~ Male Osteoporosis: The Hidden Epidemic

By Julius G. Goepp, MD

Often overlooked, male osteoporosis is a rapidly growing health problem.1 About 2 million US men have osteoporosis.2 The annual cost of male osteoporosis has been estimated at about $200 million in France alone.3 Recent articles in the scientific literature have begun to recognize that osteoporosis and bone fractures in men pose “a significant public health problem,”4 one that continues to be unrecognized by health care providers, insurers, and the public.5

In a 2002 article in the journal Urology, Dr. Mark Moyad of the University of Michigan Medical Center noted that the impact of osteoporosis in men is “significant and noteworthy,” particularly in light of the growing use of androgen deprivation therapy (ADT) for prostate cancer.6

While osteoporosis has many different causes in both women and men, male osteoporosis generally differs in important ways from female osteoporosis. Men develop osteoporosis about a decade later in life than women,7 and though men have fewer osteoporosis-related fractures than women, they are more likely to suffer serious complications or death as a result.2 About one third of all osteoporotic fractures occur in men, and experts predict that with expected increases in life expectancy, the number of fractures in men will double by the year 2025.1

People often tend to think of hip fractures as a problem of older women. In fact, as many as one third of all hip fractures occur in men,5 and elderly men have age-specific hip fracture rates that are nearly half those of women.8 Moreover, the death rate after hip fracture is even higher in men than in women.2 After the age of 80, spine fractures are equally common in men and women, and are associated with increased mortality.9

Women with osteoporosis tend to fracture their lower extremities more commonly than their arms, but men are more likely to have wrist fractures. In men, wrist fractures have been shown to be an important risk factor for having hip fractures later in life, whereas in women, a previous spine fracture is predictive of subsequent hip fractures.10

Millions of older adults around the world have neglected their bone health. The problem has become so important, in fact, that the decade between 2000 and 2010 has been designated as the “Bone and Joint Decade” by the United Nations, the World Health Organization, and 37 countries. This designation was made to encourage research into the burden of musculoskeletal disorders worldwide, in recognition of the rapid aging of the population.11

To prevent or overcome male osteoporosis, it is important to understand the many ways in which bone health is affected by growth, aging, the environment, and diet. In this article, we will look at normal bone structure and function, then examine the ways in which bone changes normally and abnormally over a lifetime. Finally, we will explore the many proven ways to maintain healthy bones that resist fractures and pain, and help maintain a vigorous and active lifestyle.

Primary Osteoporosis: “Normal” Bone Loss with Aging

The human skeleton is the single largest organ system in the body. Composed of a complex mix of organic proteins and inorganic mineral crystals, bones are much more than just structural supports. Bones are the body’s only reservoir of important minerals such as calcium and phosphorus, which are critical for virtually every other organ system. Calcium, for example, is used in every nerve and muscle cell in the body as a chemical signal. Phosphorus is used in every cell in the human body and is considered the universal energy “currency”; when fats, carbohydrates, and proteins are burned for energy, phosphate molecules move to or from carrier molecules to keep the energy flowing. Levels of calcium and phosphorus must be precisely maintained to keep tissues working properly. Because there is no other internal storage area for these minerals, the skeleton functions as a strategic reserve, absorbing or releasing minerals as required to keep blood levels virtually constant. Bones are able to fulfill this function due to their amazing complexity.

To a structural engineer, bone would be considered a “composite” material, part mineral and part living tissue. It is formed mostly of calcium phosphate arranged in crystals called hydroxyapatite, embedded in a protein matrix primarily made of collagen. This arrangement is very similar to reinforced concrete, in which strong steel bars are embedded in weaker cement. Like reinforced concrete, bone has remarkable strength when it is compressed (for example, when it supports the normal weight of a person standing or moving). Bone has relatively poor strength, however, when it is pulled or bent (such as in a fall). Dietary intake of calcium and phosphorus, as well as of protein (particularly structural proteins that go into the makeup of collagen), is critical in maintaining every element of healthy bone.

In a normal adult diet without supplementation, the amount of calcium entering the body just balances the amount that is excreted each day. This means that even a slight dietary deficiency in calcium itself, or in the vitamin D needed to absorb it, can result in a drop in total body calcium levels. Because blood levels must be maintained within a narrow range, this will result very rapidly in mobilization of calcium from bone to restore the balance. Although the entire skeleton contains large amounts of calcium, prolonged deficiency of vitamin D or calcium will rapidly deplete the stores, resulting in decreased bone mineral content and weaker bones.

