Cancer - Colorectal

Cancer - Colorectal 
Category: Health Condition/ Disease
Practice Questions
Q1: What nutrients/dietary factors are associated with a decreased risk of developing colorectal,
colon and rectal cancer?
Subcategory: Assessment
Updated: 2020-04-13
Key Practice Point #1

Recommendation
Consuming whole grains (e.g. 90 g/day) and replacing refined grains with whole grains protects against
colorectal cancer.
Evidence Summary
The 2018 WCRF/AICR Continuous Update Project reported a dose-response meta-analysis demonstrating
a 17% decreased risk of colorectal cancer for consuming each additional 90 g/day whole grains. When
stratified by cancer site, the protective effect of whole grains was observed for colon cancer but not rectal
cancer.
A 2019 systematic review and meta-analysis commission by the World Health Organization reported that
high compared to low whole grain intake was associated with a 13% reduction in colorectal cancer.
A dose-response relationship identified that each additional 15 g/day whole grains reduced the incidence
of colorectal cancer.
Grade of Evidence: B
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.
Evidence
a. The 2018 WCRF/AICR Continuous Update Project (CUP) report identified strong evidence that
consuming whole grains decreased the risk of colorectal cancer (1). This was based on six
prospective cohort studies, all of which adjusted for age, physical activity, BMI, alcohol
consumption, smoking, red meat and hormone therapy in women. A dose-response meta-
analysis (n=8320 cases) identified a decreased risk of colorectal cancer per 90 g/day whole
grains (RR, 0.83; 95%CI, 0.78 to 0.89) with low heterogeneity (I2=18%). When stratified by
cancer site, the inverse association was for colon cancer only (n=4 studies; per 90 g/day whole
grains: RR, 0.82; 95%CI, 0.73 to 092), but not rectal cancer. The CUP concluded that given the
consistent evidence with a dose-response relationship, a clear dose-response
Cancer - Colorectal
© 2021 Dietitians of Canada. All rights reserved. PAGE 1
relationship, “consumption of whole grains probably protects against colorectal cancer”.
b. A series of systematic reviews and meta-analyses commissioned by the World Health
Organization examined the relationship between carbohydrate quality and non-communicable
disease incidence, mortality and risk factors (2). Prospective cohort studies (searched to April
2017) were included that reported associations between whole grain intake and mortality,
cardiovascular disease and colorectal cancer incidence or cancer mortality. For colorectal
cancer incidence, seven cohort studies were included (n=8803 cases), four of which were in the
WCRF/AICR CUP report (1). Data was assessed using GRADE process (2). Overall results
identified that higher compared to lower intake of whole grains was associated with reduced
incidence of colorectal cancer (RR, 0.87; 95%CI, 0.79 to 0.96, moderate quality evidence). A
dose-response association was also identified (RR, 0.97; 95%CI, 0.95 to 0.99 for each additional
15 g/day whole grains consumed). For all non-communicable diseases, the authors concluded
that replacing refined grains with whole grains would be expected to benefit health.
Comments
Whole grain foods are generally required to have a similar nutrient composition to the original grain,
without considering the amount of processing (2). However, many whole grain products may be highly
processed (e.g. breakfast cereals), which may impact disease risk factors. There is a lack of
epidemiological evidence examining the impact of such processing on clinical outcomes. Therefore, the
recommendation from the WHO report was to emphasize the benefits of naturally occurring whole grains
that have been minimally processed.
Rationale
Whole grains may reduce colorectal cancer risk by contributing a source of dietary fibre, which can
produce short-chain fatty acids, reduce intestinal transit time, bind carcinogens and regulate glycemic
response (1). Furthermore, whole grains are a source of bioactive compounds, including nutrients (i.e.
vitamin E, selenium, copper, zinc) and phenolic compounds, the latter of which have been shown to
stimulate antioxidative activity in experimental studies.
References
1. World Cancer Research Fund/American Institute for Cancer Research. Continuous Update
Project Expert Report 2018. Diet, nutrition, physical activity and colorectal cancer. 2018.
Available from: https://www.wcrf.org/dietandcancer
2. Reynolds A, Mann J, Cummings J, Winter N, Mete E, Te Morenga L. Carbohydrate quality and

human health: a series of systematic reviews and meta-analyses. Lancet. 2019 Feb 2;393
(10170):434-45. doi: 10.1016/S0140-6736(18)31809-9. Epub 2019 Jan 10. Abstract available
from: https://www.ncbi.nlm.nih.gov/pubmed/30638909
Cancer - Colorectal
Recommendation
The consumption of foods containing dietary fibre protects against colorectal cancer. Fibre intake in the
range of 25-29 g/day is adequate with additional health benefits likely at intakes >30 g/day.
Evidence Summary
The 2018 WCRF/AICR Continuous Update Project reported a dose-response meta-analysis demonstrating
a 9% decreased risk of colorectal cancer for each 10 g/day fibre.
{grade_b}
A 2019 systematic review and meta-analysis commission by the World Health Organization reported that
high compared to low intake of dietary fibre was associated with a 16% reduction in colorectal cancer. A
dose-response relationship identified that each additional 8 g/day of dietary fibre reduced the incidence of
colorectal cancer. Significant inverse associations were observed for cereal fibre {grade_b} but not when
stratified by other food groups (fibre from vegetables, fruit and legumes) or subcategories (soluble or
insoluble fibre); however, this was based on very limited data. Overall results suggest that fibre intake in
the range of 25-29 g/day is adequate with additional benefits to health at intakes of >30 g/day.
{grade_c}
Grade of Evidence: B & C
Evidence
a. The 2018 WCRF/AICR Continuous Update Project (CUP) report identified strong evidence that
consuming foods containing dietary fibre decreased the risk of colorectal cancer (1). This was
based on 23 prospective cohort studies (including 13 studies reported in an earlier 2005 pooled
analysis), all of which adjusted for age and most adjusted for physical activity, BMI, alcohol
consumption, smoking, red meat and hormone therapy in women. A dose-response meta-
analysis of 21 studies (n=16,562 cases) found a nonsignificant association per 10 g/day fibre
(RR, 0.93; 95%CI, 0.87 to 1.00) with substantial heterogeneity (I2=72%). An analysis of the
results of individual studies (rather than the pooled analysis results) (n=15 studies, 14,876
cases) identified a significant dose-response association of reduced colorectal cancer per 10
g/day fibre (RR, 0.91; 95%CI, 0.88 to 0.94) with no heterogeneity (I2=0%). When stratified by sex
and geographical region, significant inverse associations were observed for colorectal cancer risk
in men and women and in North American and European populations. When stratified by cancer
site, no associations were observed for colon or rectal cancer. The CUP concluded that given the
consistent evidence “consumption of foods containing dietary fibre probably protects against
colorectal cancer”.
b. A series of systematic reviews and meta-analyses commissioned by the World Health
Organization examined the relationship between carbohydrate quality and non-communicable
disease incidence, mortality and risk factors (2). Prospective cohort studies (searched to April
2017) were included that reported associations between dietary fibre intake and mortality,
cardiovascular disease and colorectal cancer incidence or cancer mortality. For colorectal
cancer incidence, 22 cohort studies were included (n=22,920 cases) (1). Data was assessed
using GRADE process (2). Overall results identified that higher compared to lower intake of
Cancer - Colorectal
dietary fibre was associated with reduced incidence of colorectal cancer (RR, 0.84; 95%CI, 0.78
to 0.89, moderate quality evidence). A dose-response association was also identified (RR, 0.92;
95%CI, 0.89 to 0.95 for each additional 8 g/day of fibre). For sources of dietary fibre, a significant
inverse association was reported for high versus low intake of cereal fibre (n=6 studies, RR, 0.87;
95%CI, 0.81 to 0.94; moderate quality evidence), but no significant associations were observed
for other food groups (i.e. fibre from vegetables, fruit, legumes) or by subcategories of fibre (i.e.
soluble or insoluble); however, this was based on low and very low quality evidence. For all non-
communicable diseases, the authors concluded that fibre intake in the range of 25-29 g/day is
adequate, with dose response data suggesting additional benefits at intakes >30 g/day.
Comments
The WCRF/AICR CUP used the definition of dietary fibre as constituents of plant cell walls that are not
digested in the small intestine (1). As the observations in the report related to foods containing dietary
fibre, there was no distinction between fibre types, other than studies that reported separate effects for
specific food types (e.g. whole grains).
Rationale
Fibre has been hypothesized to protect against colorectal cancer through a variety of mechanisms
including decreasing transit time, increasing fecal bulk and through the production of short-chain fatty
acids resulting from colonic bacterial fermentation (1). In particular, the short-chain fatty acid butyrate has
been shown to have anti-proliferative effects in experimental studies.
References
2. Reynolds A, Mann J, Cummings J, Winter N, Mete E, Te Morenga L. Carbohydrate quality and
human health: a series of systematic reviews and meta-analyses. Lancet. 2019 Feb 2;393
(10170):434-45. doi: 10.1016/S0140-6736(18)31809-9. Epub 2019 Jan 10. Abstract available

Recommendation
There is some limited evidence for a beneficial effect of the following foods and the reduced colorectal
cancer risk:
foods containing vitamin C
fish
multivitamin supplements.
Cancer - Colorectal
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
The 2018 WCRF/AICR Continuous Update Project reported limited but generally consistent evidence for a
beneficial effect of foods containing vitamin C, fish consumption and multivitamin supplementation and the
reduced risk of colorectal cancer. Evidence was limited but consistent for an increased risk of colorectal
cancer with low intakes (<100 g/day) of fruit and non-starchy vegetables.
A 2018 systematic review and meta-analysis reported that high compared to low intake of vegetables and
fruit was associated with a small reduced risk of colon cancer. A dose-response relationship was identified
suggesting that each additional 100 g/day vegetables and fruit reduced risk of colon cancer.
Grade of Evidence: C
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).
See Additional Content:

