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1 Executive Sunday
Scientific pronouncements are usually viewed by the public as carry-
ing a rather high level of certainty. Therefore, scientists must be
especially careful in their choice of words whenever they are not total-
ly confident about their conclusions. For example, it has become abso-
lutely clear that cigarettes are the cause of approximately one-quarter
of all the fatal cancers in the United States. If the population had
been persuaded to stop smoking when the association with lung cancer was
first reported, these cancer deaths would now not be occurring. Twenty
years ago the stop-smoking message required some rather cautious word-
ing. Today, the facts are clear, and the choice of words is not so
important.
The public often demands certain kinds of information before such
information can be provided with complete certainty. For example,
weather forecasting is often not exact; nevertheless, the public asks
that the effort be made, but has learned to accept the fact that the
results are not always reliable.
The public is now asking about the causes of cancers that are not
associated with smoking. What are these causes, and how can these
cancers be avoided? Unfortunately, it is not yet possible to make firm
scientific pronouncements about the association between diet and cancer.
We are in an interim stage of knowledge similar to that for cigarettes
20 years ago. Therefore, in the judgment of the committee, it is now
the time to offer some interim guidelines on diet and cancer.
Approximately 20% of all deaths in the United States are caused by
cancer. Although the number of cancer cases is steadily increasing as
the population grows, the age-adjusted total cancer incidence and mor-
tality rates for sites other than the respiratory tract (cancers of
which are primarily due to cigarette smoking) have as a whole remained
stable during the last 30 to 40 years.
The search for the causes of cancer has been an important branch of
cancer research. Considerable effort has been devoted to studying the
influence of both environmental and genetic factors on the incidence of
cancer. In the course of this research, it has become clear that most
cancers have external causes and, in principle, should therefore be pre-
ventable. For example, blacks and Japanese residing in the United States
develop the spectrum of cancers that is typical for the United States but
different from that in Africa and Japan.
But what might these external causes be? Many factors in our en-
vironment are potential causes of cancer. They include substances in
the air we breathe, the water we drink, the regions in which we work and
1
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2 DIET, NUTRITION, AND CANCER
live, and the foods we eat. Our exposure to some of these factors var-
ies in ways that can be precisely measured. For most factors, however,
the measurement of the exposures and the assessment of their effects are
neither precise nor straightforward. Among the factors whose precise
effects are difficult to assess are the diets consumed by different
groups of people. The measurements are difficult not only because it is
hard to learn what people eat but also because the foods comprising
their diets are so complex.
Studies of the association between diet and cancer have focused on
cancers of the gastrointestinal tract, the breast and other tissues
susceptible to hormonal influence, and, to a lesser extent, the respi-
ratory tract and the urinary bladder. After assessing the resultant
literature, the committee concluded that the differences in the rates
at which various cancers occur in different human populations are often
correlated with differences in diet. The likelihood that some of these
correlations reflect causality is strengthened by laboratory evidence
that similar dietary patterns and components of food also affect the
incidence of certain cancers in animals.
Chapters 16 and 17 provide information about the trends in cancer
incidence and the relationship between diet and the incidence of cancer
at specific sites.
Epidemiologists have found it relatively easy to demonstrate a cor-
relation between diets consumed in modern affluent societies and the
incidence of cancers in such organs as the breast, colon, and uterus.
But it has proved to be much more difficult to establish causal rela-
tionships and to determine which, if any, of the dietary components is
responsible.
Similarly, difficulties are encountered in laboratory experiments.
Like humans, most animals have a significant incidence of cancer in old
age, and the rates of these cancers often tend to be affected by changes
in diet. However, the influence of diet on spontaneous and experimen-
tally induced cancers is not easily investigated because the underlying
mechanisms and molecular biology of the cancers are still not fully
understood. Indeed, the effects of diet were often regarded as a
nuisance--i.e., yet another variable standing between the investigators
and their measurement of carcinogenicity. As a consequence, researchers
have only recently returned to the study of diet as a factor in carcino-
genesis.
It is possible that research in progress will generate more defini-
tive information that will be useful in formulating dietary recommenda-
tions to minimize the risk of cancer. In the meantime, the committee
believes that the evidence at hand justifies certain interim guidelines.
These guidelines appear at the end of this chapter following a summary
of the committee's findings and the conclusions it believes can be drawn
from the scientific evidence.
