Common Myths about Osteoporosis

*As the first volume of the Osteoporosis book series (Preventing and Treating Osteoporosis: The Complete Guide Volume I: Lifestyle and Nutrition) is nearing release, I thought it might be appropriate to provide a free sample chapter: Chapter 1 – “Common Myths about Osteoporosis”.

**Hopefully, readers see that this condition is far from exclusive to old women, and more over, that prevention in both males and females should begin in youth. In the series, it will become evident that prevention and care of osteoporosis must be done holistically and below the surface, this book is also a prevention tool against diabetes, heart disease, Alzheimer’s, and many other degenerative conditions that stand in the way of a long, healthy life.

***To be alerted when the first volume is released, please feel free to sign-up for the newsletter on the left side bar!

Introduction: Common Myths about Osteoporosis

Or in other words … why this book is likely to imbue a great deal of necessary knowledge about bone disease, including the causes and mechanisms behind the loss of skeletal homeostasis and how to properly treat, or even reverse, poor bone quality and bone loss.


  • Osteoporosis is not a serious disease.


Osteoporosis is no longer a disease limited to affluent nations. Mainly a product of industrialized living, osteoporosis is increasing in prevalence in developing countries. Jordan, for example, has seen a rapid increase in osteoporosis prevalence in recent years. Considering the effects of globalization and the growing expansion in lifespan, osteoporotic fractures are expected to rise exponentially, yet some healthcare students (e.g., nursing students) around the world remain mostly unbothered concerning its significance while under the assumption that they are impervious to the disease simply based on adequate calcium and some physical activity. The debt of knowledge concerning the serious risks of osteoporosis is therefore expected to be even greater in the general public.

The sobering truth is that osteoporosis is an insidious pandemic that is growing still. Why it is especially threatening is that it progresses innocuously, hence it being dubbed a “silent killer”. Worldwide, it is predicted that 200 million people suffer from the disease. Moreover, approximately 40% of women and 13% of men are expected to suffer an osteoporotic-related fracture (e.g., hip, spine, distal forearm) after the age of 50. Other sources have found higher risks in this age group, with 1 in 2 women and 1 in 5 men expected to fracture. Worse, extreme skeletal fragility and multiple vertebral fractures (a hallmark feature of osteoporosis) can occur over a period of time unbeknownst to the sufferer. This is usually explained by a “natural” loss of height when in fact it is pathologic. Fractures are nearly impossible to prevent as fragility increases. Normal activity such as sneezing, coughing, bending forward, or twisting in some way can trigger a fracture. Fracturing in such innocent circumstances is not always met with initial pain; hence, many fractures go unnoticed and early diagnosis is hampered.

Only when looked at through rose-colored glasses by the young and healthy can osteoporosis be considered merely a disease of weakness and frailty. Early progression of bone deterioration may be silent and painless, and one of its most recognizable symptoms—height loss—may be a minor concern for many; but make no mistake: osteoporosis is a life-threatening disease that can cause pain, severe loss of quality of life, and death.

Fractures, whether or not they cause pain initially, can eventually lead to chronic pain that can cause depression. Moreover, fractures (especially vertebral and hip fractures) are associated with significant disability. Multiple spinal fractures, for example, can cause numerous health problems such as stomach complaints (due to resultant digestive issues from stomach compression), breathing problems (from severe spine compression), and hip pain (due to closer contact of the rib cage with the hip bones). Due to disability, patients suffer a reduction in quality of life as normal daily activities become increasingly restrictive. Close to half of those who suffer a hip fracture are unable to walk independently, and in worse cases, some (about one-third) are forced to forfeit independent living altogether and soon may become confined to a nursing home, where health and happiness deteriorate ever more rapidly. Multiple studies have found that the number of fractures (all fractures) inversely correlates with QOL (quality of life) scores. As skeletal strength decreases, exercise becomes limited, which further accelerates the rate of bone decline. Quality of life can also be reduced in those without fractures in later-stage osteoporosis, as fragility calls for increased precaution.

Finally, premature mortality, independent of other comorbidities, is a real possibility. More than other fractures, hip fractures have a substantial impact on mortality for several reasons (e.g., infection/pneumonia, deep vein thrombosis, pulmonary embolism, cardiovascular complications). In some cases, hip fractures can directly induce death. Lesser known is the fact that vertebral fractures are also strongly associated with increased mortality due to complications following deformity post-fracture (e.g., loss of pulmonary function, respiratory complications, possible future hip fracture with associated mortality). Because vertebral fractures are more common than hip fractures, prioritizing their prevention should be an equal concern.

