Bone is a living tissue made of a hard outer shell and spongy inner tissue. Bone is constantly reforming and resorbing. This delicate balance allows the body to remodel the bone. Resorption breaks down bone tissue before it is reformed. Osteoclasts are cells that break down the skeleton and osteoblasts are cells that build bones. In present-day humans, the entire skeleton is replaced approximately every seven years. With age, the balance shifts from formation to resorption, which means more bone is broken down than built. Peak bone mass, when bone density is at its maximum, is usually reached between the ages of 18 and 25. After that, bone loss occurs. For women at about age 30 and men a bit later in life, bone resorption will begin to outpace bone formation. When women hit menopause, bone resorption significantly exceeds formation, due to shifts in hormones. The weakening of bones can lead to osteoporosis.
When diagnosed with osteoporosis, bisphosphonate drug treatment is almost always suggested. Most patients do not give it a second thought. But they should. In journal Menopause, The North American Menopause Society suggest that management should first focus on nonpharmacologic measures, such as balanced diet, adequate supplemental nutrients, adequate exercise, avoidance of cigarette smoke, avoidance of excessive alcohol intake, and fall prevention, before pharmacological measures are considered.
As we have seen consistently since bisphosphonates were introduced, while there may be an increase in bone quantity, there certainly is not an increase in quality. Two recent studies bring the pharmacological treatment into question:
- Bisphosphonates may adversely affect bone quality and increase risk of atypical fractures of the femur when used for four or more years, according to research presented at the 2010 Annual Meeting of the American Academy of Orthopaedic Surgeons. Two separate studies revealed data suggesting that long-term suppression of bone remodeling by bisphosphonate treatments may alter the material properties of bone, potentially affecting the bone's mechanical integrity and potentially contributing to the risk of atypical fractures. "Although bisphosphonates have demonstrated an improvement in bone quantity, little if anything is known about the effects of these drugs on bone quality," said a lead researcher. The studies found that bisphosphonate use improved structural integrity early in the course of treatment, but those gains were diminished with long-term treatment.
Both studies noted that the culprit behind the diminishing results may be the fact that bisphosphonates suppress the body's natural process of remodeling bone. "Recent research suggests that suppressed bone remodeling from long-term bisphosphonate use might result in brittle bone that is prone to atypical fractures," said one of the research team. - Clinical Endocrinology, March 2010 - long-term bisphosphonate therapy may increase the risk of unusual long bone mid-shaft fractures. This is probably due to prolonged suppression of bone turnover, which could lead to accumulation of microdamage and development of hypermineralized bone. At present, the scope of this complication in the larger context of patients receiving bisphosphonate therapy remains unknown.
While most of the following is part our protocol for individualized osteoporosis prevention, we summarized the latest recommendations from The North American Menopause Society for Management of Osteoporosis.
Genetics Link
According to the newest data, the greatest influence on peak bone mass is heredity. Studies have shown up to 80% of variability of peak bone mineral density may be attributable to genetic factors. First-degree relatives of women who have had osteoporatic fractures have lower BMD than those with no family history.
Bonnie - as such, public health focus should be on preventative efforts to quell epigenetic expression in those with a family history. Pharmacological treatment is a band-aid approach. It takes environmental, lifestyle, emotional, dietary, and supplemental action to keep osteoporatic genetic expression under lock and key.
Lifestyle Factors
Several lifestyle factors are associated with the risk of low BMD and fracture. These include poor nutrition, insufficient physical activity, cigarette smoking, and heavy alcohol consumption.
Menopause Status
The increased rate of bone resorption immediately after menopause clearly indicates a hormonal influence on bone density in women. The most likely explanation for this increased resorption is the drop in ovarian estrogen production that accompanies menopause. Bone loss begins to accelerate approximately 2 to 3 years before the last menses, and this acceleration ends 3 to 4 years after menopause.
Bonnie - balancing estrogen production naturally is paramount during this stage.
Secondary Causes of Bone Loss
Various medications, disease states, and genetic disorders are associated with bone loss. There is some early evidence that certain disease states may provide a risk of fracture over and above that provided by BMD.
| Medications |
| Aromatase inhibitors |
| Cytotoxic agents |
| Excessive thyroxine doses |
| Gonadotropin-releasing hormone agonists or analogues |
| Heparin |
| Immunosuppressives (eg, cyclosporine) |
| Intramuscular medroxyprogesterone |
| Long-term use of certain anticonvulsants (eg, phenytoin) |
| Oral or intramuscular use of glucocorticoids for >3 mo |
| Genetic disorders |
| Hemochromatosis |
| Hypophosphatasia |
| Osteogenesis imperfecta |
| Thalassemia |
| Disorders of calcium balance |
| Hypercalciuria |
| Vitamin D deficiency |
| Endocrinopathies |
| Cortisol excess |
| Cushing's syndrome |
| Gonadal insufficiency (primary and secondary) |
| Hyperthyroidism |
| Primary hyperparathyroidism |
| Type 1 diabetes mellitus |
| Gastrointestinal diseases |
| Billroth I gastroenterostomy |
| Chronic liver disease (eg, primary biliary cirrhosis) |
| Malabsorption syndromes (eg, celiac disease, Crohn_s disease) |
| Total gastrectomy |
| Other disorders and conditions |
| Ankylosing spondylitis |
| Chronic renal disease |
| Lymphoma and leukemia |
| Multiple myeloma |
| Nutritional disorders (eg, anorexia nervosa) |
| Rheumatoid arthritis |
| Systemic mastocytosis |
Diet
Inflammation is the key. The hunter-gatherer diet, to which our genes are most closely related, were net-acid producing, mostly from consumption of animal protein. However, fruits, nuts, and vegetables were the only other dietary sources, which were all alkaline. The modern Western-style diet has greatly increased the acid/alkaline disparity because of increased grain, cow's milk, and processed food consumption. This does not take into account stress, which creates an acidic environment as well. As the acid load increases, so does inflammation. Inflammation creates bone imbalances. And for those who may be unaware, osteoporosis is an inflammatory disorder.
