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Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride A Meta-analysis

Niels A. Graudal, MD; Anders M. Galløe, MD; Peter Garred, DrMedSci
JAMA. 1998;279(17):1383-1391. doi:10.1001/jama.279.17.1383.
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Context.— One of the controversies in preventive medicine is whether a general reduction in sodium intake can decrease the blood pressure of a population and thereby reduce the number of strokes and myocardial infarctions. In recent years the debate has been extended by studies indicating that reduced sodium intake has adverse effects.

Objective.— To estimate the effects of reduced sodium intake on systolic and diastolic blood pressure (SBP and DBP), body weight, and plasma or serum levels of renin, aldosterone, catecholamines, cholesterols, and triglyceride, and to evaluate the stability of the blood pressure effect in relation to additional trials.

Data Sources.— MEDLINE search from 1966 through December 1997 and reference lists of relevant articles.

Study Selection.— Studies randomizing persons to high-sodium and low-sodium diets were included if they evaluated at least one of the effect parameters.

Data Extraction.— Two authors independently recorded data.

Data Synthesis.— In 58 trials of hypertensive persons, the effect of reduced sodium intake as measured by urinary sodium excretion (mean, 118 mmol/24 h) on SBP was 3.9 mm Hg (95% confidence interval [CI], 3.0-4.8 mm Hg) (P<.001) and on DBP was 1.9 mm Hg (95% CI, 1.3-2.5 mm Hg) (P<.001). In 56 trials of normotensive persons, the effect of reduced sodium intake (mean, 160 mmol/24 h) on SBP was 1.2 mm Hg (95% CI, 0.6-1.8 mm Hg) (P<.001) and on DBP was 0.26 mm Hg (95% CI, −0.3-0.9 mm Hg) (P=.12). The cumulative analysis showed that this effect size has been stable since 1985. In plasma, the renin level increased 3.6-fold (P<.001), and the aldosterone level increased 3.2-fold (P<.001); the increases were proportional to the degree of sodium reduction for both renin (r=0.66; P<.001) and aldosterone (r=0.64; P<.001). Body weight decreased significantly, and noradrenaline, cholesterol, and low-density lipoprotein cholesterol levels increased. There was no effect on adrenaline, triglyceride, and high-density lipoprotein cholesterol.

Conclusion.— These results do not support a general recommendation to reduce sodium intake. Reduced sodium intake may be used as a supplementary treatment in hypertension. Further long-term studies of the effects of high reduction of sodium intake on blood pressure and metabolic variables may clarify the disagreements as to the role of reduced sodium intake, but ideally trials with hard end points such as morbidity and survival should end the controversy.

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Figure 1.—Meta-analysis of the effect of reduced sodium intake on systolic and diastolic blood pressure (SBP and DBP) in hypertensive populations (n=58). The effect sizes (in millimeters of mercury [mm Hg]) and the 95% confidence intervals for the individual trials, the cumulative meta-analyses, and the cumulative reduction of 24-hour urinary sodium excretion are shown.
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Figure 2.—Meta-analysis of the effect of reduced sodium intake on systolic and diastolic blood pressure (SBP and DBP) in normotensive populations (n=56). The effect sizes (in millimeters of mercury [mm Hg]) and the 95% confidence intervals for the individual trials, the cumulative meta-analyses, and the cumulative reduction of 24-hour urinary sodium excretion are shown.
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Figure 3.—Operating characteristic curve of the type II error for the diastolic blood pressure effect in normotensive persons.
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Figure 4.—Regression analysis of the relation between sodium reduction and change in plasma renin (R) and change in plasma aldosterone (A) where R=0.020 × [Sodium Reduction] (95% CI, 0.018-0.022), r2=0.43, and P<.001; A=0.017 × [Sodium Reduction] (95% CI, 0.015-0.019), r2=0.41, and P<.001.

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