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take — within some range — that pro- 
duces the most beneficial nutritional 
results while minimizing the risk of 
cancer. One emerging concept is that 
those levels that optimize such tra- 
ditional nutritional effects as healthy 
growth are the same levels that mini- 
mize cancer risk. We now know that 
inappropriately low intakes of some 
nutrients may cause an enhancement 
of the cancer process, whereas with 
other nutrients inappropriately high 
intakes may create the same result. 
It should be possible to take in nu- 
trients within an optimum range by 
selecting a wide variety of readily 
available foods without resort to com- 
pensatory gimmicks. This concept, al- 
though straightforward, is too often 
ignored. There have been claims, for 
example, that unusually high nutrient 
intakes of selenium and vitamin C are 
useful in reducing the risk of cancer 
when, in fact, the experimental ob- 
servations on which the claims are 
based were made on much lower levels 
of intake. More is not necessarily bet- 
ter. (Incidentally, it is important to 
understand what constitutes an unusu- 
ally high nutrient intake, or megadose. 
For some nutrients, including sele- 
nium, vitamin A, vitamin D, protein, 
and linoleic acid [a polyunsaturated 
fatty acid], an excessive intake may 
be only a few multiples of the rec- 
ommended daily allowance, or RDA, 
established by the Food and Nutrition 
Board of the U.S. National Academy 
of Sciences. In the case of other nu- 
trients, including some of the water- 
soluble vitamins such as all the B vi- 
tamins, the difference between the 
RDA and a potentially toxic dose may 
be quite large.) 
Because nutrients, unlike nonnutri- 
ent chemicals, do not act as cancer 
initiators, we deduce that inappropri- 
ate nutrient intakes can modify the 
carcinogenic process without initiating 
it. There are numerous mechanisms 
that appear to account for these nu- 
trient modifications; in fact, each nu- 
trient affecting the carcinogenic proc- 
ess possesses its own set of unique 
characteristics. Surprisingly, this va- 
riety of mechanisms does not neces- 
sarily present a hopeless morass in 
terms of practical information; quite 
the contrary may be true. The emerg- 
ing evidence suggests that a few well- 
chosen dietary practices may serve to 
simultaneously correct a variety of nu- 
trient imbalances associated with an 
increased cancer risk. Before discuss- 
ing such food choices, let us consider 
a few recently reported examples of 
nutrient effects that illustrate this con- 
cept. 
The nutrient, other than dietary fi- 
ber, currently receiving the most at- 
tention is fat, which has been inves- 
tigated both in terms of the total 
amount and the type of fat ingested. 
In the United States, about 40 to 45 
percent of our total caloric intake is 
supplied by fat. (That compares with 
10 to 15 percent for the typical Asian 
diet.) Several epidemiological studies 
suggest positive relationships between 
the total intake of fat and cancer of 
the large bowel, breast, pancreas, and 
prostate gland. The early literature 
on these relationships tended to infer 
that the higher the total fat intake, 
the higher the incidence of cancer, 
with the data for cancer of the large 
bowel and breast being more compre- 
hensive than the data for pancreatic 
and prostatic cancer. 
More recently, there have been sev- 
eral findings that may permit a finer 
tuning of that generalization. First, 
the type of fat appears to be impor- 
tant. Although earlier human popu- 
lation studies indicated a more sig- 
nificant carcinogenic risk with sat- 
urated fat (derived largely from ani- 
mal sources) than for unsaturated fat 
(from plant sources), later animal 
model studies did not support this con- 
tention. There is now increasing evi- 
dence for enhancement of the carcino- 
genic process by the ingestion of 
linoleic acid, the only fatty acid that 
is essential in the human diet. Linoleic 
acid is present in large amounts in 
vegetable oils, such as corn oil and 
safflower oil, where it makes up one- 
half to three-fourths of the total fatty 
acids. In addition, animal studies sug- 
gest that increasing the intake of lin- 
oleic acid increases tumor yield only 
when there is already a sufficiently 
high level of total fat. In rats, as with 
human infants, the requirement for 
linoleic acid appears to be easily met 
when that chemical makes up about 
0.5 to 1.0 percent of the diet. In the 
rat studies, where an experimental car- 
cinogenic initiator was given, a diet 
containing 2.5 percent linoleic acid 
increased mammary tumor yield only 
when the total fat content was also 
high, for example, when fat content 
represented 12 to 15 percent of the 
diet by weight, or 25 to 30 percent 
of the total calories. These effects of 
linoleic acid and total fat are primarily 
exerted during the second, or modi- 
fication, phase of carcinogenesis; that 
14 