There is a pressing need for dissemination of osteoporosis awareness for both men and women of all ages. Education and preventative care of other dangerous diseases, such as breast cancer, are eagerly sought after by the public and made relevant by government bodies, when in fact the risk for hip fracture (1 in 6) is higher than that of breast cancer (1 in 9) for the main demographic (Caucasian women). In adults over 45 years of age, osteoporosis accounts for more sick days spent in the hospital than not only breast cancer, but also diabetes and myocardial infarction (i.e., heart attack). On the understanding of its potential deadly consequences, osteoporosis should therefore be treated with at least equal prominence.


  • Osteoporosis is a woman’s disease.


Men comprise a significant portion of osteoporotic patients. In fact, men sustain 20-30% of all osteoporotic fractures, and worse, this percentage is expected to increase in the upcoming decades. Hip fractures are the worst kind of fracture to sustain considering the possible consequences, yet the proportion of men suffering from osteoporotic hip fractures worldwide in 2025 are predicted to be equal to that experienced by women in 1990. By 2050, the incidence of hip fracture in men is projected to increase by 310%. That will be equivalent to over 6 million hip fractures worldwide. Similar to women, men experience slow and constant bone loss following achievement of peak BMD and, also like women, undergo an accelerated rate of bone loss in advanced age, albeit at a later age than that which corresponds to menopause in women. The average lifetime bone loss in both cortical and trabecular bone will be roughly 20-25%. In comparison to women, the absolute risk of hip fracture is higher in men, and worse, mortality from hip fractures tends to be greater in men. Therefore, men should not be excluded from osteoporosis education and preventative measures.



  • Osteoporosis runs in my family so I am doomed / Osteoporosis does not run in my family so I am safe.


Although osteoporosis and fracture risk tends to run in families, that does not guarantee developing the condition, nor does the absence of osteoporosis in the family guarantee that one will be protected. Heritability studies have found 50-85% of BMD variance to be attributed to heritable factors, and similarly, measures of bone quality such as bone geometry and microarchitecture are found to be anywhere from 33-81% heritable. But that is not the same as saying 50-85% of BMD and 33-81% of bone structure  is purely under genetic control. Even if osteoporosis was solely a genetic condition, it is a complex polymorphic phenotype influenced by multiple genes, making heritability not so simple. For example, in a family with a low incidence of osteoporosis, a mother might have a majority (~70%) of genes that confer a lower risk of osteoporosis. Let us imagine the same is true of the father. A child inherits exactly 50% of genes from each parent. It is very possible that this child could inherit a high portion of gene variants that exhibit negative effects on bone (30% from each parent) and as a result, end up with a much higher risk of osteoporosis and fracture than either parent. The same outcomes are seen with other traits such as children with light eyes being born from parents with dark eyes, children who are significantly more or less intelligent than either parent, those who become taller or shorter than both parents by adulthood, etc. Such is expected with Mendelian inheritance patterns. In other words, a lack of osteoporosis in the family does not automatically translate to a low risk of degenerative bone disease in the offspring and vice versa.

Then there are the environmental factors. Despite the fact that family and twin studies imply high heritability, identified genes and their variants all together only explained about 6% of the total variance in BMD. Much of the “missing heritability” can be explained by the “epigenetic” interactions. It is critical not to look at environmental influence as separate from genetic influence (e.g., Osteoporosis is 50% influenced by genetics, 50% influenced by the environment. Genes and environmental factors (e.g., diet, activity level, anxiety/stress, exposure to toxins, etc.) do not each operate in a vacuum, but through gene-environmental interactions, hence the term “epigenetic”. The interplay between genetic and environmental influences is based on the consistently observable evidence that external influences alter genetic expression without changing the nature of the genes themselves (e.g., genetic sequence). In actuality, environmental modification (e.g., dietary changes, stress reduction, nutritional supplements, exercise, etc.) is a natural form of gene therapy. Epigenetic modification influences all stages of life, including the crucial period of development during gestation. If osteoporosis is evident in the family, it becomes more of a priority to alter genetic behavior through modifiable means. Likewise, a predicted low risk of bone deterioration is not an excuse to forego preventative action, because epigenetics works both ways. Exposure to detrimental factors can in turn adversely modify and/or overpower the protective effects of “good” genes. Very few diseases are completely determined by gene interaction and fortunately, osteoporosis is not one of them.


  • I will worry about osteoporosis when I’m older.


For a while, it was generally believed that bone loss starts in menopausal years in women and in elderly years for men. On the contrary, it was recently shown that trabecular bone loss begins in young adults of both sexes, which accounts for one-third of total trabecular bone loss over the course of a lifetime. Before age 50, about 40% of trabecular bone loss occurs, compared to <15% for cortical bone, which is still significant over the years. It may be true that bone loss is accelerated around menopause and age-associated hormone changes in men, but clinically relevant bone loss, even osteoporosis with fractures, can occur at any stage of life, including in young adulthood and childhood (i.e., juvenile osteoporosis) in certain circumstances, such as prolonged malnutrition and wasting (e.g., anorexia), disease, some medications, and prolonged bed rest. It is also worthwhile to consider only about 70% of fractures occur among women 65 and older. Although 70% is a clear majority, the remaining 30% represents a relevantly high threat among the rest of the population when over 200 million people worldwide are estimated to be affected.

