Professional Documents
Culture Documents
Cancer - Head and Neck
Cancer - Head and Neck
Practice Questions
Q1: What are the optimal dietary strategies for managing dysphagia in adult patients receiving
cancer treatment?
Subcategory: Intervention
Updated: 2008-11-30
Grade of Evidence: C
Evidence
a. Several reviews recommend altering food consistency, taste, temperature and/or fluid consisten
consistency to aid swallowing in patients receiving radiation and/or chemotherapy (1-3), although
there is a lack of research investigating the optimal diet for dysphagia management during
cancer treatment.
b. Isenring and his group randomized 60 oncology outpatients receiving radiation treatment to the
gastrointestinal tract (GI) or head and neck (H&N) region to receive either nutrition intervention
(NI) (n=29) or usual care (UC) (n=31). NI consisted of individualized regular and intensive nutrition
counselling, including high energy high protein recommendations, from a dietitian for the 12
weeks of the study (seen weekly throughout radiation treatment and monthly thereafter for the
length of the study). UC consisted of nutrition education by nurses, although those patients
receiving radiation treatment to the H&N region were referred to the outpatient dietitian for UC
(maximum two visits). The NI group had statistically smaller deteriorations in weight (P<0.001),
nutritional status (P=0.020) and global Quality of Life (P=0.009) compared with those receiving
UC (2).
c. In his narrative review of preventing and treating dysphagia following chemoradiation for head and
neck cancer, Rosenthal recommends patients with dysphagia avoid even brief periods of NPO.
He suggests that patients should be taking the maximum tolerated size and texture of bolus to
maintain the greatest function of the swallow as possible (even in the presence of a tube feed)
(1).
d. Current practice of oncology dietitians and other trained professionals is to recommend texture
Comments
Texture modification is the appropriate management of swallowing dysfunction resulting from neurogenic,
structural, motility, or iatrogenic etiologies. Texture is modified to assist the patient with dysphagia to
maintain or achieve adequate nutrition and hydration while minimizing the risk of choking and aspiration.
For more information about swallowing dysfunction associated with cancer,
see http://www.bccancer.bc.ca/nutrition-site/Documents/Symptom%20management%
20guidelines/Dysphagia.pdf
Rationale
Dysphagia is a common symptom of cancers of the head and neck and esophageal regions as well as a
side effect of radiation and/or chemotherapy to those areas. Treatment-related side effects are typically
worse in the last two weeks of treatment and continue for at least two weeks after treatment ceases.
Causes of dysphagia during cancer treatment can be either tumor related (structural/anatomical
dysmotility, obstruction) or treatment related (mucositis, thick saliva/secretions, xerostomia,
obstruction/edema).
References
1. Rosenthal DI, Lewin JS, Eisbruch A. Prevention and treatment of dysphagia and aspiration after
chemoradiation for head and neck cancer. J Clin Oncol. 2006 [cited 2007 21 May];24:2636-43.
Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/16763277
2. Isenring EA, Capra S, Bauer JD. Nutrition intervention is beneficial in oncology patients receiving
radiotherapy to the gastrointestinal or head and neck area. Brit J Cancer. 2004[ cited 2007 21
May];91:447-52. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/15226773
3. Grobbelaar EJ, Owen S, Torrance AD, Wilson JA. Nutritional challenges in head and neck
cancer. Clin Otolaryngol. 2004 [cited 2007 21 May];29:307-13. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/15270813
4. Minasian A, Dwyer J. Nutritional implications of dental and swallowing issues in head and neck
cancer. Oncol. 1998 [cited 2007 21 May];12(8):1155-62. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/11236308
5. Gaziano JE. Evaluation and management of oropharyngeal dysphagia in head and neck cancer.
Can Contr. 2002 [ cited 2007 21 May];9(5):400-9. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/12410179
It has been suggested that the modification of food texture and bolus size may be effective in eliminating
aspiration risk for patients receiving treatment for head and neck cancer.
If a patient is unable to minimize weight loss prior to and/or during treatment, a prophylactically placed
tube feed may be recommended to maintain fluid and nutritional status. This recommendation may occur
for patients with cancers involving the oropharyngeal region and/or the esophagus.
Grade of Evidence: C
Evidence
a. Colasanto and colleagues cite the American Society for Gastrointestinal Endoscopy Guidelines
for Selecting Patients for Tube Feeding to indicate that tube feeding should be considered in
those patients with severe dysphagia but a functioning gut (1).
b. Rosenthal, et al. indicate that although there have been benefits shown with prophylactic tube
feeds for cancer treatment, it is not without potential complications (2) and the benefits remains
controversial (3).
c. Mittal, et al., through a review of the literature, recommend that limiting food textures be the last
compensatory strategy used to minimize aspiration for patients as it may be challenging for
patients and may impact nutritional status. However, they also note that in patients being treated
for head and neck cancers, bolus modification (size and consistency) may be effective in
eliminating aspiration (4).
Comments
The type of tube (i.e. gastrostomy or jejunostomy), the type of placement (i.e. surgically or radiologically),
and the timing of tube placement (i.e. prophylatically or responsively) should be determined by the degree
of swallow dysfunction at the time of diagnosis, potential worsening due to planned cancer treatment, the
location of the tumor (i.e. head and neck or esophageal) and what anatomical structures are affected by
the cancer and the planned treatment.
References
1. Colasanto JM, Prasad P, Nash MA, Decker RH, Wilson LD. Nutritional support of patients
undergoing radiation therapy for head and neck cancer. Oncol. 2005 [cited 2007 21 May];19
(3):371-87. Abstract available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15828552
3. Grobbelaar EJ, Owen S, Torrance AD, Wilson JA. Nutritional challenges in head and neck
cancer. Clin Otolaryngol. 2004 [cited 2007 21 May];29:307-13. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/15270813
4. Mittal B, Pauloski BR, Haraf DJ, Pelzer HJ, Argiris A, Vokes EE, et al. Swallowing dysfunction -
preventative and rehabilitation strategies in patients with head-and-neck cancers treated with
surgery, radiotherapy, and chemotherapy: a critical review. Int J Radiation Oncology Biol Phys.
2003 [cited 2007 21 May];57(5):1219-30. Citation available from:
https://www.ncbi.nlm.nih.gov/pubmed/14630255
Q2: What are optimal dietary strategies for managing taste changes in adult patients undergoing
cancer treatment?
Subcategory: Intervention
Updated: 2007-07-10
Grade of Evidence: C
Evidence
a. Two hundred and eighty-four patients undergoing chemotherapy completed a questionnaire on
taste changes in a cross-sectional descriptive study in eleven outpatient oncology centers. The
findings note patients frequently experienced taste changes; this side-effect had a negative
impact on their quality of life, and oncology health professionals typically did not offer self-
management suggestions to patients (1).
b. In a second paper, two experienced registered dietitians describe their role in counselling
patients with taste changes and provide practical suggestions to overcome this challenge. They
Comments
As taste changes are unique to each person and can vary over time time, an individualized approach
needs to be taken to brainstorm for tolerable foods and continued follow up. Patients may need
encouragement and support to try foods again that may have resulted in food aversions secondary to taste
changes.
References
1. Wickham RS, Rehwaldt M, Kefer C, Shott S, Abbas K, Glynn-Tucker E, et al. Taste changes
experienced by patients receiving chemotherapy. Oncol Nurs Forum 1999 [cited 2007 22
May];26: 697-705. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/10337648
2. Peregrin T. Improving taste sensation in patients who have undergone chemotherapy or radiation
therapy. J Am Diet Assoc 2006;106(10):1536-1540. Abstract available from
https://www.ncbi.nlm.nih.gov/pubmed/17000184
3. Sherry VW. Taste alterations among patients with cancer. Clini J Oncol Nurs 2002 [cited 2007
22 May];6(2):1-4. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/11889680
Grade of Evidence: C
Evidence
a. A phase III multi-institutional double-blind, placebo-controlled trial of 169 head and neck cancer
patients were given oral zinc sulfate (45 mg, three times daily) throughout their external beam
radiation treatments and for one month after. Zinc sulfate did not significantly increase the
interval to taste alterations, nor did it appear to decrease the incidence of taste alterations or the
interval to taste recovery. The dose used is higher than the tolerable upper intake level (UL) for
zinc (UL=40 mg/day) (1).
