Bingham S A
MRC Dunn Clinical Nutrition Centre, Cambridge.
Proc Nutr Soc. 1990 Jul;49(2):153-71. doi: 10.1079/pns19900021.
The cause of human colo-rectal cancer is unknown, although international and racial comparisons suggest that diet may be important. Within populations, risk of cancer is also affected by genetic factors which remain to be elucidated. Dietary fibre and NSP consumption is not always high in populations at low risk of colo-rectal cancer, but rates are fast increasing with westernization (and meat and fat consumption) in Japan. The suggestion that dietary fibre is protective in colo-rectal cancer is based on the fact that cereal fibre from bran increases faecal weight, dilutes large intestinal contents, and speeds up transit time. In animal models, bran reduces the number of tumours induced by chemical carcinogens, and cellulose may have a similar effect. The faeces of some individuals contain mutagens, some of which have been identified as fecapentaenes and heterocyclic amines. Bran reduces faecal mutagenicity, although the mutagen concerned is unknown. Most dietary fibre is fermented in the large gut by anaerobic bacteria and little remains in faecal matter. Recent observations have shown that substantial amounts of starch survive digestion in the small bowel and are available also for fermentation in the large gut. The metabolic consequences of fermentation may be important in carcinogenesis via altered N metabolism, SCFA production, and pH reduction. Methane is also produced in some individuals, but, contrary to previous findings, is not a risk factor for large bowel cancer. Starch appears to be beneficial as a substrate for fermentation because yields of the SCFA butyrate are increased both in vitro and in vivo. Butyrate is an energy substrate for the colonic mucosa and an anti-proliferative and differentiating agent in cell culture lines. Possible mechanisms whereby starch and NSP may protect against colo-rectal cancer, therefore, exist. The majority of individual case-control epidemiological studies suggest that fibre-containing foods are protective in colo-rectal cancer, although this effect is largely due to vegetable, rather than cereal, consumption. Case-control studies of diet and large bowel cancer may, however, reflect the effect rather than the cause of the disease, so that confirmation of the possible protective effects of starch and NSP is needed from accurate prospective studies both of diet and associated risk factors.
人类结直肠癌的病因尚不清楚,不过国际比较和种族比较表明饮食可能起到重要作用。在人群中,癌症风险还受遗传因素影响,而这些因素仍有待阐明。在结直肠癌低风险人群中,膳食纤维和非淀粉多糖的摄入量并非总是很高,但在日本,随着西方化进程(以及肉类和脂肪消费量的增加),这一比例正在迅速上升。膳食纤维对结直肠癌有保护作用这一观点基于以下事实:麸皮中的谷物纤维可增加粪便重量,稀释大肠内容物,并加快转运时间。在动物模型中,麸皮可减少化学致癌物诱发的肿瘤数量,纤维素可能也有类似作用。一些人的粪便中含有诱变剂,其中一些已被鉴定为粪戊烯和杂环胺。麸皮可降低粪便的诱变性,不过相关诱变剂尚不清楚。大多数膳食纤维在大肠中由厌氧菌发酵,很少残留在粪便中。最近的观察结果表明,大量淀粉在小肠消化后留存下来,也可在大肠中发酵。发酵的代谢后果可能通过改变氮代谢、短链脂肪酸生成和降低pH值,在致癌过程中发挥重要作用。一些人还会产生甲烷,但与之前的研究结果相反,甲烷并非大肠癌的风险因素。淀粉似乎作为发酵底物有益,因为体外和体内实验中短链脂肪酸丁酸盐的产量均有所增加。丁酸盐是结肠黏膜的能量底物,在细胞系中具有抗增殖和分化作用。因此,淀粉和非淀粉多糖可能预防结直肠癌的机制是存在的。大多数个体病例对照流行病学研究表明,含纤维食物对结直肠癌有保护作用,不过这种作用很大程度上归因于蔬菜而非谷物的摄入。然而,饮食与大肠癌的病例对照研究可能反映的是疾病的影响而非病因,因此需要通过准确的饮食及相关风险因素前瞻性研究来证实淀粉和非淀粉多糖可能的保护作用。