Nutrition Care process for Oncology Patients

Nutrition Care Process
for Oncology Patients
Comunicación y Gerencia
Presented by:
Salmeh Bahmanpour
Nutritionist(PhD)
PhD’s Seminar

Agenda
Section I: Introduction
Section II: Cancer-related Malnutrition
Section III: Nutrition Care process
Section IV: Practice Recommendation
Questions & Answers

Oncology
 The term “Oncology “ is derived from
the Ancient Greek onkos (bulk, mass, or
tumor), and the suffix -logy (study ).
 Oncology is a branch of medicine that
deals with cancer.

What is Cancer ?
 Cancer is actually a cluster of more than 100
disease that arise due to an uncontrolled 1
• cellular growth
• cell signalling
• cell physiological function
• cell gene expression
• cell death
 The development of tumour from cancer cells is a
multistep process occurs in three stages1:
1) Initiation(Precancerious Cell)
2) Promotion(Precancerious Lesions)
3) Progression(a Cluster of Abnormal Cell)

Click to add Title
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•6
 An estimated 12. 6 million people were diagnosed with
cancer across the world in 2008.
 The burden of cancer will increase to 22 million new cases
each year by 2030.
 Cancer Mondial 3website provides access to various
databases source containing information on the occurrence of
cancer worldwide
• World Health organization(WHO)
• GLOBOCAN
• UICC(Union International Cancer Control)
• IARC( International Agency for Research on Cancer),
• CI5 (Cancer Incidence in Five Continents)
Cancer Statistics2

Cancer –related Malnutrition
 Malnutrition, refers to the nutritional depletion
associated with uncomplicated starvation4.
 Starvation:
• Reduce Energy Expenditure
• Preserve muscle Mass
• At the Expense of Fat Mass.
• Promptly responds to nutritional supplementation
 Cancer-related Malnutrition:
• Increase Energy Expenditure
• Accelerate in Muscle & Fat Mass Depletion.
• Minimally response to Standard Nutrition Supplement.

Cancer –related Malnutrition
 Cancer-associated nutritional depletion is usually
defined as Cancer Anorexia-Cachexia
Syndrome(CACS)1.
 The term "Cachexia' is derived from Greek words
“kakos,” (bad) and “Hexis “, (condition).
 CACS is characterized by different symptoms5:
• Anorexia& Reduced Food intake
• Wasting
• Fatigue & Astenia (a reduced daily Activity)
• Impaired immune Function.

CANCER
The prominent clinical feature of cachexia is
weight loss in adults7.
The degree of cachexia (observed weight loss
within the previous 12 months (or less)is
classifyed:
–Mild: <5 %
–Moderate: 5-10%
–Severe: >10%
Diagnostic Criteria
for Cachexia6

Stages of cancer cachexia7
There are two main factor in cancer-cachexia’s staging7:
1. The rate of ongoing loss of weight in combination
2. Depletion of body protein mass
–Weight loss ≤5%
–Anorexia
–metabolic change
–Weight loss >5% or
–BMI <20 and weight loss >2%
–Sarcopenia and weight loss >2%
–Often reduced food intake
–Systemic inflammation
–procatabolic
–not responsive to
anticancer treatment
–Low performance score
–<3 months expected
survival
Spectrum of Cachexia

Cachexia
 Two most Prominent Symptoms of CACHEXIA
are Anorexia And Wasting6.
A. Pathogenesis of Anorexia :
A-1-Peripheral factors
A-2-Brain Neurochemistry
A-3-Pro-inflammatory cytokines
A-4-Hypothalamic energy metabolism
B. Pathogenesis of wasting:
B-1-Abnormalities in Carbohydrate Metabolism
B-2-Abnormalities in Protein Metabolism
B-3-Abnormalities in Fat Metabolism
B-4-Abnormalities in ENERGY Metabolism

