Looming in the future for most of us is old age, which will hopefully be filled with energy, abundance, activity, and wisdom. These can be the benefits of a life well lived, yet despite these benefits, our bodies are slowly paying the price of having spent so many years alive. No matter what we may think of bumper sticker wisdom, the one that claims, “Growing old is not for sissies” has pretty much gotten it right. Through a lifetime of stress, toxins, trauma, and malnutrition, the organ systems of our bodies gradually lose their reserves. Both men and women have a plethora of possible ills awaiting them: prostate enlargement, cardiovascular disease, weakened immunity and all that comes with it, aches and pains, meno- or andropause, and osteoporosis. Some of our clients will consider these degenerative conditions the inevitable results of aging.
Others will not go so gently into that good night and will want to learn how to reduce their risk factors in order to increase their number of healthy, active years. Aging, of course, is the ultimate degenerative condition, yet its deleterious effects can be delayed, often for decades. Our skin might wrinkle and sag, our hair grow thin and gray, but we can maintain our health and high energy levels long after these visible signs of aging have made photos of ourselves and the face in the mirror a lot less fun than they used to be.
The specter of osteoporosis is frightening and is often in the forefront of women’s worries about aging because it is so commonly a silent condition … until it isn’t, and we break a bone. And at that point it may be too late to completely recover our bone strength or even our mobility. Preying upon these fears are the multi-billion dollar medical, pharmaceutical, and supplements industries, bombarding us with a media barrage of the latest in bone density testing, bone-preserving drugs, and bone-strengthening supplements, making it difficult for us, as well as our clients, to sort fact from fiction. Yet, as you read on, you’ll come to understand that, as we step out of conventional thinking and come to see osteoporosis as part of a larger degenerative picture, it loses some of its fear factor and becomes an aging body system the health of which we can help clients support through food, supplementation, and lifestyle adjustments. We can also learn to direct our clients to appropriate testing that will give a much more well-rounded view of how the skeletal system is functioning, rather than merely determining a “disease” state.
Although many people think of the skeleton as an unchanging structure, something from which to hang clothes, strong bones are living, growing tissues and are meant to last a lifetime. Bone consists of a strong, flexible mesh of collagen fibers (proteins that form a soft framework) and calcium phosphate (a mineral that hardens the framework). Bone architecture includes trabecular bone — the porous, spongy inner structure that gives strength to the ends of weight-bearing bones — and cortical bone, which forms the solid shafts of our long bones and is denser, thicker, and stronger than trabecular bone. Throughout a person’s lifetime, new bone is added to the skeleton and old bone is removed (resorption). During the early years of life, new bone is added faster than old bone is removed. As a result, bones become larger, stronger, and denser until they reach peak bone mass (maximum bone density and strength) between the ages of 30 and 35. After this age, however, a certain amount of bone loss becomes inevitable, and if bone loss exceeds the body’s ability to rebuild, the bones can become thin and porous. However, while small amounts of bone loss are normal, osteoporosis is not a foregone conclusion for most women.
Osteoporosis, which literally means “porous bone,” is a disease of the skeleton in which the bones gradually lose density and structural integrity. People with osteoporosis have brittle bones and an increased susceptibility to fractures, especially of the hip, spine, and wrist. According to the National Institutes of Health (NIH) (2011), an estimated 40 million Americans already have osteoporosis or are at increased risk of breaking bones, due to having low bone mass, though this alone does not always correlate with structural weakness. Osteoporosis is common among the elderly, but the disease can strike at any age. And although 80% of those affected by osteoporosis are women, particularly post-menopausal women, aging men are affected as well, especially after the seventh decade of life (NIH, 2013; Colbin, 2009, p. 20).
There are two distinct types of osteoporosis:
- Primary, where there is no known mechanism or disorder leading to the condition
- Secondary, which is bone loss that occurs due to a prior existing condition or event, such as the use of medications
Primary osteoporosis is further subdivided into:
- Type I, early postmenopausal osteoporosis, characterized by an excessive loss of trabecular bone, due to loss of estrogen
Average loss about 1.3% during late perimenopause and 1.6% postmenopausally (Finkelstein et al., 2008)
- Women lose about 50% of trabecular bone and 30% of cortical bone during their lives; about half of this lost during first 10 years postmenopause (Arthritis Foundation, 2008)
- Bone loss approximately 35–55% slower in women of highest weight (>170 lb) versus the lowest weight women (<133.5 lb) (Finkelstein et al., 2008)
- Type II, loss of both trabecular and cortical bone (outer layers of bone), more age-related than Type I, and common in men, too.
