Osteoporosis (submitted by Dan Austin)
Osteoporosis, defined as a reduction of bone mass or bone density, was long viewed as a disease unique to aging women, and has been treated primarily with conjugated equine estrogens (CEE) in hopes of mitigating the decline in endogenous female hormone levels that occurs during menopause (Leong 1998, Wylie 2010). Sadly, much of what conventional wisdom held true about osteoporosis turns out to be flawed; it is now clear that osteoporosis (like many age-related conditions) is not a disease with a singular cause affecting a specific population. Rather, it is a multi-faceted disease driven by a barrage of interrelated factors, and must be addressed as such for optimal prevention and treatment (Clarke 2010).
Today we realize that osteoporosis not only impacts the lives of women, but of men as well; fully one third of those affected by the condition are males (about 2.8 million of them as of 2011), and that number is likely to grow as the population ages (Cawthon 2011, Kawate 2010, Nuti 2010). Indeed, one out of every four men will sustain an osteoporotic fracture during their lifetime (Ahmed 2009). Conventional physicians have been slow to recognize the prevalence of osteoporosis in men; as a result the diagnosis is often delayed even more than it is in women, allowing the disease to progress to an advanced stage before it is detected. (Kawate 2010).
Scientific advancements have revealed that the etiology of osteoporosis stems not only from hormonal imbalances, but oxidative stress, elevated blood sugar, inflammation, and components of the metabolic syndrome as well (Clarke 2010, Confavreux 2009, Lieben 2009; Zhou 2011).
Overlooked by mainstream medicine is the critical role that micronutrients play in bone health. For instance, emergent research on vitamin K has attracted great scientific interest through the revelation of its involvement, along with vitamin D, in both bone health and atherosclerosis, a condition to which osteoporosis is intimately related (Baldini 2005, Abedin 2004).In fact, these two conditions can be thought of as mirror images of one another (McFarlane 2004, D’Amelio 2009). Osteoporosis is characterized by loss of calcium from bones, shifting them from their healthy hard state to a diseased state of softness. Atherosclerosis, on the other hand, is characterized by excessive influx of calcium into arterial walls, shifting them from their healthy flexible state to a diseased state of hardness. Insufficiency of vitamin K contributes to this unhealthy balance.
Similarly underappreciated contributors to bone loss in both men and women are advanced glycation end products (AGE’s); byproducts of high blood sugar. AGE’s interact with proteins in bone causing impaired mineralization and increases in the number of osteoclasts – bone resorbing cells. Moreover, AGE’s encourage vascular calcification by activating a specialized receptor called RAGE, which recruits calcium into vascular smooth muscle cells, leading to hardening of the arteries. This relationship between elevated blood sugar, osteoporosis, and atherosclerosis comprises a vicious cycle linking the conditions in a manner unknown to the majority of mainstream physicians (Tanikawa 2009; Franke 2007; Hein 2006; Zhou 2011).
Pharmaceuticals, such as Actonel® or Fosamax®, have shown limited success, and are associated with some potentially serious side effects including atrial fibrillation and osteonecrosis of the jaw (Jager 2003, Howard 2010). These drugs work chiefly by inhibiting the cells responsible for breaking down bone tissue, but neglect multiple other factors responsible for osteoporosis (Roelofs 2010, Varenna 2010). Although these drugs do increase bone density, poorly appreciated is that they disrupt the natural cycle of regeneration and resorption that is important for the strength of the bone (Abrahamsen 2010).
An integrative approach, based on the human body’s finely tuned relationship with its environment and the nutrients that support bone health, makes much more sense (Confavreux 2009, Hanley 2010). This realization has led to an awakening to the tremendous potential of nutrient and mineral supplements along with hormonal optimization in the prevention and management of osteoporosis. The myriad complexities of osteoporosis necessitate the need to integrate pharmaceutical, nutritional, and lifestyle interventions in order to maintain bone health into advancing age.
