Salt Appetite, Salt Intake, and Hypertension: A Deviation of Perspective

SALT APPETITE, SALT INTAKE, AND HYPERTENSION: A DEVIATION OF PERSPECTIVE A. R. MICHELL* As a general thing, the amount of sali desired is exactly refated to the amount required. [1] If equal evidence had related salt to a similarlyfatal butfar less common disease, cancer, it would have evoked intense campaigns against it longago. [2] Hypertension affects 23,000,000 people in America alone, and, left untreated, it would cost many of them a decade oflife apart from other unpleasant consequences. Since the suggestion ofAmbard and Beaujard in 1904 [3], reinforced by Allen in 1925 [4, p. 88] and subsequently by Dahl [2], suspicion has grown that salt intake has at least some adverse effect on the development of a substantial number of these cases. Even so guarded a statement concerns the life and livelihood of millions. Others state the position more forcibly: "The existence of a relationship between sodium intake and hypertension is unquestionable. . . . What is in doubt is the mechanism ..." [5]. Strangely, what is seldom in question is the intake itself, with even nutritionists being "remarkably uninterested in salt" [2]. Yet, with a daily sodium requirement considerably below 10 meq [6, 7], Western man consumes 100-200 meq. Why? Nor is it casual consumption. Faced with the difficulty of persuading hypertensive patients to restrict their consumption, Dahl asks, "Why is it so difficult to maintain a low sodium intake?" [2]. The problem was crystallised by Von Bunge [8] nearly a century ago (he also advocated rice diets for renal disease 50 years ahead of Kemp- *Wellcome Research Fellow, Department of Physiology, Royal Veterinary College, London , NWl OTU, United Kingdom. Development of these ideas was originally encouraged by Professor Carl Pfaffmann of Rockefeller University, and the related studies were made possible, at various times, by support from the Harkness Fellowships (Commonwealth Fund of New York), the Beit Memorial Trust, the Wellcome Trust, the Medical Research Council, and by facilities generously provided by Professor F. R. Bell. Finally, it is a pleasure to acknowledge the extremely helpful influence of a year spent with Professors Adrian Katz and Marshall Lindheimer at the University of Chicago.© 1978 by The University of Chicago. 003 1-5982/78/2 103-0063$01.00 Perspectives in Biology and Medicine ¦ Spring 1978 \ 335 ner): "The a priori necessity for a constant supply of water is thus evident . But it is otherwise with salt . . . The constant supply ofsalt in considerable quantities is not a necessity for the adult." Sixty-seven years later Kaunitz [9] could do little more than endorse this conclusion: ". . . Normal metabolic processes are possible without the adding of salt to natural foodstuffs. Why then do we eat salt?" One might almost believe that, despite its physiological and clinical importance, the question had not been studied: "Maintenance of normal extracellular sodium requires not only the control of sodium excretion but also the control of sodium intake. Unfortunately we know very little about this" [10, p. 481]. In fact, a considerable amount is known [11, sec. 6, vol. 1, p. 433]; but while clinicians have grappled with excess salt consumption, the main research on salt appetite has sought to relate it to sodium deficiency. Why? The answer is rooted in the concept of homeostasis. Cannon himself wrote: "If there is need for salt in the body . . . the phenomenon of salt appetite appears . . ." [12, p. 91], yet Carlson had suggested much earlier that "need" was not implicit in such behavior [13, p. 15]. Subsequently, however, Richter [14] demonstrated the enhanced salt intake provoked by adrenalectomy and its importance in survival, and most ensuing work essentially confined itself to extending or explaining this response to sodium deficiency [15]. Indeed, sodium appetite which could not be interpreted within a simple homeostatic deficit-intake loop was often relegated to another category of "need-free" intake [16, 17]; sometimes the loop approached a circular argument: "I eat therefore I need." The purpose of this article is to suggest that it is exactly the need-free salt appetite which demands an explanation and to propose a hypothesis which encompasses it. First, it is necessary to see if there is anything distinctive about salt appetite among those who become hypertensive and to examine whether...