Comments
Recommended daily intake for Zinc is 12-15 mg/day.
References
1. Halyard MY, Jatoi A, Sloan JA, Bearden JD, Vora SA, Atherton PJ, et al. Does zinc sulfate
prevent therapy-induced taste alterations in head and neck cancer patients? Results of phase III
double-blind, placebo-controlled trial from the north central cancer treatment group. Int J
Radiation Oncology Biol Phys 2007 [cited 2007 22 May];67(5): 1318-1322. Abstract available
from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17394940&query_hl=11&itool=pubmed
_docsum
2. Ripamonti C, Zecca E, Brunelli C, Fulfaro F, Villa S,Balzarini A, et al. A randomized, controlled
clinical trial to evaluate the effects of zinc sulfate on cancer patients with taste alterations
caused by head and neck radiation. Cancer 1998 [cited 2007 22 May];82:1938-1945. Abstract
available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=9587128&query_hl=13&itool=pubmed_
DocSum
3. Leitzmann MF, Stampfer MJ, Wu K, Colditz GA, Willett WC, Giovannucci EL. Zinc supplement
use and risk of prostate cancer. J Natl Cancer Ins 2003 [cited 2007 22 May];95:1004-7. Abstract
available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12837837&query_hl=16&itool=pubmed
_DocSum
In support of the protective association of vegetables, fruits, legumes and grains against cancers of some
sites is evidence from observational studies that the intake of foods containing specific micronutrients
found in plant foods protects against cancer. Evidence is generally consistent for a protective effect of
foods containing carotenoids protect against cancers of the mouth, pharynx, larynx and lung.
Limited evidence is also available for a protective effect of the following nutrients in foods against the
following cancer sites:
Foods containing vitamin E protect against esophageal and prostate cancer.
Foods containing folate protect against esophageal and colorectal cancer.
Foods containing pyridoxine and fibre protect against esophageal cancer.
Dysphagia during cancer treatment should be managed with appropriate diet texture and/or fluid
consistency modification; both of which will depend on the exact location of the swallow dysfunction. The
goal of nutrition intervention during treatment should be to minimize weight loss (through adequate energy
and protein intakes) and to maintain hydration. Texture modification should be progressive as the
dysphagia worsens through treatment and then graduate back as the dysphagia diminishes with healing
post-treatment.
Severe dysphagia during cancer treatment, involving either the complete inability to swallow foods or fluids
or a high risk of aspiration, should be managed with an appropriately placed feeding tube. Percutaneous
gastrostomy (PEG) tube placement is frequently recommended for severe dysphagia and/or aspiration
risk.
It has been suggested that the modification of food texture and bolus size may be effective in eliminating
aspiration risk for patients receiving treatment for head and neck cancer.
If a patient is unable to minimize weight loss prior to and/or during treatment, a prophylactically placed
tube feed may be recommended to maintain fluid and nutritional status. This recommendation may occur
for patients with cancers involving the oropharyngeal region and/or the esophagus.
The Third Expert Report on Diet, Nutrition, Physical Activity and Cancer: a Global Perspective provides
evidence and recommendations on preventing and surviving cancer through diet, nutrition and physical
activity (1).
Nutrition Assessment
The nutrition assessment of a child or an adult with cancer or wanting to prevent cancer from developing
may include the parameters using NCP terminology in the table below.
Anthropometric Measurements
Height/Length
Weight
Weight Change
BMI
Body Compartment Estimates (waist circumference)
Growth pattern indices/percentile ranks
Waist As above
Circumference
Food/Nutrition-related History
Energy Needs
» Estimated energy needs
Macronutrient Needs
» Estimated fat needs
» Estimated protein needs
» Estimated carbohydrate needs
» Estimated fluid needs
Micronutrient Needs
» Estimated vitamin needs
» Estimated mineral needs
See International Dietary Reference Values Collection.
Client History
Personal History
Personal Data
Age
Patient/Client/Family Medical/Health History
Hematology/Oncology
Cancer (specify)
Primary Tumour Site
Presence of Metastases
Effect of Cancer on Ingestion, Digestion and Absorption of Nutrients
Pre-existing Other Medical Conditions
Treatments/Therapy
Nutrition Diagnosis
Sample PES Statements (problem, etiology, signs and symptoms using some NCP terminology)
These statements are provided as an example only, and will not apply to all individuals:
High meat intake due to frequent visits to fast food establishments, as evidenced by almost daily
red and/or processed meat consumption in the past year and recent development of colon
cancer.
Excessive alcohol intake related to lack of value for behaviour change or competing values, as
evidenced by regular consumption of more than two drinks per day and development of
esophageal cancer.
Nutrition Intervention
Goals
Goals for an individual wanting to prevent cancer from developing or prevent cancer reoccurrence should be
determined in conjunction with the client and should be specific to the individual. Goals that are set should
be time-sensitive, easily measured and achievable by the nutrition intervention. Examples of short- and
long-term goals include to:
lower the number of red meat servings each week from six to three serving by substituting with
more plant foods like legumes and tofu in stews and stir fries over the next three weeks.
eat a variety of vegetables and fruits through changes in eating more plant foods daily to
decrease risk of cancer.
This Summary of Recommendations and Evidence synthesizes the Key Practice Point(s) for each
Practice Question (PQ) in this Knowledge Pathway. It is organized by the Nutrition Care Process and
contains statements or recommendations that have been graded using either
the PEN or GRADE approaches to critical appraisal. For additional information on the evidence and
references, see the PQs in this Knowledge Pathway.
Content
INTERVENTION
1. Omega-3 Fatty Acid Supplementation
2. Low Iodine Diet and Radioactive Iodine Ablation
Low Iodine Diet Side-Effects
Low Iodine Diet and Cancer Recurrence and Mortality Rates
Evidence Summary
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Additional Remarks
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The above review found that there is no standardized protocol for LIDs, but most studies have used ≤50 μg
iodine/day with a duration of one to two weeks. A one-week LID may be adequate, especially if subjects
have intensive education on the LID, or reside in regions with mild iodine deficiency.
A non-randomized study published after the above review suggested that a two-week restricted iodine diet
(RID) (50-100 μg/day) was as effective in RAI ablation as a two-week LID (≤50 μg/day), but more research
is needed to confirm.
{grade_c}
Remarks
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Additional Remarks
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Another earlier review theorized that LIDs could result in radiation toxicity, especially in individuals with
impaired excretion due to renal dysfunction or advanced age, but no studies have demonstrated this
outcome.
Epidemiological data provides consistent evidence for an association between overweight/obesity and
adenocarcinoma of the esophagus and cancers of the pancreas, colorectum, breast (postmenopausal),
endometrium and kidney].
Epidemiological data provides consistent evidence that low levels of physical activity are associated with
an increased risk of colon cancer and reasonably consistent evidence for an increased risk of
postmenopausal breast cancer and endometrial cancer. In addition, sedentary living is associated with an
increased risk for weight gain, overweight and obesity, and subsequently increased cancer risk.
Epidemiological data provides consistent evidence that consumption of any type of alcoholic drink (i.e.
beer, wine, spirit/liquor) is associated with cancers of the mouth, pharynx, larynx, esophagus, colorectum
(men) and breast.
