The 1978-1979 mortality rates for cancers of the breast, prostate, ovary, and colon in 26 to 30 countries were related to the average 1979-1981 food availability data published by the United Nations. The previously described relationship between breast cancer mortality rates and animal fat consumption continues to be evident, and applies also to the other three tumor types. The correlation with breast cancer was particularly strong in postmenopausal women. Since 1964, particularly notable increases in both breast cancer mortality rate and dietary fat intake have occurred in those countries with a relatively low breast cancer risk. The international comparisons support evidence from animal experiments that diets in which olive oil is a major source of fat are associated with reduced breast cancer risk. The excess in mortality rates for breast and ovarian cancer in Israel relative to the national animal fat consumption may be due to the mixed ethnic origin of the Israeli population. Positive correlations between foods and cancer mortality rates were particularly strong in the case of meats and milk for breast cancer, milk for prostate and ovarian cancer, and meats for colon cancer. All four tumor types showed a negative correlation with cereal intake, which was particularly strong in the case of prostate and ovarian cancer. Although, in general, there was a good positive correlation between prostate and breast cancer mortality rates and between prostate cancer and animal fat, discrepancies in national ranking indicate the operation of other etiologic factors that modify risk. The observed positive correlations between the four cancer mortality rates and caloric intake from animal sources, but negative correlations for vegetable-derived calories, suggest that, of the two, animal fat and not energy is the major dietary influence on cancer risk.

International comparisons of mortality rates for cancer of the breast, ovary, prostate, and colon, and per capita food consumption

Of the known carcinogenic agents (viruses, ultraviolet and ionizing radiations, and chemicals), chemicals appear to be of major importance in the induction of human cancers. The known chemical carcinogens include a wide range of structures. Their common feature is that their ultimate forms are electrophilic reactants; in most cases, these reactants arise through metabolism in vivo. Carcinogenesis by chemicals is a multistage process. The first stage, initiation, occurs rapidly and appears to be irreversible. The available data indicate that initiation generally results from one or more mutations of cellular DNA. Covalent reactions of electrophilic derivatives of carcinogens with DNA are the major cause of these mutations. The second stage, promotion, occurs over a longer period of time. Promotion is a complex process, for which the early stages are largely reversible. The critical events appear to be epigenetic. Complete carcinogens have both initiating and promoting activities, but the ratios of these two activities for various chemicals may differ greatly. This knowledge of the mechanisms of carcinogens by chemicals provides a useful basis for approaches to the prevention of human cancer.

Mechanisms of chemical carcinogenesis.

Multi-targeted therapy of cancer by omega-3 fatty acids.

14 – Mammalian Lignans and Phyto-oestrogens Recent Studies on their Formation, Metabolism and Biological Role in Health and Disease

In their first reports on smoking and disease both the Royal College Of Physicians Of London (1962) and the US Surgeon General Of The Public Health Service (1964) concluded that cigarette smoking is causally related to lung cancer in humans and is associated with cancer of the oral cavity, larynx and urinary bladder. These conclusions were based on epidemiological data and were supported by laboratory studies. Today, 25 years later and after extensive research, epidemiological reports from more than 20 countries have led the US Surgeon General (1986 a) and the International Agency For Research On Cancer (1986) to the conclusion that smoking of cigarettes is causally related to cancer of the respiratory tract, the upper digestive tract, pancreas, renal pelvis and bladder and that cigarette smokers also face an increased risk for cancer of the cervix. Cigar and pipe smoking are also causally related to cancer of the respiratory tract, oral cavity and esophagus, although, in the case of lung cancer, not to the same extent as cigarette smoking (US Surgeon General 1986 a; IARC 1986). In addition to active smoking, involuntary smoking, i. e., the exposure to environmental tobacco smoke, has been incriminated as a risk factor for cancer of the lung in nonsmokers (IARC 1986; US National Research Council 1986; US Surgeon General 1986 a). Furthermore, chewing of tobacco and especially the oral use of snuff were found to be associated with cancer of the oral cavity (IARC 1985 a; US Surgeon General 1986 b) and possibly with cancer of the nasal cavity, kidney and bladder (Brinton et al. 1984; US Surgeon General 1986 a; Kabat et al. 1986; Goodman et al. 1986).

Advances in Tobacco Carcinogenesis

Publisher Summary Nutrition is related to the development of cancer in three ways: (1) food additives or contaminants may act as carcinogens, cocarcinogens, or both; (2) nutrient deficiencies may lead to biochemical alterations that promote neoplastic processes; and (3) changes in the intake of selected macronutrients may produce metabolic and biochemical abnormalities, either directly or indirectly, which increase the risk for cancer. Specific carcinogens play a minor role as initiators in the relationship between nutrition and the development of cancer. This chapter covers six types of cancer: large bowel cancer, colon carcinogenesis, stomach cancer, cancer of the upper alimentary and respiratory tract, cancer of the pancreas, and breast cancer. In four of these—breast, large bowel, stomach, and head and neck—the epidemiologic evidence is overwhelming that nutritional factors have a major etiological role. Dietary factors are also implicated in the etiologies of the two remaining types of cancer—pancreas and prostate—but the epidemiologic evidence is not overwhelming. The chapter also presents an evaluation of the status of the relationship between nutrition and cancer in man, discusses the use of animal models to determine if the etiological factors established for man can be modified in an experimental setting, and makes recommendations for additional research and possible preventive measures.

Nutrition and its relationship to cancer

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Nutrition and its relationship to cancer