Department of Epidemiology, Human Genetics, and Environmental Science, School of Public Health, The University of Texas Health Science Center at Houston, Houston, Texas, USA.
Division of Epidemiology, Human Genetics, & Environmental Sciences, Southwest Center for Occupational and Environmental Health, Michael & Susan Dell Center for Healthy Living, School of Public Health, The University of Texas Health Science Center at Houston, Houston, Texas, USA.
Cancer Med. 2021 Oct;10(20):7308-7319. doi: 10.1002/cam4.4256. Epub 2021 Sep 18.
The role of dietary fat consumption in the etiology of hepatocellular carcinoma (HCC) remains unclear. We investigated the associations of total fat and fatty acids with risk of HCC among US adults in a hospital-based case-control study.
We analyzed data from 641 cases and 1034 controls recruited at MD Anderson Cancer Center during 2001-2018. Cases were new patients with a pathologically or radiologically confirmed diagnosis of HCC; controls were cancer-free spouses of patients with cancers other than gastrointestinal, lung, liver, or head and neck. Cases and controls were frequency-matched by age and sex. Dietary intake was assessed using a validated food frequency questionnaire. Odds ratios (ORs) and corresponding confidence intervals (CIs) were computed using unconditional logistic regression with adjustment for major HCC risk factors, including hepatitis B virus and hepatitis C virus infection.
Monounsaturated fatty acid (MUFA) intake was inversely associated with HCC risk (highest vs. lowest tertile: OR, 0.49; 95% CI, 0.33-0.72). Total polyunsaturated fatty acid (PUFA) intake was directly associated with HCC risk (highest vs. lowest tertile: OR, 1.82; 95% CI, 1.23-2.70). Omega-6 PUFA was directly associated with HCC risk (highest vs. lowest tertile: OR 2.29; 95% CI, 1.52-3.44). Long-chain omega-3 PUFA (eicosapentaenoic acid and docosahexaenoic acid) intake was also inversely associated with HCC risk (highest vs. lowest tertile: OR, 0.50; 95% CI, 0.33-0.70). No association was observed for saturated fat and HCC risk.
Our findings support a direct association of omega-6 PUFA intake with HCC and an inverse association of MUFA and long-chain omega-3 PUFA intake with HCC.
脂肪摄入在肝细胞癌(HCC)发病机制中的作用尚不清楚。我们在一项基于医院的病例对照研究中,调查了美国成年人总脂肪和脂肪酸与 HCC 风险的相关性。
我们分析了 2001 年至 2018 年期间在 MD 安德森癌症中心招募的 641 例病例和 1034 例对照的数据。病例为病理或影像学证实的 HCC 新患者;对照为非胃肠道、肺、肝或头颈部癌症患者的无癌症配偶。病例和对照按年龄和性别进行频数匹配。饮食摄入情况使用经过验证的食物频率问卷进行评估。使用调整乙型肝炎病毒和丙型肝炎病毒感染等主要 HCC 危险因素的非条件逻辑回归计算比值比(OR)和相应的置信区间(CI)。
单不饱和脂肪酸(MUFA)摄入与 HCC 风险呈负相关(最高与最低三分位:OR,0.49;95%CI,0.33-0.72)。总多不饱和脂肪酸(PUFA)摄入与 HCC 风险呈正相关(最高与最低三分位:OR,1.82;95%CI,1.23-2.70)。ω-6 PUFA 与 HCC 风险呈正相关(最高与最低三分位:OR,2.29;95%CI,1.52-3.44)。长链 ω-3 PUFA(二十碳五烯酸和二十二碳六烯酸)摄入也与 HCC 风险呈负相关(最高与最低三分位:OR,0.50;95%CI,0.33-0.70)。未观察到饱和脂肪与 HCC 风险的相关性。
我们的研究结果支持 ω-6 PUFA 摄入与 HCC 呈正相关,MUFA 和长链 ω-3 PUFA 摄入与 HCC 呈负相关。