Alternative therapies. One of the men in the group with a long history of osteoporosis and pain from other sources has submitted a summary of his efforts to improve his health and alleviate his pain using alternative therapies. Although I normally try to confine information in this newsletter to medical results based upon sound scientific research, I think readers may benefit from this man`s experiences. This is certainly not a recommendation to try the things he has done, just an explanation of his experiences with you making a final judgment if anything he tried might interest you. See http://www.maleosteoporosis.org/alttherapy.htm for more information. I caution anyone with osteoporosis to use reason and caution before starting any exercise regimen. Get clearance from your care provider as a fracture can be a serious consequence of osteoporosis-one that you want to prevent if at all possible. On the other hand, exercise-especially weight bearing-is critically important to bone health. Choose the right exercise for you and do it with care.
Interpreting research studies. There is an educational article at the National Dairy Council Web site http://www.nationaldairycouncil.org/lvl04/nutrilib/digest/dairydigest_726.html. The important information in the article involves its explanation of the various types of research studies that are done, the strength and power of each type, and thus which you should have the most faith in to provide sound answers to nutrition and health questions. It defines and explains such terms as Observational Epidemiological Studies, Ecologic (Correlational) Studies, Cross-sectional Epidemiological Observations, Case-Control Epidemiological Studies, Cohort (long-term follow-up) Studies. Then it explains the various types of Experimental Studies, such as, Randomized controlled trials (the "Gold Standard"), and describes Basic Research Studies, and Meta-analysis. The paper concludes: "Different types of nutrition research studies vary in their strengths and weaknesses. Rarely can a single study provide evidence of a causal relationship between diet and disease. A causal relationship between diet and disease becomes more probable when relevant data from several different types of studies are consistent. Putting research findings into context and taking a moderate approach to communicating new findings can help the public better understand the evolutionary nature of nutrition science and determine whether or not a dietary change is justified." I`d suggest book marking this page to have as a reference. When you read abstracts or articles in this newsletter, or elsewhere, you will see various types of studies identified. After reading the information at the National Dairy Council Web site, you will know how much credence to give the findings in the research. This will help you decide whether your diet or lifestyle should change based upon the study`s findings.
ASBMR meeting summary online. The 23rd Annual Meeting of the American Society of Bone and Mineral Research in October 2001 has conference coverage at Medscape.com. Among many topics covered in the conference, there is a good update on men`s osteoporosis. See http://www.medscape.com/viewprogram/229 for the table of contents. Note these links aren`t necessarily permanent, so the page may not be there at some future date. Check the article entitled Treatment of Osteoporosis Using Intermittent Parathyroid Hormone for some interesting bone biopsy specimens showing the quantitative and qualitative histological results of PTH. The photos are very impressive and the article is quite interesting otherwise, too.
Ask the expert
This month`s question is for Dr. Karen Kolba, our medical expert on osteoporosis for the Men`s Osteoporosis Support Group.
Question.. I have placed an article on this Web site about one of our member`s experiences in dealing with pain using alternative medicine therapies and treatments. I wonder if you have any comments on that topic for our readers.
Answer. Yes, there are M.D.s out there who are less than competent, and even quacks, but at least there is some semblance of regulation for physicians. When you are dealing with someone not in a licensed `profession," the proportion of quackery just has to be so much higher. Otherwise, if it was such a `good thing,` it (whatever treatment) would quickly rise to the top of the heap!
We who treat arthritis patients deal with lots of `alternative,` `unproven,` or `quack` remedies. Keep in mind that these other treatments primarily deal with chronic illness, painful conditions, and diseases/conditions for which we have no documented medical cure or fix. For instance, you are simply not going to find alternative treatments for acute appendicitis! I mean, it`s surgery and that`s it (or Cipro--if you are on a nuclear submarine submerged for a 6-month tour of duty).
Now back pain, oh boy! I read an article recently by a pain specialist who demonstrated why any time `we medical people` say we "know" what the pain generator is (i.e., what structure is hurting or causing the pain) in back pain, we are wrong. Very convincing, and I felt very humble reading this! But even if we do admit ignorance, that doesn`t mean we can stop trying to help. And, we pull certain things from our bag of tricks (well, ok, knowledge) based on experience and clinical trials (whatever is available). When `alternative` treatments are used, it is too often suggested that this one technique, therapy, etc., will work no matter what the problem. When all you have is a hammer, the whole world is a nail, and I don`t find that approach terribly useful.