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Executive Summary 3
SUMMARY AND CONCLUSIONS
-
Dietary Patterns and Components of Food
Since the turn of the century, new methods of processing and storage
have resulted in a proliferation of the kinds and numbers of food items
available to the U.S. population. Unfortunately, little is known about
the ways in which such innovations have altered the specific composition
of the diet. The only components of food that have been monitored regu-
larly are the nutrients. The dietary levels of most nutrients have
changed relatively little over the past 80 years.
Attempting to determine which constituents of food might be associ-
ated with cancer, epidemiologists have studied population subgroups,
including migrants to the United States, to examine the relationship
between specific dietary patterns or the consumption of certain foods
and the risk of developing particular cancers. In general, the evidence
suggests that some types of diets and some dietary components (e.g.,
high fat diets or the frequent consumption of salt-cured, salt-pickled,
and smoked foods) tend to increase the risk of cancer, whereas others
(e.g., low fat diets or the frequent consumption of certain fruits and
vegetables) tend to decrease it. The mechanisms responsible for these
effects are not fully understood, partly because nutritive and non-
nutritive components of foods may interact to exert effects on cancer
incidence.
In the laboratory, investigators have attempted to shed light on the
mechanisms by which diet may influence carcinogenesis. They have ex-
amined the ability of individual nutrients, food extracts, or non-
nutritive components of food to enhance or inhibit carcinogenesis and
mutagenesis, thereby providing epidemiologists with testable hypotheses
regarding specific components of the diet. Because the data from both
types of studies are generally grouped according to dietary constitu-
ents, the committee found it advantageous to organize its report in a
similar fashion.
Total Caloric Intake
The committee reviewed many studies in which the variable examined
was the total amount of food consumed by humans or animals, rather than
the precise composition of the diet. This review is contained in
Chapter 4, which is entitled Total Caloric Intake, even though the
studies did not indicate whether the observed effects resulted from the
changes in the proportion of specific nutrients in the diet or from the
modification of total caloric intake.
Since very few epidemiologists have been able to examine the effect
of caloric intake per se on the risk of cancer, their reports have pro-
vided largely indirect evidence for such a relationship, and much of it
is based on associations between body weight or obesity and cancer.
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4 DIET, NUTRITION, AND CANCER
In laboratory experiments, the incidence of tumors is lower and the
lifespan much longer for animals on restricted food intake than for ani-
mals fed ad libitum. However, because the intake of all nutrients was
simultaneously depressed in these studies, the observed reduction in
tumor incidence might have been due to the reduction of some specific
nutrient, such as fat. It is also difficult to interpret experiments in
which caloric intake has been modified by varying dietary fat or fiber,
both of which may by themselves exert effects on tumorigenesis.
Thus, the committee concluded that neither the epidemiological stud-
ies nor the experiments in animals permit a clear interpretation of the
specific effect of total caloric intake on the risk of cancer. Nonethe-
less, the studies conducted in animals show that a reduction in total
food intake decreases the age-specific incidence of cancer. The evi-
dence is less clear for human beings.
Lipids (Fats and Cholesterol)
Many epidemiological and laboratory studies have been conducted to
examine the association between cancer and intake of lipids, i.e., total
dietary fat, saturated fat, polyunsaturated fat, and cholesterol.
Fats. Epidemiological studies have repeatedly shown an association
between dietary fat and the occurrence of cancer at several sites, espe-
cially the breast, prostate, and large bowel. In various populations,
both the high incidence of and mortality from breast cancer have been
shown to correlate strongly with higher per capita fat consumption; the
few case-control studies conducted have also shown this association with
dietary fat. Like breast cancer, increased risk of large bowel cancer
has been associated with higher fat intake in both correlation and case-
control studies. The data on prostate cancer are more limited, but they
too suggest that an increased risk is related to high levels of dietary
fat. In general, it is not possible to identify specific components of
fat as being clearly responsible for the observed effects, although
total fat and saturated fat have been associated most frequently.
The epidemiological data are not entirely consistent. For example,
the magnitude of the association of fat with breast cancer appears
greater in the correlation data than in the case-control data, and
several reports on large bowel cancer fail to show an association with
fat. Possible reasons for these discrepancies are apparent. These are
discussed in Chapter 5 (see pages 5-5 and 5-18~.
Like epidemiological studies, numerous experiments in animals have
shown that dietary lipids influence tumorigenesis, especially in the
breast and the colon. An increase in fat intake from 5% to 20% of the
weight of the diet (i.e., approximately 10% to 40% of total calories)
increases tumor incidence in various tissues; conversely, animals con-
suming low fat diets have a lower tumor incidence. When the intake of
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Execahve Summary 5
total fat is low, polyunsaturated fats appear to be more effective than
saturated fats in enhancing tumorigenesis. However, this distinction
becomes less prominent as total fat intake is increased.
