Radiol Oncol 2024; 58(1): 1-8. doi: 10.2478/raon-2024-0011
1
review
Sarcopenic obesity in cancer
Mihaela Jurdana
1
, Maja Cemazar
1,2
1 
Faculty of Health Sciences, University of Primorska, Izola, Slovenia
2
 Institute of Oncology Ljubljana, Ljubljana, Slovenia
Radiol Oncol 2024; 58(1): 1-8.
Received 2 November 2023 
Accepted 4 December 2023
Correspondence to: Mihaela Jurdana, Ph.D., Faculty of Health Sciences, University of Primorska, Polje 42, Izola, Slovenia.  
E-mail: mihaela.jurdana@fvz.upr.si
Disclosure: No potential conflicts of interest were disclosed. 
This is an open access article distributed under the terms of the CC-BY license (https://creativecommons.org/licenses/by/4.0/).
Background. Sarcopenic obesity is a relatively new term. It is a clinical condition characterized by sarcopenia (loss of 
muscle mass and function) and obesity (increase in fat mass) that mainly affects older adults. As the incidence of sar-
copenia and obesity increases worldwide, sarcopenic obesity is becoming a greater problem also in cancer patients. 
In fact, sarcopenic obesity is associated with poorer treatment outcomes, longer hospital stays, physical disability, and 
shorter survival in several cancers. Oxidative stress, lipotoxicity, and systemic inflammation, as well as altered expres-
sion of skeletal muscle anti-inflammatory myokines in sarcopenic obesity, are also associated with carcinogenesis. 
Conclusions. Reported prevalence of sarcopenic obesity in cancer varies because of heterogeneity in definitions 
and variability in diagnostic criteria used to estimate the prevalence of sarcopenia and obesity. Therefore, the aim of 
this review is to describe the definitions, prevalence, and diagnostic criteria as well as the mechanisms that cancer 
has in common with sarcopenic obesity. 
Key words: sarcopenia; obesity; cancer; inflammation
Introduction
Sarcopenic obesity is a clinical condition character-
ised by the coexistence of obesity, excess fat mass 
(FM) and sarcopenia (decrease in skeletal muscle 
mass and function).
1,2
 Baumgartner was the first to 
propose the term sarcopenic obesity, which is con-
sidered a unique clinical condition distinct from 
obesity and sarcopenia alone.
1
 The prevalence of 
sarcopenic obesity is expected to become a pub-
lic health problem as the prevalence of sarcopenic 
obesity in adults is rapidly increasing worldwide. 
The clinical consequences of sarcopenic obesity are 
considerably more severe than those of sarcope-
nia or obesity alone. In comparison to both, it can 
lead to physical disability, morbidity, and even 
mortality.
3
 In addition, cancer is another serious 
global health problem with increasing incidence 
and mortality worldwide.
4
 Interestingly, sarcopen-
ic obesity is more common in older adult cancer 
patients and patients with other chronic diseases, 
but its prevalence is also increased in younger 
patients with obesity and chronic diseases such 
as cancer and is associated with worse treatment 
outcomes.
5
 Sarcopenic obesity and cancer, as well 
as other chronic diseases, share some key pathoge-
netic mechanism such as inflammation, oxidative 
stress, and insulin resistance, which are considered 
key factors.
6-8
 Among these, insulin resistance is 
considered a central condition in both, cancer and 
sarcopenic obesity.
8
Several factors in sarcopenic obesity may lead 
to progressive loss of muscle mass and altered fat 
metabolism, which influence each other in a recip-
rocal pattern. Sarcopenia is known to be a common 
problem in cancer patients, especially if they are 
suffering cachexia and is associated with physical 
disability, surgical complications, increased risk 
of severe toxicity during cancer treatment, pro-
longed hospitalisation, and shortened survival.
6
 
Sarcopenia can occur at any stage of cancer and 
in any body mass index (BMI) category and is of-