Consistent evidence from a number of cohort studies suggests that consumption of red meat and
processed meat is associated with an increased risk of colorectal cancer. Current recommendations
suggest that individuals consume less than 500 grams of red meat per week and consume very little if any
processed meat (i.e. meat preserved by smoking, curing or salting or addition of chemical preservatives).
Evidence from a number of cohort and case-control studies suggests that consumption of alcoholic drinks
is associated with an increased risk of premenopausal and postmenopausal breast cancer, with no safe
limit of intake identified. The effect is from ethanol and includes any type of alcoholic beverage (beer, wine
or liquor).
Epidemiological data provides reasonably consistent evidence that greater abdominal fatness is
associated with cancers of the breast (postmenopausal) and endometrium. Furthermore, there is
reasonably consistent evidence for an association between adult weight gain and increased risk of
postmenopausal breast cancer. Avoidance of weight gain and increases in waist circumference throughout
adulthood are recommended.
Some types of breast cancer may be related to an interaction between low folate intake and alcohol
consumption. Adequate folate intakes may mitigate the increased risk of breast cancer associated with
high alcohol consumption. Epidemiologic studies examining an association between folate intake and
breast cancer are inconclusive.
Four meta-analyses examining the relationship between soy isoflavone intake from foods and breast
cancer incidence found that soy isoflavones are associated with a reduced breast cancer risk. However,
the association between soy isoflavones and breast cancer risk may be modified by menopausal status,
BMI, population studied (Asian versus Western population) and age of exposure to soy
(childhood/adolescence versus adulthood) making it difficult to definitively conclude that the consumption
of soy isoflavones reduces breast cancer risk.
The dose of soy isoflavones from food associated with a reduced risk of breast cancer also varied among
studies, and by sub-group (menopausal status, population studied). Specific soy isoflavone intake
categories (i.e. tertiles, quartiles) were unique to each study thereby challenging the ability to combine
and suggest the dose of isoflavone needed to demonstrate an association with breast cancer. A
consistent dose-response relationship was not found.
Recommendations on dietary soy intake for breast cancer prevention are likely and most logically to be
derived from epidemiological data owing to the long latency period of breast cancer, large sample sizes
required, and the associated costs and feasibility of conducting such intervention studies.
The conflicting experimental data on the effects of isoflavones on breast cancer cells in vivo and in vitro
make it difficult to conclude whether soy consumption in women is associated with decreased or
increased breast cancer risk. However, recent human observational studies suggest that this preclinical
work is of lesser significance.
Supplemental soy intake was reported in two observational studies. However, the frequency of
supplemental soy use and dose use was low, precluding the ability to assess the risk of recurrence from
soy supplement use.
[C] The following conclusions are supported by limited evidence or expert opinion:
There is probable evidence for an association between greater body fatness and decreased risk of
premenopausal breast cancer. Strong mechanistic evidence is lacking to explain this association.
However, since postmenopausal diagnosis of breast cancer is much more common than premenopausal,
any decreased risk of premenopausal breast cancer associated with increased body fatness is
outweighed by an increased risk of postmenopausal breast cancer.
Evidence is limited for an effect of any nutrient or dietary factor on a decreased risk of breast cancer, such
that a recent report on the prevention of cancer could not draw any conclusions. A recent cohort study
identified a positive association between high dietary fibre intake and reduced risk of breast cancer in
premenopausal women only. Additional studies are required to examine relationships between nutrients
and/or foods and decreased breast cancer risk.
Evidence from cohort studies shows inconsistent effects of total fat intake and increased postmenopausal
breast cancer risk, while case-control studies show a significant positive association. Overall the results
suggest limited evidence for an association between total fat intake and increased breast cancer risk in
postmenopausal women.
Epidemiological data provides reasonably consistent evidence that breastfeeding protects against
childhood overweight and obesity, which influences cancer risk if this tracks into adulthood; however, this
effect is less consistent when controlling for confounding variables (e.g. parental obesity, maternal
smoking and social class). Furthermore, the evaluation of a breastfeeding promotion intervention found no
protective effect of breastfeeding against childhood obesity.
The effect of folic acid supplements on breast cancer risk in postmenopausal women requires additional
study as both positive and negative associations have been reported.
At this time, insufficient evidence exists to suggest that breast cancer survivors who consume soy foods
have improved outcomes related to cancer recurrence or survival. More evidence is needed to specifically
recommend an increase in soy food consumption in women not habitually consuming soy to prevent
breast cancer recurrence or to see reduced mortality benefits.
Existing data in humans is insufficient to make recommendations about the effect of dietary soy on breast
cancer during treatment.
Isoflavones are naturally occurring compounds with estrogen-like activity that pose a theoretical risk to
women with breast cancer. Existing in vitro and in vivo data show evidence of both inhibition and increased
cell proliferation and an ability to negate the effects of tamoxifen under certain experimental conditions,
which raises the concern of possible harm. Existing data is not sufficiently strong to justify the use of soy
foods in the treatment of breast cancer. Health Canada’s product monograph on soybean extracts and
isolates advises against product use in women with a previous history of breast cancer and/or breast
tumours, or if there is a predisposition to breast cancer. A position statement indicates that relying on soy
supplementation alone or avoiding or delaying conventional medical care for cancer may have serious
health consequences and is not advised.
Of the few observational studies published, most studies report ginseng use to be associated with a
decreased risk of cancer incidence or cancer mortality. Additionally, observational and interventional
research reports improvement in some aspects of quality of life and fatigue with ginseng use among both
healthy populations and those with cancer.
Consistent reductions in the risk of developing breast cancer or evidence of slowing the progression of
existing breast cancer with high dietary CLA intake have not been observed in all epidemiological studies;
randomized control studies are necessary.
[D] A conclusion is either not possible or extremely limited because evidence is unavailable
and/or of poor quality and/or is contradictory:
The evidence for a beneficial effect of breastfeeding on decreased risk of adult obesity is inconsistent.
Despite new evidence, the controversy over the safety of soy for breast cancer survivors may remain.
Older, but widely cited and publicized in vitro and in vivo data demonstrated that the presence of
estrogenic compounds, known as isoflavones, in soy foods, administered as genistein-containing
products, resulted in increased cell proliferation under certain experimental conditions. These results lead
to the widely held belief that the consumption of soy foods posed a theoretical risk to women with breast
cancer.
Well-designed clinical trials are needed to determine the causal relationships between soy foods and
breast cancer outcomes. There is also a remaining need for the development and testing of improved
biomarkers in breast tissue as a surrogate endpoint to cancer recurrence, to facilitate clinical study.
However, concern has been raised regarding the potential phytoestrogen activity of ginseng because of
older case reports of individuals taking ginseng orally or topically who experienced estrogen-related side-
effects (such as postmenopausal vaginal bleeding and breast swelling and tenderness). Most of the
experimental research on estrogenic activity and the impact on breast cell cancer cell proliferation is in
vitro or animal model and it is conflicting.
An estrogenic effect of ginseng and its potential clinical consequences in humans is unclear and so a
recommendation on whether one should avoid ginseng if they have or are at risk of estrogen-receptor
positive cancers cannot be made at this time. Additional and clinical research is needed.
There are no research reports on whether dietary or supplemental CLA can improve the treatment of
existing breast cancer.
Note: See relevant practice questions in this knowledge pathway for references.
This Summary of Recommendations and Evidence synthesizes the Key Practice Point(s) for each
Practice Question (PQ) in this Knowledge Pathway. It is organized by the Nutrition Care Process and
contains statements or recommendations that have been graded using either the PEN or GRADE
approaches to critical appraisal. For additional information on the evidence and references, see the PQs in
this Knowledge Pathway.
Evidence Summary
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Remarks
Given the lack of evidence regarding the impact of consuming whole grains that have undergone
processing, it is prudent to emphasize the benefits of whole grains that have been minimally processed.
