Patel Alpa V, McCullough Marjorie L, Pavluck Alexandre L, Jacobs Eric J, Thun Michael J, Calle Eugenia E
Department of Epidemiology and Surveillance Research, American Cancer Society, National Home Office, 1599 Clifton Road NE, Atlanta, GA 30329-4251, USA.
Cancer Causes Control. 2007 Apr;18(3):287-94. doi: 10.1007/s10552-006-0081-z. Epub 2007 Jan 11.
Consumption of diets with high glycemic load has been hypothesized to increase pancreatic cancer risk by raising postprandial glucose levels and insulin secretion.
The authors analyzed data from the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort to examine the association between pancreatic cancer and glycemic load, glycemic index (GI), and intake of carbohydrates. Diet was assessed among 124,907 men and women who were cancer-free and non-diabetic at baseline in 1992 using a validated 68-item food frequency questionnaire (FFQ). During 9 years of follow-up, 401 incident pancreatic cancer cases were identified. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) adjusted for potential confounding factors.
We found no association between glycemic load, GI, or carbohydrate intake and risk of pancreatic cancer in this population. The hazard rate ratio (RR) was 1.01 (95% CI 0.75-1.37, trend P=0.80) for glycemic load, 0.92 (95% CI 0.68-1.24) for GI, and 1.10 (95% CI 0.80-1.51) for carbohydrate intake among men and women in the highest quintile compared to the lowest quintile of each measure. We also found no significant association between these measures and pancreatic cancer risk among individuals who show a greater susceptibility towards insulin insensitivity, such as those who are overweight or more sedentary.
Overall, our data do not support the hypothesis that glycemic load or index, or carbohydrate intake are associated with a substantial increase in pancreatic cancer risk; however, a weak positive association cannot be ruled out.
有假说认为，食用高血糖负荷的饮食会通过提高餐后血糖水平和胰岛素分泌来增加患胰腺癌的风险。
作者分析了美国癌症协会癌症预防研究II（CPS-II）营养队列的数据，以研究胰腺癌与血糖负荷、血糖指数（GI）和碳水化合物摄入量之间的关联。1992年，使用经过验证的68项食物频率问卷（FFQ）对124,907名基线时无癌症且无糖尿病的男性和女性进行了饮食评估。在9年的随访期间，共确定了401例胰腺癌新发病例。使用Cox比例风险模型计算经潜在混杂因素调整后的风险率比（RR）。
我们发现该人群中血糖负荷、GI或碳水化合物摄入量与胰腺癌风险之间无关联。与每种测量的最低五分位数相比，最高五分位数的男性和女性的血糖负荷风险率比（RR）为1.01（95%CI 0.75-1.37，趋势P=0.80），GI为0.92（95%CI 0.68-1.24），碳水化合物摄入量为1.10（95%CI 0.80-1.51）。我们还发现，在对胰岛素不敏感更敏感的个体中，如超重或久坐不动的个体，这些测量与胰腺癌风险之间也无显著关联。
总体而言，我们的数据不支持血糖负荷或指数、或碳水化合物摄入量与胰腺癌风险大幅增加相关的假说；然而，也不能排除微弱的正相关关系。