Do calcium and milk products impact colorectal cancer risk? Does vitamin D impact colorectal cancer
risk?
What is the effect of folate/folic acid supplements on the risk of colorectal cancer?
Evidence
a. The WCRF/AICR Continuous Update Project (CUP) report identified limited evidence for the
following foods/nutrients and colorectal cancer risk (1):
Foods containing vitamin C decreases risk. Results were based on six prospective
cohort studies (n=4391 cases), most of which adjusted for age, physical activity, BMI,
alcohol consumption, smoking, red meat and hormone therapy in women. The dose
response analysis identified a decreased risk of colon cancer per 40 mg/day vitamin C
(RR, 0.94; 95% CI, 0.89 to 0.99) with moderate heterogeneity (I2=50%). The CUP
concluded that the evidence was limited but generally consistent that consumption of
foods containing vitamin C decreases risk of colon cancer.
Low intake (<100 g/day) of fruits and non-starchy vegetables increases risk. This was
based on a dose-response meta-analysis of 10 studies (n=10,999 cases) that identified
an inverse association per 100 g/day fruit and non-starchy vegetables (RR, 0.98; 95%CI,
0.97 to 0.99). A non-linear relationship was observed with increased risks at low intakes
(<300 g/day) and decreased risk at high intakes (>500 g/day). When stratified by sex,
the inverse association was observed for men, but not women. When stratified by
cancer site, no associations were observed for colon or rectal cancer.
Cancer - Colorectal
Fish consumption decreases risk. This was based on 11 studies (n=10,356 cases)
included in the dose-response meta-analysis, which showed a reduced risk of colorectal
cancer per 100 g/day fish (RR, 0.89; 95%CI, 0.80 to 0.99). In sensitivity analysis results
were no longer significant when the EPIC study was removed, which contributed to 40%
of the weight. Furthermore, no association was observed when analysis adjusted for
meat intake. When stratified by sex, associations were significant in men only. When
stratified by cancer site, no associations were observed for colon and rectal cancer. The
CUP concluded that evidence for a beneficial effect of fish consumption was limited but
consistent.
Multivitamin supplements decrease risk. The CUP included one RCT (the Physicians’
Health study) that examined combinations of a multivitamin supplement, vitamin E,
vitamin C and beta-carotene or placebo in 14,641 male physicians >50 years. After 10
years, results showed no effect on colorectal cancer (RR, 0.89; 95%CI, 0.68 to 1.17).
The CUP also included a meta-analysis of 11 cohort studies (n=8072 cases), which
reported an association of multivitamin supplement users and reduced risk of colorectal
cancer (RR, 0.88; 95% CI, 0.79 to 0.98), but with moderate heterogeneity (I2 =47%). The
CUP concluded that evidence for benefits of multivitamin supplements was limited but
consistent.
b. A systematic review and meta-analysis (searched to April 2017) examined the relationship
between 12 major food groups (defined a priori) and colorectal cancer risk (2).
For vegetables, 20 studies (n=20,490 cases) were included comparing high versus low
intake (range 972 to 0 g/day). Results showed a small inverse association (RR, 0.96;
95%CI, 0.9 to 1.00) and a dose response relationship was identified (each additional 100
g/day vegetables: RR, 0.97; 95%CI, 0.96 to 0.98). In subgroup analyses, the
association of high versus low vegetable intake was observed for reduced risk of colon
cancer but not rectal cancer.
For fruit intake, 19 studies (n=20,148 cases) were included comparing high versus low
intake (range 1384 to 4 g/day). Results showed that high fruit intake was associated
with reduced risk of colorectal cancer (RR, 0.93; 95% CI, 0.88 to 0.98) and a dose-
response relationship was reported (each additional 100 g/day fruit: RR, 0.97; 95%CI,
0.95 to 0.99, but with heterogeneity, I2-61%). In subgroup analyses, the inverse
association was observed for colon but not rectal cancer.
For fish, 21 studies (n=19,996 cases) were included comparing high versus low fish
intake (range 280 to 0 g/day). No associations were observed comparing highest to
lowest fish intake (RR, 0.96; 95%CI, 0.90 to 1.01) and no dose-response relationship
was identified.
Comments
The WCRF/AICR recommends at least 400 g/day of non-starch vegetables and fruit (3). Examples of non-
starchy vegetables include green leafy vegetables, broccoli, okra, eggplant and non-starchy roots (e.g.
Cancer - Colorectal
carrots, rutabaga, turnips), but not starchy roots (e.g. potatoes, yams or cassava).
Rationale
Vitamin C is suggested to exert a protective effect on colorectal cancer through its potent antioxidant
activity (1). In addition to vitamin C, vegetables and fruit can provide a number of potentially anti-cancerous
agents including: fibre, carotenoids, vitamin E, folic acid, selenium, dithiolthiones, isothiocynates,
flavonoids, phenols, plant sterols and allium compounds.
References
2. Schwingshackl L, Schwedhelm C, Hoffmann G, Knüppel S, Laure Preterre A, Iqbal K, et al. Food
groups and risk of colorectal cancer. Int J Cancer. 2018 May 1;142(9):1748-58. doi:
10.1002/ijc.31198. Epub 2017 Dec 14. Abstract available
3. World Cancer Research Fund/American Institute for Cancer Research. Diet, nutrition, physical
activity and cancer: a global perspective; third expert report. 2018. Available
from: https://www.wcrf.org/dietandcancer/contents
Q2: Do calcium and milk products impact colorectal, colon or rectal cancer risk? Does vitamin D
impact colorectal, colon or rectal cancer risk?
Updated: 2020-04-14

Recommendation
Evidence from cohort studies is reasonably consistent for a beneficial effect of dairy products (including
milk and dietary calcium) and calcium supplements (200-1000 mg/day) on reduced colorectal cancer,
colon and rectal cancer risk. Limited evidence for specific dairy products suggests beneficial effects of low
fat milk, yogurt and cheese on reducing the risk of colorectal cancer, but not high fat milk; however, this
analysis is limited to fewer studies and not all cancer subsites. No adverse effects of dairy product
consumption on colorectal cancer were identified.
Evidence Summary
The WCRF/AICR Continuous Update Project (2018) reported a dose-response meta-analysis
demonstrating a decreased risk of colorectal cancer consuming dairy products, milk and dietary calcium
{grade_b}; however evidence for cheese was not strong. When stratified by cancer site, inverse
Cancer - Colorectal
associations between dairy product consumption and dietary calcium were observed for colon cancer but
not rectal cancer. When stratified by sex, an inverse association between milk intake and colorectal
cancer was reported for men, but not women. {grade_c}
The WCRF/AICR Continuous Update Project (2018) reported results from observational studies of an
inverse association between calcium supplements (200-1000 mg/day) and reduced risk of colorectal
cancer. However, one large RCT of calcium and vitamin D supplement failed to report a reduced risk of
colorectal cancer. {grade_c}
A 2019 systematic review and meta-analysis of observational studies identified an inverse relationship
between higher consumption of dairy products and milk with a 15-20% reduced risk of colorectal cancer,
colon and rectal cancer {grade_b}. Higher consumption of low fat milk, yogurt and cheese were associated
with reduced risk of colorectal cancer, but not all subsites of cancer; however this analysis was restricted
to fewer studies. No association was observed between higher consumption of high fat milk and risk of
colorectal cancer. No adverse effects of any type of dairy product on colorectal cancer risk were
observed. {grade_c}
Evidence
a. The WCRF/AICR Continuous Update Project (CUP) report identified strong evidence that the
consumption of dairy products protects against colorectal cancer (1). The CUP conclusion was
based on consistent evidence for dairy products, milk, cheese and dietary calcium; however,
evidence for cheese consumption was not significant. The CUP concluded that “consumption of
dairy products probably protects against colorectal cancer” (1). Overall results for dairy products
and specific dairy products were as follows:
For dairy products, the CUP included 14 studies, all of which adjusted for age and most
adjusted for physical activity, BMI, alcohol consumption, smoking, red meat and
hormone therapy in women. A dose-response meta-analysis of 10 studies (n=14,859
cases) found a reduced risk per 400 g/day dairy (RR, 0.87; 95%CI, 0.83 to 0.90) with
low heterogeneity between studies (I2=18%). When stratified by sex and cancer site,
significant associations were observed for colorectal cancer risk in men and women;
however, a significant inverse association was observed for colon cancer (per 400 g/day:
RR, 0.878; 95%CI, 0.81 to 0.94) but not rectal cancer.
For milk products, nine of 13 studies (n=10,738 cases) were included in the dose-
response meta-analysis, which found a reduced risk of colorectal cancer per 200 g/day
milk intake (RR, 0.94; 95%CI, 0.92 to 0.96) with no heterogeneity observed. When
stratified by sex, a significant inverse association was observed for men, but not for
women. When stratified by cancer site, significant inverse associations were reported for
both colon and rectal cancer.
For cheese, seven of nine studies (n=6,462) included in the dose-response meta-
analysis showed no association with colorectal cancer risk (RR, 0.94; 95%CI, 0.87 to
Cancer - Colorectal
1.02) with low heterogeneity among studies (I2=10%).
For dietary calcium, 13 studies (n=11,519 cases) were included in a dose-response
meta-analysis, which found a decreased risk of colorectal cancer per 200 mg/day
calcium (RR, 0.94; 95%CI, 0.93 to 0.96; I2=0%). This inverse association remained
significant when stratified by sex. When stratified by cancer site, a significant inverse
association was reported for colon, but not rectal cancer.
b. The WCRF/AICR CUP also identified strong evidence that taking calcium supplements
decreased the risk of colorectal cancer (1). One RCT (Women’s Health Initiative of >36,000
postmenopausal women) was included that randomized women to calcium (1000 mg/d) and
vitamin D (400 IU/d) or placebo for seven years. Results found no significant effect of calcium and
vitamin D compared to placebo on colorectal cancer risk (RR, 0.81; 95%CI, 0.58 to 1.13). For
prospective cohort studies, comparing highest to lowest calcium supplement intake (i.e. 200-
1000 mg/day versus 0 mg/day), six of eight cohort studies reported inverse associations with
colorectal cancer risk. The CUP concluded that evidence was generally consistent that, “taking
calcium supplements probably protects against colorectal cancer”.
c. A 2019 systematic review and meta-analysis examined the association between different types
of dairy products and the incidence of colorectal cancer (2). A total of 15 prospective cohort
studies (n=>1.3 million adults with 11,733 cases) and 14 case-control studies (n=24,319 adults)
were included. Study quality (assessed by Newcastle-Ottawa Scale, with a maximum score of 9)
excluded low quality studies with a score <6. Pooled results for the higher quality cohort studies
are summarized:
For total dairy products, eight cohort studies (n=8424 cases) identified a decreased risk
of colorectal cancer associated with high compared to low intake (RR, 0.80; 95% CI,
0.70 to 0.91). Similar inverse associations were observed when examined for colon
cancer (distal and proximal) and rectal cancer. A dose response relationship was also
identified: per 1 serving (200 g) increase in dairy products, a reduced risk of colorectal
cancer was observed (RR, 0.92; 95%CI, 0.88 to 0.96).
For total milk consumption, nine cohort studies (n=9118 cases) were included that
showed a reduced risk of colorectal cancer comparing the highest to lowest
consumption of milk (RR, 0.82; 95%CI, 0.76 to 0.88). Similar results were observed
when comparing highest to lowest total milk consumption for reduced risk of colon
cancer (proximal and distal) and rectal cancer. For whole milk, comparing the highest to
lowest consumption, no association was observed for colorectal cancer (n=3 studies:
RR, 0.97; 95%CI, 0.86 to 1.09). However for low fat milk consumption, comparing the
highest to lowest intake, a reduced risk of colorectal cancer (n=2 cohort studies: RR,
0.76; 95%CI, 0.66 to 0.88) and colon cancer (RR, 0.73; 95%CI, 0.61 to 0.87). A dose
response relationship was also identified: per 1 serving (200 g) increase in total milk, a
reduced risk of colorectal cancer was observed (RR, 0.90; 95%CI, 0.84 to 0.93).
For yogurt, four cohort studies (n=4899 cases) found a reduced risk of colorectal cancer
when comparing the highest to lowest consumption of yogurt (RR, 0.87; 95%CI, 0.66 to
1.07). No dose response relationship was identified for yogurt.
Cancer - Colorectal
For cheese, results from four cohort studies (n=8557 cases) identified a reduced risk of
colorectal cancer when comparing the highest to lowest consumption of cheese (RR,
0.85; 95%CI, 0.76 to 0.96). A dose response relationship was also identified: per 1
serving (30 g) increase in cheese, a reduced risk of colorectal cancer was observed (RR,
0.93; 95%CI, 0.88 to 0.98).
Rationale
Milk may exert an effect on colorectal cancer through its calcium content, which influences cell growth
and apoptosis (1). Calcium may also bind to bile acids and free fatty acids and prevent carcinogenic
effects on the mucosa of the colorectum and may also promote cell differentiation. In addition, milk
contains bioactive constituents (e.g. lactic acid-producing bacteria, lactoferrin), which may also play a role
in protecting against colorectal cancer.
References
2. Barrubés L, Babio N, Becerra-Tomás N, Rosique-Esteban N, Salas-Salvadó J. Association
between dairy product consumption and colorectal Cancer risk in adults: a systematic review
and meta-analysis of epidemiologic studies. Adv Nutr. 2019 May 1;10(suppl_2):S190-S211. doi:
10.1093/advances/nmy114. Abstract available