Please do not take this to mean that to reduce your acid load, you need to take reflux meds. Reflux meds block stomach acid, but do not reduce total cellular acidity. Reflux meds have also been found to increase the risk of bone fractures (the FDA just last week added this warning to PPI labels).
The way to reduce excess cellular acidity is to increase alkaline foods such as fruits, vegetables, nuts, water, and naturally-sparkling water. Do not reduce high quality, organic animal protein, however. Sufficient animal protein intake may help minimize bone loss. Dietary protein overall is positively linked to the maintenance of bone and muscle health. In the June issue of Osteoporosis International, research states that the current recommended intake of protein may be inadequate for optimum skeletal and muscle health.
Supplemental Nutrients
- Calcium is the ruler when it comes to natural bone support and many other nutrients are helpful in that they support calcium in its bone-building ways. There is no data that supports more than 1500 mg. of total calcium intake daily (total from food and supplements). Supplemental sources vary widely in absorption.
- Vitamin D is actually a steroid prohormone rather than a vitamin, as it can be produced in the human body through the interaction of sunlight with the skin. It is essential for the physiologic regulation and stimulation of intestinal absorption of calcium. Public health experts are finally coming to the realization that the majority of the human population living in the Northern Hemisphere is vitamin D-deficient.
- With 50 percent of total body magnesium found in bone, it’s no wonder that it’s essential to good bone health. Magnesium helps calcium regulation. Magnesium deficiency has been shown to alter calcium metabolism and the hormones that regulate calcium, which can lead to a reduced BMD.
- Vitamin K can help calcium do its job more efficiently. Osteoblasts produce a vitamin K-dependent protein called osteocalcin, which helps remove calcium from the blood and bind it in the bone matrix as mineral content. Osteocalcin needs vitamin K to function, and long-term deficiency in vitamin K will lead to reduced BMD and bone quality.
- Many soy foods are naturally high in calcium, which may be why it is beneficial to bone health. Soy also contains magnesium and boron. Soy isoflavones in soy foods may inhibit the breakdown of bones, but the data has been mixed. Only certified organic soy should be consumed.
- Vitamin C and Vitamin B6 are needed to make collagen, an essential part of the organic material that holds bone together.
- Fish Oil is beneficial to bone because of its anti-inflammatory properties.
- Strontium, a trace mineral, is approved as a preventative medication in very high doses in Europe. While one large study exhibited benefits, overall, the data is scant. Strontium does produce side effects when taken in doses used in the studies.
Weight-bearing and strength-training exercises are beneficial to bone development and maintenance.
Medications
Note for those with osteopenia: with the exception of estrogen, the effects of pharmacological therapies on fracture have been demonstrated only in patients with either the clinical or BMD diagnosis of osteoporosis, not osteopenia.
Current evidence does not support recommendations regarding the optimal duration of bisphosphonate therapy. This is scary considering many people have been on it for well over a decade.
Adverse Effects (in addition to recent fracture studies)
Oral bisphosphonates may cause upper GI disorders such as dysphagia, esophagitis, and esophageal and gastric ulcer. All bisphosphonates carry precautions on hypocalcemia and renal impairment. Serum calcium and serum creatinine should be measured in all patients before beginning osteoporosis therapy. A transient flu-like illness, often called an acute-phase reaction, occurs infrequently with large doses of oral or IV bisphosphonates. Jaw lesions, usually after dental extraction (known as osteonecrosis of the jaw), have been observed with bisphosphonate use.
Other pharmacologic treatments such as estrogen receptor modulators (Evista), parathyroid hormone anabolic agents (Forteo), both come with side effects and have no safety record beyond five years. Synthetic estrogen and/or progestin's awful safety record has been well studied. Experts believe the dramatic reduction in breast cancer cases coincided with the millions of women who went off hormone therapy.
Osteoporosis Testing
Fracture risk can be estimated by a variety of technologies at numerous skeletal sites. Bone Mineral Density measured by DXA is the only diagnostic technology by which measurements are made at hip, spine, and radius.
Repeat DXA testing in untreated postmenopausal women is not useful until 2 to 5 years have passed, given the rate of bone loss of 1% to 1.5% per year. Postmenopausal women, after substantial BMD losses in early postmenopause, generally lose about 0.5 T-score units in BMD every 5 years.
For women receiving osteoporosis therapy, BMD monitoring may not provide clinically useful information until after 1 to 2 years of treatment.
While often ignored, biochemical markers of bone turnover can be measured in serum or urine. They can indicate either osteoclastic bone resorption (breakdown products of type I collagen in bone: N-telopeptides, C-telopeptides, deoxypyridinoline) or osteoblast functioning (bone matrix synthesis: bone-specific alkaline phosphatase, procollagen type I N-terminal propeptide, osteocalcin). We believe bone turnover testing should be as important in osteoporosis screening as DXA.
2 comments:
I appreciate this well-rounded, well-supported information.
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