Additional Remarks
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Evidence Summary
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Remarks
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There is also limited evidence that a high intake of vegetables and fruit is associated with a reduced risk of
colon cancer and a low intake of fruit and non-starchy vegetables increases the risk of colorectal cancer.
Evidence Summary
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Remarks
Non-starchy vegetables include green leafy vegetables, broccoli, okra, eggplant and non-starchy roots
(e.g. carrots, rutabaga and turnips) but exclude starchy roots (e.g. potatoes, yams, cassava).
Additional Remarks
Evidence Summary
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Remarks
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Vitamin D
Recommendation
Limited evidence suggests that foods containing vitamin D may be associated with a decreased risk of
colorectal cancer. Vitamin D supplements do not appear to be associated with reduced risk of colorectal
cancer, suggesting that individuals should strive to meet their nutritional needs by achieving the Dietary
Reference Value for vitamin D.
Evidence Summary
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Evidence Summary
Remarks
Processed meat is meat preserved through salting, curing, fermentation and smoking (e.g. ham, salami,
bacon, hotdogs, chorizo).
Red meat includes all types of muscle meat from beef, veal, pork, lamb, mutton, horse and goat.
Additional Remarks
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Alcohol
Recommendation
Consuming alcoholic drinks (>30 g/day ethanol, about 2 drinks per day beer, wine or spirits) increases the
risk of colorectal cancer.
Evidence Summary
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Remarks
The threshold of 30 g/day alcohol applies to the risk of colorectal cancer. For breast (pre- and
postmenopausal) and esophageal cancer, no safe lower limit of alcohol consumption has been identified.
Additional Remarks
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While trials of low carbohydrate diets followed in the short term (four to eight weeks) found fair evidence
that these beneficial fermentation products decreased, limited evidence from systematic reviews of cohort
studies has not found total carbohydrate intake to be associated with colorectal cancer risk. More
research is required to enable clear conclusions on whether low carbohydrate diets increase the risk of
colorectal cancer.
Dietitians can help individuals following low carbohydrate diets get enough dietary fibre and help them
balance their greater number of protein choices so that there is not a disproportionately high amount of red
or processed meats.
Evidence Summary
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Remarks
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Evidence Summary
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6. Probiotics/Prebiotics/Synbiotics and Colorectal Cancer Prevention
Recommendation
There is no direct evidence from well-controlled intervention trials in humans that oral probiotics, prebiotics
or synbiotics are effective in the prevention of colorectal cancer.
Evidence Summary
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Additional Remarks
In support of the protective association of vegetables, fruits, legumes and grains against cancers of some
sites is evidence from observational studies that the intake of foods containing specific micronutrients
found in plant foods protects against cancer. Evidence is generally consistent for a protective effect of
foods containing carotenoids protect against cancers of the mouth, pharynx, larynx and lung.
Limited evidence is also available for a protective effect of the following nutrients in foods against the
following cancer sites:
Foods containing vitamin E protect against esophageal and prostate cancer.
Foods containing folate protect against esophageal and colorectal cancer.
Foods containing pyridoxine and fibre protect against esophageal cancer.
Dysphagia during cancer treatment should be managed with appropriate diet texture and/or fluid
consistency modification; both of which will depend on the exact location of the swallow dysfunction. The
goal of nutrition intervention during treatment should be to minimize weight loss (through adequate energy
and protein intakes) and to maintain hydration. Texture modification should be progressive as the
dysphagia worsens through treatment and then graduate back as the dysphagia diminishes with healing
post-treatment.
It has been suggested that the modification of food texture and bolus size may be effective in eliminating
aspiration risk for patients receiving treatment for head and neck cancer.
If a patient is unable to minimize weight loss prior to and/or during treatment, a prophylactically placed
tube feed may be recommended to maintain fluid and nutritional status. This recommendation may occur
for patients with cancers involving the oropharyngeal region and/or the esophagus.
Note: See relevant practice questions in this knowledge pathway for references.
This Summary of Recommendations and Evidence synthesizes the Key Practice Point(s) for each
Practice Question (PQ) in this Knowledge Pathway. It is organized by the Nutrition Care Process and
contains statements or recommendations that have been graded using either the PEN or GRADE
approaches to critical appraisal. For additional information on the evidence and references, see the PQs in
this Knowledge Pathway.
Content
1. Nutrients/Dietary Factors that Decrease Lung Cancer Risk
Fruit
Non-Starchy Vegetables
Foods Containing Carotenoids
Food Containing Retinol
Food Containing Vitamin C
Food Containing Isoflavones
Dietary Fat, Selenium and Food Containing Quercetin
2. Nutrients/Dietary Factors that Increase Lung Cancer Risk
Arsenic in Drinking Water
Beta-Carotene Supplements
Red and Processed Meat
Alcohol
Remarks
One small piece of fruit such as a banana, pear or apple weighs about 100-150 grams; 175 mL (3/4 cup) of
fruit such as berries or pineapple chunks or fruit cocktail weigh about 125-150 grams.
Additional Remarks
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Non-Starchy Vegetables
Recommendation
Limited evidence suggests that the consumption of non-starchy vegetables reduces the risk against lung
cancer in current smokers and former smokers with a maximum benefit plateauing at about 300-400
g/day.
Evidence Summary
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Remarks
The WCRF/AICR categorized non-starchy vegetables to include green leafy vegetables, broccoli, okra,
eggplant, cabbage, onions, leeks and non-starchy roots (e.g. beets, carrots, parsnips, rutabaga and
turnips), but excluded starchy roots (e.g. potatoes, yams, cassava). A 125 mL (½ cup) serving of most
cooked vegetables is equal to about 80-100 grams. One cup of lettuce weighs about 30 grams.
Additional Remarks
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Taking beta-carotene supplements is not recommended for current and former smokers. See Additional
Content: What nutrients/dietary factors are associated with an increased risk of developing lung cancer?
Evidence Summary
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Remarks
Carotenoids are fat-soluble red, orange and yellow pigments that comprise xanthophylls (i.e. lutein) and
carotenes (i.e. alpha- and beta-carotene and lycopene). They are found in varying concentrations in all
vegetables and some fruit, with the main dietary sources of carotenoids including spinach, kale, butternut
Additional Remarks
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Evidence Summary
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Remarks
Vitamin A is a fat-soluble vitamin found in animal products. Food sources of vitamin A include liver, egg
yolk, oily fish, milk, dairy products, animal fats and some fortified products. Retinol can be synthesized
from carotenoids; beta-carotene being the most efficient to be converted into retinol.
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2. Nutrients/Dietary Factors that Increase Lung Cancer Risk
Arsenic in Drinking Water
Recommendation
Strong evidence from observational studies consistently shows that high levels of arsenic in drinking water
increases risk of lung cancer.
Canada, New Zealand and the United Kingdom guidelines are in sync with the WHO provisional
guidelines.
Evidence Summary
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Remarks
See Additional Content: Food Safety – Arsenic in Rice Background.
Additional Remarks
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Beta-Carotene Supplements
Recommendation
For current and former smokers, taking beta-carotene supplements (>20 mg/day) is not recommended
since there is strong evidence showing that it is associated with an increased risk of lung cancer.
Evidence Summary
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Remarks
GSTM1 and GSTM2 are carcinogen-detoxifying enzymes. Individuals without or with less active forms of
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Results are limited as no analysis was able to be conducted by smoking. Although the studies adjusted
for smoking duration and current status, there is the potential for residual confounding due to smoking.
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Alcohol
Recommendation
There is limited evidence suggesting that consuming alcoholic drinks (>40 g/day ethanol; just over 2
drinks per day beer, wine or spirits) increases the risk of lung cancer.
