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Johns Hopkins Biographies of Disease
Aging Bones: A Short History of Osteoporosis
How osteoporosis went from a normal aging process to a disease. In the middle of the twentieth century, few physicians could have predicted that the modern diagnostic category of osteoporosis would emerge to include millions of Americans, predominantly older women. Before World War II, popular attitudes held that the declining physical and mental health of older persons was neither preventable nor reversible and that older people had little to contribute. Moreover, the physiological processes that influenced the health of bones remained mysterious. In Aging Bones , Gerald N. Grob makes a historical inquiry into how this one aspect of aging came to be considered a disease. During the 1950s and 1960s, as more and more people lived to the age of 65, older people emerged as a self-conscious group with distinct interests, and they rejected the pejorative concept of senescence. But they had pressing health needs, and preventing age-related decline became a focus for researchers and clinicians alike. In analyzing how the normal aging of bones was transformed into a medical diagnosis requiring treatment, historian of medicine Grob explores developments in medical science as well as the social, intellectual, economic, demographic, and political changes that transformed American society in the post–World War II decades. Though seemingly straightforward, osteoporosis and its treatment are shaped by illusions about the conquest of disease and aging. These illusions, in turn, are instrumental in shaping our health care system. While bone density tests and osteoporosis treatments are now routinely prescribed, aggressive pharmaceutical intervention has produced results that are inconclusive at best. The fascinating history in Aging Bones will appeal to students and scholars in the history of medicine, health policy, gerontology, endocrinology, and orthopedics, as well as anyone who has been diagnosed with osteoporosis.
304 pages, Paperback
First published June 1, 2014
2 people are currently reading
28 people want to read
About the author
Gerald N. Grob
81 books2 followersThe son of Jewish immigrants from Poland, Gerald Grob earned a bachelor's degree from the City College of New York and a master's degree from Columbia University. He earned his doctorate at Northwestern University in 1958 and taught at Clark University from 1957 until 1969 and at Rutgers University from 1969 until his retirement in 2000.
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September 24, 2018
I probably liked this book four stars’ worth because I’m looking for justification not to take medication for a diagnosis of osteoporosis. I found it.
Osteoporosis is not the first condition to get medicalized as the understanding of biology and the sophistication of the practice of medicine grew. This trend has particularly affected women, with control of the natural processes of childbirth and menopause becoming the province of specialists. Osteoporosis is a consequence of aging that affects a majority of people. Grob tells the story, study by study and meeting by meeting, how it came to be viewed as a deficiency disease requiring treatment even in those who have no symptoms.
“Study by study and meeting by meeting” suggests that this isn’t riveting reading. It’s replete with abbreviations, acronyms, statistics,* and technical terminology. Not sure who is the audience for this series; perhaps not the lay public, to which I belong. I will say up front that I have probably missed some important things and conflated other things. What follows is not a strict chronology.
I glossed over some of the numbers and verbiage to the more interesting parts, such as how the changing view of older people fed into the process of defining osteoporosis as a disease. Once respected for their experience, as life expectancy increased and older people formed a larger percentage of the population, they became seen as unproductive, unhealthy, and obstacles to the advancement of the young. There were also fears that the costs of treating untold numbers of bone fractures would overwhelm the public health system.
When hormones were discovered and as the field of endocrinology grew, menopause came to be seen as a deficiency of estrogen rather than a natural part of aging (which was, of course, undesirable and “unfeminine” in women). Luckily it could be staved off with hormone replacement therapy (HRT). The pharmaceutical industry was only too happy to develop and promote drugs for this purpose, and to fund studies that would confirm these conclusions and encourage more women to be treated. It took quite some time for the effects of HRT to become apparent: endometrial and breast cancer (and for estrogen alone, ovarian cancer), blood clots, heart disease, and stroke. Plus, many studies indicated that whatever positive effects it had disappeared when therapy stopped.
Osteoporosis followed a similar path. Increasingly sensitive imaging equipment was developed. To measure what screening showed, the World Health Organization developed the T-score scale in use today, based on standard deviations from the average bone mineral density (BMD) of white women aged 20–29. Drug companies funded research studies. HRT was shown to retard the loss of bone density, followed by the discovery of bisphosphonates (Fosamax et al.). Meetings and interest groups, like the National Osteoporosis Foundation, excluded contributions from professionals who came to different conclusions or questioned conflicts of interest. Textbooks were published promoting only the dominant concept of osteoporosis as a disease. Magazine articles and books aimed at the public popularized this concept. Drug advertisements direct to consumers were allowed, feeding demand. Women went to their general practitioners, who as nonspecialists were not equipped to evaluate their requests critically, so they prescribed what patients want. Patients want drugs, which leads to more screening, which identifies asymptomatic women, which feeds more drugs and screening.
