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Low-Sodium Diets
Dietary Electrolytes and Blood Pressure
1998;71-0146
A Statement for Healthcare Professionals From the
American Heart Association Nutrition Committee
Blood Pressure Committee Members
Theodore A. Kotchen, MD; David A. McCarron, MD
Blood pressure-associated risks ensue incrementally over a wide range of
blood pressure levels, and even among nonhypertensive persons, blood
pressure levels are predictive of morbidity and mortality from stroke, heart
disease, and end-stage renal disease.On a population basis, it has been
estimated that a reduction in diastolic blood pressure of 2 mm Hg would
result in a 15% reduction in risk of stroke and transient ischemic attacks
and a 6% reduction in risk of coronary heart disease.
Between 1971 and 1991, national health examination surveysdocumented a
downward trend in blood pressure levels and the prevalence of hypertension
in the United States. Adoption of a healthier lifestyle may have contributed
to this favorable trend. Not all subgroups have benefited equally, however,
particularly African Americans. According to the Third National Health and
Nutrition Examination Survey (NHANES III)(1988 to 1991), 24% of the US
population was classified as having hypertension. Blood pressure level and
hypertension prevalence increase with age: high-normal and high blood
pressure continue to be major contributors to cardiovascular disease.
The relationship between dietary electrolyte consumption and blood
pressure is the focus of this brief review. Evidence for a positive
association between sodium chloride (NaCl) intake and blood pressure is
discussed. Increasing evidence also suggests that dietary patterns
associated with low intakes of potassium, calcium, and possibly magnesium
also contribute to higher levels of blood pressure. An understanding of
these associations has important implications not only for the prevention
and treatment of hypertension but also for developing population-based
strategies to decrease cardiovascular disease risk by shifting the overall
blood pressure distribution toward lower levels.
Sodium Chloride
A high NaCl intake convincingly contributes to elevated arterial pressure
in a number of animal models of genetic and acquired hypertension. The
chimpanzee is phylogenetically close to the human, and it has recently been
demonstrated that the addition of NaCl (5, 10, and then 15 g/d) to the
chimpanzee's usual diet (a fruit-and-vegetable diet low in NaCl and high in
potassium) over 20 months results in significant and progressive elevations
of blood pressure. After 84 weeks of added NaCl, relative to both baseline
values and a control group, mean systolic and diastolic blood pressures
increased by 33 mm Hg and 10 mm Hg, respectively. This increase was
completely reversed within 6 months of cessation of the high NaCl intake.
Animal studies (as well as limited epidemiological and clinical
observations) suggest that diets high in NaCl may also have deleterious
cardiovascular consequences independent of blood pressure, eg, cerebral
arterial disease and stroke, left ventricular hypertrophy, renal vascular
disease, and glomerular injury.
In humans, evidence for an association between NaCl consumption and blood
pressure is based on anthropological research, observational epidemiological
studies (cross-population and within-population), and intervention
trials.The strength of the association of NaCl intake with blood pressure
increases with age, blood pressure level, and among individuals with a
family history of hypertension. In addition, the full expression of NaCl-sensitive
hypertension depends on the concomitant intake of both sodium and chloride.n
both experimental models and humans, blood pressure is not increased by a
high dietary sodium intake provided as nonchloride salts of sodium. In the
usual diet, however, most sodium is consumed as NaCl,largely from its use as
an additive in commercial food processing.
Across populations, level of blood pressure, increment in blood pressure
level with age, and prevalence of hypertension are related to NaCl intake.
The International Study of Salt and Blood Pressure (INTERSALT) is a
cross-sectional study designed to evaluate both within-population and
cross-population hypotheses on the relationship between blood pressure and
sodium excretion in >10 000 adults (aged 20 to 59 years) at 52 centers
around the world. Across the 52 populations, 24-hour sodium excretion was
significantly related to median systolic and diastolic blood pressure, the
upward slope of systolic and diastolic blood pressure with age, and the
prevalence of high blood pressure. For individuals, the within-population
analyses demonstrated that the relationship between sodium excretion and
blood pressure was similar for nonhypertensive and all participants,
indicating that varying degrees of salt sensitivity of blood pressure occur
throughout the population. Overall the principal observations in INTERSALT
are that (1) for individuals, a difference of 100 mEq (equivalent to 5.9 g
NaCl) per day in sodium intake is associated on average with a difference of
3 to 6 mm Hg in systolic blood pressure; and (2) for populations, a 100 mEq/d
lower sodium intake is associated with attenuation of the rise in systolic
blood pressure by 10 mm Hg in persons aged 25 to 55 years. As with
observations in several other isolated, preliterate populations, in 4 remote
INTERSALT samples both sodium excretion and blood pressure were low, there
was little or no upward slope of blood pressure with age, and there was
little or no hypertension.