Because it is living tissue, bone contains many different kinds of cells, each with a unique function in maintaining bone’s strength and shape. Osteoblasts are the body’s bone-forming cells. Living on or near the surface of bone, osteoblasts secrete protein to form the matrix in which hydroxyapatite crystals form. Osteoblasts are controlled by many different factors, including calcium and phosphorus levels and the sex hormones (estrogens in women and androgens in men). A different bone cell type, the osteoclast, is responsible for breaking down and absorbing bone, a function that is critical in allowing bones to adapt to changes in body size and shape. The overall state of a bone, then, is the result of a precise and delicate balance between the bone-forming work of the osteoblasts and the bone-resorbing osteoclasts. The combined process of production and resorption is called bone turnover, or remodeling.

During childhood and adolescence, bone formation is greater than bone resorption, with the result that bones grow in length, thickness, and strength. Sex hormones have a powerful impact on bone growth. At puberty, bone production increases dramatically, producing the growth spurt of the early teen years. This effect seems to be driven mostly by estrogens, the “female” hormones, in both boys and girls. Near the end of puberty, androgens, the “male” hormones, increase in both women and men. The androgen surge fuses the bone growth plates, with the result being that the bones can no longer elongate.

Young adults generally maintain a steady-state balance in which new bone formation is nearly equal to bone resorption. This process is essential in keeping the bones healthy and enabling them to respond to changes in weight, activity, and diet. Sex hormones also remain at steady levels throughout young adulthood and early middle age. After about the age of 35, however, the total amount of bone in the body begins to diminish. This is one reason that attention to diet and exercise is so important, even very early in life.

Because bone biology is so heavily influenced by sex hormones, it is not surprising that bones age differently in men and women. In aging women, bone is lost both from the inner and outer surfaces of bones, as bone resorption by osteoclasts exceeds new bone formation by osteoblasts. In men, however, new bone formation on the outer surface of bone keeps pace with resorption on the inner surface for much longer.12 This may account for the fact that men begin to suffer fractures from osteoporosis about a decade later than women.7

After middle age, bone loss accelerates. In women, the process begins fairly sharply with the onset of menopause, when estrogen levels drop dramatically. This obvious connection probably accounts for the fact that osteoporosis was thought for so long to be a problem unique to women. Because bone density in men was thought to be related to androgen levels1 and men did not appear to experience anything similar to menopause, doctors simply did not think of osteoporosis in men.

Over the past decade, a vastly different picture has emerged. Many experts now accept the reality of a male equivalent of menopause.1,4,13-17 Some scientists refer to this change as “andropause,” though a more recent and accurate term is “androgen deficiency of the aging male.”18 The distinction is important because, unlike the marked physical changes seen at menopause, the loss of androgens is more gradual and much more variable in terms of a man’s age at its onset.

Another way in which our understanding of the skeletal effects of aging has changed is the discovery that primary control of bone mineralization in both men and women is by estrogens.1 This not only changes our understanding of how osteoporosis occurs in men, but also has dramatic implications for how we can prevent and treat it. Both estrogen and testosterone are produced in the body from androstenedione, which is itself formed from dehydroepiandrosterone (DHEA).8

Causes of Secondary Osteoporosis

The previous discussion concerns “normal” bone loss with aging, or so-called primary osteoporosis. Bone loss frequently occurs due to other causes as well. Men are more likely than women to have so-called secondary osteoporosis2 related to factors including:

Corticosteroids. The most common cause of secondary osteoporosis is treatment with glucocorticoids or corticosteroids, which are often used to treat cancer and many inflammatory conditions. Steroids suppress production of the sex hormones that maintain healthy bone. Bone loss during corticosteroid treatment is very rapid and occurs right at the beginning of treatment. Without supplementation, there will be less total body calcium available to restore the bone at the end of the corticosteroid treatment.19 Even the very low doses of corticosteroids used in the inhaled form for treating asthma and other respiratory diseases have been shown to suppress serum levels of DHEA-S, the most important sex hormone building block.20

Prostate cancer and its treatment. Prostate cancer is the most common cancer in men, and major advances in early detection and treatment have made it a survivable condition for many men. Unfortunately, prostate cancer itself and its most effective treatment, androgen deprivation therapy, or ADT, both contribute to secondary osteoporosis.21 These days, many men begin receiving ADT quite early in response to an elevated or rising prostate-specific antigen (PSA) test result. Because these men are likely to live for many years after starting treatment, they should have baseline bone mineral density measurements, which should be repeated periodically.