The Truth About Osteoporosis: Multiple Causes, Multiple Targets
Most of us assume that our bones are like pieces of rocks or hard shells. However, bone is a living tissue, constantly undergoing demolition and renewal as it responds to changing forces in the environment (Martin 2009, Body 2011). Bone is also the body’s primary reservoir of the calcium needed for a wide variety of biological processes (de Baat 2005). Bone is now recognized as an endocrine organ, secreting compounds that function like hormones throughout the body (Kanazawa 2010).
Our bones are made of crystals of calcium salts in a protein matrix. Specific cells, called osteoblasts, produce the matrix and attract calcium compounds to form new bone, while a different set of cells, called osteoclasts, resorbs the bone tissue to allow new shapes and structures to form in response to gravity and the pull of muscles. This process of remodeling helps repair microdamage that occurs as a result of daily activity and prevents the accumulation of old fragile bone (Martin 2009, Mitchner 2009, Body 2011).
At the simplest level, osteoporosis occurs when more bone is resorbed than formed (Banfi 2010, Chang 2009). There are multiple causes for osteoporosis including suboptimal nutrition, age-related hormonal imbalance, and lack of weight-bearing exercise, to name a few (Body 2011).
Sedentary Life Style – Perhaps the earliest contributing lifestyle factor is lack of weight-bearing exercise, as many as 20% of young and middle aged women already have an abnormal spinal curvature related to bone loss in their vertebrae, a situation that only get worse as one ages (Dwyer 2006, Cutler 1993). A sedentary lifestyle reduces the constant forces that bone needs to experience in order to continue its normal process of remodeling (Akhter 2010). Studies show that both women and men who engage in regular exercise have much lower risk of osteoporosis and fracture (Ebeling 2004, Englund 2011).
Vital Hormones such as estrogen and testosterone promote bone formation and regulate bone resorption, and when those hormone levels drop, osteoporosis can occur. At puberty, bone production increases dramatically, producing the growth spurt of the early teen years. This effect seems to be driven mostly by estrogens, the “female” hormones, in both boys and girls (Gennari 2003, Clarke 2008). Near the end of puberty, androgens, the “male” hormones, increase in both women and men. The androgen surge fuses the bone growth plates, with the result being that the bones can no longer elongate. Young adults generally maintain a steady-state balance in which new bone formation is nearly equal to bone resorption.
Sex hormones also remain at roughly steady levels throughout young adulthood and early middle age (Clarke 2008). After about the age of 35, however, the total amount of bone in the body begins to diminish. In women, the process begins fairly sharply with the onset of menopause, when estrogen levels drop dramatically. In postmenopausal women, bone is lost both from the inner and outer surfaces of bones, as bone resorption by osteoclasts exceeds the already reduced new bone formation by osteoblasts. In men, however, new bone formation on the outer surface of bone keeps pace with resorption on the inner surface for much longer (Seeman 1999). This obvious connection probably accounts for the fact that osteoporosis was thought for so long to be a problem unique to women, and may account for the fact that men begin to suffer fractures from osteoporosis about a decade later than women (Hagino 2003), but similar factors are involved (Ducharme 2009).
The discovery that primary control of bone mineralization in both men and women is mediated by estrogens not only enhances our understanding of how osteoporosis occurs in men, but also has dramatic implications for how we can prevent and treat it (Gennari 2003).
Sex Hormone Binding Globulin (SHBG) is a protein produced primarily in the liver, and serves to bind estrogen and testosterone (Nakhla 2009). It has long been known that declining estrogen levels in both sexes are significant contributors to bone mineral loss with aging. Experts now recognize that the steady rise in SHBG with aging is directly correlated with bone loss and osteoporosis in both men and women (Hofle 2004, Lormeau 2004). As a general rule the higher the SHBG level, the less estrogen is available to contribute favorably to bone health.
