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; P trend = 0.03, especially high-grade cancer: HRquintile5vs1, 1.18; 95% CI, 1.02–1.37; P 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.

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炎症和胰岛素饮食模式：对循环生物标志物和前列腺癌风险的影响

前列腺癌在饮食习惯丰富的国家很常见，并且代表具有不同行为的异质亚型集合。专注于个体营养素或食物的还原论策略尚未明确定义风险因素。我们开发了基于机制的饮食模式，重点关注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，我们根据 3,517 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计算了高胰岛素血症的经验饮食指数 (EDIH) 和经验饮食炎症模式 (EDIP) 评分。我们在多变量调整线性回归中使用这些分数来根据相关循环生物标志物验证 EDIH 和 EDIP。在 49,317 名男性的单独样本中，我们使用多变量调整的 Cox 回归来评估 EDIH 和 EDIP 与前列腺癌（总风险和亚型）风险的关联。与五分位数 1 中的参与者相比，食用高胰岛素血症饮食最多的参与者（EDIH 五分位数 5）的 C 肽、胰岛素、C 反应蛋白、TNFα-R2 浓度显着较高，脂联素浓度较低。同样，食用促炎性饮食最多的参与者IL6、TNFα-R2、C 肽、胰岛素浓度显着升高，脂联素浓度显着降低。摄入高胰岛素饮食的男性患前列腺癌的总风险较高：HRquintile5vs1，1.11；95% 置信区间 (CI)，1.01–1.23；P 趋势 = 0.03，特别是高级别癌症：HRquintile5vs1，1.18；95% CI，1.02–1.37；P 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，EDIH 进一步预测了未来前列腺癌的风险。减少高胰岛素饮食的不利作用的干预措施可能是预防前列腺癌的一种手段。