Osteoporosis part oneOsteoporosis: Thinking Outside the Box
We are often asked to comment upon “alternative treatments” for osteoporosis. The first question one must consider is this: “alternative” to what, exactly?
Osteoporosis literally means “porous bone.” Conventional pharmaceutical treatments are typically prescribed following a diagnosis of varying degrees of osteopenia (bone loss) found by either an incidental finding of bone loss via x-ray examination or a more definitive DEXA scan (dual X-ray absorbency test) whereby the patient’s bone density is compared to that of “normal young women.” Approximately 30% of bone mineral must be lost before bone density loss can be seen on a standard x-ray, making the DEXA the currently preferred test for osteoporosis screening.
Bone Density Scanning: How Important are the Numbers?
One of the current controversies about osteoporosis treatment revolves around the actual significance of bone density. A prominent belief at this time in our medical history is that bone fractures are more likely to occur if bone density is “low” as found via the DEXA scan. In fact, it has been noted that those with lower bone density are more likely to suffer a fracture, although they will not necessary do so. Bone density appears to be a better predictor of osteoporotic spinal fracture than hip fracture: those with lower bone density are more likely to suffer fractures. The highest risk of hip fracture occurs in the lowest 10 percent of femoral hip density while the highest risk of spinal fracture is noted in the lowest 30 percent of spine density. However, while those experiencing osteoporotic fractures typically have bone densities within or below these numbers, many women within these thresholds never experience an osteoporotic fracture. In her book, Better Bones Better Body, Susan E. Brown Ph.D. points out that half of the people found to have low bone density will never suffer an osteoporotic fracture. (1)
Bone density decreases are a normal event of aging. After about age 40, there is a normal loss of bone density of about 2 percent annually. Women tend to be at higher risk than men of developing osteoporosis in later years because of a lower bone density prior to age 40. Dr. Lawrence Melton of the Mayo Clinic “suggests that 45 percent of normal Caucasian postmenopausal women have a bone density more than two standard deviations below that of normal young women at one or more sites in the hip, spine, or forearm.”(2) The definition of osteoporosis in the United States was until recently defined as bone density less than 2 standard deviations below the normal youth level. Interestingly, the World Health Organization recently redefined osteoporosis as being more than 2.5 standard deviations below the youth level, which dropped the number of Americans diagnosed with osteoporosis from 25 million to about 10 million. (3) The World Health Organization definition also includes the description of “low bone mass and micro-architectural deterioration of bone tissue, with a subsequent increase in bone fragility and susceptibility to fractures.” (4) The term “bone fragility” embodies both quality and quantity components of bone and may more accurately represent the risks of developing osteoporotic fractures than bone density alone.
Having noted these statistics, it is important to point out the fractures are an enormous concern for our elderly population and in many cases can herald a long convalescence from which the patient may never recover. Preventing this type of fracture is an enormous concern and challenge, for both conventional Western MDs and complimentary health care providers.
How do we Prevent Osteoporosis?
Prevention of osteoporosis is the preferred course of action. The influences on bone density in the younger years are most important to understand. Bone is a living, dynamic organ that is constantly undergoing breakdown (resorption) and repair by cells known as osteoclasts and osteoblasts. This dynamic process is referred to as remodeling. At birth, bone is comparatively soft and cartilaginous-like. Healthy bone is made up of about 30 percent organic components and 70 percent mineral components. The organic part is a mixture of collagen and proteins that are produced by osteoblasts. The mineral component is about 95 percent hydroxyapatite (calcium) and small amounts of magnesium, sodium, potassium, fluoride, chloride and other trace minerals. The minerals are incorporated into the organic material that mineralizes and hardens the bone. Young bones are relatively flexible and consequently susceptible to mechanical stressors such as running. However, it is also mechanical stressors that actually stimulate the bone to undergo the process of remodeling, which is a normal and healthy process ensuring healthy bone. Bone mass increases from birth and reaches its greatest density known as peak bone mass between ages of about 16 into the mid-30’s. Once peak bone mass is reached, the annual bone turnover rate is about 25 percent for the innermost portions (trabecular bone) and 3 percent for the outer portion (cortical bone). (5)
Proper nutrition and dietary habits are absolutely critical to healthy bone formation. Eating a nutritious diet may not be enough. Foods ingested must have rich absorbable sources of minerals and proteins. The overall “best” diet found to be associated with lower rates of osteoporosis is a mainly vegetarian diet. Dark green leafy vegetables (kale, collards, spinach, chard, red lettuce, etc.) offer a broad range of minerals and vitamins important for healthy bones including calcium, boron, and vitamin K1. Vitamin K1 converts the bone protein osteocalcin to its active form so it can anchor calcium molecules to its matrix forming mineralized bone. Diets that are too high in proteins stimulate excretion of calcium by the kidneys. Foods such as soft drinks, which are very high in phosphorous and lack calcium, actually lead to lower blood calcium levels, which ends up stimulating parathyroid hormone action of bone breakdown.
