Clinical Nutrition 29 (2010) 154159

Contents lists available at ScienceDirect

Clinical Nutrition
journal homepage: http://www.elsevier.com/locate/clnu

Opinion Paper

Consensus denition of sarcopenia, cachexia and pre-cachexia: Joint document

elaborated by Special Interest Groups (SIG) cachexia-anorexia in chronic wasting
diseases and nutrition in geriatrics
M. Muscaritoli a, *, n, S.D. Anker b, n, J. Argiles c, n, Z. Aversa a, n, J.M. Bauer d, o, G. Biolo e, n, Y. Boirie f, o,
I. Bosaeus g, o, T. Cederholm h, o, P. Costelli i, n, K.C. Fearon j, n, A. Laviano a, n, M. Maggio k, o,
F. Rossi Fanelli a, n, S.M. Schneider l, o, A. Schols m, n, C.C. Sieber d, o
a

Department of Clinical Medicine, La Sapienza, University of Rome, Viale dellUniversita, 37, Rome 00185, Italy
Department of Cardiology, Charite Medical School, Campus Virchow-Klinikum, Berlin, Germany
c
Departament de Bioqumica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
d
Department of Geriatric Medicine, University of Erlangen-Nuremberg, Erlangen, Germany
e
Department of Medical, Technological and Translational Sciences, Division of Internal Medicine, Molecular Medicine, AOUTS, University of Trieste, Italy
f
INRA, Centre Clermont-Ferrand-Theix, UMR 1019, Unite de Nutrition Humaine, CRNH Auvergne, Clermont-Ferrand, France
g
Department of Clinical Nutrition, Sahlgrenska University Hospital, Sahlgrenska Academy at University of Gothenburg, Goteborg, Sweden
h
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden
i
Department of Experimental Medicine and Oncology, University of Turin, Turin, Italy
j
Clinical and Surgical Sciences (Surgery), The Royal Inrmary of Edinburgh, University of Edinburgh, Edinburgh, Scotland, UK
k
Department of Internal Medicine and Biomedical Sciences, Section of Geriatrics, University of Parma, Parma, Italy
l
Gastroenterologie et Nutrition Clinique, INSERM U907, Universite de Nice Sophia-Antipolis, Nice, France
m
Department of Respiratory Medicine, University of Maastricht, Maastricht, The Netherlands
b

a r t i c l e i n f o

s u m m a r y

Article history:
Received 4 December 2008
Accepted 9 December 2009

Chronic diseases as well as aging are frequently associated with deterioration of nutritional status, loss
muscle mass and function (i.e. sarcopenia), impaired quality of life and increased risk for morbidity and
mortality. Although simple and effective tools for the accurate screening, diagnosis and treatment of
malnutrition have been developed during the recent years, its prevalence still remains disappointingly
high and its impact on morbidity, mortality and quality of life clinically signicant. Based on these
premises, the Special Interest Group (SIG) on cachexia-anorexia in chronic wasting diseases was created
within ESPEN with the aim of developing and spreading the knowledge on the basic and clinical aspects
of cachexia and anorexia as well as of increasing the awareness of cachexia among health professionals
and care givers. The denition, the assessment and the staging of cachexia, were identied as a priority
by the SIG. This consensus paper reports the denition of cachexia, pre-cachexia and sarcopenia as well
as the criteria for the differentiation between cachexia and other conditions associated with sarcopenia,
which have been developed in cooperation with the ESPEN SIG on nutrition in geriatrics.
2009 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Keywords:
Chronic diseases
Aging
Pre-cachexia
Cachexia
Anorexia
Sarcopenia

1. Introduction
The close association between chronic illnesses and the deterioration of nutritional status, impaired quality of life and increased
risk for morbidity and mortality has been long recognised.1 Indeed,
as early as in the third century B.C., the Greek physician Hippocrates
from Koos very neatly described the wasting syndrome associated

* Corresponding author. Tel.: 39 6 445 2929; fax: 39 6 446 1341.

