Nutritional magnesium supplementation does not change blood pressure nor serum or muscle potassium and magnesium in untreated hypertension. A double-blind crossover study. Effect of magnesium supplementation on blood pressure and electrolyte concentrations in hypertensive patients receiving long term diuretic treatment. Blood pressure response during long-term treatment with magnesium is dependent on magnesium status. A double-blind, placebo-controlled study in essential hypertension and in subjects with high-normal blood pressure. Effects of magnesium supplementation in hypertensive patients: assessment by office, home, and ambulatory blood pressures. Reduction of blood pressure with oral magnesium supplementation in women with mild to moderate hypertension. Chronic magnesium administration enhances oxidative glucose metabolism in thiazide treated hypertensive patients. Promising hypotensive effect of hawthorn extract: a randomized double-blind pilot study of mild, essential hypertension. Nutritional dose of magnesium in hypertensive patients on beta blockers lowers systolic blood pressure: a double-blind, cross-over study. Magnesium supplementation in mild hypertensive patients on a moderately low sodium diet. Metabolic and hemodynamic effects of magnesium supplementation in patients with essential hypertension.
The aim of this study was to evaluate if a nutritional dose of magnesium given orally changes the blood pressure in untreated hypertensive patients and if orally-given magnesium had any influence on serum and muscle magnesium and potassium. A randomized, double-blind crossover study design was followed with magnesium 15 mmol/day or placebo treatment for two months. Thirty-nine patients aged 20-59 years, were treated. Samples for magnesium and potassium in blood, muscle and urine were taken at entry time, after two months (crossover time) and after four months (end of study). Systolic and diastolic supine and standing blood pressures were measured at the same times. No significant change in blood pressure, serum or muscle concentrations of electrolytes were observed on magnesium treatment. Urine magnesium rose significantly on magnesium, and it decreased significantly on placebo. Therefore results suggest that 15 mmol magnesium/day, given to untreated mild-to-moderate hypertensives does not alter blood pressure nor the concentrations of magnesium and potassium in serum and muscle, in patients with normal magnesium turnover. nan Both experimental and epidemiological studies support the idea of magnesium supplementation in essential hypertension. We added 15 mmol Mg to a free diet in 71 subjects with mild essential hypertension or a high-normal blood pressure in a double-blind, placebo-controlled study over 6 months. The treatment, which raised urinary magnesium excretion 30%, induced no general effects on the blood pressure. However, when the changes in blood pressure in the actively treated group were related to the pretreatment magnesium status, a correlation was found between pretreatment urinary magnesium excretion and the induced change in supine blood pressure (P less than .05) with a blood pressure reduction in subjects with a low pretreatment urinary excretion of magnesium, and a pressor effect in the subjects with the highest pretreatment levels of urinary magnesium. The induced change in blood pressure was furthermore found to be inversely correlated to the changes in serum magnesium and urinary excretion of sodium (P less than .03) induced by treatment indicating that both a direct calcium antagonist action of magnesium at the cellular level as well as a diuretic effect of the increased magnesium load might be involved in the blood pressure effects of magnesium. Pretreatment serum potassium concentration also appeared to be a predictor of the induced change in standing blood pressure (P less than .03). In conclusion, magnesium supplementation does not seem to be effective in unselected mild hypertensive subjects or in subjects with a high-normal blood pressure and can therefore not be generally recommended.(ABSTRACT TRUNCATED AT 250 WORDS) An increase in magnesium intake has been suggested to lower blood pressure (BP). However, the results of clinical studies are inconsistent. We studied the effects of magnesium supplementation on office, home, and ambulatory BPs in patients with essential hypertension. Sixty untreated or treated patients (34 men and 26 women, aged 33 to 74 years) with office BP >140/90 mm Hg were assigned to an 8-week magnesium supplementation period or an 8-week control period in a randomized crossover design. The subjects were given 20 mmol/d magnesium in the form of magnesium oxide during the intervention period. In the control period, office, home, and average 24-hour BPs (mean+/-SE) were 148.6+/-1.6/90.0+/-0.9, 136.4+/-1.3/86.8+/-0.9, and 133.7+/-1.3/81.0+/-0.8 mmHg, respectively. All of these BPs were