yulius hermanto
Sodium Restriction and Cardiovascular Disease
Introduction
Blood pressure (BP)-related diseases, specifically, stroke, coronary heart disease, heart failure, and kidney disease, are leading causes of morbidity and mortality in the United States and throughout the world. In the United States, coronary heart disease and stroke are the leading causes of mortality,
whereas heart failure is the leading cause of hospitalizations.
The relation between BP and adverse health outcomes is direct and progressive with no evidence of a threshold, that is the risk of CVD, stroke, and end-stage kidney disease increases progressively throughout the range of usual BP starting at a level of 115/75 mm Hg.
Overall, elevated BP is the second leading modifiable cause of death, accounting for an estimated 395 000 preventable deaths in the United States in 2005.
Worldwide, elevated BP accounts for 54% of stroke and 47% of coronary heart disease events; importantly, about half of these events occur in persons without hypertension.
The Facts
Excess intake of salt (sodium chloride) has a major role in the pathogenesis of elevated BP. Excess sodium intake also has BP-independent effects, promoting left ventricular hypertrophy as well as fibrosis in the heart, kidneys, and arteries.
Evidence has documented that a median reduction in urinary sodium of
1800 mg/d lowered systolic/diastolic BP by 2.0/1.0 mmHg in nonhypertensive individuals and by 5.0/2.7 mmHg in hypertensive individuals. The benefits of sodium reduction in persons with poorly controlled BP are striking.
Importantly, the BP response to sodium reduction, while direct and progressive, was nonlinear. Specifically, decreasing sodium intake by 900 mg/d caused a greater reduction in BP when the starting sodium intake was 2300 mg/d than when it was3500 mg/d.
The benefits of sodium reduction in non-hypertensive individuals were recently corroborated in the GenSalt feeding study, which documented that lowering sodium intake to 1500 mg/d reduced BP in 2,000 Asian adults with mean systolic/diastolic BP 120/80 mm Hg.
Sodium reduction also blunts the age-related rise in BP. Because BP rises with age, about 90% of adults eventually become hypertensive.
Consistent with this evidence, a major trial in the United States documented that a reduced sodium intake can prevent hypertension by 20%. Evidence supporting a direct relation of sodium intake and CVD is also accumulating. In a recent meta-analysis of observational studies, a higher sodium intake was associated with an increased risk of stroke and likely CVD.
Independent of its effects on BP, an increased sodium intake has other adverse effects. These include subclinical CVD (ie, left ventricular hypertrophy, ventricular fibrosis, diastolic dysfunction), kidney damage, gastric cancer, and disordered mineral metabolism (ie, increased urinary calcium excretion, potentially leading to osteoporosis).
It is well established that sodium loading suppresses the systemic renin-angiotensin-aldosterone system by inhibiting renin release from the renal juxtaglomerular apparatus. Less well appreciated are findings that sodium loading increases oxidative stress and endothelial dysfunction and promotes mitogenic responses (fibrosis in heart, kidneys, and arteries)
resulting in cardiac and vascular remodeling.
With regard to arterial dysfunction, higher sodium intake is associated with greater increases in large elastic artery stiffness with aging, and reducing sodium intake from moderate levels by 50% to less than 1500 mg/d reduces large elastic artery stiffness in otherwise healthy middle-aged and older
adults with elevated systolic BP.
Sodium-induced increases in BP may directly induce renal injury or accelerate kidney disease caused by other conditions such as diabetes mellitus or glomerulonephritis. However, excess sodium intake also has deleterious effects on the kidneys independent of increased BP. Studies in experimental animals and in human beings have shown, for example, that high sodium intake can cause glomerular hyperfiltration and increased albumin excretion, renal oxidative stress, and renal fibrosis independent of BP.
The Recommendation
Some sodium intake is required. An Institute of Medicine Committee set 1500 mg of sodium per day as an adequate intake level, primarily to assure nutrient adequacy. Based on the DASH-Sodium trial, it is apparent that Western type
diets can provide this level of sodium intake and that such a diet also can provide adequate levels of other nutrients.
Because 90% of US adults will develop hypertension over their lifetime, the goal should be 1500 mg/d, as recommended by the scientific advisory of
the 2010 Dietary Guidelines Committee.
The health benefits apply to Americans in all groups, and there is no compelling evidence to exempt special populations from this public
health recommendation.