Certainly, the gentleman who wrote the article tried exercise in its many forms, for which I applaud him. But, while he gives credit to whatever he tried last, the truth may be much simpler: his body, given enough time, healed itself--whether through development of scar tissue, or shrinkage of a disc, or repositioning of an arthritic joint--our bodies do change. This is the very reason why randomized controlled clinical trials are the only way we have, so far, to determine what really works.
Literature review
Finding articles mentioned. To see abstracts of these articles, go to PubMed at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi and enter the numeric portion only of the PMID into the search block and click on Go or hit the enter key.
Vitamin K and bone health. There is a new excellent review of vitamin K and its effects on BMD that anyone taking vitamin K or interested in it should read. See Nutrition 2001;17:880-7, Vitamin K and Bone Health, Weber P, PMID:11684396. The author notes, "There is a consistent line of evidence in human epidemiological and interventional studies that clearly demonstrates that vitamin K can improve bone health." There is evidence that it not only increases BMD in osteoporotic people, but also decreases fracture rates. Of particular importance is that the combination of vitamins K and D in fairly low doses benefit bone health. Because of this, "The Institute of Medicine recently has increased the dietary reference intakes of vitamin K to 90 microg/d for females and 120 microg/d for males, which is an increase of approximately 50% from previous recommendations." Thus, if you have osteoporosis, you probably should be sure your vitamin supplement includes the newly recommended amount of vitamin K. Or, that your diet includes foods high in vitamin K. The article lists the vitamin K content of several foods, with green vegetables, cheese, and plant oils being highest.
Statins and BMD. Statins are drugs taken by millions of people world wide to lower serum cholesterol. I`ve reported on statins and bone health in animal and observational studies in humans in the July 2000 and April 2000 newsletters. These studies found a positive relationship between statins and BMD, however, the most important consequence of statins would be a reduction in fracture rates if that occurred. Two newer very large studies (the first case-control and the second a secondary analysis of a randomized controlled clinical trial) report no benefit as concerns fracture risk for patients taking statins. See JAMA 2001 Apr 11;285(14):1850-5, Use of statins and risk of fractures. van Staa TP and others, PMID:11308398 and Lancet 2001 Feb 17;357(9255):509-12, Effect of pravastatin on frequency of fracture in the LIPID study: secondary analysis of a randomized controlled study. Long-term Intervention with Pravastatin in Ischaemic Disease. Reid IR and others, PMID:11229669. So the final word on statins and bone health hasn`t been written yet. There certainly is no evidence strong enough to suggest taking statins solely for improved bone health. Only future studies will provide that information.
Coffee, caffeine, and BMD. The question of the influence of coffee/caffeine on BMD is one that has been around for quite some time with no definitive answer as yet provided by research. A recent study may help explain some of the reasons why some studies have found a relationship between coffee intake and BMD while others haven`t. See Am J Clin Nutr 2001 Nov;74(5):694-700, Caffeine intake increases the rate of bone loss in elderly women and interacts with vitamin D receptor genotypes. Rapuri PB, and others, PMID:11684540. To interpret this article, a basic understanding of genetics is required. Our structure and function is determined by our genetic make up. Microscopically this is governed by the make up of our chromosomes and genes. Genes are made from various combinations of deoxyribonucleic acid (DNA). The genotype is the actual genetic make up of an individual, similar to the structural make of a car, for instance. That is, a certain combination of engine, seats, tires, headlights, and other components makes a Ford, as opposed to a different set of those that makes a Chevrolet. So the different combination of genes that we all have makes our genotype, and makes us appear and function differently from other people. The way we appear is called our phenotype-the look that our microscopic genotype gives us. I hope that is somewhat clearer than mud. The Rapuri study involved a cross-sectional measurement of the BMD in 489 elderly women (aged 65-77) compared to longitudinal measurements in 96 women who were treated with placebo