Pathogenesis of Anorexia:
A-1-Peripheral factors4
 Cancer Anorexia result from the resistance of
hypothalamic neurons to peripheral signals.
 Peripheral Signals are:
1. Short-term
• Decreased Ghrelin(orexigenic)
• Increased Cholecystokinin(anorexigenic)
2. Medium-term
•Increased Polypeptide YY (anorexigenic )
3. Long-tem
•Increased Leptin(anorexigenic)
•Insuline, which cooperates with leptin

A-2-Brain Neurochemistry
There are two distinct subsets of neurons within
hypothalamus , involved in regulation of food intake .
1- Anorexigenic Neurons
•pro-opiomelanocortin (POMC)
•Melatonin
2- Orexigenic Neurons
•Neuropeptide Y(NPY)
• Agouti-related protein(AgRP)

Persistent activation of POMC, which Suppress the activity
of NPY/AgRP, were seen in Cancer Cachexia8.

A-3-Pro-inflammatory cytokines4
 Tumor Necrosis Factor-a(TNF), interleukins 1,
6(IL-1,IL-6),Interferon Gamma(INF-gamma) and
Proteolysis-Inducing Factor(PIF), are responsible
for dysfunction of the melanocortin system.
Serotonin , is a suitable potential mediator of
cancer anorexia by:
I. hyperpolarized NPY/AgRP neurons
II. suppressing postsynaptic potential in POMC
neurons.

 During Cancer, increased hypothalamic IL-1 and TNF-α followed by
expression of Serotonin, occure in conjunction, yielding the inhibition of
NPY/AgRP neuronal activity8.

A-4-Hypothalamic energy metabolism4
 Fatty Acid Metabolism(anabolism/catabolism) within
hypothalamic neurons controls food intake and energy
metabolism.
 The Fatty Acid Synthase(FAS) /Malonyl-CoA pathway
could be involved in the pathogenesis of cancer anorexia,
because of :
– Up-regulation of anorexigenic Neurons
– Down-regulation of orexigenic Neurons.
 Pro-inflammatory cytokines cause an inappropriate switch
in hypothalamic neurons from fatty acid oxidation to fatty acid
synthesis, increase [malonyl-CoA] and suppress food intake.

Pathogenesis of Wasting:
B-1-Abnormalities in carbohydrate Metabolism4
Upregulation of the GLUT1 and GLUT3 .
Insulin resistance
–the release of pro-inflammatory cytokines.
Stimulation of Glycogenolysis & Gluconeogenesis.
Enhance Glycolytic pathway
–Markedly elevated in HEXOKINASE.
–Warburg effect: in the presence of oxygen glucose
metabolize to lactic acid
Increased Cori cycle activity
‫سنگ‬ ‫تمام‬ ‫شهر‬
”‫ِترا‬‫پ‬“/‫اردن‬

B-2-Abnormalities in Protein Metabolism
Skeletal muscle(actomyosin, actin and myosin) wasting is
important in the pathophysiology of cachexia and a major
cause of fatigue6.
Oxidation of Branched Chain Amino Acids (BCAAs) has
been increased9.
There are three main proteolytic pathways that are
responsible for protein catabolism in skeletal muscle4.
1) The Lysosomal system.
2) The cytosolic Calcium-regulated Calpain.
3) The ATP Ubiquitin-Proteasome pathway, the most
significant proteolytic pathway in cancer.

B-3-Abnormalities in Fat Metabolism
 Loss of adipose tissue in cancer could be the result of
impairment in the formation and development of adipose
tissue4.
 an extensive depletion of Subcatenious fat loss(lipoatrophy)
area(Trunk,Leg, and Arm)6.
 Decreased activity of lipoprotein lipase (LPL) (Decreased
lipogenesis).
 Enhanced expression and activity of Hormone Sensitive
Lipase, lead to increased lipolysis .

