Calcium Intake and Cardiovascular Disease Risk

TO THE EDITOR: We agree that Chung and colleagues' meta-analysis (1) and the guideline from the National Osteoporosis Foundation and American Society for Preventive Cardiology (2) provide only moderate-quality evidence that calcium supplements with or without vitamin D are safe in terms of cardiovascular and cerebrovascular disease, mortality, or all-cause mortality in generally healthy adults. Of note, the guideline acknowledges that future high-quality studies may improve our confidence in the estimates. Given the widespread use of these supplements and the clinical uncertainty, further high-quality studies are warranted. Margolis and Manson's editorial (3) on what clinicians and patients need to know about calcium and cardiovascular disease provides helpful advice to a confused and confusing area of clinical practice that only a few years ago was considered to be resolved after 100 years of careful research. However, some additional insights are relevant to the debate. Using mean values of calcium intake and vitamin D status, which are commonly reported in RCTs, ignores the fact thatunlike in trials of pharmaceuticalsthe control group has already been exposed to some level of dietary calcium and vitamin D. Thus, the real question is what are the health benefits or risks of increasing total dietary and supplemental calcium intake and vitamin D status rather than simply whether someone has been exposed to these agents. The use of metaregression to consider the effect of high calcium intake is therefore reassuring because no evidence of increased risk was identified. Expert groups for the prevention of age-related bone loss continue to strongly support calcium supplements with or without vitamin D, particularly in elderly women in whom food alone cannot supply recommended dietary intakes (4). These recommendations remain in place despite Grey and Bolland's claims that pharmaceutical companies and financial self-interest control such groups (5). On the contrary, it is more likely that these expert bodies have not taken up the claims of adverse effects because of the inconsistent evidence for harm as well as criticisms of Grey and Bolland's approach, which include cherry picking certain classes of adverse events, inconsistent validation of end points, and post hoc splitting of clinical trial data that fundamentally undermines the role of randomizationall of which lead to uncertainty over whether the reported findings are real or due to chance or bias. Perhaps these latest data will allow a more rational and less emotive, evidence-based view of an important public health initiative.