The toxicity of salt.
The subject of sodium toxicity has been controversial for a long time. There is no question that the element can be noxious when consumed acutely in large quantities and there is little doubt as to cause and effect Conversely the consequences of mederate chronic sodium consumption are much harder to document. The effects are insidious and are subject to modification by a variety of environmental influences such as dietary potassium. In addition most studies of chronic sodium excess have dealt with elusive subject of "essential" hypertension. Interpretations of data have been very difficult, and conflicting reports have occurred. Nevertheless epidemiological, clinical, and animal studies show that chronic excess sodium ingestion acting upon a substrate of genetic susceptibility, is an important etiologic factor in essential hypertension and the expression of its sequelae. Positive correlations have also have been obtained between dietary salt and the incidence of stroke and gastric cancer. Dietary potassium appears to confer some degree of protection from the toxic properties of sodium through some unknown mechanism. Available evidence indicates that a  suitable intake of salt for man might be approximately 3.5 g/day and probably less. Salt consumption in most developed countries ranges between 8 to 40 g/day, and modern methods of food processing and preparation deplete the protective potassium. The incidences of hypertension in these countries range between 15 to 40% of their populations, and it exacts a dreadful toll. Recognition of the toxic properties of sodium and knowledge of the mechanisms involved in its toxicity offer great possibilities in the area of preventive medicine It may be possible by the sorting out of hypertension-prone subjects and dietary intervention to prevent or minimize the development of hypertension in susceptible individuals. This says nothing of other aspects of sodium toxicity, of which we are largely ignorant.
D000818:Animals; D001693:Biological Transport, Active; D001808:Blood Vessels / Q000503:physiopathology; D002395:Catecholamines / Q000502:physiology; D004032:Diet; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000139:chemically induced / Q000453:epidemiology / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism / Q000502:physiology; D012964:Sodium / Q000378:metabolism / Q000502:physiology; D012965:Sodium Chloride / Q000009:adverse effects*; D013649:Taste; D014883:Water-Electrolyte Imbalance / Q000139:chemically induced
D002395:Catecholamines; D012965:Sodium Chloride; D012964:Sodium; D011188:Potassium