Accelerometer-based sedentary time and physical activity with MASLD and liver cirrhosis in 2684 British adolescents

Evidence on the long-term relationship of sedentary time (ST), light physical activity (LPA) and moderate-to-vigorous PA (MVPA) with liver steatosis, fibrosis, cirrhosis, and changes in liver enzymes in the paediatric population is limited. This study examined the associations of cumulative ST, LPA and MVPA from childhood with longitudinal changes in liver indices and enzymes. From the Avon Longitudinal Study of Parents and Children (ALSPAC), UK birth cohort, 2684 children aged 11 years who had at least one follow-up time-points accelerometer-measured ST, LPA and MVPA over a period of 13 years, and liver indices and enzymes measures at age 24 years clinic visit were included. Liver steatosis and fibrosis were assessed by transient elastography and staged as fibrosis stage F0-F4 and steatosis grade (S0-S3) at age 24 years. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transferase (GGT) were assayed at ages 17 and 24 years. Longitudinal associations were examined using generalized linear mixed-effect models, while mediation analyses were conducted with structural equation models. Among 2684 children (mean [SD] age, 11.75 [0.24] years; 1537 [57.3%] females]), the prevalence of liver steatosis at age 17 years was 2.6% and 20.5% at age 24 years. The cumulative 1-minute/day increase in ST from ages 11–24 years was associated with higher odds of liver cirrhosis (odds ratio 1.004 [95% CI 1.002–1.005] p < 0.001) and severe liver steatosis (1.001 [1.001–1.002] p = 0.002) at age 24 years. Increased ST from childhood was directly associated with progressively increased ALT, AST and GGT from ages 17 to 24 years. Cumulative 1-min/day LPA was associated with lower odds of liver cirrhosis (0.990 [0.990–0.991] p < 0.001) and severe liver steatosis (0.999 [0.998–0.999] p < 0.001) at age 24 years, as well as decreased liver enzymes. Cumulative 1-min/day MVPA was associated with associated with lower odds of severe liver steatosis (0.996 [0.994–0.998] p < 0.001) but not liver cirrhosis at age 24 years. MVPA effect on lowering liver steatosis was significantly suppressed (64% suppression) by increased fat mass. In conclusion, increasing LPA, sustaining MVPA and decreasing ST from childhood may independently attenuate and reverse the risk of severe liver steatosis and liver cirrhosis by young adulthood.