Men`s Osteoporosis Support Group
Volume II, Issue 3	July 1, 1998

Summer time greetings

What`s new?

I plan on devoting this newsletter to report on the latest research information that I have found either on the Web, LunarNews, the medical library, or that has been suggested by members of the group. Thanks for the e-mails and calls from those who have had questions or suggestions.

LunarNews notes

LunarNews is an excellent free quarterly publication from Lunar Corporation, 313 West Beltline Hwy., Madison, WI 53713. (800) 445-8627. Back issues of the newsletter are also linked from the Men`s Osteoporosis Support Group Web site http://www.maleosteoporosis.org/. Each issue is a thorough review of the latest research publications that have impact on osteoporosis. Covered are such areas as: Calcium, vitamin D, osteoporosis therapy with antiresorptive or bone-forming drugs, bone densitometry, etc. The most recent issue has several very interesting discussions that I want to mention here.

Calcium and prostatic cancer risk. An article on calcium on page 1 and 2 of the June 1998 LunarNews points to a study by Giovannucci and others(1) that was conducted as an 8-year prospective study of 47,781 Health Professionals in the U.S. The study found that, "The risk of any prostatic cancer was increased 2.5X, while risk of metastatic prostate cancer was increased 4.5X, by calcium intakes >2,000 mg/day." Further, the LunarNews article states, "Calcium supplements in men should be discontinued until their long-term safety is demonstrated." LunarNews also mentions, "A high vitamin D intake, and/or elevated 1,25 D levels, reduce the risk of several cancers (most particularly prostate, colon, and breast cancer)." There is, however, no mention of a reference for this statement in the article.

The maximum recommended calcium intake for men, according to the National Institutes of Health (NIH), is 1,500 mg. That would be for men up to age 24 and 65 and older. All others have a recommended dose of 1,000 mg per day. Note, these numbers are your DAILY REQUIREMENT, not the amount of supplemental calcium you should take. So assuming your normal diet has 500-1,000 mg of calcium, the calcium supplement should be 1,000 or 500 mg respectively to reach the recommended daily calcium requirement. Don`t make the mistake of thinking that the NIH requirement is 1,500 mg of supplemental calcium. Rather, it is the total calcium intake of supplements plus dietary calcium. The first Men`s Osteoporosis Support Group newsletter describes the calcium content of many foods. Use that to figure your dietary calcium intake each day, and supplement accordingly to reach the recommended daily allowance.

In summary, it appears that until further studies are done, the safest route is to keep daily calcium intake below 2,000 mg and always take from 400-800 IU vitamin D per day when taking the calcium.

Fracture Risk and Bone Density. I often see quotations that someone has an increased fracture risk of, e.g., two or three times normal due to their lost BMD. I`m not sure exactly how they quantify that fracture risk. References from page 10 of the June 1998 LunarNews shed some light on the problem. All the studies involve women, as is so often the case, so I can`t assure you the results apply exactly to men, but they should be about the same.

A 1993 study (2) found that in people older than age 65, each standard deviation (SD) of decrease in femoral neck bone density increased the age-adjusted risk of hip fracture 2.6 times. Women in the lowest quartile had an 8.5-fold greater risk of hip fracture than those in the highest quartile. Additionally, bone density of the femoral neck was the best predictor of fracture compared to the spine, radius or calcaneus. These figures don`t necessarily apply to younger individuals with less risk of osteoporosis. Kroger et al (3) looked at 3,000 50-year-old women and found the risk of hip fracture was 1.4 per SD decrease in BMD. So there is apparently a qualitative factor of bone strength that is lost with age and onset of osteoporosis not reflected in the younger women of equal BMD. These studies appear to question the use of a simple fracture risk factor just related to BMD.

Here is another confounding issue. On page 15 there is a discussion of the skeletal side effects of corticosteroids. As you all know, these medications, particularly if used continually and at high doses, stimulate osteoporosis. LunarNews points out, "Oral corticosteroids not only stimulate loss of BMD, but decrease bone quality. Even the doubling of a bone loss at low prednisone doses of 5 mg/day can be problematic, since fracture rates are doubled in these patients(4). Patients on corticosteroids at any given BMD level have twice the risk of fracture, including hip fracture, compared to age-matched peers at the same BMD level. In other words, patients on oral doses exceeding 5 mg/day should be viewed as having a T-score 1 SD lower than that which actually is observed."