A recent review of a limited number of observational and intervention
studies suggests that there also is an association between NaCl consumption
and blood pressure level in children and adolescents. In a randomized,
double-blind trial conducted in 1980 among 476 newborn Dutch infants, blood
pressure was lower in infants fed a diet low in NaCl than in infants fed a
diet with normal NaCl intake during the first 6 months of life.In a cohort
of these same subjects at 15-year follow-up, adjusted systolic blood
pressure was lower in children who had been assigned in infancy to the low-NaCl
group compared with the control group.
On the basis of results of acute NaCl depletion or loading protocols,
depending on arbitrary definitions of NaCl sensitivity, it has been
estimated that approximately 30% to 50% of hypertensive persons and a
smaller percentage of nonhypertensive persons are NaCl sensitive, ie,
arterial pressure is decreased by NaCl depletion and/or increased by NaCl
loading.Blood pressure responses to acute protocols are reproducible. In 40
nonhypertensive and hypertensive subjects, it has been reported that blood
pressure response to an acute volume expansion-volume contraction protocol
correlates (r=.40, P<.01) with the change in blood pressure in response to a
low-sodium diet.Nevertheless, the arbitrary designation of salt sensitivity
based on blood pressure responses to acute protocols in a limited number of
subjects may not reflect long-term blood pressure responses to dietary NaCl
in a population. Such a designation of salt sensitivity, however, does
highlight the heterogeneity of response to acute changes in NaCl balance,
although intervention studies have not identified a bimodal blood pressure
response to NaCl reduction. On a population basis, the average change in
blood pressure in response to NaCl reduction may be more meaningful than
identification of "salt-sensitive" individuals.
Randomized, controlled trials provide compelling evidence for a causal
relationship between dietary NaCl and blood pressure. Despite reservations
about the limitations of meta-analyses (including criteria for inclusion and
exclusion of trials, different study designs and approaches to data analysis
among individual trials, and variable documentation of adherence to study
diets), 2 recent meta-analyses document consistent reductions in blood
pressure in response to lowered intake of NaCl.In 1 meta-analysis of 32
trials, estimated median reductions of 24-hour urine sodium excretion across
trials were 76 mmol (range 56 to 105) and 106 mmol (range 60 to 210) in
hypertensive subjects and nonhypertensive subjects, respectively; overall
reductions of systolic and diastolic blood pressure were -1.9/-1.1 mm Hg in
nonhypertensive subjects and -4.8/-2.5 mm Hg in hypertensive subjects.In a
second meta-analysis of 52 trials, estimated median reductions of sodium
excretion across trials were 79 mmol (range 71 to 119) for hypertensive
subjects and 133 mmol (range 95 to 156) for nonhypertensive subjects;
overall reductions of blood pressure were -1.6/-0.5 mm Hg in nonhypertensive
subjects and -5.9/-3.8 mm Hg in hypertensive subjects.The reductions in
blood pressure by a diet lower in NaCl are more prominent in hypertensive
than in nonhypertensive individuals, and greater reductions of blood
pressure have been observed in trials lasting >=5 weeks than in shorter
trials. Although the blood pressure reductions in these short-term trials
are relatively modest for individuals, it is estimated that lowering a
population's blood pressure to this degree would translate into a
significant reduction in cardiovascular disease mortality.
