Bone-Headed
If we are all little angels and always observe our doctors’ prescriptions, then why is something as simple as taking a daily calcium supplement and vitamin D so perplexing? Why can’t we prevent that irritating rattle of our bones? Why do we so fear that fall that may signal an end to our physical autonomy? Finally, why do we look to medical miracles like once a month, once a year, or once a life treatment regimens with such subliminal desperation, as if we could erase with a snap of the fingers the expiration date that the Almighty, Nature, and the relentless course of time have so eloquently fixed in the pages of our twilight existence? Bone-headed, we’re not. Headed for bone is another story. We desire an improved quality of life for as long as we can sustain it, and building strong bones and muscles just makes good sense. Navigating advice columns and Internet websites to find clear-cut answers and remedies, however, is an exercise in Zen, and frayed nerves and couch-potato restlessness demand answers to questions and a realistic approach to intervention. So, as is usually stated in these columns, let’s keep it simple. If we follow the rules outlined here, our lives, physically and osteogenically speaking, will be a lot less tedious and worry-ridden. Not following them will initiate the slippery slide to and through osteoporosis. The decision is ours and ours alone.
While no one likes to be reminded of the unpleasant, a jolt is sometimes needed. Here are the stats. More than 10 million people (8 million women and 2 million men) in the U.S. are affected by osteoporosis, but only a small proportion are diagnosed and treated. If that were not bad enough, an additional 18 million individuals have bone mass levels that put them at increased risk for developing the malady. Osteoporosis is defined technically a bone density that falls 2.5 standard deviations (SD) below the mean for young healthy adults of the same race and gender (so-called T-score < –2.5), and increased risk is set at bone mass T-score < –1.0. Now, that’s all well and good, but we are more interested in effects and results than simple statistics. For example, what is this thing we call osteoporosis, and how does it affect us?
Osteoporosis results from bone loss due to both normal aging and an exaggeration of the process of bone remodeling. The process of bone growth, remodeling, and repair is somewhat complicated and involves many players, but can be simplified by thinking of bone as a bank or repository of calcium, with deposits and withdrawals made daily. When there is an imbalance between the two in favor of withdrawals, we eventually go bankrupt and our bones break. Decreased activity of the bone-forming cells, called osteoblasts, and increased activity of bone-degrading cells, called osteoclasts, results in activation of bone remodeling, bone loss, decrease in biomechanical strength, more porous bone, and, finally, osteoporotic fracture, to the tune of 1.5 million fractures (300,000 hip fractures, 700,000 vertebral crush fractures, 250,000 wrist fractures, and 300,000 fractures of other bones such as the distal radius of the forearm) each year in the U.S. as a consequence of osteoporosis.
So, where does osteoporosis come from, and should we resign ourselves to the fact that it is just another inevitable sign of old age that we can do nothing about? The answer is a resounding “No!” We can do something about it, but we must first come to know our enemy. Contributing to its onslaught are inadequate calcium intake, vitamin D deficiency, estrogen deficiency in women, inactivity and lack of exercise, genetic and acquired diseases (anorexia nervosa diabetes mellitus, liver disease, rheumatoid arthritis, lymphoma and leukemia, emphysema, and multiple sclerosis, to name a few), medications such as glucocorticoids, anticonvulsants, and immunosuppressants (check with your doctor on that score), and cigarette consumption, of course.
Being less bone-headed means getting off our duffs and having our bone mineral density (BMD) measured by one of a battery of noninvasive techniques approved by the U.S. Food and Drug Administration (FDA), such as dual-energy x-ray absorptiometry (DXA), single-energy x-ray absorptiometry (SXA), quantitative computed tomography (CT), and ultrasound. All fancy names for relatively simple techniques that should be performed in postmenopausal women with risk factors for osteoporosis and in all women by age 65. If BMD is found to be > 2.5 SD below the mean value for young adults (i.e., T-score < –2.5), we play the treatment card.
