Nutrition 24 (2008) 443– 450

www.elsevier.com/locate/nut
Applied nutritional investigation

Cancer cachexia: Measured and predicted resting energy expenditures

for nutritional needs evaluation
Gyasi Johnson, M.S.a, Agnès Sallé, M.Db, Gérard Lorimier, M.D.c,
Laurent Laccourreye, M.D.d, Bernard Enon, M.D.e, Vincent Blin, M.D.e,
Yann Jousset, M.D.e, Jean-Pierre Arnaud, M.D.f, Yves Malthièry, M.D.a,
Gilles Simard, M.D.a, and Patrick Ritz, M.D.a,b,*
a
Institut National de la Santé et de la Recherche Médicale, Unité 694, Université d’Angers; Laboratoire de biochimie et biologie moléculaire, Centre
Hospitalier Universitaire, Angers, France
b
Pôle des maladies métaboliques et médecine interne, Centre Hospitalier Universitaire, Angers, France
c
Centre régional de lutte contre le cancer Paul Papin, Angers, France
d
Pôles des spécialité et des neurosciences, Centre Hospitalier Universitaire, Angers, France
e
Pôle thorax-vaisseaux, Centre Hospitalier Universitaire, Angers, France
f
Pôle digestif, Centre Hospitalier Universitaire, Angers, France

Manuscript received September 13, 2007; accepted January 21, 2008.

Abstract Objective: Cancer cachexia is associated with weight loss, poor nutritional status, and systemic
inflammation. Accurate nutritional support for patients is calculated on resting energy expenditure
(REE) measurement or prediction. The present study evaluated the agreement between measured
and predicted REE (mREE and pREE, respectively) and the influence of acute phase response
(APR) on REE.
Methods: Thirty-six patients with cancer were divided into weight-stable (WS; weight loss ⬍2%)
and weight-losing (WL; weight loss ⬎5%) patients. Measured REE was measured by indirect
calorimetry and adjusted for fat-free mass (FFM). The Bland-Altman approach was used to assess
the agreement between mREE and pREE from the Harris-Benedict equations (HBE). Blood levels
of C-reactive protein were assessed.
Results: There was no difference in mREE between groups (WS 1677 ⫾ 273, WL 1521 ⫾ 305)
even when mREE was adjusted for FFM (WS 1609 ⫾ 53, WL 1589 ⫾ 53). In WL patients,
FFM-adjusted REE correlated with blood C-reactive protein levels (r ⫽ 0.471, P ⫽ 0.048). HBEs
tend to underestimate REE in both groups.
Conclusion: WL and WS patients with cancer had similar REEs but were different in terms of
APR. APR could contribute to weight loss through enhancing REE. In a clinical context, HBE was
in poor agreement with mREE in both groups. © 2008 Elsevier Inc. All rights reserved.

Keywords: Cancer; Weight loss; Energy expenditure; Predictive equations; Inflammatory state

Introduction
Cancer cachexia is a syndrome in which complex me-
tabolism disorders occur. It appears in about half of patients
with cancer and is associated with a poor prognosis [1].
Cancer-related cachexia is characterized by progressive
* Corresponding author. Tel.: ⫹33-241-35-4499; fax: ⫹33-241-35-
4969.
E-mail address: patrick.ritz@wanadoo.fr (P. Ritz).
weight loss from fat and skeletal muscle tissues, anorexia,
asthenia, alteration of immune functions, and dysfunction of
lipid, protein, and carbohydrate metabolisms [2,3]. Survival
of patients with cancer cachexia is related to their metabo-
lism abnormalities [4]. Cachexia leads to death in 10 –20%
of cancer cases, with death occurring owing to progressive
nutritional status degradation [5–7].
During cancer cachexia, weight loss may occur early,
even when anorexia is absent; this points out that the de-
crease of food intakes is not the sole cause of weight loss

0899-9007/08/$ – see front matter © 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.nut.2008.01.013
444 G. Johnson et al. / Nutrition 24 (2008) 443– 450