Dietary fat appears to have a promoting effect on tumorigenesis.
For example, some studies suggest that the development of colon cancer
is enhanced by the increased secretion of certain bile steroids and bile
acids that accompanies high levels of fat intake. Nonetheless, there is
little or no knowledge concerning the specific mechanisms involved in
tumor promotion. This lack of understanding contributes to our overall
uncertainty about the mechanisms that underlie the effect of diet on
carcinogenesis. Although most of the data suggest that dietary fat has
promoting activity, there is not enough evidence to warrant the complete
exclusion of an effect on initiation.
The committee concluded that of all the dietary components it
studied, the combined epidemiological and experimental evidence is most
suggestive for a causal relationship between fat intake and the occur-
rence of cancer. Both epidemiological studies and experiments in ani-
mals provide convincing evidence that increasing the intake of total fat
increases the incidence of cancer at certain sites, particularly the
breast and colon, and, conversely, that the risk is lower with lower
intakes of fat. Data from studies in animals suggest that when fat
intake is low, polyunsaturated fats are more effective than saturated
fats in enhancing tumorigenesis, whereas the data on humans do not
permit a clear distinction to be made between the effects of different
components of fat. In general, however, the evidence from epidemiolog-
ical and laboratory studies is consistent.
Cholesterol. The relationship between dietary cholesterol and
cancer is not clear. Many studies of serum cholesterol levels and
cancer mortality in human populations have demonstrated an inverse
correlation with colon cancer among men, but the evidence is not con-
clusive. Data on cholesterol and cancer risk from studies in animals
are too limited to permit any inferences to be drawn.
Chapter 5 contains a more detailed discussion of these studies.
Protein
At,
The relationship between protein intake and carcinogenesis has been
studied in human populations as well as in the laboratory. These stud-
ies are discussed in Chapter 6.
Results of epidemiological studies have suggested possible associa-
tions between high intake of dietary protein and increased risk for can-
cers at a number of different sites, although the literature on protein
is much more limited than the literature concerning fats and cancer. In
addition, because of the very high correlation between fat and protein
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6 DIET, NUTRITION, AND CANCER
in the diets of most Western countries, and the more consistent and
often stronger association of these cancers with fat intake, it seems
likely that dietary fat is the more active component. Nevertheless,
the evidence does not completely preclude the existence of an inde-
pendent effect of protein.
In most laboratory experiments, carcinogenesis is suppressed by
diets containing levels of protein at or below the minimum required
for optimal growth. Chemically induced carcinogenesis appears to be
enhanced as protein intake is increased up to 2 or 3 times the normal
requirement; however, higher levels of protein begin to inhibit car-
cinogenesis. There is some evidence to suggest that protein may affect
the initiation phase of carcinogenesis and the subsequent growth and
development of the tumor.
Thus, in the judgment of the committee, evidence from both epidemio-
logical and laboratory studies suggests that high protein intake may be
associated with an increased risk of cancers at certain sites. Because
of the relative paucity of data on protein compared to fat, and the
strong correlation between the intakes of fat and protein in the U.S.
diet, the committee is unable to arrive at a firm conclusion about an
independent effect of protein.
Carbohydrates
As discussed in Chapter 7, information concerning the role of carbo-
hydrates in the development of cancer in humans is extremely limited.
Although some studies suggest that a high intake of refined sugar or
starch increases the risk of cancer at certain sites, the results are
insufficient to permit any firm conclusions to be drawn.
The data obtained from studies in animals are equally limited,
providing too little evidence to suggest that carbohydrates (possibly
excluding fiber) play a direct role in experimentally induced carcino-
genesis. However, excessive carbohydrate consumption contributes to
caloric excess, and this in turn has been implicated as a modifier of
carcinogenesis.
Dietary Fiber
Considerable effort has been devoted to studying the effects of
dietary fiber and fiber-containing foods (such as certain vegetables,
fruits, and whole grain cereals) on the occurrence of cancer (see
Chapter 8~.
Most epidemiological studies on fiber have examined the hypothesis
that high fiber diets protect against colorectal cancer. Results of
correlation and case-control studies of dietary fiber have sometimes
supported and sometimes contradicted this hypothesis. In both types of
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Executive Summary 7
studies, correlations have been based primarily on estimates of fiber
intake obtained by grouping foods according to their fiber content.