So what’s the problem if all this is beneficial? Well, perhaps it’s not necessarily helpful and may even cause harm.
First, the values of BMD measurements are arbitrary. How does the T-score based on young white women work for men and children, who do get osteoporosis from causes other than normal aging, or for women of nonwhite ethnicities? Also, Grob stated that at least as of the late 1990s, there is no industry standard to compare machines that measure BMD. How do we know what a good or bad value is, and how can we rely on a value obtained from screening? There is some suggestion that DXA screening equipment is not as accurate in people of smaller stature.
If the object of treatment is to avoid fractures: Vertebral compression fractures (an original concern of osteoporosis) are often asymptomatic and always difficult to identify when they have occurred. Along the way, emphasis got rerouted to fractures resulting from trauma (especially hip fractures), which can have many causes but are easier to count than vertebral fractures. By itself, low BMD is a poor predictor of future fractures. Many people with low BMD don’t suffer fractures, and many people who do not have osteoporosis do. The rate of hip fractures varies greatly among countries, for unknown reasons but suggesting that something other than a disease process is at work.
Low bone mineral density is only one of several risk factors for fractures resulting from falls. Others are vision problems; multiple, inappropriate, or psychotropic medications; and other medical or cognitive problems. The FRAX (Fracture Risk Assessment) tool includes other risk factors besides BMD screening, but as a patient who has fended off recommendations to take bisphosphonates for years, I have never had this tool mentioned to me by a doctor.
As happened with HRT, a longer period of use of bisphosphonates started to reveal associations with serious drawbacks. Brittle bones, femur fractures not resulting from trauma, and necrosis of the jaw have been reported. Indeed, there have been recommendations to limit the amount of time one takes these drugs. And does the effect wear off when therapy is stopped, as with HRT?
While we have been learning more about bone physiology, I gather that it is still not completely understood. The people who were the foundation of early studies grew up during the World Wars and the Great Depression, a period of nutritional deprivation when they should have been laying down bone. Generations since then have been better nourished, are more physically active, and are in generally better health. What if the predicted fracture rates don’t hold true going forward? For unexplained reasons but not attributable to treatment, the rate of hip fractures has been declining, for both genders and in several countries.
Part of this rush to treatment has been concern about the costs of treating fractures as the population ages, but there have been few studies of the cost-effectiveness of mass screening and prescription drugs. Of those studies, some have determined that it is not at all cost effective. Our market-dominated medical system rewards tests and interventions, whether these improve health or not, and there is little brake on ineffective treatment.
We are medicating asymptomatic people for what may not be a disease at all. History may correct this. In the book’s final chapter, Grob notes how the classification of diseases has changed over time and how many standard treatments in decades past have been discredited as ineffective or even harmful. Partly, it’s just the course of science, where after repeated studies the evidence eventually falls on one side or the other. (Meanwhile, the public gets whiplash as coffee, eggs, alcohol, calcium and vitamin D supplements, screening for prostate cancer, you name it, yo-yo between good and bad.) Attitudes toward aging are slowly changing, and women are pushing back against the paternalism of medicine as it has been practiced. Grob quotes Nortin Hadler, who called osteoporosis “one of the best examples of disease mongering” and whose book, Rethinking Aging, I read and liked. Grob sounds like he’s keeping an open if critical mind, and so will I, but in the meantime I will not be taking any medications for the state of my bones.
*Drug studies and advertising can make risk seem higher than the data warrant. See
Calculating Absolute Risk and Relative Risk.
Osteoporosis is not the first condition to get medicalized as the understanding of biology and the sophistication of the practice of medicine grew. This trend has particularly affected women, with control of the natural processes of childbirth and menopause becoming the province of specialists. Osteoporosis is a consequence of aging that affects a majority of people. Grob tells the story, study by study and meeting by meeting, how it came to be viewed as a deficiency disease requiring treatment even in those who have no symptoms.
“Study by study and meeting by meeting” suggests that this isn’t riveting reading. It’s replete with abbreviations, acronyms, statistics,* and technical terminology. Not sure who is the audience for this series; perhaps not the lay public, to which I belong. I will say up front that I have probably missed some important things and conflated other things. What follows is not a strict chronology.
I glossed over some of the numbers and verbiage to the more interesting parts, such as how the changing view of older people fed into the process of defining osteoporosis as a disease. Once respected for their experience, as life expectancy increased and older people formed a larger percentage of the population, they became seen as unproductive, unhealthy, and obstacles to the advancement of the young. There were also fears that the costs of treating untold numbers of bone fractures would overwhelm the public health system.