Radiol Oncol 2024; 58(1): 1-8.
Jurdana M et al. / Sarcopenic obesity and cancer 2
ten associated with obesity. In addition, obesity, 
particularly abdominal obesity, can independently 
lead to loss of muscle mass and function due to 
the negative effects of oxidative stress, inflamma-
tion, and insulin resistance, all of which negatively 
impact muscle mass.
7
 Recently, there has been an 
increasing interest in utilizing body composition 
phenotype as an additional indicator of cancer 
prognosis. Because the burden of sarcopenia and 
obesity are concurrent, they can be expected to 
have a combined impact on health outcomes in 
several clinical settings, including cancer.
6
 
As the prevalence of sarcopenic obesity with 
poor prognosis is rapidly increasing in cancer 
patients, in this review we discuss definitions, 
prevalence, mechanisms and management strate-
gies for sarcopenic obese patients in oncology. This 
review aims to provide clinician’s with additional 
evidence helping them to make rational decisions 
that will improve patients’ outcome. 
Identification of sarcopenic 
obesity and diagnostic criteria 
Sarcopenic obesity has been identified using vari-
ous definitions and diagnostic criteria. Screening 
for sarcopenic obesity is based on the simultane-
ous presence of increased BMI or waist circumfer-
ence with ethnicity-specific cut-offs and surrogate 
parameters of sarcopenia (clinical symptoms, vali-
dated questionnaires -SARC-F in the elderly). In 
addition, altered body composition is required to 
make a definitive diagnosis.
9,10
Many studies have investigated the prevalence 
of sarcopenic obesity in different cohorts of can-
cer patients, including oropharyngeal
11
, lung
12,13
, 
gastrointestinal
14,15-24
, liver and pancreatic
25,26
, uri-
nary
27-29
, breast
30
, melanoma
31
 and lymphoma.
32
 
On the other hand, the lack of uniform diagnos-
tic criteria for sarcopenic obesity hampers the 
identification of patients and the assessment of 
associated outcomes and, consequently, nega-
tively affects the development of prevention and 
treatment strategies for sarcopenic obesity. The 
prevalence of sarcopenic obesity in studies that in-
clude cancer patients varies from 1-29% in studies 
of patients in all BMI categories and from 15% to 
36% in studies of overweight/obese patients.
6
 The 
lowest prevalence of sarcopenic obesity is found 
in early disease stages and the highest in locally 
advanced or metastatic disease.
6
 Heterogeneity 
in diagnostic criteria between studies, as well as 
the metabolic impact of different cancer types, 
other patient characteristics such as ethnicity, 
and concurrent comorbidities, limit interpretation 
of results. In addition, The European Society for 
Clinical Nutrition and Metabolism (ESPEN) and 
the European Association for the Study of Obesity 
(EASO) confirmed heterogeneity in definition and 
diagnostic approaches for sarcopenic obesity, due 
to different definition of obesity and sarcopenia, 
differences in methodologies to assess body com-
position and function, as well as in the applied 
references values for variables used.
9
 Regardless of 
this variability, most studies report that sarcopenic 
obesity is an important problem in cancer patients 
and a negative prognostic factor.
Commonly used technics in 
oncology setting 
Various techniques and body composition parame-
ters with different cut off as well as muscle function 
parameters have been used to identify sarcopenic 
obesity. Body composition is traditionally meas-
ured using Dual Energy X-ray Absorptiometry 
(DEXA) or Bioelectrical Impedance Analysis (BIA) 
but is known to have some limitations.
9
 Currently, 
computed tomography (CT) and magnetic reso-
nance imaging (MRI) are considered the gold 
standard methods. Both CT and MRI are not rou-
tinely used to assess sarcopenia and obesity due 
to high costs and radiation concerns for CT.
33,34
 
CT should be used when possible (e.g., in patients 
undergoing a scan for diagnostic reasons in oncol-
ogy).
9
 In cancer patients, the CT scan provides the 
highest available precision in determining body 
composition parameters by measuring the cross-
sectional area of total skeletal muscle at the third 
lumbar vertebra (L3), which correlates strongly 
with total body skeletal muscle mass.
35
 
