Diet and Cancer
Diet and Cancer
learning objectives
After completing this chapter, the student should be able to:
1.
List several correlations between dietary intake and can cers of specific sites.
2.
Interpret dietary guidelines for the prevention of cancer.
3.
Identify reasons
that population correlations may not apply to subgroups
or to individuals .
4.
Name several factors thought to contribute to loss of appetite in cancer clients.
5.
Discuss measures
to increase oral intake for clients
with cancer.
|
cancer.
Definitions
and Statistics
Cancer
means "crab," for the creeping way in which it spreads. Cancer is a general term for more than 100 typ es of malignant neoplastic disease.
Terminology
A neoplasm, is a new and abnormal formation of tissue (tumor) that grows at the expense of the healthy organism. Two main divisions of neoplasms are malignant or cancer ous tumors , which infiltrate surrounding tissue and spread to distant sites of the bo dy, and benign tumors , which are localized but potentially dangerous
if located in vital organs.
Two of the chief types of cancer are sarcomas and car cinomas. Sarcomas arise from connective tissue, such
as muscle or bone, and
are more common in young people . Carcinomas occur in epithelial tissue , including cancers of the
lung, breast, prostate, and colon, and are more com-
Occurrence and Mortality
Cancers in general are more common in older people . In 1999 to 2000, the prevalence of cancer by age group was as follows:
• Ages 18 to 44 years
- 2 percent
• Ages 45 to 64 years - 7.4
percent,
• Ages 65 to 74 years -
17.3 percent,
• Ages 75 years or older - 22.8 percent (National Center,
2004).
Cancer is
the second most common cause of
death in the United States after diseases of the
heart and is expected to
become the leading
cause of death in the next decade. In 2001, the
age-adjusted death rate for cancer already exceeded
that for heart disease in
four states: Alaska,
Minnesota, Montana, and Oregon . In 1990 to 2000, the
five primary sites with the highest age-adjusted death rates for males were lung/ bronchus , prostate, colon/rectum, pancreas, and leukemia; for females , lung / bronchus , breast , colon / rectum , pancreas , and
ovary. Overall, cancer mor tality
is higher among men compared with
women and higher among black populations compared with whites (Centers for
Disease Control, 2004). The incidence of
the five most common cancers
for men and
women is illustrated in Figure 23-1, which shows that lung cancer, colorectal cancer,
and non-Hodgkin's lymphoma occupy the same ranks regardless of gender. Figure 23-2 exhibits the
mortality rates by gender for whites and blacks for all cancers in the United States
Clients who are alive and without
recurrence of cancer
5 years after diagnosis are considered cured.
This is termed
the 5-year survival rate. Depending on the site in which the cancer occurs, the survival rates vary greatly, but socioeconomic status affects the stage at which the cancer is diagnosed
as well as survival
rates . In a Michigan
Clinical Application 23-1
Transformation of Normal Cells Into Cancer Cells
Cancer is basically uncontrolled replication of cells. Normal cells divide in the processes of growth and maintenance but stop dividing at appropriate points.
Even in normal cell division,
mistakes in deoxyribonucleic acid (DNA) transcription are made and corrected. Hundreds
of incidents of oxidative damage to cell components, such as DNA, are estimated
to occur in a cell daily, but this oxidative damage
has not been directly linked
to cancer.
Obviously, not all of these mistakes go on to turn cells cancerous. Multiple enzyme systems inactivate the damaging elements, and various mechanisms repair the DNA (Slupphaug, Kavli, and Krokan, 2003) Deficiencies in DNA-damage signalin g and repair pathways are fundamental to the etiology of most, if not all, human cancers (Khanna and Jackson, 2001 ). Several genes within a cell must be changed or mutated for cancer to occur.
Transformation of normal
cells into cancer cells is a two-step
process. The first step is initiation
. The second step is promotion. Physical forces, chemicals, or biologic
agents can damage
genes. If the damage is not repairable, the gene has mutated, and if cancer develops later, the cancer cells are descendants of that mutated
cell (Weinberg, 1996). The
alteration may not be
significant until the second step of the conversion to cancerous
cells,
promotion, takes place. The time period between initiation and
promotion in some cases
is 10 to 30 years but may
be shorter if a mutated
cancer-causing gene is inherited from a parent. Substances that enhance the expression of the
altered gene are called promoters. They must be present at high levels for a prolonged period Promoters are tissue specific,
such as saccharin for cancer of the
urinary bladder (in rats) and bile acids for colon cancer. In contrast to initiation, which results in permanent change, the process of promotion is reversible. Reducing
exposure to
high levels of promoters allows the body to repair the damaged cells.
