Effect of oral calcium supplementation on blood pressure in patients with previously untreated hypertension: a randomised, double-blind, placebo-controlled, crossover study. Dietary calcium supplementation as a treatment for mild hypertension. Double-blind randomized, crossover trial of calcium supplementation in essential hypertension. Blood pressure response to oral calcium in persons with mild to moderate hypertension. A randomized, double-blind, placebo-controlled, crossover trial. Calcium supplementation reduces the risk of pregnancy-induced hypertension in an Andes population. The blood pressure effects of calcium supplementation in humans of known sodium responsiveness. Calcium supplementation reduces blood pressure during pregnancy: results of a randomized controlled clinical trial. Controlled trial of long-term oral calcium supplementation in essential hypertension. Calcium supplementation in patients with essential hypertension: assessment by office, home and ambulatory blood pressure.
It has been claimed that calcium lowers BP. The present randomised, double-blind, placebo-controlled crossover study is the first to investigate the effect on BP of a high oral dose of calcium given for a long period to patients with previously untreated hypertension. Elemental calcium (2 g) was administered for 12 weeks interchanging with a period of 12 weeks of placebo. Twenty patients completed the protocol. There was no significant difference in change of BP during the period of additional calcium intake when compared with placebo (P = 0.33). The risk of not detecting a real BP-lowering effect of calcium of at least 3 mmHg was < 5%. No evidence for the existence of a subgroup of 'responders' was found. It is concluded that a high daily dose of calcium supplementation given for 12 weeks does not decrease BP in previously untreated patients with mild to moderate hypertension. The blood pressure responses of 19 mildly hypertensive (diastolic blood pressure 90-104 mmHg) individuals to treatment with either 1200 mg of elemental calcium supplementation or placebo were assessed weekly in a 6-month randomized, double-blind, placebo-controlled crossover study. Both groups showed a decrease in blood pressure (calcium treated: 6 +/- 12 mmHg systolic, 7 +/- 7 mmHg diastolic; and placebo controlled: 9 +/- 14 mmHg systolic, 9 +/- 8 mmHg diastolic). Differences between the two groups were not significant (P greater than 0.1). There were no adverse effects to either treatment. This study does not support the hypothesis that dietary calcium supplementation is more effective than placebo in reducing blood pressure in mildly hypertensive individuals. In a double-blind, randomized, placebo-controlled, crossover trial, 23 middle-aged patients with mild to moderate essential hypertension were given an oral calcium supplement (1 g/day) for 8 weeks. At the end of this period, eight patients continued with this treatment for an additional 2 weeks but were also given 0.5 micrograms/day of 1,25-(OH)2 vitamin D3. In the 21 patients who completed the study, arterial pressure during the calcium-supplemented phase was almost identical to that of the placebo phase. In eight patients, mean arterial pressure (MAP) had changed by greater than 5 mmHg at the end of the calcium-supplemented period, compared with the end of the placebo phase (six patients showed an increase in MAP and two a decrease). Changes in arterial pressure were unrelated to age, plasma ionized calcium, parathyroid hormone (PTH), plasma renin activity (PRA), plasma aldosterone, 24-h urinary calcium, sodium and potassium and were only weakly related to body weight. In the eight patients who continued with the treatment of calcium plus 1,25-(OH)2 vitamin D3 after the 8-week study period, arterial pressure changed very little and not significantly. These results do not support the suggestion that calcium supplements lower arterial pressure in middle-aged subjects with mild to moderate essential hypertension. The blood pressure response of 48 hypertensive persons and 32 normotensive persons to elemental calcium (as the carbonate or citrate salt), 1000 mg/d for 8 weeks, was assessed in a randomized, double-blind, placebo-controlled, crossover trial. Compared with placebo, Ca2+ significantly lowered supine systolic blood pressure by 3.8 mm Hg, standing systolic blood pressure by 5.6 mm Hg (p less than 0.02), and supine diastolic blood pressure by 2.3 mm Hg (p less than 0.05) in hypertensive persons. The response in normotensive persons differed significantly from that in hypertensives (p less than 0.03) as their blood pressure was unchanged. Twenty-one (44%) hypertensive and 6 (19%) normotensive persons achieved a reduction in standing systolic arterial pressure of 10 mm Hg or greater. Reported adverse effects were similar between calcium and placebo phases and did not necessitate withdrawal of any patient from the trial. Treatment with 1000 mg/d of oral Ca2+ for 8 weeks represents a safe, well-tolerated, nonpharmacologic intervention that lowers blood pressure in selected patients with mild to moderate hypertension. Previous studies have suggested that increased dietary calcium is associated with a decreased occurrence of pregnancy-induced hypertension. In this study 106 young healthy nulliparous women, residing in Quito, Ecuador, were enrolled in a double-blind, randomized, controlled clinical trial. From 24 weeks gestation until delivery they received either 2 g of elemental calcium per day or a placebo. Calcium supplementation was associated with a significantly decreased risk of pregnancy-induced hypertension, with 4.1% developing pregnancy-induced hypertension in the treatment group versus 27.9% in the placebo group. Treatment was associated with a decrease in both systolic and diastolic blood pressure over the course of pregnancy. In addition, there was a small but significant increase in serum ionized calcium levels in the calcium-supplemented group during the treatment period. We examined the interactions between sodium and calcium responsiveness of blood pressure by studying the effects of calcium supplementation in 46 normotensive and hypertensive subjects who had been previously characterized as salt sensitive or salt resistant on the basis of their blood pressure responses to rapid sodium and extracellular volume expansion and contraction. The calcium supplementation study