Dietary inflammatory and insulinemic potential, risk of hepatocellular carcinoma, and chronic liver disease mortality.

Dietary inflammatory and insulinemic potential, risk of hepatocellular carcinoma, and chronic liver disease mortality.
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DOI:
10.1093/jncics/pkad023
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发表时间:
2023-03-01
影响因子:
4.4
通讯作者:
--
中科院分区:
其他
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饮食调节炎症和胰岛素反应,可能是肝细胞癌(HCC)和慢性肝病(CLD)一级预防中的重要可变因素。我们开发了经验性饮食炎症模式(EDIP)和高胰岛素血症经验性饮食指数(EDIH)评分,以评估饮食的炎症和胰岛素血症潜力。我们前瞻性研究了基线EDIP和EDIH与以下HCC风险和CLD死亡率的相关性。自1995年以来,我们在美国国立卫生研究院-美国退休人员饮食与健康研究协会中跟踪了485931人。使用考克斯比例风险回归计算多变量风险比(HR)和95%置信区间(CI)。我们确认了635例HCC病例和993例CLD死亡。EDIP最高四分位数的参与者与EDIP最低四分位数的参与者相比,发生HCC的风险高1.35倍(95% CI = 1.08 - 1.70,Ptrend = 0.0005),CLD死亡率高1.70倍(95% CI = 1.41 - 2.04,Ptrend <0.0001)。对于相同的比较,具有最高EDIH的参与者的HCC(HR = 1.53,95%CI = 1.20至1.95,Ptrend = 0.0004)和CLD死亡率(HR = 1.72,95%CI = 1.42至2.01,Ptrend <0.0001)的风险增加。在女性和男性中观察到类似的评分与HCC风险和CLD死亡率的正相关。此外,与两个最低三分位数相比,EDIP和EDIH最高三分位数的个体HCC风险增加92%(95%CI = 1.43至2.58),CLD死亡率增加98%(95%CI = 1.27至3.08)。我们的研究结果表明,炎症和高胰岛素血症是联系饮食与HCC发展和CLD死亡率的潜在机制。
Diet modulates inflammation and insulin response and may be an important modifiable factor in the primary prevention of hepatocellular carcinoma (HCC) and chronic liver disease (CLD). We developed the empirical dietary inflammatory pattern (EDIP) and empirical dietary index for hyperinsulinemia (EDIH) scores to assess the inflammatory and insulinemic potentials of diet. We prospectively examined the associations of EDIP and EDIH at baseline with the following HCC risk and CLD mortality. We followed 485 931 individuals in the National Institutes of Health–American Association of Retired Persons Diet and Health Study since 1995. Cox proportional hazards regression was used to calculate multivariable hazard ratios (HRs) and 95% confidence intervals (CIs). We confirmed 635 incident HCC cases and 993 CLD deaths. Participants in the highest compared with those in the lowest EDIP quartile had a 1.35 times higher risk of developing HCC (95% CI = 1.08 to 1.70, Ptrend = .0005) and a 1.70 times higher CLD mortality (95% CI = 1.41 to 2.04, Ptrend < .0001). For the same comparison, participants with the highest EDIH were at increased risk of HCC (HR = 1.53, 95% CI = 1.20 to 1.95, Ptrend = .0004) and CLD mortality (HR = 1.72, 95% CI = 1.42 to 2.01, Ptrend < .0001). Similar positive associations of scores with HCC risk and CLD mortality were observed for both women and men. Moreover, individuals in both the highest EDIP and EDIH tertiles had a 92% increased HCC risk (95% CI = 1.43 to 2.58) and 98% increased CLD mortality (95% CI = 1.27 to 3.08) compared with those in both lowest tertiles. Our findings suggest that inflammation and hyperinsulinemia are potential mechanisms linking diet to HCC development and CLD mortality.
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