Of course, as medical anthropologist and nutritionist Susan Brown, Ph.D., claims, all cases of osteoporosis are secondary, because they are all caused by something (Brown, 2013), be it aging, menopause, drugs, diet, or lifestyle (see “Risk Factors,” below).
Osteoporosis is a potentially crippling disease when it is characterized by weak bones and not just low bone density. The most recent Surgeon General’s Report on osteoporosis indicates that it is responsible for more than 1.5 million fractures annually, with approximately 40% of women above the age of 50 experiencing a fracture of the hip, wrist, or spine (HHS, 2004). Men, too, suffer this fate, though at a lower rate — about 13% (HHS, 2004). Unfortunately (or fortunately for these men and women), the statistics may be extremely skewed. Why? Because three decades since we began defining osteoporosis as a specific level of bone density, it has become apparent that there is little correlation between bone density alone and broken bones. In fact, the Study of Osteoporotic Fractures, a large, long-term, multi-center cohort study of women over 65 years old, found that while all types of fractures were increased in women with low bone mineral density (BMD), the proportion of fractures attributable to osteoporosis ranged from just 10% (ankle fractures) to 44% (clavicle fractures) (Stone et al., 2003). That means that a majority of fractures occurred in women without osteoporosis. In this group of over 7,000 non-African American women, who were followed for 8.5 to over 10 years, fractures from trauma, such as automobile accidents, were eliminated, leaving only those that were spontaneous or resulting from low-impact falls. The authors have concluded that “…finding effective prevention strategies for fractures in older women will require additional interventions besides treatment for osteoporosis…” (Stone et al., 2003). Two subsequent studies have reported that while BMD in women is associated with fractures, it is specifically micro-architectural decay of the cortical and trabecular bone in both men and women that results in fractures, independently of BMD (Ostertag et al., 2009; Sornay-Rendu, Cabrera-Bravo, Boutroy, Munoz, & Delmas, 2009). And even the World Health Organization has stated that “…the risk of fracture is very high when osteoporosis is present, but by no means negligible when BMD is normal” (WHO, 2007).
As in other areas of our health, our bone strength seems to be dependent not solely on the quantity of bone, but equally on its quality.
Risk Factors (IOF, 2014; Sanson, n.d., unless otherwise noted)
There is no one single cause of osteoporosis in most cases. Rather, its onset occurs due to accumulation of damage incurred from several factors known to increase risk. Other than being female, older, and being menopausal, risk factors for osteoporosis can include the following, many of which are modifiable by diet and lifestyle changes:
- Being Caucasian or Asian
- Being small and thin
- Insufficient peak bone mass around age thirty
- Family history of osteoporosis
- Certain diseases, such as hyperthyroidism, kidney disorders, Crohn’s disease, ulcerative colitis, and celiac disease — these speed bone turn-over or create malabsorption issues
- Malignancies that directly affect the bones (multiple myeloma, bone cancer)
- Gastrointestinal conditions, such as cirrhosis of the liver, gastrectomy, gastric bypass, or insufficient hydrochloric acid — create malabsorption
- Hormonal disturbances that might interfere with mineralization:
- Chronic stress; cortisol
- Low estrogen in women; low testosterone in men
- Magnesium, essential for bone health; almost certainly low in all diabetics, which may be one contributing mechanism
- Never having menstruated or given birth to a child
- Delayed puberty (male or female) or early menopause
- Being thin or underweight, including having had anorexia nervosa — bone-preserving estrogen is also formed in fatty tissues, which may be particularly important after menopause
- Chronic inflammation — causes increased bone resorption (Garg & Wood, 2013). Consider when clients present with:
- Low estrogen
- Insulin resistance/diabetes, cardiovascular disease
- Chronic stress, which elevates cortisol, leading to inflammation
- Long-term use of medications including:
- Glucocorticoids (steroid hormones). Cortisol — natural or synthetic — speeds bone breakdown.
- Diuretics (medications that promote excretion of urine)
- Antibiotics — alter GI flora, inhibiting vitamin K absorption
- Immune system suppressants
- Aluminum-containing antacids — inactivate HCl, necessary for mineral absorption
- Gonadotropin releasing hormone analogs (used to treat endometriosis). Use of these medications should be directed by your physician.