E-mail address: maurizio.muscaritoli@uniroma1.it (M. Muscaritoli).
n
SIG cachexia-anorexia in chronic wasting diseases.
o
SIG nutrition in geriatrics.

with terminal disease: The esh is consumed and becomes water,.

the abdomen lls with water, the feet and the legs swell, the shoulders,
clavicles, chest and thighs melt away. This illness is fatal.2
The spectrum of metabolic and nutritional abnormalities
secondary to chronic diseases is indeed wide and multifactorial in
origin.3,4 Consensus exists, however, that the pathogenesis of
malnutrition shares analogies and bear diversities among the
causative underlying conditions.5 The progressive knowledge of the
negative impact of malnutrition on patients prognosis has led to
the development of simple but effective tools which allow for the
accurate screening, diagnosis and treatment of malnutrition.6,7 This
notwithstanding, the prevalence of malnutrition in hospital and the

0261-5614/$ see front matter 2009 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
doi:10.1016/j.clnu.2009.12.004

M. Muscaritoli et al. / Clinical Nutrition 29 (2010) 154159

community still remains disappointingly high,1,8 underdiagnosed

and frequently left untreated until extreme pictures may develop,
which are currently referred to as cachexia, cachectic states or
severe wasting. On the other hand, it is well recognized that such
advanced clinical pictures are scarcely responsive to the available
nutritional and pharmacological treatments,9,10 suggesting that
once a critical point is reached, the complex interplay between
underlying disease, metabolic alterations and reduced availability
of nutrients will eventually and ineluctably cause the patients
death. This underscores the urgent need for the development of
early and effective interventions aimed at preventing rather than
treating those abnormalities ultimately leading to the clinical
picture of cachexia.
Based on these premises, in 2005, the Special Interest Group
(SIG) on cachexia-anorexia in chronic wasting diseases was created
within ESPEN. The main aims of this SIG are the development and
diffusion of knowledge on the basic and clinical aspects of cachexia
and anorexia. The secondary aims are to increase the awareness of
cachexia among health professionals and caregivers and to develop
clinical guidelines for the prevention/treatment of cachexia. This
would ultimately allow to promote appropriate interventions at the
institutional and political levels.
The denition, the assessment and the staging of cachexia, was
identied as a priority by the SIG. The lack of a simple and
commonly accepted denition for cachexia still represents a main
clinical issue, leading to clinically relevant mistakes, lack or delay in
identication, inadequate prevention and frequently ineffective
treatments.
This consensus paper reports the denition of cachexia and precachexia. Moreover, the criteria for the differentiation between
cachexia and other conditions associated with sarcopenia (i.e. loss
of muscle mass) are reported, which have been developed in
cooperation with the ESPEN SIG on nutrition in geriatrics.
The SIG nutrition in geriatrics was created in 2006 to focus on
nutritional disorders of specic relevance for the elderly. Agerelated sarcopenia is a concept that describes the loss of muscle
mass and muscle strength associated with aging. In its advanced
stages it causes disability and dependence. In order to implement
diagnostic and therapeutic strategies, a denition for this entity is
urgently needed. For that purpose, the SIG joined forces with the
SIG on cachexia-anorexia in chronic wasting diseases for a common
ESPEN position paper.

2. How to dene sarcopenia?

The term sarcopenia is derived from the Greek words sarx (esh)
and penia (poverty). Sarcopenia is a condition characterized by loss
of muscle mass and muscle strength.11,12 Muscle accounts for 60% of
the bodys protein stores. Muscle mass decrease is directly
responsible for functional impairment with loss of strength,
increased likelihood of falls, and loss of autonomy.13,14 Respiratory
function is also impaired with a reduced vital capacity.15 During
a metabolic stress situation muscle protein is rapidly mobilized in
order to provide the immune system, liver and gut with amino
acids, especially glutamine. The sarcopenic subject has a decreased
availability of such protein depotes.16 Although sarcopenia is
primarily a disease of the elderly.17 its development may be associated with conditions that are not exclusively seen in older
persons, like disuse, malnutrition and cachexia (Figure 1). Like
osteopenia, it can also be seen in younger patients such as those
with inammatory diseases.18 The loss of muscle mass and muscle
strength caused by such conditions is usually functionally less
relevant in younger individuals, as their muscle mass and muscle
strength is higher before it is affected by these conditions.

155

Fig. 1. Conditions potentially leading to sarcopenia. Sarcopenia can be observed at

any age resulting from inammatory diseases, malnutrition, disuse or endocrine
disorders. These conditions may act as accelerants of underlying causes of age-related
sarcopenia.