In the only case-control study and the only correlation study in which
total fiber consumption was quantified rather than estimated from the
consumption of high fiber foods, no association was found between high
fiber intake and a lower risk of colon cancer. However, the correla-
tion study indicated that the incidence of colon cancer was inversely
related to the intake of one fiber component--the pentosan fraction,
which is found in whole wheat products and other food items.
Laboratory experiments also have indicated that the consumption of
some high fiber ingredients (e.g., cellulose and bran) inhibits the in-
duction of colon cancer by certain chemical carcinogens. However, the
results are inconsistent. Moreover, they are difficult to equate with
the results of epidemiological studies because most laboratory investi-
gations have focused on specific fibers or their individual components,
whereas most epidemiological studies have been concerned with fiber-
containing foods whose exact composition has not been determined.
Thus, the committee found no conclusive evidence to indicate that
dietary fiber (such as that present in certain fruits, vegetables,
grains, and cereals) exerts a protective effect against colorectal
cancer in humans. Both epidemiological and laboratory reports suggest
that if there is such an effect, specific components of fiber, rather
than total fiber, are more likely to be responsible.
Vitamins
.
In recent years, there has been considerable interest in the role of
vitamins A, C, and E in the genesis and prevention of cancer. In con-
trast, less attention has been paid to the B vitamins and others such as
vitamin K. Chapter 9 contains more detailed information on the evidence
summarized below.
Vitamin A. A growing accumulation of epidemiological evidence indi-
cates that there is an inverse relationship between the risk of cancer
and the consumption of foods that contain vitamin A (e.g., liver) or its
precursors (e.g., the carotenoids in green and yellow vegetables). Most
of the data do not show whether the effects are due to carotenoids, to
vitamin A itself, or to some other constituent of these foods. In these
studies, investigators found an inverse association between estimates of
vitamin A intake and carcinoma at several sites, e.g., the lung, the
urinary bladder, and the larynx.
Studies in laboratory animals indicate that vitamin A deficiency
generally increases susceptibility to chemically induced neoplasia and
that an increased intake of the vitamin appears to protect against car-
cinogenesis in most, but not all cases. Because high doses of vitamin A
are toxic, many of these studies have been conducted with its synthetic
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8 DIET, NUTRITION, AND CANCER
analogues (retinoids), which lack some of the toxic effects of the
vitamin. Retinoids have been shown to inhibit chemically induced
neoplasia of the breast, urinary bladder, skin, and lung in animals.
The committee concluded that the laboratory evidence shows that
vitamin A itself and many of the retinoids are able to suppress chemi-
cally induced tumors. The epidemiological evidence is sufficient to
suggest that foods rich in carotenes or vitamin A are associated with
a reduced risk of cancer. The toxicity of vitamin A in doses exceed-
ing those required for optimum nutrition, and the difficulty of epi-
demiological studies to distinguish the effects of carotenes from those
of vitamin A, argue against increasing vitamin A intake by the use of
supplements.
Vitamin C (Ascorbic Acid). The epidemiological data pertaining
to the effect of vitamin C on the occurrence of cancer are not exten-
sive. Furthermore, they provide mostly indirect evidence since they
are based on the consumption of foods, especially fresh fruits and
vegetables, known to contain high concentrations of the vitamin, rather
than on actual measurements of vitamin C intake. The results of several
case-control studies and a few correlation studies suggest that the con-
sumption of vitamin-C-containing foods is associated with a lower risk
of certain cancers, particularly gastric and esophageal cancer.
In the laboratory, ascorbic acid can inhibit the formation of car-
cinogenic N-nitroso compounds, both in vitro and in viva. On the other
hand, studies of its inhibitory effect on preformed carcinogens have not
provided conclusive results. In recent studies, the addition of ascor-
bic acid to cells grown in culture prevented the chemically induced
transformation of these cells and, in some cases, caused reversion of
transformed cells.
Thus, the limited evidence suggests that vitamin C can inhibit the
formation of some carcinogens and that the consumption of vitamin-C-
containing foods is associated with a lower risk of cancers of the
stomach and esophagus.
Vitamin E (~-Tocopherol). Because vitamin E is present in a variety
-
of commonly consumed foods (particularly vegetable oils, whole grain
cereal products, and eggs), it is difficult to identify population
groups with substantially different levels of intake. Consequently, it
is not surprising that there are no epidemiological reports concerning
vitamin E intake and the risk of cancer.
