Men`s Osteoporosis Support Group
Volume V, Issue III	July 1, 2001

Summertime Greetings

What`s new?

Forteo. I have mentioned human parathyroid injections in many past newsletters. Clinical trials have shown them to be quite effective at increasing bone mineral density (BMD), and at reducing fracture risk. The drug Forteo is produced by Eli Lilly and Company and will be the marketed form of human parathyroid, so watch for developments on this in the lay press. I still have no word as to a final approval date by the FDA, but expect it will be sometime this year or early next year.

FreeFind search engine reminder. I want to remind readers that FreeFind is located on the home page of the Men`s Support Group Web site. This is a search engine for items on the Web site. Here is how to use it most efficiently. Type the search word into the query block, highlight it with the mouse, and hit Ctrl-C to copy that word to memory. Then hit or click on Find. If the word is anywhere on the site, you will see an active link to that page to click to open the page. Then click on Edit, Find on this page, or hit Ctrl-F. That will bring up a menu to search on the open page. Place the cursor in the Find what block, hit Ctrl-V to paste the text you had copied previously, and hit or click on Find Next. This will bring you directly to the text and prevent you from reading through the entire document to find the terms you are looking for. Use this for all Internet search engines to speed finding text on large Web pages.

Women on HRT and osteoporosis. I rarely discuss females osteoporosis in this newsletter since that topic is covered so well elsewhere, and it is not pertinent to men`s osteoporosis issues normally. However, since many of us have wives, girl friends, mothers, daughters, female friends and acquaintances etc., who might get osteoporosis, I wanted to briefly mention what happened to a friend of mine. She is in her sixties and has been on hormone replacement therapy (HRT) since menopause. A recent DXA showed she had rather severe osteoporosis, and she is not of slight build, and has no other osteoporosis risk factors other than a history of avoiding calcium supplements. I mention her case because I have always assumed-not based on any literature, just a pure assumption-that once on HRT, a woman was protected from getting osteoporosis. Obviously, she could have a metabolic disorder or some disease that has caused or contributed to her osteoporosis such as celiac sprue, hyperthyroid, parathyroid disorder, etc. But, so far in my friend`s case, none of these problems has been implicated. Thus, the point I want to make is that just because a women is on HRT, she is not guaranteed to be protected from osteoporosis. An occasional DXA, heel ultrasonometry, and use of biochemical markers of bone turn over might be in order even on women on HRT. In fact, Adler points out that, "One final caution comes from the PEPI trial. Almost 10% of the women on estrogen replacement continued to lose bone. It is imperative that treatment be monitored by periodic measurement of BMD, perhaps supplemented with measurement of bone turnover markers." See Clin Lab Med 2000 Sep;20(3):54958, vii, Adler RA, Sex steroids and osteoporosis. The role of estrogens and androgens. PMID 10986620.

New links from the Men`s Osteoporosis Support Group Web site. Evan Prost, our expert consultant to the group on physical therapy, moderates the listserve for men with osteoporosis on Yahoo. I`ve added that link from the osteoporosis links page. For men to browse and join the listserve, go to http://groups.yahoo.com/group/osteoporosismen. Once people have joined, the email address that services the listserve is osteoprososismen@yahoogroups.com. So I encourage you to join this if you would like to have direct e-mail contact with men with osteoporosis. Ira Potell, poodle.25722@home.com, one of our members, sent me several excellent links pertaining to pain control and I have created a link to them from both our osteoporosis links page and the other health-oriented links Web page. If you are dealing with pain, back problems, etc., I strongly suggest you check out these sites as they are excellent resources. Thanks to Ira for offering this information. One of the questions I`m asked most often is to suggest a physician who treats men with osteoporosis. Thus, I have placed links on the osteoporosis links page to locate an endocrinologist or rheumatologist in your area. To others who read this newsletter, please don`t hesitate to offer suggestions that might provide our readers with helpful information.

