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超加工食品摄入量与代谢功能障碍相关脂肪性肝病之间的横断面关联。

The cross-sectional association between ultra-processed food intake and metabolic dysfunction-associated steatotic liver disease.

作者信息

Sun Natalie, Prescott Brenton, Ma Jiantao, Xanthakis Vanessa, Quatromoni Paula A, Long Michelle T, Walker Maura E

机构信息

Department of Internal Medicine, Boston Medical Center, USA.

Section of Preventive Medicine and Epidemiology, Department of Medicine, Chobanian and Avedisian School of Medicine, Boston University, USA.

出版信息

Clin Nutr ESPEN. 2025 Apr;66:215-220. doi: 10.1016/j.clnesp.2025.01.045. Epub 2025 Jan 27.

DOI:10.1016/j.clnesp.2025.01.045
PMID:39880205
Abstract

BACKGROUND AND AIMS

The prevalence of Metabolic Dysfunction-Associated Steatotic Liver Disease has increased in parallel with a rise in consumption of ultra-processed foods (UPF), but little is known about their association.

METHODS

We cross-sectionally examined associations of UPF with hepatic steatosis and fibrosis in 2458 (mean age 54 years; 55.9 % women) community-dwelling adults who completed vibration-controlled transient elastography and a food frequency questionnaire. Dietary intake was categorized into levels of food processing via the NOVA system. We used multivariable-adjusted logistic regression models to evaluate the association of energy-adjusted UPF intake (per 1-SD unit and by quintile) with clinical hepatic steatosis (Controlled Attenuation Parameter [CAP]≥ 290 dB/m) and fibrosis (Liver Stiffness Measurement [LSM] ≥ 8.2 kPa) and tested for linear trends of UPF intake with CAP and LSM. We adjusted for age, sex, smoking, alcohol intake, physical activity, and intake of minimally processed foods. Additional models adjusted for diet quality index or body mass index (BMI).

RESULTS

Higher intake of UPF was directly associated with higher odds of hepatic steatosis (Odds Ratio 1.33 [95 % Confidence Interval 1.21, 1.46] per standard deviation increase). UPF intake and CAP had a dose-response relation (P <0.001). There were 2.50 times higher odds of hepatic steatosis (Confidence Interval 1.81, 3.45) with a 19.49 (standard error: 3.73) unit increase in CAP (P < 0.001) when comparing quintile 5 to quintile 1 of UPF consumption. Higher UPF was not significantly associated with hepatic fibrosis. Adjustment for BMI attenuated the strength of all UPF-hepatic associations.

CONCLUSIONS

UPF consumption was positively associated with hepatic steatosis. Longitudinal studies are needed to assess whether lowering consumption of UPF can decrease odds of hepatic fibrosis.

摘要

背景与目的

代谢功能障碍相关脂肪性肝病的患病率随着超加工食品(UPF)消费量的增加而上升,但对它们之间的关联知之甚少。

方法

我们对2458名(平均年龄54岁;55.9%为女性)社区居住成年人进行了横断面研究,这些成年人完成了振动控制瞬时弹性成像检查和食物频率问卷调查,以研究UPF与肝脂肪变性和肝纤维化之间的关联。通过NOVA系统将饮食摄入量分为食品加工水平类别。我们使用多变量调整逻辑回归模型来评估能量调整后的UPF摄入量(每1个标准差单位和按五分位数)与临床肝脂肪变性(控制衰减参数[CAP]≥290dB/m)和肝纤维化(肝脏硬度测量[LSM]≥8.2kPa)的关联,并检验UPF摄入量与CAP和LSM的线性趋势。我们对年龄、性别、吸烟、饮酒、身体活动以及最低加工食品的摄入量进行了调整。其他模型对饮食质量指数或体重指数(BMI)进行了调整。

结果

较高的UPF摄入量与肝脂肪变性的较高几率直接相关(每增加1个标准差,优势比为1.33[95%置信区间1.21,1.46])。UPF摄入量与CAP呈剂量反应关系(P<0.001)。当比较UPF消费量的第5五分位数与第1五分位数时,CAP每增加19.49(标准误:3.73)个单位,肝脂肪变性的几率高2.50倍(置信区间1.81,3.45)(P<0.001)。较高的UPF与肝纤维化无显著关联。对BMI进行调整后,所有UPF与肝脏的关联强度均减弱。

结论

食用UPF与肝脂肪变性呈正相关。需要进行纵向研究以评估减少UPF的消费量是否能降低肝纤维化的几率。

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