B-3-Abnormalities in Energy Metabolism4
There are futile energy expending cycle
include:
1.The Na+K+ATP ase transporter leakage.
2.Mitochondrial Membrane protein(UCPs) in Brown
Adipose Tissue(BAT) : which released energy as
heat instead of ATP.
3.Cori cycle (a 300 Kcal/day energy loss).
4.Pro-inflammatory cytokines (IL-6 and TNF-α
,PIF).
In cancer patients there is an uncoupling
of the balance between energy
production and energy intake in favour
of increased energy production(Heat) 4.

The majority of cancer patients (40% and 80% )
experience Wasting, Anorexia and weight loss as their
disease progresses10.
Cancer cachexia5 has been implicated in the deaths of
30–50% of all cancer patients.
The consequences of Cancer Cachexia may include
– an increased risk of complications,
–decreased response and tolerance to treatment,
–a lower quality of life,
– reduced survival,
– higher health-care costs.

What is the Oncology science look for?
 Oncology is concerned with:
• Screening efforts: of populations or the
relatives of patients.
• The diagnosis of any cancer in a person
• Therapy
• Follow-up of cancer patients after successful
treatment.
 Oncology-related nutritional issues are best
addresses within the context of Nutrition Care
process(NCP).

 The Nutrition Care Process is a systematic
approach to providing high quality nutrition
care11.
 American Dietetic Association(ADA) adopted
the NCP in 2003 as a framework for dietetics
professionals to use to support decision making
in a variety of care settings11.

 The NCP consists of four distinct,
inter-related steps11:
1) Assessment
2) Diagnosis
3) Intervention
4) Monitoring and Evaluation

Nutrition Screening
 How should patients be identified for referral to the
dietitian in order to maximise nutritional intervention
opportunities?
 Although nutrition screening is not considered part of the
Nutrition Care Process but it is a vital support to the NCP10 .
 The American Dietetics Association(ADA) and The
American Society for Parenteral and Enteral
Nutrition(ASPEN) recommend that all Cancer patients
undergoes Nutrition Screening as a component of their initial
evaluation.

Nutrition Screening
 Many nutritional screening tools generally use a
questionnaire format.
 Several nutrition screening tools have been used in
the cancer population10:
1. Malnutrition Universal Screening
Tool(MUST)
2. Mini Nutritional Assessment (MNA)
3. Nutrition Risk Screening(NRS 2002)
4. Malnutrition Screening Tool (MST)
5. Nutrition Risk intake(NRI)

Nutrition Screening Tools
 Nutrition screening tools should be
tested for their Sensitivity and
Specificity.
 Sensitivity: Ability to identify those who are at risk
of malnutrition.
 Specificity: Ability to detect those who are not at
risk of malnutrition.

Authors Objective Result
Ravasco
et al
(2003)12
Calculating Sensitivity &
Specificity
80% Sensitivity
89% Specificity
Read et
al
(2005)13
Compare the MNA against PG-
SGA
97% Sensitivity
54% Specificity
Slaviero
et al
(2003)14
Compare the MNA against
unintentional weight loss of
greater than 10% in 3 month
33% Sensitivity
90% Specificity
 Several Studies evaluated the use of the scored
Mini Nutritional Assessment(MNA) in cancer
patients

 Several Studies evaluated the use of the scored
Malnutrition Screening Tool(MST) in cancer
patients.
Ferguson et
al (1999)15
Compare the MST against PG-
SGA
100%
Sensitivity
81% Specificity
Isenring et
al
(2006)
Compare the MST against
against PG-SGA in patients
undergoing chemotherapy
100%
Sensitivity
92% Specificity
 The Malnutrition Screening Tool (MST) is a
quick , simple and reliable and an effective
screening tool for identifying patients with
cancer in the radiotherapy and chemotherapy
setting16.

