One of the unintended consequences of breast cancer therapies is an increased risk of osteoporosis due to accelerated bone loss. To offset this unwanted side effect, women undergoing breast cancer treatment cancer are widely prescribed calcium and vitamin D supplements to prevent and manage osteoporosis. However, new research from Wake Forest Baptist Medical Centerfinds that the recommended daily doses of these supplements may not prevent loss of bone mineral density (BMD) in these women.
There are a variety reasons why breast cancer treatment may be at increased risk for osteoporosis and fracture. While estrogen has a protective effect on bone, reduced levels of the hormone trigger bone loss. As a direct result of chemotherapy or surgery, many breast cancer survivors experience a loss of ovarian function which leads to a drop in estrogen levels. However, a number of studies suggest that chemotherapy may also have a direct negative effect on bone. Finally, breast cancer itself may stimulate the production of osteoclasts, the cells that break down bone and reduce bone density.
Gary Schwartz, Ph.D., a cancer epidemiologist at Wake Forest Baptist and one of the authors of the paper, said that the purpose of the study was to examine whether a seemingly common sense prescribing practice actually works. “We evaluated clinical trial evidence for calcium and vitamin D supplementation in maintaining skeletal health of women with breast cancer,” he explained. “At the doses recommended, the data show that these supplements are inadequate to prevent loss of BMD.”
The data show that at the recommended daily doses these supplements are inadequate to prevent loss of bone mineral density.
Schwartz and co-author Mridul Datta, Ph.D., a postdoctoral fellow at Wake Forest Baptist, reviewed data from clinical trials that evaluated the effect of antiresorptive drugs on BMD and used the “before-after” data from the comparison group to assess change in BMD in pre- and in post-menopausal women.
Overall, the results from 16 trials indicate that 500-1500 mg calcium and 200-1000 IU vitamin D, the doses commonly recommended, do not prevent loss of BMD in women with breast cancer. Despite supplementation, women lost BMD in virtually every clinical trial reviewed.
The study appears online ahead of print this month in the journal Critical Reviews in Oncology/Hematology.
Risk of fractures
Women with breast cancer lose BMD at a higher rate than their healthier counterparts, increasing their risk of fractures which are associated with significant declines in function and health-related quality of life, and in higher mortality rates.
Fractures from osteoporosis can result in significant pain and disability. In the United States, more than 40 million people either already have osteoporosis or are at high risk due to low bone mass.
To help limit the consequences of osteoporosis, it is a common practice to prescribe calcium and vitamin D supplements to these women, a low intensityintervention that seems to make sense, Datta said, although it’s never really been tested. In the clinical trials reviewed, BMD in the women was measured at the beginning and end of the studies, Datta said, so if the supplementation worked to prevent BMD loss, “You should be able to see that in the data, and we clearly didn’t.”
Datta said it is possible that the BMD deficits could be worse in the absence of the supplements, but the results are concerning overall because cardiovascular disease is the main cause of mortality in women with breast cancer. There is growing evidence that calcium supplements may increase the risk of heart attack and stroke.
“The take-home message is that this very common practice of supplementation doesn’t really seem to be working,” Schwartz noted. “Future trials are needed to evaluate the safety and efficacy of calcium and vitamin D supplementation in women undergoing breast cancer therapy.”
For more information:
Datta M, Schwartz GG.Calcium and vitamin D supplementation and loss of bone mineral density in women undergoing breast cancer therapy.Crit Rev Oncol Hematol. 2013 Aug 7. pii: S1040-8428(13)00152-2. doi: 10.1016/j.critrevonc.2013.07.002. [Epub ahead of print][Article][PubMed]
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