HCP Live
Contagion LiveCGT LiveNeurology LiveHCP LiveOncology LiveContemporary PediatricsContemporary OBGYNEndocrinology NetworkPractical CardiologyRheumatology Netowrk

High Salt Intake Implicated in NAFLD

A recent study suggests that high salt intake is closely associated with elevated risks of developing non-alcoholic fatty liver disease (NAFLD).

A Korean study in PLOS One suggests that high salt intake is closely associated with elevated risks of developing non-alcoholic fatty liver disease (NAFLD).

The finding is important, because NAFLD is the most common metabolic liver disease in developed countries, and its incidence has been increasing rapidly along with the worldwide increase in obesity rates. NAFLD is a major risk factor for various metabolic disorders including type 2 diabetes mellitus, dyslipidemia and cardiovascular disease.

Also, patients with nonalcoholic steatohepatitis (NASH) may develop cirrhosis and its complications. The risks posed by sodium intake are well-known in terms of obesity and hypertension, but the current study is among the first to make a definitive link between elevated risks of NAFLD and NASH. Notably, the elevated risk is independent of factors such as body fat and insulin resistance.

The researchers analyzed data from 27,433 participants in the Korea National Health and Nutrition Examination Surveys taken from 2008 to 2010. The total amount of sodium excretion in 24-hour urine was estimated using Tanaka’s equations from spot urine specimens. Subjects were defined as having NAFLD when they had high scores in previously validated NAFLD prediction models such as the hepatic steatosis index (HSI) and fatty liver index (FLI).

The participants were classified into three groups according to estimated 24-hour urinary excretion tertiles. The prevalence of NAFLD as assessed by both FLI and HSI was significantly higher in the highest estimated 24-hour urinary sodium excretion tertile group -- even after adjustment for confounding factors including body fat and hypertension.

“The significant relationship between high salt intake and NAFLD could be explained by several possible mechanisms,” the study authors wrote. “First, high salt intake may result in the dysregulation of the renin—angiotensin system, leading consequently to the development of NAFLD and progression to NASH... Second, high salt intake is generally the result of consumption of high energy foods with a high salt content, such as cheese and chips, which consequently increase the total energy intake and ultimately increase body fat. In addition, the production of inflammatory cytokines and oxidative stress, which are both induced by increased body fat, may also be involved in the development of NAFLD.”

Limitations of the study include that because it was cross-sectional rather than longitudinal, a causal relationship between high salt intake and NAFLD could not be definitively established. Second, the study did not include hepatic imaging or biopsies, so the researchers used indirect methods to define NAFLD or advanced fibrosis based on several predictive models that have been well validated.