The Trials of Hypertension Prevention (TOHP) evaluated the effects of
nonpharmacological therapy on blood pressure in adults with high-normal
blood pressure. In phase I, systolic and diastolic blood pressure were
significantly reduced in separate groups treated with weight loss or
reduction of NaCl intake over 18 months but not by dietary supplementation
with calcium, magnesium, or potassium for 6 months.The results of phase I
were the basis for phase II of TOHP, which more extensively evaluated the
effects of weight loss and reduced NaCl intake, alone and in combination, on
blood pressure over 3 to 4 years in overweight adults with high-normal blood
pressure.Compared with blood pressures in a usual-care control group, at 6
months, systolic and diastolic blood pressure were both significantly
reduced by weight loss alone (-6.0/-5.5 mm Hg) and lowered NaCl intake alone
(-5.1/-4.4 mm Hg), although the effects of the 2 interventions on average
blood pressure reduction were not additive. At 6 months, hypertension
incidence was 7.3% in the usual-care group, 4.2% in the weight loss group,
4.5% in the reduced-NaCl group, and 2.7% in the combined weight
loss-reduced-NaCl group. Beyond 6 months, the interventions were less
effective for maintaining both weight loss and lowered NaCl intake, and
impact on blood pressure was lessened. At termination of the study there
were small but significant reductions in systolic blood pressure in the
weight loss and low-NaCl group, whereas reduction of systolic blood pressure
in the combined-intervention group (weight loss and low NaCl) did not
achieve statistical significance. Reduction of diastolic blood pressure was
significant only in the weight loss group. The incidence of hypertension
during the entire course of the study was significantly lower in each of the
3 intervention groups (approximately 38%) than in the usual-care group
(44%).
Experimental models of hypertension and increasing information on humans
provide convincing evidence for genetic susceptibility and resistance to the
effects of dietary NaCl on arterial pressureIn the United States, a larger
proportion of both nonhypertensive and hypertensive African Americans are
NaCl sensitive compared with non-Hispanic whites.In response to acute NaCl
loads, African Americans excrete sodium less efficiently than whites, and it
has been estimated that >50% of hypertensive African Americans in the United
States are NaCl sensitive. The prevalence of diuretic-sensitive (and
presumably NaCl-sensitive) blood pressures in African Americans approaches
75%.Clinically there is evidence for heritability of sodium excretion,
levels of hormones that regulate sodium excretion, and NaCl sensitivity of
blood pressure in both Caucasians and African Americans.It is likely that
research over the next several years will identify multiple genetic
polymorphisms that contribute to interindividual and possibly
interpopulation variability of blood pressure responses to NaCl.
Environmental factors, including differences in other dietary mineral
contents and socioeconomic status, may also contribute to the apparently
greater prevalence of salt sensitivity among African Americans.
Potassium, Calcium, and Magnesium
Observational studiesdocument inverse associations of blood pressure with
dietary potassium, calcium, and magnesium consumption. On the basis of these
observations, however, it is difficult to relate blood pressure levels to
specific nutrients because of strong correlations among dietary intakes of
potassium, magnesium, fiber, and, to a lesser extent, calcium.Furthermore,
an inverse relationship between calcium intake and blood pressure has not
been observed in all studies,and a recent critical review has highlighted
methodological issues that complicate interpretation across these studies.
The inverse relationship between calcium intake and blood pressure is more
convincing at low levels of calcium consumption, ie, 300 to 600 mg/d.
The impact of dietary NaCl on blood pressure may be affected by
consumption of potassium or calcium. The urine sodium-potassium ratio is a
stronger correlate of blood pressure than either sodium or potassium alone.
In addition, high sodium intake is associated with higher blood pressure
levels among persons consuming low-calcium diets.
Results of 2 recent meta-analyses of clinical trials support the
conclusion that oral potassium supplements (60 to 120 mEq/d) lower blood
pressure. The magnitude of the blood pressure-lowering effect is greater in
hypertensive than in nonhypertensive persons and more pronounced in persons
consuming a diet high in NaCl. In an analysis of 19 trials of hypertensive
subjects, blood pressure was lowered on average -8.2/-4.5 mm Hg. In a
separate analysis of 33 trials, blood pressure was lowered on average by
-1.8/-1.0 mm Hg in nonhypertensive subjects and -4.4/-2.5 mm Hg in
hypertensive subjects.
Two meta-analyses of controlled clinical trials have shown that calcium
supplementation (1000 to 2000 mg/d) results in small but significant
reductions of systolic (-4.3 and -1.7 mm Hg, respectively) but not diastolic
blood pressure, and only in hypertensive individuals.Calcium supplementation
may preferentially lower blood pressure in patients with NaCl-sensitive
hypertension.Contrary to earlier evidence of a benefit of calcium
supplementation in high-risk pregnancy, results of a recent randomized
multicenter trial indicate that calcium supplementation during pregnancy
does not prevent preeclampsia or pregnancy-associated hypertension in
healthy nulliparous women.
