News Release

Studies Link Calcium Problem To Atherosclerosis And Osteoporosis

Peer-Reviewed Publication

American Heart Association

DALLAS, Sept. 16 -- Two diseases -- atherosclerosis and osteoporosis -- may be linked by a common problem in how the body uses calcium, according to two reports in American Heart Associations journals. One report is published in Stroke, the other is in today's Circulation.

Calcium is found in the crusty plaques that form on the inner of the artery and over time the plaque can obstruct and trigger heart attacks and strokes. Calcium deficiency has also been linked to osteoporosis, in which bones become weak or brittle.

Osamu Uyama, M.D., Ph.D., the lead author of the study appearing in this month's Stroke, says that the two diseases have been thought of as unrelated, but "the increase in atherosclerosis among women as they develop osteoporosis suggests that the two illnesses may be more closely related than previously realized."

Uyama and his colleagues at the division of pathobiology of the College of Nursing Art and Science in Hyogo, Akashi, Japan, examined the carotid arteries of 30 postmenopausal women between 67 and 85 years of age living in an upper-middle-class senior citizens' residence. Carotid arteries, located in the neck, supply blood to the brain. Carotid atherosclerosis is a major cause of stroke.

The researchers used X-ray absorption tests to measure bone mineral density and ultrasound to check the amount of atherosclerotic narrowing in each woman's carotid arteries. They found that bone mineral density declined as atherosclerotic plaque increased. Low bone density, which causes osteoporosis, results in weakened or brittle bones that may fracture easily.

California investigators tried to tease out the underlying problem that may explain the association. They suspected osteoporosis and atherosclerosis might be related to a problem in handling calcium. Lead author of the Circulation report, Karol E. Watson, M.D., a clinical instructor of medicine at the University of California at Los Angeles School of Medicine, says calcium deposits on the plaques have always been thought to be a "passive process that was simply a natural part of aging. But recent research suggests that it is something we can control and this could open up new treatments."

While osteoporosis has been linked to prolonged calcium deficiency, it is also a symptom of oral vitamin D overdose. Oral vitamin D is given to encourage bone-growth in people with osteoporosis, and it is added to dairy products in several countries including the United States. The way the body uses the oral form is quite complex. Unless a person is vitamin-deficient, the kidneys convert only a fraction of dietary vitamin D into a form usable to cells. However, the system can be overridden with megadoses of oral vitamin D -- hence the possibility for overdose in patients being treated with the substance.

Watson and colleagues studied 173 men and women who were either at high or moderate risk for coronary heart disease. Calcification in the blood vessels near the heart and blood levels of 1,25-vitamin D were examined. This is the form of the vitamin made in a two-step process involving activation by sunlight in the skin and enzymes in the kidney. This form is most likely to be active in the body's regulatory processes of calcium.

The researchers used a relatively new, non-invasive imaging tool called electron beam computed technology (EBCT) which is the only way to see calcium deposits in the heart's coronary arteries. Its use in the past five years has made scientists appreciate how common artery calcification is, she says.

The California researchers were surprised by their study's results. "We thought the development of atherosclerotic calcification would respond in the same way as bone -- that high vitamin D would lead to higher calcium absorption, but serum vitamin D seems to have an opposite effect on the skeleton as it does on the vessels," she says. "The lower the vitamin 1,25-D level the higher the level of calcification in the blood vessels."

In separate "test tube studies" Watson found more evidence that bone and artery calcification are different but related processes. In one experiment, fats were exposed to both artery cells and bone cells. "The bone cells stopped calcifying whereas the artery cells increased calcification," she says.

They see their results, though confusing, as somewhat promising because they do provide a bases for the idea that the diseases could occur together and this "might point the way to new treatments," she says.

Uyama agrees. "I doubt there will be one magic bullet to treat both conditions but it certainly will make us think about how one treatment for one affects the other."

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Media advisory: Dr. Uyama can be reached by fax 81-078-925-0878 or e-mail (uyama@kh.rim.or.jp). Dr. Watson's phone number is (310) 206-2677. (Please do not publish numbers.)


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