Malnutrition Screening Tool (MST):
1. Have you Lost weight recently without trying?
2. If above Q is YES, How Much weight(Kilograms) have
you lost?
3. Have you been eating poorly because of a decreased
Appetite ?
Mini Nutritional Assessment (MNA)
Screening 6 Questions:
 Food intake
 Weight history
 Activity
 Psychological stress
 Neuropsychological problems
 BMI
Assessment 12 Questions.
Have you lost weight recently without trying?
–If no 0
–If unsure 2
–If yes, how much weight (kg) have you lost?
0.5–5.0 1
>5.0–10.0 2
>10.0–15.0 3
>15.0 4
Unsure 2
Have you been eating poorly because of a decreased appetite?
No 0
Yes 1
RESULT:
If score 0 or 1 not at risk of malnutrition
score ≥2 at risk of malnutrition

 The NCP consists of Four distinct,
inter-related steps:
1) Assessment
2) Diagnosis
3) Intervention
‫ِیتو‬‫پ‬ ‫آتشفشانی‬ ‫های‬ ‫کوه‬‫ن‬
(‫ایسلند‬)

1)Assessment
Nutrition assessment is the First Step of
the NCP and involves the collection and
analysis of data that identify the nature
and cause of nutrition problems11.
How should Nutritional Status be
assessed?

1)Assessment
 Comprehensive Assessment are clustered in the
following groups10:
1. Nutrition Assessment
2. Biochemical assessment
3. Anthropometric assessment
4. Functional assessment
5. Client History
• Food consumption
• Nutrition and health awareness and management
• Physical activity and exercise
• Food availability
 Hepatic Transporter Protein
– Albumin, prealbumin, transferrin
 C-Reactive Protein(CRP)
 Haemoglobin
 Blood Glucose
 Baselines, during treatment, and following treatment weight
 Baselines, during treatment, and following treatment height
 Dual Energy X-ray Absortiometry(DEXA),
 Triceps SkinFold Thickness (TSF);
 Corrected Arm Muscle Area(CAMA)
 Bioelectrical Impedance Analysis(BIA) can be used to assess total
body water (TBW).
Karnofsky Performance Status
Eastern Cooperative Oncology Group (ECOG)
European Organisation for Research and Treatment of
Cancer(EORTC) QLQ-C30,
Functional Assessment of Cancer Therapy (FACT)
The Short Form Health Survey(SF 36)
5.Client History:
I. The individual’s medical and surgical history
II. Current treatments plan
III. Medications
IV. Socioeconomics data

Nutrition Assessment Tool
Very few validated tools have been developed to
assess nutrition status in patients with cancer.
Patient-Generalized Subjective Global
Assessment (PG-SGA) is thought of as the gold
standard for nutrition assessment in the cancer
population due to its high sensitivity and
specificity17.

Several Studies evaluated the use of the scored PG_SGA in cancer
patients.
Authors Objective Study
Population
Duration of
study
Result
Thoresen et
al (2002)18
Compare the PG-
SGA against Objective
Method(anthropometr
ic and assays of serum
proteins)
80 patients 3 month 96%
Sensitivity
83%
Specificity
Bauer et al
(2002)17
Compare the PG-
SGA against SGA
71 patients 11
month
98%
Sensitivity
82%
Specificity
Ravasco et al
(2003)12
Calculating Sensitivity
& Specificity
200
patient
attending
radiothera
py
80%
Sesnitivity
89%
Specificity

Nutrition Assessment Tool
The PG-SGA consists of two section:
I. A four-question patient-completed
— Weight History
— Presence of nutrition-related Symptoms
— Food intake
— Activity/functional Level.
II. Healthcare professional
— Evaluate metabolic Demand
— Disease and its relation to nutrition requirement
— Elements of physical exam.

1) Assessment
2) Diagnosis
3) Intervention
‫ایتزا‬ ‫چیچن‬(‫مایا‬ ‫تمدن‬/)‫مکزیک‬

2- Diagnosis
 The process of assessment results in a
diagnosis.
 The Nutrition Diagnosis is Identification and
Labeling that describe11:
• the actual occurrence of a nutrition-related
problem
• the risk of occurrence of a nutrition-related
problem
• the potential for developing a nutrition-related
problem.

2- Diagnosis
 The nutrition Diagnosis, labels Nutrition
problem in 3 domains 11 :
• Intake Domain
• Clinical Domain
• Behavioral- Environmental Domain
 A nutrition Diagnostic System is Written in a
PES format that states the Problem(P), the
Etiology(E), the Sign & Symptoms(S)11.