In summary, fracture risk is a complex issue. BMD, age, and particularly, history of corticosteroid use, are very important to help assess fracture risk. It appears especially important for physicians treating patients, and the patients themselves who are on corticosteroids, to be aware of their much higher fracture risk at a given BMD. Also, note that risk of hip fracture relates only to BMD in the hip, not necessarily to low BMD in the spine or other areas.

Update: Bisphosphonates. It is interesting that one of the most common perceptions I see on Web bulletin boards and questions from people just diagnosed with osteoporosis is that Fosamax causes stomach problems. It is true that it can be a gastric irritant, but clinical trials show few differences in side effects compared to placebo. I interpret this to mean that if YOU THINK that Fosamax or a sugar pill will cause you stomach irritation, there is a chance they will. If Fosamax is taken incorrectly without a full glass of water, and, if the person lays down before eating, the chance of gastric irritation is greatly increased. Additionally, there should be a minimum of one-half hour wait (and more, if possible) before eating or the drug is not properly absorbed into the system.

Since Merck has publicized the possible risk of gastric irritation from Fosamax to presumably lower the risk of law suits, it appears there will always be the stigma of gastric irritation attached to the taking of the drug. On page 19 of LunarNews, there is an interesting alternative dosing method suggested. " A 40 mg tablet of alendronate given once per week could be as protective as a dose of 5 to 10 mg given daily." Their rationale for this method is, "Since the half-life of bisphosphonates in vivo is many months, intermittent doses should be just as effective as daily dosing." NOTE: This recommendation is not backed by reference to a research study, it is just based upon their idea of a logical approach to Fosamax dosing. Obviously, the once per week dose would be more convenient, too, in light of the long wait to eat or take other medications after taking Fosamax. So, this method may be one you would want to discuss with your physician for convenience reasons, too.

A recent study by McClung et al (5) showed that treatment with 5 mg/day of Fosamax for three years prevented bone loss in women within 3 years of menopause. Actually, there was increased spine and femur neck BMD during the study. I wonder if these results might suggest that lower doses of Fosamax might be indicated in later years in osteoporosis patients that, e.g., have had BMD brought to within 1 S.D. of young adults or some similarly improved BMD level.

Update: Vitamin D. A recent study by Thomas and others(6) showed that 57% of 290 sequential patients hospitalized in a general medicine ward had low vitamin D levels. 22% were severely deficient. On page 21 of LunarNews June 1998 issue it is noted, "Vitamin D deficiency, and resultant secondary hyperparathyroidism, is the major factor responsible for hip fracture in older subjects, particularly those who are housebound or institutionalized. Supplementation of the elderly with 700 to 800 IU of the ordinary vitamin D precursor augments femur BMD by a few percent, comparable to the more potent antiresorptives, and halves the rate of hip fractures." They cite several studies to back up this statement that I will not list as references. An editorial in the same issue of the New England Journal of Medicine recommended vitamin D supplements should be increased to 700 to 1,000 IU daily for patients over 70 years of age. Thomas and others (6) also mention that it appears that currently recommended daily doses of vitamin D appear inadequate. The population they studied was patients appearing in a general medical ward and were not housebound or institutionalized patients. Since almost 60% of them had hypovitaminosis D, there appears to be inadequate vitamin D intake in the general population.

In summary, adequate vitamin D is protective of bone fractures in older patients. Daily doses should be increased in the general population, too, to alleviate the hypovitaminosis D that is prevalent.