Hemochromatosis and osteoporosis

Hemochromatosis is a genetic condition of abnormal iron metabolism. This allows too much absorption of iron, even from a normal diet, and it can result in very large amounts of iron absorption in diets high in iron and/or vitamin C intake. This condition is quite prevalent with an incidence of one in eight people as single gene carriers and one in 200 people have both genes, that is, they have hemochromatosis. This makes hemochromatosis one of the most common genetic disorders with about 35 million Americans carrying one or both genes, yet most people who have it are undiagnosed and do not know they are carrying this silent killer. There are literally millions of people walking the streets today who, to all appearances, appear healthy, but are walking time bombs. People of Celtic heritage with ancestors from Ireland, Wales, Scotland, or Great Britain are at very high risk for hemochromatosis. But, people of other ethnic backgrounds can have the genetic defect, too. The problem is that this iron overload, if allowed to continue, can cause serious health problems, and even death as the iron builds up in body organs and causes illness and injury. Any such damage is needless, since treatment is totally effective if started early. Many people have no symptoms, especially in the early years when it is best to diagnose the condition. Don`t wait for symptoms to have diagnostic testing done--it may be too late. Early diagnosis and treatment assures individuals that they will not have permanent injury from the iron overload if they have proper therapy. There are some symptoms often associated with hemochromatosis, but these may not be noted until an individual is 40-50 years old, and even later for females, as they have lost iron from menstruation. Here is a list of some of the signs and symptoms often ascribed to hemochromatosis: Chronic fatigue, liver cirrhosis or cancer, arthritis or joint pain, impotence/sterility/infertility, hair loss, diabetes, cancer, abdominal pain and swelling, weight loss, frequent colds/infections, headaches, hypothyroidism; heart irregularities etc. Unfortunately some of these are vague symptoms that many people have without having hemochromatosis, so how can you find out if your symptoms might relate to the genetic defect? The answer is to undergo iron profile lab tests. These include Serum Iron, Total Iron Binding Capacity (TIBC), Serum Iron percent of saturation, and Serum Ferritin. Percent of saturation greater than 40% and Serum Ferritin greater than 150 ng/ml is diagnostic-or at least suggestive of hemochromatosis. If the iron profile is abnormal, then you can have genetic testing done to verify whether or not you are a carrier, have the condition, or don`t have it. It is important to note that a single lab test that is normal is not a guarantee of normal future tests, so annual retesting is suggested. Also, if one family member discovers they have the genetic defect, all blood relatives should have the genetic testing done. Additionally, there is concern that another as yet undiagnosed gene may sometimes cause the problem, so the routine lab studies can be important as a precaution even if your genetic testing proves normal. Most important: Have lab tests done whether you have symptoms or not, in fact, preferably without symptoms.

The key to good health after the diagnosis of hemochromatosis is proper treatment. This involves phlebotomies to remove blood and lower iron levels. Initially blood is taken from the person every week until normal iron levels are reached. After that, 3-4 times yearly blood is taken to maintain the normal levels. There is no cure, but treatment is effective and palliative if continued indefinitely.

There is a terrific Web site devoted to educating people about hemochromatosis by the American Hemochromatosis Society at http://www.americanhs.org/. Spend some time there to educate yourself and then pass the information onto others who may not realize the risk they have for this condition. Obviously, to prevent passing this onto other generations, genetic testing must be done. And remember, early treatment is the only method to prevent the serious damage and death that can occur if hemochromatosis is not diagnosed and treated. I urge you to ask for TIBC and serum iron diagnostic blood tests on your next medical visit.

If you read the brochures about osteoporosis diagnosis and treatment, you won`t find hemochromatosis listed as a risk factor very often, if at all. Liver disease is often listed, however, and that is one complication of hemochromatosis. But, osteoporosis is a possible complication of hemochromatosis, so this is another reason to get proper diagnosis and treatment. In fact, I heard from a gentleman (I`ll call him Ed, not his name) recently who has hemochromatosis and osteoporosis. Here is a synopsis of his case history for your information.

Ed, now 57 years old, found out he had hemochromatosis four years ago when an ayurvedic doctor had his iron level tested when she noted reddish discoloration on his shins. A liver biopsy followed and it was noted that he had seventeen times normal liver iron concentration, but fortunately no cirrhosis yet. After one and one-half years of phlebotomies which took about one pint of blood per week, his blood iron levels returned to normal and he now maintains that with four phlebotomies per year. He thought everything was returning to normal, when last year he was diagnosed with osteoporosis. There are no family risk factors, his serum testosterone levels are normal, along with all other diagnostic tests. So, he concludes that the hemochromatosis is the source of his osteoporosis.

