Dietary Salt

Note: The following abstracts are written in extremely technical language and include technical research and case studies. References are provided. For 'user-friendly' informative reading, check out the health topics presented by Dr. Martin and Dr. Davenport. Feel free to contact us for more information or if you have any questions.

Salt skirmishes

Dietary salt intake continues to occupy believers and nonbelievers alike. Fortunately a large quantity of excellent data have accrued in the last decade, so that the quality of the ammunition has undoubtedly improved. The numbers of clinical intervention trails has practically doubled and several meta-analyses are available. Interestingly, the results from the advocates for strict salt restriction and those from authors with more liberal views are fairly consistent; namely, salt reduction would decrease blood pressure in normotensive persons slightly, and in the hypertensive patients by about 5 mm Hg. Recently, almost an entire issue of a prestigious medical journal was devoted to salt and hypertension-related issues. The editors made their point of view clear by interspersing various articles with commentaries of their own. One of the topics was related to the 'right' of authors to restrict access to data accrued through public funding with the argument that only they have the wisdom to analyze and interpret the data properly. This was the case with intersalt. Through litigation, some of the Intersalt data were made available to persons associated with the salt industry. Their interpretation and the counter-editorial make for interesting reading. A public-interest group termed Consensus Action on Salt and Hypertension has been founded, to admonish the living to eat less salt. I recommend shortening the advice to: 'eat less'.

Kidney-Blood-Press-Res. 1997; 20(2): 71-3

Dietary salt and hypertension

Sodium restriction is the most commonly used lifestyle modification for control of hypertension. Nevertheless, there is no consensus on the relative importance of salt in the development of hypertension, nor is the physiological mechanism(s) responsible for salt-induced elevations of blood pressure clearly understood. This review focuses on new research developments in this area.

Hatton-DC; McCarron-DA
Curr-Opin-Nephrol-Hypertens. 1996 Mar; 5(2): 166-9

Role of dietary salt in hypertension

Hypertension is the most common chronic disease in the United States and, untreated, results in disability or death due to stroke, heart failure or kidney failure. Fortunately the results of hypertension can be avoided to a large extent by proper treatment. One treatment which is effective in some cases is the restriction of dietary NaCl intake. This review considers the role of dietary NaCl in the genesis, therapy and prevention of hypertension. Most people can eat as much NaCl as they like; they have good kidneys which, within about 24 hours, excrete the NaCl as fast as it is taken in and nothing happens to blood pressure. A few, especially those with kidney disease, do not excrete it as fast as it is taken in and blood pressure rises. They are "salt sensitive". Once hypertension is established, the proportion who are "NaCl sensitive" is much higher. About 60% of people with hypertension respond to a high NaCl intake with a rise in pressure and to NaCl restriction with a fall in pressure and reduction in the need for antihypertensive medication. These are the same people that respond to diuretics with a fall in blood pressure. Many are black and elderly and have low plasma renin activity (low-renin hypertension) but some have normal or high plasma renin activity (normal or high-renin hypertension). Evidence suggests that very early they have a subtle kidney defect which causes them to excrete NaCl and water more slowly, e.g., even before they become hypertensive, black and elderly subjects excrete intravenously administered NaCl more slowly than white and young subjects. How does NaCl retention raise blood pressure? One possibility is that the NaCl retention causes water retention which releases a digitalis-like substance that increases the contractile activity of heart and blood vessels. Another is that the sodium itself penetrates the vascular smooth muscle cell, causing it to contract. "Salt sensitive" hypertension also responds to increased potassium and calcium intakes, perhaps in part because they increase NaCl urinary excretion.

Haddy-FJ; Pamnani-MB
J-Am-Coll-Nutr. 1995 Oct; 14(5): 428-38

Calcium supplementation attenuates an enhanced platelet function in salt-loaded mildly hypertensive patients

We designed this study to evaluate the effect of low versus high calcium intake on platelet function in salt-loaded patients with mild hypertension. After a 7-day period of dietary salt restriction, 19 patients were placed on a high salt (300 mmol/d), low calcium (6.25 mmol/d) diet for 7 days; 10 of these patients were given 54 mmol/d of supplementary calcium, and 9 patients were given placebo. At the end of the low and high salt regimens, we evaluated changes in blood pressure, platelet aggregation, and the platelet release reaction measured as plasma beta-thromboglobulin and platelet factor 4 levels. With high salt intake, significant increases in mean blood pressure (P < .02), red blood cell sodium (P < .01), and platelet aggregation induced by 3 mumol/L ADP (P < .01) and by 3.0 mg/L epinephrine (P < .05) were observed in the placebo-treated patients but not in the calcium-supplemented ones. Compared with the placebo-treated patients, calcium-supplemented patients had a smaller weight gain (P < .05) but excreted more sodium and calcium (P < .01) at the end of the high salt regimen. Calcium supplementation resulted in decreases in beta-thromboglobulin (P < .05), platelet factor 4 (P < .01), and plasma and urinary excretions of norepinephrine (P < .02) during the high salt, low calcium regimen. The decrease in plasma norepinephrine correlated positively with the decreases in beta-thromboglobulin (r = .72, P < .02) and platelet factor 4 (r = .85, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Saito-K; Sano-H; Kawahara-J; Yokoyama-M
Hypertension. 1995 Jul; 26(1): 156-63

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