The DEXA method, which is considered inex-
pensive, is the most accurate method for measur-
ing appendicular muscle mass, and exposes the 
patient to minimal radiation, but is not widely 
available. The BIA method is an alternative, inex-
pensive, and readily available method, but results 
are easily confounded by various factors, espe-
cially fluid status.
34
 All these techniques provide 
anatomic information about the patient but not 
functional information, because loss of muscle 
function is also required to diagnose sarcopenia.
36
 
Therefore, the diagnostic process must include a 
direct assessment of altered skeletal muscle func-
tion parameters along with altered body compo-
sition. Thereafter, individuals with a positive di-

Radiol Oncol 2024; 58(1): 1-8.
Jurdana M et al. / Sarcopenic obesity and cancer 3
agnosis should be classified into two stages: Stage 
I, when no clinical complications are present, and 
Stage II, with clinical complications such as chron-
ic disease (e.g. cancer), dietary events (weight loss, 
decreased food intake), immobility, falls, and other 
complaints associated with altered body compo-
sition and muscle function.
9
 All procedures are 
summarized in Table 1.
Biological pathways leading to 
sarcopenic obesity 
The biological pathway leading to sarcopenic 
obesity includes changes in body composition re-
lated to ageing, hormonal changes, the interplay 
between metabolism and inflammation, environ-
mental factors such as poor nutrition and lack of 
exercise and chronic diseases.
37-40
 This results in 
a decrease in oxidative capacities, mitochondrial 
number, atrophy of fast type II muscle fibres and 
neurodegeneration, decrease in protein synthesis 
and increase muscle protein degradation.
41
Metabolic disfunctions
Both, skeletal muscle mass and adipose tissue 
interplay with several cancers at metabolic lev-
els.
42-45
 Few studies have investigated the path-
way between sarcopenia, obesity and cancer. The 
mechanisms involved in pathogenesis of metabolic 
imbalances associated with obesity are in part com-
mon with pathway modulating cancer related sar-
copenia.
5
 Inflammation promoted by cancer and/or 
inadequate intake of essential nutrients could con-
tribute to the presence of fatigue and decrease in 
physical activity and mobility of cancer patients.
6
 
Physical inactivity can lead to skeletal muscle 
loss by reduced protein anabolic pathway and 
activation of proteolytic pathway.
5,6
 In addition, 
inadequate food intake can also impair muscle 
anabolic pathway due to low omega -3 (n-3) fatty 
acid intake. Namely, it was demonstrated that low 
level of n-3 fatty acids is associated with loss of 
muscle mass and skeletal muscle fat infiltration 
or myosteatosys.
46
 In addition, atrophy of fast type 
II muscle fibre and switch to slow type I muscle 
fibre increase the lipid deposition into the mus-
cle.
6
 Importantly, myosteatosis is associated with 
metabolic muscle disfunction and muscle function 
loss and is widespread in cancer associated mal-
nourished patients.
47,48
 A vicious cycle between 
myocytes and adipocytes is responsible for sarco-
penic obesity. Specifically, adipose tissue inflam-
mation and dysfunction leads to overproduction 
of fatty acids which in combination with low oxi-
dation capacity of skeletal muscle stimulate the 
formation of intramyocellular lipid (IMCL).
49
 This 
process blocks the translocation of glucose trans-
porter type 4 (GLUT4) to the surface of the muscle 
fiber and therefore hampers uptake of glucose by 
skeletal muscle resulting in a decrease of glucose 
utilization and increase of fatty acid oxidation in 
mitochondria, which leads to impaired insulin 
sensitivity of skeletal muscle, inhibition of mito-
chondrial respiration, increase in reactive oxygen 
species formation (ROS), myocyte toxicity, inflam-
mation and finally sarcopenia.
5,6
 Various forms 
of fat accumulation in skeletal muscle have been 
associated with insulin resistance, mitochondrial 
dysfunction and decreased muscle contracting 
force.
50
 Based on these mechanisms, myosteato-
sis is a potentially important factor in sarcopenic 
obesity in the cancer setting, which could contrib-
ute to further muscle dysfunction in sarcopenic 
obese cancer patients and is an independent pre-
dictor of reduced survival in cancer patients.
47, 51
 
