BoneKEy-Osteovision | Commentary
Calcium: Good for your bones, good for your heart?
Commentary on:. Reid IR, Mason B, Horne A, Ames R, Clearwater J, Bava U, Orr-Walker B, Wu F, Evans MC, Gamble GD. Effects of calcium supplementation on serum lipid concentrations in normal older women: a randomized controlled trial. Am J Med. 2002 Apr 1;112(5):343-7.
Calcium supplementation has come of age, thanks to a vast consensus between physicians, nutritionists and their patients. There is consensus that the calcium intake of older people is often insufficient for skeletal health (), and oral calcium supplements increase bone mass (). Calcium supplementation (with or without vitamin D) also decreases the risk of vertebral fracture (), nonvertebral fracture () and hip fracture (). The principal risk to be weighed against these benefits is a small increase in the incidence of kidney stones (). Although these favorable effects upon the skeleton give us reason enough to recommend calcium supplements, a recent article reports another potential benefit, an increase in the level of HDL cholesterol (HDL-C) ().
Reid et al. conducted a randomized controlled trial of the effects of calcium supplementation on serum lipid levels as a substudy of a larger trial designed to look at calcium supplementation and fracture risk (). They assigned 223 postmenopausal women with a normal bone mass for age (Z-score > -2) to receive either one gram of calcium daily as calcium citrate or placebo. Women receiving therapy for hyperlipidemia were excluded from the substudy. At the end of one year of therapy, women treated with calcium citrate experienced a 7% increase in HDL-C, a nonsignificant 6% decline in calculated LDL-C levels, and no change in the level of triglycerides.
High HDL levels have a powerful cardioprotective effect. HDL particles remove cholesterol from cells, including those in atherosclerotic plaques, and the core protein of HDL, apolipoprotein A-1, mobilizes cholesterol ester stores in macrophages. Besides its role in reverse cholesterol transport, HDL also has antioxidant and anti-inflammatory properties. The mechanism by which oral calcium would increase HDL levels is unknown, but it has been reported that oral calcium inhibits the absorption of dietary fats and bile acids by binding them in the gut (). The possibility that citrate has its own effects on HDL also deserves consideration.
Low plasma HDL-C levels are powerful predictors of coronary heart disease (CHD), particularly in women (). Observational studies have shown a curvilinear relationship of HDL-C and CHD, but on average a population increase of 1% in HDL-C is associated with an relative reduction in the risk of coronary events of 2% in men and 3% in women ().
How then does the 7% increase in HDL-C that was reported by Reid et al. compare with the effects of traditional hypolipidemic therapy? Quite favorably with the effects of HMG-CoA reductase inhibitors (statins). For example, pravastatin therapy was associated with a 5% increase in the levels of HDL-C in the West of Scotland Coronary Prevention Study () and simvastatin treatment with an 8% increment in HDL-C in the Scandinavian Simvastatin Survival Study ().
Fibrates have similar effects on HDL-C. Gemfibrizol therapy achieved a 9% increase in HDL-C in the Helskinki Heart Study, and this was associated with a 34% reduction in the incidence of coronary events (). Every 1% increase in HDL-C on therapy was associated with a 3% reduction in coronary events, independent of changes in other lipids - thus the quantitative cardiovascular benefit of raising HDL-C levels with gemfibrizol agreed well with the the relationship between HDL-C and coronary events that was previously found in observational studies (). In VA-HIT, a VA Cooperative Study of men with very low HDL-C levels (32 mg/dl, or 0.83 mmol/l) but normal levels of LDL-C (111 mg/dl), treatment with gemfibrizol achieved a 6% increase in HDL-C that was also associated with a substantial reduction in coronary events ().
By this yardstick the 7% increase in HDL-C reported by Reid () is impressive. Should we recommend calcium supplementation to our patients as a hypolipidemic therapy on this basis? Probably not until these results have been confirmed and extended in several ways. Two previous randomized trials differed in their conclusions about the effect of oral calcium on HDL-C (); the results of Reid et al. require confirmation. It will also be important to extend these observations to a population of men. Finally, the subjects in the Reid study had high HDL-C levels at baseline, averaging 63.1 mg/dl (1.65 mmol/l), and it will be essential to determine the effects of calcium treatment on low HDL levels in subjects who are at substantially increased risk of coronary events. In the meantime, it is good to think that calcium, which has already achieved the status of motherhood and apple pie in the estimation of most boneheads, may be even better than we thought.
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