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4 TotalCaloncIntake
This chapter reviews the many experiments in which the variable
studied is the total amount of food humans or animals eat, rather than
the precise composition of their diet. It is entitled Total Caloric
Intake, although it is difficult to determine whether the effects
brought about by changing the quantity of a diet are due to the result-
ing changes in caloric intake or to the changed distribution of specific
nutrients.
A number of factors complicate the interpretation of the effect of
caloric intake on cancer incidence. Caloric density can be modified
either by modifying the ratio of fat (9.5 kcal/g) to carbohydrate (4.0
kcal/g) or by varying the concentration of nonnutritive bulk (fiber).
Since dietary fat and fiber may also affect carcinogenesis, it becomes
difficult to measure any independent effect of calories.
It is also not possible to identify the effect of caloric intake on
cancer incidence in studies of humans. Although total caloric intake by
two populations can be compared, the interpretation of the data is lim-
ited by the same considerations that apply to experiments in animals. It
is also difficult to interpret studies in which the prevalence of obesity
is compared with cancer incidence. Obesity is related to the balance
between caloric intake and caloric expenditure. However, the proportion-
al contributions of caloric intake and caloric expenditure to cancer risk
are not known. Furthermore, there is evidence that obesity is related to
the consumption of diets with increased caloric density. Thus, the contri-
butions of fat, fiber, and carbohydrate cannot be readily measured inde-
pendently.
EPIDEMIOLOGICAL EVIDENCE
There are few epidemiological data relating total caloric intake to
cancer risk, partly because most dietary studies have been based on
preselected food lists, which do not permit the quantification of total
dietary intake.
Berg (1975) pointed out that the international distribution of hor-
mone-dependent cancers has generated suspicion that these cancers may
be related to affluence. He suggested that diets typical of affluent
populations, when ingested since childhood, could overstimulate the en-
docrine system, lead to aberrations in metabolic processes, and result
in cancer.
66
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Total Caloric Intake 67
Gregor et al. (1969) analyzed data on caloric intake and the inci-
dence of gastric and intestinal cancers. They concluded that as the per
capita food intake (or gross national product) increases, the mortality
rates for gastric cancers fall and those for intestinal cancer rise.
Hill _ al. (1979), who studied mortality from colorectal cancer in three
socioeconomic groups in Hong Kong, found that the most affluent group had
more than twice the mortality of the poorest group, i.e., 26.7/100,000
vs. 11.7/100,000. The relative proportions of nutrients in their diets
were similar, but estimated daily caloric intake was 2,700 in the lowest
socioeconomic group and 3,900 in the highest.
In a correlation study conducted by Armstrong and Doll (1975), per
capita total caloric intake was examined in relation to cancer incidence
in 23 countries and to cancer mortality in 32 countries. Significant
correlation coefficients (r >0.70) were found for total calories and
rectal cancer incidence in males, leukemia in males, and mortality from
breast cancer in females. Notably, the per capita intake of calories was
highly correlated with intakes of total fat, total protein, and animal
protein. The finding for breast cancer was reproduced by Gaskill et al.
(1979), who analyzed data on mortality from breast cancer in relation to
per capita intake for foods by state within the United States. However,
there was no correlation when they controlled for age at first marriage
(to reflect age at first pregnancy) in the analysis.
In two case-control studies, a number of dietary variables, including
total caloric and fat intake, were estimated for subjects with cancer of
the breast (Miller _ al., 1978), for subjects with cancer of the colon
and rectum (Jain et al., 1980), and for matched controls. For breast
cancer cases, Miller and colleagues found no association with caloric
intake and a weak association with total dietary fat. Jain and coworkers
reported direct associations with caloric intake for both colon and rec-
tal cancer, but the associations were not as strong as they were for in-
take of saturated fat. The authors concluded that the relevant variable
in each study was more likely to be dietary fat than caloric intake.
