Randomised Controlled Trial of a No-Added-Sodium Diet for Mild Hypertension

Beard, Trevor C.; Gray, WendyR.; Cooke, HelenM.; Barge, Ray

doi:10.1016/s0140-6736(82)90491-3

Cited by 146 publications

(37 citation statements)

References 17 publications

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“…There was no significant difference in mean arterial pressure between the periods on slow sodium and placebo tablets, despite a difference of 56 nmmol in 24 hour urinary sodium excretion and a twofold difference in plasma renin activity. In contrast, in a virtually identical study MacGregor et a!2 observed a fall of 7-1 mm Hg in mean arterial pressure between the fourth week of slow sodium and the fourth week of placebo, in association with a fall of 76 mmol in 24 hour urinary sodium excretion and a similar difference in plasma renin activity.…”

Section: Order Effectsmentioning

confidence: 71%

“…In contrast, in a virtually identical study MacGregor et a!2 observed a fall of 7-1 mm Hg in mean arterial pressure between the fourth week of slow sodium and the fourth week of placebo, in association with a fall of 76 mmol in 24 hour urinary sodium excretion and a similar difference in plasma renin activity. Making this comparison in the 13 patients who reduced their sodium intake satisfactorily in our study, we found no significant difference in mean arterial pressure despite a fall of 57 mmol in sodium excretion: the 95l, confidence interval extended from a rise of 3-0 mm Hg to a fall of 5 4 mm Hg.…”

Section: Order Effectsmentioning

confidence: 92%

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Dietary sodium restriction for mild hypertension in general practice.

Watt¹,

Edwards²,

Hart³

et al. 1983

BMJ

124

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Section: Order Effectsmentioning

confidence: 71%

Section: Order Effectsmentioning

confidence: 92%

Dietary sodium restriction for mild hypertension in general practice.

Watt¹,

Edwards²,

Hart³

et al. 1983

BMJ

124

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“…Stamler and colleagues 39 conducted a similar trial, the Hypertension Control Program, with similar results over a 4-year period; however, the multifactor intervention precluded identification of a specific effect of sodium. Some of the same investi- 42 have compared sodium reduction to drug treatment and have generally found similar blood pressure control, but some of these trials are difficult to interpret due to drug treatment in both arms. Finally, there have been three community intervention trials 43 -45 testing the effects of nutritional education or environmental alteration of available dietary sources of salt.…”

Section: Discussionmentioning

confidence: 99%

An overview of randomized trials of sodium reduction and blood pressure.

et al. 1991

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To test for effects on systolic and diastolic blood pressure and to provide precise estimates of their magnitude, we conducted an overview of randomized clinical trials that aimed to reduce the intake of sodium in human subjects. We excluded from pooled analyses trials with confounded designs, those that compared intake levels beyond the usual range in the population, and those without published reports. Two reviewers abstracted information in duplicate and differences were reconciled. Twenty-three trials with outcome data from an aggregate of 1,536 subjects were included. Data were pooled both separately for hypertensive and nonnotensive subjects and for all trials combined. With the use of sample size weighting, blood pressure reductions (net of controls) were 4.9±13/2.6±0.8 mm Hg (systolic and diastolic, respectively, with 95% confidence limits) in hypertensive subjects and 1.7 ±1.0/1.0 ±0.7 mm Hg in nonnotensive subjects. The combined blood pressure reductions were 2.9±0.8/1.6±0.5 mm Hg. These changes were associated with mean reduction of urinary sodium excretion ranging from 16 to 171 mmol/24 hr for individual trials. A dose-response relation across trials was found, both in nonnotensive and in hypertensive subjects. These results indicate that sodium reduction lowers mean blood pressure in both hypertensive and nonnotensive individuals for periods of at least several months. The findings are highly consistent with results of observational epidemiological studies and have implications for preventive strategies of blood pressure control. {Hypertension 1991;17[suppl I]:I-27-I-33) R andomized intervention trials, properly conducted, provide the best test of an effect of prophylactic or therapeutic treatments. 1 Although the blood pressure effects of reducing dietary sodium have been studied since early in the century, 2 randomized trials have been reported only within the past 17 years, 3 largely the past 10 years. Trials have both increased in frequency and become more varied and complex in design. These changes reflect the importance of the question for public health and biology but also pose a challenge for summarizing and interpreting results. Several reviews have been published in recent years, 4 -5 but they did not present pooled analyses of all relevant trials to the time of the reviews, and several trials have since been completed. We favor pooling as part of a review because it formalizes the objective of including all relevant trials and an explicit method of combining their results. It also furnishes a quantitative estimate of the effect, which

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“…103 Of the 20 published studies I have been able to find in which pretreatment or control blood pressures and the fall in blood pressure with sodium restriction alone are given, it can be seen that the higher the blood pressure, the greater the effect of salt restriction irrespective of the degree of sodium restriction To examine this relationship further, we studied 103 subjects, including normotensive and hypertensive subjects who had not been treated for 2 months. 120 They were studied 1) while receiving their normal sodium diet (approximately 150 mmoL/day), 2) after 5 days of a high salt diet (approximately 350 mmol/day), and 3) after 5 days on a low sodium diet (10 mmol/ day); no subject was admitted to hospital.…”

Section: Does Reducing Sodium Intake Lowermentioning

confidence: 99%

Sodium is more important than calcium in essential hypertension.

Macgregor¹

1985

Hypertension

168

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There is much circumstantial and some direct evidence in humans to suggest that a high consumption of salt predisposes communities and individuals to the development of essential hypertension. Recent work has suggested possible mechanisms whereby a high salt intake could cause a rise in blood pressure in genetically susceptible persons. Restriction of salt intake in the diet lowers blood pressure in many subjects with high blood pressure and this fall in blood pressure is mediated in part by a diminished renin response to sodium restriction as hypertension develops. The effect of sodium restriction, like diuretics, is additive to most blood pressure lowering drugs, particularly those that inhibit the renin system such as beta-blockers and angiotensin converting enzyme inhibitors. Claims that a slight reduction in calcium intake may be important in the development of high blood pressure are disputed. Furthermore, no satisfactory hypothesis has been put forward to explain how a small reduction in dietary calcium intake could cause high blood pressure. Large increases in calcium intake have been reported to lower blood pressure in both normotensive and hypertensive humans. The three published studies, however, are not in agreement.

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Randomised Controlled Trial of a No-Added-Sodium Diet for Mild Hypertension

Cited by 146 publications

References 17 publications

Dietary sodium restriction for mild hypertension in general practice.

Dietary sodium restriction for mild hypertension in general practice.

An overview of randomized trials of sodium reduction and blood pressure.

Sodium is more important than calcium in essential hypertension.

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