Vitamin E, like ascorbic acid, inhibits the formation of nitrosa-
mines in viva and in vitro. However, there are no reports about the
effect of this vitamin on nitrosamine-induced neoplasia. Limited evi-
dence from studies in animals suggests that vitamin E may also inhibit
the induction of tumorigenesis by other chemicals.
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Execahve Summary 9
The data are not sufficient to permit any firm conclusion to be
drawn about the effect of vitamin E on cancer in humans.
The B Vitamins. No specific information has been produced by epi-
demiological studies, and there have been only a few inadequate labora-
tory investigations to determine whether there is a relationship between
various B vitamins and the occurrence of cancer. Therefore, no conclu-
sion can be drawn.
Minerals
Of the many minerals present in the diet of humans, the committee
reviewed the evidence for nine that have been suspected of playing a
role in carcinogenesis. The assessment was severely limited by a pau-
city of relevant studies on all but two minerals--selenium and iron.
Where data on dietary exposure and carcinogenesis were insufficient,
the committee used information from studies of occupational exposure or
laboratory experiments in which the animals were exposed through routes
other than diet. Chapter 10 contains more detailed information on the
evidence summarized below.
Selenium. Selenium has been studied to determine its role in both
the causation and the prevention of cancer. The epidemiological evi-
dence is derived from a few geographical correlation studies, which have
shown that the risk of cancer is inversely related to estimates of per
capita selenium intake, selenium levels in blood specimens, or selenium
concentrations in water supplies. It is not clear whether this relation-
ship applies to all types of cancer or only to cancer at specific sites
such as the gastrointestinal tract. There have been no case-control or
cohort studies.
Experiments in animals have also demonstrated an antitumorigenic
effect of selenium. But the relevance of these results to cancer in
humans is not apparent since the selenium levels used in most of the
studies far exceeded dietary requirements and often bordered on levels
that are toxic. Earlier reports suggesting that selenium was carcino-
genic in laboratory animals have not been confirmed.
Therefore, both the epidemiological and laboratory studies suggest
that selenium may offer some protection against the risk of cancer.
However, firm conclusions cannot be drawn from the limited evidence.
Increasing the selenium intake to more than 200 ~g/day1 by the use
of supplements has not been shown to confer health benefits exceeding
The upper limit of the Range of Safe and Adequate Daily Dietary
Intakes published in the Recommended Dietary Allowances (see Chapter
10~.
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10 DIET, NUTRITION,AND CANCER
those derived from the consumption of a balanced diet. Such supple-
mentation should be considered an experimental procedure requiring
strict medical supervision and is not recommended for use by the public.
Iron. Iron deficiency has been related to an increase in the risk
of Plummer-Vinson syndrome, which is associated with cancer of the upper
alimentary tract. Some evidence suggests that iron deficiency may be
related to gastric cancer, also through an indirect mechanism. Although
epidemiological reports have suggested that inhalation exposures to high
concentrations of iron increase the risk of cancer, there is no evidence
pertaining to the effect of high levels of dietary iron on the risk of
cancer in humans. The limited evidence from animal experiments suggests
that a deficiency of dietary iron may increase susceptibility to some
chemically induced tumors.
The data are not sufficient for a firm conclusion to be drawn about
the role of iron in carcinogenesis.
Copper, Zinc, Molybdenum, and Iodine. Some epidemiological studies
suggest that dietary zinc is associated with an increase in the inci-
dence of cancer at certain sites; others suggest that blood and tissue
levels of zinc in cancer patients are lower, and those of copper are
higher, than in the controls. Results of experiments in animals are
also inconclusive. Different levels of dietary zinc either enhance or
retard tumor growth, depending on the specific test design. High levels
of copper have been observed to protect against chemical induction of
tumors.
There is some epidemiological evidence that a deficiency of molyb-
denum and other trace elements is associated with an increased risk of
esophageal cancer. Limited experiments in animals suggest that dietary
molybdenum supplementation may reduce the incidence of nitrosamine-
induced tumors of the esophagus and forestomach.
Studies conducted in Colombia, Iceland, and Scotland indicated that
iodine deficiency, and also excessive iodine intake, may increase the
risk of thyroid carcinoma. These observations have not been confirmed
in other countries or in other studies. In general, the results of
studies in animals support the association between iodine deficiency and
thyroid cancer.
The committee concluded that the data concerning dietary exposure to
zinc, copper, molybdenum, and iodine are insufficient and provide no
basis for conclusions about the association of these elements with cancer
risk.