3. What is age-related sarcopenia?

Age-related sarcopenia is the loss of muscle mass and muscle
strength that is associated with aging.11,12 Features of sarcopenia
include: decreased muscle mass and cross-sectional area, inltration of muscle by fat and connective tissue, decrease of type 2 ber
size and number, but also of type 1 bers, accumulation of internal
nuclei, ring bers and ragged bers, disarrangement of myolaments and Z-lines, proliferation of the sarcoplasmic reticulum and
t-tubular system, accumulation of lipofuscin and nemaline rod
structures and decreased number of motor units.19 The pathophysiology of sarcopenia in the elderly is complex. There is
a multitude of internal and external processes that contribute to its
development. With regard to internal processes the most important inuences are reductions of anabolic hormones (testosterone,
estrogens, growth hormone, insulin like growth factor-1), increases
of apoptotic activities in the myobers, increases of proinammatory cytokines (esp. TNF-a, IL-6), oxidative stress due to
accumulation of free radicals, changes of the mitochondrial function of muscle cells and a decline in the number of a-motoneurons.20 Among external inuences a decient intake of energy and
protein will contribute to loss of muscle and function. Reduced
intake of vitamin D has been associated with low functionality in
the elderly. Acute and chronic co-morbidities will also contribute to
the development of sarcopenia in older persons. Co-morbidities
may on one hand lead to reduced physical activity and periods of
bedrest, and on the other hand to increased generation of proinammatory cytokines that play important triggering roles for
proteolysis (see cachexia). Obviously there are considerable overlaps between cachexia and sarcopenia in older patients. Therefore,
it may be impossible to distinguish which component is the most
relevant in the individual patient.
4. How to diagnose sarcopenia?
Diagnosis of sarcopenia is based on the combined presence of
the two following criteria:
I. A low muscle mass, i.e. a percentage of muscle mass 2
standard deviations below the mean measured in young adults of
the same sex and ethnic background.
Subjects aged 1839 years in the 3rd NHANES population13
might be used as reference. The suggested T-score-based diagnosis
of sarcopenia relates closely to the diagnosis of osteoporosis. Like

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M. Muscaritoli et al. / Clinical Nutrition 29 (2010) 154159

for osteopenia/osteoporosis, much needed reference values in

various populations, based on ethnicity, age, sex and location, will
help us to specify more accurately the diagnosis in the future.
II. Low gait speed, e.g. a walking speed below 0.8 m/s in the 4-m
walking test.21
However, it can be replaced by one of the well-established
functional tests utilized locally as being part of the comprehensive
geriatric assessment.
5. How to dene cachexia?
` s (bad)
The term cachexia is derived from the Greek words kako
and hexis (condition). Cachexia may be dened as a multifactorial
syndrome characterized by severe body weight, fat and muscle loss
and increased protein catabolism due to underlying disease(s).
Cachexia is clinically relevant since it increases patients morbidity
and mortality. Contributory factors to the onset of cachexia are
anorexia and metabolic alterations, i.e. increased inammatory
status, increased muscle proteolysis, impaired carbohydrate,
protein and lipid metabolism. The Cachexia Society has recently
made available a clinical denition of cachexia.22 These Special
Interest Groups agree with this denition and are promoting its
clinical application. However, considering the wide range of clinical
manifestations of cachexia, a staging of this syndrome is warranted.
5.1. Does inammation have a role in the pathogenesis of cachexia?
Yes. Systemic inammation is a common feature of chronic
diseases.23 Inammation does play a pivotal role in the pathogenesis of cachexia and its presence allows for cachexia identication.3,24 An imbalance between proinammatory (e.g. tumor
necrosis factor-a [TNF-a], interleukin-1 [IL-1], interleukin-6 [IL-6],
interferon-g [IFN-g]) and antiinammatory (e.g. IL-4, IL-12, IL-15)
cytokines25 is currently believed to contribute to cachexia. Moreover, high levels of IL-6 correlate with high C-reactive protein (CRP)
values and concomitant body weight loss.26,27
5.2. Is there a difference between cachexia and malnutrition?
Yes. Cachexia is to be considered the result of the complex
interplay between underlying disease, disease-related metabolic
alterations and, in some cases, the reduced availability of nutrients
(because of reduced intake, impaired absorption and/or increased
losses, or a combination of these). Malnutrition is a state of nutrition in which a deciency or excess (or imbalance) of energy,
protein, and other nutrients causes measurable adverse effects on
tissue/body form (body shape, size and composition) and function,
and clinical outcome.28,29 Reduced nutrient availability, however,
may be a component of and play a role in the pathogenesis of
cachexia. Indeed, it is noteworthy that while not all malnourished
patients are cachectic, all cachectic patients are invariably
malnourished.5
5.3. What is anorexia and what is its role in cachexia?
Anorexia is dened as the reduced desire to eat. Unlike anorexia
nervosa, secondary (i.e. disease-related) anorexia is a rather
common symptom, and frequently accompanies chronic diseases.10
The pathogenesis of secondary anorexia is complex and multifactorial and is believed to result from inammation-driven resistance
of the hypothalamus to appropriately respond to orexigenic (i.e.
appetite stimulating) and anorexigenic (i.e. satiety stimulating)
signals. Anorexia and reduced food intake are frequently underdiagnosed and may signicantly contribute to the nutritional