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
The WCRF/AICR reported a dose-response meta-analysis demonstrating a decreased risk of colorectal
cancer for consuming foods containing vitamin D and a decreased risk of colon cancer for vitamin
D supplements. No association was reported for plasma vitamin D and colorectal cancer risk.
{grade_c}
A 2017 systematic review and meta-analysis of RCTs reported no overall effect of vitamin D supplements
compared to placebo on colorectal cancer occurrence or colorectal adenomas {grade_b}; however, results
of additional studies are needed to examine the effect of vitamin D supplements on overall cancer
occurrence and mortality {grade_c}.
Cancer - Colorectal
Evidence
a. The 2018 WCRF/AICR Continuous Update Project (CUP) identified limited evidence that vitamin D
D (including foods and supplemental vitamin D) was associated with a decreased risk of
colorectal cancer (1). For foods containing vitamin D, the CUP referenced the 2010 dose-
response meta-analysis of 10 studies (n=5171 cases) that reported a decreased risk of
colorectal cancer per 100 IU/day vitamin D (RR, 0.95; 95%CI, 0.93 to 0.98, with low
heterogeneity). For vitamin D supplements, a total of three cohort studies were included; the
2010 dose-response meta-analysis of two studies (n=415 cases) reported a decreased risk of
colon cancer per 100 IU/day (RR, 0.93; 95% CI, 0.88 to 0.98). For serum vitamin D, 11 studies
(n=4801 cases) were included in a dose-response meta-analysis that found no association per
30 nanomoles per litre (RR, 0.92; 95%CI, 0.85 to 1.00) with moderate heterogeneity (I2=54%),
which was explained by the direction of the effect. The panel commented that serum vitamin D
status could be influenced by sun exposure, season, obesity, smoking and measurement error.
Overall, the report concluded that evidence for vitamin D was limited but generally consistent for
foods containing vitamin D and supplemental vitamin D for reducing colorectal cancer risk.
b. A systematic review and meta-analysis (searched to 2017) examined evidence from RCTs
regarding the effect of vitamin D supplementation on non-skeletal disorders (2). As relates to
cancer outcomes, the authors identified two meta-analyses from 2014, both of which found no
effect of vitamin D supplements on the incidence of all cancer or any specific cancer. In
particular, a 2014 Cochrane, which reported results from five trials (n=45,598 participants), found
that vitamin D supplements (400-2000 IU/day) had no effect on colorectal cancer occurrence
(RR, 1.11; 95%CI, 0.92 to 1.34, with no heterogeneity). Results from three trials (n=4967 adults)
not included in the earlier meta-analyses were uncertain for an effect of vitamin D supplements
on any cancer occurrence as one study showed a trend for reduced risk. One of the trials
(n=2259 adults) that specifically examined incidence of colonic polyps, which can give rise to
colorectal cancer, found no effect of vitamin D supplementation (1000 IU/day) over three to five
years compared to placebo (2). A recently reported five-year follow-up to this study in 1121
adults found no effect vitamin D versus placebo on colorectal adenomas (RR, 1.04; 95%CI, 0.93
to 1.17) (3). The authors of the review suggest that results of ongoing trials are needed before
any firm conclusions can be made about the effect of vitamin D supplements on cancer
occurrence or mortality (2).
References
2. Autier P, Mullie P, Macacu A, Dragomir M, Boniol M, Coppens K, et al. Effect of vitamin D
supplementation on non-skeletal disorders: a systematic review of meta-analyses and
randomised trials. Lancet Diabetes Endocrinol. 2017 Dec;5(12):986-1004. doi: 10.1016/S2213-
Cancer - Colorectal
8587(17)30357-1. Epub 2017 Nov 5. Abstract available
3. Calderwood AH, Baron JA, Mott LA, Ahnen DJ, Bostick RM, Figueiredo JC, et al. No evidence
for posttreatment effects of vitamin D and calcium supplementation on risk of colorectal
adenomas in a randomized trial. Cancer Prev Res (Phila). 2019 May;12(5):295-304. doi:
10.1158/1940-6207.CAPR-19-0023. Epub 2019 Mar
4. https://www.ncbi.nlm.nih.gov/pubmed/30833381
Q3: What nutrients and dietary factors are associated with an increased risk of developing
colorectal, colon and rectal cancer?
Updated: 2020-04-14

Recommendation
Limiting the consumption of processed meat (little to none) may reduce the risk of colorectal cancer.
Limiting the consumption of red meat (<350-500 g/week cooked) or foods containing heme iron (including
red and processed meat, fish and poultry) has smaller and uncertain benefits on reducing the risk of
colorectal cancer.
Evidence Summary
Processed Meat
The World Cancer Research Fund/American Institute of Cancer Research Continuous Update Project
(2018) reported a dose-response meta-analysis suggesting a 16% increased risk of colorectal cancer
associated with consuming each additional 50 g/day of processed meat.
{grade_b}
A 2018 systematic review and meta-analysis reported that for processed meat, high compared to low
consumption was associated with a 17% increased risk of colorectal cancer. A dose-response
relationship suggested that each additional 50 g/day of processed meat was associated with a 17%
increased risk of colorectal cancer.
{grade_b}
A 2019 systematic review and meta-analysis identified that reducing the intake of processed meat by 3
servings (150 g)/week was associated with a 7% reduction in colorectal cancer incidence. Reducing
intake of red meat by 3 servings (360 g)/week was associated with little to no effect on colorectal cancer
incidence.
{grade_c}
Red Meat
Cancer - Colorectal
(2018) reported a dose-response meta-analysis suggesting a 12% increased risk of colon cancer only
associated with each additional 100 g/day of red meat.
{grade_b}
A 2018 systematic review and meta-analysis reported that for red meat, high compared to low
consumption was associated with a 12% increased risk of colorectal cancer. A dose-response
relationship suggested that each additional 100 g/day red meat was associated with a 12% increased risk
of colorectal cancer.
{grade_b}
A parallel 2019 systematic review based on RCTs included only one eligible trial comparing low fat and
usual fat diets. From this trial, the authors reported very low certainty of evidence that restricted red meat
in diets had little to no effect on colorectal cancer incidence.
{grade_c}
Foods Containing Heme Iron (Including Red and Processed Meat, Fish and Poultry)
(2018) reported limited evidence suggesting a 9% increased risk associated with consuming each
additional >0.6 mg/day of heme iron (e.g. 90 g cooked sirloin steak contains 2.09 mg heme iron).
{grade_c}
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.
500 g of cooked red meat is about 700-750 g raw meat.
Evidence
a. The WCRF/AICR continuous update project (CUP) examined evidence for associates between red
red and processed meat and the risk of colorectal cancer (1):
Processed meat (i.e. meats preserved by smoking, curing or salting or addition of
chemical preservatives) was judged to have strong, convincing evidence for an increased
risk of colorectal cancer. This was based on 10 prospective cohort studies (n=10,738
cases) that were included in a dose-response meta-analysis. Most but not all studies
adjusted for smoking, alcohol consumption, BMI, physical activity, age and sex. None of
the studies adjusted for barbecuing. Pooled results estimated an increased risk of
colorectal cancer per 50 g/day increase processed meat (RR, 1.16; 95%CI, 1.08 to
1.26) with low heterogeneity (I2=20%). When stratified by sex, associations were not
significantly different. When stratified by cancer site, a positive association was
Cancer - Colorectal
observed for colon cancer (n=12 studies; per 50 g/day processed meat: RR, 1.23; 95%
CI, 1.11 to 1.35), but not rectal cancer (n=10 studies; per 50 g/day processed meat:
RR, 1.08; 95%CI, 1.00 to 1.18). The CUP concluded that given the consistent evidence
of a dose-response relationship, “consumption of processed meat is a convincing cause
of colorectal cancer”.
Red meat (i.e. beef, pork, lamb and goat from domesticated animals) was judged to
have strong, probable evidence for increased risk of colorectal cancer. A total of eight
studies (n=6662 cases) were included in the dose-response meta-analysis that did not
show a significant association with colorectal cancer per 100 g/day increase red meat
(RR, 1.12; 95% CI, 1.00 to 1.25) with low heterogeneity (I2=24%). No significant
associations were observed when stratified by sex. When stratified by cancer site, a
positive association was observed for colon cancer (n=11 studies; per 100 g/day red
meat: RR, 1.22; 95%CI, 1.06 to 1.39; I2=12%). Most but not all studies adjusted for
smoking, alcohol consumption, BMI, physical activity, age and sex. Despite the lack of
overall association observed for colorectal cancer, the CUP concluded
that “consumption of red meat is a probable cause of colorectal cancer” (1); however,
significant results were for colon cancer only.
Foods containing heme iron (including red and processed meat, fish and poultry): limited
evidence was found suggesting an increased risk of colorectal cancer. This was based
on six studies (n=6070 cases) included in a dose-response meta-analysis. Although no
association was observed in the meta-analysis (RR, 1.04; 95%CI, 0.98 to 1.10; I2=0%
and 5/6 studies observed non-significant associations), there was evidence of a non-
linear association with increased risk at intakes >0.6 mg/day heme iron (RR, 1.09; 95%
CI, 1.05 to 1.13). As an example, 90 g of cooked sirloin steak contains 2.09 mg heme
iron. No significant associations were observed when stratified by sex or cancer site.
Given that the evidence was based on the non-linear association at higher levels of
intake, the CUP judged that evidence suggesting heme iron intake increases risk of
colorectal cancer was limited.
Based on these and other cancer risk studies, the WCRF/ AICR Third Expert Report
recommended consuming very little, if any processed meat; if red meat is eaten the
recommendation is to limit amount to 3 servings (350-500 g)/week (2).
b. A systematic review and meta-analysis (searched to April 2017) examined the relationship
between 12 major food groups (defined a priori) and colorectal cancer risk (3). Risk of bias was
assessed in all studies with consideration given to certainty of exposure, adequacy of outcome
assessment, adequacy of follow-up (≥10 years) and adjustment for confounders (including age,
sex, education, BMI, smoking, activity and energy intake).
For processed meat, 18 studies (n=20,283 cases) were included comparing high versus
low intake (range 122 to 0 g/day). Results showed a positive association when
comparing high to low intake (RR, 1.14; 95% CI, 1.06 to 1.21 with low heterogeneity). A
dose response relationship was identified, which estimated that each additional 50
g/day processed meat increased risk of colorectal cancer (RR, 1.17; 95%CI, 1.10 to
Cancer - Colorectal
1.23 with no heterogeneity). In subgroup analyses, the positive association persisted for
both colon and rectal cancer.
For red meat, 25 studies (n=22,286 cases) were included comparing high versus low
intake (range 203 to 0 g/day). Results showed a positive association (RR, 1.12; 95%CI,
1.06 to 1.18 with high heterogeneity). A dose-response relationship was identified that
found each additional 100 g/day red meat increased risk of colorectal cancer (RR, 1.12;
95%CI, 1.06 to 1.19 with no significant heterogeneity). In subgroup analyses, the
positive association persisted for both colon and rectal cancer.
When the researchers included only lower risk of bias studies, the estimates were
smaller but still observed a positive association between red and processed meat and
risk of colorectal cancer. The authors concluded that a diet characterized by low
amounts and red and processed meat was associated with lower risks of colorectal
cancer.
c. A 2019 systematic review examined the relationship between intake of processed and red meat
and cancer mortality and incidence (4). A total of eight articles were identified for colorectal
cancer mortality and 35 articles examining colorectal cancer incidence. The authors conducted a
dose-response meta-analysis calculating the pooled risk for an effect of reducing intake by three
servings per week as this was likely to be the maximum reduction for most people (1 serving=50
g processed meat or 120 g red meat). The authors used GRADE process to examine certainty of
evidence.
For processed meat, results from only one study (n=39,867 participants) found
uncertain effects of processed meat on colorectal cancer mortality (RR, 0.88; 95%CI,
0.67 to 1.14; very low certainty of evidence). For colorectal cancer incidence, results
from n=15 studies (n=>1.6 million participants) found that reducing intake of processed
meat may result in a small decrease in colorectal cancer (RR, 0.93; 95% CI, 0.89 to
0.95; low certainty of evidence due to observational study design).
For red meat, no studies examined colorectal cancer mortality. For colorectal cancer
incidence, results from n=5 studies (n=322,502 participants) found that reduced intake
of red meat had little to no effect on colorectal cancer (RR, 1.00; 95%CI, 0.92 to 1.09;
low certainty of evidence due to observational study design).
Overall the authors concluded that the possible effects of reducing intake of processed
meat and red meat on cancer mortality and incidence are very small and the certainty of
evidence is low.
d. A parallel 2019 systematic review and meta-analysis by the same research group (4), included
only RCTs to examine the effect of lower versus higher intake of red meat on cardiometabolic
disease and cancer outcomes (5). For colorectal cancer, only one trial was eligible, which was
the Women’s Health Initiative of 48,835 postmenopausal women who were randomized to a low
fat (20% of kcal) or usual diet and followed up to 12 years. Results from this trial found little to no
effect of a diet low in red meat on colorectal cancer incidence (hazard ratio 1.04; 95%CI, 0.90 to
Cancer - Colorectal
1.20). The evidence assessed by GRADE was very low certainty because of high risk of bias due
to missing data, and indirectness as the trial did not reduce red meat intake directly and there
was a very small gradient between groups (i.e. only about 1.4 servings/week difference in meat
consumption between the intervention and control groups). The authors concluded that there was
very low certainty of evidence that diets restricted in red meat had little or no effect on colorectal
cancer incidence.
Comments
Heterocyclic amines are formed when muscle meats (e.g. beef, pork, chicken and fish) are cooked at very
high temperatures (e.g. by frying, grilling and barbecuing) causing amino acids and creatine to react
together (6). To date, 17 different heterocyclic amines have been identified as being formed when muscle
meats are cooked at high temperatures. In contrast, oven roasting and baking that involve lower
temperatures or microwaving before cooking will cause lower levels of heterocyclic amines; however, gravy
made from meat drippings from any cooking method contains substantial amounts (6), possibly due to
high temperature used in preparation.
Polycyclic aromatic hydrocarbons (PAHs) comprise a group of over 100 different chemicals formed when
organic substances such as meat are burnt incompletely (e.g. grilling, broiling, or barbecuing) (6). When
fat drops from meat, chicken or fish onto a hot fire, PAHs are produced that adhere to the food. The more
intense the heat, the higher level of PAHs and using wood creates more of these chemicals than charcoal.
Cereals contaminated with PAH (e.g. air pollution particulate on crops from petroleum or coal tar products)
also a common source of PAHs in the diet and although levels are lower than in meat, their overall
contribution to the diet may be larger due to greater amounts consumed (7).
Despite the fact that heterocyclic amines and PAHs are potential carcinogens, the WCRF/AICR third
expert report did not make any conclusions about an association between methods of food preparation
and cancer risk (2). The report recommends that if red meat is eaten it should be limited to 350-500
g/week cooked weight; 500 g of cooked red meat is about 700-750 g raw meat.
The WCRF/AICR report describes processed meat as meat preserved through salting, curing, fermentation
and smoking (e.g. ham, salami, bacon, hotdogs, chorizo) (2). Red meat includes all types of muscle meat
from beef, veal, pork, lamb, mutton, horse and goat.
Rationale
Nitrates added as preservatives to processed meats are suspected mutagens and carcinogens that are
produced both endogenously in the low pH of the stomach and added as preservatives to processed
meats (6). Other mechanisms suggested for the carcinogenic potential of processed meats include the
high levels of salt and nitrite and the content of heterocyclic amines and polycyclic aromatic hydrocarbons
if they are cooked at high temperatures (1).
Since many processed meats are red meats, other potential mechanisms for an association between red
meat consumption and colorectal cancer risk include the generation of potentially carcinogenic N-nitroso
compounds and the heme content, which promotes the formation of N-nitroso compounds and also
contains iron that can lead to the production of free radicals (8,9). In addition, some meats are cooked at
Cancer - Colorectal
high temperatures (e.g. frying, grilling and barbecuing), leading to the production of heterocyclic amines
and polycyclic aromatic hydrocarbons.
References
2. World Cancer Research Fund/American Institute for Cancer Research. Third Expert Report, Diet,
nutrition, physical activity and cancer: a global perspective. 2018. Available
from: https://www.wcrf.org/dietandcancer/about
3. Schwingshackl L, Schwedhelm C, Hoffmann G, Knüppel S, Laure Preterre A, Iqbal K, et al. Food
groups and risk of colorectal cancer. Int J Cancer. 2018 May 1;142(9):1748-58. doi:
10.1002/ijc.31198. Epub 2017 Dec 14. Abstract available
4. Han MA, Zeraatkar D, Guyatt GH, Vernooij RWM, El Dib R, Zhang Y, et al. Reduction of red and
processed meat intake and cancer mortality and incidence: a systematic review and meta-
analysis of cohort studies. Ann Intern Med. 2019 Oct 1. doi: 10.7326/M19-0699. [Epub ahead of
print]. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/31569214
5. Zeraatkar D, Johnston BC, Bartoszko J, Cheung K, Bala MM, et al. Effect of lower versus higher
red meat intake on cardiometabolic and cancer outcomes: a systematic review of randomized
trials. Ann Intern Med. 2019 Oct 1. doi: 10.7326/M19-0622. [Epub ahead of print]. Abstract
available from: https://www.ncbi.nlm.nih.gov/pubmed/31569236
6. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. Washington,
D.C.: AICR; 2007. Link not available.
7. Kazerouni N, Sinha R, Hsu CH, Greenberg A, Rothman N. Analysis of 200 food items for benzo
[a]pyrene and estimation of its intake in an epidemiologic study. Food Chem Toxicol. 2001
May;39(5):423-36. Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/11313108
8. Kim E, Coelho D, Blachier F. Review of the association between meat consumption and risk of
colorectal cancer. Nutr Res. 2013 Dec;33(12):983-94. Abstract available
from: http://www.ncbi.nlm.nih.gov/pubmed/24267037
9. Shaughnessy DT, Gangarosa LM, Schliebe B, Umbach DM, Xu Z, MacIntosh B, et. al. Inhibition
of fried meat-induced colorectal DNA damage and altered systemic genotoxicity in humans by
crucifera, chlorophyllin, and yogurt. PLoS One. 2011;Apr 25;6(4):e18707. Abstract available