Arsenic, Cadmium, and Lead. Occupational exposure to these elements
is associated with an increased risk of cancer at several sites. Expo-
sure to high concentrations of arsenic in drinking water has been linked
with skin cancer. However, the evidence for cancer risk resulting from
exposure to the normally low levels of these elements in the diet is not
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Executive Summary 11
conclusive. No carcinogenic effects of dietary cadmium and arsenic have
been observed in laboratory experiments, whereas high intakes of certain
lead compounds appear to increase the incidence of cancer in mice and
rats.
On this basis, the committee believes that no firm conclusions can
be drawn about the risk of cancer due to normal dietary exposure to
arsenic, cadmium, and lead.
Inhibitors of Carcinogenesis
Foods and numerous nutritive and nonnutritive components of the
diet have been examined for their potential to protect against carcino-
genesis. In epidemiological studies, investigators have attempted to
correlate the intake of specific foods (and by inference, certain vita-
mins and trace elements) and the incidence of cancer. In laboratory
experiments, vitamins, trace elements, nonnutritive food additives, and
other organic constituents of foods (e.g., indoles, phenols, flavones,
and isothiocyanates) have been tested for their ability to inhibit
neoplasia (see Chapter 15~.
The committee believes that there is sufficient epidemiological
evidence to suggest that consumption of certain vegetables, especially
carotene-rich (i.e., dark green and deep yellow) vegetables and cru-
ciferous vegetables (e.g., cabbage, broccoli, cauliflower, and Brussels
sprouts), is associated with a reduction in the incidence of cancer at
several sites in humans. A number of nonnutritive and nutritive com-
pounds that are present in these vegetables also inhibit carcinogenesis
in laboratory animals. Investigators have not yet established which,
if any, of these compounds may be responsible for the protective effect
observed in epidemiological studies.
Alcohol
The effects of alcohol consumption on cancer incidence have been
studied in human populations. In some countries, including the United
States, excessive beer drinking has been associated with an increased
risk of colorectal cancer, especially rectal cancer. This observation
has not been confirmed in other studies. There is limited evidence that
excessive alcohol consumption causes hepatic injury and cirrhosis, which
in turn may lead to the formation of hepatomas (liver cancer). When
consumed in large quantities, alcoholic beverages appear to act syner-
gistically with inhaled cigarette smoke to increase the risk for cancers
of the mouth, larynx, esophagus, and the respiratory tract. The studies
of alcohol consumption and cancer are discussed in Chapter ll.
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12 DIET, NUTRITION, AND CANCER
Naturally Occurring Carcinogens
In addition to nutrients, a variety of nonnutritive substances
(e.g., hydrazines) are natural constituents of foods. Furthermore,
metabolites of molds (e.g., mycotoxins such as the potent carcinogen
aflatoxin) and of bacteria E.g., carcinogenic nitrosamines) may con-
taminate foods. Many of these are occasional contaminants, whereas
others are normal components of relatively common foods. In Chapter
12, the committee examines evidence linking consumption of some of
these substances to carcinogenesis.
The committee concluded that certain naturally occurring contami-
nants in food are carcinogenic in animals and pose a potential risk of
cancer to humans. Noteworthy among these are mycotoxins (especially
aflatoxin) and N-nitroso compounds, for which there is some epidemio-
logical evidence. Studies in animals indicate that a few nonnutritive
constituents of some foods, such as hydrazines in mushrooms, are also
carcinogenic.
The compounds thus far shown to be carcinogenic in animals have
been reported to occur in the average U.S. diet in small amounts; how-
ever, there is no evidence that any of these substances individually
makes a major contribution to the total risk of cancer in the United
States. This lack of sufficient data should not be interpreted as an
indication that these or other compounds subsequently found to be car-
cinogenic do not present a hazard.
Mutagens in Foods
Mutagens are substances that cause heritable changes in the genet-
ic material of cells. If a chemical is mutagenic to bacteria or other
organisms, it is generally regarded as a suspect carcinogen, although
carcinogenicity must be confirmed in long-term tests in whole animals.
As is evident from the discussion in Chapter 13, considerable
attention has recently been directed toward mutagenic activity in
foods. Many vegetables contain mutagenic flavonoids such as quercetin,
kaempferol, and their glycosides. Furthermore, some substances found
in foods can enhance or inhibit the mutagenic activity of other com-
pounds. Mutagens in charred meat and fish are produced during the
pyrolysis of proteins that occurs when foods are cooked at very high
temperatures. Mutagens can also be produced during normal cooking of
meat at lower temperatures. Smoking of foods as well as charcoal
broiling results in the deposition of mutagenic and carcinogenic poly-
nuclear organic compounds such as benzo~a~pyrene on the surface of the
food.