significantly lower in the magnesium supplementation period than in the control period, although the differences were small (office, 3.7+/-1.3/1.7+/-0.7 mmHg; home, 2.0+/-0.8/1.4+/-0.6 mmHg; 24-hour, 2.5+/-1.0/1.4+/-0.6 mm Hg). Serum concentration and urinary excretion of magnesium increased significantly with magnesium supplementation. Changes in 24-hour systolic and diastolic BPs were correlated negatively with baseline BP or changes in serum magnesium concentration. These results indicate that magnesium supplementation lowers BP in hypertensive subjects and this effect is greater in subjects with higher BP. Our study supports the usefulness of increasing magnesium intake as a lifestyle modification in the management of hypertension, although its antihypertensive effect may be small. In a double-blind controlled trial, 91 middle-aged and elderly women with mild to moderate hypertension who were not on antihypertensive medication were randomly assigned to treatment with magnesium aspartate-HCl (20 mmol Mg/d) or placebo for 6 mo. Magnesium aspartate-HCl in the given dose was well-tolerated and was not associated with an increased frequency of diarrhea compared with placebo. At the end of the study, systolic blood pressure had fallen by 2.7 mm Hg (95% CI -1.2, 6.7; P = 0.18) and diastolic blood pressure by 3.4 mm Hg (1.3, 5.6; P = 0.003) more in the magnesium group than in the placebo group. Blood pressure response was not associated with baseline magnesium status, as measured by dietary magnesium intake and urinary magnesium excretion. Urinary magnesium excretion in the magnesium group increased by 50% during the intervention period. No changes were seen in other biochemical indexes, including serum concentrations of total and high-density-lipoprotein cholesterol. The findings suggest that oral supplementation with magnesium aspartate-HCl may lower blood pressure in subjects with mild to moderate hypertension. In newly-diagnosed untreated (n = 24) and thiazide treated (n = 18) hypertensive patients erythrocyte ion content and plasma ion and metabolite levels were determined. Thiazide treated patients had lower arterial blood pressure, plasma ion levels, erythrocyte magnesium and potassium content but higher fasting plasma insulin (66 +/- 7 v 87 +/- 8 pmol/L P < .02), triglycerides (1.88 +/- 0.24 v 2.34 +/- 0.44 mmol/L P < .05), free fatty acids (0.68 +/- 0.11 v 0.81 +/- 0.18 mmol/L P < .05). Subsequently, in a double-blind fashion and in random order thiazide diuretic treated patients were assigned to two groups: the first (n = 9) taking magnesium (15.8 mmol/day) and the other (n = 9) a placebo. Each treatment period lasted 8 weeks. At the end of each treatment period, each patient underwent blood sampling for determination of erythrocyte ion content and plasma ion and metabolite levels and was submitted to an euglycemic hyperinsulinemic (1 mU/kg/min for 120 min) glucose clamp. In this latter test D-3-H glucose infusion and indirect calorimetry allowed determination of glucose turnover parameters and substrate oxidation respectively. Chronic magnesium administration (CMA) raised fasting plasma (0.79 +/- 0.03 v 0.83 +/- 0.02 mmol/L, P < .05) and erythrocyte (1.98 +/- 0.08 v 2.35 +/- 0.03 mmol/L, P < .01) magnesium content. Along with insulin infusion, CMA improved glucose uptake, glucose metabolic clearance rate, and oxidative glucose metabolism. In the multiple linear regression analysis of the pooled basal data (n = 42), erythrocyte magnesium content displayed an independent correlation with basal plasma insulin levels (t = -2.08, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS) This pilot study was aimed at investigating the hypotensive potential of hawthorn extract and magnesium dietary supplements individually and in combination, compared with a placebo. Thirty-six mildly hypertensive subjects completed the study. At baseline, anthropometric and dietary assessment, as well as blood pressure measurements were taken at rest, after exercise and after a computer 'stress' test. Volunteers were then randomly assigned to a daily supplement for 10 weeks of either: (a) 600 mg Mg, (b) 500 mg hawthorn extract, (c) a combination of (a) and (b), (d) placebo. Measurements were repeated at 5 and 10 weeks of intervention. There was a decline in both systolic and diastolic blood pressure in all treatment groups, including placebo, but ANOVA provided no evidence of difference between treatments. However, factorial contrast analysis in ANOVA showed a promising reduction (p = 0.081) in the resting diastolic blood pressure at week 10 in the 19 subjects who were assigned to the hawthorn extract, compared with the other groups. Furthermore, a trend towards a reduction in anxiety (p = 0.094) was also observed in those taking hawthorn compared with the other groups. These findings warrant further study, particularly in view of the low dose of hawthorn extract used.