Evidences indicate that the SHBG molecule itself plays another key role in the body: conveying essential signals to the heart, the brain, the bone and adipose (fat) tissue that ensure their optimal function (Caldwell 2009). There’s even a special SHBG receptor molecule on cell surfaces that functions much like the ubiquitous vitamin D receptor protein, helping cells communicate with one another (Adams 2005, Andreassen 2006). In other words, SHBG itself functions much like a hormone.
New studies are finding a direct role for SHBG and its cell surface receptor in bone loss (Hoppe 2010). The association is so strong that some experts are now suggesting routine measurement of SHBG as a useful new marker for predicting severity of osteoporosis (Hoppe 2010).
Insulin Resistance, Blood Sugar & Glycation- Bone functions as an endocrine organ secreting compounds that act like hormones (Kanazawa 2010). Healthy production of bone matrix protein increases insulin sensitivity in other tissues (Kanazawa 2010, de Paula 2010). Conversely, people with the metabolic syndrome who are insulin resistant have poorer bone quality and an increased risk of osteoporotic fracture (Hernandez, McClung 2010). Metabolic syndrome also raises SHBG levels, further reducing bioavailable levels of estrogen and testosterone (Akin 2009).
Research suggests that advanced glycation end products, or AGEs, are implicated in bone loss. AGEs are formed when proteins interact with glucose molecules to form damaged structures in the body. One study examined the proteins in osteoporotic bones to determine if there was damage by AGEs. More AGEs present resulted in fewer bone-building osteoblasts (Hein 2006). It is suggested that limiting AGE formation by maintaining a healthy blood sugar level may slow the osteoporotic process (Valcourt 2007).
Oxidation & Inflammation – Oxidation of fatty acids and other molecules produces reactive oxygen species that directly and indirectly impair new bone formation and promote excessive bone resorption (Graham 2009, Maziere 2010). In a similar fashion, chronic inflammation hastens the absorption of existing bone while impeding normal production of new bone (Chang 2009). Fat cells produce a steady efflux of inflammatory cytokines while diminishing cells’ insulin sensitivity; both factors further impede normal bone production (Mundy 2007, Kawai 2009).
Vitamin K- For healthy, mineral-rich bone to form, healthy bone matrix protein must be produced (Bugel 2008, Wada 2007). Over the past decade scientists have realized that vitamin K is an essential co-factor for production of the major bone protein, osteocalcin (Bugel 2008, Iwamoto 2006). Vitamin K-dependent enzymes produce changes in osteocalcin that allow it to tightly bind to the calcium compounds that give bone its incredible strength (Bugel 2008, Wada 2007, Rezaieyazdi 2009).
Calcium & Vitamin D – Many other environmental and nutritional factors contribute to the gradual development of osteoporosis. The role of low intake of vitamin D and calcium are well known (Cherniack 2008, Lips 2010). Adequate calcium intake is required to allow healthy bone remodeling and prevent osteoporosis. Vitamin D promotes intestinal absorption of calcium, and also regulates how much calcium enters and leaves bone tissue in response to the body’s other calcium requirements.
Trace Minerals – While bone is primarily composed of matrix protein and calcium compounds, small amounts of other trace minerals are essential for normal bone function. These include magnesium, which regulates calcium transport; silicon, which reverses loss of calcium in the urine; and boron, which interacts with other minerals and vitamins and also has anti-inflammatory effects (Aydin 2010 Mizoguchi 2005, Kim 2009, Li 2010, Spector 2008, Scorei 2011).
The conventional model of osteoporosis predicts that simple restoration of declining sex hormone levels and provision of modest amounts of calcium and vitamin D should be sufficient to prevent osteoporosis. When those steps fail (which they inevitably do), conventional medicine resorts to suggesting that osteoporosis must be an inevitable consequence of aging.
Life Extension’s position, however, is much more nuanced and incorporates the truth about the complex, interrelated factors that genuinely contribute to osteoporosis. Life Extension recommends a lifelong commitment to an active lifestyle, and supplementation with targeted vitamins, minerals and nutrients that quench reactive oxygen species (ROS), reduce inflammation, control obesity and insulin resistance, promote healthy bone matrix protein synthesis, and supply sufficient trace minerals to support healthy bone.