Recommendation
Cancer - Colorectal
Consuming alcoholic drinks (>30 g/day ethanol, about 2 drinks per day beer, wine or spirits) increases the
risk of colorectal cancer.
Evidence Summary
The WCRF/AICR continuous update project (2018) reported a dose-response meta-analysis demonstrating
a 7% increased risk of colorectal cancer for consuming each additional 10 g/day ethanol. Similar
significant positive associations were observed for wine, beer and spirits. A non-linear dose-response
relationship identified increased risk at intakes >30 g/day. When stratified by sex, the significantly
increased risk was observed in men only.
Grade of Evidence: B
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.
See International Alcohol Guideline CollectionInternational Alcohol Guideline Collection
Evidence
a. The WCRF/AICR continuous update project (CUP) report identified strong evidence that
consuming alcoholic drinks (>30 g/day increases the risk of colorectal cancer (1). Results were
based on 16 studies (n=15,896 cases) included in a dose-response meta-analysis which
identified an increased risk of colorectal cancer per 10 g/day ethanol (RR, 1.07; 95%CI, 1.05 to
1.08 with no heterogeneity). When examined by type of drink, similar and significant positive
associations were observed for wine, beer and spirits. A non-linear dose-response relationship
was identified with no increased risk at low levels of intake (<20 g/day), but increased risk at
intakes >30 g/day (e.g. 30 g/day RR, 1.15; 95%CI, 1.06 to 1.26; 60 g/day RR, 1.60; 95%CI, 1.51
to 1.69). When stratified by sex, the positive association was significant in men only. When
stratified by cancer site, significant positive associations were observed for colon and rectal
cancer.
Comments
Although the WCRF/AICR third expert report indicated that there is no safe lower limit of alcohol
consumption for pre- and postmenopausal breast cancer and esophageal cancer, using non-linear dose-
response analysis has made possible the ability to identify that increased risk of some cancers is
apparent at intakes >30 g/day alcohol (as ethanol) for colorectal cancer and >45 g/day for stomach and
liver cancers (2).
Rationale
Alcohol may contribute to colorectal cancer risk through its metabolites (e.g. acetaldehyde) that may be
carcinogenic to colonocytes (1). Alcohol may also induce adverse effects through the increased
production of reactive oxygen species, generating free radicals and acting as a solvent to enhance the
penetration of carcinogens into cells. In addition, alcohol may act as a solvent for penetration of dietary or
Cancer - Colorectal
environmental (e.g. tobacco) carcinogens into cells, affect hormone metabolism or interfere with
metabolism of folate and DNA repair (3).
References
Project Expert Report 2018. Alcoholic drinks and the risk of cancer. 2018. Available
from: https://www.wcrf.org/dietandcancer/exposures/alcoholic-drinks
3. Varela-Rey M, Woodhoo A, Martinez-Chantar ML, Mato JM, Lu SC. Alcohol, DNA methylation,
and cancer. Alcohol Res. 2013;35(1):25-35. Abstract available
Q4: Does a low carbohydrate diet (LCD) increase the risk for colorectal cancer?
Updated: 2017-03-21