The overall antihypertensive response to magnesium supplementation among
hypertensive individuals is small, and several trials have failed to show a
significant effect of magnesium supplementation on blood pressure.One
placebo-controlled, 6-month trial in hypertensive women found that magnesium
supplementation (20 mmol/d) significantly lowered diastolic (-3.4 mm Hg) but
not systolic blood pressure.
Dietary Approaches to Stop Hypertension Trial
Persons consuming vegetarian diets tend to have lower blood pressure than
nonvegetarians. For Americans, fruits and vegetables are a main source of
potassium, magnesium, and fiber, and dairy products are a main source of
calcium.n a randomized, multicenter study, the Dietary Approaches to Stop
Hypertension (DASH) trialevaluated the effects on blood pressure of 3
dietary patterns over 8 weeks in 459 adults with high-normal blood pressure
or mild hypertension. The dietary interventions were (1) a control diet with
potassium, calcium, and magnesium levels close to the 25th percentile of US
consumption; (2) a diet rich in fruits and vegetables; and (3) a
"combination" diet rich in fruits, vegetables, and fat-free or low-fat dairy
products.
The study diets were relatively high in potassium, calcium, and magnesium
content. Compared with the control diet, the study diets also were higher in
fiber, protein, carotenoid, and folate, and lower in total fat, saturated
fat, and cholesterol. NaCl content was equivalent in all 3 diets (7.5 g/d).
Caloric intake was adjusted so that weight change was avoided. Persons
consuming >14 alcoholic beverages per week were excluded from the study.
Systolic and diastolic blood pressure were significantly reduced by the
diet enriched with fruits and vegetables (-2.8/-1.1 mm Hg) and, compared
with the control diet, were reduced to an even greater extent by the
combination diet (-5.5/-3.0 mm Hg). The greater effect of the combination
diet was manifest in both hypertensive (-11.4/-5.5 mm Hg) and
nonhypertensive (-3.5/-2.1 mm Hg) persons, although reductions in blood
pressure were more pronounced in hypertensive persons. Blood pressure
reductions were similar in men and women and across ethnic groups.
Although not designed to identify the effective nutrients of the diets,
the DASH trial convincingly reaffirms the importance of multiple factors in
the diet for blood pressure control.
Conclusion
The beneficial effects of diet on blood pressure can be maximized by
avoiding high intake of NaCl and ensuring adequate intake of fruits,
vegetables, and fat-free and low-fat dairy products. Such diets are rich in
potassium, calcium, magnesium, and protein and low in total fat, saturated
fat, and cholesterol. Although not discussed here, additional nutritional
strategies for optimizing the effect of diet on blood pressure are
prevention and treatment of obesity, and for people who drink alcohol,
avoiding consumption of >2 drinks per day.
Any population-based guideline for an upper limit of NaCl is arbitrary
and should represent a reduction that is acceptable and safe. For the
general population, the AHA recommends that the average daily consumption of
NaCl by adults not exceed 6 g. This recommendation is consistent with the
guidelines of a number of other agencies in both the United States and
abroad. Although total cholesterol and LDL cholesterol may be slightly
increased by short-term "excessive sodium reduction," there is no evidence
that limiting NaCl consumption to 6 g per day poses any health risk. A lower
NaCl intake may be recommended for hypertensive persons. Although there is
insufficient evidence to recommend high intake of calcium for prevention or
treatment of hypertension, calcium deficiency should be avoided. Primarily
for prevention of osteoporosis, the National Academy of Sciences recently
recommended the following calcium intakes as adequate: 1300 mg/d for
adolescents (9 to 18 years); 1000 mg/d for persons aged 19 to 50 years; and
1200 mg/d for persons older than 50. It remains to be determined whether the
blood pressure-lowering capacity of fruits, vegetables, and low-fat dairy
products can be explained entirely by their electrolyte content.
References
-
Stamler J, Stamler R, Neaton JD. Blood
pressure, systolic and diastolic, and cardiovascular risks. Arch Intern
Med.1993;153:598-615.
-
Klag MJ, Whelton PK, Randall BL, Neaton JD,
Brancati FL, Ford CE, Shulman NB, Stamler J. Blood pressure and end-stage
renal disease in men. N Engl J Med. 1996;334:13-18.
