Nutrition in Clinical Practice Ebook
Chapter 12
Diet and Cancer
The link between diet and cancer, supported by in vitro, animal, and epidemiologic studies, is convincing. Decisive intervention trials are for the most part lacking, however, because of the protracted time course of carcinogenesis and a lack of reliable surrogate markers in most cases. An exception is studies in populations with well-defined nutrient deficiencies that increase the risk of specific cancers, where supplementation may dramatically reduce risk; the Linxian study in rural China is noteworthy (1,2). Most reviews of diet and cancer cite the work of Doll and Peto (3) and suggest that one-third or more of all cancer is related to nutritional factors and potentially preventable by nutritional means. Dietary factors may influence cancer initiation, promotion, and progression via direct effects on DNA, indirect effects on immune function (see Chapter 11), and overall vitality (see Chapter 45).
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Diet and Cancer
The link between diet and cancer, supported by in vitro, animal, and epidemiologic studies, is convincing. Decisive intervention trials are for the most part lacking, however, because of the protracted time course of carcinogenesis and a lack of reliable surrogate markers in most cases. An exception is studies in populations with well-defined nutrient deficiencies that increase the risk of specific cancers, where supplementation may dramatically reduce risk; the Linxian study in rural China is noteworthy (1,2). Most reviews of diet and cancer cite the work of Doll and Peto (3) and suggest that one-third or more of all cancer is related to nutritional factors and potentially preventable by nutritional means. Dietary factors may influence cancer initiation, promotion, and progression via direct effects on DNA, indirect effects on immune function (see Chapter 11), and overall vitality (see Chapter 45).
As is the case for atherogenesis, the process of carcinogenesis may be affected
both favorably and unfavorably by micronutrients and macronutrients. Initiation
is fostered by mutagenic exposures, including nutrient compounds, and
forestalled by immunosurveillance, the robustness of which is influenced by
dietary pattern. Cancer promotion and progression appear to be more meaningfully
associated with macronutrient intake and overall health than specific nutrient
compounds, although the aggregate influence of certain nutrient groups, such as
antioxidants and essential fatty acids may be considerable. Procarcinogens in
the diet include heterocyclic amines and polycyclic aromatic hydrocarbons that
result from pyrolysis (i.e., charring); acrylamide formed when starchy foods are
cooked at high temperature (4); nitrosamines used or
produced in the curing of meats; naturally occurring contaminants, such as
aflatoxin B-1; naturally occurring chemicals in plants; and chemicals added to
the food supply as a result of agricultural practices and food handling. While
all of potential importance, the net effect of carcinogenic compounds in foods is generally thought to be small relative to the effects of
dietary pattern on general health, and its profound influence on cancer risk.
This contention is highlighted by the presence of naturally occurring mutagens
in many plant foods, yet a consistent and strong inverse association between the
consumption of such foods and cancer risk. Also germane is the issue of chemical
contamination of food; there is widespread concern that pesticide residues on
produce, for example, may at times be carcinogenic (5). If
so, voluminous data largely from observational trials suggest that the benefits
of a generally nutritious diet clearly outweigh any harmful effects of such residues on otherwise healthful foods. Nonetheless, a potential
benefit from choosing organic alternatives—particularly in certain food groups
(6)—is worthy of both consideration and study.
