vitamin D, and ursolic acid, as monotherapy
or in combination therapy due to the multifactorial pathogen-
esis of the disease. However, the performing of clinical trials
of novel drugs requires careful consideration because of the
multiple adverse events related to these medications, especial-
ly in aging populations.
Bariatric surgery
There are limited data on the effect of bariatric surgery in pa-
tients with sarcopenic obesity. Again, the risk of excessive loss
328
of muscle mass exists, especially if weight loss is rapid and if
bariatric surgery is not followed by a regular exercise program
[88]. Since there is no available RCT for bariatric surgery in
patients with sarcopenic obesity, the best evidence to date
comes from a 12-month prospective cohort study in which the
effect of bariatric surgery (gastric bypass or sleeve gastrectomy)
is evaluated in sarcopenic compared with non-sarcopenic mor-
bidly obese [89]. Bariatric surgery resulted in similar weight
loss and similar improvement in comorbidity (i.e., T2DM,
NAFLD, hypertension, dyslipidemia, obstructive sleep apnea
syndrome, and arthritis) in both groups. Importantly, despite
baseline differences in muscle mass between the sarcopenic
and non-sarcopenic obese, muscle mass was not different be-
tween groups 12 months after surgery, thus implying that
sarcopenic patients did not lose more muscle mass despite sim-
ilar weight loss [89]. Nevertheless, until further relevant data are
published, it is recommended that bariatric surgery be carefully
considered in patients with sarcopenic obesity.
Closing remarks
Sarcopenic obesity is a growing diagnostic and therapeutic
challenge because of aging populations, the current obesity
epidemic, and changes in lifestyle, especially in the industri-
alized world. The study of sarcopenic obesity, however, is still
in its early stages. The first step towards a more in-depth study
of the disease and its consequences should be a consensus on
its definition. This is of paramount importance, since the new
studies to be carried out must be focused on the same disease
and their interpretation needs to apply the same “language”.
By following different definitions, as mentioned above, the
results of the studies referred to a similar but not an identical
disease, thus they cannot be generalized. In this regard, while
the use of DXA is necessary to evaluate both fat and muscle
mass, evaluation of muscle strength and/or physical perfor-
mance should be combined with DXA for sarcopenic obesity.
Mechanistic studies are additionally required to better eluci-
date the pathogenesis of this multifactorial disease. The next
step could be the establishment of simple diagnostic bio-
markers not only to screen populations but also to aid in the
follow-up of affected individuals. Lastly, RCTs are required to
determine what is the optimal management of the disease.
Recently, Cushing’s syndrome was suggested as a model
for sarcopenic obesity [90], a rational proposal, since abdom-
inal obesity and loss of muscle mass are common in patients
with Cushing’s syndrome [90]. The authors proposed
Cushing’s syndrome as an alternative model for the study of
sarcopenic obesity, possibly less affected by the comorbidities
and polypharmacy of older individuals with sarcopenic obe-
sity [90]. However, it must be borne in mind that sarcopenic
obesity in Cushing’s syndrome develops more rapidly than
sarcopenic obesity in the elderly; thus, any results should be
Hormones (2018) 17:321–331
interpreted with caution before being extrapolated to
sarcopenic obesity of the elderly. Furthermore, the pathophys-
iology of glucocorticoid-induced myopathy and adipose tis-
sue distribution in Cushing’s syndrome may differ from that
of sarcopenic obesity.
An important question that remains to be answered is
whether the consequences of sarcopenic obesity are more se-
vere than those of sarcopenia alone or obesity alone, in other
words, whether a synergistic effect of sarcopenia and obesity
exists. Although there are several studies comparing
sarcopenic obesity with sarcopenia alone and/or obesity alone
[15, 43, 49, 56, 61], the existing data are few to draw any firm
conclusions. For example, sarcopenic obesity was shown to
increase all-cause mortality in the aforementioned meta-
analysis [6]; however, it has not as yet been clearly shown
whether sarcopenic obesity increases mortality more than
sarcopenia alone or obesity alone, which have both been sep-
arately associated with increased all-cause mortality [91, 92].
If sarcopenic obesity does not have a greater impact than
sarcopenia alone or obesity alone on long-term consequences
and hard end-points (e.g., CVD and mortality), then even the
existence of sarcopenic obesity as a separate entity will be
questionable.
It should be highlighted that since sarcopenic obesity is a
multifactorial disease, its management cannot be based on
consideration of a single pathogenetic factor, but needs to be
multifactorial. As mentioned above, concomitant weight loss
together with adequate protein intake and exercise are essen-
tial, because weight loss alone possibly results in further mus-
cle loss [71, 72]. In this regard, in our opinion, a single ther-
apeutic agent is unlikely to be capable of treating sarcopenic
obesity, despite the promising results of myostatin antibody
[84]. Furthermore, given that the emerging pharmaceutical
treatment of sarcopenic obesity may be costly, healthcare sys-
tems will be unable to cover these expenses. Moreover, it is
known that among the old, it is difficult to attempt to reverse
age-related diseases, both because of their general disability,
but also due to the unwillingness of older individuals to un-
dergo lifestyle changes and adhere to medication on a long-
term basis. For these reasons, prevention of sarcopenic obesity
rather than its treatment is certainly the more rational choice.
A healthy diet and adequate exercise, which are the corner-
stones of preventive measures, must start at a young age and
be followed lifelong. Although it remains to be shown, it is
expected that these measures may decrease the prevalence and
impact of sarcopenic obesity.
To sum up, sarcopenic obesity is a chronic condition that
has metabolic consequences but also impacts physical capac-
ity, QoL, and possibly the mortality of affected individuals. A
consensus on its definition is considered an important step that
will greatly facilitate the setting up of mechanistic studies and
clinical trials to expand our knowledge, thus improving the
management of affected individuals in the near future.
Hormones (2018) 17:321–331
Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict of
interest.
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