he mainstream medical establishment is still fixated on the effects of dietary salt (sodium chloride) on blood pressure. However, evidence going back over three decades clearly shows that in normal healthy individuals salt does not cause an increase in blood pressure, even if consumed in high amounts. The reason for this is that a healthy individual is able to regulate water and salt balance and the kidney is able to excrete any sodium chloride that is not required for normal physiological function. Ingesting more salt results in excretion of the excess with the kidney easily able to handle the amount of salt found in a typical Western diet. However, strong evidence does implicate calcium in the aetiology of hypertension. Rather than an excess of calcium, it appears that a chronic deficiency of dietary calcium, leading to a decrease in plasma levels, may be a primary driver of blood pressure rises.
The ability of calcium supplementation to lower blood pressure in those with hypertension has been demonstrated in the nutritional literature. For example, researchers1 showed that administration of 1500 mg per day of calcium using a randomised double-blind placebo controlled study design caused significant reductions in blood pressure over 12 weeks of supplementation, when compared to the placebo group. Other intervention studies have found similar effects and epidemiological studies show an inverse association between calcium intake and blood pressure. However, the results of some studies have been inconclusive, and although in some cases this can be attributed to method design flaws, there is some consistent evidence that populations studied may contain non-responders. When comparisons have been performed between subjects which respond to supplementation and those who do not, clear differences exist.
For example, in one study1, comparison of the calcium responders (defined as those with a decrease in blood pressure of more than 5 mm Hg in mean arterial pressure) to non-responders, showed that the responders were older, had higher mean arterial pressure, lower total plasma calcium and higher parathyroid hormone. This suggests that those with a calcium deficient diet, reflected in the low plasma calcium levels and high parathyroid levels, respond to calcium supplementation. In other words, one of the symptoms of a calcium deficiency is high blood pressure. Interestingly, high calcium intakes are inversely associated to abdominal weight gain and obesity, and increasing calcium intake may improve insulin sensitivity through the prevention of the calcium paradox (whereby low calcium intakes cause high cellular calcium levels and interference in the insulin signal cascade). Therefore calcium supplements may affect blood pressure through modulation of the action of insulin.
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