2- Diagnosis
Intake Domain11
Problem Etiology Sign/Symptoms
Inadequate oral intake Pelvic radiation Therapy -Diarrhea
-Weight loss in a week
Inadequate Enteral
Nutrition(EN) infusion
Intolerance of EN -Nausea
- Abdominal distention
- 7 kg Weight loss in 5 day
Malnutrition Cancer cachexia -Wasting of the muscle
- weight loss of more than
7.5% in 3 month

2- Diagnosis
Clinical Domain11
Altered GI Function Recent ileostomy surgery - 2 L/day ostomy diarhhea
output
Altered GI Function Biweekly chemotherapy -Nausea
-Vomiting
-Anorexia
Swallowing Difficulty Obstruction esophageal
tumor
- Dysphasia
-Odynophagia
-5 kgWeight loss

2- Diagnosis
Behavioral – Environmental Domain11
Limited access to
nutrition-related supplies
Lack of insurance &
financial resources
-Not using the prescribed
amount of tube feeding
formula
-Continued weight loss to
80% of usual weight
Intake of unsafe food Exposure to contaminated
food while neutropenic
-hospitalization
-Diarhhea
-Positive stool culture for
Salmonella
Undesirable food choices An unwilling to apply
nutrition information
-Ongoing Diarrhea
-Diet history of continued
high fiber food intake
while undergoing pelvic
radiation therapy.

1) Assessment
2) Diagnosis
3) Intervention
‫کانزای‬ ‫فرودگاه‬(‫ژاپن‬)

3- Intervention
 Nutrition interventions are to the specific actions, taken
intended to address and correct the nutrition diagnosis.
 The aspects of intervention are10 :
1. What are the Goals of nutrition intervention for
patients with cancer cachexia?
2. What is the nutrition Prescription to achieve these
goals?
3. What are effective methods of Implementation to
ensure positive outcomes?

1. What are the Goals of nutrition intervention for patients
with cancer cachexia?
 Traditionally, Treatment has focused on Weight Gain.19
 Recently, Weight Stabilisation is an appropriate goal for
weight losing cancer patients.20
2. What is the nutrition Prescription to achieve these goals?
 Energy Requirement
 Protein Reqiurement
 Fluid Requirement
 Eicosapentaenoic Acid (EPA)
3. What are effective methods of Implementation to ensure
positive outcomes?
 Counselling to maximise food intake.

What is the nutrition Prescription to achieve goals 4?
 The following guideline are recommended for
estimating Energy Requirement for cancer patients:
• Cancer –specific (bedridden): 20-25 kcal/kg/day
• Obese patient :21-25 kcal/kg/day
• Normo-metabolic patient : 25-30 kcal/kg/day
• Hyper-metabolic patients: 30-35 kcal/kg/day
• Cancer-specific(Ambulant): 30-35 kcal/kg/day.
Guidelines for protein requirements are as follows:
• Cancer- specific(Ambulant): 1 g/kg per day.
• Cancer-specific(bedridden): 1.2-2 g/kg per day.
• Non-stressed: 1-1.5 g/kg per day.
• Hypermetabolic or protein-losing enteropathy
conditions: 1.5-2.5 g/kg per day.
 In cancer , there is a severe Fall in plasma leucine
and glutamate level and Rise in plasma
phenylalanine and tryptophan level.
Fluid Requirement
 Dehydration is prevalent in many cancer patients,
especially those who Receive chemotherapy
and/or radiation therapty.
 The fluid needs of cancer patients are similar to
those of other patient population without renal
disease(30-35 ml/kg/day).
 Although, fluid needs may also be greater in the face of
increased fluid losses.