Table 1 Predicted REEs were calculated from the Harris-Benedict

Sites of tumors equations (HBEs) [30]. In addition, we evaluated the influ-
Patients ence of weight loss and APR on mREE.
Weight stable Weight losing
(n ⫽ 18) (n ⫽ 18)
Materials and methods
Tumor locations and types
Lung (non–small cell) 5 6
Gastrointestinal* (adenocarcinoma) 3 8
Subjects
Head and neck (epidermoid carcinoma) 10 4
The study population consisted of patients with clinically
* All were colon adenocarcinomas except in one weight-losing patient
who had a pancreatic adenocarcinoma.
stable cancer and solid tumor referred for surgical tumor re-
section. According to Union Internationale Contre le Cancer
criteria, all patients selected were at stage II of the disease
[8,9]. Nevertheless, cachectic patients are malnourished and (local spread). Patients were recruited consecutively in three
therefore at risk for nutrition-related problems [10]. surgery departments (lung, digestion, and ear, neck, and
Appropriate energy and nutritional support recommen- throat). Patients were referred to surgeons and included into a
dations for patients with cancer should be set on energy weight group if they had no exclusion criteria, volunteered to
expenditure estimation. Because patients with cancer and participate, and until there were 18 patients in each group.
cancer cachexia are known to present disturbed metabo- Patients were categorized as WL patients if they had lost more
lisms, it is of clinical importance to assess accurately their than their preillness body weight over the previous 6 mo and
energy requirements to avoid negative outcomes due to WS patients if they had lost less than 2% of their preillness
over- or underfeeding [11]. The calculation of total energy body weight over this period. Exclusion criteria were surgery
expenditure from the measurement of resting energy expen- within 6 mo before the study, hypo-/hyperthyroidism, any
diture (REE) enables the calculation of energy requirements other anticancer treatment, chronic renal failure, diabetes, or
and the adjustment of nutritional support. Indirect calorim- human immunodeficiency virus. No patients had ascites or
etry is the technique commonly used to assess REE [12,13]. ankle edema. The aim was to exclude any conditions that could
Unfortunately, for clinical use, these methods are impracti- interfere with energy expenditure. Thirty-six patients with can-
cal because they are expensive, time consuming, and require cer were selected and categorized into two groups according to
trained technicians. Therefore, prediction equations [14] are their degree of weight loss. Half of the group (n ⫽ 18) pre-
useful to estimate REE from easily measurable clinical sented marked weight loss and the other half was weight
variables (e.g., weight, height, age, and gender). Some of stable. Characteristic of patients are listed in Tables 1 and 2.
these equations have been adjusted for particular illnesses All patients underwent weight and height measurements, blood
known to increase energy expenditure (surgery, sepsis, acute phase protein measurements, and body composition and
trauma, burns, etc.) by including injury (or stress) factors REE assessments.
[15,16]. Furthermore, new equations have been developed The WL patients were separated in two groups according
for specific diseases [17,18]. to C-reactive protein (CRP) blood levels. One group had a
It is commonly held that patients with cancer present an mean CRP level up to the upper normal limit (10 mg/L) and
elevated REE compared with healthy persons [19 –21]. Sim- the other with a CRP mean level above 10 mg/L.
ilarly, cancer-related cachexia is widely thought to increase
REE [22–24]. Yet, this may not be the case for total energy Table 2
expenditure because physical activity level could be dimin- Cancer patient group characteristics*
ished and as a result reduce total energy expenditure [25]. Patients P (t test)†
Few studies have evaluated the difference between weight- Weight stable Weight losing
stable (WS) and weight-losing (WL) patients with cancer (n ⫽ 18) (n ⫽ 18)
[26,27] with respect to weight loss related to REE and the
Male/female 17/1 11/7
acute phase response (APR). Moreover, few have evaluated Age (y) 59.4 ⫾ 12 61.2 ⫾ 13 NS
the accuracy of predictive equations to assess REE during Height (cm) 172 ⫾ 15 170 ⫾ 9 NS
cancer-related weight loss. Weight (kg) 77.2 ⫾ 21 65.3 ⫾ 14 0.058
During cancer, the APR is thought to contribute to an BMI (kg/m2) 26.6 ⫾ 6 22.4 ⫾ 5 0.055
FFM (kg) 58.9 ⫾ 11 51.8 ⫾ 9 0.046
enhanced REE [28], which is believed to promote weight
BF (%) 22.3 ⫾ 8 19.5 ⫾ 10 NS
loss [1,24,29]. Nevertheless, these results were obtained by Skeletal muscle 37.3 ⫾ 6 37.4 ⫾ 9 NS
comparing cancer patients with non-cancer patients but not mass (%)
by comparing WL with WS patients with cancer. Weight loss (kg) 0.44 ⫾ 0.68 (0–2) 6.3 ⫾ 2.4 (4–14) ⬍0.001
Therefore, the aim of this study was to assess the agree- BF, body fat; BMI, body mass index; FFM, fat-free mass.
ment between predicted and measured REE (pREE and * Values are numbers of patients, means ⫾ SDs (ranges).
mREE, respectively) for WL and WS patients with cancer. †
Weight-losing versus weight-stable patients.
 G. Johnson et al. / Nutrition 24 (2008) 443– 450
All patients gave written informed consent. The study