After consultation with our health care providers and laboratory evaluation for secondary causes of osteoporosis, we proceed to the intervention phase in which we reduce risk factors, supplement our diets with calcium (taken in doses of ≤600 mg at a time), vitamin D (400-600 IU daily), vitamin K, and magnesium, exercise by walking at least three times a week, and begin pharmacologic therapy. Our doctors will know how to best advise us regarding the latter, as we navigate a maze of television commercials touting the benefits of agents that specifically treat osteoporosis (bisphosphonates, calcitonin, parathyroid hormone) and others having broader effects (selective estrogen response modulators or SERMS). For those of us adverse to popping pills on a daily basis, two potent bisphosphonates, zoledronate (Zometa) and ibandronate (Boniva), have unique administration regimens (once yearly intravenously, once monthly orally).
Our money, our choices, our lives. Let’s not be bone-headed!
© 2007, Albert M. Balesh, M.D. All rights reserved.
While no one likes to be reminded of the unpleasant, a jolt is sometimes needed. Here are the stats. More than 10 million people (8 million women and 2 million men) in the U.S. are affected by osteoporosis, but only a small proportion are diagnosed and treated. If that were not bad enough, an additional 18 million individuals have bone mass levels that put them at increased risk for developing the malady. Osteoporosis is defined technically a bone density that falls 2.5 standard deviations (SD) below the mean for young healthy adults of the same race and gender (so-called T-score < –2.5), and increased risk is set at bone mass T-score < –1.0. Now, that’s all well and good, but we are more interested in effects and results than simple statistics. For example, what is this thing we call osteoporosis, and how does it affect us?
Osteoporosis results from bone loss due to both normal aging and an exaggeration of the process of bone remodeling. The process of bone growth, remodeling, and repair is somewhat complicated and involves many players, but can be simplified by thinking of bone as a bank or repository of calcium, with deposits and withdrawals made daily. When there is an imbalance between the two in favor of withdrawals, we eventually go bankrupt and our bones break. Decreased activity of the bone-forming cells, called osteoblasts, and increased activity of bone-degrading cells, called osteoclasts, results in activation of bone remodeling, bone loss, decrease in biomechanical strength, more porous bone, and, finally, osteoporotic fracture, to the tune of 1.5 million fractures (300,000 hip fractures, 700,000 vertebral crush fractures, 250,000 wrist fractures, and 300,000 fractures of other bones such as the distal radius of the forearm) each year in the U.S. as a consequence of osteoporosis.
So, where does osteoporosis come from, and should we resign ourselves to the fact that it is just another inevitable sign of old age that we can do nothing about? The answer is a resounding “No!” We can do something about it, but we must first come to know our enemy. Contributing to its onslaught are inadequate calcium intake, vitamin D deficiency, estrogen deficiency in women, inactivity and lack of exercise, genetic and acquired diseases (anorexia nervosa diabetes mellitus, liver disease, rheumatoid arthritis, lymphoma and leukemia, emphysema, and multiple sclerosis, to name a few), medications such as glucocorticoids, anticonvulsants, and immunosuppressants (check with your doctor on that score), and cigarette consumption, of course.
Being less bone-headed means getting off our duffs and having our bone mineral density (BMD) measured by one of a battery of noninvasive techniques approved by the U.S. Food and Drug Administration (FDA), such as dual-energy x-ray absorptiometry (DXA), single-energy x-ray absorptiometry (SXA), quantitative computed tomography (CT), and ultrasound. All fancy names for relatively simple techniques that should be performed in postmenopausal women with risk factors for osteoporosis and in all women by age 65. If BMD is found to be > 2.5 SD below the mean value for young adults (i.e., T-score < –2.5), we play the treatment card.
After consultation with our health care providers and laboratory evaluation for secondary causes of osteoporosis, we proceed to the intervention phase in which we reduce risk factors, supplement our diets with calcium (taken in doses of ≤600 mg at a time), vitamin D (400-600 IU daily), vitamin K, and magnesium, exercise by walking at least three times a week, and begin pharmacologic therapy. Our doctors will know how to best advise us regarding the latter, as we navigate a maze of television commercials touting the benefits of agents that specifically treat osteoporosis (bisphosphonates, calcitonin, parathyroid hormone) and others having broader effects (selective estrogen response modulators or SERMS). For those of us adverse to popping pills on a daily basis, two potent bisphosphonates, zoledronate (Zometa) and ibandronate (Boniva), have unique administration regimens (once yearly intravenously, once monthly orally).
Our money, our choices, our lives. Let’s not be bone-headed!
© 2007, Albert M. Balesh, M.D. All rights reserved.
posted by Dr. Al at
7/30/2007 12:27:00 PM
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