The Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute, Columbus, Ohio.
Division of Medical Oncology, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio.
Cancer Prev Res (Phila). 2020 Oct;13(10):841-852. doi: 10.1158/1940-6207.CAPR-20-0236. Epub 2020 Jul 12.
Prostate cancer is common in countries with affluent dietary patterns and represents a heterogeneous collection of subtypes with varying behavior. Reductionist strategies focusing on individual nutrients or foods have not clearly defined risk factors. We have developed mechanisms-based dietary patterns focusing upon inflammation and chronic insulin hypersecretion, processes that are hypothesized to impact prostate carcinogenesis. In the Prostate, Lung, Colorectal, and Ovarian cancer cohort, we calculated the empirical dietary index for hyperinsulinemia (EDIH) and empirical dietary inflammatory pattern (EDIP) scores from food frequency questionnaire data among 3,517 men and women who provided a blood sample at enrollment. We used these scores in multivariable-adjusted linear regression to validate EDIH and EDIP against relevant circulating biomarkers. In a separate sample of 49,317 men, we used multivariable-adjusted Cox regression to evaluate associations of EDIH and EDIP with prostate cancer (total and subtypes) risk. Participants consuming the most hyperinsulinemic diets (EDIH quintile 5) had significantly higher concentrations of C-peptide, insulin, c-reactive protein, TNFα-R2, and lower adiponectin, than those in quintile 1. Similarly, participants consuming the most proinflammatory diets had significantly higher concentrations of IL6, TNFα-R2, C-peptide, insulin, and lower adiponectin. Men consuming hyperinsulinemic diets were at higher total prostate cancer risk: HRquintile5vs1, 1.11; 95% confidence interval (CI), 1.01-1.23; trend = 0.03, especially high-grade cancer: HRquintile5vs1, 1.18; 95% CI, 1.02-1.37; trend = 0.06. The EDIP was not associated with prostate cancer risk. In summary, EDIH and EDIP predicted concentrations of known insulinemic and inflammatory biomarkers, and EDIH further predicted risk of future prostate cancer. Interventions to reduce the adverse role of hyperinsulinemic diets may be a means of prostate cancer prevention.
前列腺癌在饮食模式富裕的国家很常见，代表了具有不同行为的多种亚型的集合。关注个别营养素或食物的简化策略并没有明确界定风险因素。我们已经开发了基于机制的饮食模式，侧重于炎症和慢性胰岛素分泌过多，这些过程被假设会影响前列腺癌的发生。在前列腺癌、肺癌、结直肠癌和卵巢癌队列中，我们从 3517 名在入组时提供血液样本的男性和女性的食物频率问卷数据中计算了高胰岛素血症的经验性饮食指数 (EDIH) 和经验性饮食炎症模式 (EDIP) 得分。我们在多变量调整线性回归中使用这些分数来验证 EDIH 和 EDIP 与相关循环生物标志物的相关性。在另一组 49317 名男性中，我们使用多变量调整 Cox 回归来评估 EDIH 和 EDIP 与前列腺癌 (总发病率和亚型) 风险的关联。食用最具高胰岛素血症饮食的参与者 (EDIH 五分位 5) 的 C 肽、胰岛素、C 反应蛋白、TNFα-R2 浓度显著较高，而 adiponectin 浓度显著较低。同样，食用最促炎饮食的参与者的 IL6、TNFα-R2、C 肽、胰岛素浓度显著较高，而 adiponectin 浓度显著较低。食用高胰岛素血症饮食的男性患总前列腺癌的风险更高：HR 五分位 5vs1，1.11；95%置信区间 (CI)，1.01-1.23；趋势=0.03，尤其是高级别癌症：HR 五分位 5vs1，1.18；95%置信区间 (CI)，1.02-1.37；趋势=0.06。EDIP 与前列腺癌风险无关。总之，EDIH 和 EDIP 预测了已知的胰岛素和炎症生物标志物的浓度，而 EDIH 进一步预测了未来前列腺癌的风险。减少高胰岛素血症饮食的不良作用的干预措施可能是预防前列腺癌的一种手段。