A search of PubMed turned up many articles that show a relationship between hemochromatosis and osteoporosis or osteopenia. A study in 1997 is particularly pertinent. It was done by Sinigaglia L and others and reported in J Rheumatol 1997 Sep;24(9):1809-13. Bone and joint involvement in genetic hemochromatosis: role of cirrhosis and iron overload. PMID 9292808. The authors investigated multiple risk factors as the source of bone or joint involvement in 28 men and four women with hemochromatosis. They found osteoporosis in nine patients, and noted that condition was highly related to the degree of iron overload. There was no relationship of the cirrhosis or iron overload to joint problems, although 81.3% of the people exhibited joint involvement. The authors note, "In contrast, in univariate analysis the risk of osteoporosis was significantly increased by liver cirrhosis. With multivariate analysis we found that osteoporosis was highly influenced by the degree of iron overload, playing an independent role in accelerating bone loss in patients with genetic hemochromatosis." Another pertinent article is a review in 1998 by Isaia G and others, in Forum (Genova) 1998 Jan-Mar;8(1):28-38, Bone disorders in cholestatic liver diseases. PMID 9514992. The authors note that osteopenia is a common finding (from 10-56% of the time) in cholestatic liver diseases; hemochromatosis is one form of this disease. They point out the importance of bone density measurement in this population as the best way to determine the degree of bone mineral involvement. So, physicians need to perform routine laboratory testing to diagnose people who have hemochromatosis, and then must do bone density testing to assure they are not osteoporotic as a result of the genetic iron overload problem.

Ask the experts

We have questions for three of our expert contributors this month. The first is for Dr. Karen Kolba, Rheumatologist, with input from Evan Prost, Physical Therapist, and involves corticosteroids, compression fractures, and osteoporosis.

Question: My husband has osteoporosis after taking high-dose corticosteroids for other medical problems and is currently on about 10 mg/day of steroids and he takes Fosamax for his osteoporosis. He has a history of spinal compression fractures that had been under control since he started the Fosamax. However, recently he apparently injured another vertebra while just reaching for something and is in pain. He has been given no advice on how to treat this acute painful phase. Should he just lay down and take it easy or will exercise hurt his back or make it better?

Answer: While Fosamax and Actonel do decrease fractures by 50%, that means there are still 50% of folks that have fractures, especially vertebral, and especially after steroid therapy. X-rays should be taken to verify that this is indeed another compression fracture and not something else.

The first bit of advice is: continue Fosamax, along with enough calcium and possibly high doses of Vitamin D (50,000 IU twice a week). The Vitamin D may be particularly useful while a person is taking any dose of steroids, and when off of these, return to the usual recommended doses of 800-1200 IU per day. [See the American College of Rheumatology Guidelines for Treatment of Steroid-induced Osteoporosis.]

The second bit of advice is find an orthopedist who is actively doing kyphoplasty and get on with it! This procedure must be done early or it can`t be done at all. For more information about vertebroplasty and kyphoplasty see http://pages.prodigy.net/jerryd3001/pv.htm. The trick is to find a surgeon or a center with enough experience. Clearly, this is a procedure where outcomes improve as the surgeon gains experience. Ideally, one would find a surgeon who has done at least 100 of these; but I would say that 30 procedures would be my personal rock-bottom minimum. A person may have to hunt around to find this sort of expertise. Ask locally, especially if the person lives near a big city/medical center. If not, it may be worth contacting the manufacturers of the devices as they certainly know which surgeons are their best customers, and generally are happy to refer patients in that direction. [Editor`s note: www.kyphon.com, the manufacturer of kyphoplasty equipment, has a physician locator on their Web site and they have both U.S. and International Web sites.]

The bottom line on the surgery is clearly up to the surgeon. It is not the right procedure for everyone--in fact, I`m struggling in my own practice to figure out who might benefit from this sort of referral. But, this person`s situation may be it. While the surgery only stabilizes the one or two vertebrae that are worked on, it improves the mechanics of the spine and posture, and this may be a way to go. It should certainly be investigated to get the facts and to find if it will be beneficial in each case.

In the acute stages of fracture, pain medicine is really key and there is no reason that 90% of the pain can`t be controlled. This allows a person to remain functional (not in bed) and prevents complications like pneumonia, blood clots, etc.--and depression!