Genes are carried in
the DNA of the chromosomes in the cell nucleus.
Two classes of genes play maior roles in
the life cycle of cells: pronto-oncogenes and tumor suppressor genes. In normal cells, pronto-oncogenes support
the growth and division of the cell, whereas
tumor-suppressor genes inhibit those processes. Both pronto-oncogenes
and tumor-suppressor genes may be mutated and thus contribute to cancer development.
The pronto-oncogenes become carcinogenic oncogenes that stimulate
excessive reproduction, and the tumor suppressor genes become
inactivated and unable to stop the multiplication of cells.
As more is learned about the molecular basis of cancer,
therapies can be developed that targe t the aberrant cells
much more accurately than the treatments currently available.
Several genes within a cell must undergo mutation for cancer to occur.
and rectum, corpus and uterus, and
non -Hodgkin 's lymphoma. The race/ethnicity groupings are w hit e,
black, Hispanic
,
Asian /Pacific Islander , and American Indian /Alaskan native. (Data derived from Nation al
Cancer Institute, 2004.)
study of female breast , cervix, lung , pro state , and colon carcinoma , persons over 65 years of age who were in surfed by Medic aid had the greatest risk of late-stage diagnosis and death (Bradley, Given, and Rob er ts , 2001). Similarly,
national cervical cancer incidence and mortality rates in cr eased with increasing poverty and decreasing education levels for the total population as well as for non Hispanic white, black , American Indian, Asian/Pacific Island er, and Hispanic women. Patients in low er socioeconomic census tracts had significantly higher rates of lat e st age cancer diagnosis and l owe r rates of cancer survival (Singh et al, 2004).
The causes of cancer are complex often incompletely understood. Certain cancers appear in great numbers in particular countries.
Clinical application 23-2 summarizes some of the findings.
In addition to people.
Cancer mortality rates by state economic area (age -adjusted 1970 US population)
Mortality rates for
all cancers in the United States , 1970-1994, by
race and sex. Depicted here are
mortality rates for all cancers
for (a) white males, (b) black males, (c) white females , and
(d) black females.
Note that the legend colors
denote
different rates per 100,000 age-adjusted
population for each map . The brightest
red is assigned to the highest 10 percent of each group
, so that it indicates rates of 230 to
266/100,000 population for white males but 339 to
908/100,000 for
black males . This Web site
also contains maps
of mortality rates
for about 50 specific
cancers, maps by
county, and maps for
the years 1950-1969 (Devesaet al, 1999).
Clinical Application 23-2
History of Diet-Cancer Links in Various Populations
Particular cancers occur
with greater frequency in some countries than others. When this was noted, the search began for dissimilarities in environment that
could explain the differences. Because hereditary factors
can confound the results when dissimilar populations
are compared, the study of immigrants is especially enlightening.
In Japan there is more stomach cancer and less prostate and colon
cancer than in the United States. In second-generation
Japanese immigrants to the
United States, however, the distribution of cancers becomes
similar to that of other
Americans. Similar findings are reported in Polish men for prostate cancer. On the other hand, migrants from Asia to
the West, who maintain their traditional diet, do not have an increased risk of prostate
cancer, attributed in part to phytoestrogens in vegetarian
Asian diets (Vij and Kumar, 2004 ). See Clinical
Application 23-6
for more information on phytoestrogens. Immigration, and presumed adoption of a Western diet, affects cancer development: age-adjusted breast cancer incidence rates per 100,000 Japanese women were 14
in
Japan, 44 in Hawaii, and 57 in Los Angeles (Tomlin-son, 1994)
Stomach and esophageal cancers are common where nitrates and nitrites are prevalent in food
and water and where
cured and pickled foods are
popular. These areas include China, Japan, and Iceland.
In Yangzh ong, China, frequent intake of allium vegetables (garlic, onion, Welsh
onion, and Chinese chives), raw vegetables, tomatoes, snap beans, and tea decreased the risk of stomach and esophageal cancer (GAO et al, 1999) Vitamins C and E and
green tea can prevent formation
of carcinogenic nitrosamines and nitrosamides (Greenwald, 1994; Ho
et al, 1994; Kim et al, 1994) In Linxian County, China , where residents have one of the world's
highest rates of esophageal and gastric cardia cancer; a 5-year trial of
beta-carotene, vitamin E, and selenium reduced stomach cancer
incidence by 20 percent and total mortality
by 10 percent (Albert's and Garcia, 1995).