was approved by the medical school ethical committee.
Measurement protocol
For each patient, height without shoes was measured to
the nearest 0.1 cm and weight was measured to the nearest
0.1 kg while wearing light clothing on a weighing scale
(SECA 901, Hamburg, Germany). REE was measured in a
thermoneutral environment by indirect calorimetry (Vmax
229, SensorMedics; Yorba Linda, CA, USA) after a fasting
period of at least 6 h by using a ventilated-hood system.
Patients rested for 30 min before measurement. The system
was calibrated before each assessment in accordance with
the manufacturer’s instructions. With the patient in the
supine position, whole-body oxygen consumption and car-
bon dioxide production were measured for at least 30 min
(including a steady-state period of at least 10 min). The
calorimetry procedure was identical for all patients.
Total body water was calculated with equations from
Segal et al. [31]: total body water (L) ⫽ 0.454796 ⫻ (height
[cm])2/Z100 ⫹ 0.139523 ⫻ weight (kg) ⫹ 3.432026, where
Z100 is impedance at 100 kHz measured by hand-to-foot
bioelectrical impedance analysis with Bodystat Quadscan
4000 (Bodystat Ltd., Doubles, Isle of Man, United King-
dom). Fat-free mass (FFM) was estimated from total body
water assuming a constant hydration level of 73.2% [32] be-
cause this equation was found to be acceptable for measuring
body composition of groups of patients with cancer [33].
Muscle mass was estimated according to the equation of
Janssen et al. [34]. Blood was obtained in the fasting state,
immediately after REE measurement. Biochemical mea-
surement on blood samples were performed by immunotur-
bimetric assays (Tina-quant, Roche Diagnostics, Mann-
heim, Germany) on a Modular system (Roche Diagnostics,
Basle, Switzerland). The APR was screened through the
measurement of blood levels of CRP. The level of albumin,
as a negative APR protein, was also assessed.
Predicted equations
The pREE was estimated from the HBEs [30] for both
groups:
Male: BMR (kcal ⁄ d) ⫽ 66.4730 ⫹ 13.7516 W
⫹ 5.0033 H ⫺ 6.7550 A
Female: BMR (kcal ⁄ d) ⫽ 655.0.955 ⫹ 9.5634 W
⫹ 1.8496 H ⫺ 4.6756 A
where BMR represents basal metabolic rate, W represents
weight, H represents height, and A represents age.
Considering that the energy cost of the disease theoret-
ically consists of the difference between mREE and pREE
[35,36], factors were calculated for each group of the study
as the ratio of their measured energy expenditure to their
predicted energy expenditure using the HBE [15].
445
Statistical analysis
All measured variables were normally distributed ex-
cepted CRP and weight loss. Variables were expressed as
mean ⫾ standard deviation. Independent-samples t tests
were used to assess differences between WL and WS pa-
tients. CRP levels and weight loss were compared with the
Mann-Whitney test. The influence of APR on REE in the
WL group was tested with Spearman’s correlation. A gen-
eral linear modeling technique (analysis of covariance) was
used for the regression analysis to adjust the association
between mREE and weight-loss status for differences in
absolute FFM between the two groups.
The Bland-Altman approach [37] was used to assess the
agreement between mREE and pREE. The trend in the
magnitude of the bias with increasing mREE was assessed
with Pearson’s correlation coefficients. We calculated the
proportion of patients with pREE within clinically accept-
able limits, i.e., mREE would fall within ⫾10% of pREE
[38]. Data were analyzed with SPSS 13.0 for Windows
(SPSS Inc., Chicago, IL, USA).
Results
Thirty-six patients (28 male, 8 female) with lung (non–
small cell), colon, or head and neck cancer (Table 1) were
selected. None received chemo- or radiotherapy.
Although body weight and body mass index tended to be
lower for WL patients, these were not statistically different
from those of WS patients (Table 2). Age and height were
similar in both groups. The absolute weight loss over the
previous 6 mo was greater for WL than for WS patients.
There was no significant difference in FFM or skeletal
muscle mass between the groups. For WL patients, CRP
levels were higher than the upper limits of the normal range
and were significantly higher than those of WS patients
(Table 3). Orosomucoid levels were significantly higher in
WL patients with cancer than in WS patients. Although
albumin levels were unchanged, transthyretin levels were
lower in WL patients.
There was no significant difference in mREE between
WL and WS patients (Table 4). When adjusted for FFM,
REE remained similar between the two groups. The pREE
calculated from the HBEs was significantly lower for WL
than for WS patients. Predicted values were lower than
mREE for both groups but this was significant only for WL
patients (⫺10%, P ⬍ 0.01). The pREE adjusted for FFM
did not statistically differ when both groups were compared.
In the WL group, CRP levels were positively correlated
to mREE (r ⫽ 0.471, P ⫽ 0.048). Moreover, mREE ad-
justed for FFM of patients with a high APR (mean CRP
⬎10 mg/L) was significantly higher (21%, P ⫽ 0.006) than
in patients with a low APR (mean CRP ⬍10 mg/L; Table 5).
The Bland-Altman approach [37] was used to assess the
level of agreement between pREE and mREE. Although the
446 G. Johnson et al. / Nutrition 24 (2008) 443– 450

