Background & Aims

Coffee is associated with a reduced risk of liver disease. This association is limited by important sources of confounding such as recall bias, healthy user bias, and indirect measures of liver outcomes or health. We aimed to examine the impact of coffee consumption with liver fibrosis and steatosis in a nationally representative sample.

Methods

We evaluated 4510 subjects 20 years and older from the 2017 to 2018 National Health and Nutrition Examination Survey study who underwent both transient elastography and two 24-hour dietary recall examinations. We tested the associations between liver stiffness measurements (LSM) of 9.5 kpa or greater or controlled attenuation parameter (CAP) and coffee consumption. We used decaffeinated coffee and tea consumption as controls. As a sensitivity analysis, we included all drinks in 1 model, examined the impact of caffeine consumption, and adjusted for the Healthy Eating Index-2015 and sugar-sweetened beverage consumption as separate models.

Results

The study sample described was aged 48 ± 0.6 years, 73% were overweight or obese, 10.6% had diabetes, 47.5% reported participation in vigorous physical activity, and 23% drank 2 or more alcoholic drinks per day. After multivariate adjustment, there was no association between coffee and controls with CAP. Subjects who drank more than 3 cups of coffee, but not other drinks, had a 0.9 lower kPa (95% CI, -1.6 to -0.1; P = .03). More than 3 cups of coffee were protective for LSM of 9.5 kpa or higher (odds ratio, 0.4; 95% CI, 0.2–1.0; P = .05). Accounting for all beverages in the same model, only consuming more than 3 cups of coffee remained independently associated with LSM (odds ratio, 0.5; 95% CI, 0.2–0.9; P = .03). Caffeine was not associated significantly with LSM at any dose. Finally, adjusting for sugar-sweetened beverage consumption and Healthy Eating Index-2015, coffee consumption remained associated with a lower LSM. The protective nature of coffee consumption therefore is not attributable to caffeine and persists in participants regardless of their diet quality.

Conclusions

Coffee is associated with lower liver stiffness, but not steatosis, as measured by CAP among US adults.

中文翻译：

---

咖啡消费与降低肝脏硬度有关：一项全国代表性研究

背景与目标

咖啡与降低患肝病的风险有关。这种关联受到重要混杂因素的限制，例如回忆偏差、健康用户偏差以及肝脏结果或健康的间接测量。我们的目的是在全国代表性样本中研究咖啡摄入对肝纤维化和脂肪变性的影响。

方法

我们评估了 2017 年至 2018 年国家健康和营养检查调查研究中 4510 名 20 岁及以上的受试者，他们接受了瞬时弹性成像和两次 24 小时饮食回忆检查。我们测试了 9.5 kpa 或更高的肝脏硬度测量值 (LSM) 或受控衰减参数 (CAP) 与咖啡消耗量之间的关联。我们使用不含咖啡因的咖啡和茶消费作为对照。作为敏感性分析，我们将所有饮料纳入 1 个模型，检查咖啡因消耗的影响，并根据 2015 年健康饮食指数和含糖饮料消耗作为单独的模型进行调整。

结果

所描述的研究样本年龄为 48 ± 0.6 岁，73% 的人超重或肥胖，10.6% 的人患有糖尿病，47.5% 的人报告参加过剧烈的体育活动，23% 的人每天喝 2 杯或更多酒精饮料。经过多变量调整后，咖啡和对照组与 CAP 之间没有关联。喝超过 3 杯咖啡但不喝其他饮料的受试者的 kPa 降低 0.9（95% CI，-1.6 至 -0.1；P  = .03）。超过 3 杯咖啡对 9.5 kpa 或更高的 LSM 具有保护作用（比值比，0.4；95% CI，0.2–1.0；P  = .05）。考虑到同一模型中的所有饮料，仅饮用超过 3 杯咖啡仍与 LSM 独立相关（比值比，0.5；95% CI，0.2–0.9；P  = 0.03）。任何剂量的咖啡因与 LSM 均无显着相关性。最后，根据含糖饮料消费量和 2015 年健康饮食指数进行调整后，咖啡消费量仍然与较低的 LSM 相关。因此，饮用咖啡的保护性质并不归因于咖啡因，并且无论参与者的饮食质量如何，这种保护性质都会持续存在。

结论

根据美国成年人 CAP 的测量，咖啡与降低肝脏硬度有关，但与脂肪变性无关。