Higginbotham Susan, Zhang Zuo-Feng, Lee I-Min, Cook Nancy R, Giovannucci Edward, Buring Julie E, Liu Simin
Department of Epidemiology, University of California at Los Angeles, USA.
J Natl Cancer Inst. 2004 Feb 4;96(3):229-33. doi: 10.1093/jnci/djh020.
Although diet is believed to influence colorectal cancer risk, the long-term effects of a diet with a high glycemic load are unclear. The growing recognition that colorectal cancer may be promoted by hyperinsulinemia and insulin resistance suggests that a diet inducing high blood glucose levels and an elevated insulin response may contribute to a metabolic environment conducive to tumor growth. We prospectively followed a cohort of 38 451 women for an average of 7.9 years and identified 174 with incident colorectal cancer. We used baseline dietary intake measurements, assessed with a semiquantitative food-frequency questionnaire, to examine the associations of dietary glycemic load, overall dietary glycemic index, carbohydrate, fiber, nonfiber carbohydrate, sucrose, and fructose with the subsequent development of colorectal cancer. Cox proportional hazards models were used to estimate relative risks (RRs). Dietary glycemic load was statistically significantly associated with an increased risk of colorectal cancer (adjusted RR = 2.85, 95% confidence interval [CI] = 1.40 to 5.80, comparing extreme quintiles of dietary glycemic load; P(trend) =.004) and was associated, although not statistically significantly, with overall glycemic index (corresponding RR = 1.71, 95% CI = 0.98 to 2.98; P(trend) =.04). Total carbohydrate (adjusted RR = 2.41, 95% CI = 1.10 to 5.27, comparing extreme quintiles of carbohydrate; P(trend) =.02), nonfiber carbohydrate (corresponding RR = 2.60, 95% CI = 1.22 to 5.54; P(trend) =.02), and fructose (corresponding RR = 2.09, 95% CI = 1.13 to 3.87; P(trend) =.08) were also statistically significantly associated with increased risk. Thus, our data indicate that a diet with a high dietary glycemic load may increase the risk of colorectal cancer in women.
尽管人们认为饮食会影响结直肠癌风险,但高血糖负荷饮食的长期影响尚不清楚。越来越多的人认识到高胰岛素血症和胰岛素抵抗可能会促进结直肠癌,这表明导致高血糖水平和胰岛素反应升高的饮食可能会促成有利于肿瘤生长的代谢环境。我们对38451名女性进行了平均7.9年的前瞻性随访,确定了174例新发结直肠癌患者。我们使用通过半定量食物频率问卷评估的基线饮食摄入量测量值,来研究饮食血糖负荷、总体饮食血糖指数、碳水化合物、纤维、非纤维碳水化合物、蔗糖和果糖与随后结直肠癌发生之间的关联。使用Cox比例风险模型来估计相对风险(RRs)。饮食血糖负荷与结直肠癌风险增加在统计学上显著相关(调整后的RR = 2.85,95%置信区间[CI] = 1.40至5.80,比较饮食血糖负荷的极端五分位数;P(趋势)=.004),并且与总体血糖指数相关,尽管在统计学上不显著(相应的RR = 1.71,95% CI = 0.98至2.98;P(趋势)=.04)。总碳水化合物(调整后的RR = 2.41,95% CI = 1.10至5.27,比较碳水化合物的极端五分位数;P(趋势)=.02)、非纤维碳水化合物(相应的RR = 2.60,95% CI = 1.22至5.54;P(趋势)=.02)和果糖(相应的RR = 2.09,95% CI = 1.13至3.87;P(趋势)=.08)也与风险增加在统计学上显著相关。因此,我们的数据表明,高饮食血糖负荷的饮食可能会增加女性患结直肠癌的风险。