Each thoracic compression fracture can be associated with a permanent 7% decrease in pulmonary function, just based on the change in the shape of the chest wall. So, I think that people with recurrent fractures are probably the appropriate candidates for kyphoplasty. Chronic pain seems to be improved, and I would hope that in the long run, lung function is preserved.

And now to get at the root cause of the osteoporosis in this individual-high dose corticosteroids. Physicians who prescribed the high doses (or any dose, really) of steroids for a prolonged period without prescribing concomitant medications to prevent bone loss should be severely chastised. No matter what the underlying disease, preventing further harm is absolutely key, and we`ve had drugs to do this since 1995. I know that it is often hard for a patient to tell this to their physician, especially if they are still being treated and don`t want to make the physician mad. But, believe me, unless you educate that physician, it will happen again to someone else. My suggestion is to send a typed, well thought out letter about what happened as a result of the steroids, and what might have been done to prevent it. Don`t threaten to sue - you may find yourself looking for a new physician. Ask for a response (between office visits) and maybe include some printed info from the National Osteoporosis Foundation, www.nof.org, or the Arthritis Foundation, www.arthritis.org, on steroid-induced osteoporosis. This gives a chance to save face, and may actually cause the physician to rethink his/her treatment methods. [Editor`s note: See below a list of PubMed abstract references starting in 1994 showing that bisphosphonates prevent corticosteroid-induced bone loss. You may want to get copies of these from PubMed, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi, and attach them to your letter. Also, see the Literature Review section of this newsletter for an article showing that, unless you are seeing a rheumatologist, your chances of getting proper osteoporosis prevention advice and medications are only about 50:50 if you have been prescribed corticosteroids]

References showing bisphosphonates are effective in preventing steroid-induced osteoporosis: Rheumatol Int 2001 Feb;20(2):65-9 PMID: 11269535; Arthritis Rheum 2001 Jan;44(1):202-11, PMID 11212161; Calcif Tissue Int 1996 Mar;58(3):166-9, PMID 8852571; J Bone Miner Res 2001 Jan;16(1):104-12, PMID 11149473; Kurume Med J 2000;47(3):219-24, PMID 11059223; Calcif Tissue Int 2000 Oct;67(4):277-85, PMID 11000340; J Bone Miner Res 2000 Jun;15(6):1006-13, PMID 10841169; Arthritis Rheum 1999 Nov;42(11):2309-18, PMID 10555025; J Rheumatol 1999 Jul;26(7):1545-9, PMID 10405943; Scand J Rheumatol 1999;28(3):152-6, PMID 10380836; Thorax 1998 May;53(5):351-6, PMID 9708225; J Clin Endocrinol Metab 1998 Apr;83(4):1128-33, PMID 9543129; Scand J Rheumatol Suppl 1996;103:91-3, PMID 8966498; Am J Med 1995 May;98(5):459-63, PMID 7733124; J Rheumatol 1994 Oct;21(10):1922-6, PMID 7837160; Am J Respir Crit Care Med 1994 Aug;150(2):394-7, PMID 8049820; Br J Rheumatol 1994 Apr;33(4):348-50, PMID 8156307.

Answer from Evan Prost, PT: I can offer some general information about managing compression fractures. The information can be found at my web site http://web.missouri.edu/~proste/osteoporosis/. This site is in it`s very early stages, but it does have some information relevant to this person. Also, note that you can e-mail Evan from his site.

The next question is for our radiology and bone densitometry expert, Dr. James Schuster.

Question. The hip DXA computer report lists readings for multiple parts of the hip, often including the Wards, trochanter, neck, and some reports include a total reading. What is the significance of a low BMD reading in one portion of the hip vs. another.

Answer. The total reading is the most important. But, I also look for any "low spots" and certainly look at Wards when assessing response to therapy, as it is the trabecular portion most likely to respond to treatment. The neck is the weakest, or at least the most commonly fractured. I would hesitate to diagnose osteoporosis unless the TOTAL T-score was abnormal. In terms of the spine, we usually only "throw out" a level if it is spuriously high, for example due to spurring, calcified aneurysm, etc. If one level was significantly lower than the others, I would wonder about a benign intervertebral lesion like a lipoma, hemangioma, etc.

Literature review

To find PubMed abstracts mentioned here, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi and type the PMID information, numeric portion only, into the search block.

