A dose-response relationship exists between salt intake and the risk of obesity, and this association is partly mediated by increased body fat mass, suggests a China study.
“In this large Chinese cohort, salt intake was positively associated with adiposity and risks of overweight and central obesity, with body fat mass partly explaining these relationships,” the investigators said. “These results highlight salt reduction as a potential public health intervention that could help curb both obesity and cardiometabolic risk.”
The study used longitudinal data from a cluster-randomized controlled trial involving 7,372 adults with 12,800 observations. Spot urine samples were collected to estimate 24-h salt intake. Adiposity was evaluated using BMI, body roundness index (BRI), body fat mass, overweight, and central obesity.
The investigators explored the relationship between salt intake and adiposity using generalized linear mixed-effects models. They also conducted mediation analyses to calculate the proportion of associations mediated by body fat mass.
At baseline, the mean 24-h salt intake was 9.88 g/day. Participants in the highest (≥11.2 g/day) vs lowest (<8.4 g/day) quartile of salt intake had higher BMI (difference, 1.14 kg/m2, 95 percent confidence interval [CI], 1.03‒1.25), BRI (difference, 0.31, 95 percent CI, 0.26‒0.35), and body fat mass (difference, 1.88 kg, 95 percent CI, 1.69‒2.07). [Nutrients 2026;18:976]
Individuals with the highest salt intake were also more likely to be overweight (odds ratio [OR], 2.82, 95 percent CI, 2.47‒3.22) and have central obesity (OR, 2.78, 95 percent CI, 2.42‒3.20) than those with the lowest intake.
Longitudinally, reductions in salt intake (>1 g/day) resulted in decreases in BMI (‒0.21 kg/m2, 95 percent CI, ‒0.33 to ‒0.09), BRI (‒0.04, 95 percent CI, ‒0.09 to 0.00), and body fat mass (‒0.14 kg, 95 percent CI, ‒0.36 to 0.07). This effect was more pronounced in women and adults aged <40 years (p<0.05).
Notably, body fat mass mediated 56.93 percent to 84.73 percent of these associations.
“Our findings indicate that salt intake is not only a concern for hypertension prevention but may also play a meaningful role in the development of obesity,” the investigators said.
Earlier evidence
Previous studies have also reported positive associations between salt intake and adiposity indices. [Am J Clin Nutr 2019;109:139-147; Am J Clin Nutr 2019;110:34-40; Obes Facts 2025;18:1-656; BMC Nutr 2018;4:47]
However, the 0.22-kg/m2 increase in BMI per 1 g/day higher salt intake observed in the current study was lower than that seen in the NHANES analysis (1.49 kg/m2) and higher than that found in the INTERMAP study (0.10 kg/m2). [Am J Clin Nutr 2019;109:139-147; Am J Clin Nutr 2019;110:34-40]
“Moreover, we observed 2.82-fold higher odds of overweight among participants in the highest quartile vs lowest quartile of salt intake, which was higher than the 1.93-fold increase observed in the NHANES study, yet lower than the 4.30-fold increase reported in Finnish adults,” the investigators said.
“The heterogeneity between studies may attribute to the difference in study population, sample size, and methods used to estimate salt intake,” they added.
Mechanism
Although the underlying mechanism of the association between salt intake and obesity remains unclear, one study suggests that high salt intake co-occurs with the consumption of processed energy-dense food or increases in the intake of sugar-sweetened beverages driven by thirst. [Br J Nutr 2021;126:409-427]
On the other hand, previous studies reported a robust association between salt intake and adiposity irrespective of energy intake or beverage consumption. [Am J Clin Nutr 2019;109:139-147; Am J Clin Nutr 2019;110:34-40; Hypertension 2015;66:843-849]
“Our results similarly showed that adjustment for multiple metabolic and lifestyle factors did not attenuate the associations,” the investigators said.
Moreover, animal experiments suggest that high salt intake could activate the aldose reductase‒fructokinase pathway in the liver and hypothalamus. This promotes endogenous fructose production with the development of leptin resistance and hyperphagia, resulting in obesity insulin resistance, and fatty liver disease. [Hypertension 2015;66:843-849; Proc Natl Acad Sci USA 2018;115:3138-3143]
“The observed increased body fat mass related to higher salt intake and the mediating role of body fat mass in the salt–obesity association supported this hypothesis,” the investigators said. “Future studies are needed to validate these pathways in human populations.”