From the Departments of Medicine Y (Dr Graudal) and Cardiology P (Dr Galløe), Gentofte Hospital, and Tissue Typing Laboratory, Department of Clinical Immunology, Rigshospitalet (Drs Graudal and Garred), University of Copenhagen, Copenhagen, Denmark.
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
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.
Graudal NA, Galløe AM, Garred P. Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and TriglycerideA Meta-analysis. JAMA. 1998;279(17):1383–1391. doi:10.1001/jama.279.17.1383