Additionally, ectopic fat deposition surrounding 
muscle accelerate proteolysis in muscle tissue lead-
ing to further muscle loss and worsen outcome.
47
Another consequence of insulin resistance is 
the reduction in the uptake of amino acids by mus-
cle cells, altering the balance of protein synthesis/
degradation in favour of proteolysis. It is proposed 
TABLE 1. Selected criteria to identify sarcopenic obesity. Altered skeletal muscle function parameters considering muscle 
strength and physical performance and altered body composition parameters should be present to assess sarcopenic obesity
SCREENING DIAGNOSIS STAGES 
High BMI and WC
(based on ethnic cut-points)
Altered skeletal muscle strength  
(HGS, chair stand test)
STAGE 1: Without complications
Surrogate markers of sarcopenia:
(clinical symptoms or validated 
questionaries’ e.g. SARC-F)
Altered body composition  
(increased FM, decrease MM)
STAGE 2: One or more 
complications attributable to 
sarcopenic obesity
BMI = body mass index; FM = fat mass; HGS = hand grip strength; MM = muscle mass; SARC-F = strength, assistance in walking, rise from a chair, 
climb stairs, and falls; WC = waist circumference;

Radiol Oncol 2024; 58(1): 1-8.
Jurdana M et al. / Sarcopenic obesity and cancer 4
that the amino acids released by muscle proteoly-
sis in sarcopenia contribute to the supply of tumor 
growth.
8
Hormonal imbalances
Furthermore, cancer is associated with an altera-
tion in hormones that severely affects skeletal mus-
cle and fat metabolism.
6
 The body composition of 
cancer patients is associated with insulin, insulin 
resistance, and the hormone ghrelin, the levels of 
which are modulated in obese patients and affect 
skeletal muscle metabolism. In addition, increased 
levels of stress hormones and a decrease in andro-
gens and estrogens affect the anabolic and catabolic 
conditions for muscle protein metabolism and lead 
to alterations in the production and metabolism of 
anabolic hormones (growth hormone, insulin-like 
growth factor (IGF-1)) that may result in a sarco-
penic obese phenotype.
52,53
 Increasing insulin re-
sistance is associated with an increase in intramyo-
cellular fat mass and loss of muscle function.
54
Cytokine imbalances
The systemic inflammatory condition in sar-
copenic obesity as well as the altered expression 
of myokines and adipokines are also involved in 
carcinogenesis. Skeletal muscle and adipose tissue 
are considered endocrine organs due to release an-
ti-inflammatory myokines and pro -inflammatory 
cytokines, respectively.
55
 Myokines are proteins re-
leased by muscle cells in response to contractions. 
They play autocrine, paracrine, and endocrine roles 
in many exercise-induced adaptations (e.g., muscle 
hypertrophy and cancer protection).
55,56
 The re-
lease of pro- and anti-inflammatory cytokines by 
adipose and muscle tissue has a strong influence 
on skeletal muscle and adipose tissue metabolism 
and is involved in various cancer related changes 
in body composition.
5
 Dysregulation of pro- and 
anti-inflammatory cytokines is responsible for 
muscle intracellular adipose tissue. They contrib-
ute to the secretion of myostatin a negative regu-
lator of muscle mass secreted by skeletal muscle 
cells, tumor necrosis factor –α (TNF- α), proin-
flammatory interleukin -6 (IL-6), interleukin -1β 
(IL-1β), mononuclear chemoattractant protein-1 
(MCP-1), and downregulate the secretion of anti-
inflammatory adiponectin, leading to lipotoxic-
ity and insulin resistance.
8,37 ,57-59
 Inflammatory 
cytokines directly affect skeletal muscle and accel-
erate muscle proteins degradation and apoptosis 
and induces muscle tissue reduction and fat tissue 
accumulation.
5,6,8
 Levels of IL -6 and TNF- α are 
further increased by the hormone leptin, reduc-
ing the anabolic pathway of IGF-1 and enhancing 
lipotoxicity. The cytokine-like hormone leptin is 
a classic adipokine that is secreted by adipocytes, 
its blood concentration correlates with triglyceride 
accumulation in adipocytes.
60
 In addition to this, 
the impaired secretion of skeletal muscle anti-in-
flammatory myokines such as interleukin -15 (IL-
15), irisin, muscle derived IL-6 accelerate muscle 
atrophy and disfunction.
8,56,59,61
 
