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Weight-reducing diets and sodium intake.
Author(s) -
Pasquale Strazzullo
Publication year - 1986
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.8.4.357
Subject(s) - sodium , food science , high sodium , medicine , fluid intake , dietary sodium , zoology , chemistry , endocrinology , biology , organic chemistry
To THE EDITOR: I have the following comments to the recent article by Fagerberg et al. In this stimulating article, the authors reported the effects of caloric restriction with or without concomitant reduction of sodium intake on the blood pressure (BP) and sympathetic nervous system activity of obese hypertensive men (see also Reference 2). Based on their results, Fagerberg et al. concluded that hemodynamic adjustment and BP reduction were associated with weight loss only when dietary sodium was restricted, although a decrease in sympathetic tone seemed to occur both in men on the low energy-unchanged sodium regimen (Group I) and in those on the low energy-low sodium diet (Group II). In this regard, I should like to observe that there was actually some BP reduction not only in Group II but also in Group I: average BP fall in Group I was 4.7/5.0 mm Hg in the first report (n = 13)' and 7.5/6.1 mm Hg in the second report (n = 10). Despite the small sample size, this result cannot be overlooked, at least from an epidemiological point of view. My second observation is that, judging from the reduction in urinary norepinephrine (NE) excretion, a more marked decrease in sympathetic discharge seemed to occur in the low energy-unchanged sodium group (Group I), a finding also supported by the concomitant significant decrease in plasma renin activity in this group. Based on the findings of the NE infusion test, the authors concluded that this effect of the low energy diet was counteracted by an increase in the vascular sensitivity to NE, probably due to up-regulation of adrenergic receptors, whereas such unfavorable adjustment would have been prevented in Group II by the concomitant reduction of sodium intake. Accordingly, in their interpretation, BP fell only (or to a greater extent) in Group II. It has been repeatedly suggested that sodium restriction per se may enhance the sympathetic discharge"; if this is true, then the depressing effect of low energy intake on sympathetic tone might have been balanced at least partly in Group II by the contrasting effect of reduced sodium intake. Thus, I wonder whether the unchanged reactivity to exogenous NE in Group II might simply reflect a lesser reduction in sympathetic discharge compared with that in Group I. If so, other explanations must be sought for the greater BP fall in this group. (In fact no statistical relationship was found between BP changes and changes in reactivity to NE infusion.) An alternative interpretation of the data is that a volume factor related to sodium restriction adds to the effect of caloric restriction alone in Group II, resulting in a more pronounced BP fall in this group. I believe that the lack of a demonstrable difference in blood volume in the two groups does not rule out this possibility. This view is supported by the finding that the BP reduction was traced to reduced cardiac output (and cardiac index) in Group II, although total peripheral resistance was unchanged (a finding difficult to reconcile with the interpretation proposed by the authors). What also puzzles me in this context is the role of the carbohydrate (CHO) content of weight-reducing diets with respect to their hemodynamic effects. In another recent article the authors reported on the lack of effect on BP and sympathetic nervous system activity of a diet identical to the one adopted in this study (i.e., >50% of total intake supplied as carbohydrates). They found instead that an isocaloric diet with much lower CHO content (CHO < 30% of total intake) reduced BP through a reduction of sympathetic tone (and with no need for sodium restriction). Thus, they concluded that a relatively high CHO content prevented the BP lowering effect of caloric restriction, while reduction of CHO to less than 30% of total intake significantly reduced sympathetic tone and BP. I wonder why in this later study they used a diet with 50 to 60% of total intake from carbohydrates, which was likely to be ineffective according to their own previous experience It seems to me that they could have obtained more definite information had they tested the additive effect of sodium restriction with respect to a low calorie and low CHO diet.

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