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the claim
The heart disease risk arising from dietary salt is mediated entirely by blood pressure.
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REFUTED
the evidence says no
refutedsupported
the weight of evidence
0 sources for · 1 against

A peer-reviewed meta-analysis on dietary salt and vascular function refutes the claim that heart disease risk is mediated entirely by blood pressure.

Evidence against · 1
2025 · cited by 0
Abstract Introduction Excessive dietary salt intake has been a serious cardiovascular risk factor for years. Approximately 1.7 million cardiovascular deaths are directly related to a high-salt diet each year. Excessive sodium intake is most often associated with cardiovascular risk through its effect on blood pressure. Nevertheless, sodium directly damages the vascular endothelium and participates in the pathogenesis of atherosclerotic diseases, also in people with normal blood pressure [1-3]. Aim of the study: The aim of the study was to assess the effect of a low- and high-salt diet and urinary sodium excretion on vascular function parameters: carotid IMT (cIMT), carotid to femoral pulse wave velocity (cf-PWV) and Augmentation Index (AIx). Material and methods We conducted a comprehensive search of PubMed, Scopus, and Web of Science from their creation until January 2025. The search approach incorporated a blend of keywords and MeSH terms: "salt intake," "sodium excretion," "carotid intima-media thickness," "pulse wave velocity," "augmentation index," "cIMT," "cf-PWV," and "AIx." Furthermore, we conducted a thorough review of the reference lists of chosen papers to uncover additional pertinent studies. We performed statistical analyses using Review Manager (RevMan) version 5.4 and Stata version 16.0. Results The meta-analysis of cIMT included 2 studies that analyzed low and high salt intake (n=2013 participants) and 5 studies that compared urinary sodium excretion (n=1984 participants) and showed no significant association between the assessed parameters (WMD = -2.24; 95% CI: -6.66, 2.18 and WMD = -0.00; 95% CI: -0.02, 0.02, respectively) (Fig. 1A.). Similarly, in the case of cf-PWV, no significant effect of dietary salt was demonstrated, either as assessed by comparison of low and high dietary salt intake (17 studies with 8276 participants, WMD = -0.12; 95% CI: -0.28, 0.04). Higher urinary sodium excretion was associated with better cf-PWV (4 studies with 2431 participants, WMD = 1.01; 95% CI: 0.28, 1.74) (Fig. 1B.). Furthermore, no significant effect of dietary salt on AIx was demonstrated, either as assessed by salt intake (13 studies with 2078 participants, WMD = -1.84; 95% CI: -4.95, 1.27) or urinary sodium excretion (in studies with 549 participants, WMD = -1.20; 95% CI: -6.38, 3.98) (Fig. 1C.). Conclusions The meta-analysis performed did not show the influence of excessive dietary salt intake, assessed as low versus high intake or 24-hour urinary sodium excretion, on arterial function parameters such as cIMT, cf-PWV and AIx. Analysis of the relationship between dietary salt intake and arterial function requires further studies, preferably with a longer intervention period and a more accurate assessment of the actual amount of salt intake.Figure 1 A-C
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rails:sufficiency:refuted:single_source:for=0+0p:against=1+0p | v55:sufficiency

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  1. Dietary salt on vascular function - a meta-analysispeer-reviewedno side taken
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first checked01 Aug 2026
judged → INSUFFICIENT EVIDENCE · 001 Aug 2026
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