-
Klag MJ, Whelton PK, Randall BL, Neaton JD,
Brancati FL, Stamler J. End-stage renal disease in African-American and
white men. JAMA. 1997;277:1293-1298.
-
Cook NR, Cohen J, Hebert P, Taylor JO,
Hennekens CH. Implications of small reductions in diastolic blood pressure
for primary prevention. Arch Intern Med.1995;155:701-709.
-
Burt VL, Cutler JA, Higgins M, Horan MJ,
Labarthe D, Whelton P, Brown C, Roccella EJ. Trends in the prevalence,
awareness, treatment, and control of hypertension in the adult US
population: data from the Health Examination Surveys, 1960 to 1991.
Hypertension. 1995;26:60-69.
-
Burt VL, Whelton P, Roccella EJ, Brown C,
Cutler JA, Higgins M, Horan MJ, Labarthe D. Prevalence of hypertension in
the US adult population: results from the Third National Health and
Nutrition Examination Survey, 1988-1991. Hypertension.1995;25:305-313.
-
Kannel WB. Blood pressure as a cardiovascular
risk factor. JAMA.1996;275:1571-1576.
-
Denton D, Weisinger R, Mundy N, Wickings EJ,
Dixson A, Moisson P, Pingard AM, Shade R, Carey D, Ardaillou R, Paillard
F, Chapman J, Thillet J, Michel JB. The effect of increased salt intake on
blood pressure of chimpanzees. Nat Med. 1995;1:1009-1016.
-
MacGregor GA. Salt--more adverse effects. Am J
Hypertens. 1997;10:37S-41S.
-
INTERSALT Cooperative Research Group.
INTERSALT: an international study of electrolyte excretion and blood
pressure. Results for 24 hour urinary sodium and potassium excretion. Br
Med J. 1988;297:319-328.
-
Law MR, Frost CD, Wald NJ. By how much does
dietary salt reduction lower blood pressure? I: analysis of observational
data among populations. Br Med J.1991;302:811-815.
-
Frost CD, Law MR, Wald NJ. By how much does
dietary salt reduction lower blood pressure? II: analysis of observational
data within populations. Br Med J.1991;302:815-818.
-
Law MR, Frost CD, Wald NJ. By how much does
dietary salt reduction lower blood pressure? III: analysis of data from
trials of salt reduction. Br Med J. 1991;302:819-824.
-
Overlack A, Ruppert M, Kolloch R, Gobel B,
Kraft K, Diehl J, Schmitt W, Stumpe KO. Divergent hemodynamic and hormonal
responses to varying salt intake in normotensive subjects. Hypertension.
1993;22:331-338.
-
Boegehold M, Kotchen TA. Importance of dietary
chloride for salt sensitivity of blood pressure.
Hypertension.1991;17(suppl I):I-158-I-161.
-
Luft FC, Fineberg NS, Sloan RS. Overnight
urine collections to estimate sodium intake. Hypertension.1982;4:494-498.
-
National Research Council, Committee on Diet
and Health, Food and Nutrition Board, Commission on Life Sciences. Diet
and Health: Implications for Reducing Chronic Disease Risk. Washington,
DC: National Academy Press; 1989.
-
Evans M, Cohen JD, Kumanyika S, Cutler JA,
Roccella EJ, for the Planning Committee and Participants of the Workshop.
Implementing Recommendations for Dietary Salt Reduction: A Summary of an
NHLBI Workshop. Bethesda, Md: US Dept of Health and Human Services,
National Institutes of Health, National Heart, Lung, and Blood Institute;
1997. NIH publication No. 55-728N.
-
Elliott P, Stamler J, Nichols R, Dyer AR,
Stamler R, Kesteloot H, Marmot M, for the INTERSALT Cooperative Research
Group. INTERSALT revisited: further analyses of 24 hour sodium excretion
and blood pressure within and across populations. Br Med J.
1996;312:1249-1253.
-
Stamler J. The INTERSALT Study: background,
methods, findings, and implications. Am J Clin
Nutr.1997;65(suppl):626S-642S.
-
Simons-Morton DG, Obarzanek E. Diet and blood
pressure in children and adolescents. Pediatr Nephrol. 1997;11:244-249.
-
Hofman A, Hazebroek A, Valkenburg HA. A
randomized trial of sodium intake and blood pressure in newborn infants.