Evidence Summary
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Remarks
The threshold of 40 g/day alcohol applies to risk of lung cancer. For breast (pre- and postmenopausal) and
esophageal cancer, no safe lower limit of alcohol consumption has been identified. For colorectal cancer,
the threshold is 30 g/day alcohol and 45 g/day for stomach and liver cancers.
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This Summary of Recommendations and Evidence synthesizes the Key Practice Point(s) for each
Practice Question (PQ) in this Knowledge Pathway. It is organized by the Nutrition Care Process and
contains statements or recommendations that have been graded using either the PEN or GRADE
Content
1. Nutrients/Dietary Factors and Decreased Prostate Cancer Risk
2. Nutrients/Dietary Factors and Increased Prostate Cancer Risk
3. Foods/Nutrients/Supplements and Prostate Cancer Progression
4. Dietary Patterns and Prostate Cancer Progression
5. Flaxseed and Prostate Cancer Treatment
6. Flaxseed and Prostate Cancer Reoccurrence
Glycemic Index
A small number of RCTs and cohort studies consistently suggest that while glycemic index may affect
prostate cancer risk, glycemic load does not.
Selenium
Although there is mixed evidence regarding the effect of dietary and supplemental selenium intake on the
risk of prostate cancer, the highest quality studies show that selenium supplementation likely has no
effect.
There is not enough evidence to suggest that the following factors have an effect on the risk of prostate
cancer:
selenium
alpha-tocopherol/vitamin E supplements
pulses (beans, legumes, lentils).
Remarks
See Additional Content: What health-related outcomes and safety concerns are associated with green tea
consumption, including both beverage and supplement forms, among adults?
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Beta-Carotene
There is strong evidence to suggest that beta-carotene has no effect on the risk of prostate cancer.
Fat Intake
Consistent, moderate quality studies suggest that fat intake (total, saturated, monounsaturated or
polyunsaturated) has no effect on the risk of prostate cancer. The evidence regarding individual omega-3
fatty acids is less clear, with a possible association between prostate cancer incidence and both long-
chain omega-3 fatty acids (i.e. eicosapentaenoic acid (EPA) and docosapentaenoic acid (DPA)) and
alpha-linolenic acid (ALA). That said, circulating docosapentaenoic acid (DPA) levels has been linked to a
decreased risk of prostate cancer. More evidence is necessary to solidify this conclusion.
Folate
Inconsistent, low quality evidence suggests that folate intake has no effect on prostate cancer risk, but
that high serum folate may be associated with an increased risk. More evidence is necessary to clarify
these findings.
Evidence Summary
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Remarks
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3. Foods/Nutrients/Supplements and Prostate Cancer Progression
Recommendation
No foods, nutrients or dietary supplements are currently recommended to slow disease progression or
improve mortality outcomes in men with prostate cancer.
Multivitamin Supplement
Another placebo-controlled RCT assessed a multivitamin supplement containing soy (62.5 mg), lycopene
(15 mg), selenium (128 μg), coenzyme Q10 (4 mg) and various vitamins and minerals and found similar
results.
Evidence Summary
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Remarks
PSA is a commonly used surrogate marker of prostate cancer disease activity, diagnosis and survival, as
tests for PSA are widely available. However, it has not been proven to be a completely reliable proxy
measure in assessing the effect of long-term interventions.
Following a Mediterranean or vegetarian diet has not been associated with the risk of prostate cancer,
although this finding may be partially related to inconsistent definitions of both diets across existing
research.
Evidence Summary
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Remarks
The DII uses a point system to score a person’s dietary pattern on a scale from anti-inflammatory (lowest
score) to pro-inflammatory (highest score). Each of 45 dietary components (e.g. vitamin A, iron,
cholesterol, flavonols, turmeric, garlic) is rated by its effect on serum inflammatory markers and given a
score of +1 if they raise inflammatory biomarkers, -1 if they lower inflammatory biomarkers and zero if they
have no effect on inflammatory biomarkers. A person’s overall dietary score is totalled, with a negative
score indicating a more anti-inflammatory diet and a positive score indicating a more pro-inflammatory
diet.
Additional Remarks
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5. Flaxseed and Prostate Cancer Treatment
Evidence Summary
To date, there are no flaxseed intervention trials in men with prostate cancer undergoing cancer treatment
such as hormone blocking therapy or radiotherapy. The limited studies that are available have been done
in men with a diagnosis of prostate cancer awaiting surgery. Therefore, no recommendations can be made
regarding the consumption of flaxseed during prostate cancer treatment.
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Additional Information
References
1. World Cancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical
activity, and the prevention of cancer: a global perspective. Continuous update project expert
report 2018. Washington, D.C.: AICR; 2018. Available from: http://www.dietandcancerreport.org
This toolkit provides an overview of practice recommendations that have been summarized from relevant
key practice points contained in PEN® Knowledge Pathways. To view the key practice points (including
the associated references) see the following Knowledge Pathways:
Cancer
Cancer - Breast
Cancer - Lung
Cancer - Colorectal
Cancer - Head and Neck
Cancer - Prostate
In addition, the source of the NCP terminology used in this toolkit is: The Academy of Nutrition and
Dietetics. eNCPT: Nutrition Terminology Reference Manual. 2018. Available from: Nutrition Care Process
and Terminology Web Links.
Background
Cancer - Head and Neck Background
The levels of evidence for the practice guidelines were assessed using the level of evidence rating system
recommended by the National Health and Medical Research Council and quality ratings utilizing the
Academy of Nutrition and Dietetics quality criteria checklist (2008). The evidence rating system has been
determined to be comparable and of similar quality to the system used by PEN®. The full methodology for
the guideline development is described on the Clinical Oncological Society of Australia wiki platform.
Etiology
Most head and neck cancers are squamous cell in origin and develop in the mucosa of the upper digestive
tract (1). Squamous cell carcinomas in the head and neck have similar etiologies, diagnoses and
treatments. Head and neck cancer sites include the oral cavity, nasopharynx, oropharynx, hypopharynx,
larynx, nasal cavity and paranasal sinuses and salivary glands (1).
A number of risk factors are involved in the development of squamous cell carcinomas (SCC) in the head
and neck (1). SCCs develop in the head and neck from the combination of exposure to risk factors,
usually over long periods of time, and the host's body response to the exposure (2). There are many
potential risk factors that are associated with the development of SCC in the head and neck. These risk
factors include tobacco, alcohol and betel nut chewing; old age; genetic predisposition; nutritional status;
chronic inflammation and irritation; viruses; and industrial and occupational exposure (2,3). It has been
suggested that tobacco use and high alcohol consumption are responsible for up to 80% of all head and
neck cancers (3).
Many studies have demonstrated an association between the use of tobacco, both smoke and smokeless
products, and head and neck cancer (1,2). Heavy smokers have five to 25 times the risk of developing
head and neck cancer compared to non-smokers, and the risk seems to be dose dependent (4,5). Even
though the association is strong, it is not known which carcinogen(s) are involved and the mechanism(s)
are not well understood (2). Also, smokers are often exposed to other risk factors, especially poor
nutritional status and alcohol use (2). Environmental exposure to tobacco smoke in the home or workplace
may also pose a risk. One study demonstrated an increased risk of tongue cancer in women who did not
smoke or drink heavily but were exposed to second-hand smoke (6).
Heavy alcohol consumption has been shown to increase the risk of head and neck cancer independent of
tobacco use (3), although tobacco and alcohol seem to have a synergistic effect and repeated exposure
over time can increase the risk of developing primary and secondary SCCs particularly in the oral cavity
(1,2). The carcinogen acetaldehyde is a primary metabolite of alcohol and is thought to be one of the main
metabolites of alcohol involved in the development of SCCs. Acetaldehyde can be detected in the mouth
for up to 10 minutes after using an alcohol-based mouthwash (7). However, no association has been found
between the use of alcohol-based mouthwashes and head and neck cancers.