for three years. For each woman the vitamin D receptor (VDR) genotype was determined and classified as TT, Tt, or tt. Caffeine intake was stratified as low is <300 mg/d or high if >300 mg/d. Changes in BMD in the hip and spine were measured with Lunar DPX-L, dual-energy X-ray absorptiometry (DXA). Results showed women with the high caffeine intake had significantly higher rates of bone loss at the spine than did those with low intake (-1.90 + 0.97% compared with 1.19 + 1.08%;P=0.038). Comparing VDR genotype and caffeine intake showed women with the tt genotype had significantly (P=0.054) higher rates of bone loss at the spine (-8.14 + 2.62%) than did women with the TT genotype (-0.34 + 1.42%f) when caffeine intake was > 300 mg/d. These findings are interesting and appear to show a strong relationship between caffeine intake and bone mineral loss in older women with the tt VDR genotype. Note that the tt genotype was found in only approximately 5% of the population studied, meaning those at risk for BMD problems due to excess caffeine intake is relatively small. Whether men, or younger women with that VDR genotype would be affected similarly is unknown. If that relationship was found to be true in those populations that could be a contributing factor in some peoples` unexplainable BMD loss. As pointed out in an editorial in the same Nov 2001 Am J Clin Nutr by Massey, LK, page 569, moderation as concerns caffeine intake appears to be the wisest route-particularly for elderly individuals. She points out that, "Moderate caffeine consumption seems likely to be <300 mg, approximately 16 oz (473 mL) brewed coffee, 32 oz (946 mL) brewed tea, or 6, 12-oz (355-mL) cans of most caffeinated soft drinks. It wouldn`t appear to be a hardship to drink less than those amounts of beverages for individuals concerned about bone health.
Series of articles on male osteoporosis. Calcif Tissue Int 2001;69(4) has an extensive series of articles dealing with male osteoporosis. If you can get copies, they will make a nice reference set. Here are some of the topics, all dealing with men and the subject of: Fluoride; parathyroid hormone; alendronate; androgen replacement; biochemical markers; quantitative ultrasound densitometry; assessment of bone mass; diagnosis of osteoporosis and fracture threshold; bone microarchitecture and fragility; genetics; secondary causes of osteoporosis; mortality, morbidity, and assessment of fracture risk; and prevalence of osteoporosis: gender and racial comparison. I will further discuss two that I found particularly interesting.
1. Risedronate`s effect on BMD in men on corticosteroid therapy. See pages 242-247 for the article, Risedronate increases bone density and reduces vertebral fracture risk within one year in men on corticosteroid therapy. Reid DM and others, PMID:11730260. This study involved a total of 184 men in two double-blind, placebo-controlled, 1-year studies to verify the effects of risedronate (Actonel) on patients either beginning corticosteroid therapy or continuing long-term therapy. They received either placebo, risedronate (2.5 or 5 mg), and calcium supplements (500-1000 mg/d). All men were receiving at least 7.5 mg/d prednisone or equivalent. Actually, the mean daily corticosteroid dosage was 19.4 mg and 14.2 mg before and after enrollment, respectively. Results showed that 5 mg risedronate significantly increased BMD at the lumber spine (4.8%), femoral neck (2.1%), and femoral trochanter (2.6%) compared to baseline levels in the treatment group at one year. The difference between the placebo group at 1 year was significant at only the lumbar spine. In the prevention study, the placebo group lost about 3.3% of BMD at all three studied sites, while the 5-mg risedronate group maintained BMD. Nine of 38 (24%) of the placebo group had spinal fractures compared with none in the 2.5% risedronate treatment group and 3 of 33 (9%) in the 5 mg risedronate group. Combining the treatment groups showed 82.4% reduction in fractures (P=0.008). Adverse events were similar between placebo and risedronate. Interestingly, 96% of the placebo group and about 92% of the risedronate group reported adverse events. And, for gastrointestinal events, 10% of the placebo group reported them vs. 1.6% of the 2.5-mg and 7.9% of the 5-mg risedronate groups. In every category of adverse events the placebo group is higher. These results show the continued excellent outcomes for men with risedronate as concerns increasing BMD, reducing fracture rates, and its excellent safety profile. Although the men were all taking corticosteroids, there is no reason to believe the results would not be similar for other causes of low BMD.
