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

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.