The chewing of betel nut, which is common in parts of Asia, is an independent risk factor for head and
neck cancer (2,3). It has a synergistic affect when combined with alcohol and tobacco use (3).
There is evidence Epstein-Barr virus (EBV), human papillomavirus (HPV) and human immunodeficiency
The role of nutrition in the etiology of head and neck cancers has been difficult to determine because there
are often confounding variables such as smoking, alcohol or the potential for an individual to have HPV (2).
The consumption of fruit and vegetables has been associated with a reduced risk of developing SCCs
(1,3,9,10). An observational study concluded that smokers have lower fruit and vegetable intakes and
higher intake of calories from fat than non-smokers (11). Nasopharyngeal carcinomas are significantly
more frequent in individuals who regularly consume processed meats containing nitrites (12).
Chronic inflammation and irritation (e.g. from rough teeth, poorly fitting dentures or fillings) have been
described as a risk factor by some authors. Poor oral hygiene is associated with oral SCCs, especially
when combined with heavy alcohol use and smoking (2). Individuals with the rare genetic conditions of
xeroderma pigmentosum, epidermolysis bullosa, or Bloom’s syndrome have a higher risk of developing
oral cancer independent of alcohol and tobacco use (2,3). Individuals with dystrophic epidermolysis
bullosa have an 80% mortality rate within five years of diagnosis and two-thirds of people die from
metastatic disease (13,14).
Several observational studies have investigated whether there is an association or increased risk between
individuals exposed to industrial chemicals in certain professions and different head and neck cancers (15-
23). These professions include dry cleaners; the textile or electronic industry; workers exposed to fumes
or gases from paint, rubber or plastics; wood, metal and leather workers; farmers; workers exposed to
pesticides and asbestos, formaldehyde and polycyclic aromatic hydrocarbons. Most of the studies had
small sample sizes and were based on subjective surveys (2). Some of the smaller studies reported a
relationship or increased risk, while larger studies found few associations. Further larger long-term studies
are needed to determine if particular industrial agents are related to an increased incidence of head and
neck cancer. Arsenic has been found to increase the risk of developing SCCs, both cutaneous and head
and neck mucosal, and other cancers (2,24). Of note, Chinese medicines were found to be the major
source of arsenic in one small Chinese study (24). Other major sources of arsenic can be contaminated
water, especially from wells (2).
Screening/Diagnosis
Medical Diagnosis and Staging
The initial medical assessment for diagnosing head and neck cancer involves the treating physician taking
a thorough case history followed by visual inspection, palpation, an indirect mirror examination and direct
endoscopy of the relevant anatomical areas in the head and neck (25). If a tumour is suspected or located,
further examination and a biopsy is recommended under anesthesia to determine the extent and type of
the tumour.
The Tumor Node Metastases (TNM) Staging System is used to classify head and neck cancers (25). The
staging system is classified by the location or site of the primary tumour. The sites include oral cavity,
nasopharynx, oropharynx, hypopharynx, larynx, nasal cavity and paranasal sinuses and salivary glands.
The global cancer statistics in 2008 estimated there were 128,000 deaths and 263,900 new cases of oral
cavity cancer (27). The highest prevalence of oral cancer was in Melanesia, South Central Asia and
Central and Eastern Europe. The lowest prevalence is in East Asia, Central America and Africa. It is
estimated 42% of deaths from oral cavity cancer are from tobacco use, while alcohol consumption
accounts for 16% of deaths globally. In developed countries, it is estimated 70% of deaths are from
tobacco use and 30% from heavy alcohol consumption. Oral cavity cancer rates are decreasing in the U.S
and U.K. as smoking rates decrease, but the rates are increasing in Eastern Europe, which is a reflection
Globally there was an estimated 84,000 people diagnosed and 51,600 deaths from nasopharyngeal cancer
(NPC) in 2008 (27). There are large differences in the distribution of nasopharyngeal carcinoma, both
demographically and geographically. Rates of NPC are higher in males both in developed and developing
countries. An estimated 92% of new cases are in developing countries, with the highest rates occurring in
South East Asia. There are also high incidence rates in South East China and parts of Southern Asia.
NPC is also relatively common in Inuit populations and Chinese and Filipino migrants living in the United
States. Individuals from high risk populations who migrate to low risk countries retain their higher risk of
developing nasopharyngeal carcinoma. This trend suggests that there could be both genetic and
environmental components. Certain associations have been identified between nasopharyngeal carcinoma
and risk factors such as EBV and certain processed foods that contain nitrogen-based compounds such
as fish preserved with sodium nitrate.
The global estimate of the number of new cases of laryngeal cancer diagnosed in 2008 was 150,000 (28).
In the U.K. there were 2,300 diagnosed in 2010; 1900 men and 400 women. This male to female ratio is
consistent with the suggestion that it is five times more common in men than in women. Seventy-five per
cent of the cases being diagnosed in individuals over 60 years of age. Smoking and alcohol are believed to
contribute to the incidence of laryngeal cancer.
Symptoms
The symptoms of head and neck cancer may vary depending on the site of the SCC and the presentation
of the head and neck cancer in the individual.
General tumours in the oral cavity may present as ulcers that do not heal (25). Symptoms may include
loose teeth or dentures, oral dysphagia, weight loss, localized bleeding, and otalgia or earache. Lip cancer
excluding skin cancers is the most common site and usually presents with an ulcerative lesion on the
bottom lip, which results in localized bleeding and pain or in some cases numbness from nerve
impairment (1). Tongue cancer is an infiltrative lesion, which causes localized pain and in some cases oral
dysphagia.
Symptoms of oropharyngeal cancers may include localized pain or bleeding, obstructive sleep apnea
and/or snoring and a neck mass (25). Individuals who are HPV positive often present with a cystic neck
mass. Ninety per cent of individuals with nasopharyngeal cancers have a neck mass. The most common
symptoms are hearing loss and otitis or ear infection, tinnitus or ringing in the ear, pain and impaired
muscle and nerve function as the tumour grows into surrounding tissues. Individuals with hypopharygeal
cancers are often asymptomatic until the later stages of the disease. Common symptoms include
dysphagia, weight loss, a neck mass and pain during swallowing.
Symptoms of laryngeal cancer depend where the tumour is located and may include long-term
hoarseness, dysphagia, ear pain, a chronic cough with or without blood and stridor (25). Subglottic
cancers are rare and occur with airway obstructions, dyspnea and stridor.
Co-Morbidities/Associated Diseases
The frequency of co-morbidities is high in individuals with head and neck cancer compared to other
cancers because of the risk factors of smoking, heavy alcohol use and HPV (29). There are no typical co-
morbidities associated with different head and neck cancers. Rather, associations have been
demonstrated between moderate to severe co-morbidities and reduced survival, primarily with early
detection and treatment of tumours rather than late stage tumours (29,30). Increased co-morbidity is
independently associated with poorer levels of survival in oropharyngeal, oral cavity, early stage laryngeal
and nasopharyngeal cancers (29,31). Co-morbidities associated with head and neck cancer influence the
prognosis, treatment and the decision to initiate palliative care rather than only relying on the diagnosis
and staging of the tumour and the individual's decision (29,30,32). For this reason, several instruments
have been developed and validated to assess the presence of co-morbidities in individuals with head and
neck cancer (30). Some authors have even suggested that co-morbidities should be included in the TMN
staging system because of their importance and improvement in determining the prognosis and treatment
(29,33). One study demonstrated that in oropharyngeal cancer, comorbidity combined with HPV status,
was found to be a better predictor of survival than co-morbidity and staging (29). Most studies investigating
co-morbidity and head and neck cancer use a retrospective cross-sectional design. There is a need to
investigate co-morbidity, treatment and outcome in longitudinal prospective studies (30).
