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Review
. 2021 Sep 12;13(9):3177.
doi: 10.3390/nu13093177.

Sodium Intake as a Cardiovascular Risk Factor: A Narrative Review

David A Jaques  1 , Gregoire Wuerzner  2 , Belen Ponte  1
Affiliations
Review

Sodium Intake as a Cardiovascular Risk Factor: A Narrative Review

David A Jaques et al. Nutrients. .

Abstract

While sodium is essential for human homeostasis, current salt consumption far exceeds physiological needs. Strong evidence suggests a direct causal relationship between sodium intake and blood pressure (BP) and a modest reduction in salt consumption is associated with a meaningful reduction in BP in hypertensive as well as normotensive individuals. Moreover, while long-term randomized controlled trials are still lacking, it is reasonable to assume a direct relationship between sodium intake and cardiovascular outcomes. However, a consensus has yet to be reached on the effectiveness, safety and feasibility of sodium intake reduction on an individual level. Beyond indirect BP-mediated effects, detrimental consequences of high sodium intake are manifold and pathways involving vascular damage, oxidative stress, hormonal alterations, the immune system and the gut microbiome have been described. Globally, while individual response to salt intake is variable, sodium should be perceived as a cardiovascular risk factor when consumed in excess. Reduction of sodium intake on a population level thus presents a potential strategy to reduce the burden of cardiovascular disease worldwide. In this review, we provide an update on the consequences of salt intake on human health, focusing on BP and cardiovascular outcomes as well as underlying pathophysiological hypotheses.

Keywords: blood pressure; cardiovascular; hypertension; salt; sodium.

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Conflict of interest statement

Authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Pathophysiological pathways linking sodium intake to target organ damage independently of BP-mediated effects.
Figure 2
Figure 2
Schematic representation of potential pathways involved in sodium-induced cellular injury. SA-beta-gal, senescence-associated β-galactosidase; AIF, apoptosis-induced factor; Nox, NADPH oxidase; ASK1, apoptosis signal-regulating kinase 1.
Figure 3
Figure 3
Schematic representation of potential pathways involved in sodium-induced vascular alterations. VSM, vascular smooth muscle; NOS, NO synthase; NO, nitric oxide; cGMP, cyclic GMP; 20-HETE, 20-hydroxyeicosatetraenoic acid.
See this image and copyright information in PMC

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