All these cytokines are known to be involved in 
several cancer induced alteration of body compo-
sition.
62
 Altered fat metabolism promotes inflam-
mation, having an important role in cancer and 
non-cancer muscle wasting
63
 creating a vicious 
cycle for sarcopenic obesity, leading to morbidity 
and mortality.
Sarcopenic obesity and carcinogenesis, there-
fore, are mediated by mechanisms, such as insu-
lin resistance, adiposity, proteolysis, myosteatosis, 
inflammation, oxidative stress, imbalance of adi-
pokines and myokines (Figure 1).
Therapeutic strategies
Patients with cancer and sarcopenic obesity have 
several specific adverse clinical outcomes, includ-
ing higher risk of dose-limiting toxicity, surgical 
complications, prolonged hospitalisation, physi-
cal disability, and shorter survival. This was dem-
onstrated for several cancers.
6
 Chemotherapy has 
been shown to alter body composition by reducing 
lean mass, thus favouring the development of sar-
copenic obesity.
64
 Low muscle mass and strength is 
common in any cancer stage and is clearly consid-
ered an independent predictor for cancer progres-
sion, making it a preferred target in the treatment 
of sarcopenic obesity. On the other hand, obesity 
is not univocally associated with worse outcome 
in cancer patients regardless of the cancer type.
65
 
Although obesity is considered an important risk 
factor for the development of various cancers, the 
presence of moderate obesity paradoxically ap-
pears to be a protective factor that may improve 
response to treatment and consequently survival in 
patients but there are conflicting and controversial 
results.
66
Several therapeutic strategies, exercise and nu-
tritional exists to counteract sarcopenic obesity. 
Prado et al. have shown that poor nutritional sta-
tus in cancer is primarily manifested by a severe 
loss of muscle mass, which can occur at any stage 

Radiol Oncol 2024; 58(1): 1-8.
Jurdana M et al. / Sarcopenic obesity and cancer 5
(from curative to palliative treatment) and often 
co-exists with obesity. They have addressed the 
role of diet in preventing and reversing sarcopenia 
in cancer patients, which may also apply to sar-
copenic obesity.
67
 Nutritional strategies comprise 
the importance of adequate intake of macro- and 
micronutrients, including high-quality proteins, 
branched-chain amino acids (leucine), β-hydroxy-
β-methylbutyrate, glutamine, carnitine, creatine, 
fish oil/eicosapentanoic acid (EPA and DHA), vi-
tamins/minerals (e.g., vitamin D), and multimodal 
approaches (diet, exercise, and medications) to 
counteract low muscle mass in cancer.
Moreover, physical activity could be an impor-
tant and effective treatment strategy to reverse 
sarcopenia by promoting insulin sensitivity, re-
ducing oxidative stress and inflammation, and 
stimulating mitochondrial biosynthesis. Both re-
sistance training and aerobic exercise have been 
shown to improve muscle mass and physical per-
formance.
68,69
 We note that standard treatment 
recommendations derived from studies in the el-
derly and certain diseases may not be applicable 
to cancer patients due to fatigue or pain. However, 
many intervention studies of physical activity in 
cancer indicate some benefit of exercise for mus-
cle strength and endurance.
70
 In addition, cancer 
obese individuals, who exercise more and are not 
insulin resistant or hypertensive might then have 
a lower mortality risk.
8
Another effective treatment for sarcopenic obe-
sity in older adults and cancer patients is skeletal 
muscle electrostimulation. It causes contraction 
of muscle fibres via neuromuscular activation 
and can induce a change in body composition.
71
 