Medical Treatment
Given that the vast majority of head and neck cancers are squamous cell carcinomas, treatment using
surgery and/or radiation therapy is successful in about 60-65% of individuals with head and neck SCC.
Successful treatment depends on the size, site and tissue infiltration of the tumour and HPV status
(34,35). Surgery is most frequently used for oral cavity SCCs because of the ease of accessibility and
ability to resect or reconstruct the oral cavity to minimize loss of function (36). However, radiation therapy
in combination with surgery is often recommended particularly with advanced stage disease. Radiation
therapy alone, with or without systemic therapy (chemotherapy and non-chemotherapy agents including
EGFR-inhibitors/MABs) is performed when surgical resection is not possible. In contrast, organ sparing
approaches (radiotherapy and/or chemotherapy) rather than surgical resection are preferred for resectable
SCCs of the oropharynx, hypopharynx and larynx.
Thirty to 40% of individuals present with early stage (stage I and II) head and neck SCC (35) and they have
a 60 to 90% chance of being cancer-free five years after treatment (34,36). The greatest risk to these
individuals is the development of a second malignancy (36,37), especially if the cancer is related to
tobacco and alcohol use (35).
Individuals with more advanced head and neck cancers (stage III and IVA and IVB) are treated with both
surgery and radiation therapy or chemotherapy and radiotherapy (34). Local therapy alone, that is surgery
and/or radiation therapy, historically resulted in high levels of recurrence and considerable morbidity such
as loss of tongue and speech and/or dysphagia. There is a 60% chance of developing local or regional
recurrences and a 20% chance of developing metastases or secondary primaries (34). When surgery is
not possible to remove the tumour and radiation therapy is the primary treatment, the survival rate is less
In the past, chemotherapy has been used for palliative care to relieve symptoms mainly when the head
and neck cancer has metastasized (34). Some sources suggest that in some stage III and IV SCC of the
head and neck combining chemotherapy and radiation therapy results in increased survival and reduced
morbidity (36). A meta-analysis of 10,741 individuals from 63 trials investigated individuals who had
received local and regional treatment with or without chemotherapy (38). The individuals who received
chemotherapy had a significant 4% survival benefit at two and five years. There was no significant benefit
of adjuvant or neoadjuvant chemotherapy.
16. What are the complications from gastrostomy tube placement and is there a preferred method of
placement?
Definitions
Adjuvant Chemotherapy: assists in the attempt to prevent, ameliorate or cure the disease usually after
surgery or in addition to radiation therapy in head and neck cancer (39).
Nasopharyngeal: upper part of the pharynx continuous with the nasal passages (39).
Neoadjuvant Chemotherapy: the administration of chemotherapy before the main therapy, which is
surgery and/or radiation therapy in head and neck cancer (39).
Canada
Title: The Role of the Registered Dietitian in Dysphagia Assessment and Treatment: A Discussion Paper
Description: The role of the registered dietitian in dysphagia assessment and treatment is described
including knowledge and skills needed for conducting swallowing assessments and providing therapy.
United Kingdom
Title: Guidance on Cancer Services: Improving Outcomes in Head and Neck Cancers - The Manual
Description: Framework from the National Institute of Health and Clinical Excellence (NICE) for the
management of head and neck cancers through a multidisciplinary approach including nutrition
intervention.
References
1. Stenson KM, Brockstein BR. Overview of head and neck cancer. UpToDate. 2013 [cited 2013
May10]. Available from http://www.uptodate.com/contents/overview-of-head-and-neck-cancer?
source=search_result&search=head+and+neck+cancer&selectedTitle=1~150
2. Monroe, M. Head and neck cancer: squamous cell carcinoma. Medscape. 2013 [cited 2013
May 10]. Available from: http://emedicine.medscape.com/article/1965430-overview
3. Stenson KM. Overview of head and neck cancer. UpToDate. 2013 [cited 2013 May10]. Available
from: http://www.uptodate.com/contents/epidemiology-and-risk-factors-for-head-and-neck-cancer?
source=search_result&search=head+and+neck+cancer+epidemiology&selectedTitle=1~150
4. Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin S, et al.
Epidemiology and risk factors for head and neck cancer. Semin Oncol. 1994 Jun [cited 2013
May 10];21(3):281-8. Citation available from: https://www.ncbi.nlm.nih.gov/pubmed/8209260
5. Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin S, et al. Smoking
and drinking in relation to oral and pharyngeal cancer. Cancer Res. 1988 Jun [cited 2013 May
10]:1;48(11):3282-7. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/3365707
6. Tan EH, Adelstein DJ, Droughton ML, Van Kirk MA, Lavertu P. Squamous cell head and neck
cancer in nonsmokers. Am J Clin Oncol. 1997 Apr [cited 2013 May 10];20(2):146-50. Abstract
available from: https://www.ncbi.nlm.nih.gov/pubmed/9124188
7. Lachenmeier DW. Alcohol-containing mouthwash and oral cancer--can epidemiology prove the
absence of risk? Ann Agric Environ Med. 2012 [cited 2013 May 10];19(3):609-10. Citation
available from: https://www.ncbi.nlm.nih.gov/pubmed/23020065
8. Sturgis EM, Cinciripini PM. Trends in head and neck cancer incidence in relation to smoking
prevalence: an emerging epidemic of human papillomavirus-associated cancers? Cancer. 2007
[cited 2013 Oct 7];110(7):1429-34. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/17724670
9. Freedman ND, Park Y, Subar AF, Hollenbeck AR, Leitzmann MF. Schatzkin A, et al. Fruit and
vegetable intake and head and neck cancer risk in a large United States prospective cohort
study. Int J Cancer. 2008 May 15 [cited 2013 May 10];122(10):2330-6. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/18092323
10. Boeing H, Dietrich T, Hoffmann K, Pischon T, Ferrari P, Lahmann PH, et al. Intake of fruits and
vegetables and risk of cancer of the upper aero-digestive tract: the prospective EPIC-study.
Cancer Causes Control. 2006 Sep [cited 2013 May 10];17(7):957-69. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/16841263
35. Fortin A, Couture C, Doucet R, Albert M, Allard J, Tetu B. Does histologic grade have a role in
the management of head and neck cancer? J Clin Oncol. 2001 [cited 2013 May10];19:4107-
4116. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/11689578
36. Carneiro BA, Brockstein BE, Stenson KM, Song S. Overview of treatment for head and neck
squamous cell cancer. UpToDate. 2013 [cited 2013 May10]. Available from:
http://www.uptodate.com/contents/overview-of-treatment-for-head-and-neck-squamous-cell-
cancer?source=search_result&search=treatment+head+and+neck+cancer&selectedTitle=2~150
37. Leon X, Quer M, Orris C, del Prado Venegas M. Can cure be achieved in patients with head and
neck carcinomas? The problem of second neoplasm. Expert Rev Anticancer Ther. 2001 [cited
2013 May10];1:125-33. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/12113119
38. Pignon JP, Bourhis J, Domenge C, Designe L. Chemotherapy added to locoregional treatment for
head and neck cancer squamous-cell car- cinoma: three meta-analyses of updated individual
data. MACH-NC Collaborative Group. Meta-analysis of chemotherapy on head and neck cancer.
Lancet. 2000 Mar [cited 2013 May10];355:949-55. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/10768432
39. MedlinePlus. National institute of health: US national library of medicine. 2012. [Cited 2013 May
16]. Link not available.
