1. Anderson, John J.B. PhD

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Use of calcium supplements by adults has been widely accepted, because the supplements are intended to help maintain bone mass and density and prevent late-life fractures.1 Unfortunately, several reports have demonstrated that such supplements have little or no effect on skeletal retention and osteoporotic fracture prevention.2,3 Only 1 classic report, based on supplements of calcium phosphate salts and vitamin D, has shown major reductions of hip fractures in older women with more than 6 months' therapy.4 This study has not been replicated, however and therefore, remains an outlier when compared with numerous other published data.5


A few years ago, the US Preventive Services Task Force recommended against the use of calcium and vitamin D supplements taken by adults without recommendation of a clinician for the purpose of preventing osteoporotic fractures.6 The report implies that decisions for taking supplemental calcium should rest with the physician and patient, based on the patient's clinical status. This change in advice resulted from increasing data showing the potential adverse effects of supplemental calcium salts, typically calcium carbonate, as being associated with renal stones7 and coronary artery calcification (CAC)8 in older adults of both genders.


Much concern about effects of the supplemental calcium salts revolves around the far more common CAC, also known as atherosclerotic calcification, which is a process that contributes to cardiovascular disease,9 especially in those older than 60 years. In all likelihood, he arteries of the heart and other major organs such as the brain10 and kidney11 also may become calcified at common sites of plaque formation. New bone formation occurs in arteries only after pathological changes, that is plaque, is established at specific sites. Prevalence data of CAC suggest that by the age of 50, as high as 50% of healthy adults have this abnormality of new bone formation in arterial walls, that is, at highly inappropriate locations outside the skeleton,8 and it typically progresses with age. Although mechanisms underlying the genetic conversion of vascular intimal cells to bone-like osteoblast cells are not established, the switch only occurs in the plaque-laden intimal layers of arteries.12


Calcium salts may be handled differently by the body largely because of the differences in the chemical state between dietary and supplemental calcium. A matrix exists in food sources for calcium, but no such matrix accompanies mineral salts such as calcium carbonate and others. Intestinal absorption of calcium in supplements is more rapid; serum calcium increases acutely, and distribution in the blood is more prompt compared with matrix-based calcium sources.13,14 Absorbed calcium ions also tend to suppress parathyroid hormone (PTH) secretion because the supplemental calcium load is higher for longer time frames than when calcium is consumed from foods.13 Much remains to be learned about the effect of suppressed PTH on organs other than bone, where the relative lack of circulating PTH suppresses both bone formation and resorption. Such adynamic bone does not take up calcium ions from blood because new bone formation is practically nonexistent during these time frames.15 The question then becomes "where do the extra calcium ions go?" Much excess is sent to the kidneys for excretion, a limited exit route, and the remainder travels to distal organs in blood for potential uptake by soft tissues for ectopic calcification, especially at sites in arteries where plaques already have formed.15 Because of their potential risks, calcium supplements should not be clinically used in the routine therapy for the prevention of osteoporotic fractures.16


Questions as to whether the CAC damage results primarily from supplemental calcium salts or from any combination of high calcium intakes, including both calcium salts and matrix-bound calcium in foods, arises, but 1 recent report suggests that the CAC damage results largely from supplements and that food calcium can be consumed at a fairly high level without inducing CAC.8 Therefore, despite new data on the adverse effects of high amounts of supplemental calcium, that is, about 1000 mg per day, in stimulating CAC, additional prospective human investigations are needed to sort out the physiological and pathological differences, if any, between the calcium sources, supplemental versus food-borne, that contribute to the generation of bone in inappropriate locations and increases the risk of cardiovascular diseases.




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