Osteoporosis has been part of the human condition since there was a human condition. It doesn’t fit into the characteristics of a disease or an illness. It’s not an infection, nor yet a cellular mutation like cancer. It’s not caused by trauma of any kind. It’s a condition that goes along with aging. The essentials of the process that leads to osteoporosis affect everybody who lives long enough, but (thankfully!) it doesn’t result in harm to everyone. This process was taking place in the bones of Pithecanthropus erectus and it continues to take place in our bones today. Java man (as P. erectus is known) didn’t live long enough to experience the ill effects of osteoporosis, but as we live longer and longer (again, thankfully!) this entirely normal condition affects more and more of us.

Osteoporosis contradicts the way many people consider their bones. We view our skeletons as relatively solid structures that do the job of supporting our organs and muscles in their proper place, like the reinforced concrete and steel structures that support the structure of skyscrapers. But many of us are surprised to learn that, in fact, as long as we are alive, our bones are also alive. Tiny blood vessels run through our bones, carrying nutrients and oxygen. The bones themselves are mostly composed of a mesh of protein fibers called collagen. This mesh is suffused with molecules composed of calcium and phosphate ions, which, mixed with water, make a paste which hardens – in fact, very much like concrete. That substance makes up the solid part of our bones, providing structure and strength.

But our bones are constantly changing. It’s as if the builders who put together your house stay on the job perpetually, examining every brick and beam for signs of weakness or decay, and when a brick or beam looks vulnerable, they zero in on it, take it out of the structure of your house, and replace it with a new, sturdier brick or beam.

In our bones, there are two groups at work. One bunch consists of cells named osteoclasts, whose job it is to remove the more decayed particles of that calcium/phosphate paste, which they release into the bloodstream. The osteoblasts are another group. They release collagen into the spaces vacated by the decayed particles, and the calcium and phosphate ions in the collagen particles harden into new, healthy, solid bone. The process is called “bone remodeling.”

This is the way our bones stay strong and healthy. That is, as long as the osteoblasts can keep up with the osteoclasts.

When they don’t – and there are multiple reasons why the osteoblasts fall behind – what happens is that our bones lose density and we are prone to developing osteoporosis, which means “porous bones.”

These porous bones put us at a very high risk of experiencing fractures. About one in two women and one in four men in their lifetimes will experience a fracture due to osteoporosis. In women in particular, the incidence of an osteoporosis-caused fracture is greater than the risk of a heart attack, a stroke, and breast cancer combined.

The great majority – four out of five – of people who have a bone fracture due to osteoporosis do not find out that they have osteoporosis until after they experience the fracture.

It’s evident that the process of bone remodeling has been a part of our physiology since we first evolved from our predecessors, and it’s likely that the same process is present in many or most other species. The structure of our bones is similar to that of most other mammals. Bones consist of two types of tissue. The exterior of the bone is a highly compact form of tissue, composed of units called osteons. These are like tiny ribbons wound very tightly into tubular forms. Through the center of each osteon runs a capillary, which supplies oxygen and nutrients to the osteons.

The interior of the bone is made of a different type of tissue, composed of beams and plates that form a lattice, which is spongier in consistency than the exterior bone. If you are a meat-eater, you might recognize that type of tissue as bone marrow. The scientific name for it is trabecular bone.

All bones are composed of both compact and trabecular tissue, in different proportions. Overall, there is more compact than trabecular tissue, with a ratio favoring the compact bone tissue of about four to one in most bones. Long bones, in our arms, legs and ribs, are mostly compact bone. But some bones, such as the pelvis, the vertebrae, and the chunky ends of arm and leg bones, consist mostly of trabecular tissue.

It is the trabecular tissue that is particularly susceptible to the slowdown in bone remodeling that constitutes the disease process in osteoporosis, which is why osteoporosis is a major risk factor for fractures of the pelvis and the vertebrae.

A bit of history

In the first part of the 19th century, John Hunter, a British surgeon, found that old bone tissue is constantly being eliminated and being replaced by new bone tissue – the process that came to be known as bone remodeling. And around the same time Jean Lobstein, a French pathologist, found that the bones of some people have bigger holes in them, making them porous. He named the disease that causes this condition osteoporosis.

According to my OED, the earliest use of the word “osteoporosis” in the English language was in 1846: “A specimen of osteoporosis growing in the cranium of an aged person.” (G. E. Day, in Simon’s Anim. Chem. II) A use of the word more in line with the condition as we recognize it today dates from 1896: “If the compact osseous tissue becomes porous from the widening of the Haversian canals, the condition is termed osteoporosis.”