Oral Mucositis
Oral mucositis is the inflammation of the mucosal membranes that line the mouth, throat and esophagus
(1). This inflammation can cause pain with swallowing (odynophagia), alterations in taste (dysgeusia),
mouth dryness (xerostomia) and increase the risk of infections, such as oral thrush (2). Oral mucositis is
a common side-effect of radiation treatments directed towards the head and neck region, with the severity
directly related to dosage, volume and overall duration of treatment. Oral mucositis can also be caused by
some cytotoxic chemotherapeutic agents, such as high dose melphalan (used in hematopoietic stem cell
transplantation (HSCT)) or anti-metabolites, such as fluorouracil (5-FU, commonly used in the treatment of
bowel cancers). Oral mucositis can develop in up to 100% of individuals receiving these treatments (1).
The causes of oral mucositis are multifactorial but most likely the damage caused by chemo(radio)
Stomatitis is a term previously used in the literature to describe oral inflammation or oral infections that
develop as a result of chemotherapeutic agents (2). At a clinical level, the terms stomatitis and oral
mucositis are frequently used interchangeably, but the use of oral mucositis to describe both conditions is
now common. However, stomatitis technically refers to any inflammation of the oral cavity, inclusive of the
mucosa, dentition/periapices, periodontium or infections of the oral tissue. Oral mucositis is instead
defined as the inflammation of the oral mucosa that results from chemotherapeutic agents or ionizing
radiation.
Taste Changes
Taste changes include dysgeusia (distorted taste perception), hypergeusia (enhanced taste sensitivity),
hypogeusia (diminished taste sensitivity) and ageusia (complete loss of taste). The etiology of taste
changes is currently unknown and often described as multifactorial (2). Individuals receiving radiation to
the head and neck region frequently experience changes in taste both during and after treatment. Gradual
recovery of taste can take up to two years post-radiation and thus can result in secondary complications
such as poor oral intake, weight loss and decreased quality of life (4,5).
Those individuals who receive six to eight weeks of curative-intent radiotherapy at a dose >60 Gy often
experience a permanent loss of taste, due to the damage caused by radiation on the major salivary glands
(6). Individuals who also develop xerostomia (see below) may also experience taste changes due to the
change in both the amount and composition of salivary secretions produced (2).
Certain chemotherapeutic drugs have also been associated with a high risk of causing taste changes
(including cisplatin, carboplatin, cyclophosphamide, doxorubicin and 5-FU) (6). High dose
chemotherapeutic agents such as melphalan, often used in HSCT, also may lead to altered taste
perceptions and change.
Other contributing factors for taste change development include surgery to the oral cavity and/or tongue
and other medications, such as antibiotics, antidepressants, antihypertensives and analgesics (2,7). The
presence of smoking, poor oral hygiene practices and an advancing age have also been implicated (7).
Xerostomia and thick saliva often co-exist, because they are both direct consequences of a reduction in
the amount of and/or type of saliva produced (2,6). During radiotherapy to the head and neck region, thick
and ropey saliva often presents within the first two weeks, progressively worsening throughout treatment.
Most of the saliva in the mouth is produced by the parotid, submandibular and sublingual glands, and each
gland produces a different type of saliva as they are comprised of different cell types and thus have
differing degrees of sensitivity to the effects of radiotherapy (10,11). The majority of salivary production is
produced by the parotid glands (60-65%), with the submandibular glands producing 20-30% and the
sublingual glands 2-5% (10). The parotid glands are primarily made up of serous cells, and therefore
produce more watery salivary secretions; whereas the submandular and sublingual glands are comprised
of a mixture of serous cells and mucous acini, resulting in the production of thicker, stickier salivary
secretions. Serous cells are the most sensitive to radiation; thus, as a result, radiation causes a reduction
not only in the amount of watery salivary secretions produced but also an imbalance in the proportions of
watery and thick saliva (with more thick saliva and less watery saliva) and a reduction in total salivary
secretion volume produced. The degree of salivary gland compromise depends on the total dose of
radiation and the degree of salivary gland involvement in the radiation field (10). Xerostomia and thick saliva
have been identified as the most persistent long-term symptom in individuals who have received head and
neck radiation (11).
Screening/Diagnosis
Individuals receiving treatment for cancer should undergo a full nutrition assessment, ideally before the
treatment starts, and be regularly screened for nutrition-related side-effects throughout the duration of the
treatment (12).
Prevalence
The prevalence of cancer-related mouth changes is hard to establish, given differences seen for cancer
type, treatment regimens used, time frames of followup, methods of assessment and the specific patients
populations studied.
Symptoms
Nutrition related cancer side-effects that affect the mouth are as follows:
Oral Mucositis
mouth pain/burning sensation in the mouth
redness of the mouth (sign of inflammation)
red, raw patches, sores or ulcers in the mouth
dry, cracked or blistered tongue and/or lips
bleeding of the lips, gums, or oral cavity
increased risk of infection (oral thrush)
alterations in taste
heightened sensitivity to hot and cold foods
mouth dryness
Taste Changes
dysgeusia (distorted taste perception, i.e. foods tasting metallically/foul/salty/rancid/bitter)
hypergeusia (enhanced taste sensitivity, i.e. extremely sweet/sour/bitter)
hypogeusia (diminished taste sensitivity, i.e. foods tasking bland/plain/blunted/no taste at all)
ageusia (complete loss of taste, i.e. unable to distinguish between different foods) (4-7,14).
Co-Morbidities/Associated Diseases
The major co-morbidity is the cancer that necessitated the treatment causing the side-effects (2). The
management of other co-morbidities such as diabetes may also be affected if the symptoms of thick
saliva, mucositis, taste changes and mouth dryness are not effectively addressed.
With xerostomia and oral mucositis, there is an increased risk of both local and systemic infection and
dental disease. Malnutrition as a result of these side-effects can also develop in severe cases.
Medical Treatment
Oral Mucositis
The medical treatment for oral mucositis involves meticulous oral care (involving good oral hygiene, denture
care and lip care), fluoride treatments, and frequent oral rinsing (1,2). Topical anesthetics may be used to
manage mouth pain, and if infection is present, antibiotics may be needed (1). If mucositis is so severe
that individuals find it too painful to eat, nutritional support (i.e. enteral nutrition support) may be needed
(16).
Taste Changes
At present there are no medical treatments identified for the management of taste changes in individuals
with cancer (2,17). Self-management strategies to deal with taste changes are often not addressed by
research and largely rely on anecdotal evidence. More research is needed to study the usefulness of
recommended strategies for taste changes and the impact on the individual’s quality of life during and after
cancer treatment.
Nutrition Care
See Additional Content: Cancer – Nutritional Implications of Treatment Toolkit.
Definitions
Nil
Other
Nil
References
1. Lalla RV, Bowen J, Barasch A, Elting L, Epstein, J, Keefe D et al. MASCC/ISOO clinical
practice guidelines for the management of mucositis secondary to cancer therapy:
MASCC/ISOO Mucositis Guidelines. Cancer. 2014;120:1453-61. doi: 10.1002/cncr.28592. Epub
2014 Feb 25. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/24615748
2. PDQ® Supportive and Palliative Care Editorial Board. PDQ oral complications of chemotherapy
and head/neck radiation. Bethesda, MD: National Cancer Institute; 2016. Available from:
https://www.cancer.gov/about-cancer/treatment/side-effects/mouth-throat/oral-complications-hp-
pdq
3. Keefe DM, Schubert MM, Elting LS, Sonis ST, Epstein JB, Raber-Durlacher JE, et al. Updated
clinical practice guidelines for the prevention and treatment of mucositis. Cancer. 2007;109:820-
31. doi: 10.1002/cncr.22484. Abstract available from: https://pubmed.ncbi.nlm.nih.gov/17236223
4. Ruo Redda MG, Allis S. Radiotherapy-induced taste impairment. Cancer Treatment Reviews.
2006;32:541-7. doi: 10.1016/j.ctrv.2006.06.003. Abstract available from:
https://www.ncbi.nlm.nih.gov/pubmed/16887272
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