utilized a placebo-controlled, double-blind, randomized crossover design. Subjects received calcium carbonate supplementation (1.5 g/day) for 8 weeks or matching placebo, with 2-week placebo lead-in and crossover periods. For the entire group, no significant blood pressure changes were seen with calcium supplementation. When the subjects were separated on the basis of race or prior salt sensitivity, significant differences were seen. Blacks and salt sensitive subjects exhibited a significant (P < .05) blood pressure decrease when compared to their counterparts. Calcium sensitive subjects had significantly (P < .02) lower levels of plasma renin activity than those not demonstrating a decrease in blood pressure with added calcium. When urinary calcium excretion of subjects previously defined as salt sensitive or salt resistant were compared, the former had significantly (P < .001) higher calcium excretion values at baseline as well as during the placebo and calcium supplementation periods than did the latter. There were no known differences in dietary calcium intake to account for the striking urinary findings. These observations confirm the heterogeneity of blood pressure response to calcium supplementation and demonstrate congruity between sodium and calcium responsiveness of blood pressure in normal and hypertensive humans.(ABSTRACT TRUNCATED AT 250 WORDS) Fifty-two healthy pregnant women were enrolled in a double-blind, randomized, controlled clinical trial. After the 26th week of gestation, the women were given either 1.5 g of elemental calcium per day or a placebo. Subjects in the calcium group, after adjustment for race and initial blood pressure (BP), had a term mean systolic and diastolic BP value of 4-5 mmHg lower than those in the placebo group (P less than .05). The incidence of pregnancy-induced hypertension was 11.1% in the placebo group and 4.0% in the calcium group, a nonsignificant difference. Combining these values with previous data, we found a dose-effect relationship between calcium intake and BP reduction during the third trimester of pregnancy. Further research should be directed at understanding the mechanism of this effect and trying to demonstrate a reduction in pregnancy-induced hypertension with calcium supplementation in a larger population. A randomized, double-blind, placebo-controlled crossover trial of oral calcium supplementation was carried out in 18 patients with uncomplicated essential hypertension. After 15 weeks of oral calcium supplementation, 1 g/day, of the patients' habitual diet, the only blood pressure change (compared with the results of placebo treatment) was in the average standing systolic blood pressure, which was significantly reduced (-8.6 mm Hg; p less than 0.01). The 24-hour urinary calcium excretion and the total serum calcium concentration increased significantly during calcium supplementation (p less than 0.05), indicating good compliance with the treatment. The individual blood pressure changes with high calcium intake were found to be inversely related to basal 24-hour urinary calcium excretion (r = -0.69, p less than 0.001 for standing systolic pressure; r = -0.55, p less than 0.002 for standing diastolic pressure). This correlation was independent of age, basal blood pressure, serum calcium concentration, basal 24-hour urinary sodium excretion, and body weight changes during the trial. In particular, a subgroup of six patients, who had a basal 24-hour urinary calcium excretion higher than the mean + 2 SD of a reference healthy population previously described, showed a substantial average blood pressure fall at variance with the other patients in the study. These results do not support the usefulness of an oral calcium supplement in the majority of subjects with mild essential hypertension; however, they suggest that a group of patients with a previously reported abnormality of calcium metabolism may be responsive to this therapeutic measure. To study the effects of a high calcium intake in hypertensive patients by blood pressure monitoring.
                In a randomized crossover study, patients were assigned to an 8-week calcium supplementation period and an 8-week control period. The subjects were given 25 mmol/day (1 g/day) of calcium as calcium carbonate during the intervention period.
                A hypertension clinic in a tertiary teaching hospital.
                Sixty untreated or treated hypertensive patients (35 men and 25 women, mean age 58 years) with office systolic/diastolic blood pressure > or = 140/90 mmHg.
                Office blood pressure, home blood pressure (last 7 days), and ambulatory 24 h blood pressure (every 30 min using TM-2421).
                The serum calcium concentration and urinary calcium excretion increased significantly with calcium supplementation. Office, home and 24 h blood pressure were lower in the calcium period than in the control period, although the differences were small (mean +/- SEM office blood pressure: 1.2+/-1.2/1.1+/-0.7 mmHg; home blood pressure: 1.9+/-0.7/1.3+/-0.6 mmHg; 24 h blood pressure: 1.2+/-0.8/0.9+/-0.5 mmHg,), and significant only for home systolic and diastolic blood pressures. The difference in home systolic blood pressure was inversely correlated with the level of home blood pressure in the control period and with the difference in urinary calcium. The difference in 24 h systolic blood pressure was positively correlated with the control level of urinary calcium. Age, sex, antihypertensive medication, drinking habit, sodium intake or order of treatment did not significantly influence the effects of calcium supplementation.
                An increase in calcium intake tends to lower office, home and ambulatory blood pressure in hypertensive patients. However, the antihypertensive effect is too small to support the general application of a high calcium intake in the treatment of hypertension.
Due to poor quality of included trials and heterogeneity between trials, the evidence in favour of causal association between calcium supplementation and blood pressure reduction is weak and is probably due to bias. This is because poor quality studies generally tend to over-estimate the effects of treatment. Larger, longer duration and better quality double-blind placebo controlled trials are needed to assess the effect of calcium supplementation on blood pressure and cardiovascular outcomes.