But it wasn’t until the 1940s that an American endocrinologist, Fuller Albright, found the association between osteoporosis and menopause. He instituted the treatment of menopausal women with estrogen in order to prevent bone loss.

And it wasn’t until 1984 that the NIH declared osteoporosis to be a significant threat to health and raised the possibility that good nutrition and exercise, coupled with estrogen therapy in women, might slow the pace of bone loss.

Several drugs, including the class of bisphosphonates and also selective estrogen receptor modulators were introduced, starting in the 1970s, raising the hopes that osteoporosis-related fractures might no longer be a major threat, especially to women. Those hopes, as we will see, have been tempered by other factors.

What causes osteoporosis?

Our osteoblasts and osteoclasts are at it from our earliest years. For the first 20 years of our lives, the osteoblasts are building bone strength much faster than the osteoclasts are removing bone. By age 20, most women have built about 98% of their bone mass. By age 30, almost all men and women have reached their maximum bone mass. During the next ten years or so, until about age 40, new bone creation by osteoblasts and bone removal by osteoclasts stays about even. Starting in the 40s, bone removal gradually outpaces bone creation in both men and women. In women, bone loss is accelerated during menopause, and by around age 70, many women pass over the warning line where the degree of bone loss significantly increases the risk of fracture – i.e., osteoporosis.

Why does this happen? In a certain sense, the process is natural. We need to build strong bones in our youth. Once we’ve reached maturity, bone-building slows down, and as time goes on the main activity of the bone-remodeling process is osteoclasts carrying off those decayed bone particles. The osteoblasts do less and less as we age.

A number of factors play into this process. One is that we have reduced levels of calcium in the bloodstream. As we age, our intestines absorb less calcium from food, and our kidneys are less efficient in conserving calcium. Less calcium reaches the bloodstream, and more calcium is excreted in feces and urine, so that the body (which requires calcium for a number of other metabolic functions) needs to get some of that calcium from our bones. Also, as we age, we tend to consume less calcium in our diets for a range of reasons. People shun milk, butter, and cheese because they are fattening or because of lactose intolerance.

Another is a reduction in the production of vitamin D, which, as we know, our bodies can generate, depending on exposure to sunlight. Vitamin D is what tells our intestines to absorb calcium in what we eat, so if we don’t get enough vitamin D, eating calcium-rich foods doesn’t do us much good.

A number of medical conditions can accelerate normal bone loss beyond what normally happens with aging. The Harvard Medical School’s treatise on osteoporosis lists 60 medical conditions, some rare and some common, such as diabetes, epilepsy, heart failure, lupus, and multiple sclerosis.

Some medications are also known to cause bone loss. The most common of these are corticosteroids, such as prednisone. These drugs are used to treat conditions such as asthma, rheumatoid arthritis, and chronic obstructive pulmonary disease (COPD).

Many women with breast cancer take a class of drugs called aromatose inhibitors, including anastrozole (Arimidex), exemestane (Aromasin) and letrozole (Femara). What the drugs do is block the production of estrogen, which tends to stimulate the growth of their cancers. However, estrogen plays an important part in slowing bone loss, so blocking estrogen production can speed bone loss.

Men who are being treated for prostate cancer sometimes take drugs that suppress the production of androgen, the male sex hormone. Androgen tends to accelerate the development of prostate cancers, but androgen also causes the growth of new bone mass, so the suppression of androgen can cause bone loss. In one study, about 20% of men who had androgen suppression therapy experienced bone fractures, compared with about 13% of the men who did not have androgen suppression therapy.

Other classes of drugs that can lead to bone loss include diabetes drugs such as canaglifozin (Invokana), piolitazone (Actos), and rosiglitazone (Avandia). Proton pump inhibitors used to reduce stomach acids such as omeprazole (Prilosec) can reduce the absorption of calcium.

It may be a good idea to check with a physician on the effects of any drug on the absorption of calcium and possible consequences leading to bone loss.

How common is osteoporosis?

In the US, according to a report by the Surgeon General, about 10 million people have osteoporosis, and about 34 million more are at risk of osteoporosis, due to low bone mineral density, called osteopenia, which is a condition preceding osteoporosis. Those figures are carefully calculated estimates. In fact, only a small percentage of people have the tests that determine low bone mineral density, perhaps as low as 10%.

Bone fractures due to osteoporosis are very common. In the US, between 1.5 million and 2.0 million persons per year experience fractures due to bone fragility resulting from osteoporosis. A study in the UK (where the prevalence of osteoporosis is similar to that in the US) estimated that that one in two women and one in five men over the age of 50 years will have a bone fracture due to osteoporosis in their lifetime.

