About this Research Topic
Hypertension exists in about a third of the population and poses major risks for stroke, cardiovascular disease, kidney and liver abnormalities, dementia, and death. While some progress has been made in reducing and controlling hypertension, health experts have been disappointed with overall progress. Behavioral interventions such as reducing salt intake appear to be a simple and straightforward way to decrease or prevent hypertension. Indeed, it is believed that even a modest reduction in salt intake will dramatically reduce the percentage of the general population with hypertension and the enormous health-related costs. Accordingly, the public constantly receives recommendations from health organizations such as the American Heart Association and the US Department of Health and Human Services to reduce salt consumption. These efforts have met with little success, even though most people consume far more salt than the recommended amounts.
The association between increased salt consumption and elevated blood pressure – termed salt-sensitivity or salt-sensitive hypertension – has been studied extensively for decades and yet continues to be debated vigorously. The controversy and confusion stem largely from conflicting results on the effects of low- or high-salt consumption and on the large individual variability in the blood-pressure response to changes in dietary salt. The reality is that salt sensitivity is multifactorial, with genetic and non-genetic causes. In salt-sensitive hypertensives, the kidney fails to respond appropriately in adjusting sodium excretion. Thus, mutations in renal sodium transporters have been linked to salt sensitivity. It also has been shown that salt intake affects the renin-angiotensin-aldosterone (RAAS) and endothelin (ET) systems, with significant consequences for sodium excretion. Moreover, interesting interactions between the RAAS, salt intake, and insulin have been suggested. Some studies have linked salt-sensitivity with genetic differences, with blacks having a higher prevalence than whites. Other studies suggest that age and/or gender may contribute to salt sensitive hypertension, as evidenced by the increased rate of hypertension in postmenopausal women. In this regard, the RAAS and ET systems have been implicated in sex differences associated with blood pressure, and there are major differences in renal function and disease between males and females. Finally, epigenetic effects are receiving increasing attention, as consuming excess salt during pregnancy not only can affect fetal development, but also has been linked to hypertension in offspring.
Given the conflicting findings about the role of dietary salt in hypertension and the myriad factors that may modulate the contribution of salt to blood pressure control, it is perhaps not surprising that recommendations reflecting a “one-size-fits-all” policy of reducing salt intake to reduce hypertension are viewed with skepticism. Better understanding and more accurate information about dietary salt, blood pressure control, and health in general will be greatly beneficial for the general public. At the same time, an integrated series of scientific papers will be instructive for those working on elements of this subject. Therefore, a Research Topic on salt sensitivity focusing on the issues described above would add to the scientific literature and increase understanding by scientists, physicians, and the lay public.
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