Independent associations of breast cancer with body weight and height
were found by de Waard and Baanders-van Halewijn (1974) in a cohort study
of postmenopausal women in the Netherlands. Also, differentials in
weight between cases of breast cancer and controls were found in Taiwan
(tin _ al., 1971) and in Sao Paula, Brazil (Mirra et al., 1971~. Thus,
de Waard (1975) suggested that susceptibility to breast cancer could be
related to body mass (which, in turn, could be related to nutrition), but
this hypothesis has not been accepted universally (MacMahon, 1975~. Sub-
sequently, de Waard et al. (1977) examined the influence of height and
weight on age-specif~c incidence of breast cancer in the Netherlands and
Japan and computed age-specific incidence curves for different height and
weight groups. The heavier and taller postmenopausal women had the high-
est incidence of breast cancer. However, there appeared to be little
independent effect of weight if there was an adjustment for its correla-
tion with height. In his earlier study, de Waard (1975) suggested that
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68 DIET, NUTRITION, AND CANCER
lean body mass may be the important variable. However, if height is
critical (and it is critical to the calculation of lean body mass),
nutritional factors, if relevant, must begin to operate during adoles-
cence or earlier, as was pointed out by MacMahon (1975~. De Waard et al.
(1977) suggested that approximately one-half of the differences in inci-
dence of breast cancer between Holland and Japan can be attributed to
differences in body weight and height.
In an analysis based on a long-term prospective study conducted by
the American Cancer Society from 1959 to 1972, Lew and Garfinkel (1979)
examined the relationship between mortality from cancer and other
diseases and variation in weight among 750,000 men and women selected
from the general population. Cancer mortality was significantly elevated
in both sexes only among those 40% or more overweight. For men, most of
the excess mortality resulted from cancer of the colon and rectum; for
women, cancer of the gallbladder and biliary passages, breast, cer-
vix, endometrium, and ovary were the major sites. It was not possible
to evaluate the relative importance of overweight in comparison to total
caloric intake or intake of other nutrients. Therefore, it cannot be
assumed that obesity as such is the major risk factor. Nonetheless, most
studies confirm a relationship between obesity and caloric intake, and in
the absence of definitive information from studies that have separated
the effects of caloric intake and fat intake, e.g., Miller et al. (1978)
and Jain et al. (1980) (discussed above), it is reasonable to assume that
high total caloric intake is a risk factor for some sites identified in
other studies.
EXPERIMENTS IN ANIMALS
Tannenbaum (1942a,b, 1944, 1945a,b) examined the effects of caloric
restriction upon the development of spontaneous and chemically induced
tumors in several strains of mice. Growth of benzota~pyrene-induced
tumors was inhibited by caloric restriction to different extents in ABC,
Swiss, or DBA mice (Tannenbaum, 1942a). The level of dietary fat
affected growth of skin tumors or spontaneous and chemically induced
breast tumors, but not of sarcomas or lung tumors (Tannenbaum, 1942b).
Caloric intake was restricted by controlling the amount of starch added
to a diet containing commercial ration and skim milk powder. Mice whose
daily dietary intake was 11.7 calories exhibited 25% more spontaneous
mammary tumors than mice whose intake was 9.6 calories (Tannenbaum,
1945a). The incidence of benzpyrene-induced tumors was similar in mice
ingesting 11.7 and 9.6 calories per day, but when caloric intake dropped
to 8.1 calories daily, tumor incidence fell by 38% (Tannenbaum, 1945a).
Among mice ingesting 11.7 calories daily, those receiving 18% of the
calories from fat developed 70% more spontaneous mammary tumors than
those whose diets contained only 2% (approximately 4% of calories) fat.
Tannenbaum concluded that dietary fat exerted a specific influence over
and above its caloric contribution (Tannenbaum, 1945b).
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Total Caloric Intake 69
The influence of caloric restriction was also tested in a study of
3-methylcholanthrene-induced skin tumors in mice fed ad libitum and in a
control group on a restricted diet. The carcinogen was painted on the
skin for 10 weeks, and the mice were then observed for 1 year. On the
basis of this experiment and earlier studies, Tannenbaum (1944, 1945b)
concluded that the carcinogen-induced changes occur regardless of diet,
but that the ad libitum ingestion of diet promotes tumor development.