Table 3 Table 5
Blood parameter levels* Measured REE of weight-losing patients with low or high APR*
Patients Normal Weight-losing patients P
range
High APR Low APR
Weight stable Weight (n ⫽ 9) (n ⫽ 9)
losing
Serum C-reactive 56.5 (19–210) 8.8 (3–17) ⬍0.001
C-reactive 6.8 ⫾ 6.5 (3–26) 32.7 ⫾ 48† ⬍10 mg/L protein (mg/L)
protein (3–210) mREE (kcal/d) 1624 ⫾ 308 1418 ⫾ 283 0.11
Orosomucoid 0.9 ⫾ 0.21 1.3 ⫾ 0.49‡ 0.44–1.2 g/L mREE ajusted for FFM 1666 ⫾ 64 1376 ⫾ 64 0.006
Transthyretin 0.26 ⫾ 0.08 0.18 ⫾ 0.06‡ 0.20–0.4 g/L (kcal · kg⫺1 · d⫺1)
Albumin 40.8 ⫾ 3 37.9 ⫾ 6 35–50 g/L
APR, acute phase response; FFM, fat-free mass; mREE, measured rest-
* Values are means ⫾ SDs (ranges). ing energy expenditure.
†
P ⬍ 0.05, weight-losing versus weight-stable patients. * Values are means ⫾ SDs (ranges).
‡
P ⬍ 0.01, weight-losing versus weight-stable patients.

patients and was not in good agreement with measured

mean bias of pREE was higher for WL (⫺150 ⫾ 203
kcal/d) than for WS (⫺91 ⫾ 191 kcal/d) patients, the mean
biases of both groups were within clinical acceptable limits
of ⫾10% of mREE (Table 6). Nevertheless, at an individual
level, pREE produced wide limits of agreement for WL
(⫺37% to 17%) and WS (⫺28% to 17%) patients with
cancer.
The HBEs predicted REE within clinical acceptable lim-
its for only 61% of WL and 56% of WS patients.
No statistically significant trend was observed in the
spread of bias with increasing REE values between pREE
and mREE for WS (r ⫽ 0.222, P ⫽ 0.377; Fig. 1a) or WL
(r ⫽ ⫺0.457, P ⫽ 0.056; Fig. 1b) patients.
Factors calculated for each group from the ratio of
mREE to pREE were 1.11 for WL patients and 1.06 for WS
patients.
Discussion
In this study, no detectable difference in mREE was
found between WS and WL patients with cancer even when
mREE was adjusted for FFM. In the WL group, high blood
levels of CRP were associated with elevated mREE or
FFM-adjusted mREE. The prediction of REE of patients
with cancer with the HBE underestimated REE in WL
values for both groups.
Acute phase response
The role of CRP as a survival predictor has been dem-
onstrated for different tumor types [39]. The CRP level was
higher in the WL group. Thus, early in the malignant dis-
ease course, the groups were distinct in terms of APR, with
WL patients demonstrating a higher CRP level (Table 3) as
previously described for advanced cancer [39].Moreover,
WL patients clearly had a higher inflammatory response
because orosomucoid levels were increased in WL com-
pared with WS patients. WL patients had a similar albumin
concentration as WS patients, but had a lower transthyretin
level, suggesting that they were calorie restricted. Because
weight loss may occur early in the development of the
tumor [40 – 42], we examined patients at the onset of weight
loss (i.e., 5–10% weight loss). Although WL patients were
not grossly undernourished, their weight loss associated
with the APR may represent early forerunners of cancer
cachexia. Our results agree with previous studies correlating
weight loss and systemic inflammatory response in patients
with cancer [29,43,44].
Measured resting energy expenditure
In our study, mREE and pREE were adjusted for FFM
because it is the main determinant of REE [45]. We ob-