deterioration of cachexia, if not properly treated either pharmacologically or nutritionally.30

5.4. How to diagnose the presence of anorexia?
Anorexia is clinically dened as the reduction/loss of appetite.31
Based on this denition, the presence of anorexia is generally investigated by assessing whether patients report a subjective reduction of
appetite. This simple qualitative assessment identies patients at
higher risk of complications in different clinical settings.32,33 A more
objective evaluation of appetite loss could be obtained by simultaneously providing patients with a visual analogue scale, either
anchored or not anchored, although its specic and autonomous
relevance for diagnosing anorexia is limited unless a reference value
obtained in age- and sex-matched healthy individuals is available for
comparison.
In cancer patients, specic tools to diagnose anorexia have been
developed, mainly based on a comprehensive assessment of
appetite and appetite-related symptoms. The most frequently used
are the Functional Assessment of Anorexia/Cachexia Therapy
(FAACT) questionnaire and the North Central Cancer Treatment
Group (NCCTG) Anorexia/Cachexia questionnaire. Both tools
provide a qualitative and quantitative assessment of anorexia in
cancer patients. The FAACT questionnaire has been validated to
assist clinicians in testing the efcacy of anti-anorexia/cachexia
therapies.34 The questionnaire is divided into ve sections and
comprehends 39 items, 12 of which directly related to nutritional
issues, including appetite. Similarly, the NCCTG Anorexia/Cachexia
questionnaire includes 15 items, 10 of which directly related to
nutritional issues, including appetite.35 Similar questionnaires
providing a qualitative and quantitative assessment of appetite are
also available for patients with chronic renal failure.36
Disease-associated anorexia results from a number of symptoms
which are related to changes in the physiological mechanisms
controlling eating behavior, but depression and psychological
discomfort, as well as pain and difculty in swallowing, may well be
involved in its pathogenesis. Although it is acknowledged that the
clinical consequences are the same, i.e. reduced food intake and
weight loss, it could be clinically relevant trying to distinct the
anorexia secondary to psychological distress and dysphagia from
that secondary to altered brain neurochemistry, in order to develop
more specic therapies. A number of symptoms have been identied contributing to the development of anorexia, including nausea/
vomiting, meat aversion, early satiety, changes in taste and smell,
and it has been proposed that patients reporting at least one of
these symptoms could be dened as anorexic.37 Although this
symptom-based questionnaire is not widely utilized, a number of
studies in different clinical settings showed that this diagnostic
approach is able to identify patients with deteriorated nutritional
status and likely altered brain neurochemistry which is compatible
with deranged control of eating behavior.3840 Also, early satiety
per se has been demonstrated to represent a robust predictor of
worse outcome in cancer patients.41 More studies are needed to
strengthen the reliability of the symptom-based questionnaire in
identifying anorexic patients and predicting clinical outcomes.
6. Why is the staging of cachexia necessary?
One of the innovative aspects of the present re-appraisal of
cachexia in chronic diseases is the attempt to stage cachexia. The
SIGs felt the staging of cachexia as necessary, based on a number of
reasons that are listed below:
(a) late-stage cachexia is substantially untreatable with currently
available tools42;

M. Muscaritoli et al. / Clinical Nutrition 29 (2010) 154159

(b) increasing the awareness of conditions potentially leading to

cachexia is mandatory;
(c) staging may facilitate identication of early markers of
cachexia;
(d) there is emerging consensus that preventative rather than
therapeutic strategies for cachexia are warranted9;
(e) there is not linear time course between early-stage and latestage cachexia;
(f) staging may support the pursue of good timing and treatment
modalities.
The SIGs also agreed that the staging of cachexia into many
grades might generate confusion among health professionals and
caregivers, potentially leading to delayed diagnosis. Therefore it
was nally proposed that cachexia should be graded into cachexia
(see paragraph #5) and pre-cachexia.