Risk Factors for Osteoporosis
The risk factors for osteoporosis, like those for all chronic, multifactorial conditions, are many, and they interact with one another. Here is a summary of those we understand best, and that we can take steps to incorporate in our prevention strategies.
Gender- Women are more likely to develop osteoporosis than men. This difference is related to several reasons including: the abrupt loss of estrogen at menopause, women start with a lower bone density and lose bone more quickly than men and women live longer than men.
Age -Increasing age is associated with falling production of estrogen and testosterone, which increases osteoporosis risk. Levels of sex hormone binding globulin (SHBG) rise with age, binding to the sex hormones and reducing their total bioavailable levels, which further aggravates bone loss. Advancing age also means longer total exposure to chronic oxidant stress and inflammation, both of which contribute to development of osteoporosis (Mundy 2007, Maziere 2010, Seymour 2007, Ruiz-Ramos 2010).
Ethnicity- Caucasian and South Asian people have greater risk of osteoporosis (Dhanwal 2011, Golden 2009).
Family History- A family history of hip fracture carries a twofold increased risk of fracture among descendants (Ferrari 2008).
Estrogen Exposure- Women with late puberty or early menopause are at higher risk due to a decrease in estrogen exposure over their lifetime (Vibert 2008, Sioka 2010).
Vertigo- Several recent studies have shown an association between “benign positional vertigo” (BPV) and lower bone mineral density (Vibert 2008, Jeong 2009, Vibert 2003). The inner ear, where balance is maintained, contains tiny bone particles (otoconia) that may be affected in osteoporosis (Vibert 2008). Some experts recommend that people with BPV should undergo screening for osteoporosis (Jeong 2009).
Slim stature (underweight) – People with a body mass index of 19 or less or have small body frames tend to have a higher risk because they may have less bone mass to draw from as they age (El Maghraoui 2010).
Obesity- Increased body fat was long thought to be protective against osteoporosis (Bredella 2010). Accumulating evidence, however, suggests that obesity-related components such as insulin resistance, hypertension, increased triglycerides, and reduced high-density lipoprotein cholesterol are all risk factors for low bone mineral density (Bredella 2010, Kim 2010).
Cardiovascular Disease- Cardiovascular disease and mortality are associated with osteoporosis and bone fractures (Baldini 2005). That’s not surprising since the two conditions share many mechanisms and risk factors, such as oxidant damage and inflammation (Baldini 2005, Vermeer 2004).
Chronic Stress & Depression- Both condition increase cortisol production, leading to suppression of sex hormone production, increased insulin resistance, and enhanced release of inflammatory cytokines (Kiecolt-Glaser 2003, Kaplan 2004, Berga 2005). All of these effects increase the risk of bone mineral loss and osteoporosis (Berga 2005, Bab 2010, Diem 2007, Haney 2007).
Other risk factors for osteoporosis include: HIV infection (Ofotokun 2010), anorexia (Mehler 2011), cancer (Ewertz 2011, Lim 2007), smoking (Kanis 2009), caffeine (Tsuang 2006, Tucker 2006), and alcholism (Matsui 2010).
Medication Use- A variety of medications increase one’s risk for osteoporosis. These include:
Corticosteroids. These immune-suppressive drugs mimic the effect of stress-induced cortisol, with all of its suppression of sex hormones, weight gain, and insulin resistance.
Selective Serotonin Reuptake Inhibitors (SSRIs). Both depression and medications used in its treatment, such as SSRIs, increase the risk of osteoporosis (Bab 2010).
“Blood thinning” Medications (Anticoagulants). The drug Coumadin, used to prevent clot formation in patients with cardiovascular disease, acts to block the beneficial effects of vitamin K and is associated with decreased bone mineralization in some patients (Deruelle 2007). Low molecular weight heparin, an unrelated blood thinner, can also cause reduced bone mineral content (Rezaieyazdi 2009).
