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Health Protocols

Osteoporosis

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.

Testosterone

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).

Bisphosphonates

Bisphosphonate drugs, such as risedronate (Actonel) and alendronate (Fosamax), are chemical mimetics of a naturally occurring molecule, inorganic pyrophosphate, which regulates mineral metabolism. Bisphosphonates are used to help prevent loss of bone density (Hinshaw 2016). What many do not know is bisphosphonates work by limiting additional bone loss rather than building more bone. When taken up by osteoclasts, 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 after prolonged use, which may contribute to atypical fractures (Abrahamsen 2010, Seeman 2009; Ma 2017). Bisphosphonate drugs were found, in a laboratory and an animal study, to increase oxidative stress and inflammatory processes (Enjuanes 2010, Karabulut 2010).

While bisphosphonates are a leading therapy for osteoporosis and bone loss, they are associated with a number of serious though rare side effects. These include osteonecrosis of the jaw, atypical fractures, low blood calcium, kidney toxicity, and musculoskeletal pain; reflux, esophagitis, and ulcers with oral treatment; and flu-like symptoms with intravenous administration (Whitaker 2012; Diab 2010). Some studies have concluded that longer treatment with bisphosphonates increases the risk of fractures and some adverse effects (Drieling 2016; Jung 2018). Since bisphosphonates remain in bone for years after treatment, and can continue to have therapeutic efficacy after being discontinued, “drug holidays” lasting up to several years have been proposed in those who are candidates for long-term bisphosphonate therapy (Brown 2014; Lee 2015; Adler 2016).

Reports of osteonecrosis of the jaw secondary to bisphosphonate therapy indicated patients receiving bisphosphonates orally were at a negligible risk of developing osteonecrosis of the jaw compared with patients receiving bisphosphonates intravenously. In a study of 208 patients who had taken alendronate, 70 mg once weekly for 1‒10 years, nine (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).

Another rare (up to 1% of users) side effect of some bisphosphonates is orbital inflammation, a painful condition that affects the eye and eye socket. Orbital inflammation affects up to 1% of bisphosphonate users, and requires prompt evaluation and management (Chehade 2019; Altundag 2017; Lee 2018). Numerous case reports have described instances of bisphosphonate-associated orbital inflammation, and it is believed that as more individuals are treated with bisphosphonates, cases will increase (Chehade 2019; Tan 2018; Lefebvre 2016; Boni 2013; Pirbhai 2015; Vora 2014). Bisphosphonate-induced orbital inflammation tends to affect individuals in their mid-60s, and can usually be resolved with a course of corticosteroid anti-inflammatory medication. Once the inflammation is resolved, a retrial of another bisphosphonate is often tolerated without problems (Chehade 2019). This complication has only been associated with the newer class of aminobisphosphonates, such as alendronate and zoledronate (Reclast), and not with the older class of non-aminobisphosphonates that includes edidronate (Didronel) and clodronic acid (Chehade 2019; Marcus 2013).

There is some evidence that prolonged bisphosphonate treatment (more than five years) is associated with increased risk for esophageal cancer (Green 2010). Experts generally advise a critical reassessment of fracture risk, a risk versus benefit evaluation, and consideration of a drug holiday after 3‒5 years of bisphosphonate therapy (Abrahamsen 2010; Brown 2014).

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

  • Osteoporosis is a condition in which healthy bone is lost through decreased new bone formation and increased resorption of existing bone
  • Osteoporosis was long thought to result simply from age-related reductions in sex hormones, primarily estrogen. As a result osteoporosis was only considered a disease of postmenopausal women.
  • Life Extension recognizes that osteoporosis is in fact the ultimate consequence of a host of modifiable factors that accumulate over time, including chronic oxidant stress, inflammation, insulin resistance and obesity, chronic life stress that increases cortisol secretion, and nutritional deficiencies or insufficiencies of a host of vitamins, minerals and other compounds
  • As a result, Life Extension recommends a multi-targeted approach to osteoporosis prevention, one that includes regular resistance exercise, weight loss, stress reduction, hormone restoration, and strategic use of nutritional supplements to restore or maintain a more youthful body milieu.
  • Life Extension’s supplement regimen goes beyond the simple recommendations for calcium and vitamin D provided by conventional medicine, adding supplements that promote healthy bone protein formation, and those that reduce inflammation, protect against oxidant stress, and supply adequate amounts of trace and ultra-trace minerals.
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