Recommendation
Because dietary fibre comes primarily from carbohydrate-containing foods, concerns have been raised that
low carbohydrate diets could be low in fibre and that the potential benefits of sufficient dietary fibre on
colon health would be compromised. Fermentation byproducts of fibre; such as short-chain fatty acids,
phenolic compounds and certain bacterial populations like bifidobacteria; are thought to be healthy and
protective for the large intestine and thereby potentially help lower the risk of colon cancer. Additionally,
undigested protein, such as from red meat, in the colon could result in production of harmful nitrogenous
metabolites such as nitrosamines and heterocyclic amines.
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
A systematic review of cohort studies did not find total carbohydrate intake to be associated with
Cancer - Colorectal
colorectal cancer risk in the general population. There was no significant difference between higher and
lower carbohydrate intake and the risk of colorectal cancer.
{grade_c}
Randomized controlled trials among adults with overweight and obesity found that short-term (four to eight
weeks) lower carbohydrate diets (~5-35% of energy from carbohydrate, ~30-35% protein) resulted in
potentially adverse changes in the fecal metabolites and biomarkers that are associated with healthy
colonic function and colonic mucosal health such as the following: {grade_b}
decreased short chain fatty acids, particularly butyrate and especially with the lower
carbohydrate levels in the diet
increased fecal pH
decreased bacteria populations like Bifidobacteria, Roseburia/Eubacterium rectale
decreased phenolic acid levels
decreased fecal output.
(See Comments and Rationale for further details of colonic metabolites and biomarkers).
Low dietary fibre intakes (6-22 g/day) in the lower carbohydrate diets, which is below most
recommendations, likely contributed to the adverse changes outlined above. The higher carbohydrate diets
(40-50% calories from CHO) had significantly higher fibre intakes (22 to 31.5 g per day). (See Comments
for dietary fibre recommendations).
Remarks
There is no consensus in the literature on the definition of a very low carbohydrate (CHO) diet (VLCD),
a low CHO diet (LCD), a moderate CHO diet or a high CHO diet.
Evidence
a. A 2012 systematic review of 14 cohort studies examined the relationship between total
carbohydrate (CHO) intake and colorectal cancer risk (1). Meta-analysis of 12 cohort studies
(n=806,647) found no significant difference in relative risk (RR) of colorectal cancer between
higher versus lower carbohydrate diets (RR=0.93, 95%CI, 0.84 to 1.04, moderate heterogeneity).
Dose-response analysis of 10 cohort studies (n=783,980) found no significant difference in
relative risk of colorectal cancer per 100 grams carbohydrate intake per day (RR=0.95, 95%CI,
0.84 to 1.07, moderate heterogeneity).
b. A 2015 Italian prospective cohort study investigated the relationship between colorectal cancer
and total carbohydrate intake, glycemic index (GI) and glycemic load (GL) (2). The study
followed 47,749 adult participants for median of 11.7 years and 421 colorectal cancer cases were
identified. The study found no association between total carbohydrate intake and colorectal
cancer risk. However, the study did find that increasing high GI intake was significantly
associated with increasing colorectal cancer risk and increased lower GI carbohydrate intake
was significantly associated with reduced risk of colorectal cancer.
c. A 2013 Swedish population-based, prospective cohort study (n= 62,528 adults, median 9.7 years
Cancer - Colorectal
follow up) examined the relationship between moderately lower carbohydrate, moderately higher
protein (LCHP) intakes (as assessed with FFQ) and the incidence of cancers, including
colorectal cancer (3). Regression analysis found that LCHP intakes were not associated with
increased risk of colorectal cancer. However, multivariate subgroup analysis found that among
women with high saturated fat intakes lower CHO/higher PRO intakes were associated with a
lower risk of colorectal cancer and that among men where elevated protein intakes came mostly
from vegetable protein that the lower CHO/higher PRO intakes were associated with a greater
risk of colorectal cancer. The authors concluded that their data did not support that higher animal
protein intake increased risk of colorectal cancer. They further noted, however, that the
macronutrient distribution ranges did not vary that much in the study and so it does not speak to
more extreme or strict lower carbohydrate/higher protein diets.
d. Investigators examined the effect of reduced carbohydrate, high protein diets on fecal matter
metabolites that are linked to colon health (phenolic metabolites, short-chain fatty acids
(SCFAs), and nitrogenous compounds) (4). In a cross-over design, 17 obese men were
randomized to four weeks of either a high protein, moderate CHO (HPMC; 28% of energy from
PRO or 139 g/d, 35%CHO or 181 g/d, 37% FAT or 82 g/d, and 22 g/day fibre) or a high protein,
low CHO weight loss diet (HPLC; 29% PRO or 137 g/d, 5% CHO or 22 g/d, 66% fat or 143 g/d,
and 13 g/day fibre). All food was provided. Diets were compared to each other and to a one-week
control diet that provided 13% PRO or 85 g/d, 50% CHO or 360 g/d, 37% FAT or 116 g/d, and 22
g/day fibre. There was a significant decrease in total SCFAs and butyrate in the HPLC diet
compared with the control diet. There was no significant change in butyrate or total SFCAs in the
HPMC versus control diets. The concentrations and proportions of the branched chain fatty acids
(BCFAs) isovalerate and isobutyrate significantly increased in both the HPMC and HPLC
compared to the control diet. Fecal pH was higher on HPLC than on control or HPMC diet. Both
the HPMC and HPLC diets resulted in significantly increased proportions of N-Nitroso
compounds compared to the control diet and the HPLC had an even greater increase than the
HPMC diet. There was a significant reduction in Roseburia/Eubacterium rectale bacteria on the
HPLC diet versus control diet. There was also a reduction in fiber-derived, antioxidant phenolic
acids with HPLC compared to the control diet; in particular ferulic acid (FA) and its derivatives.
This was not observed in the HPMC versus control diet. Indole concentrations were significantly
lower and indole-3-pyruvic acid concentrations were significantly higher on the HPMC diet versus
control and HPLC. No significant change was seen in bile concentrations or ammonia across the
three diet groups. The authors concluded that the reduced total carbohydrate diets resulted in
significant decreases in fecal cancer-protective metabolites and increased concentrations of
hazardous metabolites (4). (See Comments for a description of how each marker is associated
with risk). A key limitation of the study was that there was no washout period between the
HPMC and HPLC diets, which may affect the stool concentrations. Another limitation is that the
control diet was of one-week duration compared to the modified carbohydrate diet interventions,
which were four weeks duration. This one-week duration is a short period for bowel adaptation to
occur and the study may have provided different results if the control and intervention durations
length were the same.
e. In a 2009 RCT, 91 overweight and obese participants were randomized to either a very low
carbohydrate (LC) or high carbohydrate diet (HC) for eight weeks (5). The diets were isocaloric
Cancer - Colorectal
and calorie-restricted (~1500 kcal). The HC diet provided 45% of energy from CHO; 24% PRO,
28% FAT and 31.5 g/day of total fibre. The LC diet provided 5% CHO, 35% PRO, 58% FAT and
13 g/d total fibre. Compared with the HC group, the LC group had significant reductions in fecal
output (HC -21 g versus LC -61 g), butyrate concentrations, and total SCFAs concentration. Total
SCFA concentration and fecal output were significantly positively correlated with fibre and
carbohydrate intake. No correlation was found between fecal output and protein and fat intake
when controlled for carbohydrate and fibre intake. There was a significant decrease in counts of
fecal bifidobacteria in the LC group. Fecal form, pH, ammonia concentration and numbers of
coliforms and Escherichia coli did not change with either diet. No significant difference in change
in fecal moisture, or defecation frequency was found between groups, but self-reported defecation
and flatulence frequency was lower in the LC group. There were no differences between the diets
for incidence of adverse gastrointestinal symptoms, e.g. bloating, ease of laxation or cramping. A
key limitation of the study is that despite the link between decreased fibre intake and change in
the biomarkers of bowel health and function, fat, protein and carbohydrate were all significantly
different between the HC and LC, so it is unclear if reduced or increased carbohydrate intake
resulted in the differences between the two groups.
f. Investigators randomized 19 healthy, obese participants to follow a HPLC diet or HPMC diet for
four weeks in a crossover design (6). The HPLC provided 4% of energy from CHO, 30% PRO,
66% FAT, 6.1 g fibre) and the HPMC provided 35% CHO, 30% PRO, 35% FAT, 11.7 g fibre).
Between the HPMC and the HPLC there was a three-day washout where participants followed
the baseline diet of 52% CHO, 13% PRO, 35% FAT, 27.9 g fibre. All food was provided in the
study and daily intakes were recorded by weight. Total SCFAs concentrations were lower on the
two reduced CHO diets compared to baseline and washout intakes. SCFA isovalerate and
ammonia concentrations dropped significantly only on the HPLC diet. There was no significant
difference in total SCFA, isovalerate, formate, isobutyrate, lactate, acetate, valerate,
propopionate or ammonia concentrations between the HPLC and HPMC diets. However, when
the SCFA butyrate decreased in the two experimental diets, it decreased more so in the HPLC
diet (control =18 mmol/L, HPMC=9 mM, and HPLC=4 mM). The percentage of fecal bacteria
Roseburia spp. and Eubacterium rectale concentrations significantly decreased with the
decreasing carbohydrate intake. The concentrations of butyrate-producing bacteria related to
Roseburia spp. and E. rectale was correlated with a decline in fecal butyrate (r 0.68) and
decreasing carbohydrate intakes. The total bacterial count and bifidobacteria were significantly
decreased on the two reduced CHO diets but was not significantly different between those diets.
Comments
National guidelines recommend 25-30 g dietary fibre daily (7-9).
Increases in the following colonic metabolites and biomarkers is associated with increased risk of
colorectal cancer (4,5):
fecal pH (less acidic)
N-Nitroso compounds
» nitrosamine
» heterocyclic amines
Cancer - Colorectal
ammonia.
Decreases in the following colonic metabolites and biomarkers are associated with increased risk of
colorectal cancer (4,5):
short chain fatty acids (SCFAs) butyrate
» isovalerate
» formate
» isobutyrate
» lactate
» acetate
» valerate
» propopionate
colonic bacterial species:
» Bifidobacteria
» Lactobacilli
» Roseburia
» Eubacterium
stool mass
fecal moisture content and fecal frequency
phenolic acids including ferulic acid (FA) and its compounds.
(See Rationale for further discussion).
There is no consensus in the literature on the definition of a very low carbohydrate (CHO) diet (VLCD),
a low CHO diet (LCD), a moderate CHO diet or a high CHO diet. However, suggested definitions are
highlighted below for a 2000kcal diet (6):
Very low CHO ketogenic diet (VLCKD) or VLCD
20-50 g CHO per day
OR <10% calories from CHO
Low CHO diet
<130 g CHO per day
OR < 26% calories from CHO
Moderate CHO diet
130-230 g CHO per day
OR 26-45% calories from CHO
High CHO diet
> 230 g CHO per day
OR >45% calories from CHO.
Rationale
Due to the association between decreased colorectal cancer risk and diets high in dietary fibre
(particularly cereal and whole grains), there is concern that lower carbohydrate diets, which are lower in
dietary fibre and whole grains, would increase colorectal cancer risk (5,10). Low carbohydrate diets restrict
intake of plant foods including fruit, some vegetables and grains, which are the main source of dietary fibre
Cancer - Colorectal
and non-digestible carbohydrates in the diet. Insoluble and soluble fibres are important for the stool bulk,
laxation, stool transit time, as well as fermentation, and byproducts of fermentation (5). Important end
products of fermentation include short chain fatty acids (SCFA) such as butyrate that are suspected to be
important for healthy colon function and colonic mucosal health due to lowering of the pH of the luminal
environment (5). Butyrate, a SCFA, is also the main energy source for colonocytes, which are thought to
have a key role in preventing colorectal cancer by promoting gene stability and apoptosis of colorectal
cancer cells (4). Mechanisms proposed for increased colorectal cancer include decreased fecal and
colonic bacteria, carcinogens/metabolites exposure, lower total stool mass, lower frequency of bowel
movements, reduced large bowel fermentation; the latter of which decreases the concentration of SCFAs
and can lead to an unfavorable shift in fecal microflora with reductions in the bifidobacteria count (5).
Microbial fermentation of plant fibre also releases many phenolic compounds into the colon that show
antioxidant and anti-cancer activities (4).
Also, with increased protein on a low carbohydrate diet, it is proposed that undigested protein, such as
from red meat, could increase production of harmful nitrogenous metabolites such as nitrosamine and
heterocyclic amines (4). Increased colorectal cancer is associated with high red meat consumption and
production of nitrogenous metabolites (4).
A small number of RCTs have shown that resistant starch (a type of dietary fibre) may protect against the
carcinogenic effect of high red meat intakes (11,12). When consumed with high red meat intakes, the
increased butyrate levels from resistant starch fermentation prevent the expression of microRNA in
colorectal cancer cells and thus reducing colorectal cancer risk (11).
References
1. Aune D, Chan DS, Lau R, Vieira R, Greenwood DC, Kampman E, et al. Carbohydrates, glycemic
index, glycemic load, and colorectal cancer risk: a systematic review and meta-analysis of
cohort studies. Cancer Causes Control. 2012; 23(4):521-35. Abstract available
2. Sieri S, Krogh V, Agnoli C, Ricceri F, Palli D, Masala G, et al. Dietary glycemic index and
glycemic load and risk of colorectal cancer: results from the EPIC-Italy study. Int J Cancer.
2015;136 (12):2923-31. Abstract available from: http://www.ncbi.nlm.nih.gov/pubmed/25403784
3. Nilsson LN, Winkvist A, Johansson I, Lindahl B, Hallmans G, Lenner P, et al. Low-carbohydrate,
high-protein diet score and risk of incident cancer; a prospective cohort study. Nutr J. 2013;12
(58). Abstract available from: http://www.ncbi.nlm.nih.gov/pubmed/23651548
4. Russell WR, Gratz SW, Duncan SH, Holtrop G, Ince J, Scobbie L, et al. High-protein, reduced-
carbohydrate weight-loss diets promote metabolite profiles likely to be detrimental to colonic
health. Am J Clin Nutr. 2011 May;93(5):1062-72. Abstract available
5. Brinkworth GD, Noakes M, Clifton PM, Bird AR. Comparative effects of very low-carbohydrate,
high-fat and high-carbohydrate, low-fat weight-loss diets on bowel habit and faecal short-chain
Cancer - Colorectal
fatty acids and bacterial populations. Br J Nutr. 2009 May;101(10):1493-502. Abstract available
6. Duncan SH, Belenguer A, Holtrop G, Johnstone AM, Flint HJ, Lobley GE. Reduced dietary
intake of carbohydrates by obese subjects results in decreased concentrations of butyrate and
butyrate-producing bacteria in feces. Appl Environ Microbiol. 2007;73(4):1073-8. Abstract
available from: http://www.ncbi.nlm.nih.gov/pubmed/17189447
7. Institute of Medicine. National Academies Press. 2005. Available
from: https://www.nap.edu/catalog/10490/dietary-reference-intakes-for-energy-carbohydrate-fiber-
fat-fatty-acids-cholesterol-protein-and-amino-acids-macronutrients
8. National Health & Medical Research Centre (NHMRC) & New Zealand Ministry of Health (NZ
MOH). Nutrient Reference Values: dietary fibre. Australia. 2006. Available
from: https://www.nrv.gov.au/nutrients/dietary-fibre
9. British Nutrition Foundation. Nutrition requirements. 2015. Available
from: https://www.nutrition.org.uk/nutritionscience/nutrients-food-and-ingredients/nutrient-
requirements.html
10. Aune D, Chan DS, Lau R, Vieira R, Greenwood DC, Kampman E, et al. Dietary fibre, whole
grains, and risk of colorectal cancer: systematic review and dose-response meta-analysis of
prospective studies. BMJ. 2011;343:d6617. Abstract available
11. Humphreys KJ, Conlon MA, Young GP, Topping DL, Hu Y, Winter JM, et al. Dietary
manipulation of oncogenic microRNA expression in human rectal mucosa: a randomized trial.
Cancer Prev Res (Phila). 2014;7(8):786-95. Abstract available
12. Le Leu RK, Winter JM, Christophersen CT, Young GP, Humphreys KJ, Hu Y, et al. Butyrylated
starch intake can prevent red meat-induced O6-methyl-2-deoxyguanosine adducts in human
rectal tissue: a randomised clinical trial. Br J Nutr. 2015; 114(2):220-30. Abstract available
Q5: What is the effect of folate/folic acid supplements on the risk of colorectal cancer?
Subcategory: Intervention
Updated: 2020-04-14