2. Therapy of Male Osteoporosis with Parathyroid Hormone. See pages 248-251 for the article, Therapy of male osteoporosis with parathyroid hormone, Bilezikian JP and Kurland ES, PMID:11730261. This article points to the importance for men of having an agent that will build bone (anabolic) rather than just those that will prevent or slow resorption, especially for those men with idiopathic osteoporosis. They point out that parathyroid hormone (PTH) is normally thought of as a catabolic (bone-destructive) agent since PTH usually acts within the body to cause bone loss when it is present in excess, as in hyperparathyroidism. It, however, can have a site-specific effect that is anabolic and catabolic for cancellous and cortical bone, respectively. Researchers have taken advantage of the anabolic aspects of PTH to treat osteoporosis. In the history of PTH treatment for men with osteoporosis, the first positive results were shown in 1986. Then, in 2000, a randomized, controlled trial for men with idiopathic osteoporosis showed excellent results. This study by Kurland ES and others was reported in J Clin Endocrinol Meta 2000 Sep;85(9):3069-76, Parathyroid hormone as a therapy for idiopathic osteoporosis in men: effects on bone mineral density and bone markers. PMID:10999788. The study involved 23 men aged 30-68 with idiopathic osteoporosis who received either placebo or 400 IU PTH-(I-34) plus 1,500 mg calcium and 400 IU vitamin D daily. There was no change in BMD in the spine for the control group, but the PTH-treated group had a marked 13.5% increase in BMD. Additionally, femoral neck BMD increased 2.9% in the treatment group. Interesting histological results of the bone after PTH therapy were noted, too. These showed not only quantitative improvements, but also significant qualitative bone improvement in the cancellous bone structure. It was thought that the cortical bone might not fare as well, but internal cortical bone increases were also noted. These qualitative improvements have not been noted with any antiresorptive medications before. There are no large studies to indicate reduced fracture incidence in men after PTH therapy, but that has been shown in women. These excellent results should do much to have men included in the approval of PTH for treatment of osteoporosis by the FDA. (See the 18th newsletter for possible prostate cancer implications of PTH therapy).
Alendronate and male osteoporosis. Another study has shown the effectiveness of alendronate (Fosamax) for treating men with osteoporosis. See J Clin Endocrinol Metab 2001 Nov;86(11):5252-5. Alendronate treatment of established primary osteoporosis in men: results of a 2-year prospective study, Ringe JD and others, PMID 11701687. This study involved 134 men with primary osteoporosis who received either 10-mg alendronate/d or alfacalcidol (1 microg/d ). All patients also received 500-mg calcium/d during the two-year study. BMD of the lumbar spine and femoral neck was checked each six months via DXA and yearly spinal X-rays were taken to check for vertebral fractures, defined as any 20% decrease in vertebral height.. The results showed 88% of the patients completed the trial. There was a 2.8% improvement in spinal BMD in the alfacalcidol group and a 10.1% improvement in the alendronate group. Femoral neck improvement was 2.2% and 5.2% respectively. Vertebral fractures occurred in 7.3% of the alendronate group and 18.2% of the alfacalcidol group, amounting to a 64% reduction in vertebral fracture risk for the alendronate group. Both treatment regimens were generally well tolerated with no loss of patients from the study due to adverse events. The 2-year 64% reduction in fracture risk is an important element of this study that should be comforting to men taking alendronate. Whether long-term results will show additional reduction in fracture risk is not known.