Human parathyroid hormone. Two new studies continue to show the effectiveness of human parathyroid (PTH) to treat osteoporosis. The first is in J Bone Miner Res 2001 May;16(5):925-31, Parathyroid hormone added to established hormone therapy: effects on vertebral fracture and maintenance of bone mass after parathyroid hormone withdrawal. Cosman F and others. PMID 11341338. In this study they compared 25 women on HRT alone, to 27 women on HRT and PTH in a random group assignment study with three years for the treatment trial and one year of follow up. Biochemical markers of bone turnover and DXA were used to evaluate results. The authors found, "Subjects in the PTH + HRT group increased bone mass by 13.4 +/- 1.4% in the spine, 4.4 +/- 1 % in the total hip, and 3.7 +/- 1.4% in the total body. Bone density measurements remained stable one year after discontinuation of PTH without any significant loss while women continued HRT." Additionally, "PTH + HRT reduced the percent of women who had vertebral fractures from 37.5% to 8.3% (using a 15% height reduction criterion) and from 25% to 0% (using a 20% height reduction criterion) compared with women receiving HRT alone (p<0.02 for both)." So this combination therapy`s ability to reduce vertebral fractures by 75-100% compared to HRT alone, is very exciting. Whether this study applies to men remains to be seen. The key will be whether PTH can be combined with bisphosphonates in a similar manner, and that won`t be known until clinical trials are done. It also appears possible that bisphosphonates might be able to retain increased BMD gained using PTH if the bisphosphonates are started when PTH therapy stops. This is an interesting area ripe for a lot of research, and I hope some of it will apply to men. As mentioned in the last newsletter, there is some concern about PTH promoting cancer in men-especially prostate cancer--so research must look at that possibility, too.

The second study is by Neer RM and others and is reported in N Engl J Med 2001 May 10;344(19):1434-41. Effect of parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis. PMID 11346808. This is a very large multicenter trial involving 1637 postmenopausal women with prior vertebral fractures who received either 20 or 40 micrograms of parathyroid hormone (1-34) or placebo via daily subcutaneous injection for 21 months. The authors found, "New vertebral fractures occurred in 14 percent of the women in the placebo group and in 5 percent and 4 percent, respectively, of women in the 20-microg and 40-microg groups. . ." They concluded, "Treatment of postmenopausal osteoporosis with parathyroid hormone (1-34) decreases the risk of vertebral and nonvertebral fractures; increases vertebral, femoral, and total-body bone mineral density; and is well tolerated." So, there are now many studies that have found PTH effective in increasing BMD and decreasing fracture risk. We now await FDA approval, and what the final guidelines will be for administering the drug once it is approved.

Physicians` opinion, does it affect patient choices? This interesting study was done in Belgium by Rozenberg S and Ham h. It is in Eur J Obstet Gynecol Reprod Biol 2001 Jun;96(2):215-7. Effect of physicians` opinion on patients` choice of treatment. PMID 11384811. The authors developed two different letters to send to patients who were hypothetically 55 years old and at high risk for osteoporosis. Each letter described the options of two medications for treatment, but one letter favored HRT and the other favored a selective estrogen receptor (SERM), both backed by scientific studies as references for using that medication. 58 nurses randomly received the letters and were asked to choose which treatment they preferred. 23/30 women receiving the version favoring HRT preferred HRT, and 26/28 of the women receiving the version favoring SERM preferred that method. The authors conclude:, "The content of the information provided and its wording have a great influence on the patients` decision." Thus, unless you are willing to do personal investigation, you are probably going to be influenced by the bias of your physician. Hopefully that bias is based upon research and the latest valid medical information available.