Table 4 Table 6
REE values in weight-stable and weight-losing patients* Bias and limits of agreement for predicted REE versus mREE in WS
(1677 ⫾ 273 kcal/d) and WL (1521 ⫾ 305 kcal/d) cancer patients*
Patients with cancer
Patients with cancer
Weight stable Weight losing
WS WL
mREE (kcal/d) 1677 ⫾ 273 1521 ⫾ 305
mREE adjusted for FFM (kcal/d) 1609 ⫾ 53 1589 ⫾ 53 Bias (kcal/d) ⫺91 ⫾ 191 ⫺150 ⫾ 203
pREE (kcal/d) 1586 ⫾ 331 1372 ⫾ 209† Limit of agreement of mREE (%) ⫺28 to 17 ⫺37 to 17
pREE adjusted for FFM (kcal/d) 1501 ⫾ 31 1457 ⫾ 31 Patients within clinical acceptable 55.6 61.1
limits (%)
FFM, fat-free mass; mREE, measured resting energy expenditure;
pREE, predicted resting energy expenditure. mREE, measured resting energy expenditure; WL, weight-losing; WS,
* Values are means ⫾ SDs. weight-stable.
†
P ⬍ 0.05, weight-losing versus weight-stable patients. * Values are means ⫾ SDs.
 G. Johnson et al. / Nutrition 24 (2008) 443– 450 447