7. How to dene pre-cachexia?

Pre-cachexia is dened based on the presence of all the
following criteria:
(a) underlying chronic disease;
(b) unintentional weight loss 5% of usual body weight during the
last 6 months;
(c) chronic or recurrent systemic inammatory response;
(d) anorexia or anorexia-related symptoms.
Pre-cachexia includes therefore patients with a chronic disease,
small weight loss, a chronic or recurrent systemic inammatory
response and anorexia. Inammation is indicated by elevated
serum levels of inammatory markers like C-reactive protein.43,44
Early metabolic alterations (e.g. impaired glucose tolerance
according to an oral glucose tolerance test,45,46 anaemia related to
inammation or hypoalbuminemia) may also be present in
pre-cachexia. A decreased spontaneous food intake, i.e. anorexia is
revealed by visual analogue scales, specic questionnaires30 and/or
reduced nutrient intake below <70% estimated needs. In particular,
the section AC/S-12 of the FAACT questionnaire assesses anorexiarelated symptoms and differentiates their severity by assigning
a score ranging from 0 to 4.34 Therefore, it could be proposed that
a score 24 may be sufcient to make diagnosis of anorexia
(see Table 1).
Table 1
Symptom-based assessment of anorexia (adapted from AC/S-12 of FAACT
questionnaire).

I have a good appetite

The amount I eat is sufcient to
meet my needs
I am worried about my weight
Most food tastes unpleasant to me
I am concerned about how thin
I look
My interest in food drops as soon
as I try to eat
I have difculty eating rich or
heavy foods
My family or friends are
pressuring me to eat
I have been vomiting
When I eat, I seem to get fully
quickly
I have pain in my stomach area
My general health is improving

Not
at all

A little
bit

Somewhat

Quite
a bit

Very
much

0
0

1
1

2
2

3
3

4
4

0
4
4

1
3
3

2
2
2

3
1
1

4
0
0

4
4

3
3

2
2

1
1

0
0

4
0

3
1

2
2

1
3

0
4

157

Pre-cachexia denition will allow for large multicenter

epidemiological and intervention studies aimed at preventing or
delaying changes in body composition and nutritional complications linked to chronic diseases. The diseases potentially associated
to pre-cachexia are listed in Table 2.
8. Is cachexia associated with changes in body composition?
Yes. One of the hallmark of cachexia is loss of body weight,
which is brought about by loss of both lean and fat mass.47 In
advanced cachexia, water retention may occur as a consequence of
severe hypoalbuminemia. The water retention may then account
for an increase in body weight in spite of severe body wasting.48
The same may occur in patients with severe heart failure, liver
cirrhosis or renal failure, in whom loss of body weight may be
obscured by uid retention.49
Loss of skeletal muscle mass should be considered the most
clinically relevant phenotypic feature of cachexia, irrespective of
the underlying causative illness. Progressive skeletal muscle loss
has negative clinical consequences on muscle strength, respiratory
function,50 functional status, disability risk and quality of life.51 The
imbalance between anabolic and catabolic rates within muscle is
responsible for accelerated muscle loss, with increased muscle
protein degradation playing the prominent role.52 Systemic
inammation is believed to be causally involved in the derangement of the whole muscular machinery typical of cachexia, but
hormones,5355 tumor-derived factors such as proteolysis-inducing
factor (PIF),56 bedrest and inadequate nutrient intake48 may
contribute as well.
Muscle loss is not specic for cachexia. Aging,57 starvation and
malnutrition,58 bedrest, prolonged physical inactivity,59 denervation, space ight60 are also associated with relevant segmental or
systemic skeletal muscle atrophy. Cachexia must therefore be
distinguished from other forms of muscle depletion, in particular
age-related sarcopenia.
9. Can an obese person be dened as pre-cachectic?
Within the frame of our denition of pre-cachexia, muscle
wasting may be frequently observed in obese or overweight
patients exhibiting unintentional weight loss and systemic
inammatory response due to underlying disease, such as cancer.61
These patients exhibit signicant muscle loss despite fat mass is
still increased. This condition is therefore dened as sarcopenic
obesity. The current denition of obesity is anthropometric and
based on body mass index and does not take into account body
composition, i.e. fat-free mass and fat mass. On the other hand,
sarcopenia itself refers to body composition. Thus, sarcopenic
obesity is currently dened by increased body mass index associated with depleted lean body mass and function.62 Nonetheless,
sarcopenic obesity, as anthropometric denition, is not necessarily
the same as cachexia or pre-cachexia in an obese person because it
is not necessarily associated with a specic disease state, since it
may be the consequence of insulin resistance,63 physical inactivity
Table 2
Chronic diseases associated with pre-cachexia and cachexia.