Diet and Lifestyle Factors
- Sedentary lifestyle (lack of exercise)
- Bone is dynamic tissue; gets stronger when stressed by weight-bearing exercise
- Nutrient deficiencies:
- Minerals, esp. calcium, magnesium, zinc, manganese, copper, boron, silicon
- Vitamins, esp. B complex, C, D, K2
- Excess vitamin A (as retinol, not carotenoids), combined with low vitamin D. Women with vitamin D deficiency (<20 ng/mL), and highest levels of serum retinol, had 8 times greater risk for osteoporosis than those with lowest serum retinol (Mata-Granados, Cuenca-Acevedo, Luque de Castro, Holick, & Quesada-Gómez, 2013).
- Phytonutrients, esp. flavonoids, involved in complex signaling activity that modulates bone metabolism (Horcajada & Offord, 2012)
- Oxidative stress from:
- Nutrient deficiencies, esp. antioxidants and phytochemicals
- Heavy caffeine use
- Smoking cigarettes — depletes estrogen (Fallon & Enig, 2000)
- Excessive alcohol consumption
- Environmental toxins: metals, air pollution, agricultural chemicals
- Excessive exercise
A Word on pH Balance
For decades, popular thought has placed metabolic acidosis as the central villain in osteoporosis generation in what is known as the “acid-ash hypothesis.” This states that if one eats a diet loaded with meats, grains, and dairy, and low in vegetables and fruits, one’s body will become overly acidic and will have to dip into bone mineral reserves for calcium in order to alkalinize the body’s tissues, including the blood. While no one questions the foolishness of such a diet, it turns out that the scientific research that initially made these claims was interpreting information gleaned from subjects with chronic kidney disease (CKD), whose buffering systems are not working properly (Bonjour, 2013). In healthy individuals, acid-base homeostasis is maintained through other processes. In the words of a recent review article,
Any influence of nutritional origin that slightly disrupts the acid–base equilibrium is at once corrected by biochemical buffering systems operating in both the extracellular and intracellular compartments . Then…..come into play the homeostatic systems involved in the regulation of pulmonary ventilation and urinary acid excretion via modulation of the renal tubular reabsorption (Bonjour, 2013).
To paraphrase, we have several lines of defense against metabolic acidosis, including the intracellular and extracellular environments, the lungs, and, especially, the kidneys. Bones do not appear to lose any of their minerals in order to keep us metabolically alkaline.
A 2011 systematic review and meta-analysis of 55 studies, with very strict inclusion criteria, found that while higher protein, dairy, and grain diets do indeed increase urinary calcium excretion, “…higher protein intakes were not detrimental to calcium retention since higher protein increased calcium absorption in similar quantity to the rise in urine calcium, even when calcium intakes were low” (Fenton, Tough, Lyon, Eliasziw, & Hanley, 2011).
The study authors cite numerous studies that have demonstrated no negative impact on calcium retention from higher protein intakes and animal protein (Fenton et al, 2011). Their conclusion: “A causal association between dietary acid load and osteoporotic bone disease is not supported by evidence and there is no evidence that an alkaline diet is protective of bone health.” However, plant foods, most of which do alkalinize our urine, definitely support the health of our bones. It is, however, for reasons other than pH regulation.
Determining Bone Density and Diagnosing Osteoporosis
Bone mineral density relates to the quantity not the quality of bone. It reveals nothing about the strength, micro-architecture, rate of remodeling, size or shape of bone — all factors which contribute to fragility. (Sanson, n.d.)
|OSTEOPOROSIS IS NOT||OSTEOPOROSIS IS|
|Merely thin bones||Thin and substandard
|Common throughout the
|Common only in
|Something that strikes
just the elderly
|Becoming more common
among the young
|An isolated disorder||One manifestation of
Adapted from Brown, 2009
Prior to 1994, osteoporosis was considered a condition of fragile bones, diagnosed only after someone had broken a bone in a non-traumatic fall (in other words, they didn’t fall off a cliff or get hit by a car; they simply tripped and went down). In 1994, with the advent of bone mineral density scans, a panel of experts from the World Health Organization set the standards for diagnosing osteoporosis that are used today (WHO, 2007):
- Recommended using BMD as the sole means to diagnose osteoporosis
- Defined normal bone:
- Has the average bone density of 25 year-old adults, + 1.0 standard deviation below that
- 2.5 standard deviations below the average defined as osteoporosis, regardless of whether there’s been a bone fracture or not
- Created new definition of osteopenia to describe bone loss between 1.0 and 2.5 standard deviations below average
The problem with these diagnostic criteria is that osteoporosis is a disease of bone fragility, not simply low bone density, and not everyone with low density is osteoporotic.
