Sodium in relation with nonalcoholic fatty liver disease: A systematic review and meta‐analysis of observational studies

Abstract

Findings on the association of sodium with nonalcoholic fatty liver disease (NAFLD) are conflicting. The present systematic review and meta‐analysis study aimed to assess the association between salt or sodium intake or serum sodium levels and NAFLD risk. Relevant articles were identified by searching PubMed, Web of Knowledge, Scopus, Proquest, and Embase databases through May 1, 2021, without language restriction. The pooled odds ratio (OR) and 95% confidence interval (CI) were estimated using Der‐Simonian and Laird method and random‐effects meta‐analysis. The certainty of the evidence was rated using the GRADE method. Out of 6470 documents, 7 epidemiological/observational (1 cohort, 1 case–control, and 5 cross‐sectional) studies on the relationship between dietary salt/sodium intakes and NAFLD risk met our inclusion criteria. The meta‐analysis of all studies showed a significant positive association between the highest salt/sodium intake and NALFD risk (OR = 1.60, 95% CI: 1.19–2.15) with a meaningful heterogeneity among studies (I2 = 96.70%, p‐value <.001). The NAFLD risk was greater in the studies with higher quality (OR = 1.81, 95% CI: 1.24–2.65) or using the equation‐based methods for NAFLD ascertainment (OR = 2.02, 95% CI: 1.29–3.17) or urinary sodium collection as a sodium intake assessment (OR = 2.48, 95% CI: 1.52–4.06). The overall certainty of the evidence was very low. In conclusion, high sodium intake seems to be related to increased NAFLD risk. Further well‐designed studies are needed to clarify this association and shed light on the underlying mechanisms.

Dietary Sodium and Nonalcoholic Fatty Liver Disease: A Systematic Review

“…During the preparation of this review, Shojaei-Zarghani et al [ 5 ] published a systematic review with a meta-analysis evaluating the effect of sodium on NAFLD prevalence that mostly agreed with our thoughts. The main results of the study by Shojaei-Zarghani et al [ 5 ] were: higher risk of developing NAFLD in high- sodium intake compared to low intake (OR = 1.6, 95% CI: 1.19–2.15); surveys using predictive formulas (FLI) to assess NAFLD showed a higher effect size (OR = 2.02, 95% CI: 1.29–3.17) than those assessing disease by FibroScan or ultrasonography (OR = 1.81, 95% CI: 1.24–2.65); studies with sodium excretion (24 h and <24 h) showed a higher risk of developing NAFLD (OR = 2.48, 95% CI: 1.52–4.06, I2 = 96.00%) compared with dietary assessments of sodium (OR = 1.23, 95% CI: 1.15–1.32). It is important to point out that these data refer to the uncorrected risk ratio and that the assessment of the certainty of the evidence (assessed by the GRADE method) was considered very low, so these data should be evaluated with great caution.…”

“…There are few human and animal studies dealing with the influence of sodium consumption on the development of NAFLD. Shojaei-Zarghani et al [ 5 ], in a systematic review and meta-analysis of observational studies, found that people with a high-sodium intake have a 60% greater risk of developing NAFLD compared to those with low consumption. Xu and Mao [ 6 ] reviewed the potential mechanisms for this relationship: elevation of caloric consumption, hyperosmolarity induced by salt, insulin resistance, endogenous fructose synthesis, and dysfunction of the RAAS.…”

The effect of DASH diet on glycemic response, meta-inflammation and serum LPS in obese patients with NAFLD: a double-blind controlled randomized clinical trial

“…Previous studies have also demonstrated that high sodium intake is associated with the risk of NAFLD [ 60 ] . Uetake et al [ 61 ].…”

Alleviation of Metabolic Disturbance by Substituting Kanjang High in Bacillus for Salt through Modulation of Gut Microbiota in Estrogen-Deficient Rats

“…Furthermore, estrogen deficiency induces metabolic disturbance in energy, glucose, lipid, and bone metabolism [21]. A high salt intake exacerbates metabolic dysfunction [13,31]. Although their relationship remains controversial, a high salt intake induces hypertension in salt-sensitive persons.…”

“…Estrogen or phytoestrogen intervention prevented the estrogen-deficient-related symptoms [21,22,29]. On the other hand, a high sodium intake increases the salt sensitivity to hypertension, exacerbating metabolic syndrome, even though women are salt insensitive before menopause [31]. Furthermore, the salt sensitivity to hypertension is inversely correlated with the circulating ovarian hormones [37].…”