Nutritional factors and behaviors inimical to bone development that do not cause osteopenia or osteoporosis in youth can still affect risk later in life by interfering with peak bone mass if severe enough. For example, osteoporosis and osteopenia are dramatically increased among Holocaust survivors, more so in those who were exposed to the Holocaust before 18 years of age. Similarly, studies find that BMD remains significantly reduced in middle-aged anorexia patients who have been fully recovered for an average of 21 years.

More commonly, the combination of poor lifestyle practices that begin in youth that are maintained chronically, such as a processed and nutritionally poor diet, low physical activity, high caffeine and sugar consumption, stress, and inadequate sleep, can also sabotage bone accrual and confer a higher risk of osteoporosis later in life.

Skeletal health is impacted as early as in utero by the maternal diet . Food and lifestyles conducive to bone health are best ingrained during childhood and adolescence when active bone growth is occurring. It is never too early to implement healthful measures that positively influence bone health and better minimize risk rather than attempting to reverse years of skeletal deterioration after middle age. To put it bluntly: the earlier, the better.


  • The higher the bone density, the stronger the bone.


Believe it or not, there is not a linear relationship between bone density and bone strength, nor does a high bone density guarantee strength and protection from fracture. Conversely, low bone density does not automatically mean bones will be weak and prone to fracture. Being osteopenic versus osteoporotic should not allow one to worry any less about fracture. In actuality, there are more osteopenic people than osteoporotic people, and thus, most fractures occur in osteopenic individuals. A non-negligible portion of fractures also occurs in those with normal and even those with high BMDs (see: Bone Quality).


  • Osteoporosis is essentially a calcium deficiency disease.


This assertion is only partially correct, and it is more incorrect than correct, leading to widespread calcium over-supplementation that is not corrective of underlying bone loss and sometimes exacerbates bone disease and leads to other harmful consequences (e.g., constipation, kidney stones). If osteoporosis were simply a matter of a lack of calcium and vitamin D, it would not be the (growing) problem it is today. At best, calcium, even when supplemented alongside vitamin D, does not improve fracture risk in most cases. Osteoporosis can be more accurately termed a calcium absorption disease, and calcium absorption is not only remedied by vitamin D supplementation. Contrary to popular belief, vitamin D is required for calcium intestinal absorption, but calcium absorption into the bone involves more minerals, hormones, vitamins, protein, other nutritional compounds, and especially, exercise. Furthermore, adverse metabolic states (i.e., acidosis), organ dysfunction, and certain medications can interfere with calcium uptake independent of vitamin D uptake. Most importantly, bone consists of other minerals and components that influence its density and resilience independent of their effects on calcium retention.


  • Exercise is good for bone.


Like the relationship with calcium and bone, this statement is partially true, but not all exercises are created equal. In fact, depending on which exercises are done and at what intensity and frequency they are performed, exercise can serve as a source for bone loss in some instances. Exercises need to be targeted for bone health, including those that are high impact and weight bearing (see: Exercise).


  • There are plenty of medications already available for treating osteoporosis.


There are indeed a number of anti-osteoporosis drugs, but they do not effectively “treat” osteoporosis and, in some cases, further damage the quality of bones. Drug treatment is not effective for a few reasons. Antiresorptive agents (i.e., bisphosphonates) are the most popular drugs used for the treatment of osteoporosis, yet these drugs only stop or slow down the rate of bone loss; they do not improve the lack of bone formation, which is a crucial component to most bone disease. Loss of bone mineral density will invariably slow down or, as in many cases, reverse by stopping bone resorption from occurring, but improving bone mineral density is not the be-all and end-all of correcting bone disease, as previously explained, and even then, effects of drug treatment on BMD are modest. Rather, eliminating bone resorption will merely lead to the accumulation of inflexible, old bone that is even more susceptible to fracture. There  are a slew of other harmful side effects from antiresorptive medication including osteonecrosis of the jaw and upper gastrointestinal effects. These drugs are also not suitable for pregnancy and have been associated with shortened gestational age, low birth weight, spontaneous abortions, etc. There are more recent “anabolic” drugs that target bone formation, but treatment with these drugs are confined to only a few years due to later emergence of bone cancer observed during animal testing. Finally, osteoporosis drugs have limited utility in fully addressing the risk factors for fractures, such as poor bone quality, weak muscle strength, joint flexibility, and balance, unlike natural interventions such as exercise.



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