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Barry D. Dickinson, PhD; Stephen Havas, MD, MPH, MS

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We thank Premaor and colleagues for reinforcing the fact that sodium intake affects calcium disposition, and that resulting physiologic compensatory mechanisms may contribute to the pathogenesis of high blood pressure, as well as changes in body mass index, in some individuals. Both blood pressure and salt intake are independent predictors of urinary calcium excretion.¹ The average urinary calcium loss is approximately 1 mmol per 100 mmol of sodium. Patients with high blood pressure have a higher urinary calcium excretion for a given urinary sodium excretion than normotensive people, as well as a tendency for lower ionized calcium and higher parathyroid hormone concentrations.² Such changes have been linked with the development of hypertension, especially in women.³

Although the long-term effects of dietary sodium on bone mineral density are unknown, short-term increases in sodium intake increase bone resorption in postmenopausal women.^4-5 . . . [Full Text of this Article]

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RELATED LETTER

Cardiovascular Disease, Sodium Intake, and Urinary Calcium Loss
Melissa O. Premaor, Roberta Vanacour, and Tania W. Furlanetto
Arch Intern Med. 2008;168(3):332.
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