Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA.
Department of Epidemiology and Biostatistics, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, P.R. China.
JNCI Cancer Spectr. 2023 Mar 1;7(2). doi: 10.1093/jncics/pkad023.
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.
饮食可调节炎症和胰岛素反应，可能是原发性肝细胞癌 (HCC) 和慢性肝病 (CLD) 一级预防的重要可调节因素。我们开发了经验性饮食炎症模式 (EDIP) 和经验性饮食高胰岛素血症指数 (EDIH) 评分，以评估饮食的炎症和胰岛素生成潜力。我们前瞻性地研究了基线时 EDIP 和 EDIH 与以下 HCC 风险和 CLD 死亡率的相关性。
我们自 1995 年以来对美国国立卫生研究院-美国退休人员协会饮食与健康研究中的 485931 名参与者进行了随访。使用 Cox 比例风险回归计算多变量风险比 (HR) 和 95%置信区间 (CI)。
我们证实了 635 例 HCC 新发病例和 993 例 CLD 死亡病例。与 EDIP 四分位最低组相比，最高组发生 HCC 的风险增加了 1.35 倍（95%CI=1.08 至 1.70，Ptrend=0.0005），CLD 死亡率增加了 1.70 倍（95%CI=1.41 至 2.04，Ptrend<0.0001）。对于相同的比较，EDIH 最高的参与者患 HCC 的风险增加（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）。在女性和男性中，分数与 HCC 风险和 CLD 死亡率的正相关关系相似。此外，EDIP 和 EDIH 最高三分位数的个体 HCC 风险增加了 92%（95%CI=1.43 至 2.58），CLD 死亡率增加了 98%（95%CI=1.27 至 3.08），与最低三分位数的个体相比。
我们的研究结果表明，炎症和高胰岛素血症可能是饮食与 HCC 发生和 CLD 死亡率相关的潜在机制。
