To the Editor: Calcium and vitamin D play a central role in preventing osteoporosis and fractures,1 so a recent study published in the BMJ claiming that calcium supplements increased the risk of heart attacks and strokes in postmenopausal women2 naturally received widespread media attention — so much so that many patients are already stopping calcium treatment.

The study, based on a previously published randomised controlled trial of calcium supplementation in 1471 healthy women,3 showed that self- or family-reported heart attack, stroke or sudden death was significantly more common in those taking calcium than in the placebo group (P = 0.008). This conflicted with the findings of a much larger study.4 Further, the difference became non-significant when the analysis was corrected for covariables (P = 0.08), or when the analysis was repeated using data on cardiovascular events obtained from medical records (P = 0.08). Yet, it still gained a place in a leading medical journal.

The small excess of cardiovascular events in the women taking calcium could be due to chance and needs to be tested further; one way of doing this is to examine available data for evidence of mortality in patients taking calcium. We have done this. In the 29 randomised trials in a recent meta-analysis of the effect of calcium and vitamin D in fracture risk,1 five trials comprising 12 609 subjects provided crude mortality data.5-9 When these mortality data were pooled using a random effects model, there was no evidence that calcium supplementation increased mortality (Box).

We find it hard to believe that calcium can have a significant adverse effect on cardiovascular disease without increasing mortality. Our reservations about this study are further strengthened by the weak theoretical basis of the case against calcium. Metastatic calcification in renal failure, which the authors quote as an analogy,2 is due to the high serum calcium–phosphorus (CaxP) product levels caused by hyperphosphataemia, which may be aggravated by calcium supplementation. In women without this condition, this degree of oversaturation cannot be reached by the 5% rise in plasma calcium10 resulting from the recommended dose of calcium citrate used for supplementation.

Moreover, coronary blockage is not due to calcification of atheromatous vessels, which is a dystrophic calcification secondary to tissue damage, but rather to ruptured atheromatous plaques and the thrombi which form upon them.

Thus, it is premature to conclude that calcium supplementation should not be given to older women.

Effect of calcium supplementation on mortality, data pooled by a random effects model