Most mutagens detected in foods have not been adequately tested for
their carcinogenic activity. Thus, the committee believes that it is
not yet possible to assess whether such mutagens are likely to contrib-
ute significantly to the incidence of cancer in the United States.
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Executive Summary 13
Food Additives
In the United States, nearly 3,000 substances are intentionally
added to foods during processing. Another estimated 12,000 chemi-
cals (e.g., vinyl chloride and acrylonitrile, which are used in food-
packaging materials) are classified as indirect (or unintentional)
additives, and are occasionally detected in some foods. Large amounts
of some additives, such as sugar, are consumed by the general popula-
tion, but the annual per capita exposure to most indirect additives
represents only a minute portion of the diet. Although the Food Safety
Provisions and, in many cases, the "Delaney Clause" of the Federal Food,
Drug, and Cosmetic Act prohibit the addition of known carcinogens
to foods, only a small proportion of the substances added to foods
have been tested for carcinogenicity according to protocols that are
considered acceptable by current standards. Moreover, except for the
studies on nonnutritive sweeteners, only a few epidemiological studies
have been conducted to assess the effect of food additives on cancer
incidence.
Chapter 14 contains detailed information on certain additives,
i.e., selected nonnutritive sweeteners, antioxidants, and additives
used in packaging or for promoting the growth of animals used for
food. Particular attention is given to substances to which humans
are widely exposed.
Of the few direct food additives that have been tested and found
to be carcinogenic in animals, all except saccharin have been banned
trom use in the food supply. Only minute residues of a few indirect
additives that are known either to produce cancer in animals (e.g.,
acrylonitrile) or to be carcinogenic in humans (e.g., vinyl chloride
and diethylstilbestrol) are occasionally detected in foods.
The evidence reviewed by the committee does not suggest that the
increasing use of food additives has contributed significantly to the
overall risk of cancer for humans. However, this lack of detectable
effect may be due to their lack of carcinogenicity, to the relatively
recent use of many of these substances, or to the inability of epide-
miological techniques to detect the effects of additives against the
background of common cancers from other causes.
Environmental Contaminants
Very low levels of a large and chemically diverse group of environ-
mental contaminants may be present in a variety of foods. The dietary
levels of some of these substances are monitored by the Market Basket
Surveys conducted by the Food and Drug Administration. Many of them
have been extensively tested for carcinogenicity.
2Sec. 402(a)~2~(C) and Sec. 409(c)~1~(A), respectively.
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14 DIET, NUTRITION, AND CANCER
In Chapter 14, the committee has summarized the evidence concern-
ing exposure of humans to, and the carcinogenicity of, selected pesti-
cides, some industrial chemicals, and other environmental contaminants.
As with food additives, consideration was given primarily to compounds
to which humans are widely exposed.
The results of standard chronic toxicity tests indicate that a num-
ber of environmental contaminants (e.g., some organochlorine pesticides,
polychlorinated biphenyls, and polycyclic aromatic hydrocarbons) cause
cancer in laboratory animals. The committee found no epidemiological
evidence to suggest that these compounds individually make a major con-
tribution to the risk of cancer in humans. However, the possibility
that they may act synergistically and may thereby create a greater car-
cinogenic risk cannot be excluded.
Contribution of Diet to Overall Risk of Cancer
-
By some estimates, as much as 90% of all cancer in humans has
been attributed to various environmental factors, including diet (see
Chapter 18~. Other investigators have estimated that diet is respon-
sible for 30% to 40% of cancers in men and 60% of cancers in women.
Recently, two epidemiologists suggested that a significant proportion
of the deaths from cancer could be prevented by dietary means and that
dietary modifications would have the greatest effect on the incidence
of cancers of the stomach and large bowel and, to a lesser extent, on
cancers of the breast, the endometrium, and the lung.
The evidence reviewed by the committee suggests that cancers of
most major sites are influenced by dietary patterns. However, the
committee concluded that the data are not sufficient to quantitate the
contribution of diet to the overall cancer risk or to determine the
percent reduction in risk that might be achieved by dietary modifica-
tions.
