CALCIUM AND COLORECTAL EPITHELIAL CELL PROLIFERATION

有希望，但尚未决定性的证据已经积累， 表明膳食中钙含量足够，可能是一种保护性 对大肠癌的因素-特别是对于那些消费典型的 高脂肪的西式饮食。现在也有证据支持结肠 上皮细胞增殖，如氚化胸苷[3 H]dTh - 将细胞标记为生物标志物或潜在的前驱病变， 结肠息肉和结肠癌。这些细胞可以通过 通过简单非准备直肠活检进行的研究反映了肿瘤形成的风险， 发生在结肠上方此外，现在也有证据表明， 结肠粘膜的过度增殖可以通过 钙补充剂的管理和结肠癌的风险 从而减少。迄今为止，有三项关于钙的影响的非对照试验， 对人类结肠上皮细胞增殖的影响。所有 其中三项已显示大幅减少。然而，迄今为止， 已经报道了对照试验或使用不同剂量的试验。 此外，没有连续或长期随访的效果 钙对结肠上皮细胞增殖的影响，以确定 是否能迅速地获得全部益处，或者是否适应性过程 可能会发生这种情况，随着时间的推移，这种影响会减弱。另外，在这一点上， 关于结肠的可能的自然波动知之甚少， 结肠癌高危人群上皮细胞增殖 腺瘤性息肉本研究拟采用随机双盲 安慰剂对照临床试验将通过以下方式解决这些差距： 对照组（执行双重功能，也是高风险 自然史组），具有两种不同的钙补充水平 组，并在三个月后对每组进行直肠活检 不同的时代因此，这项研究将提供所需的数据， 钙离子与结肠上皮细胞增殖的关系， 腺瘤性息肉和结肠癌。这项研究也将提供一个基础 为进一步研究结肠上皮细胞增殖的价值 作为结肠息肉和结肠癌的后续发展的生物标志物， 癌症和其他饮食干预措施，包括 评价饮食相互作用，如钙与脂肪的相互作用， 维生素D3和纤维

Promising, but as yet inconclusive evidence has been accumulating to indicate that dietary calcium in sufficient quantity, may be a protective factor against colorectal cancer--particularly for those consuming typical high fat Western-style diets. Evidence now also exists to support colonic epithelial cell proliferation as indicated by tritiated thymidine [3H]dTh - labeling of the cells as a biomarker or potential precursor lesion for colonic polyps and colonic cancer. These cells which can be obtained for study by simple non-prep rectal biopsies reflect risk for neoplasia that has occurred higher in the colon. Furthermore, evidence now also exists that this hyperproliferation in the colonic mucosa can be reversed by administration of calcium supplementation and the risk of colonic cancer thereby reduced. To date three uncontrolled trials on the effect of calcium on colonic epithelial cell proliferation in humans have been conducted. All three have shown important reductions. However, to date no randomized controlled trials or trials utilizing different dosages have been reported. Furthermore, there has been no serial or long term follow-up of the effect of calcium on colonic epithelial cell proliferation to determine how quickly a full benefit is achieved or whether or not an adaptive process may occur which would lessen the effect over time. Also, at this point, little is known regarding the possible natural fluctuation of colonic epithelial cell proliferation in high risk humans with previous colonic adenomatous polyps. This proposed randomized double-blind placebo-controlled clinical trial would address these gaps by having a control group (which performs a dual function of also being a high risk natural history group), having two different calcium supplementation level groups and by following up each group with rectal biopsies at three different times. This study therefore will provide needed data on the relationship between calcium and colonic epithelial cell proliferation, adenomatous polyps and colonic cancer. This study will also provide a basis for further studies of the value of colonic epithelial cell proliferation as a biomarker of subsequent development of colonic polyps and colonic cancer and for other dietary interventions on this marker including the evaluation of dietary interactions such as those of calcium with fat, vitamin D3, and fiber.