Antwi Samuel O, Oberg Ann L, Shivappa Nitin, Bamlet William R, Chaffee Kari G, Steck Susan E, Hébert James R, Petersen Gloria M
Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, 200 First Street SW, Charlton 6-243, Rochester, MN 55905, USA and.
Cancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA.
Carcinogenesis. 2016 May;37(5):481-90. doi: 10.1093/carcin/bgw022. Epub 2016 Feb 12.
Epidemiologic studies show strong associations between pancreatic cancer (PC) and inflammatory stimuli or conditions such as cigarette smoking and diabetes, suggesting that inflammation may play a key role in PC. Studies of dietary patterns and cancer outcomes also suggest that diet might influence an individual's risk of PC by modulating inflammation. We therefore examined independent and joint associations between inflammatory potential of diet, cigarette smoking and long-standing (≥5 years) type II diabetes in relation to risk of PC. Analyses included data from 817 cases and 1756 controls. Inflammatory potential of diet was measured using the dietary inflammatory index (DII), calculated from dietary intake assessed via a 144-item food frequency questionnaire, and adjusted for energy intake. Information on smoking and diabetes were obtained via risk factor questionnaires. Associations were examined using multivariable-adjusted logistic regression. Higher DII scores, reflecting a more proinflammatory diet, were associated with increased risk of PC [odds ratio (OR)Quintile 5 versus 1 = 2.54, 95% confidence interval (CI) = 1.87-3.46, P trend < 0.0001]. Excess risk of PC also was observed among former (OR = 1.29, 95% CI = 1.07-1.54) and current (OR = 3.40, 95% CI = 2.28-5.07) smokers compared with never smokers, and among participants with long-standing diabetes (OR = 3.09, 95% CI = 2.02-4.72) compared with nondiabetics. Joint associations were observed for the combined effects of having greater than median DII score, and being a current smoker (OR = 4.79, 95% CI = 3.00-7.65) or having long-standing diabetes (OR = 6.03, 95% CI = 3.41-10.85). These findings suggest that a proinflammatory diet may act as cofactor with cigarette smoking and diabetes to increase risk of PC beyond the risk of any of these factors alone.
流行病学研究表明,胰腺癌(PC)与炎症刺激或状况(如吸烟和糖尿病)之间存在密切关联,这表明炎症可能在胰腺癌中起关键作用。对饮食模式与癌症结局的研究还表明,饮食可能通过调节炎症来影响个体患胰腺癌的风险。因此,我们研究了饮食的炎症潜能、吸烟和长期(≥5年)II型糖尿病与胰腺癌风险之间的独立关联和联合关联。分析纳入了817例病例和1756例对照的数据。饮食的炎症潜能通过饮食炎症指数(DII)来衡量,该指数根据通过144项食物频率问卷评估的饮食摄入量计算得出,并针对能量摄入进行了调整。吸烟和糖尿病信息通过风险因素问卷获得。使用多变量调整逻辑回归分析关联。较高的DII分数反映了更具促炎作用的饮食,与胰腺癌风险增加相关[五分位数5与1相比的优势比(OR)= 2.54,95%置信区间(CI)= 1.87 - 3.46,P趋势< 0.0001]。与从不吸烟者相比, former(OR = 1.29,95% CI = 1.07 - 1.54)和 current(OR = 3.40,95% CI = 2.28 - 5.07)吸烟者中也观察到胰腺癌的额外风险,与非糖尿病患者相比,长期糖尿病患者(OR = 3.09,95% CI = 2.02 - 4.72)中也观察到该风险。对于DII分数高于中位数、 current吸烟者(OR = 4.79,95% CI = 3.00 - 7.65)或长期糖尿病患者(OR = 6.03,95% CI = 3.41 - 10.85)的联合效应观察到了联合关联。这些发现表明,促炎饮食可能与吸烟和糖尿病共同作用,增加胰腺癌风险,其风险超过任何单一因素单独作用时的风险。