JAMA. 1983;250:370-373.
-
Geliejnse JM, Hofman A, Witteman JCM,
Hazebroek AJM, Valkenburg HA, Grobbee DE. Long-term effects of neonatal
sodium restriction on blood pressure. Hypertension.1996;29:913-917.
-
Weinberger MH, Miller JH, Luft FC, Grim CE,
Fineberg NS. Definitions and characteristics of sodium sensitivity and
blood pressure resistance. Hypertension. 1986;8(suppl II):II-127-II-134.
-
Sullivan JM, Prewitt RL, Ratts TE. Sodium
sensitivity in normotensive and borderline hypertensive humans. Am J Med
Sci. 1988;295:370-377.
-
Luft FC, Weinberger MH. Heterogeneous
responses to changes in dietary salt intake: the salt-sensitivity
paradigm. Am J Clin Nutr. 1997;65(suppl):612S-617S.
-
Weinberger MH, Stegner JE, Fineberg NS. A
comparison of two tests for the assessment of blood pressure responses to
sodium. Am J Hypertens. 1993:6:179-184.
-
Cutler JA, Follmann D, Allender PS. Randomized
trials of sodium reduction: an overview. Am J Clin
Nutr.1997;65(suppl):643S-651S.
-
Midgley JP, Matthew AG, Greenwood CM, Logan
AG. Effect of reduced dietary sodium on blood pressure: a meta-analysis of
randomized controlled trials. JAMA. 1996;275:1590-1597.
-
The Trials of Hypertension Prevention
Collaborative Research Group. The effects of non-pharmacological
interventions on blood pressure of persons with high normal levels:
results of the Trials of Hypertension Prevention (Phase I).
JAMA.1992;267:1213-1220.
-
Yamamoto M, Applegate WB, Klag MJ, Borhani NO,
Cohen JE, Kirchner KA, Lakatos E, Sacks FM, Taylor JO, Hennekens CH, for
the Trials of Hypertension Prevention (TOHP) Collaborative Research Group.
Lack of blood pressure effect with calcium and magnesium supplementation
in adults with high-normal blood pressure: results from Phase I of the
Trials of Hypertension Prevention (TOHP). Ann Epidemiol. 1995;5:96-107.
-
The Trials of Hypertension Prevention
Collaborative Research Group. Effects of weight loss and sodium reduction
intervention on blood pressure and hypertension incidence in overweight
people with high-normal blood pressure: the Trials of Hypertension
Prevention, Phase II. Arch Intern Med. 1997;157:657-667.
-
Miller JZ, Weinberger MH, Christian JC,
Daugherty SA. Familial resemblance in the blood pressure response to
sodium restriction. Am J Epidemiol. 1987;126:822-830.
-
Weinberger MH, Miller JZ, Fineberg NS, Luft
FC, Grim CE, Christian JC. Association of haptoglobin with sodium
sensitivity and resistance of blood pressure.
Hypertension.1987;10:443-446.
-
Grim CE, Wilson TW. Salt, slavery, and
survival: physiological principles underlying the evolutionary hypothesis
of salt-sensitive hypertension in western hemisphere blacks. In: Fray JCS,
Douglas JG, eds. Pathophysiology of Hypertension in Blacks. New York, NY:
Oxford University Press; 1993:25-49.
-
Freis ED, Reda DJ, Masterson BJ. Volume
(weight) loss and blood pressure response following thiazide diuretics.
Hypertension. 1988;12:244-250.
-
Grim CE, Luft FC, Weinberger MH, Miller JZ,
Rose RJ, Christian JC. Genetic, familial, and racial influences on blood
pressure control systems in man. Aust N Z J Med. 1984;14:453-457.
-
Morris RC, Sebastian A. Potassium responsive
hypertension. In: Laragh JH, Brenner BM, eds. Hypertension:
Pathophysiology, Diagnosis, and Management. 2nd ed. New York, NY: Raven
Press Publishers; 1995:2715-2726.
-
Harlan WR, Harlan LC. Blood pressure and
calcium and magnesium intake. In: Hypertension: Pathophysiology,
Diagnosis, and Management. 2nd ed. New York, NY: Raven Press Publishers;
1995:1143-1154.
-
Witteman JCM, Willett WC, Stampfer MJ, Colditz
GA, Sacks FM, Speizer FE, Rosner B, Hennekens CH. A prospective study of
nutritional factors and hypertension among US women. Circulation.
