Editorials

Increased calcium intake may reduce risk of primary hyperparathyroidism

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e6646 (Published 18 October 2012) Cite this as: BMJ 2012;345:e6646
  1. James Norman, chief of surgery
  1. 1Norman Parathyroid Center, Tampa, FL 33606, USA
  1. jnorman{at}parathyroid.com

Moderate calcium supplementation in women should be encouraged

In recent years, many basic science and clinical studies have provided evidence that untreated primary hyperparathyroidism is associated with an increased incidence of hypertension, cardiomyopathy, myocardial infarction, atrial fibrillation, stroke, and even breast and prostate cancer.1 2 3 4 5 6 Primary hyperparathyroidism is now known to exacerbate or underpin many more diseases and conditions than the classic osteoporosis and kidney stones. Physicians no longer wait until one of the classic complications arises but take a more proactive approach and recommend parathyroidectomy once the diagnosis has been secured. Such an approach is now easier because parathyroidectomy has become available as an outpatient procedure over the past decade.7

A linked cohort study by Paik and colleagues (doi:10.1136/bmj.e6390) provides the first clinical evidence that calcium intake may play a role in the pathogenesis of sporadic primary hyperparathyroidism.8 More specifically, their study suggests that parathyroid adenomas may be induced by chronic calcium deficiency in the diet. The authors examined daily calcium intake in more than 58 000 nurses over a 22 year period and found that the incidence of sporadic primary hyperparathyroidism was significantly lower in women with a higher intake of dietary calcium. Low calcium diets and a lack of daily calcium supplementation were associated with a higher incidence of parathyroid adenoma formation. Importantly, supplementation with only 500 mg of daily calcium was associated with a decreased incidence of developing primary hyperparathyroidism.

At least 95% of cases of primary hyperparathyroidism are caused by one or more parathyroid adenoma, true tumors that are a monoclonal proliferation of a single parathyroid cell.9 The authors have postulated that years of suboptimal calcium intake is the trigger for a parathyroid cell to become activated and begin multiplying. About 20% of patients have two concurrent parathyroid adenomas while having two normal dormant glands at the time of parathyroidectomy, and this provides further support to the authors’ theory of a chronic slow stimulation of parathyroid hormone production induced by a subclinical lack of dietary calcium intake.7 9 The proposed mechanism is quite different from the more aggressive parathyroid gland stimulation seen with chronic kidney disease that leads exclusively to four gland hyperplasia—never formation of a monoclonal adenoma.

Most clinicians do advise patients to take adequate calcium and have done for decades given its known benefits on bone health. In the past couple of years the wisdom of calcium supplementation has come into question as evidence has emerged that taking supplemental calcium may be associated with a higher incidence of myocardial infarction.10 11 Some patients now question whether they should take supplemental calcium even when they have overt osteoporosis. Paik and colleagues found that even a dose as low as 500 mg a day was associated with a decreased incidence of primary hyperparathyroidism. This is important because such a modest dose is less likely to be controversial.

Paik and colleagues’ study provides evidence to support physicians in confidently encouraging female patients to take calcium supplements. Daily calcium supplements in modest doses are likely to provide more benefits than risks given that even mild primary hyperparathyroidism has important clinical associations and, over many years, even a moderate increase in calcium concentration probably helps reduce the incidence of parathyroid tumors.

Notes

Cite this as: BMJ 2012;345:e6646

Footnotes

  • Research, doi:10.1136/bmj.e6390
  • Competing interests: The author has completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

  • Provenance and peer review: Commissioned; not externally peer reviewed.

References