Bingham S A
Medical Research Council, Dunn Nutrition Unit, Cambridge, UK.
Proc Nutr Soc. 1999 May;58(2):243-8. doi: 10.1017/s0029665199000336.
Up to 80% of breast, bowel and prostate cancers are attributed to dietary practices, and international comparisons show strong positive associations with meat consumption. Estimates of relative risk obtained from cohort investigations are in the same direction, although generally weak, and red and processed meats rather than white meat seem to be associated with elevated risk of colon cancer. In breast cancer, there are consistent associations with total meat intake and there is evidence of a dose response. Despite these associations with meat, existing studies suggest that vegetarians do not have reduced risk of breast, bowel or prostate cancer, but there are no quantitative estimates of amounts of meat consumed by meat eaters in these cohort studies. Possible mechanisms underlying epidemiological associations include the formation of heterocyclic amines in meat when it is cooked. These heterocyclic amines require acetylation by P450 enzymes, and individuals with the fast-acetylating genotype who eat high amounts of meat may be at increased risk of large-bowel cancer. NH3 and N-nitroso compounds (NOC) formed from residues by bacteria in the large bowel and probably also important. NH3 is a promotor of large-bowel tumours chemically induced by NOC, and some of the chromosomal mutations found in human colo-rectal cancer are consistent with effects of NOC and heterocyclic amines. However, the type, amount, and cooking method of meat or protein associated with increased risk are not certain. The effects of high levels of meat on NH3 and NOC output are not reduced by increasing the amount of fermentable carbohydrate in the diet, but interaction between meat, NSP and vegetable intakes on the risk of cancer has not been studied comprehensively. The interaction between dietary low-penetrance genetic polymorphic and somatic mutation factors has also been investigated to a limited extent. Current Department of Health (1998) recommendations are that meat consumption should not rise, and that consumers at the top end of the distribution should consider a reduction in intakes.
高达80%的乳腺癌、肠癌和前列腺癌都与饮食习惯有关，国际比较显示这些癌症与肉类消费之间存在很强的正相关。队列研究得出的相对风险估计值方向相同，尽管通常较弱，而且红肉和加工肉而非白肉似乎与结肠癌风险升高有关。在乳腺癌方面，总肉类摄入量与之存在持续关联，并有剂量反应的证据。尽管存在这些与肉类的关联，但现有研究表明素食者患乳腺癌、肠癌或前列腺癌的风险并未降低，不过在这些队列研究中没有对肉食者的肉类消费量进行定量估计。流行病学关联背后的可能机制包括肉类烹饪时形成杂环胺。这些杂环胺需要通过P450酶进行乙酰化，食用大量肉类的快速乙酰化基因型个体可能患大肠癌的风险增加。大肠中细菌由残留物形成的NH3和N-亚硝基化合物（NOC）可能也很重要。NH3是NOC化学诱导的大肠肿瘤的促进剂，在人类结直肠癌中发现的一些染色体突变与NOC和杂环胺的作用一致。然而，与风险增加相关的肉类或蛋白质的类型、数量和烹饪方法尚不确定。增加饮食中可发酵碳水化合物的量并不能降低大量肉类对NH3和NOC产出的影响，但肉类、非淀粉多糖和蔬菜摄入量之间对癌症风险的相互作用尚未得到全面研究。饮食低穿透性基因多态性与体细胞突变因素之间的相互作用也仅在有限程度上得到了研究。英国卫生部（1998年）目前的建议是肉类消费量不应增加，处于分布顶端的消费者应考虑减少摄入量。