Cancer
COPD
Chronic heart failure
Chronic renal failure
Liver failure
AIDS
Rheumatoid arthritis

See ref.

70

and

71

for review.

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M. Muscaritoli et al. / Clinical Nutrition 29 (2010) 154159

and overfeeding,64 as it may be frequently observed in aging.62

Conversely, our denitions of pre-cachexia and cachexia imply the
presence of specic disease-related mechanisms, in turn responsible for progressive body wasting. Thus, an obese patient with
underlying disease and unintentional 5% weight loss, may well be
pre-cachectic, despite his still elevated BMI value. Diagnosis of precachexia may indeed be particularly difcult in obese patients
because an increase in fat mass may obscure a loss of lean body
mass.65 These patients therefore carry the risk of null or delayed
appropriate metabolic intervention.

10. Is it possible to differentiate cachexia from other

sarcopenic conditions?
Not always. Loss of muscle mass is a feature of cachexia, whereas
most sarcopenic subjects are not cachectic. Persons with no weight
loss, no anorexia, no measurable systemic inammatory response
may well be sarcopenic. Sarcopenia may be accelerated after an
acute inammatory stress, and may also involve, in the elderly,
a low-grade systemic inammatory response or insulin resistance.6668 However, none of these inammatory conditions match
the denition of cachexia. As inammation is a key feature of
cachexia, one can expect a treatment of cachexia to at least partially
improve cachexia-related sarcopenia.

11. Conclusion
A universally accepted denition of the clinical syndrome of
cachexia would represent a major achievement in clinical medicine,
allowing for early recognition, prevention and timely-appropriate
treatment of this devastating condition. Cachexia has been long
considered a late and ineluctable event complicating the natural
history of many chronic diseases such as cancer, chronic heart
failure, COPD, chronic renal failure, etc. Moreover, the negligible
response of cachexia to available pharmacological and nutritional
interventions has lead to the misconception that the complex
metabolic picture of cachexia is uniquely amenable to palliative
care. However, recent clinical and experimental evidences clearly
indicate that those mechanisms ultimately leading to the severe
wasting of cachexia are operating early during the natural history of
disease, suggesting that appropriate interventions might be effective in preventing or delaying the onset of this syndrome. Consistently with the progressive knowledge of its biochemical and
molecular mechanisms, the role of nutritional impairment in
cachexia has become increasingly clear. This underscores the need
for appropriate combined interventions (pharmacological and
nutritional) to prevent the evolution of pre-cachexia into
cachexia.69 In this respect, the staging of cachexia has major practical implications since it may help in the better denition of
screening and intervention plans. Urgent next steps are to undertake longitudinal observational studies to conrm the diagnostic
and predictive accuracy of the suggested pre-cachexia criteria, as
well as to design the targeted interventional studies.
Moreover, with this document we put forward a denition and
diagnostic criteria for age-related sarcopenia comprised by the
combined presence of muscle mass loss and reduced muscle
strength. The condition responds readily to resistance training. In
addition, new nutritional and pharmacological treatment options
are under way.
The next aim of the Special Interest Groups is to devise practical
guidelines for the prevention, diagnosis and treatment of cachexia
of chronic diseases and sarcopenia. A mission that will entirely rely
on the work performed so far.

Conict of interest statement

None declared.
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