Hypomagnesemia: exploring its multifaceted health impacts and associations with blood pressure regulation and metabolic syndrome

Abstract

This article provides a comprehensive and in-depth exploration of the multifaceted effects of Hypomagnesemia on human health, with a specific focus on its intricate associations with mechanisms regulating blood pressure and metabolic syndrome. Firstly, the fundamental concept of hypomagnesemia is elucidated, followed by a detailed analysis of its prevalence, risk factors, and Magnesium Deficiency Score. Furthermore, this article delves into the intricate relationship between hypomagnesemia and blood pressure regulation, encompassing its impact on endothelial function, vascular calcification, oxidative stress and inflammatory response, sympathetic nervous system activity as well as the renin-angiotensin-aldosterone system (RAAS). Additionally, it explores the correlation between hypomagnesemia and insulin resistance, metabolic syndrome along with other health issues. Notably noteworthy is that this paper also places special emphasis on exploring the potential role of hypomagnesemia in specific diseases such as renal hypertension and preeclampsia while providing novel insights for their prevention and treatment. Finally, this article summarizes the diverse effects of hypomagnesemia on health while anticipating future research directions. Future studies should further investigate the pathogenesis underlying hypomagnesemia while optimizing assessment methods for magnesium deficiency to develop targeted intervention strategies aimed at offering improved treatment options alongside preventive measures for patients.

Keywords: Health; Hypertension; Hypomagnesemia; Metabolic syndrome.

Fig. 1

Magnesium deficiency weakens calcium antagonism, enhances NADPH oxidase activity, leading to increased oxidative stress [22], inhibits eNOS activity, and reduces NO production, causing endothelial dysfunction [49]. Simultaneously, it diminishes the inhibition of calcium channels, increases calcium influx, and vasoconstriction of vascular smooth muscle, and exacerbates vascular tension by reducing Na⁺-K⁺-ATPase activity [57]. Furthermore, low magnesium activates the RAAS, elevating Ang II levels, which directly contracts blood vessels and promotes sodium and water retention [113]. Ang II further aggravates oxidative stress, creating a vicious cycle. The concomitant metabolic disorders also contribute to elevated blood pressure