The impact of sodium and fructose on blood pressure and inflammation

Date
2024
Journal Title
Journal ISSN
Volume Title
Publisher
University of Delaware
Abstract
Increased dietary sodium is associated with hypertension. Yet, many young healthy adults have “sodium-resistant” blood pressure (BP), meaning that increased dietary sodium is not associated with increased BP. This is because normal functioning kidneys can excrete excess dietary sodium, preventing a sodium-induced expansion of the extracellular fluid volume (ECV) and consequent increase in BP. However, rodent studies demonstrate that increased dietary fructose impairs renal sodium handling, which is associated with increased BP and hypertension risk. Moreover, both dietary salt and fructose have been shown to be pro-inflammatory. ☐ The immune mechanisms underlying the pro-inflammatory effects of sodium and fructose are poorly understood. The impact of the Western diet on the peripheral blood mononuclear cells (PBMCs) has garnered attention due to associations with vascular-related diseases. There is evidence demonstrating that increased dietary sodium induces pathogenic subtypes of PBMCs, resulting in an exacerbated production of proinflammatory interleukins. In rodents fed increased sodium, T-cell infiltration in the kidneys was increased in conjunction with higher levels of reactive oxygen species (ROS). Moreover, increased fructose consumption is linked to elevated de novo lipogenesis and plasma triglyceride levels, both contributing to increased oxidative stress. ☐ The combined consumption of increased dietary sodium and fructose, prevalent in typical Western diets, may exacerbate hypertension and inflammation more than sodium loading alone. While numerous rodent studies support these associations, few have sought to validate them in humans. This research gap is significant, given the prevalence of Western dietary patterns and their link to cardiovascular health. Here we hypothesize that 1) the combination of increased dietary fructose and sodium will increase BP in normotensive adults by preventing the kidneys from properly excreting excess sodium and 2) the combination of increased dietary fructose and sodium will induce increased ROS and inflammation resulting in an impairment in endothelium function when compared to an increased sodium alone. To investigate our hypotheses, we gathered data from 36 participants using a randomized double-blind clinical trial. Our study demonstrates that within a single week of consuming increased dietary fructose in conjunction with high sodium, healthy normotensive adults display a modest reduction in urinary sodium excretion and an increase in BP. Additionally, we find that the combination of increased fructose and sodium induces a greater pro-inflammatory (e.g., TNF alpha and IL-6) and oxidative stress (e.g., intracellular ROS) response when compared to sodium loading alone. Overall, these data demonstrate that increased sodium and fructose lead to alterations in renal function while promoting inflammation in young healthy adults.
Description
Keywords
Blood pressure, Fructose, Inflammation, Salt, Hypertension, Extracellular fluid volume
Citation