Recommendation
Evidence is too limited to draw a conclusion regarding dietary folate intake and the risk of colorectal
cancer. Folic acid supplements do not appear to affect colorectal cancer risk.
Cancer - Colorectal
Evidence Summary
A 2018 systematic review and meta-analysis of RCTs found that folic acid supplements had no effect on
the risk of colorectal cancer or the risk of adenoma {grade_b}. For folate status, the same review of
observational studies found that total folate intake was associated with a reduced risk of colorectal cancer;
however, no association was reported between circulating folate levels and the risk of colorectal cancer.
{grade_c}
The WCRF/AICR Continuous Update Project (2018) reported that the evidence was too limited to draw
a conclusion for an effect of folate on colorectal cancer. {grade_c}
Evidence
a. A systematic review and meta-analysis (searched to 2016) examined the association between
folic acid or folate and colorectal cancer risk (91).
For folic acid supplements, 11 RCTs (n=35,761 subjects) were included using a dose of
0.5 to 5 mg/day for a duration of two to nine years. Study quality assessment identified
six high quality studies (Jadad Score=5). Pooled results showed no effect of folic acid
compared to placebo on the risk of colorectal cancer (n=4 studies: RR, 1.07; 95%CI,
0.86 to 1.43) or on the risk of adenoma (n=6 studies: RR, 1.00; 95%CI, 0.86 to 1.51).
For folate status, 22 studies were included (n=>2.5 million subjects in cohort studies
and 12,000 in case-control studies). Study quality assessment identified five high quality
studies (Newcastle-Ottawa Scale=9). Folate was assessed by total/dietary folate intake
(method not specified) or circulating folate levels. Pooled results found that total folate
intake was associated with reduced risk of colorectal cancer in cohort studies (RR,
0.71; 95%CI, 0.59 to 0.86) and in case-control studies (OR, 0.77; 95%CI, 0.62 to 0.95);
however, no association was reported between rbc/plasma folate levels and risk of
colorectal cancer (RR, 1.05; 95%CI, 0.85 to 1.30).
The authors concluded that the lack of beneficial effects of folic acid supplements compared to
dietary folate may be due to differences in bioavailability and metabolism of synthetic folic acid.
Furthermore, variation in methods of assessing folate status may explain different results.
b. The WCRF/AICR CUP report identified no new evidence and confirmed that evidence was too
limited to draw a conclusion for an effect of folate on colorectal cancer risk (2).
References
1. Moazzen S, Dolatkhah R, Tabrizi JS, Shaarbafi J, Alizadeh BZ, de Bock GH, et al. Folic acid
intake and folate status and colorectal cancer risk: a systematic review and meta-analysis. Clin
Nutr. 2018 Dec;37(6 Pt A):1926-34. doi: 10.1016/j.clnu.2017.10.010. Epub 2017 Oct 28. Abstract
available from: https://www.ncbi.nlm.nih.gov/pubmed/29132834
Project Expert Report 2018. Diet, nutrition, physical activity and colorectal cancer.
Cancer - Colorectal
2018. Available from: https://www.wcrf.org/dietandcancer
Q6: Are probiotics, prebiotics and synbiotics effective in the prevention of colorectal cancer?
Subcategory: Intervention
Updated: 2020-04-14

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
No studies were identified that examined the effect of probiotics, prebiotics or synbiotics on colorectal
cancer incidence.
{grade_d}
Clinical trials evaluating the effect of probiotic or prebiotic supplemented diets have not demonstrated
consistent benefits on clinical biomarkers of colorectal cancer risk (e.g. cell proliferation, development of
adenomas) or secondary markers (e.g. fecal microflora, bacterial enzyme activity.
{grade_c}
Grade of Evidence: C & D
Evidence
a. A 2012 systematic review examining the effect of prebiotics on biomarkers of colorectal cancer in
humans identified nine studies (n=7 RCTs, one randomized crossover and one nonrandomized
controlled trial) (1). Prebiotics included inulin, oligofructose, lactulose and resistant starch given
for two weeks to up to three years. Overall most studies showed no effect of prebiotics on cell
proliferation, gene expression or DNA methylation. Of the two studies that assessed adenoma
development, one showed no effect and the other reported a reduction in adenoma recurrence;
however, the latter study received a low quality rating. Overall the authors concluded that
evidence is weak that diets supplemented with prebiotics lower colorectal cancer risk.
b. A narrative review examined the effect of probiotics on gastrointestinal cancers (2). For colorectal
cancer, three clinical trials (n=75 healthy adults and 10 individuals with colorectal cancer) were
identified that examined effects of probiotics (two using Lactobacillus strains and one using
Bifidobacterium for four to 12 weeks) on secondary markers of intestinal carcinogenesis. Results
were inconsistent with one study finding no change in fecal microflora with probiotics, one study
showing a reduction in bacterial enzyme activity considered to be beneficial and the third study
showing an improvement in the intestinal environment in patients with colorectal cancer taking
probiotics compared to healthy controls. The authors concluded that human clinical trials with
Cancer - Colorectal
adequate follow up and reporting relevant outcomes are needed to identify potential benefits of
probiotics for preventing or treating cancer.
c. A 2017 systematic review and meta-analysis examining the effect of dietary supplements on the
primary prevention of cardiovascular disease and cancer included a search for probiotics,
prebiotics and synbiotics (3). Included trials were RCTs with placebo or another supplement
provided for a minimum of 12 months and assessing incidence of any cancer or cancer mortality.
No studies were identified that included prebiotics, probiotics or synbiotics.
Rationale
Probiotics are thought to have potential for cancer prevention through modulating microbiota and the
immune system, reducing bacterial translation and enhancing the gut barrier, all of which can contribute to
reduced tumour formation (2).
Prebiotics resist digestion in the small intestine and are fermented in the colon by gut microflora producing
short-chain fatty acids (notably butyrate), thought to be protective against colon cancer (1). Epidemiologic
studies do not typically evaluate prebiotic consumption, making it a challenge to examine association with
colorectal cancer incidence.
Synbiotics are simultaneous doses of probiotics and prebiotics that may have cumulative benefits beyond
probiotics and prebiotics alone (1).
References
1. Clark MJ, Robien K, Slavin JL. Effect of prebiotics on biomarkers of colorectal cancer in humans:
a systematic review. Nutr Rev. 2012 Aug;70(8):436-43. doi: 10.1111/j.1753-4887.2012.00495.x.
Abstract available from: https://www.ncbi.nlm.nih.gov/pubmed/22835137
2. Javanmard A, Ashtari S, Sabet B, Davoodi SH, Rostami-Nejad M, Esmaeil Akbari M, et al.
Probiotics and their role in gastrointestinal cancers prevention and treatment; an overview.
Gastroenterol Hepatol Bed Bench. 2018 Fall;11(4):284-95. Abstract available
3. Schwingshackl L, Boeing H, Stelmach-Mardas M, Gottschald M, Dietrich S, Hoffmann G, et al.
Dietary supplements and risk of cause-specific death, cardiovascular disease, and cancer: a
systematic review and meta-analysis of primary prevention trials. Adv Nutr. 2017 Jan 17;8(1):27-
39. doi: 10.3945/an.116.013516. Print 2017 Jan. Abstract available
Summary of Recommendations and Evidence

Cancer - Colorectal Summary of Recommendations and Evidence
Last Updated: 2020-05-01
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
Cancer - Colorectal
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 and Decreased Colorectal Cancer Risk
Whole Grains
Dietary Fibre
Fish/Vitamin C/Vitamin Supplements
2. Milk Products/Vitamin D and Colorectal Cancer Risk

Milk Products
Vitamin D
3. Nutrients/Dietary Factors and Increased Colorectal Cancer Risk

Meat
Alcohol
4. Low Carb Diet and Increased Colorectal Cancer Risk

5. Folate Supplements and Colorectal Cancer Risk
6. Probiotics/Prebiotics/Synbiotics and Colorectal Cancer Prevention

Whole Grains
Recommendation
colorectal cancer.
Evidence Summary
Toggle content
Remarks
Cancer - Colorectal
Additional Remarks
Toggle content
Dietary Fibre
Recommendation
Evidence Summary
Toggle content
Remarks
Toggle content
Vitamin C/Fish/Vitamin Supplements

Recommendation
cancer risk:
fish
Evidence Summary
Toggle content
Remarks

risk?
Cancer - Colorectal
Additional Remarks
Toggle content

Milk Products
Recommendation
Evidence Summary
Toggle content
Remarks
Toggle content
Vitamin D
Recommendation
Evidence Summary
Toggle content

Meat
Recommendation
Cancer - Colorectal
colorectal cancer.
Evidence Summary
Toggle content
Remarks
Additional Remarks
Toggle content
Alcohol
Recommendation
Evidence Summary
Toggle content
Remarks
See International Alcohol Guideline Collection: International Alcohol Guideline Collection
Additional Remarks
Toggle content

Recommendation
Cancer - Colorectal
colorectal cancer.
or processed meats.
Evidence Summary
Toggle content
Remarks
Toggle content

Recommendation
Evidence Summary
Toggle content
Recommendation
Evidence Summary
Toggle content
Cancer - Colorectal
Additional Remarks
Toggle content
Practice Guidance Toolkit

Cancer Practice Guidance Toolkit
Last Updated: 2020-11-29
Key Nutrition Issues
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).
This toolkit discusses the following key nutrition issues:

effects of fish oil or omega-3 fatty acid supplementation on nutritional, functional and clinical
outcomes of individuals with cancer
a low iodine diet (e.g. ≤50 μg iodine/day) for adults with well-differentiated thyroid cancer prior to
radioactive iodine (RAI) ablation treatment or scanning
effect of folate/folic acid supplements with alcohol and breast cancer risk
effect of soy on prevention, reoccurrence and treatment of breast cancer
benefits of breastfeeding on cancer prevention for mother and infant
relationship of ginseng use and breast cancer
conjugated linoleic acid (CLA) or high CLA intake and breast cancer development risk and
treatment
probiotics and colorectal cancer prevention
nutrients/dietary and lifestyle factors associated with increasing and decreasing the risk of
developing:
» breast cancer
» colorectal cancer
» head or neck cancer
» lung cancer
» prostate cancer
strategies for managing dysphagia and taste changes in adults undergoing cancer treatment
flaxseed effect on prostate cancer during treatment and preventing reoccurrence.

