Food Lipids: Chemistry, Nutrition, and Biotechnology

studies contains equal amounts (40–45%) of the c9,t11, and t10,c12 modifications.
CLA has been shown to inhibit atherogenesis in cholesterol-fed rabbits [89] and
hamsters [90]. Of greater interest is the observation that feeding 1% CLA to rabbits
with preestablished atherosclerosis leads to significant regression [91] of lesions.
III. LIPIDS AND CANCER
In 1930 Watson and Mellanby [92] showed that the incidence of coal tar–induced
skin tumors in mice rose from 34% to 57% when 12.5–25.0% butter was added to
the basal diet that normally contained 3% fat. Baumann et al. found that high-fat
diets increased the yield of ultraviolet radiation–induced or chemically induced skin
tumors in mice [93]. They also found saturated fats to be less cocarcinogenic than
unsaturated fats [94]. Carroll and Khor [95] made a similar observation. The reason
that unsaturated fat enhanced carcinogenesis was found by Ip et al. [96] to be due
to the tumor’s requirement for linoleic acid as a growth factor. This finding may
explain why rats fed fish oils [97] or fats high in trans unsaturated [98,99] fatty acids
also show a reduced incidence of tumors.
Armstrong and Doll [100] published a thorough review correlating cancer incidence
in over 30 countries with diet, gross national product (GNP), physician
density, population density, and use of solid or liquid fuel. They found positive
associations between breast and colorectal cancers and total fat consumption. They
also found a strong association between these cancers and GNP. In their conclusion
they state, ‘‘It is clear that these and other correlations should be taken only as
suggestions for further research and not as evidence of causation or as bases for
preventive action.’’ Several studies carried out in the 1970s found correlations between
fat intake and risk of breast cancer [101,102]. The association between dietary
fat and risk of breast cancer appears to be weakening [103]. Goodwin and Boyd
[104] reviewed a large number of studies and found that 7 of 13 international comparisons
found a correlation between fat intake and breast cancer risk but only 1 of
14 case-control studies did. Hirohata et al. found no association between dietary fat
intake and breast cancer in Japan [105] or Hawaii [106]. The NHANES I reported
on 99 cases of breast cancer, as opposed to 5386 noncases, and found no differences
in fat or fatty acid intake [107]. Willett et al. [108] studied a cohort of more than
89,000 American women whose fat intake ranged from 32% to 44% of calories and
found a slight decrease in relative risk with increasing fat intake.
As in the case of breast cancer, local (case-control) studies of fat intake and
colon cancer risk show minimal correlations with fat intake [109–111] whereas international
studies find strong correlation [100,112]. Rogers and Longnecker [113]
reviewed diet and cancer and in a summary of 24 cases of colon cancer found a
small, but inconsistent, association between fat intake and risk of colon cancer.
Stocks and Karn [114] in an early (1933) study of colon cancer and diet in England
found dairy foods to be negatively correlated with risk. Jensen et al. [115] in studying
colon cancer and diet in Finland and Denmark found saturated fat to be inversely
correlated with risk. Stemmermann et al. [116] made a similar observation in Hawaii.
Others [117,118] reported that risk increased with increasing intake of saturated fat.
Tuyns et al. [119] in a Belgian study suggested that the dietary factor leading to
increased risk was oligosaccharides and not fat. It should be evident from the fore-
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