A connection between bone mineral content and high-risk prostate cancer?


New data published in the July issue of the British Journal of Urology International suggest the possibility of a connection between a man’s bone mineral density and his risk for prostate cancer, most particularly the more aggressive and dangerous forms of the disease.

Loeb et al. hypothesized that — because advanced forms of prostate cancer tend to show up most commonly as metastases in the bones — there might be some form of connection between bone physiology and the progression of prostate cancer over time. As an initial way to test this idea, they decided to see if there were any differences between the bone mineral content (BMC) of men who developed life-threatening types of prostate cancer and men with prostate cancer but no indication of metastasis. To do this, they went back to look at data collected as part of the Baltimore Longitudinary Study of Aging — a study that has been tracking health-related data for more than 50 years for hundreds of people in the Baltimore area.

Specifically, Loeb and her collegues were able to identify 519 men whose bone mineral content was measured between 1973 and 1984 as part of the aging study. They then looked for any association between the serial BMC data and the development of overall and high-risk prostate cancer over the next 30 years. For all prostate cancer cases, BMC was censored at the time of diagnosis.

The core results of their study showed the following:

  • Median overall follow-up was 21.1 years (range, 0.2–35.0 years) after the last BMC measurement.
  • 76/519 men (14.6 percent) were later diagnosed with prostate cancer (18 with high-risk and 58 with low- or intermediate-risk disease).
  • BMC decreased more with age in the healthy (control) men than among men diagnosed with prostate cancer (P = 0.018).
  • BMC tended to decline less with age in men with high-risk prostate cancer thqan in men were were not high-risk cases.

The authors conclude that, in this study population, there was a statistically significant difference in the distribution of BMC men who did and men who did not develop prostate cancer, over an extended follow-up. Furthermore, they note that,  “BMC appeared to decline to a greater extent with age among healthy controls than in men with prostate cancer, especially high-risk disease.”

However, as noted in a media release from Johns Hopkins Medicine about this study, Loeb et al. do not believe that bone density scans can be used as a method to test for  risk of prostate cancer. This study was both retrospective in natuire and too small to produce generalizable resulst. The researcher’s initial goal was only “to better understand the link between prostate cancer and bone.” The key learning from this study at this time is only that the same factors that influence bone density (e.g., level of  sex hormones or growth factors in bone may also be stimulating prostate cancer to develop and metastasize.

An additional fact provided in the media release, however, is that the study results remained valid even after the researchers accounted for lifestyle factors that might influence bone density, such as smoking, body mass index, and intake of dietary calcium and vitamin D.

2 Responses

  1. Thanks as always for picking up interesting studies, such as this one.

    The key findings — greater early bone density (well before diagnosis) in men who later develop prostate cancer, and greater early bone density among men with high risk compared to lower risk cases of prostate cancer — run against the grain of my own understanding of bone density and prostate cancer: that decreased bone density is virtually epidemic among prostate cancer patients. Here are my thoughts in attempting to understand this, but at this point I’m puzzled.

    The statistical association is strong, at p = 0.018, probably indicating only about a 2% likelihood that the results are due to chance rather than to a real phenomenon. That favors the odds that the authors have detected a real phenomenon. Dr. H. Ballentine Carter is one of the authors, and that adds credibility to me.

    I’m puzzled by the fact that only 778 bone density observations were taken for these 519 men, about 1.5 scans per man over the 11-year period between 1973 and 1984. Obviously that is not enough observations to even suggest trends, let alone bone density near the date of diagnosis, but it is enough for an early snapshot, many years before diagnosis. As the authors state, more study is needed.

    In trying to explain the findings to myself, one possibility comes to mind involving calcium and vitamin D. We know that calcium is key to bone mineral density; we know that low levels of vitamin D are associated with prostate cancer; and we know that excessive calcium can cause a decrease in vitamin D. I’m wondering whether a high amount of calcium in the diets of the men diagnosed with prostate cancer was causing a low level of vitamin D that increased the risks of both developing prostate cancer and developing high risk prostate cancer. On the other hand, adequate vitamin D is needed to drive calcium into the bones to help increase and maintain density. I’m wondering if the Baltimore Longitudinal Study of Aging database has sufficient dietary data and data on calcium and 25-hydroxy vitamin D levels to explore this possible connection.

    Another thought is that the bone density testing was during a period well before PSA testing. Is it possible that many of the men later found to have prostate cancer, especially high risk prostate cancer, already had the disease — many with bone metastases, and that these typically bone-density-increasing metastases (typical for prostate cancer) were increasing the bone density measurements.

    My own case has had a substantial bone density aspect. After about 10 months of hormonal blockade, I had my first DEXA scan, and the result was a diagnosis of osteopenia. Over the next 10 years the degree of osteopenia varied (with the L4 vertebra scoring well into the osteoporosis range) as I cycled on and off intermittent hormonal therapy, with continuous Fosamax, later Boniva, with calcium and quality vitamin D3 as well as regular weight bearing/resistance exercise in support, also including 25-hydroxy vitamin D tests and nearly annual DEXA scans. (I have no signs of arthritis or vascular calcification that can throw off DEXA scan results, so it is likely that the results are valid.) My last DEXA scan this spring, at the end of my third cycle of full triple blockade (and after 10.25 years of intermittent hormonal therapy overall), showed my bone density had returned to normal!

  2. Dear Jim:

    (1) The high probability of reduced bone density in men treated with hormone therapy is not a relevant factor in this study. This study is about a correlation between high bone density in early adulthood (when these men were in their 30s and 40s and highly unlikely to have advanced prostate cancer) and later risk for progressive and metastatic disease as compared to localized and indolent disease.

    (2) I don’t think you can necessarily make the assumption that this potential correlation has anything at all to do with calcium or vitamin D. It seems to me that — if it is real at all — it is likely to have a great deal more to do with human genetics, epigenetics, and childhood nutrition and exercise, in that done density in one’s 40s is probably much more highly dependent on those multi-influential factors than on levels of any one specific biochemical. Just look at how nutrition of children over the past 60 years has affected average weight and height. Prior to World War II, men > 6’3″ tall were relatively uncommon. Today they are relatively commonplace … as are women of > 5’10”.

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