Mildred S. Seelig, M.D - "Arterial Damage of Magnesium Deficiency, Intensified by High Calcium and Vitamin D Intakes"

High dietary calcium/magnesium dietary ratios have uniformly increased the susceptibility to the symptoms and signs of magnesium deficiency. It is important to remember that high intakes of calcium interfere with magnesium intestinal absorption and increase its renal excretion, and that high intakes of vitamin D also favor calcium retention over that of magnesium (Reviews: Seelig, 1964, 1971).

Cardiovascular changes, similar to those seen in "pure" magnesium deficiency, developed in rats fed 400-650 times as much calcium as magnesium (versus 40/1 in controls, which is also a much higher than normal Ca ratio). There were small inflammatory and necrotic myocardial lesions (suggestive of disease of the small coronary arteries) with increased tissue calcium and sodium, but no significant change in serum calcium, and low tissue and serum magnesium and potassium (Mishra, 1960a; Ko et al., 1962). Adding sufficient magnesium to lower the Ca/Mg ratio to 3/1 prevented the lesions (Mishra, 1960a). In a study designed to show how much magnesium is necessary to prevent macroscopically manifest intimal calcific plaques in dogs on Ca/Mg intakes of 33-50/1, Bunce et al. (1962a) found a little more than a twofold increase in grossly visible aortic intimal lesions in dogs receiving 0.6% of calcium (Ca/Mg = 33/1). Most of the dogs on high calcium/low magnesium intakes had intimal plaques.

Since vitamin D normally increases serum calcium levels and increases magnesium requirements, it is of interest that magnesium-deficient dogs on normal calcium intakes showed minimal coronary arterial calcification unless they were given vitamin D or an intravenous calcium load (Syllm-Rapoport and Strassburger, 1968; Unglaub et al., 1959). An early study (Handovsky and Goormaghtigh, 1935) showed that moderately high doses of vitamin D significantly raised the blood pressure in dogs; that vitamin D excess causes arteriosclerosis has been known even longer (Kreitmair and Moll, 1928). Like the arterial lesions of magnesium deficiency, those of experimental hypervitaminosis D (Gillman and Gilbert, 1956) involve medial and elastica degeneration and calcification (Review: Seelig, 1969), but the predominant lesions described were of the larger arteries, rather than of the coronaries. Rats on toxic doses of vitamin D also developed hypercholesterolemia, hypertension, and aortic calcification; the latter changes were prevented by high-dosage magnesium supplementation (Sos et al., 1960; Rigo, 1965; Rigo et al., 1965a; Sos, 1965).

When calves were fed low-magnesium diets that were usually comprised of whole milk or a comparable synthetic diet (both supplemented with vitamin D) for prolonged periods, they developed neuromuscular signs of magnesium deficiency and endocardial and intimal plaques, and fragmentation, degeneration, and calcification of the elastic fibers of both endocardium and arteries, and phlebothrombosis and focal myocardial necrosis (Moore et al., 1936, 1938; Blaxter et al., 1954). The magnesium-deficiency syndrome was prevented by magnesium supplementation: 30-40 mg/kg/day (Huffman et al., 1930; Duncan et al., 1935; Moore et al., 1936, 1938; Blaxter et al., 1954). Like human infants, despite these calves' high calcium intakes, their serum calcium remained normal or slightly low. In addition to the endocardial and intimal calcification, calves on a whole-milk diet developed high serum cholesterol levels (J. W. Thomas, 1959).

Source: Mildred S. Seelig, M.D. “MAGNESIUM DEFICIENCY IN THE PATHOGENESIS OF CARDIOVASCULAR DISEASES” Part II: Chapter 6 http://www.mgwater.com/Seelig/Magnesium-Deficiency-in-the-Pathogenesis-of-Disease/chapter6.shtml#toc6-5-1