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膳食脂肪摄入量与前列腺癌、肺癌、结直肠癌和卵巢癌筛查试验中胰腺癌风险的关系。

Dietary fat intake and risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.

机构信息

Department of Chronic Disease Epidemiology, Yale University School of Public Health, New Haven, CT, USA.

出版信息

Ann Epidemiol. 2013 Sep;23(9):571-5. doi: 10.1016/j.annepidem.2013.06.006. Epub 2013 Jul 23.

Abstract

PURPOSE

Epidemiologic and experimental studies suggest that dietary fat intake may affect risk of pancreatic cancer, but published results are inconsistent.

METHODS

We examined risk associations for specific types of dietary fat intakes and related food sources among 111,416 participants in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. We used Cox proportional hazards regression to examine associations between fat intake and pancreatic cancer risk.

RESULTS

Over a mean 8.4 years of follow-up, 411 pancreatic cancer cases were identified. We observed an inverse association between saturated fat intake and pancreatic cancer risk (hazard ratio [HR], 0.64 comparing extreme quintiles; 95% confidence interval [CI], 0.46-0.88), but the association became weaker and nonsignificant when individuals with fewer than 4 years of follow-up were excluded to avoid possible reverse causation (HR, 0.88; 95% CI, 0.58-1.33). Total fat intake showed a similar pattern of association, whereas intakes of monounsaturated and polyunsaturated fats and fats from animal or plant sources showed no associations with risk.

CONCLUSIONS

These results do not support the hypothesis of increased pancreatic cancer risk with higher fat consumption overall or by specific fat type or source. Dietary changes owing to undetected disease may explain the observed inverse association with saturated fat.

摘要

目的

流行病学和实验研究表明,饮食中的脂肪摄入量可能会影响胰腺癌的风险,但已发表的结果并不一致。

方法

我们在前列腺癌、肺癌、结直肠癌和卵巢癌筛查试验中检查了 111416 名参与者中特定类型的饮食脂肪摄入量和相关食物来源的风险关联。我们使用 Cox 比例风险回归来检查脂肪摄入量与胰腺癌风险之间的关联。

结果

在平均 8.4 年的随访期间,确定了 411 例胰腺癌病例。我们观察到饱和脂肪摄入量与胰腺癌风险呈负相关(风险比[HR],极端五分位数之间比较为 0.64;95%置信区间[CI],0.46-0.88),但当排除随访时间少于 4 年的个体以避免可能的反向因果关系时,关联变得较弱且无统计学意义(HR,0.88;95%CI,0.58-1.33)。总脂肪摄入量表现出相似的关联模式,而单不饱和脂肪和多不饱和脂肪以及来自动物或植物来源的脂肪摄入量与风险没有关联。

结论

这些结果不支持脂肪摄入量总体增加或特定脂肪类型或来源增加会增加胰腺癌风险的假设。由于未检测到疾病而导致的饮食变化可能解释了与饱和脂肪观察到的负相关。

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