1989;80:1320-1327.
-
Stamler J, Caggiula AW, Grandits GA. Relation
of body mass and alcohol, nutrient, fiber, and caffeine intakes to blood
pressure in the special intervention and usual care groups in the Multiple
Risk Factor Intervention Trial. Am J Clin Nutr. 1997;65(suppl):338S-365S.
-
Geleijnse JM, Witteman JCM, den Breeijen JH,
Hofman A, de Jong PTVM, Pols HAP, Grobbee DE. Dietary electrolyte and
intake and blood pressure in older subjects: the Rotterdam Study. J
Hypertens. 1996;14:737-741.
-
Osborne CG, McTyre RB, Dudek J, Roche KE,
Scheuplein R, Silverstein B, Weinberg MS, Salkeld AA. Evidence for the
relationship of calcium to blood pressure. Nutr Rev. 1996;54:365-381.
-
Pryer J, Cappuccio FP, Elliott P. Dietary
calcium and blood pressure: a review of the observational studies. J Hum
Hypertens. 1995;9:597-604.
-
McCarron DA. Epidemiological evidence and
clinical trials of dietary calcium's effect on blood pressure. Contrib
Nephrol. 1991;90:2-10.
-
McCarron D, Morris C, Henry H, Stanton JL.
Blood pressure and nutrient intake in the United States.
Science.1984;224:1392-1398.
-
Khaw K-T, Barrett-Conner E. The association
between blood pressure, age, and dietary sodium and potassium: a
population study. Circulation. 1988;77:53-61.
-
Hamet P, Mongeau EK, Lambert J, Bellavance F,
Daignault-Gelinas M, Ledoux M, Whissell-Cambiotti L. Interactions among
calcium, sodium, and alcohol intake as determinants of blood pressure.
Hypertension. 1991;17(suppl I):I-150-I-154.
-
Cappuccio FP, MacGregor GA. Does potassium
supplementation lower blood pressure? A meta-analysis of published trials.
J Hypertens. 1991;9:465-473.
-
Whelton PK, He J, Cutler JA, Brancati FL,
Appel LJ, Follmann D, Klag MJ. Effects of oral potassium on blood
pressure: meta-analysis of randomized controlled clinical trials. JAMA.
1997;277:1624-1632.
-
Bucher HC, Cook RJ, Guyatt GH, Lang JD, Cook
DJ, Hatala R, Hunt DL. Effects of dietary calcium supplementation on blood
pressure: a meta-analysis of randomized controlled trials. JAMA.
1996;275:1016-1022.
-
Allender PS, Cutler JA, Follmann D, Cappuccio
FP, Pryer J, Elliott P. Dietary calcium and blood pressure: a
meta-analysis of randomized clinical trials. Ann Intern Med.
1996;124:825-831.
-
Bucher HC, Guyatt GH, Cook RJ, Hatala R, Cook
DJ, Lang JD, Hunt KD. Effect of calcium supplementation on
pregnancy-induced hypertension and preeclampsia: a meta-analysis of
randomized controlled trials. JAMA. 1996;275:1113-1117.
-
Levine RJ, Hauth JC, Curet LB, Sibai BM,
Catalano PM, Morris CD, DerSimonian R, Esterlitz JR, Raymond EG, Bild DE,
Clemens JD, Cutler JA. Trial of calcium to prevent preeclampsia. N Engl J
Med. 1997;337:69-76.
-
Witteman JCM, Grobbee DE, Derkx FHM, Bouillon
R, de Bruijn AM, Hofman A. Reduction of blood pressure with oral magnesium
supplementation in women with mild to moderate hypertension. Am J Clin
Nutr. 1994;60:129-135.
-
Appel LJ, Moore TJ, Obarzanek E, Vollmer WM,
Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin P-H,
Karanja N, for the DASH Collaborative Research Group. A clinical trial of
the effects of dietary patterns on blood pressure. N Engl J Med.
1997;336:1117-1124.
-
The Sixth Report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure. Arch Intern Med. 1997;157:2413-2446.
-
Graudal NA, Galloe AM, Garred P. Effects of
sodium restriction on blood pressure, renin, aldosterone, catecholamines,
cholesterols, and triglyceride: a meta-analysis. JAMA. 1998;279:1383-1391.
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