Cancer - Head and Neck Background
Cancer - Nutritional Implications of Treatment: Mouth Changes Background
Cancer - Nutritional Implications of Treatment: Constipation, Nausea and Vomiting Background
Cancer - Nutritional Implication of Cancer Treatment: Diarrhea Background
Cancer- Nutrition Implications of Treatment Practice Guidance Toolkit
Cancer - Colorectal
Cancer - Neutropenia Background
Cancer – Neutropenia Practice Guidance Toolkit
Cancer – Prostate Cancer Background
Cancer – Thyroid Background
Nutrition Care Process and Terminology Background.
Nutrition Assessment, Monitoring and Evaluation
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.
Nutrition Monitoring and Evaluation

Some of the indicators that were measured in the nutrition assessment using the table below can be
repeated in the nutrition monitoring and evaluation step.
Anthropometric Measurements
Height/Length
Weight
Weight Change
BMI
Body Compartment Estimates (waist circumference)
Growth pattern indices/percentile ranks
Anthropometric Comparative Standards – Adult
Measure NCP Terminology
Adult BMI Weight and Growth Recommendation

» Recommended body weight/BMI
Ideal/reference body weight (IBW)
Recommended BMI
Waist As above
Circumference
Anthropometric Comparative Standards – Children
Cancer - Colorectal
Measure Recommendation NCP Terminology
Birth to 24 The WHO Child Growth Weight and Growth

months Standards/Reference: Recommendation
Length-for-age For Birth to 5 years » Recommended body
Weight-for-age For 5 to 19 years weight/BMI/growth
Weight-for-length Desired growth
Head pattern
Circumference
2 to 19 years of
age Growth Charts (WHO and
Height-for-age CDC)
Weight-for-age
BMI-for-age
Child BMI WHO Growth Charts Adapted

for Canada
UK-WHO 0-4 years

UK Growth 2-18 years
Food/Nutrition-related History
Food and Nutrient Intake

» Energy intake
Total energy intake
» Food and beverage intake
Fluid/beverage intake
Food intake
» Macronutrient intake
Fat and cholesterol intake (omega-3 fats)
Protein intake
Carbohydrate intake
Fibre intake
» Micronutrient intake
Vitamin intake
Mineral/element intake (iodine)
Food and Nutrient Administration
Cancer - Colorectal
» Diet history
» Diet order
» Diet experience
» Eating environment
Medication and Complementary/Alternative Medicine Use
» Complementary/alternative medicine
Nutrition-related complementary/alternative medicine use
Physical Activity and Function
» Physical activity
Food/Nutrition-related Comparative Standards
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.
Nutrition-focused Physical Findings
Overall Appearance (underweight, overweight or obesity)
Biochemical Data, Medical Tests and Procedures
Mineral Profile, Iodine, Urinary Excretion
Client History
Personal History
Personal Data
Age
Patient/Client/Family Medical/Health History
Hematology/Oncology
Cancer (specify)
Cancer - Colorectal
Primary Tumour Site
Presence of Metastases
Effect of Cancer on Ingestion, Digestion and Absorption of Nutrients
Pre-existing Other Medical Conditions
Treatments/Therapy
Medical Treatment/Therapy (chemotherapy, radiation therapy)
Surgical Treatments
Social History
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
Nutrition Prescription Examples

Modified Diet
» Energy/nutrient modification
Calorie modification (e.g. to prevent weight loss)
Mineral intake (e.g. iodine ≤50 μg iodine/day for 1-2 weeks)
Fibre level (increase)
Food intake (e.g. increase whole grains, vegetables and fruit, legumes, fish
consumption)
Food and/or Nutrient Delivery Example

Meals and Snacks
» General/healthful diet
» Composition of meals/snacks
Protein-modified diet (e.g. avoid processed meats)
Carbohydrate-modified diet (e.g. consume whole grains)
Fat-modified diet (e.g. avoid prepared foods that contain trans fats, replace with
foods containing mono- and polyunsaturated fats)
Fibre-modified diet (e.g. sources of viscous fibre)
Diets modified for specific foods or ingredients (plant-based eating pattern)
Specific foods/beverages or groups (e.g. increase vegetables and fruit, legumes)
Cancer - Colorectal
Nutrition Education Example
Content
» Purpose of the nutrition education
» Nutrition relationship to health/disease
» Recommended modifications (e.g. calorie modification to prevent weight loss, more
plant foods, limit iodine before RAI ablation therapy)
Nutrition Counselling Example

Strategies
» Goal setting
» Problem-solving
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.
Cancer Summary of Recommendations and Evidence
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
1. Omega-3 Fatty Acid Supplementation

Recommendation
Omega-3 fatty acid supplementation has not been consistently shown to benefit individuals with cancer
Cancer - Colorectal
but has not been associated with serious adverse effects in clinical trials.
Evidence Summary
Toggle content
Remarks
As most studies exclude subjects receiving anticoagulants, individuals should check with their doctor or
pharmacist before commencing fish oil supplements due to the potential increase in bleeding risk.
Additional Remarks
Toggle content
2. Low Iodine Diet and Radioactive Iodine Ablation

Evidence Summary
Evidence from a review on the benefit of a low iodine diet (LID) on the efficacy of radioactive iodine (RAI)
ablation therapy is conflicting, mainly because of retrospective study designs and a lack of objective
measurements of urinary iodine levels. Additional research from RCTs is needed to better understand the
effectiveness of an LID in RAI ablation and on longer survival without disease in differentiated thyroid
cancer.
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
Toggle content
Additional Remarks
Toggle content
Low Iodine Diet Side-Effects

Evidence Summary
Evidence from a review of case reports found that hyponatremia was the main side-effect of LIDs, with age
over 65 years, female gender, and taking thiazide diuretics increasing the risk. Other risk factors included
a prolonged hypothyroid state and the presence of several metastases. One retrospective chart review
published after the review found that LIDs did not increase the risk for hyponatremia (either in frequency or
severity). Nonetheless, monitoring serum sodium levels in high risk subjects and the use of non-iodized
salt during RAI therapy has been recommended, as it was found that despite availability of non-iodized
salt, some subjects restricted sodium during the LID.
Cancer - Colorectal
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.
A report of dietary intake from subjects on an LID compared to their usual diet found lower intakes of
sodium and most other nutrients, including energy. This suggests that dietary counselling is needed on
a LID diet to ensure the provision of sufficient calories and overall nutrients.
{grade_d}
Low Iodine Diet and Cancer Recurrence and Mortality Rates

Evidence Summary
At the present time, there are no human or animal studies that have evaluated the effect of a LID prior
to RAI treatment or scanning on long-term thyroid cancer recurrence or mortality rates.
{grade_d}
Cancer - Breast Summary of Recommendations and Evidence
[A] The following conclusions are supported by good evidence:
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
Cancer - Colorectal
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).
Cohort and case-control studies provide consistent evidence that lactation protects against
premenopausal and postmenopausal breast cancer. It is recommended that mothers aim to exclusively
breastfeed their infants for about six months, followed by continued breastfeeding with complementary
feeding.
[B] The following conclusions are supported by fair evidence:
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.
Cancer - Colorectal
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.
Emerging evidence from large-scale prospective observational studies have consistently shown that the
consumption of approximately two servings/day of soy foods is not associated with an increase in the risk
of breast cancer recurrence or lower risk of survival in women with breast cancer. The protective
association appears more pronounced in postmenopausal women. However, the reduced risk of
recurrence results should be interpreted with caution given the modest effect and wide confidence intervals
for most studies and the lack of dose response relationship in one positive study.
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.
Cancer - Colorectal
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.
There is a lack of human intervention studies that directly examine the effect of soy supplementation on
breast cancer risk. However, there are a number of studies that have evaluated various risk factors (often
referred to as surrogate markers) that are known to be associated with breast cancer development, such
as serum estrogen concentration, breast tissue/mammographic density and breast cell proliferation. The
mixed findings of these studies are difficult to interpret and it is unclear what impact the changes in
surrogate markers may have on long-term breast cancer risk. Therefore, soy supplements therefore cannot
be recommended for breast cancer prevention.
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.
Cancer - Colorectal
[D] A conclusion is either not possible or extremely limited because evidence is unavailable
and/or of poor quality and/or is contradictory:
For premenopausal women, no conclusions could be reached regarding an effect of total fat intake and
breast cancer risk.
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.
Cancer - Colorectal Summary of Recommendations and Evidence
Cancer - Colorectal
Content
Whole Grains
Dietary Fibre
Fish/Vitamin C/Vitamin Supplements

Milk Products
Vitamin D

Meat
Alcohol


Whole Grains
Recommendation
colorectal cancer.
Evidence Summary
Toggle content
Remarks
Cancer - Colorectal
Additional Remarks
Toggle content
Dietary Fibre
Recommendation
Evidence Summary
Toggle content
Remarks
Toggle content
Vitamin C/Fish/Vitamin Supplements

Recommendation
cancer risk:
fish
Evidence Summary
Toggle content
Remarks

Cancer - Colorectal
risk?
Additional Remarks
Toggle content

Milk Products
Recommendation
Evidence Summary
Toggle content
Remarks
Toggle content
Vitamin D
Recommendation
Evidence Summary
Toggle content

Meat
Recommendation
Cancer - Colorectal
colorectal cancer.
Evidence Summary
Toggle content
Remarks
Additional Remarks
Toggle content
Alcohol
Recommendation
Evidence Summary
Toggle content
Remarks
See International Alcohol Guideline Collection: International Alcohol Guideline Collection
Additional Remarks
Toggle content
Cancer - Colorectal
Recommendation
colorectal cancer.
or processed meats.
Evidence Summary
Toggle content
Remarks
Toggle content

Recommendation
Evidence Summary
Toggle content
Recommendation
Evidence Summary
Cancer - Colorectal
Toggle content
Additional Remarks
Toggle content
Cancer - Head and Neck Summary of Recommendations and Evidence
[A] The following conclusions are supported by good evidence:

Epidemiological data provides consistent evidence that the 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.
[B] The following conclusions are supported by fair evidence:

Epidemiological studies generally provide consistent evidence to suggest that the consumption of non-
starchy vegetables (i.e. green leafy, cruciferous and allium vegetables or raw vegetables) protect against
cancers of the mouth, larynx, pharynx, esophagus and stomach. Data primarily from case-control studies
is generally consistent for a protective effect of fruits in general (and citrus fruits) against cancers of the
mouth, pharynx and larynx, esophagus, lung and stomach.
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.
[C] The following conclusions are supported by limited evidence:

Epidemiological studies generally provide limited evidence to suggest that the consumption of non-
starchy vegetables (i.e. green leafy, cruciferous and allium vegetables or raw vegetables) protect against
cancers of the nasopharynx, lung, colorectum, ovary and endometrium. For specific vegetables, there is
limited evidence to suggest that carrots protect against cervical cancer. Limited evidence suggests that
fruits also protect against cancers of the nasopharynx, pancreas, liver and colorectum. Current
recommendations are that individuals should eat at least five servings per day of a variety of non-starchy
vegetables and fruits (i.e. vegetables and fruits of different colours including red, green, yellow, white,
purple and orange, including tomato-based products and allium vegetables such as garlic).
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
Cancer - Colorectal
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.
Note: See relevant practice questions in this knowledge pathway for references.
Cancer - Lung Summary of Recommendations and Evidence
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
Cancer - Colorectal
1. Nutrients/Dietary Factors that Decrease Lung Cancer Risk
Fruit
Recommendation
Limited evidence suggests that greater consumption of fruit can reduce the risk of cancer in current and
former smokers. A daily amount of 200-300 grams of fruit is recommended.
Evidence Summary
Toggle content
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
Toggle content
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
Toggle content
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
Toggle content
Foods Containing Carotenoids