 Nutrition interventions should be recognised as an integral
part of cancer therapy to improve clinical outcomes and
quality of life21.
 A Specific Nutritional Ingredients has developed to support
the immune system , modulate weight, Lean Body Mass
loss , change anorexia, in cancer cachexia21.
 The active nutritional ingredients is :
1. Fish Oil
2. Branch Chain Amino Acid (Leucine)
3. High Protein
4. Specific Oligosaccharide Mixture (SOM)

Authors Study Population LBM
assessment
Result
Murphy et
al
(2011)22
-16 Intervention , 4 capsules per day
(2.5 g EPA + DHA)
- 24 Control : no intervention
-duration 10 weeks
CT I:maintenance of weight &skeletal
muscle,
-69% gained muscle.
C: weight loss (2.3 kg) muscle loss
(1 kg)
Weed et al
(2011) 23
-31 Weight-losing patients (Two cans
enriched-oral nutritional supplement per
day (2.2 g EPA)./ Duration 5 week
BIA - Significant increase in LBM (+3.2
kg)
van der
Meij
et al
(2010)24
19 patient with cancer
- Two cans of enriched-ONS per
day (2 g EPA + 0.9 g DHA)
14 in control: Mean intake: 1.0 can per
day.
- Duration 5 weeks.
BIA,
MUAC
I:- Weight maintenance,
- increased MUAC,
- decreased serum IL-6& CRP
-Greater decrease of REE in I vs
C.
-Milderdecrease of FFM in I vs C.
Ryan et al
(2009) 25
28 in intervention EPA-enriched enteral
feed (2.2 g EPA per day)
25 in control: iso-caloric, iso-
nitrogenous
standard feed.
Duration: 26 day.
BIA I: Maintenance of LBM.
-Muscle loss >5% of body weight
8%(vs 39% in C.)
No difference in CRP, albumin or
IL-6 between groups
 Summary of recent Clinical Trials on the effect of EicosaPentaenoic Acid (EPA)on
Lean Body Mass(LBM).

Proteolysis:
Reduced muscle apoptosis and necrosis
Down regulation of ubiquitin proteosome pathway
Decreased production of pro-inflammatory cytokines
Protein synthesis:
Improved insulin sensitivity
Increased protein and caloric intake
Indirect effects :
Reduced side effects from chemotherapy
Enhanced response to chemotherapy
EPA affects LBM via several diverse mechanisms26:

2. Branch Chain Amino Acid (Leucine)
Authors Objective Study Population Result
Gomes-
Marcondes27
MC. et al
(2003)
- Effect of A leucine-
supplemented diet on
protein content of skeletal
muscle in young tumor-
bearing rats.
Duration: 12 day.
Control: 18% protein
Intervention:15%
protein+3% leucin
Wistar rats (25
days old) N =
36,
-a small reduction in
myosin content in I vs C.
-Body fat was especially
reduced( I group)
- Body weight was
reduced too (I group)
- leucine-supplemented
diet could prevent, in
part, the more expected
Weight & LBM loss.
-prevent hypoglycemia
Cangiano C.
et al 28(1996)
- Effects of oral BCAA on
anorexia and caloric intake
in cancer patients
- BCAA supplement
[14.4g/day(7.1 g Leucine)
]for 7 consecutive days.
cancer patients
(n = 28)
-increased plasma BCAA
-Decreased tryptophan
-45 % decreased in
anorexia
Skeletal muscle was the tissue most severely affected in terms of
wasting.
The Branched Chain Amino Acids(BCAA)29:
–act as substrates for protein synthesis
–modulate several elements of the protein synthetic
machinery.
BCAA have a clear inhibitory action on proteolysis in skeletal
muscle30.
 Leucine is the most potent of the three branched chain amino
acids in this regard.
Leucine supplementation could better preservation of body
weight gain, food intake and muscle protein31.