Symptoms and Diagnostic Tests
Anyone who losing height with age may have osteoporosis, unfortunately, osteoporosis typically has no symptoms at all until a serious fracture occurs, usually from a relatively minor injury (Walker 2010, Azagra 2011). All the while, however, the disease is actually progressing, which is why early prevention is so important (Kawate 2010). Diagnosis and treatment are often substantially delayed, especially in men, because the concept of male osteoporosis is still unfamiliar to many practitioners as well as patients (Kawate 2010).
In women, the “dowager’s hump” that is classically associated with the disease is actually also a late finding, caused by gradual collapse of the front portion of the bones of the spinal column (Cutler 1993). It is predictive of decreased mobility over the coming years (Katzman 2011). Once fractures are evident, of course, they are associated with symptoms such as pain and immobility. If the hip is fractured, patients are often bedridden for weeks or months, putting them at major risk of pneumonia and blood clots. Hip fracture continues to be a leading cause of death in older adults (Dhanwal 2011).
The current gold standard for diagnosis of osteoporosis, the so-called DEXA scan, uses dual energy X-ray absorptiometry to determine the relative bone mineral content (Santos 2010). The DEXA test is most commonly used because there are more DEXA testing devices in doctors’ offices than the more advanced quantitative computed tomography (QCT), another x-ray based equipment for determining bone mineral density. However, studies suggest that the QCT test is much more sensitive (Smith 2001).
In one clinical study, osteoporosis was present in 63 percent of men at the time of diagnosis of prostate cancer, prior to any therapy. In this landmark paper, the investigators evaluated DEXA bone mineral density testing and compared it to QCT bone mineral density testing in the same patients. A significantly greater percentage of men were found to have osteoporosis by the QCT methodology than by means of the DEXA approach. DEXA bone mineral density evaluation detected osteoporosis in only 5 percent of men, whereas with QCT technology, 63 percent of men were diagnosed with osteoporosis. Using QCT technology, bone density abnormalities (osteopenia and osteoporosis) were found in 95 percent of men, compared to 34 percent of men evaluated with DEXA (Smith MR et al 2001).
Although QCT testing exposes patients to more radiation than DEXA does, the amount of radiation associated with QCT for determining bone density is roughly equivalent to that of a dental series and is approximately 50 percent that of a mammogram (depending on the technique used). Most important, QCT generates far less radiation exposure—orders of magnitude less than a contrast-enhanced abdominal CT scan.
The results of bone density testing are given in T-scores. These scores are developed by comparing the person being tested to a young adult of the same gender between 25 and 45 years of age. A T-score of -2.5 or lower indicates high fracture risk, or a 60 percent chance of fracturing a hip. For every decrease of 1 in T-score, there is a twofold increase in risk of fracture. Individuals with a T-score of -1.1 to -2.5 are diagnosed with osteopenia, or mild bone loss. Results are also given as Z scores, which measures individual results against people of the same age, gender, and race.
DEXA and QCT scans require specialized equipment, keeping them from more widespread use in rural areas. As a result, a variety of predictive scales and scores are being developed that have similar predictive accuracy at substantially less cost. Ultrasonometric scaner (Gueldner 2008), Osteoporosis Prescreening Risk Assessment tool (OPERA) (Salaffi 2005), and Osteoporosis Self-Assessment Tool (OST) (Perez-Castrillon 2007) are a few examples.
The problem, however, with using any of these modalities is that they are useless until substantial bone mineral loss has already occurred (because they rely on measuring that loss). In most people these findings occur only after years of progressive exposure to the chronic, underlying causes of osteoporosis, such as oxidant stress, inflammation, insulin resistance, and insufficiency or deficiency of vitamins D and K.
Conventional Treatments and Associated Risks
HRT (Hormone replacement therapy) – 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 treatment – 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 (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, which 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 supplements – these 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.