1. Giovannucci E et al. 1998. Cancer Res 58:442-7.

2. Cummings SR et al. 1993. Lancet Jan 9;341(8837):72-5.

3. Kroger H et al. 1995. J Bone Miner Res 10:302-6.

4. Saag KG 1997. Am J Med 103:31S-39S.

5. McClung et al. 1998. Ann Intern Med 128:253-261.

6. Thomas MK et al. 1998. N Engl J Med 338:777-783.

Osteoporosis odds and ends

Tennis anyone? One problem for some, even while on Fosamax, is rebuilding hip bone. A recent study (1) shows one way to build hip bone mass, and spine bone mass, too. When comparing nine male professional tennis players to nonplaying controls, they found lumbar spine BMD was 15% greater in the tennis players. The tennis players` femoral neck BMD was 10-15% greater than controls. An obvious conclusion is that playing a lot of tennis in young adult life should provide an excess of BMD to draw upon in later life as a means of preventing osteoporosis. It is also possible that playing tennis in later life will aid in rebuilding lost hip BMD in those of us who didn`t play professional tennis and have osteoporosis. It is unknown how much tennis would need to be played a day/week/month to obtain these benefits. There is the added possibility of falls with the chance of fractures that could occur while playing tennis. So, there is no easy answer concerning playing tennis if you have osteoporosis. You should use your own judgment and consult your physician or exercise therapist, especially if you have very low BMD. But it might offer an effective and enjoyable BMD-building alternative to simple calisthenics and walking for some men.

What is/was your job? Israeli investigators (2) looked at the effect of the position you assume while working on hip BMD. They compared 55 clerks who sat while working with 44 nurses who stood on their job. The spine BMD was similar, apparently since the weight on the spine is similar whether sitting or standing. The hip BMD of the nurses was 0.6-0.8 SD greater than the clerks` BMD. The authors concluded, ". . . that prolonged working in a sitting position may induce a low hip BMD, and thereby increase the risk for osteoporotic hip fracture." The results also suggest that those of us with low hip BMD should probably spend a lot more time each day in a standing position. We may be asking too much of a 30-minute walk and some floor exercises to increase hip BMD.

The spine or the hip? As you may know, most of us develop osteophytes on the spine as we develop osteoarthritis with advancing age. Is it possible that these bone growths, and other bone changes that occur in osteoarthritis, may affect the outcome of bone density test results? To see if this might occur, Liu and others (3) looked at lumbar spine and hip radiographs and dual-energy X-ray absorptiometry (DXA) results for 120 men and 314 women aged 60-99. They found 75% of men and 61.1% of women were affected by lumbar spine osteophytes. There were 31.7% of men and 27.4% of women affected by hip osteophytes. The authors found osteoporosis at the hip in 33.1% of women and 25.8% of men, however, at the lumbar spine, it was present in only 24.2% of women and 4.2% of men. This disparity is apparently due to the effect of osteophytes that are present in the lumbar spine and not the hips. The DXA apparently interprets the excess osteophyte bone as normal spine bone. The authors conclude, ". . . that the lumbar spine osteophytes affect most subjects over the age of 60 years, and contribute substantially to lumbar spine BMD measured in the anteroposterior position by DXA." Additionally, they state, "Diagnosis of osteoporosis and assessment of osteoporotic fracture risk in the elderly should be based on hip BMD and not on anteroposterior lumbar spine, unless spinal osteoarthritis has been excluded." My interpretation of this is that if you have spinal osteoarthritis, you also may not be able to rely as heavily on results of lumbar spine follow-up DXA to interpret the effect of osteoporosis medications. The hip appears to be a more reliable site. Note, that this is just in individuals that are age 60 or older. There should be no problem as long as you are young enough not to have spinal osteophytes.

A new testosterone patch. There was an announcement on the Doctors Guide to the Internet Web site recently about the Testoderm(R) TTS (Testosterone Transdermal System) patch. This is a prescription therapy in testosterone-deficient men that is now available in the United States. Patches have been available for some time, but they were difficult to apply and had problems staying in place if sweating occurred. The Testoderm(R) TTS features a proprietary adhesion technology that allows the patch to be removed before and reapplied after swimming, bathing, or exercising. In addition, men can stay with a preferred application site including the back, arms, or upper buttocks and don`t need to rotate to different sites. In clinical trials 94% of men achieved serum testosterone levels within the normal range. This patch appears to be a significant improvement that you may want to discuss with your physician if you use testosterone.

