Editorials
Health services administration Cardiovascular diseases Endocrinology
Volume 194 - Issue 1

In defence of calcium

Author:  B E Christopher Nordin

Med J Aust 2011; 194 (1): 3-4. || doi: 10.5694/j.1326-5377.2011.tb04133.x
Published online: 3 January 2011
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Reports of adverse events related to calcium supplementation should be supported by rigorous evidence

Calcium is an essential nutrient, not only because of its major role in bone, where 99% of it is stored, but because of its central role in neuromuscular function. It is this latter role that explains why ionised calcium in the blood and tissue fluids is one of the most tightly controlled analytes of those that are commonly measured.1 However, maintenance of the calcium level in tissue fluids carries with it the penalty of continuous loss of calcium through the kidneys, bowel and skin, even on a low calcium intake, which is why the recommended daily calcium allowance for adults is relatively high, at 1000 mg.2

Nutritional deficiencies of other minerals, such as magnesium and phosphate, are rare because their tissue fluid levels are not tightly controlled but vary with intake and, therefore, so does their excretion. Calcium is different; reducing calcium intake has a marginal effect on extracellular calcium (and therefore on calcium excretion) because bone is mobilised to maintain the calcium level, which leads sooner or later to the development of osteoporosis. This is the case in laboratory animals3 and, by implication, in humans. Osteoporosis is therefore the index disease for calcium deficiency,4 just as rickets and osteomalacia are the index diseases for vitamin D deficiency; however, there is some overlap between them because the secondary hyperparathyroidism associated with hypovitaminosis D5 increases bone resorption. This is not to suggest that all adult osteoporosis is due to calcium deficiency, but simply to point out that the increase in bone resorption which follows menopause6 can be largely or wholly explained by the fall in calcium absorption and rise in obligatory calcium excretion which occur at this time,7 and also occur in oophorectomised animals.8,9 (The loss of a direct antiresorptive action of oestrogen on bone at menopause cannot be excluded but is probably quantitatively much less important.) For these reasons, it has become standard practice to recommend calcium supplementation to postmenopausal women, increasingly with vitamin D, to prevent or delay bone loss and reduce fracture risk. In the largest meta-analyses, calcium with vitamin D in adequate dosage reduces fracture risk by 25% or more, but vitamin D alone is not effective.10,11

Until very recently, calcium supplementation was not thought to cause any significant side effects. However, a New Zealand team recently reported an increase in the mean rate of mainly self-reported myocardial infarction in participants who were allocated to receive calcium supplements in five prospective trials for which patient-level information was available.12 Although the effect was not significant in any of the trials individually, it was significant at the 5% level in the whole series and has attracted sufficient media attention to endanger the use of calcium in the prevention of osteoporosis in postmenopausal women. An extension of this case against calcium recently appeared in this Journal, in a position statement on fracture prevention in aged-care facilities that was co-authored by one member of the New Zealand team.13 The article not only ignores the seminal work of Chapuy and colleagues on fracture prevention with vitamin D and calcium in aged care homes,14 but specifically opposes the general use of calcium supplementation on four separate grounds, none of which are directly referenced. The first is that long-term compliance with calcium supplementation is very poor, whereas in most trials it is not significantly different from compliance with placebo.15 The second is that the anti-fracture efficacy of calcium is marginal, despite overwhelming evidence to the contrary in the largest meta-analyses.10,11 The third is a bizarre claim that calcium could increase the rate of hip fracture; this is only supported by one trial (by one of the co-authors of the position statement) in which the adverse effect was not remotely significant in participants who complied with calcium supplementation,15 which is widely regarded as an anomaly and is contradicted by a later meta-analysis.16 The final is that calcium supplementation could increase the risk of myocardial infarction, which is highly contentious and negated by the latest meta-analysis of 17 trials.17

These negative statements about calcium (which are not reflected in the article’s abstract) are coupled with the promotion of bisphosphonates — particularly the intravenous variety — despite the fact that virtually all the bisphosphonate trials have incorporated calcium supplements. It may therefore be relevant that this article arose from a meeting financed by a pharmaceutical company that happens to market an intravenous bisphosphonate and gave some form of assistance to six of the 10 authors.13 Since it is clearly stated that this meeting was endorsed by the Royal Australian College of General Practitioners, the Australian and New Zealand Bone and Mineral Society and Osteoporosis Australia, there is a strong implication that these bodies also support the article itself. It is questionable whether such public bodies should lend their authority to a position statement of uneven quality and which runs the risk of being seen as commercially driven.

Author

  • B E Christopher Nordin MD, FRACP, DSc1,2
  • 1. Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA.
  • 2. Discipline of Medicine, University of Adelaide, Adelaide, SA.

Correspondence: christopher.nordin@imvs.sa.gov.au

References

View this article on Wiley Online Library