In the US, hip fractures frequently lead to mortality. In men over 50 years of age hospitalized after hip fracture, the mortality rate is approximately 8%. In women with the same characteristics, the mortality rate is significantly lower, only 3%. No specific reasons for this difference are given, but the speculation is that in men the hip fractures leading to hospitalization are more severe than those in women.

A recent report issued by the US National Osteoporosis Foundation estimated that 2 million Americans had 2.3 million osteoporotic fractures in 2015. In the first 2–3 years post fracture, a second fracture occurred in 307,000 of these individuals incurring a cost of in excess of $6.3 billion.

The overall economic burden of osteoporosis-related fracture is significant, costing approximately $17.9 billion and £4 billion per year in the USA and UK, respectively.

In spite of the fracture risks described above, many people underestimate the risk associated with osteoporosis. Osteoporosis is thought by many, especially women, to be an almost inevitable consequence of aging. If asked what they fear more, osteoporosis or breast cancer, most women would surely respond that breast cancer is much more scary than osteoporosis. And yet, if we consider the statistics, it’s by no means so open and shut. For one thing, the incidence of osteoporosis is higher than that of breast cancer – about 15.4% across all age brackets for osteoporosis in women, versus 12.4% for breast cancer. And, since 1990, breast cancer mortality has declined significantly, by 39%. That decline has resulted in 322,000 deaths averted. Currently, the 5-year mortality rate for women diagnosed with breast cancer is about 10%.

In contrast, about half of women with osteoporosis will experience some kind of fracture, and these fractures can have dire consequences. Studies of mortality in women following hip fractures report significantly higher mortality rates than in women with breast cancer. A study in elderly patients with hip fractures reported a one-year mortality rate of 21.2%, which is, as you will note, doubles the five-year mortality with breast cancer. Another study found a five-year mortality of 32.3% in individuals following hip fracture.

About a third of all patients who experience hip fractures are discharged to a nursing home, and most of these do not recover the level of activity they enjoyed before their fracture. Moreover, individuals who have osteoporotic fractures, whether of the hip or the vertebrae, are at three times the risk of another fracture due to the frailty of their bones.

All in all, it would not be an exaggeration to say that osteoporotic fractures present far more of a risk to life and to quality of life than breast cancer.

Managing bone loss and osteoporosis

Topping the list is the common injunction: “know your risk factors.” Yes, age and gender are first in line as risk factors. As we’ve noted, bone loss starts at about age 40 and in women accelerates at menopause.

A risk factor that is often ignored is race. Caucasian and Asian people are at significantly higher risk than Africans, because Africans tend to have larger and thicker bones. Asians in particular have thinner bones, perhaps because their diets are lower in calcium, and lactose intolerance is more common in Asians. Because of the connection between vitamin D and calcium metabolism, the less sunshine a person is exposed to (meaning less vitamin D synthesis) the higher the risk of bone loss.

Simply being a member of the female gender increases the chances of developing osteoporosis by a factor of about 3.5. The overall prevalence of osteoporosis in men is about 4.3%, compared with the 15.4% prevalence in women. The prevalence in each gender increases with age, reaching 34.9% in women over the age of 80 and 10.9% in men in the same age range.

But gender is only one of many factors. Here’s a list of just some of those factors:

• Cigarette smoking significantly increases the risk of osteoporosis
• Lack of exercise – weight-bearing exercise adds mass to the bones
• Any condition that prevents or hinders normal walking
• General nutritional deficiencies, especially a lack of sufficient calcium in the diet
• Vitamin D deficiency either because it is lacking in the diet or insufficient exposure to sunlight
• Being underweight and with small body frame
• Excessive alcohol consumption
• Having sustained fractures as an adult
• Family history of osteoporosis
• Chronic inflammation, such as in inflammatory bowel disease, rheumatoid arthritis, some diseases of the liver
• Conditions resulting in malabsorption of nutrients, such as celiac disease
• In women, chronically low estrogen levels, which may occur in menopause, but also with early removal of both ovaries, or with some forms of chemotherapy that can have toxic effects on the ovaries
• In women, interruption of menstrual cycle, which may be due to excessive exercise training or diets leading to very low body fat, as in anorexia
• In men, low testosterone levels (hypogonadism)
• Thyroid and parathyroid malfunctions

Some of the things you can do to avoid bone loss and prevent the onset of osteoporosis sound a lot like general health advice relating to life-style habits. You’ve heard them before, probably many times. But they may be a bit different when it comes to osteoporosis. For example, a person diagnosed with osteoporosis is advised to take a brisk walk for about 30 minutes every day. The bones respond to weight-bearing exercise – each step when you put your foot down and your full body weight is supported sends a message to your bones that they have to stay strong to support this activity.