Elsewhere, a low rate of colon cancer is seen in Africa. The diet there is high in fiber, and the Africans pass bulky stools. The theory put forth was
that the fiber both dilutes the carcinogens in
the feces and pushes them out of the body
faster than a low-fiber diet
would. New research shows that black South Africans consume less than the RDA for fiber, so the low risk for colon cancer was then attributed to avoidance of excess animal protein and fat (O'Keefe
et al, 1999). Avoidance is probably unintentional. The populations with
high fiber intakes and low colon cancer rates also are seen in poor countries where obesity is uncommon, meat consumption is
low, and physical activity is high.
This type of research is intriguing and offers a starting point
for other
investigations, but it cannot establish causation
no matter how large the study.
in a given country possibly being innuenced by similar environmental factors, including diet, they also may have genes that are similar compared with those found in people else
where . This
chapter describes some examples of
the associations
that have been found and shows the difficulty of pinpointing the causative links and
thus the difficulty of identifying a dietary behavior to adopt or
to avoid with the goal of preventing cancer.
In the United States, about 33 percent of the 500,000
yearly cancer deaths are
associated with cigarette smoking and about 33 percent with inappropriate nutritional and activity habits
(Byers et al, 2002). This chapter considers diet and cancer. The
relationship of diet to the development
of cancer is explored first, followed
by the nourishment of clients with cancer.
Dietary Components Associated With Cancer
It is difficu lt to assess the role of dietary components with out also considering other
factors that might contribute to the development of cancer. Outside of
tobacco use, diet is probably the
most important fac tor in the etiology of human cancer,
thought to be responsible for about
one-third of all cases in developed
countries (Blackburn et al, 2003; Ferguson,
2002). Illustrating the limits of present knowledge, however, despite an overall
healthy lifestyle and long life expectancy, Adventist
populations have high rates of breast and
prostate cancers (Willett, 2003). Over time, the relation ship of diet to breast cancer has become
clearer, and it is elaborated upon in Clinical Application 23-3.
Excesses of Certain Substances
Some substances and practices are associated with higher cancer rates. This is the case with energy and
fatty acid intake, meat, alcohol, and certain cooking and preparation methods.
These topics are addressed in the following
section.
Energy and Fatty Acid Intake
Some of the end products of fat metabolism are thought to be carcinogenic, but
dietary fat may contribute to the risk of cancer because of its energy density.
Overweight and obesity increase the risk for cancers of the breast (post menopausal), colon, endometrium, gallbladder, esophagus,
pancreas, and kidney; however, moderate-to-vigorous exercise reduces colon
and breast cancer risks independent of the effect of activity on weight (Byers et al, 2002). Obesity contributes to a poorer prognosis: men with BMls of 40 or more had 52 percent higher
death rates from all cancers than normal-weight men; for women, the corresponding rates were
62 percent higher (Calle et al, 2003).
Public health recommendations to decrease total fat intake for the prevention of cancer appear largely unwar ranted (Kushi and Giovannucci, 2002), but additional infor mation is needed regarding specific fatty acids in relation to causing or preventing cancer in particular sites. A high total fat intake is associated with a 24 percent increased risk of ovarian cancer whereas diets high in animal fat increased risk 70 percent, pointing out a need to need clarify the.
Clinical Application 23-3
Breast Cancer and Diet
Mutations in certain genes greatly increase
breast cancer risk,
but these account
for a minority
of cases (Key, Verkasalo , and Banks , 2001). In fact, eight of
nine
women who
develop breast cancer do not have an affected first degree relative
with the disease (Collaborative Group, 2001).
Large prospective studies have not found dietary fat per se or a diet high in red meats to be associated
with breast cancer (Moyad,
2002; Terry,
et al, 2001).
Populations with high fat intakes generally
have high rates of breast cancer, but studies of individual women have not confirmed an association of high-fat diets with
breast cancer risk. The major risk factors for breast cancer are hormone-related, and the only generally recognized dietary risk factors
are obesity and alcohol consumption .