Recall that about 30 percent of bone is made up of various proteins, while the remainder is composed of minerals. Mineral absorption and assimilation is dependent on several factors: minerals must be broken down into an absorbable form by stomach acid in order to be absorbed in the intestine. If one is taking an “acid blocker” such as Protonix®, Nexium®, Tums®, or another “proton pump inhibitor,” acid production in the stomach is greatly reduced, thereby reducing the body’s ability to break down minerals. Vitamin D, which is normally formed in the skin by the action of sunlight, stimulates the actual absorption of calcium by the intestines. If one is living indoors or in areas beleaguered by inclement weather (either too hot or too cold) and is not outside in the sun, vitamin D production is greatly reduced. Sunscreen, while protecting against the very real dangers of skin cancer, effectively blocks production of vitamin D.
There is a constant interplay between bone remodeling and the endocrine system. Calcium levels in the blood are strictly maintained by interaction between the hormones estrogen, calcitonin and parathyroid hormones. Estrogen is the major hormone regulator of bone remodeling and it inhibits bone resorption by helping to regulate osteoclast and osteoblast activity. Reduced levels of estrogens lead to increased activity of the osteoclasts and in increased levels of proinflammatory cytokines. (Read more on this in part 2) It is this pivotal role in bone metabolism that is what lead researchers to recommend the supplementation of estrogens and progesterones in postmenopausal women. If blood calcium decreases, parathyroid hormone is secreted which stimulates the osteoclasts to breakdown bone and release calcium, decreases secretion of calcium by the kidneys, and stimulates the conversion of vitamin D to its active form in the kidneys. Vitamin D stimulates the absorption of calcium in the intestines. If calcium levels become elevated, calcitonin is secreted from the thyroid and parathyroid glands, which antagonizes the action of parathyroid hormone and inhibits bone resorption. Overall thyroid function needs to be carefully monitored since both hyperthyroidism and hypothyroidism are major risk factors for osteoporosis. (6) Hyperthyroidism can cause elevated blood levels of calcium and a secondary lowering of parathyroid hormone, leading to eventual bone loss through increased urinary excretion of calcium. Hypothyroidism can also contribute to bone loss. Elevated cortisol, an adrenal steroid hormone and reduced levels of DHEA have been related to osteoporosis. Cortisol is released in response to stress. The effects of chronically elevated cortisol or reduced DHEA can be similar to those of exogenous steroids. (7)
Risk Factors for developing Osteoporosis
There is no one test or risk factor that will definitively determine whether one is going to experience the dreaded result of osteoporosis: fracture. However, we can assess overall risk by adding up some of the combined elements that are present in your history. Here is a list of some of the considerations commonly used to assess risk:
* Gender: females are much more at risk, although men are catching up
* Characteristics: short, slender, fair skinned, blonde, blue-eyed
* Age: post-menopausal
* Early menopause: physiologic, surgical, or iatrogenic (caused by drug treatment): lower exposure to estrogens
* History of amenorrhea, late menstrual onset, or anovulation: lower exposure to estrogens
* Nulliparous (no children borne): no prolonged periods of exposure to high estrogens
* Race: Caucasian or Asian: unknown genetic factor?? Make less vitamin D in their skin due to sunscreen use??
* Family history of osteoporosis
* History of Anorexia Nervosa, diabetes mellitus, Cushing’s disease, hyperthyroidism, or hyperparathyroidism
* Digestive Problems: gall bladder disease, fat malabsorption, cirrhosis, low stomach acid, lactose intolerance, celiac disease
* Kidney disease and kidney stones, rheumatoid arthritis, multiple myeloma, COPD, scoliosis, underweight/nourished
* Dietary factors: high intake of caffeine, sodium, phosphate (soft drinks), or animal protein. Inadequate intake of vitamin D and calcium (especially during pregnancy).
* History: stress fractures, prolonged bed rest or wheelchair bound, fractures after age 45, bone loss in the jaw, dentures before age 60
* Surgeries: total thyroidectomy, removal of part or all of intestine, intestinal bypass surgery for weight control.
* Medications: Furosemide, Heparin, INH, Tetracycline, anticonvulsants, Steroids such as cortisone or prednisone, and aluminum containing antiacids.
* Lifestyle: sedentary, moderate (or more) alcohol intake, cigarette smoking.8
The presence of any of these risk factors means one may wish to take more proactive steps in preventing a potential onset of osteoporosis and increased bone fragility therefore an elevated risk of fractures later in life. To see some of the methods we might recommend to reduce the risks of fractures, see part two of this article.
1 Brown, Susan E., Better Bones Better Body: Beyond Estrogen and Calcium, (2000):209-215.
4 McCormick, Keith R., “Osteoporosis: Integrating Biomarkers and other Diagnostic Correlates into the Management of Bone Fragility,” Alternative Medicine Review (2007): 113-145.
5 O’Connor, Deirdre J., “Understanding Osteoporosis and Clinical Strategies to Assess, Arrest, and Restore Bone Loss,” Alternative Medicine Review (1997): 36-47.
6 Murray, Michael T., “osteoporosis Prevention and Treatment—Beyond Calcium,” Natural Medicine Journal (1999): 5-13
7 McCormick, Keith R., “Osteoporosis: Integrating Biomarkers and other Diagnostic Correlates into the Management of Bone Fragility,” Alternative Medicine Review (2007): 113-145.
8 Hudson, Tory S., “Osteoporosis: An Overview for Clinical Practice,” Journal of Naturopathic Medicine (Vol 7, Number 1): 27-34.