Weisburger J H
American Health Foundation, Valhalla, NY 10595, USA.
J Am Diet Assoc. 1997 Jul;97(7 Suppl):S16-23. doi: 10.1016/s0002-8223(97)00725-6.
The primary nutritionally linked diseases are coronary heart disease, stroke and cancers of the stomach, colon, pancreas, prostate, breast, ovary, and endometrium. Dietary fats operate through a promoting mechanism. An S-shaped dose-response curve with a threshold has been demonstrated in models of breast and colon cancer in which the standard Western fat intake of 40% of energy yields a high level of promotion, and reduction of fat to 10% to 20% of energy (the traditional Japanese fat intake) has a low promoting action. In models of breast and colon cancer, saturated fats such as beef fat or lard, and monounsaturated oils, such as olive oil, display only a weak promoting effect, with the incidence of induced tumors being similar at intake levels of 40% and 10% of energy. On the other hand, the n-6-polyunsaturated oils display a strong promoting effect. Such findings may have a parallel in the low but definitely increasing slope of postmenopausal breast cancer incidence in the past 30 years as the American public decreased saturated fat intake to avoid heart disease and increased use of the n-6-polyunsaturated oils. Mechanisms underlying the cancer-promoting effect in the colon stem from increased hepatic production of bile acids, which are transferred to the intestinal tract via the bile. Ingestion of 40% fat calories yields higher concentrations of bile acids in the colon than lower levels of dietary fat ingestion. Cancer in the mammary gland is promoted through higher concentrations of fats and phospholipids in the gland as well as increased levels of estrogen secondary to production by the ovary and other endocrine tissues that, in turn, affect the generation of pituitary hormones such as prolactin and growth hormone. The n-3-fats, as found in fish and fish oils, have a pronounced inhibitory effect in models of colon and breast cancer, presumably through their shifting of prostaglandin metabolism to the generation of prostaglandins, which lower cell proliferation potential and, thus, decrease promotional effects. The role of dietary fat as a promoter can be modified by other nutritional components. Finally, one of the best pieces of evidence for an enhancing effect of many dietary fats in the nutritionally linked cancers is the current increase in the incidence of these diseases in Japan as the nutritional habits of people in that country become more Westernized.
主要的营养相关疾病包括冠心病、中风以及胃癌、结肠癌、胰腺癌、前列腺癌、乳腺癌、卵巢癌和子宫内膜癌。膳食脂肪通过促进机制发挥作用。在乳腺癌和结肠癌模型中已证实存在一条有阈值的S形剂量反应曲线，其中标准的西方脂肪摄入量（占能量的40%）会产生高水平的促进作用，而将脂肪摄入量降至能量的10%至20%（传统日本脂肪摄入量）则具有低促进作用。在乳腺癌和结肠癌模型中，牛肉脂肪或猪油等饱和脂肪以及橄榄油等单不饱和油仅显示出微弱的促进作用，在能量摄入量为40%和10%时诱导肿瘤的发生率相似。另一方面，n-6多不饱和油显示出强烈的促进作用。过去30年中，随着美国公众减少饱和脂肪摄入量以预防心脏病并增加n-6多不饱和油的使用，绝经后乳腺癌发病率呈现出低但明显上升的趋势，这些发现可能与此类似。结肠中促进癌症发生的机制源于肝脏胆汁酸生成增加，胆汁酸通过胆汁转移到肠道。摄入40%的脂肪热量时结肠中胆汁酸的浓度高于较低水平的膳食脂肪摄入。乳腺中的癌症是通过腺体中较高浓度的脂肪和磷脂以及卵巢和其他内分泌组织产生的雌激素水平升高来促进的，而雌激素水平升高又会反过来影响催乳素和生长激素等垂体激素的生成。鱼类和鱼油中含有的n-3脂肪在结肠癌和乳腺癌模型中具有显著的抑制作用，推测是通过将前列腺素代谢转向生成前列腺素来实现的，前列腺素可降低细胞增殖潜能，从而减少促进作用。膳食脂肪作为促进剂的作用可被其他营养成分改变。最后，许多膳食脂肪在营养相关癌症中具有增强作用的最佳证据之一是，随着日本民众的营养习惯变得更加西化，该国这些疾病的发病率目前正在上升。
