We thank Liu and colleagues for their interest in our work,1 and we read with great interest their letter examining associations between accelerated biological ageing, quantified using PhenoAge, and liver steatosis and fibrosis in the NHANES cohort.2 The authors demonstrate that biological age is associated with metabolic dysfunction–associated steatotic liver disease (MASLD) and liver fibrosis. These findings prompted two related questions: first, whether biological ageing behaves similarly in high-risk populations, and second, whether ageing-related vulnerability extends across the full SLD spectrum.
We thank Liu and colleagues for their interest in our work,1 and we read with great interest their letter examining associations between accelerated biological ageing, quantified using PhenoAge, and liver steatosis and fibrosis in the NHANES cohort.2 The authors demonstrate that biological age is associated with metabolic dysfunction–associated steatotic liver disease (MASLD) and liver fibrosis. These findings prompted two related questions: first, whether biological ageing behaves similarly in high-risk populations, and second, whether ageing-related vulnerability extends across the full SLD spectrum.