Blood pressure (BP)-related diseases, specifically, stroke, coronary heart disease, heart failure, and kidney disease, are leading causes of morbidity and mortality in the United States and throughout the world. In the United States, coronary heart disease and stroke are the leading causes of mortality,
whereas heart failure is the leading cause of hospitalizations.
The relation between BP and adverse health outcomes is direct and progressive with no evidence of a threshold, that is the risk of CVD, stroke, and end-stage kidney disease increases progressively throughout the range of usual BP starting at a level of 115/75 mm Hg.
Overall, elevated BP is the second leading modifiable cause of death, accounting for an estimated 395 000 preventable deaths in the United States in 2005.
Worldwide, elevated BP accounts for 54% of stroke and 47% of coronary heart disease events; importantly, about half of these events occur in persons without hypertension.
The Facts
Excess intake of salt (sodium chloride) has a major role in the pathogenesis of elevated BP. Excess sodium intake also has BP-independent effects, promoting left ventricular hypertrophy as well as fibrosis in the heart, kidneys, and arteries.
Evidence has documented that a median reduction in urinary sodium of
1800 mg/d lowered systolic/diastolic BP by 2.0/1.0 mmHg in nonhypertensive individuals and by 5.0/2.7 mmHg in hypertensive individuals. The benefits of sodium reduction in persons with poorly controlled BP are striking.
Importantly, the BP response to sodium reduction, while direct and progressive, was nonlinear. Specifically, decreasing sodium intake by 900 mg/d caused a greater reduction in BP when the starting sodium intake was 2300 mg/d than when it was3500 mg/d.
The benefits of sodium reduction in non-hypertensive individuals were recently corroborated in the GenSalt feeding study, which documented that lowering sodium intake to 1500 mg/d reduced BP in 2,000 Asian adults with mean systolic/diastolic BP 120/80 mm Hg.
Sodium reduction also blunts the age-related rise in BP. Because BP rises with age, about 90% of adults eventually become hypertensive.
Consistent with this evidence, a major trial in the United States documented that a reduced sodium intake can prevent hypertension by 20%. Evidence supporting a direct relation of sodium intake and CVD is also accumulating. In a recent meta-analysis of observational studies, a higher sodium intake was associated with an increased risk of stroke and likely CVD.
Independent of its effects on BP, an increased sodium intake has other adverse effects. These include subclinical CVD (ie, left ventricular hypertrophy, ventricular fibrosis, diastolic dysfunction), kidney damage, gastric cancer, and disordered mineral metabolism (ie, increased urinary calcium excretion, potentially leading to osteoporosis).
It is well established that sodium loading suppresses the systemic renin-angiotensin-aldosterone system by inhibiting renin release from the renal juxtaglomerular apparatus. Less well appreciated are findings that sodium loading increases oxidative stress and endothelial dysfunction and promotes mitogenic responses (fibrosis in heart, kidneys, and arteries)
resulting in cardiac and vascular remodeling.
With regard to arterial dysfunction, higher sodium intake is associated with greater increases in large elastic artery stiffness with aging, and reducing sodium intake from moderate levels by 50% to less than 1500 mg/d reduces large elastic artery stiffness in otherwise healthy middle-aged and older
adults with elevated systolic BP.
Sodium-induced increases in BP may directly induce renal injury or accelerate kidney disease caused by other conditions such as diabetes mellitus or glomerulonephritis. However, excess sodium intake also has deleterious effects on the kidneys independent of increased BP. Studies in experimental animals and in human beings have shown, for example, that high sodium intake can cause glomerular hyperfiltration and increased albumin excretion, renal oxidative stress, and renal fibrosis independent of BP.
The Recommendation
Some sodium intake is required. An Institute of Medicine Committee set 1500 mg of sodium per day as an adequate intake level, primarily to assure nutrient adequacy. Based on the DASH-Sodium trial, it is apparent that Western type
diets can provide this level of sodium intake and that such a diet also can provide adequate levels of other nutrients.
Because 90% of US adults will develop hypertension over their lifetime, the goal should be 1500 mg/d, as recommended by the scientific advisory of
the 2010 Dietary Guidelines Committee.
The health benefits apply to Americans in all groups, and there is no compelling evidence to exempt special populations from this public
health recommendation.