Obesity increases breast
cancer risk in postmenopausal women
by about 30 percent, probably by increasing serum concentrations of bioavailable estradiol (Key et al, 2003).
Breast cancer is associated with early menarche and late menopause, both effects of high
estrogen levels, and with
obesity in postmenopausal women since fat cells can produce estrogen. In Washington and New Mexico, women with BMls
above 30 had 130 percent higher
concentrations of estradiol
as those with BM
ls lower than 22. Lastly, overweight and obese women with breast cancer have poorer
survival compared with thinner
women (McTiernan et al, 2003) Worldwide, 25 percent of breast cancer cases are due to overweight, obesity, and sedentary
habits.
Women who exercise 3 to 4 hours per week at a moderate to vigorous level have a 30 to 40 percent
lower risk for breast cancer than sedentary women (McTiernan, 2003).
Moderate alcohol intakes increase breast cancer risk by about 7 percent per alcoholic drink per day, perhaps also by increasing estrogen levels (Key et al, 2003). Alcohol use, even at moderate levels (two drinks per day), increases risk for both premenopausal and postmenopausal breast cancer (M cTie rnan, 2003) because the metabolism of alcohol produces DNA-damaging reactive oxygen species that subject cells to oxidative stress (Ambrosone, 2000) and mediates an increase in estradiols that may be partly responsible for breast cancer risk (Poschl and Seitz, 2004). Adequate folate levels may be particularly important for women who are at higher risk of breast cancer because of high alcohol consumption (Zhang, 2004).
Specific dietary components have been investigated without changing the aforementioned
relationships.
No strong association was found
between the ingestion of milk or other dairy products and breast cancer risk (Moorman and Terry, 2004) Similarly, analysis of eight prospective studies discerned no significant association between intakes of total meat, red meat, white meat, total dairy fluids, or total dairy solids and breast cancer risk and an inconsistent relationship was found
between egg consumption and risk
of breast cancer (Missmeret al, 2002) While high bone mineral density (BMD) in elderly women is related to higher rates of breast cancer, BMD is also regarded as a marker for lifetime estrogen exposure (Van der Klift et al, 2003)
Although not obtained
through diet, some deriva- tives of vitamin D have been developed
that may inhibit proliferation of cells, including those of breast cancer
(O'Kelly and Koeffler, 2003) . These synthetic
products have the growth-regulating effects but not the calcium-mobilizing actions of vitamin D, thus avoiding the hypercalcemia caused by large doses of the natural vitamin (Colston
and Hansen, 2002 ).
factors th at might contribute to the d is parity (Hun charek and Ku pelni c k, 2001). In th e case of bowel cancer, for instance, increased concentrations of
short-chain fatty acids and eicosano pentaenoic acid (EPA) seem to protect against colorectal cancer,
but increased concentrations
of medium-cha i
n fatty acids and arachidonic acid (AA) may
be associated with increased risk (Nkondjock et al, 2003). Long -chain omega-3 polyunsaturated
fatty acids
from fish show promise asnutrients to possibly prevent prostate cancer, but in contrast, another omega -3 PUFA, alpha linolenic acid, might be a risk
factor (Astorg , 2004). Consuming one or more servings
of fish per week protected against digestive tract cancers in
Italy (Fernandez et al,
1999); however, to
what extent th e
fish-containing meals reduce d meat consumption was not re ported, but once again, the evidence supports the health fulness of a varied diet.
Prolonged high consumption of re d and processed meat may increase the risk of cancer in the distal portion of the large intestine. Over a ten year period, people consuming processed meat at the highest levels had a 50 percent higher risk of distal colon cancer than those consuming at the lowest levels . Likewise, high consumption of red meat was associated with a 40 percent higher risk of rectal cancer (Chao et al, 2005) . Seventh Day Advent its and Mormons have a lower incidence of bowel cancer than other Americans , eve n when caffeine and alcohol differences between the study groups are equalized. Some Seventh Day Advent instead meat, but those who did had higher rates of colon and prostate cancer than vegetarian members of the sect, and those who consumed the most beef had a higher risk of bladder cancer than those who consumed less (Fraser, 1999).
Alcohol
Alcohol intake greater than two drinks per day substantially increases risk for cancers of the mouth , pharynx, larynx, esophagus , liver, and breast and may be related to increased risk of colon cancer (Byers et al, 2002). Contrary to earlier reports linking alcohol to head and
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