Advanced liver fibrosis, but not MASLD, is associated with accelerated biological aging: a population-based study

Background: The process of biological aging in patients diagnosed with chronic liver disease remains unclear.

Aim: The current study aims to investigate if there is an accelerated biological aging process in participants with advanced fibrosis (AF) and metabolic dysfunction-associated steatotic liver disease (MASLD).

Methods: Data from the 2017-2018 NHANES cycle were analyzed. AF was determined based on the values of liver stiffness measurement (LSM) and MASLD was defined according to new consensus nomenclature. Klemera-Doubal method biological age (KDM bioage) and Phenotypic age (Phenoage) were adopted to quantify biological age. Phenoage advancement (Phenoage_advance) and KDM advancement (KDM_advance) were generated as the difference between the calculated biological age and chronological age, and a positive residual was regarded as an indicator of accelerated biological aging.

Results: A total of 3974 participants was enrolled. The weight mean KDM_advance and phenoage_advance in AF group was 4.22 years (95%CI: 2.96-5.49 years) and 2.61 years (95%CI: 1.80-3.41 years), while in MASLD group was 0.37 years (95%CI: -0.28-1.03 years) and 0.04 years (95%CI: -0.64-0.72 years), respectively. Multivariate linear regression analysis showed that participants with AF had older KDM_advance and phenoage_advance compared with those without AF (1.50 years (95%CI: 0.23-2.77 years), P = 0.02; 1.00 years (95%CI: 0.18-1.82 years), P = 0.02; respectively), in models adjusting demographic characteristics, socioeconomic status, lifestyle factors, and comorbidities. No significant association was found between MASLD and KDM_advance and phenoage_advance.

Conclusions: AF, not MASLD, was independently associated with accelerated biological aging in adults from a US representative sample.