Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC.
Cancer Prevention and Control Program, University of South Carolina, Columbia, SC.
Int J Cancer. 2018 Jun 15;142(12):2461-2470. doi: 10.1002/ijc.31271. Epub 2018 Feb 2.
Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet. We aimed to examine the association between the inflammatory potential of diet, assessed with the Dietary Inflammatory Index (DII®), and pancreatic cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial prospective cohort. Our study included 101,449 participants aged 52-78 years at baseline who completed both baseline questionnaire and a diet history questionnaire. Energy-adjusted DII (E-DII) scores were computed based on food and supplement intake. Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with participants in the lowest E-DII quintile (most anti-inflammatory scores) as referent. After a median 8.5 years of follow-up, 328 pancreatic cancer cases were identified. E-DII scores were not associated with pancreatic cancer risk in the multivariable model (HR = 0.94; 95% CI = 0.66-1.35; p-trend = 0.43). Time significantly modified the association (p-interaction = 0.01). During follow up <4 years, there was suggestive evidence of an inverse association between E-DII and pancreatic cancer (HR = 0.60; 95% CI = 0.35-1.02; p-trend = 0.20) while there was a significant positive trend in the follow up ≥4 years (HR = 1.31; 95% CI = 0.83-2.08; p-trend = 0.03). Similar results were observed for E-DII from food only. Our study does not support an association between inflammatory potential of diet and pancreatic cancer risk; however, heterogeneous results were obtained with different follow-up times. These divergent associations may result from the influences of undetected disease in the short-term.
炎症在胰腺癌的病因学中起着核心作用，并且可以通过饮食进行调节。我们旨在研究饮食的炎症潜能与前列腺癌、肺癌、结直肠癌和卵巢癌筛查试验前瞻性队列中胰腺癌风险之间的关联。我们的研究包括 101449 名年龄在 52-78 岁的参与者，他们在基线时完成了基线问卷和饮食史问卷。根据食物和补充剂的摄入量计算了能量调整后的 DII（E-DII）评分。使用 Cox 比例风险模型和时间依赖 Cox 模型，以最低 E-DII 五分位数（抗炎评分最高）的参与者作为参考，估计风险比（HR）和 95%置信区间（CI）。在中位随访 8.5 年后，确定了 328 例胰腺癌病例。多变量模型中，E-DII 评分与胰腺癌风险无关（HR=0.94；95%CI=0.66-1.35；p 趋势=0.43）。时间显著改变了这种关联（p 交互=0.01）。在随访<4 年期间，E-DII 与胰腺癌之间存在反向关联的提示性证据（HR=0.60；95%CI=0.35-1.02；p 趋势=0.20），而在随访≥4 年期间呈显著正趋势（HR=1.31；95%CI=0.83-2.08；p 趋势=0.03）。仅从食物中获取 E-DII 也得到了类似的结果。我们的研究不支持饮食炎症潜能与胰腺癌风险之间的关联；然而，不同的随访时间得到了不同的结果。这些不一致的关联可能是由于短期未检测到疾病的影响。