Prevention of glucocorticoid-induced osteoporosis. As noted in the Ask the Expert section of this newsletter, prescription of long-term and high-dose corticosteroids is a continuing cause of osteoporosis in the world. This in spite of the fact the literature reports since at least 1994 have shown that bisphosphonates, and/or vitamin D and calcium can prevent that bone loss. Here is another article to demonstrate the depth of the problem. See Arch Intern Med 2001 May 289;161(10):1322-7, Prevention of glucocorticoid-induced osteoporosis: experience in a managed care setting. Yood RA and others, PMID 11371261. The authors examined patient records in a managed care setting for patients prescribed oral glucocorticoid prescriptions from October 1997 to September 1998. Of the 224 patients seen, 62% had at least one documented intervention aimed at osteoporosis prevention. An intervention could be counseling about or prescription for medications, exercise, or bone mineral density testing. There was no better chance of an intervention on greater than 10 mg/day dose than less than 5 mg/day. The breakdown of interventions by specialty was: 90% of rheumatologists, 48% of internists, 55% of pulmonologists, and 46% of all other physicians. The authors point out, "Currently available guidelines indicate that patients receiving long-term glucocorticoid therapy should receive measures to prevent osteoporosis." They conclude, "A substantial proportion of patients receiving long-term glucocorticoid therapy do not receive preventive therapy for osteoporosis. Efforts should be made to reduce barriers to such treatment and increase the proportion of patients given preventive therapy." If you have received long-term or high-dose corticosteroids and haven`t been counseled about osteoporosis, you must ask your physician why not? This is the only way to assure that future patients will get proper care and avoid getting osteoporosis totally unnecessarily.

Members bone density results after long-term Fosamax therapy. Clinical results after long-term Fosamax. Two of the members of the Men`s Osteoporosis Support Group have submitted Dual-energy X-ray Absorptiometry (DXA) results this quarter. Both men have been treated for osteoporosis for several years, one being diagnosed in 1991 and the other in 1994.

Member number one (M1). This man is 62 years old and had his first bone density test done in 1991. The machine was different from those used for subsequent tests, so the reliability of the figures is somewhat questionable. He takes Fosamax, 70 mg/once weekly, testosterone injections, .25 mcg vitamin D daily, and 200 mg Citracal daily. He is going to increase the Citrical dosage up to 600-800 mg as he didn`t realize he was only taking 200 mg. Additionally, he works out with free weights once weekly, and is in an exercise class that uses a large ball for core conditioning. He does little walking. He reports having a pretty bad fall recently, but no fractures from it, so that is anecdotal evidence of increased bone strength along with the increased bone mineral density (BMD).

Member number two (M2). This man is 57 years old and was diagnosed with osteoporosis in 1994. He has also had tests done on two different machines but a correlation DXA was done on the original machine to assure results were comparable. He has been on Fosamax since February 1996, and testosterone injections since late 1994. He also takes at least 500 mg of calcium supplements daily with 200-400 IU of vitamin D, has a diet with plenty of calcium in it, and spends several hours outside daily. His exercise includes walking carrying a golf bag that weighs about 15-20 pounds 3-5 days a week, biking for about an hour every other day, and on alternate days, free weights for about one-half hour. Until knee arthritis stopped him about four months ago, he had been doing hill climbing and running for about one hour on days when he didn`t bike. Here are both their DXA results in gm/cm2:

M1 Lumbar Spine Avg	M1 Lumbar Spine Avg	M1 Hip Avg	M2 L2-L4	M2 L2-L4	M2 Hip neck
1991: 0.835 2001: 0.962 Increase: 15%	1995: 0.89 2001: 0.962 Increase: 8.1%	1995: 0.956 2001: 1.033 Increase: 8.1%	1994: 0 .957 2001: 1.163 Increase: 21.5%	1998: 1.154 2001: 1.163 Increase: 0.78%	1995: 0.89 2001: 0 .899 Increase: 1.01%

Summary. These results follow the general tendency noted in most studies of marked improvement in spinal BMD, often with lesser improvement in the hip. The most dramatic improvement occurred in the first couple of years-especially on M2. And, in spite of pretty rigorous physical activity, improvement during the last two years has been minimal. But, a man his age would normally lose some BMD, so that makes the recent small improvement look better. Also, M2`s results aren`t reported for the total hip, so it is hard to compare both member`s results. M1`s spinal T-score is now -1.170, consistent with osteopenia, not osteoporosis and his femur neck T-score is -1.75, also osteopenic. M2 has a spinal T-score of -0.64 which is now in the normal range, and his femur neck T-score is -1.31, osteopenic. So both men have moved out of the osteoporosis T-score range of -2.5 S.D. These results are exciting and show that Fosamax can have both short- and long-term positive benefits on BMD, which should reduce fracture risk also. These findings confirm those of many studies, but bring those results closer to home since they are on members of our group.

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.

EDITOR

Jerome C. Donnelly

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