The PSA prostate cancer screening test. There has been a lot of press lately about the PSA test. I have heard both positive and negative comments. The negative particularly related to its reliability and predictability. That is why I was interested to come across a National Institutes of Aging (NIA) press release that referred to a 1996 study (4) of the benefits of PSA screening. This study looked at 26 men with no history of prostate disease, 29 men with benign prostatic hypertrophy, and 23 men with prostate cancer. This is a longitudinal study ongoing since 1958. The current PSA tests total PSA, but there are actually two forms: free and bound PSA. The total PSA test gave a four-year alert that prostate cancer was developing. When the ratio of free PSA to total PSA was used, however, a continuously decreasing ratio was noted among cancer cases for 10 years before cancer developed. The authors give exact PSA ratios that physicians can use as a signal for concern.

I have never had anything but a total PSA test during my examination visits. Therefore, I sent a copy of the press release from NIA to my physician just in case he was not aware of these findings. This new PSA test may be particularly important for men taking prescription testosterone, since prostate cancer is a known risk factor.

Update on human parathyroid hormone therapy. In the fourth newsletter, Dr. Cosman discussed the clinical trials she was involved with using human parathyroid (PTH) hormone to treat osteoporosis. This hormone stimulates bone formation and may be nearing approval by the FDA. Dr. Cosman published two new papers on the topic. The first (5) is a review that I will list here if you would be interested in getting a copy to read. The second (6) may have significance to men taking alendronate since it shows that the two drugs may be combinable with additive effects. The study involved 10 women already on 10 mg/day of alendronate. Five continued on only that therapy throughout the study while five were given 400IU/day of subcutaneous human PTH (1-34) along with the alendronate for six weeks. Those women given the PTH showed a significant increase in biochemical markers for bone formation. These results indicate PTH can stimulate bone formation in the presence of alendronate, a drug that blocks bone resorption. Although the study involved only women, there appears to be nothing gender specific in either medication. So, this may be a potent drug combination, particularly for those with severe osteoporosis needing powerful therapy.

Space-age bone densitometry. Here is a quick summary of what sounds like very exciting new x-ray and bone density equipment that I found on the Doctors Guide to the Internet Web site. The announcement, dated December 1, 1997, describes the Digital OsteoView(R) 2000. Here is a quote from Dr. Michael Davis, M.D., D.Sc, professor of radiology and director of radiologic research at the University of Massachusetts Medical Center. "We are now at the threshold of having a machine that just a few years ago seemed to be a dream, an instantaneous osteoporosis and arthritis detection and monitoring device that every physician can afford." The machine uses amorphous silicon flat panel technology that should replace X-ray film and expensive image intensifying tubes. It will greatly reduce patient X-ray exposure and be an instant analysis that will allow image enhancement, transmission, and archiving. It is hoped to be approved by the FDA in the second half of 1998. Keep your eyes open for announcements on this new technology, it sounds like it has tremendous potential.

Questions from a member. Here are a couple of questions from a new member to the support group. He wants to know if any of you have noted a lessening of pain over the years since taking osteoporosis medications, starting exercise programs, and making dietary changes? Additionally, have any of you noted pain in the feet upon arising in the morning that you could relate to osteoporosis? If you wouldn`t mind e-mailing, writing, or calling me with answers to this, I`ll post the response in the next newsletter. Thanks in advance.

1. Calbet JA et al. 1998. Calcif Tissue Int Jun;62(6):491-96.

2. Weiss M et al. 1998. Calcif Tissue Int Jan;62(1):47-50.

3. Liu G et al. 1997. Osteop Int 7(6):564-69.

4. Pearson JD et al. 1996. Urology Dec;48(6A):4-9

5. Cosman F, Lindsay R. 1998 Calcif Tissue Int Jun;62(6):475-80

6. Cosman F, et al. 1998. J. Bone Miner Res Jun;13(6):1051-1055.

Disclaimer

Diagnosis and treatment of osteoporosis are the responsibility of the patient and his or her physician. Nothing in this newsletter is to be interpreted as a recommendation for treatment or to change treatment that your physician has prescribed. Although we attempt to assure that information in this newsletter is factual, errors will occur. It is the responsibility of the reader to verify that information they are acting on is factual. There is no relationship between this newsletter and any national osteoporosis group, including the National Osteoporosis Foundation. All references to any such groups are for informational purposes only.

Jerome C. Donnelly
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