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The French have a high-fat diet; the Japanese have a low-fat diet. Both have lower caloric intake and longer life expectancies than Americans.
Any time we start thinking about the effect of a change in a diet constituent on health, we should first think about what effect the change has on total caloric intake. A high vegetable intake usually lowers total caloric intake. A high-fat diet usually increases it. This factor is often ignored; yet it is the one factor that significantly increases longevity in rodent models and now in a primate model [Weindruch R. The retardation of aging by caloric restriction: studies in rodents and primates. Toxicol Pathol 1996;24:742–5]. In addition, it dramatically delays onset of chronic diseases.
Dr Weisburger: I agree. In the United States 30 y ago, 1 in 4 of us were obese. Today it is 1 in 3. The lack of exercise contributes to this increase. We need to instruct people more adequately on this topic and to develop foods that seem to be filling but are low in caloric content. Water and tea have no calories, but they can satisfy hunger pangs.
Dr Milner: There certainly is an impact of caloric intake on reducing risk of chronic diseases. I am not convinced, however, that it has a bigger impact than some of the things we have talked about today, such as soybeans or lycopene. In the earlier animal studies, there was about a 40% reduction in caloric intake, a massive reduction, and a 25–40% reduction in cancer incidence.
Dr Weisburger: Yes, we all agree that weight control is part of a healthful diet program. On the other hand, in women, fat cells generate estrogen, which protects them against heart disease. I do not know whether there are data to suggest that obese women have less heart disease.
Dr Arab: No, I don't think so.
Dr Milner: When you plot body mass index against some measure of survival, there is generally a J-shaped curve. At a level beyond 20% greater than desired body weight, risk of coronary heart disease or death increases. So I am not sure that the relation between body weight and the protective effect of estrogen is more important than the relation between body weight and susceptibility to coronary heart disease.
Dr Dwyer: The newer data on Helicobacter pylori and gastric cancers are interesting. Current evidence suggests that gastric cancer may be triggered by chronic infection and inflammation and that H. pylori is a good marker of such processes, even if it is not causative. Nutritional explanations alone now appear too simplistic. Nevertheless, it seems to me there is still a place for the kind of oxidative processes you discussed to contribute to the development of cancer. What are your thoughts as to how those 2 fit together? I think we have to consider interactions of various pathogens with dietary substrates.
Dr Weisburger: Let me respond by discussing a study by Chung [Chung FL, Xu Y. Increased 8-oxodeoxyguanosine levels in lung DNA of A/J mice and F344 rats treated with the tobacco-specific nitrosamine 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone. Carcinogenesis 1992;13:1269–72], who fed a tobacco carcinogen to mice and induced the development of lung tumors. He studied the alkylation of DNA in the lung and found little difference between the carcinogen-derived DNA adducts in tea drinkers and control subjects drinking water. However, when he studied 8-hydroxy-dG in the lung, tea dramatically lowered its formation. When the mice drank tea, they had lower oxidative modification of DNA in parallel with the lower incidence of lung cancer.