Fig. 1. Bland-Altman plot for difference against the mean of mREE and pREE in weight-stable patients (a) and weight-losing patients (b) showing mean
bias (large dashed lines), 95% limits of agreement (small dashed lines), and regression line (solid line). mREE, measured resting energy expenditure; pREE,
predicted resting energy expenditure.
448 G. Johnson et al. / Nutrition 24 (2008) 443– 450
served that, among WL patients with cancer, those with a
high acute phase parameter (CRP) had higher mREE and
FFM-adjusted mREE. This strongly suggests that the in-
flammatory response may contribute to hypermetabolism
and metabolism alterations seen in WL patients with cancer.
This is in accordance with the study of Falconer et al. [28]
who found an elevated REE in cachectic patients with
cancer with an APR compared with cachectic patients with
cancer without an APR. Moreover, the present correlation
between APR and REE in WL patients was observed in a
heterogeneous tumor-site group and this may be generalized
to tumor locations other than what was previously observed
in single tumor-site studies [28,43]. Hypermetabolism can
result from the energetic cost of substrate turnover such as
stimulation of the adrenergic system [46] or an alteration in
mitochondrial production of energy.
Resting energy expenditure was similar in WL and WS
patients with cancer despite their differences in weight.
Adjusted REEs (for differences in FFM) were similar, sug-
gesting that in WL patients there is no hypermetabolism that
can be seen at the whole-body level. Some degree of APR
participates in minimizing the expected difference in REE
between the two groups (WS and WL). An alternative
explanation can be that the degree of weight loss was not
enough to distinguish the two groups. Indeed, the duration
of malignancy has an impact on REE, with longer duration
of disease correlating with hypermetabolism [47,48]. Thus,
the contribution of REE to weight loss may progressively
appear along the disease course, being not significant for
patients with newly detected cancer or at weight-loss onset
but obvious in advanced cancer. WL patients may have
similar mREEs to WS patients with cancer but have differ-
ent metabolism regulations leading to tissues wasting. Fe-
aron et al. [27] observed no difference of mREE between
WS and WL patients with cancer. However, although
mREEs were similar in their study groups, WL patients with
cancer had 50 –70% higher rates of whole-body protein
turnover. If some energy costs are increased and others are
decreased, mREE at the whole-body level may not be in-
creased.
Agreement of pREE
Energy requirements of hospitalized patients are often
estimated from pREE. This estimation is usually made from
REE unadjusted for FFM because FFM is seldom assessed
in the clinical context. Therefore we evaluated the accuracy
of HBEs to predict unadjusted mREE. A good correspon-
dence of an REE-predictive method with measured values is
achieved when the bias is minimal with narrow limits of
agreement and an absence of correlation between residuals
and means of mREE and pREE. We observed that the mean
bias in each group was within clinical acceptable limits
(⫾10%). However, limits of agreement were wide, indicat-
ing a potentially poor prediction of REE for individual
patients in both groups. Although not statistically signifi-
cant, the bias observed in the WL group showed a tendency
toward underestimation of mREE with increasing REE val-
ues. The HBEs were intended to assess basal metabolism
rates of healthy persons but overestimate REE by 5–15%
[49,50] and underestimate REE in malnourished patients
[51]. Nevertheless, HBEs are still routinely used for persons
with diseases [36]. In our study, HBEs tended to underes-
timate REEs in both groups, especially in WL patients
(⫺10%). FFM is the main determinant of REE, whereas fat
mass contributes little, if any, to REE. In situations where
percentage of FFM in the body increases, an equation based
on weight underestimates true REE. In WL patients, fat
mass loss occurs first so that percentage of FFM increases.
This is reflected in the present group by the relatively low
percentage of body fat for a 60-y-old population. This un-
derestimation could be of clinical importance because en-
ergy requirements of patients may be underestimated, lim-
iting the nutritional-support positive effect. Our data agree
with previous studies in which HBEs were shown to under-
estimate REE in WS or WL patients with cancer [52,53]. In
addition, our limits of agreement for WS patients with
cancer were similar to those previously described [38].
Hence, in a clinical setting, HBEs are not suitable for REE
prediction in WL or WS patients with cancer. Indeed, for an
individual, HBE may predict an REE as much as 28 –37%
lower or 17% above mREE. Moreover, with HBE predic-
tion, only 55.6% of WS and 61.1% of WL patients were
within clinical acceptable limits.
To improve the estimation of REE with HBEs, studies
have set stress factors [15,16]. In patients with cancer, when
HBE is used with an injury factor of 1.3, REE is overesti-
mated [38]. From our data, we calculated injury factors for
WS (1.06) and WL (1.11) patients to be used with HBE. The
agreement of such a method remains be tested with a new
patient sets.
This study has limitations. We made the assumption that
lean tissue hydration was constant at 73%. Nevertheless,
changes in fluid distribution may occur in patients with
cancer and bias bioelectrical impedance analysis of body
compartments [54]. Although the patients included had
no clinical fluid abnormalities, this did not exclude subclin-
ical fluid disorders, which could represent a limitation. In
each group, gender distribution had no effect on mREE
adjusted or unadjusted for FFM (data not shown). Never-
theless, because body composition differs with gender, val-
idation of stress factors on a larger group is desirable.
In addition, mean mREEs of WS and WL patients were
statistically similar but differed by about 156 kcal/d. This is
approximately 10% of mREE and could be of clinical im-
portance. Therefore, larger samples are needed to limit
variation in body size in both groups and to provide more
statistically powerful observations. Comparison of groups
that are clearly distinct with respect to body weight, as in
early and advanced cancer stages, may reveal more discrep-
ancies.
 G. Johnson et al. / Nutrition 24 (2008) 443– 450
In conclusion, despite having a slightly lower weight,
WL patients had similar FFM-adjusted REEs, thus ruling
out a major hypermetabolism. Patients with a positive APR
had a higher REE despite similar weight loss. There was
some degree of calorie restriction in WL patients. All to-
gether, as suggested by Hansell et al. [26] and Fearon et al.
[28], REE of patients with cancer poorly contribute to weight
loss. Estimation of energy requirements with HBEs are not
recommended unless a correction factor is applied. The
proposed factor needs validation on an independent group.
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