Addressing potential calcium and/or vitamin D deficiencies, supplements only go so far. On the whole, it works better to get those required nutriments in the diet.

And there are medications that work quite well in protecting persons who have developed osteoporosis from the bone-fracture consequences. But before we get to those, we need to discuss the crucial matter of detecting osteoporosis.

Is there a way of anticipating the onset of osteoporosis?

The most common is dual-energy X-ray absorptiometry (DEXA), which was developed in the 1990s by Dr Richard Cameron and Dr Richard Mazzes. The concept of dual-energy X-ray made it possible to discriminate more accurately between soft tissues and bone, so as to enhance the precise measurement of the bone boundaries. This was a major advancement in the accuracy of bone health diagnosis.

The DEXA scan usually measures bone density at three spots in the body – the spine in the lower back (lumbar spine), the total hip, and the top of the thighbone (the femur). DEXA scans do this with about one-tenth of the radiation of a standard X-ray.

The DEXA scan results are summarized as T-scores. If a T-score is no lower than a minus 1, the results are considered normal. A T-score between a minus 1 and a minus 2.5 indicates low bone density, called osteopenia, but not osteoporosis. A T-score of minus 2.5 or lower points to osteoporosis.

Questions about who should have DEXA scans and how often are complicated and can be contentious. To my knowledge, the USPSTF (Preventive Services Task Force) has not weighed in on this subject. At this point, Medicare will pay for one DEXA scan every two years, or more often if the physician deems it medically necessary. For persons under the Medicare age, the decision depends largely on risk factors.

In spite of the value of the information provided by a DEXA scan, a comparatively small number of persons have availed themselves of this method of assessing their chances of developing osteoporosis and the accompanying fracture risk. It is estimated that fewer than 10% of persons presenting with an osteoporosis-linked fracture had any idea, based on a bone scan, that they were at risk.

What can we do to prevent osteoporosis?

A petite white woman, well past menopause, whose mother, also a petite white woman, had osteoporosis, fell and broke her hip, and died in a nursing home a year later, is evidently at a higher risk of osteoporosis than many of her fellow human beings. That doesn’t mean that she’s destined to the same fate. But what can she do?

If we look at that unsettling list of factors contributing to osteoporosis, there are some that are clearly modifiable. Our petite white woman can, for one thing, quit smoking. She can keep moving – go for walks, ride her bike, dig weeds out of her garden, take out the garbage while her lazy bum of a husband watches TV…. She can stop being super-careful about eating cheese and butter and all those calcium-rich dairy products that might make her gain weight and lose her sylph-like silhouette. Some things are more important than having a figure like Twiggy.

When she goes to her regular MD for her annual physical (assuming she has a regular MD and gets an annual physical) she should ask this MD about her risk of developing osteoporosis. But the assumption that she has a regular MD and an annual physical is risky. Only about 21% of the US population has an annual preventive physical examination. The percentage of women who get an annual gynecological exam drops to 18%. Gynecologists are frequently the physicians who advise their patients regarding the risk of osteoporosis, since the onset of osteoporosis is frequently linked with menopause and the decline in estrogen levels. But many women, as they advance in age, discontinue regular visits with their gynecologists. After all, the USPSTF has proclaimed that PAP smears are no longer needed after age 65, so why go to the gynecologist?

All this means that many fewer women get any sort of advice on how to prevent osteoporosis. The general advice, to repeat what has already been said above, is to remain physically active, stop smoking, and make sure that the diet includes foods that contain calcium and vitamin D. If the trend in bone scans points to a significant decline in bone mass, there are nutritional supplements that could make up the deficiencies. And, indeed, in the past quarter of a century or so, effective medications have emerged.

The next installment of the Doc Gumshoe serial will discuss the supplements and medications in considerable detail. This installment has gone on long enough. I thank you for sticking with it to the end.

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Also, many thanks for your comments, which keep me with my nose to the grindstone and my shoulder to the wheel. Be well! Michael Jorrin (aka Doc Gumshoe)

[ed note: Michael Jorrin, who I dubbed “Doc Gumshoe” many years ago, is a longtime medical writer (not a doctor) and shares his commentary with Gumshoe readers once or twice a month. He does not generally write about the investment prospects of topics he covers, but has agreed to our trading restrictions.  Past Doc Gumshoe columns are available here.]