Even before ADT is started, many men with prostate cancer have pre-existing osteopenia and osteoporosis.22 This finding has concerned experts because of the additional bone loss experienced during ADT, and has served to alert the medical community to the higher-than-expected frequency of osteoporosis in men overall.21,23 It makes sense, then, for all men to ensure the best possible degree of bone mineralization through regular intake of nutrients known to promote strong bone structure.

Vitamin D deficiency. Skin’s exposure to sunlight is a critical element for activating vitamin D. As people age, their skin’s ability to perform this crucial function diminishes, and less active people may not get out into the sun enough to promote the conversion. In fact, people who live in latitudes north of San Francisco may receive inadequate UVB radiation for several months of the year.24 Because both the kidneys and liver are important in activating vitamin D, impairment in either of these organs makes less of the vitamin available.

Miscellaneous causes. There are a host of other causes of osteoporosis. Any condition or treatment that impairs calcium metabolism anywhere along the complex pathways that control it will make osteoporosis likely. These conditions include kidney disease, organ transplants, smoking, and anticoagulants.25-28 Poor nutrition or the need for parenteral nutrition (intravenous “feeding”) are two possible causes of osteoporosis.29-31 While the nature of the relationship is unclear, osteoporosis is also related to depression.32 Interestingly, many of the things known to help prevent depression—such as good diet, regular exercise, and ample exposure to natural light—also help prevent osteoporosis.


There are two tests used to measure bone mineral density. The dual energy X-ray absorptiometry (DEXA) test is most commonly used because there are more DEXA testing devices in doctors’ offices than the more advanced quantitative computed tomography (QCT).

In a report by Smith et al, osteoporosis was present in 63% of men at the time of diagnosis of prostate cancer, prior to any therapy.87 In this landmark paper, the investigators evaluated DEXA bone mineral density testing and compared it to QCT bone mineral density testing in the same patients. A significantly greater percentage of men were found to have osteoporosis using the QCT methodology versus the DEXA approach. DEXA bone mineral density evaluation detected osteoporosis in only 5% of men, whereas with QCT technology, 63% of men were diagnosed with osteoporosis. Using QCT technology, total bone density abnormalities (osteopenia and osteoporosis) were found in 95% of men, compared to 34% of men evaluated with DEXA. This study corroborates the epidemic of bone loss faced by aging males.

Studies by prostate oncologists Drs. Stephen Strum and Mark Scholz have confirmed the results of Smith et al. Drs. Strum and Sholz found either osteoporosis (50%) or osteopenia (50%) in 100% of the men they studied with QCT. In the same men, using DEXA, they found only 5% with osteoporosis and 50% with osteopenia.88 A reasonable question to ask is, “Why are there such differences in detection using the two techniques?” One answer is that the DEXA scan may pick up degenerative changes involving the bone and joint tissues, as well as calcium deposits within blood vessels, and read these as bone density, whereas the QCT reads only calcium deposits in bone itself.89-93

Although QCT testing exposes patients to more radiation than DEXA, the amount of radiation associated with QCT for determining bone density is roughly equivalent to that of a dental series, and is roughly 50% less than that of a mammogram (depending on the technique used). Most important, QCT generates far less radiation exposure—orders of magnitude less—than a contrast-enhanced abdominal CT scan.

If you are going to have your bone density checked, the QCT test provides a more effective analysis than DEXA. First, it does not place the patient in harm's way due to the likelihood of underestimating bone density because of falsely high readings related to the reasons previously mentioned. Second, because QCT assesses the patient's status more accurately, this directs medical strategy to resolve the multiple medical problems encountered by the aging patient. Such problems may include bone aches and pain, vertebral compression fractures, and fractures of the hip, wrist, and other bones, as well as the problems commonly encountered by cancer patients at the time of diagnosis and during treatment.

Call Mindways 1-877-646-3929 (www.qct.com) or Image Analysis at 1-800-548-4849 (www.image-analysis.com) for QCT sites nearest you.

Tests, Treatments, and Supplements

Continued . . .

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