A review of long-term effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol and triglyceride
- Correspondence to Maureen McCormick Covelli
College of Nursing, University of Central Florida, 12201 Research Rarkway, Suite 300, Orlando, FL 32826, USA;
Implications for practice and research
■ Low sodium diet in normotensive Caucasians showed less than 1% decrease in systolic blood pressure (SBP) and 3.5% decrease in hypertensive Caucasian populations.
■ Further controlled studies are needed on the effect of sodium reduction among Blacks and Asians.
■ Sodium reduction diet resulted in significant increase in lipids (plasma cholesterol and triglycerides) and hormones (renin, aldosterone, and catecholamine).
■ Research on long-term hormonal and lipid effects of sodium restriction diets is needed.
Low sodium diets have been a major hypertension prevention and treatment theme. Evidence supporting interventions of reduced sodium intake as a generalised hypertension prophylaxis initiative remains ambiguous.1 Although a diet high in sodium has been associated with development of hypertension and cardiovascular disease, population study data have been conflicting and showed direct harmful effects in patients with heart failure and diabetes. Sodium intake has been shown to effect the renin-angiotensin-aldosterone system, catecholamines and serum lipids that are surrogate markers of cardiovascular disease, thus questioning the generalised advisability of reduced sodium intake recommendations.2
The systematic review and meta-analysis included randomised, controlled, intervention studies (1950–2009) of 2–4 weeks or longer duration, to estimate the influence of low versus high dietary sodium on SBP, diastolic BP, mean BP, concentrations of renin, aldosterone, catecholamines, cholesterol, high-density lipoproteins, low-density lipoproteins, and triglyceride to evaluate the suitability of sodium reduction as a prophylaxis initiative and treatment of hypertension. Healthy normotensive and hypertensive participants, irrespective of age or race, were included.
The type of intervention was changed sodium intake (estimated by 24 h urinary sodium excretion) and allocated low and high sodium-intake groups. Levels of BP (normotension and hypertension) were stratified according to race. Separate meta-analysis was performed for each outcome measure. Treatment effect was determined by the difference between baseline to end of treatment measurements during a low and a high sodium diet.
Intervention studies (167) were reviewed. The median age of hypertensive persons was 51 years, the mean 24 h sodium excretion for high salt groups was 196 mmol; the low salt group was 71 mmol. The median age of normotensive persons was 27 years, mean 24 h sodium excretion for high salt groups was 206 mmol; the low salt group was 50 mmol. A baseline 24 h sodium excretion rates not influenced by diets was 157 mmol. Low salt diets reduced SBP by 1% in normotensive Caucasians and 3.5% in hypertensive Caucasians. The limited number of trials that included Asians (three trials) and Blacks (six trials) revealed the following: hypertensive Asians and both normotensive and hypertensive Blacks had greater BP effects. All reduced sodium diet groups had significant increase in plasma renin, aldosterone, noradrenaline, adrenaline, a 2.5% cholesterol increase, and a 7% tryglyceride increase.
The general therapeutic initiative for prevention and management of hypertension has emphasised dietary sodium reduction (eg, DASH diet)2 and yet, in clinical practice, maintenance of low sodium diet is generally difficult to maintain and the support evidence is based on short-term interventions.3 Long-term outcomes are in question.
This meta-analysis of 167 clinical long-term dietary sodium reduction intervention studies compared the effects of dietary sodium reduction intake levels lower than the normal range (below 120 mmol) to high normal sodium intake (150–200 mmol) within healthy normotensive and hypertensive participants.
The limited SBP effect of a generally normal to subnormal dietary sodium reduction intervention in normotensive Caucasians (1% SBP decrease) and those with hypertension (3% SBP decrease) does not support a general recommendation to reduce sodium intake for a prolonged period. Results suggest that the SBP effect of low sodium intake was greater in Black and Asian patients than Caucasians. The increase in BP effect in African–Americans may be related to normal physiologic adaptive mechanisms. However, the number of studies in Black and Asian patients was insufficient for different recommendations.
Elevated hormonal and lipid responses to low sodium intake is clinically noteworthy. Effects may be attributed to compensatory, homeostatic, physiological responses of neurohormonal regulators to maintain normal sodium levels. Sodium-restricted diets resulted in increases in hormones (renin, aldosterone, noradrenaline, adrenaline) and lipids (cholesterol and triglycerides), thereby, eliminating or minimising the long-term BP effects. The increased hormonal and lipid responses may have important long-term cardiovascular and endocrine disease complications and implications.