Lavik and Baumann (1943) studied the promoting action of different
levels of dietary fat on 3-methylcholanthrene-induced skin tumors in
mice. A low fat, low calorie diet resulted in the fewest tumors. Lard
with high (saturated) and low (unsaturated) melting points produced
similar results, and the addition of riboflavin to the diet had a slight
promoting effect; but the principal effect on carcinogenesis was produced
by high caloric intake.
The studies of Tannenbaum and those by Lavik and Baumann could be
profitably extended since we have identified a variety of possible car-
cinogens and promoters and have gained a greater understanding of food
composition in recent decades.
SUMMARY AND CONCLUSIONS
Epidemiological Evidence
The epidemiological evidence supporting total caloric intake as a
risk factor for cancer is slight and largely indirect. Much of it is
based on associations between body weight or obesity and cancer. Studies
that have evaluated both caloric and fat intake suggest that fat intake
is the more relevant variable.
Experimental Evidence
Studies in animals to examine the effect of caloric intake on car-
cinogenesis have been few and are difficult to interpret. In these
experiments, animals on restricted diets developed fewer tumors and their
lifespan far exceeded that of animals fed ad libitum, thereby indicating
a decrease in the age-specific incidence of tumors. However, because the
intake of all nutrients was simultaneously depressed in these studies,
the observed reduction in tumor incidence or delayed onset of tumors
might have been due to the reduction of other nutrients 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 them-
selves exert effects on tumorigenesis.
Thus, neither the epidemiological nor the experimental studies
permit a clear interpretation of the specific effect of caloric intake
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7@ DIET' NUTRITION' AND CANCER
on the risk of cancer. Nonetbeless, the studies conducted in animals
show that a reduction in total food intake decreases the age-specific
incidence of cancer" The evidence for humans is less clear.
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Total Caloric Intake 71
REFERENCES
Armstrong, B., and R. Doll. 1975. Environmental factors and cancer
incidence and mortality in different countries, with special
reference to dietary practices. Int. J. Cancer 15: 617-631.
Berg, J. W. 197 5. Can nutrition explain the pattern of international
epidemiology of hormone-dependent cancers? Cancer Res.
35: 3345-3350.
de Waard, F. 1975. Breast cancer incidence and nutritional status with
particular reference to body weight and height. Cancer Res.
35: 3351-3356.
de Waard, F., and E. A. Baanders-van Halewijn. 1974. A prospective
study in general practice on breast-cancer risk in postmenopausal
women. Int. J. Cancer 14 :153-160.
de Waard, F., J. P. Cornelis, K. Aoki, and M. Yoshida. 1977. Breast
cancer incidence according to weight and height in two cities of
the Netherlands and in Aichi prefecture, Japan. Cancer
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Gaskill, S. P., W. L. McGuire, C. K. Osborne, and M. P. Stern. 1979.
Breast cancer mortality and diet in the United States. Cancer
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Gregor, O., R. Roman, and F. Prusova. 1969. Gastrointestinal cancer
and nutrition. Gut 10:1031-1034.
Hill, M., R. MacLennan, and K. Newcombe. 1979. Letter to the Editor:
Diet and large-bowel cancer in three socioeconomic groups in Hong
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Lavik, P. S., and C. A. Baumann. 1943. Further studies on the tumor-
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, E. A., and L. Garfinkel. 1979. Variations in mortality by weight
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72 DIET, NUTRITION, AND CANCER
MaclIahon, B. 1975. Formal discussion of Breast cancer incidence and
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Miller, A. B., A. Kelly, N. W. Choi, V. Matthews, R. W. Morgan,
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Tannenbaum, A. 1942b. The genesis and growth of tumors. III. Effects
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Tannenbaum A. 1944. The dependence of the genesis of induced skin
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Tannenbaum, A. 1945a. The dependence of tumor formation on the
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Representative terms from entire chapter:
breast cancer