INTERIM DIETARY GUIDELINES
It is not now possible, and may never be possible, to specify a diet
that would protect everyone against all forms of cancer. Nevertheless,
the committee believes that it is possible on the basis of current evi-
dence to formulate interim dietary guidelines that are both consistent
with good nutritional practices and likely to reduce the risk of cancer.
These guidelines are meant to be applied in their entirety to obtain
maximal benefit.
1. There is sufficient evidence that high fat consumption is linked
to increased incidence of certain common cancers (notably breast and
colon cancer) and that low fat intake is associated with a lower inci-
dence of these cancers. The committee recommends that the consumption
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Execahve Summary 15
of both saturated and unsaturated fats be reduced in the average U.S.
diet. An appropriate and practical target is to reduce the intake of
fat from its present level (approximately 40%) to 30% of total calo-
ries in the diet. The scientific data do not provide a strong basis
for establishing fat intake at precisely 30% of total calories. Indeed,
the data could be used to justify an even greater reduction. However,
in the judgment of the committee, the suggested reduction (i.e., one-
quarter of the fat intake) is a moderate and practical target, and is
likely to be beneficial.
2. The committee emphasizes the importance of including fruits,
vegetables, and whole grain cereal products in the daily diet. In
epidemiological studies, frequent consumption of these foods has been
inversely correlated with the incidence of various cancers. Results
of laboratory experiments have supported these findings in tests of
individual nutritive and nonnutritive constituents of fruits (especially
citrus fruits) and vegetables (especially carotene-rich and cruciferous
vegetables).
These recommendations apply only to foods as sources of nutrients--
not to dietary supplements of individual nutrients. The vast litera-
ture examined in this report focuses on the relationship between the
consumption of foods and the incidence of cancer in human populations.
In contrast, there is very little information on the effects of various
levels of individual nutrients on the risk of cancer in humans. There-
fore, the committee is unable to predict the health effects of high and
potentially toxic doses of isolated nutrients consumed in the form of
supplements.
3. In some parts of the world, especially China, Japan, and Ice-
land, populations that frequently consume salt-cured (including salt-
pickled) or smoked foods have a greater incidence of cancers at some
sites, especially the esophagus and the stomach. In addition, some
methods of smoking and pickling foods seem to produce higher levels of
polycyclic aromatic hydrocarbons and N-nitroso compounds. These com-
pounds cause mutations in bacteria and cancer in animals, and are sus-
pected of being carcinogenic in humans. Therefore, the committee recom-
mends that the consumption of food preserved by salt-curing (including
salt-pickling) or smoking be minimized.
4. Certain nonnutritive constituents of foods, whether naturally
occurring or introduced inadvertently (as contaminants) during pro-
duction, processing, and storage, pose a potential risk of cancer to
humans. The committee recommends that efforts continue to be made to
minimize contamination of foods with carcinogens from any source. Where
such contaminants are unavoidable, permissible levels should continue to
be established and the food supply monitored to assure that such levels
are not exceeded. Furthermore, intentional additives (direct and indi-
rect) should continue to be evaluated for carcinogenic activity before
they are approved for use in the food supply.
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16 DIET, NUTRITION, AND CANCER
5. The committee suggests that further efforts be made to identify
mutagens in food and to expedite testing for their carcinogenicity.
Where feasible and prudent, mutagens should be removed or their con-
centration minimized when this can be accomplished without jeopardizing
the nutritive value of foods or introducing other potentially hazard-
ous substances into the diet.
6. Excessive consumption of alcoholic beverages, particularly com-
bined with cigarette smoking, has been associated with an increased risk
of cancer of the upper gastrointestinal and respiratory tracts. Consump-
tion of alcohol is also associated with other adverse health effects.
Thus, the committee recommends that if alcoholic beverages are consumed,
it be done in moderation.
* * *
The committee suggests that agencies involved in education and pub-
lic information should be encouraged to disseminate information on the
relationship between dietary and nutritional factors and the incidence
of cancer, and to publicize the conclusions and interim dietary guide-
lines in this report. It should be made clear that the weight of evi-
dence suggests that what we eat during our lifetime strongly influences
the probability of developing certain kinds of cancer but that it is not
now possible, and may never be possible, to specify a diet that protects
all people against all forms of cancer. The cooperation of the food
industry should be sought to help implement the dietary guidelines de-
scribed above.
Since the current data base is incomplete, future epidemiological
and experimental research is likely to provide new insights into the
relationship between diet and cancer. Therefore, the committee suggests
that the National Cancer Institute establish mechanisms to review these
dietary guidelines at least every 5 years.
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Representative terms from entire chapter:
fat intake