Exercise and BMD. In a cross-sectional population-based study involving 4,254 men aged 20-59 years, men who jogged had increased femoral neck BMD compared to men who didn`t jog (P = .01) This study was part of the Third National Health and Nutrition Examination Survey (NHANES III). Men who jogged nine or more times per month had higher BMD levels than those who jogged 1-8 times per month (P = .01). The authors conclude: "Jogging is associated with higher femoral neck BMD in men. Additional large-scale studies that measure all aspects of jogging are warranted." See Am J Public Health 2001 Jul;91(7):1056-9. Jogging and bone mineral density in men: results from NHANES III, Mussolino ME and others. PMID:11441731. Note that these men didn`t have osteoporosis, so the results don`t necessarily apply to those of us who do. Additionally, these tended to be younger men mainly in their 30s. Did they increase their BMD because of long-term jogging starting at a younger age, or would they have done so had they started when older? Obviously additional studies are needed to find these answers. But, we know from a lot of research that weight-bearing exercise benefits BMD, but exercise increases BMD mainly from exercise done early in life. Another recent study done in Finland lends credence to this notion. See Osteop Int 2001;12(5):349-55, Regular physical exercise and bone mineral density: a four-year controlled randomized trial in middle-aged men. The DNASCO study. Huuskonen J and others, PMID:11444081. A total of 140 men from 53-62 years old were randomly assigned into exercise and reference groups with DXA of the proximal femur and lumbar spine performed at 2 and 4 years from the study start. Aerobic fitness increased by 13% in the exercise group indicating compliance with the test guidelines while the control group`s aerobic fitness declined by 2%. There was, however, no association between the increase in aerobic threshold and change in BMD. The authors found, "In the entire group, age-related bone loss was seen in the femoral neck BMD and BMDvol (p < 0.01)." Another finding was, "An increased rate of bone loss at the femoral neck was observed in men with a low energy-adjusted calcium intake (p = 0.003). A decrease in body height associated with decreased total femoral BMD r = 0.19, p = 0.04) and the change in body height was a predictor of bone loss in the femoral neck (beta = .201)." Thus, in this study, increased aerobic activity didn`t increase femoral neck BMD in middle-age men. The authors point out that long-term physical activity could have beneficial qualitative effects on bone that might reduce fracture risk without an identifiable increase in BMD. To me the noteworthy finding that is often overlooked as concerns osteoporosis is the correlation between decreased height and lost femoral neck BMD. Could there be a cheaper and easier test than height measurement, either by individuals themselves, or at the physician`s office, to look for early osteoporosis? (See below for additional review of articles on this subject). There should be more emphasis placed upon this simple diagnostic tool with early height loss followed up immediately with DXA to rule out osteoporosis. The increased rate of bone loss in those with low energy-adjusted calcium intake is noteworthy, too. Even though there is no obvious improvement in femoral neck BMD from aerobic exercise, there are probably undetectable qualitative changes to bone, improvements in flexibility and coordination, and other benefits. These suggest that aerobic exercise should probably be done by all those who are physically capable of it, and who have the approval of their physician. Obviously the more extensive your loss of BMD, the more caution you should use when deciding to start an aerobic program and when doing the exercises.
Height loss relationship to BMD. We often hear that height loss is a predictor of osteoporosis, and can see for ourselves the humped back and shortened stature of older men and women who have osteoporosis who were not diagnosed and treated early enough. But, how much height loss is significant, and at what point would DXA be warranted if height loss is detected ? I`ve searched the PubMed literature to see if any definitive studies have been done to suggest parameters of significance of height loss as concerns BMD and osteoporosis risk. The study by Huuskonen J and others,PMID:11444081, mentioned above, found a significant correlation between height loss and decreased total femoral BMD. Another recent study by Versluis RG and others noted a correlation between height loss and osteoporosis. See Br J Gen Pract 2001 Oct;51(471):806-10. Clinical risk factors as predictors of postmenopausal osteoporosis in general practice. PMID:11677703. This study found, "Three risk factors-a low body mass index, fragility fractures, and severe kyphosis and/or loss of height-were associated significantly with osteoporosis; they were present in 33% of women and identified 60% of those with osteoporosis." I could only find one study dedicated to detecting the relationship between height change and BMD. See Orthop Nurs 1996 May-Jun;15(3):57-64. The relationship between height change and bone mineral density. Hunt AH. PMID:8788647. This was a pilot study to determine if height loss would serve as an effective screening tool for osteoporosis. The author found, "Results indicate that excessive height loss does reflect low bone mass and may predict osteoporosis-related fractures." Additional studies are indicated in this area. If a test so simple and cheap as height measurement could detect early, treatable loss of BMD, it could be used by virtually everyone at home as a preventative and diagnostic tool for osteoporosis. Studies need to define what is "normal" height loss, what is "significant" height loss (that point where a DXA should be done to rule out osteoporosis), relate that to age, gender, etc., and define as accurately as possible the percentage of people that could be diagnosed and treated early with this diagnostic tool with its universal use. I`m seen by a physician at least twice yearly and my height is rarely measured. My guess is that means others don`t have this simple test done often enough either-and particularly don`t pay close enough attention to any changes in height as a means of osteoporosis diagnosis.
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.
