Salt intake: potential deleterious effects excluding blood pressure.
Increasing evidence from animal, epidemiological, intervention studies and treatment trials all clearly point to the important role that salt intake plays in determining blood pressure (BP). Of more current interest is whether salt may have other deleterious effects independent of its role in high BP. For instance, salt intake plays an important role in left ventricular hypertrophy independent of its effect on BP. Experimental evidence and some epidemiological evidence also suggest that salt intake may have an adverse effect on stroke mortality which may be independent of its effect on BP. In animal models of renal failure, dietary salt restriction has been found to slow the progression of the renal impairment, but no studies as yet have been reported in humans. Salt intake has also been associated with asthma, stomach and nasopharyngeal cancer. Increasing salt intake produces changes in the chemical composition of urine, particularly an increase in calcium excretion which will predispose to kidney stone formation and has also been shown to increase hydroxyproline excretion indicating increased bone resorption. It is likely that a high salt intake may be one of several factors aggravating osteoporosis. This may be particularly relevant in patients with essential hypertension who already have an increased urinary calcium excretion and may in the long term be at greater risk of osteoporosis. Restriction of salt intake reduces urinary calcium excretion and, perhaps, like thiazide diuretics may be beneficial in the long-term prevention of bone demineralisation.
D000818:Animals; D001249:Asthma / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000401:mortality; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D007668:Kidney / Q000187:drug effects; D007669:Kidney Calculi / Q000209:etiology; D010024:Osteoporosis / Q000209:etiology; D012965:Sodium Chloride / Q000009:adverse effects*; D016019:Survival Analysis; D014652:Vascular Diseases / Q000209:etiology
D012965:Sodium Chloride