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Experimental epidemiology of chronic sodium chloride toxicity and the protective effect of potassium chloride

1958; Elsevier BV; Volume: 25; Issue: 5 Linguagem: Inglês

10.1016/0002-9343(58)90009-3

1555-7162

George R. Meneely, Con O.T. Ball,

Sodium Intake and Health

T HE origin of the human custom of adding sodium chloride to food is still hidden in pre-history. Throughout the historical period of man, salt is found in use in almost all civilizations. Concurrently there have always been speculations that extra salt was not needed, even some suspicions it might be harmful. The rich and varied literature on salt and humankind has been scanned by others and by us [l-lo]. Only in the present century did evidence begin to accumulate for a relation between salt and hypertension in man [II--781. Research by Selye [79], Sapirstein [ZO], Fukuda [27] and others showed by animal experiment the hypertensigenic action of sodium chloride. Thompson [22] has complained of a lack of candor among scientists to tell what really was the inception of some worthwhile line of research, suggesting instead of the portentous “In view of the recent evidence concerning . . . ” the more factual “ . . . we happened to be fooling around one day when . . . ” Real efforts at candor, however, are likely to be awkward or embarrassing or both, and suffer from the added demerit that an excess of candor usually does, of leaning backward from the facts as far as specious reason may lean into them. At the outset of these studies, early in 1951, Robert G. Tucker had come to join William J. Darby and us for the purpose of engaging in medical research. For reasons probably not even known to himself, one of us developed at that time a curiosity about the long term effect of added sodium chloride in the diet. A search of the literature revealed an immense number of publications pertaining to salt and concomitant variables, very little about salt alone. The fine work of Sapirstein [Zo] had not yet come to our attention and we failed also to find the important paper of Fukuda with Selye [27]. We designed an experiment intended to test increased sodium chloride as the sole variable in a purified diet. The rats immediately added a variable of their own by altering their fluid intake according to the salt intake, a phenomenon reported in Pliny’s Natural History somewhat earlier. We had in mind the possibility that excess salt might manifest itself as a source of degenerative disease, nature unspecified. Our minds were open, even perhaps blank. It is the purpose of this article to review in one place what we have found so far, most of which we have reported piecemeal elsewhere [Z&34]. Before doing so it is appropriate to relate the participation of those who worked in these studies. Stewart Auerbach joined the investigation and throughout the early years dealt with the microscopical-anatomical phases of the study. Later, Ernest Goodpasture devoted a period of intensive study to the high salt eating animals of experiment I. His report has been drawn upon for some comments later in this paper but the main body of his findings are not yet published. Ross C. Kory developed the technic for electrocardiography employed, established criteria for interpretation of the rat electrocardiograms and studied the entire colony. Further electrocardiographic investigations were conducted by Thomas M. Blake and he participated in the pathological studies. When Robert Tucker moved on from the group, Janet Lemley-Stone assumed general charge of the animal colony and the biochemical and radioisotope phases of the investigation.