Blood Selenium and Liver Health: Divergent Associations with Fibrosis and Steatosis
Poster #: 155
Session/Time: B
Author:
Neda Rehan, BS
Mentor:
Rehan Qayyum MBBS MHS
Research Type: Public Health
Abstract
INTRODUCTION:
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a spectrum of hepatic conditions characterized by metabolic dysfunction and ranging from simple steatosis to steatohepatitis, fibrosis, and cirrhosis. Selenium, an essential trace element incorporated into 25 selenoproteins with key antioxidant and anti-inflammatory functions, has been implicated in metabolic and hepatic processes, including regulation of oxidative stress, apoptosis, and endoplasmic reticulum stress. Prior studies have suggested potential associations between selenium status and fatty liver disease or fibrosis, but findings remain inconsistent and limited, often relying on modest sample sizes. To address this gap, we examined the relationship between blood selenium levels and both liver steatosis and fibrosis, assessed by controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) respectively using vibration-controlled transient elastography.
METHODS:
We performed a cross-sectional analysis of U.S. adults aged ≥19 years using publicly-available NHANES data from 2017-2023. Demographic, socioeconomic, lifestyle, and clinical characteristics were obtained through standardized interviews, examinations, and laboratory assessments. Liver steatosis and fibrosis were assessed using vibration-controlled transient elastography (using FibroScan® 502 V2 Touch). Liver stiffness measurement (LSM, expressed in kilopascals) was derived from shear wave velocity using the Young modulus, while hepatic steatosis was quantified with the controlled attenuation parameter (CAP, 100-400 dB/m). Blood selenium concentrations were measured by inductively coupled plasma-mass spectrometry. Covariates included age, sex, race/ethnicity, education, household income, smoking, alcohol consumption, body mass index, and diabetes status. Associations between blood selenium and liver outcomes were evaluated using sample-weighted linear regression models, with stepwise adjustment for demographic and clinical factors.
RESULTS:
A total of 13,241 adults were included. Participants in higher selenium quartiles were more likely to be male and of middle-age (p<0.001 for both). Median liver stiffness was modestly lower in quartiles 2-3 compared with the lowest quartile (p=0.005), whereas controlled attenuation parameter (CAP) increased progressively with selenium status (p<0.001). In sample-weighted regression analyses, higher selenium was inversely associated with liver stiffness, indicating lower fibrosis burden with higher selenium levels. Compared with the lowest quartile, adjusted differences in stiffness were −0.46 kPa (95%CI: −0.76, −0.17; p=0.003) for quartile 3 and −0.53 kPa (95%CI: −0.88, −0.19; p=0.003) for the highest quartile. In contrast, selenium was positively associated with hepatic steatosis. Adjusted CAP values were 9.00 dB/m (95%CI: 5.51, 12.50; p<0.001) higher in quartile 3 and 9.30 dB/m (95%CI: 5.59, 13.02; p<0.001) in the highest quartile relative to the lowest. Associations for quartile 2 were not significant.
CONCLUSION:
Higher selenium status was independently associated with reduced liver stiffness, suggesting a potential protective effect against fibrosis, but concurrently with greater hepatic steatosis. These findings highlight a complex, bidirectional role of selenium in liver health and underscore the need for mechanistic and longitudinal studies to clarify causal pathways and inform targeted nutritional or therapeutic strategies.
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a spectrum of hepatic conditions characterized by metabolic dysfunction and ranging from simple steatosis to steatohepatitis, fibrosis, and cirrhosis. Selenium, an essential trace element incorporated into 25 selenoproteins with key antioxidant and anti-inflammatory functions, has been implicated in metabolic and hepatic processes, including regulation of oxidative stress, apoptosis, and endoplasmic reticulum stress. Prior studies have suggested potential associations between selenium status and fatty liver disease or fibrosis, but findings remain inconsistent and limited, often relying on modest sample sizes. To address this gap, we examined the relationship between blood selenium levels and both liver steatosis and fibrosis, assessed by controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) respectively using vibration-controlled transient elastography.
METHODS:
We performed a cross-sectional analysis of U.S. adults aged ≥19 years using publicly-available NHANES data from 2017-2023. Demographic, socioeconomic, lifestyle, and clinical characteristics were obtained through standardized interviews, examinations, and laboratory assessments. Liver steatosis and fibrosis were assessed using vibration-controlled transient elastography (using FibroScan® 502 V2 Touch). Liver stiffness measurement (LSM, expressed in kilopascals) was derived from shear wave velocity using the Young modulus, while hepatic steatosis was quantified with the controlled attenuation parameter (CAP, 100-400 dB/m). Blood selenium concentrations were measured by inductively coupled plasma-mass spectrometry. Covariates included age, sex, race/ethnicity, education, household income, smoking, alcohol consumption, body mass index, and diabetes status. Associations between blood selenium and liver outcomes were evaluated using sample-weighted linear regression models, with stepwise adjustment for demographic and clinical factors.
RESULTS:
A total of 13,241 adults were included. Participants in higher selenium quartiles were more likely to be male and of middle-age (p<0.001 for both). Median liver stiffness was modestly lower in quartiles 2-3 compared with the lowest quartile (p=0.005), whereas controlled attenuation parameter (CAP) increased progressively with selenium status (p<0.001). In sample-weighted regression analyses, higher selenium was inversely associated with liver stiffness, indicating lower fibrosis burden with higher selenium levels. Compared with the lowest quartile, adjusted differences in stiffness were −0.46 kPa (95%CI: −0.76, −0.17; p=0.003) for quartile 3 and −0.53 kPa (95%CI: −0.88, −0.19; p=0.003) for the highest quartile. In contrast, selenium was positively associated with hepatic steatosis. Adjusted CAP values were 9.00 dB/m (95%CI: 5.51, 12.50; p<0.001) higher in quartile 3 and 9.30 dB/m (95%CI: 5.59, 13.02; p<0.001) in the highest quartile relative to the lowest. Associations for quartile 2 were not significant.
CONCLUSION:
Higher selenium status was independently associated with reduced liver stiffness, suggesting a potential protective effect against fibrosis, but concurrently with greater hepatic steatosis. These findings highlight a complex, bidirectional role of selenium in liver health and underscore the need for mechanistic and longitudinal studies to clarify causal pathways and inform targeted nutritional or therapeutic strategies.