Leucine supplementation increases protein synthesis through insulin-
dependent pathway which lead to activation of mTOR pathway32.
Gallagher P. et al, 2007 . . FASEB J. 21:895.10
p70S6K: Ribosomal protein
4E-BP1: Elongation factor
eIF4G: Initiation factor
PKB/Akt: protein kinase B
mTOR:
mammalian Target Of Rapamycin

Faber J.
et al
(2008)5
- Beneficial immune modulatory effects of a specific
nutritional Combination for cancer cachexia
-26 rat.
-Duration: 20 day.
-Control Diet:
•126 gr Protein(Casein)
•699 gr CHO
•52.5 gr Fat( corn oil)
–Experiment Diet:
•210 gr protein(189 g casein+ 21g Leucin)
•561 gr CHO
•52.5 gr fat
 20.2 g corn
10.2 gcanola
22.1g Fish oil provide 6.9g EPA ,
3.1g DHA)
•18 g short-chain galacto-oligosaccharides
•2g short-chain fructo-oligosaccharides
Experimen Diet show:
-Improved Th1 immuno
response.
-Significantly Increased in :
-Weight of Skelatal Muscle
-Epididymus Fat Weight
-Body Weight
-- Significant decreased in :
-PGE2
-TNF-a
-IL-6

Faber J.
et al
(2008)5
–Experiment Diet:
•210 gr protein(189 casein+ 21 Leucin)
•561 gr CHO
•52.5 gr fat
 20.2 g corn
10.2 g canola
22.1 g Fish oil provide 6.9 g EPA
, 3.1 g DHA)
When Fish Oil in
combination with high
protein/leucine was added
to the diet, BW, weights of
epididymus fat and the
skeletal muscle improved
significantly
Norren
K Van.
et al.
(2009)9
Dietary supplementation with a specific
combination of high protein, leucine, and fish oil
on muscle function in cachectic mice.
Duration :20 day
-Control Diet :
•126g protein(casein)
•727 g CHO
•40 g Fat(soy oil)
– Experimental Diet:
–151 gr Casein + 16 gr leucin
–22 g Fish oil(provided 6.9 g EPA, 3.1 g
DHA)
-Reduction of inflammatory
state by fish oil
-Improve sensitivity of
cachectic mice to anabolic
stimuli like Leucine
-High protein Diet , resulting
in improved maintenance of
Muscle protein Mass.
It is important to provide nutritional intervention with
immuno-modulating properties;
Because, impaired immune function is affected before
the onset of weight loss, in Cancer Cachexia.
High protein –high leucine did not result in significant
weight gain, Unless FISH OIL was added.
Reduction of inflammation by Fisah Oil 33, improved the
sensitivity of the muscle to anabolic stimuli like ,Leucine.
Also better immuno responses against infection , achieved
through Specific oligosaccharid Mixture(SOM)9.
Overally

What are effective methods of Implementation (‫اقدامات‬) to
 Counseling to Encourage high protein/energy
supplements as an essential component of
treatment34.
 Try serving 6 smaller meals/snacks per day.
 Discuss good sources of protein in the diet
 If vegan/vegetarian ensure adequate alternative
sources of protein.
 Fortify foods by adding milk powder, cream, cheese

What are effective methods of Implementation (‫اقدامات‬) to
 Patients with chewing and swallowing difficulties,
modified protein mixture: e.g. minced meats, pureed
meat/chicken/fish , scrambled or poached eggs,
mashed beans, peanut paste, lentil/bean soups10.
 Ensure adequate quantity consumed of High protein
energy nutrition supplements enriched with EPA10.
 To develop gastrointestinal tolerance, fish oil and
high protein energy supplements should increase
gradually.
 Consumption of high protein energy supplement
enriched with EPA over a period of at least 8 weeks10.

1) Assessment
2) Diagnosis
3) Intervention
‫پالمیرا‬ ‫شهر‬(‫سوریه‬)

4- Monitoring & Evaluation
 Nutrition intervention may lead to a variety of outcomes10.
Intermediate outcomes include
– changes in dietary intake,
– changes in symptoms,
– changes in biochemistry, anthropometric measures
– changes in nutrition status
Clinical/Cost/patient outcomes include:
– Mortality( length of hospital stay + quality of life)
– Morbidity(Complication)

Agenda
Section I: Introduction
Section II: Cancer-related Malnutrition
Section III: Nutrition Care process
Section IV: Practice Recommendation
Questions & Answers
Libya

Practice Recommendation:
Screening :
–Malnutrition Screening Tool has been validated.
Assessment :
–The PG-SGA should be used in patients
with cancer cachexia.