Whole-body vibration therapy has been shown to 
significantly increase muscle strength and func-
tion in older adults.
72
 Further clinical studies are 
needed to verify its efficacy in clinical practise.
Conclusions
The prevalence of sarcopenic obesity is considered 
a novel factor of great clinical relevance in cancer 
patients, leading to postoperative complications, 
worse functional status, and shorter survival pos-
sibly mediated by interactions among patho-
SARCOPENIC OBESITY
Aging
Obesity
Physical in ac�vity
Muscle mass and strenght
An �-in flammatory myokines
GLUT 4
IGF
IMCL
Fat mass, visceral fat
In flammatory cytokines
Lep �n
Adiponec �n
Cancer
In flammatory cytokines
Inadequate food intake
Fa �gue
Physical ac�vity and mobility
Myokine de ficiency
Proteolysis Insuline resistance
In flamma �o n Oxida �ve stress
Lipotoxicity
Myosteatosis
SKELETAL MUSCLE ATROPHY AND DISFUNCTION
MORTALITY
..
FIGURE 1. Main pathophysiological mechanisms in cancer patients with sarcopenic obesity. Body composition (low skeletal muscle mass and 
strength, increase in fat mass), inflammation, insulin resistance, myosteatosis, myokine dysregulation, and oxidative stress in sarcopenic obese 
cancer patients significantly induce muscle proteolysis, leading to muscle wasting and dysfunction and premature mortality.

Radiol Oncol 2024; 58(1): 1-8.
Jurdana M et al. / Sarcopenic obesity and cancer 6
physiological mechanisms (inflammation, insulin 
resistance, dysregulation of myokines and pro-
inflammatory cytokines). Specific prevention and 
treatment strategies are needed to address sarco-
penic obesity in cancer patients. One of the major 
challenges in prevention strategies is to maintain 
skeletal muscle mass and function and reduce fat 
mass, because the combination of decreasing skel-
etal muscle mass and increasing fat mass leads to 
physical limitations that worsen the prognosis for 
chronic disease, including cancer. Exercise and 
proper nutrition are two key components in the 
prevention and treatment of sarcopenic obesity, 
but effective interventions should be explored for 
cancer patients.
3,4,6,56,73
 The key question is how to 
maintain muscle anabolism in an energy deficit 
situation to avoid a high percentage of weight loss 
in the form of lean mass in this muscle loss prone 
population. 
The underestimated prevalence of sarcopenic 
obesity in cancer are the consequence of the lack of 
standard methods and definitions used in previ-
ous studies. Therefore, further studies need to fo-
cus on screening sarcopenic obesity in cancer pa-
tients, and additional studies are needed to clarify 
the pathogenesis of sarcopenic obesity, with em-
phasis on identifying new markers. 
In conclusion, the development of standard-
ised diagnostic criteria is urgently needed. Up to 
now the identification of sarcopenia by measuring 
muscle mass and strength as a physical function 
has been done only in few studies, while in all oth-
ers muscle mass was used as the only criteria. 
ESPEN and EASO have launched an initiative to 
reach expert consensus on diagnostic procedures 
that include an assessment of skeletal muscle func-
tion followed by an assessment of body composi-
tion. Individuals with sarcopenic obesity should 
be classified into stages 1 and 2 based on clinical 
complications associated with body composition 
or muscle dysfunction. The proposed definition 
should be implemented in routine clinical practice. 
In addition, validation and prospective follow-up 
studies and secondary analyses of existing co-
horts are proposed and encouraged by ESPEN and 
EASO.
9
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