OsteoporosisLife Extension Suggestions
Conventional Treatments and Associated Risks
Hormone Replacement Therapy (HRT)
For many years, while osteoporosis was thought of as primarily a disease of post-menopausal women, treatment included conventional hormone replacement therapy (HRT) using conjugated equine estrogen (CEE) and the synthetic progestogen - medroxyprogesterone acetate (MPA). Early termination of the large Women’s Health Initiative trial in 2002 revealed the dramatic faults in that approach, demonstrating increased rates of breast cancer and heart attack risk in women using conventional HRT (Sveinsdóttir 2006, Archer 2010). As a result, conventional HRT fell out of favor, because of risks associated with stroke, heart disease, and some types of cancer.
In an effort to recoup some of the beneficial effects of conventional HRT, drug companies have brought out a new class of single-targeted drugs called selective estrogen receptor modifiers, or SERMs. These drugs mimic the beneficial effects of estrogen on bone density in postmenopausal women (Silverman 2010, Ko 2011). Raloxifene is an example of this drug class, approved for women with osteoporosis, not men. SERMs theoretically should reduce both osteoporosis and breast cancer. While they show some promise, these drugs remain expensive and associated with side effects such as blood clots, hot flashes, and leg cramps (Ohta 2011).
Life Extension suggests that women talk to their doctor about bioidentical hormone replacement instead, for details please read our Female Hormone Restoration protocol.
When a man has osteoporosis because of low testosterone production, testosterone treatment may be recommended. The positive effects of testosterone on lumbar bone density in men were consistent (Tracz 2006, Isidori 2005). A common misconception is that testosterone administration necessarily increases the risk of prostate cancer, in a causal fashion similar to the risk of HRT and breast cancer in women. However, a careful review of the medical literature reveals otherwise. For example, in a landmark review article published in the New England Journal of Medicine, the authors report “there appears to be no compelling evidence at present to suggest that men with higher testosterone levels are at greater risk of prostate cancer or that treating men who have hypogonadism [low testosterone] with exogenous androgens increases this risk” (Rhoden 2004). However, since testosterone stimulates cell growth in androgen-responsive tissues, it may accelerate the growth of existing prostate cancer. Cancer-screening tests such as a PSA test are necessary before replacement therapy. Testosterone-replacement therapy is contraindicated in men with active prostate cancer (Morgentaler 2011).
Bisphosphonate drugs (Actonel® and Fosamax®) are chemical mimetics of one of the mineral components of bone structure, and they help prevent bone density loss (Drake 2010). What many people do not know is that bisphosphonate focus on limiting additional bone loss, rather than building more bone. When taken up by osteoclasts, the bisphosphonates impair those cells’ ability to resorb bone minerals (Drake 2010). The result is an increase in bone mineral density, but since the remodeling process is reduced, the bone may accumulate microdamage and after prolonged use can result in atypical fractures (Abrahamsen 2010, Seeman 2009).
Most recently, bisphosphonate drugs have been found to increase oxidant stress in the liver, as well as expression of components of the inflammatory system involving NF-kappa-B, a critical inflammation-regulator (Karabulut 2010, Enjuanes 2010). That may imply that these drugs are aggravating one of the fundamental underlying processes that contribute to osteoporosis, inflammation, while superficially treating only the end result.
Few studies with this drug class have actually followed patients for more than 5 years, yet bisphosphonate drugs are generally considered safe by the conventional medical community (Abrahamsen 2010, Seeman 2009). Oral bisphosphonates can cause upset stomach, inflammation, erosion of the esophagus, and intravenous bisphosphonates have been associated with influenza-like illness (Katsumi 2010). More serious, rare side effects include a condition called osteonecrosis of the jaw, and an increase in atrial fibrillation, a heart rhythm disturbance (Jager 2003, Howard 2010).
Reports of osteonecrosis of the jaw (ONJ) secondary to bisphosphonate (BP) therapy indicated that patients receiving BPs orally were at a negligible risk of developing ONJ compared with patients receiving BPs intravenously; a landmark study of 208 patients who had taken alendronate, 70 mg once per week for one to 10 years, 9 (4%) developed jaw bone osteonecrosis. None of more than 13,500 dental patients who had not taken alendronate developed jaw bone osteonecrosis (Sedghizadeh 2009). In patients taking bisphosphonates, 3-5% developed atrial fibrillation and 1-2% developed serious atrial fibrillation, with complications including hospitalization or death (Miranda 2008).
There is also some evidence that prolonged treatment (more than 5 years) with bisphosphonates is associated with increased risk for esophageal cancer (Green 2010). Experts currently advise a critical reassessment of bone density and the risk versus benefit of bisphosphonate therapy after 3-5 years of use (Abrahamsen 2010).
Calcitonin, a hormone made by the thyroid gland, inhibits the cells that break down bone. An intranasal salmon calcitonin (50 to 200 IU/day) plus oral calcium supplements was administered for 1 to 5 years to postmenopausal women for prevention of osteoporosis. The results showed bone mineral density of the lumbar spine increased by approximately 1% to 3% from baseline. In contrast, postmenopausal women receiving only oral calcium supplements typically had reductions in bone mineral density about 3 to 6% (Plosker 1996).
A newly developed oral formulation of salmon calcitonin provides increased efficacy on bone based on Phase I and II clinical trials data, as compared with the nasal formulation (Henriksen 2010).
Stem Cell Therapy
Mesenchymal stem cells are easily obtainable from bone marrow by means of minimally invasive approach and can be expanded in culture and permitted to differentiate into the desired lineage. Experimental investigations of the clinical application of the adult bone marrow derived mesenchymal stem cells with bioactive molecules, growth factors have become promising (Chanda 2010). A case report of mesenchymal stem cells, when percutaneously injected into knees, resulted in significant cartilage growth, decreased pain and increased joint mobility in the patient (Centeno 2008).
Another study investigated the effects of systemic transplantation of human adipose-derived stem cells (hASCs) in ovariectomized mice. hASCs induced an increased number of both osteoblasts and osteoclasts in bone tissue and thereby prevented bone loss (Lee 2011).
Scientists believe that stem cells could halt osteoporosis, promote bone growth - and new pathways that controls bone remodeling (zur Nieden 2011).
Calcium and Vitamin D
Calcium and vitamin D supplements may help older patients lower their risk of hip fractures (details in prevention protocol). Most people in North America, however, lack sufficient sunlight exposure to produce adequate amounts of vitamin D, so vitamin D insufficiency is widespread (Drake 2010).
What You Need To Know