Insights from the Amol Cohort Study on the relationship between allostatic load score, ultrasonographically detected hepatic steatosis, and hepatic steatosis index in Iranian adults

Allostatic load score (ALS), a composite measure of cumulative physiological dysregulation, may be associated with hepatic steatosis. This study aimed to investigate the association of ALS with ultrasonographically detected hepatic steatosis and, exploratorily, with elevated hepatic steatosis index (HSI) among Iranian adults. This cross-sectional analysis included 3,120 participants from the Amol Cohort Study. Hepatic steatosis was assessed by ultrasonography, and HSI was calculated using its established formula. ALS was derived from metabolic, cardiovascular, and inflammatory parameters, and participants were categorized into tertiles. Regression models were used to examine associations between ALS and ultrasonographically detected hepatic steatosis and elevated HSI, adjusting for demographic, lifestyle, and dietary factors. Higher ALS was associated with a higher prevalence of ultrasonographically detected hepatic steatosis (adjusted PR per one-unit increase = 1.15; 95% CI: 1.14–1.16) and elevated HSI (HSI > 36.0; adjusted PR = 1.14; 95% CI: 1.13–1.15) in Adjusted Model 1. Compared with participants in the lowest ALS tertile (T1), those in the highest tertile (T3) had higher prevalence ratios for ultrasonographically detected hepatic steatosis (adjusted PR = 4.67; 95% CI: 4.05–5.39) and elevated HSI (adjusted PR = 5.03; 95% CI: 4.42–5.74). All associations were statistically significant ( P < 0.001). ALS showed an AUC of 0.77 for discriminating ultrasonographically detected hepatic steatosis within the study sample. Higher ALS was associated with a higher prevalence of ultrasonographically detected hepatic steatosis among Iranian adults. The association with elevated HSI should be interpreted as exploratory because of potential structural and metabolic overlap between the indices. Given the cross-sectional design and the lack of systematic exclusion of alternative causes of hepatic steatosis, these findings do not establish causality or support conclusions regarding NAFLD specifically. Further longitudinal studies are warranted.