**Background:** Obesity prevalence has tripled globally between 1975 and 2016, and while high energy intake is the primary driver, emerging evidence suggests high sodium intake may independently contribute to weight gain. However, the scientific evidence for a sodium-obesity association is limited by the methods used to assess sodium intake. Twenty-four-hour urine collection is the gold standard, but many studies use less accurate methods such as spot urine, overnight urine, or dietary recall. This review of systematic reviews aimed to synthesize the evidence on the association between dietary sodium intake and obesity in adults, and to examine whether the association differs by sodium intake assessment method.
**Methods:** The authors searched PubMed (from inception to October 24, 2022) for systematic reviews (with or without meta-analysis) that examined the association between dietary sodium intake and obesity-related outcomes (BMI, body weight, waist circumference, abdominal obesity) in adults. Two reviewers independently screened abstracts and full texts. Risk of bias was assessed using the ROBIS tool. Re-meta-analyses of individual studies from the included systematic reviews were performed using random-effects models. Heterogeneity was assessed using the I² index. Subgroup analyses were conducted by sodium intake assessment method (24-hour urine, spot urine, overnight urine, dietary methods).
**Key Results:** Three systematic reviews were included (two with meta-analyses, one without), comprising 39 unique observational studies (35 cross-sectional, 4 longitudinal) and 15 RCTs. One systematic review was rated as high risk of bias (Kang et al., 2016); the other two were low risk. The re-meta-analysis of 28 cross-sectional studies (38 effect sizes) showed that BMI was significantly higher in the highest versus lowest sodium intake group (mean difference = 1.52 kg/m²; 95% CI, 1.24–1.80; P < 0.001; I² = 97%). Subgroup analysis by assessment method revealed: 24-hour urine (mean difference = 2.27 kg/m²; 95% CI, 1.59–2.51; P < 0.001; I² = 77%), spot urine (mean difference = 1.34 kg/m²; 95% CI, 1.13–1.55; P < 0.001; I² = 95%), overnight urine (mean difference = 1.00 kg/m²; 95% CI, 0.48–1.52; P < 0.001), and dietary methods (mean difference = 0.85 kg/m²; 95% CI, 0.18–1.51; P < 0.05; I² = 95%). Higher sodium intake was significantly associated with increased risk of overweight/obesity (OR, 1.75; 95% CI, 1.40–2.18; P < 0.001; I² = 72%), with the strongest effect in 24-hour urine studies (OR, 2.44; 95% CI, 1.67–3.56; P < 0.001; I² = 59%). Body weight was significantly greater in the high-sodium group (mean difference = 8.28 kg; 95% CI, 6.69–9.86; P < 0.001; I² = 66%), again strongest in 24-hour urine studies (mean difference = 9.00 kg; 95% CI, 7.53–10.48; P < 0.001; I² = 46%). Waist circumference was significantly greater with higher sodium intake (mean difference = 4.99 cm; 95% CI, 4.00–5.99; P < 0.001; I² = 89%), with 24-hour urine studies showing the largest effect (mean difference = 6.34 cm; 95% CI, 5.27–7.42; P < 0.001; I² = 0%). Higher sodium intake was significantly associated with increased risk of abdominal obesity (OR, 2.05; 95% CI, 1.72–2.44; P < 0.001; I² = 67%). In 15 RCTs, reduced-sodium diets showed non-significant effects on body weight compared to usual or control diets. Four longitudinal studies showed no change in body weight with higher sodium intake, though one study reported increased body fat and decreased fat-free mass per 100 mmol/d sodium increase.
**Clinical Implications:** This review demonstrates a consistent positive cross-sectional association between dietary sodium intake and multiple obesity outcomes, with the strongest associations observed when sodium intake was measured using 24-hour urine collection. Less accurate methods (spot urine, overnight urine, dietary recall) systematically underestimate the sodium-obesity association, which may explain inconsistencies in the literature. These findings suggest that public health recommendations to reduce sodium intake may have additional benefits for obesity prevention beyond their well-established cardiovascular benefits. However, the lack of significant findings from RCTs and longitudinal studies limits causal inference. The authors call for more high-quality prospective cohort studies and RCTs using 24-hour urine collection to establish whether the relationship is causal. Potential biological mechanisms include salt-induced adipogenesis and lipogenesis, increased endogenous fructose production, elevated fasting ghrelin levels stimulating appetite, and reduced diet-induced thermogenesis.