Practice Recommendation:
Intervention:
–To Improve Immune System Function
–To Maintain Lean Body Mass
–Stabilisation of Weight
•provide Specific Nutritional Combination.
•Fish Oil (Generally Recognised As Safe(GRAS1) = 3g/day )+
High protein Diet+ Leucine+ Specific
Oligosaccharid
•Counseling
Monitoring & Evaluation:
–The outcome of intervention should be
Monitoring

References:
1. Marian m., [book].[Cancada].Jones and Bartlett Publishers; (2009) 461p.
2. Bray F, et al. Lancet Oncol. (2012)
3. Ferlay J, et al. GLOBOCAN (2008)
4. Shaw C, .[hardcover book].[(2011) 1.398p.
5. Faber J., et al . British Journal of Cancer (2008) 99, 2029 – 2036.
6. Evans WJ et al. Clin Nutr, (2008)
7. Kenneth Fearon et al.Lancet Oncol (2011) 12: 489–95
8. Laviano A., et al. .Nature Clinical Practice Oncology, (2005) 2;3-158-165
9. Norren van K. et al.. British Journal of Cancer (2009) 100, 713 – 722
10.Linda Tapsell et al..Nutrition & Dietetics (2006); 63 (Suppl. 2): S5–S32.
11.L. Kathleen Mahan.[text book] (2012).1227p.
12.Ravasco,p. et al. Clinical oncology (2003) 15(80, 443-450.
13.Read, J.A. et al. Nutrition and Cancer (2005) 53(1),51-56.
14.Slaviero K.A., et al. Nutrition and cancer (2008) 46(2), 148-157.
15.Ferguson M.L. Australasian radiology (1999) 43(30, 325-327.
16.Ferguson, m., et al .Nutrition (1999) 15(6), 458-464.
17.Bauer, J.A., European journal of Clinical Nutrition (2009) 56, 779-785.

References:
18.Thoresen, L., et al. Palliative Medicine (2002) 16(10,33-42.
19.Bruera E, et al . J Clin Oncol (2008); 21: 129–34.
20.Jatoi A, et al. J Clin Oncol (2004); 22: 2469–76.
21.van Bokhorst-de et al. Eur J Oncol Nurs (2005) 9(Suppl 2):S74–S83.
22.Murphy RA, et al.Cancer (2011) 117: 1775–1782.
23.Weed HG, et al. Head Neck (2011) 33(7): 1027–1033.
24.van der Meij BS,et al. J Nutr (2010) 140: 1774–1780.
25.Ryan AM, et al. Ann Surg (2009) 249: 355–363 .
26.Murphy RA. et al. British Journal of Cancer (2011) 105, 1469 – 1473.
27.Gomes-Marcondes MC, et al. Braz J Med Biol Res (2008) 36: 1589–1594.
28.Cangiano C, et al. J Natl Cancer Inst (1996) 88: 550–552.
29.Kobayashi H, et al. J Nutr (2006) 136: 234S–236S.
30.Busquets S, et al. Journal of Cellular Physiology, (2000) 184: 380-384.
31.Anthony JC, et al. J Nutr (2000);130: 2413–2419.
32.Gallagher P, et al. FASEB J. (2007) 21:895.10.
33.Tisdale M. J. et al . Nutr Clin Pract (2006) 21: 168-174.
34.Bauer j. European Oncological Disease (2007),12-14

–Dr Bauer has presented research related to nutrition screening, assessment
and cancer at national and international conferences .
–She is also an Adjunct Associate Professor in the School of Public Health,
Queensland University of Technology.
–Dr. Judy Bauer she has over 40 publications in national and international
journals.
–

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