Recommendation
Limited evidence suggests that the consumption of foods containing carotenoids including beta-carotene
(e.g. red and orange vegetables and fruit) reduces the risk of lung cancer.
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
Cancer - Colorectal
Toggle content
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
squash, pumpkin, red peppers, carrots, tomatoes, sweet potatoes and cantaloupe.
Additional Remarks
Toggle content
Food Containing Retinol

Recommendation
There is limited evidence that retinol (vitamin A)-containing foods reduces the risk of lung cancer.
Evidence Summary
Toggle content
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.
Additional Remarks
Toggle content
Food Containing Vitamin C

Recommendation
Limited evidence suggests that the consumption of foods containing vitamin C are associated with a
reduced risk of lung cancer in current smokers but not former smokers or for those that have never
smoked. Vitamin C intake in the range of 40 mg/day is adequate with additional health benefits likely up to
100 mg/day.
Evidence Summary
Toggle content
Remarks
Toggle content
Food Containing Isoflavones

Recommendation
A higher consumption of foods containing isoflavones is associated with a decreased risk of lung cancer in
those who never smoked but not former smokers or current smokers.
Cancer - Colorectal
Evidence Summary
Toggle content
Remarks
Toggle content
Additional Remarks
Toggle content
Dietary Fat, Selenium and Food Containing Quercetin

Recommendation
Evidence is too limited to draw a conclusion regarding dietary fat, butter, selenium, selenium supplements
and food containing quercetin intake and the risk of lung cancer.
Evidence Summary
Toggle content
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.
Country-Specific Guidelines for Maximum Arsenic Levels in Drinking Water:

Australia: 0.007 mg/L
Canada: 0.010 mg/L
New Zealand: 0.010 mg/L
United Kingdom: 0.010 mg/L
Canada, New Zealand and the United Kingdom guidelines are in sync with the WHO provisional
guidelines.
Evidence Summary
Toggle content
Remarks
See Additional Content: Food Safety – Arsenic in Rice Background.
Additional Remarks
Toggle content
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.
Cancer - Colorectal
Evidence Summary
Toggle content
Remarks
GSTM1 and GSTM2 are carcinogen-detoxifying enzymes. Individuals without or with less active forms of
these enzymes due to genetic variation are less able to metabolize toxins and have a higher risk of
cancer.
Additional Remarks
Toggle content
Red and Processed Meat

Recommendation
Evidence is limited but consistent suggesting that the consumption of red and processed meat increases
the risk of lung cancer.
Evidence Summary
Toggle content
Remarks
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.
Additional Remarks
Toggle content
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
Toggle content
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.
See Additional Content: International Alcohol Guideline Collection.
Additional Remarks
Toggle content
Cancer - Colorectal
Cancer - Prostate Summary of Recommendations and Evidence
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
1. Nutrients/Dietary Factors and Decreased Prostate Cancer Risk

Recommendation
The evidence is heterogeneous regarding the following dietary factors, but overall the evidence suggests an
association with a decreased risk of prostate cancer:
glycemic index (score of 40-60)
total and unfermented soy foods
tomatoes (cooked, sauces) and lycopene
dried fruit (>5 days/ week)
green tea (>7 cups/day)
coffee (>4 cups/day).
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.
Vitamin E and Tocopherols

No significant associations have been found between prostate cancer risk and dietary vitamin E, dietary
alpha-tocopherol or serum gamma-tocopherol. It is possible that a low plasma concentration of alpha-
tocopherol may be associated with an increased risk of prostate cancer, although evidence is limited.
Cancer - Colorectal
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).
Evidence Summary
Toggle content
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?
Additional Remarks
Toggle content
2. Nutrients/Dietary Factors and Increased Prostate Cancer Risk

Recommendation
Dairy, Calcium and Alcohol
There are conflicting results regarding the following dietary factors, but overall the evidence suggests that
they may be associated with an increased risk of prostate cancer:
high dairy intake/high calcium diets
alcohol.
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
Toggle content
Cancer - Colorectal
Remarks
Toggle content
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.
Pomegranate, Broccoli, Turmeric and Green Tea Supplement

Three high quality RCTs showed promise in slowing prostate-specific antigen (PSA) progression in men
with prostate cancer. One found that a combined supplement containing 100 mg each pomegranate,
broccoli, turmeric and green tea powders delayed PSA progression compared to placebo.
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.
Low Fat Diet Plus Flaxseed

The third found that a low fat diet (<20% total kcal from fat) plus flaxseed (30 g/day) decreased
proliferation rate from baseline in men with prostate cancer. Additional studies are needed to confirm both
results.
Alpha-Linolenic Acid, Saturated Fat, Meat, Poultry, Calcium and Folate

Alpha-linolenic acid (ALA), saturated fat, meat (red, processed, grilled, barbecued, very well done),
poultry, calcium and low folate intake have been associated with an increased risk of disease progression
or mortality in men with prostate cancer, although evidence is sparse and sometimes conflicting.
Additional studies are needed to confirm these results.
Evidence Summary
Toggle content
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.

What nutrients/dietary factors are associated with an increased risk of prostate cancer?
What nutrients/dietary factors are associated with a decreased risk of prostate cancer?
4. Dietary Patterns and Prostate Cancer Progression
Recommendation
Risk of Prostate Cancer
Dietary inflammatory index (DII) score may be associated with prostate cancer risk, with a 10% decrease
in risk for every one-point decrease DII score. Similarly, a “healthy” dietary pattern has been associated
Cancer - Colorectal
with a reduced risk of prostate cancer, in contrast to a “Western” dietary pattern or a dietary pattern high
in refined carbohydrates, both of which have been associated with an increased risk of prostate cancer.
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.
Prostate Cancer-related Mortality

Only a Mediterranean-style diet has been studied in relation to cancer-related mortality among prostate
cancer survivors. Following a Mediterranean diet was not found to have an effect on prostate cancer-related
mortality, although it did lead to a 22% decrease in all-cause mortality among prostate cancer survivors.
Evidence Summary
Toggle content
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.
Definitions of Mediterranean were inconsistent across studies.
Additional Remarks
Toggle content
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.
{grade_d}
6. Flaxseed and Prostate Cancer Reoccurrence

Evidence Summary
There have been no rigorous studies undertaken to examine the effect of dietary flaxseed on the risk of
prostate cancer recurrence in humans. Thus, the role of flax in the primary or secondary prevention of
prostate cancer or during cancer therapy remains uncertain. Consuming moderate amounts of dietary flax
and flax-containing products as part of a diet rich in vegetables and fruit that is consistent with Healthy
Eating Guidelines remains prudent.
{grade_d}
Cancer - Colorectal
Nutrition Monitoring and Evaluation
Nutrition Education and Professional Resources
Education materials for clients, practice guidelines and other professional tools and resources can be
found under the following tabs:
Cancer - Related Tools and Resources
Cancer – Breast Related Tools and Resources
Cancer – Colorectal Related Tools and Resources
Cancer - Head and Neck Related Tools and Resources
Cancer – Lung Related Tools and Resources
Cancer – Prostate Related Tools and Resources
Use the Audience, Country and Language sort tabs to narrow your search.
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.
Disclaimer: The information included on this website is based on the best available evidence at the time of writing. It
has been independently researched, written and reviewed by dietitians and other health professionals using established
protocols, to assist practitioners to make practice decisions. It should be used to complement, not replace, sound clinical
Cancer - Colorectal
judgment. While every effort is made to ensure information contained on this website is accurate and up-to-date, errors
may occasionally occur. Neither Dietitians of Canada nor any dietetic associations contributing to or licensing the content
in PEN: Practice-based Evidence in Nutrition® assumes any responsibility or liability arising from any error in or omission
of information, or from the use of any information or advice contained within this website or provided by your health care
professional. Because PEN® content is updated regularly, printed web pages or PDF documents may become obsolete.
PEN® users should ensure that they are referring to the most recent version available. The PEN® website may contain
links to other external websites that do not fall under the pennutrition.com domain. Pennutrition.com is not responsible for
the privacy practices or the content of such external websites. Neither Dietitians of Canada nor any dietetic associations
contributing to or licensing the content in PEN® endorses the content, products or services on other websites. All PEN®
authors and reviewers are required to complete a Declaration of Affiliations and Interests Form that is kept on file with
Dietitians of Canada.
© Dietitians of Canada 2005-21. All rights reserved. While individual copies of documents may be reproduced for the
convenience of the licensed subscriber according to the end user license, distribution to non subscribers or
reproduction of multiple copies of PEN content is strictly prohibited without prior written permission. Licensed
subscribers may download, duplicate and distribute copies of the PEN branded client handouts for educational use with
their own clients. Institutions must have sufficient numbers of site licenses in order to make multiple copies to meet client
needs. The PEN website may also contain information which is copyrighted by others; multiple copies of these
documents may not be reproduced without the prior written permission of the copyright holder.
Cancer - Colorectal

Cancer - Colorectal

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Cancer - Colorectal

Uploaded by

Copyright:

Available Formats

Cancer - Colorectal 

Category: Health Condition/ Disease

Key Practice Point #1

2. Reynolds A, Mann J, Cummings J, Winter N, Mete E, Te Morenga L. Carbohydrate quality and

Key Practice Point #2

Grade of Evidence: B & C

Key Practice Point #3

See Additional Content:

Key Practice Point #1

Grade of Evidence: B & C

Key Practice Point #2

Key Practice Point #1

Grade of Evidence: B & C

500 g of cooked red meat is about 700-750 g raw meat.

Key Practice Point #2

See International Alcohol Guideline CollectionInternational Alcohol Guideline Collection

Key Practice Point #1

Grade of Evidence: B & C

Key Practice Point #1

Grade of Evidence: B & C

Key Practice Point #1

Grade of Evidence: C & D

Summary of Recommendations and Evidence

2. Milk Products/Vitamin D and Colorectal Cancer Risk

3. Nutrients/Dietary Factors and Increased Colorectal Cancer Risk

4. Low Carb Diet and Increased Colorectal Cancer Risk

6. Probiotics/Prebiotics/Synbiotics and Colorectal Cancer Prevention

1. Nutrients/Dietary Factors and Decreased Colorectal Cancer Risk

Vitamin C/Fish/Vitamin Supplements

See Additional Content:

2. Milk Products/Vitamin D and Colorectal Cancer Risk

3. Nutrients/Dietary Factors and Increased Colorectal Cancer Risk

500 g of cooked red meat is about 700-750 g raw meat.

See International Alcohol Guideline Collection: International Alcohol Guideline Collection

4. Low Carb Diet and Increased Colorectal Cancer Risk

5. Folate Supplements and Colorectal Cancer Risk

Practice Guidance Toolkit

This toolkit discusses the following key nutrition issues:

See Additional Content:

Nutrition Assessment, Monitoring and Evaluation

Nutrition Monitoring and Evaluation

Anthropometric Comparative Standards – Adult

Measure NCP Terminology

Adult BMI  Weight and Growth Recommendation

Anthropometric Comparative Standards – Children

Birth to 24 The WHO Child Growth  Weight and Growth

Child BMI WHO Growth Charts Adapted

UK-WHO 0-4 years

 Food and Nutrient Intake

Food/Nutrition-related Comparative Standards

Nutrition-focused Physical Findings

 Overall Appearance (underweight, overweight or obesity)

Biochemical Data, Medical Tests and Procedures

 Mineral Profile, Iodine, Urinary Excretion

Nutrition Prescription Examples

Food and/or Nutrient Delivery Example

Nutrition Counselling Example

Cancer Summary of Recommendations and Evidence

 Low Iodine Diet and Cancer Recurrence and Mortality Rates

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

Cancer - Breast Summary of Recommendations and Evidence

Adult BMI Weight and Growth Recommendation

Birth to 24 The WHO Child Growth Weight and Growth

Food and Nutrient Intake

Overall Appearance (underweight, overweight or obesity)

Mineral Profile, Iodine, Urinary Excretion

Low Iodine Diet and Cancer Recurrence and Mortality Rates

Fish/Vitamin C/Vitamin Supplements