                Copyright 2002 John Wiley & Sons, Ltd. To evaluate if magnesium alters blood pressure in hypertensive patients treated with beta blockers and if such effect can be coupled to a change in potassium and magnesium levels in muscle, serum and urine.
                A randomized double-blind, cross-over study with magnesium and placebo taken orally, each for 8 weeks.
                Outpatient clinic, University Hospital, Umeå, Sweden.
                Thirty-nine patients aged 26-69 years with moderate essential hypertension, treated before entry and during the study with continuous, unchanged beta blockers completed the study.
                Random allocation to receive magnesium aspartate or placebo. Daily magnesium dose was 15 mmol (365 mg) distributed three times a day over 8 weeks.
                Blood pressure, serum, urine and muscle magnesium and potassium. Measurements performed at the start, after 8 and 16 weeks.
                Systolic supine and standing blood pressure significantly decreased when magnesium was supplemented following placebo but not when magnesium was given at start. When magnesium and placebo groups were independently compared there was no significant change in supine and standing systolic and diastolic pressure. Serum and urine magnesium and serum potassium were significantly higher after magnesium treatment, whilst no change was present in urine potassium or in muscle magnesium and potassium.
                This study showed that 15 mmol magnesium day-1 given to mild to moderate hypertensive patients treated with beta blockers could be the cause of a significant decrease in supine and standing systolic blood pressure. 1. The effect of oral magnesium supplementation was assessed in a group of untreated, mild hypertensive subjects who were following a moderately low sodium diet (baseline urinary sodium 86 +/- 6 mmol/day). 2. Thirteen patients were allocated placebo and 12 were allocated magnesium aspartate (10 mmol/day) in a double blind fashion for 8 weeks. 3. There was no fall in blood pressure with magnesium supplementation and no significant difference in blood pressure between groups at the end of the study. 4. In the magnesium group there was an increase in urinary magnesium (4.4 +/- 0.6 to 6.1 +/- 1 mmol/day P less than 0.001), and urinary calcium (4.3 +/- 0.7 to 5.5 +/- 0.9 mmol/day P less than 0.01). There was no change in plasma or red cell magnesium or plasma renin activity with supplementation. 5. Magnesium supplementation does not appear to have an additive hypotensive effect in mild hypertensive subjects on a reduced sodium intake. The effect of magnesium supplementation on blood pressure, erythrocyte cation metabolism, and serum lipids was evaluated in 13 patients with mild hypertension. After randomization and a 3-wk placebo run-in period, seven patients received 40 mmol Mg aspartate (20 mmol elemental Mg twice daily) and six received placebo for 3 mo. In comparison with placebo treatment, magnesium aspartate therapy had no effect on blood pressure, lipid concentrations, or erythrocyte cation metabolism. These results demonstrate that in magnesium-repleted hypertensive subjects, magnesium supplementation does not affect blood pressure or lipids probably because magnesium has no effect on cellular cation metabolism in magnesium-replete individuals.
In view of the poor quality of included trials and the heterogeneity between trials, the evidence in favour of a causal association between magnesium 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 magnesium supplementation on blood pressure and cardiovascular outcomes.