Abstract

Beyond the physiological effects of sodium and potassium strong evidence from animal, clinical and epidemiological studies, has implicated excess dietary sodium and low potassium intake as major factors associated with the development of hypertension and increase in stroke risk. Daily salt intake of 5–6 g 85–100 mmol was recommended for the general population i.e. 2.0–2.4 g Na along with K intake to at least 90 mmol d 3.51 g perd. Randomized trials demonstrate that salt reduction and potassium increase in diet lowers blood pressure and reduces the risk of brain damage and cardiovascular disease. Population studies showed that 15 percent reduction of salt intake from 9.5 g/day was associated with a 40 percent reduction of stroke and CHD mortality. Potassium lowers BP via multiple mechanisms, by acting directly on the vasculature and by triggering a signalling cascade mediated by endothelium and also reduces salt-sensitivity. A meta-analysis of 21 RCTs reported that increasing potassium intake lowers BP 3.5/2.0 mm Hg and the risk of stroke. Eating more than 11 g of salt /day was associated with 2.5 times more likely to have a stroke than those who got less than 4.5 g /day. Switching from regular salt to a salt substitute reduced the risk for stroke, major CV events and death in a large trial of adults in rural China with a history of stroke or high risk for stroke. High salt intake reduces resting cerebral blood flow and induces endothelial dysfunction in mice and impairs vasodilatory responses of cerebral vessels. Gut-brain relation links dietary salt to cognitive impairment though a gut-initiated adaptative immune response damaging brain function via increase in circulating IL-17. A high potassium diet reduces cerebral infact size and improves vascular function independently of BP changes. Thus high salt and low potassium intake interfere in multtiple brain vascular strutural complex processes including fluid homeostasis and inflammatory mechanisms, immune responses and gut-microbiome-brain axis.

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