When hormones were discovered and as the field of endocrinology grew, menopause came to be seen as a deficiency of estrogen rather than a natural part of aging (which was, of course, undesirable and “unfeminine” in women). Luckily it could be staved off with hormone replacement therapy (HRT). The pharmaceutical industry was only too happy to develop and promote drugs for this purpose, and to fund studies that would confirm these conclusions and encourage more women to be treated. It took quite some time for the effects of HRT to become apparent: endometrial and breast cancer (and for estrogen alone, ovarian cancer), blood clots, heart disease, and stroke. Plus, many studies indicated that whatever positive effects it had disappeared when therapy stopped.
Osteoporosis followed a similar path. Increasingly sensitive imaging equipment was developed. To measure what screening showed, the World Health Organization developed the T-score scale in use today, based on standard deviations from the average bone mineral density (BMD) of white women aged 20–29. Drug companies funded research studies. HRT was shown to retard the loss of bone density, followed by the discovery of bisphosphonates (Fosamax et al.). Meetings and interest groups, like the National Osteoporosis Foundation, excluded contributions from professionals who came to different conclusions or questioned conflicts of interest. Textbooks were published promoting only the dominant concept of osteoporosis as a disease. Magazine articles and books aimed at the public popularized this concept. Drug advertisements direct to consumers were allowed, feeding demand. Women went to their general practitioners, who as nonspecialists were not equipped to evaluate their requests critically, so they prescribed what patients want. Patients want drugs, which leads to more screening, which identifies asymptomatic women, which feeds more drugs and screening.
So what’s the problem if all this is beneficial? Well, perhaps it’s not necessarily helpful and may even cause harm.
First, the values of BMD measurements are arbitrary. How does the T-score based on young white women work for men and children, who do get osteoporosis from causes other than normal aging, or for women of nonwhite ethnicities? Also, Grob stated that at least as of the late 1990s, there is no industry standard to compare machines that measure BMD. How do we know what a good or bad value is, and how can we rely on a value obtained from screening? There is some suggestion that DXA screening equipment is not as accurate in people of smaller stature.
If the object of treatment is to avoid fractures: Vertebral compression fractures (an original concern of osteoporosis) are often asymptomatic and always difficult to identify when they have occurred. Along the way, emphasis got rerouted to fractures resulting from trauma (especially hip fractures), which can have many causes but are easier to count than vertebral fractures. By itself, low BMD is a poor predictor of future fractures. Many people with low BMD don’t suffer fractures, and many people who do not have osteoporosis do. The rate of hip fractures varies greatly among countries, for unknown reasons but suggesting that something other than a disease process is at work.
Low bone mineral density is only one of several risk factors for fractures resulting from falls. Others are vision problems; multiple, inappropriate, or psychotropic medications; and other medical or cognitive problems. The FRAX (Fracture Risk Assessment) tool includes other risk factors besides BMD screening, but as a patient who has fended off recommendations to take bisphosphonates for years, I have never had this tool mentioned to me by a doctor.
As happened with HRT, a longer period of use of bisphosphonates started to reveal associations with serious drawbacks. Brittle bones, femur fractures not resulting from trauma, and necrosis of the jaw have been reported. Indeed, there have been recommendations to limit the amount of time one takes these drugs. And does the effect wear off when therapy is stopped, as with HRT?
While we have been learning more about bone physiology, I gather that it is still not completely understood. The people who were the foundation of early studies grew up during the World Wars and the Great Depression, a period of nutritional deprivation when they should have been laying down bone. Generations since then have been better nourished, are more physically active, and are in generally better health. What if the predicted fracture rates don’t hold true going forward? For unexplained reasons but not attributable to treatment, the rate of hip fractures has been declining, for both genders and in several countries.
Part of this rush to treatment has been concern about the costs of treating fractures as the population ages, but there have been few studies of the cost-effectiveness of mass screening and prescription drugs. Of those studies, some have determined that it is not at all cost effective. Our market-dominated medical system rewards tests and interventions, whether these improve health or not, and there is little brake on ineffective treatment.
We are medicating asymptomatic people for what may not be a disease at all. History may correct this. In the book’s final chapter, Grob notes how the classification of diseases has changed over time and how many standard treatments in decades past have been discredited as ineffective or even harmful. Partly, it’s just the course of science, where after repeated studies the evidence eventually falls on one side or the other. (Meanwhile, the public gets whiplash as coffee, eggs, alcohol, calcium and vitamin D supplements, screening for prostate cancer, you name it, yo-yo between good and bad.) Attitudes toward aging are slowly changing, and women are pushing back against the paternalism of medicine as it has been practiced. Grob quotes Nortin Hadler, who called osteoporosis “one of the best examples of disease mongering” and whose book, Rethinking Aging, I read and liked. Grob sounds like he’s keeping an open if critical mind, and so will I, but in the meantime I will not be taking any medications for the state of my bones.
*Drug studies and advertising can make risk seem higher than the data warrant. See
Calculating Absolute Risk and Relative Risk.
Displaying 1 of 1 review