Bone mineral density testing, as performed by dual energy x-ray absorptiometry (DEXA, also seen as DXA) scans, is considered the medical industry standard for measuring bone density and diagnosing osteoporosis, yet there are several problems with this technology:
- Bone density does not necessarily correlate with bone strength and is NOT predictive of future fractures, and bones that appear dense may still be susceptible to fracture (Brown, 2009), especially in those who have been treated either with fluoride or with bisphosphonates.
- Bone and body size, height, and weight make a difference in bone density testing, and current bone density testing underestimates the bone density of thin or small individuals, resulting in incorrect diagnoses of osteopenia and osteoporosis (NOF, n.d.).
- Inaccuracies are common, due to differences in readings caused by factors such as levels of surrounding adipose tissue (Tothill, Weir, & Loveland, 2014), or due to positioning errors or partial clothing coverage, i.e., operator errors (Krueger et al., 2013). These appear to be quite common.
- DEXA machines are manufactured by three different companies that do not give standardized readings, and it is not recommended to compare readings between different machines (Fan, Lu, Genant, Fuerst, & Shepherd, 2010; Ozdemir & Uçar, 2007).
- Health History and Risk Assessment Questionnaires
- HCl Assessment
- Check for zinc deficiency (low Alkaline Phosphatase on blood tests or zinc taste test), often indicative of low HCl
- Can be checked medically, too
- Stomach acid required for ionization and absorption of minerals
- Especially important in the over-50 population
- Serum Testing
- Alkaline Phosphatase (ALP) — elevations MAY indicate increased bone turnover. If elevated, individual isoenzymes can be tested to confirm.
- Calcium (Ca) — If below 9.2 mg/dL, look at albumin reading (low albumin leads to low calcium). If calcium is low, with normal albumin, calcium and its cofactors may need supplementing.
- Calcium cofactors: adequate HCl; vitamin D3; macrominerals phosphorus and magnesium (all must be in balance); trace minerals manganese, boron, copper, zinc, potassium
- Low Ca may also indicate need for medical appraisal of parathyroid function
- Ionized Ca testing also available. Measures free, i.e., metabolically active, Ca levels.
- Vitamin D3 (serum or blood spot) — inexpensive and can be ordered through client’s doctor or directly from on-line sites, including ZRT Labs
- Required for utilization of calcium
- Optimal levels now considered by some to be 50–80 ng/ml (www.vitamindcouncil.org)
- Bone Mineral Density test
- If a client wishes to have it performed, or if there appears to be risk of osteoporosis, by all means let DEXA scans help determine bone density. This test does not, however, serve well as a stand-alone assessment, as described above.
- This test subjects women (and men) to radiation, which, on top of the recommended yearly mammograms, semi- or yearly dental x-rays, and any other diagnostic radiation-based screenings your clients may have, can add up to a dangerous toxic load.
- Quantitative Ultrasound (QUS)
- A safer means of imaging than x-rays
- Usually performed on the heel bone
- Looks at a “snapshot” of bone, as do DEXA scans, to see what bones look like today. Neither gives information regarding rate of bone loss, but QUS has been verified through a meta-analysis as an accurate means of predicting fractures (Moayyeri et al., 2012).
- Bone Turnover Markers (BTM)
- Two most commonly tested urinary markers of bone resorption are Pyrilinks-D (measures deoxypyridinoline [Dpd]) and N-telopeptide (NTx)
- Used to monitor bone turnover in post-menopausal women and in those being treated medically for osteoporosis
- Safe and noninvasive; patients can request through doctor
- Studies currently underway to establish efficacy of serum carboxy terminal telopeptide of collagen type I (s-CTX) and serum procollagen type I N-terminal propeptide (s-PINP) — markers of resorption and bone formation, respectively — to enhance fracture prediction (Lee & Vasikaran, 2012)
- International Federation of Clinical Chemistry (IFCC) and International Osteoporosis Foundation (IOF) planning for the standardization of commercial assays for s-CTX and s-PINP, so these probably represent additional tests that will one day be standard (along with DEXA scans)
- Two most commonly tested urinary markers of bone resorption are Pyrilinks-D (measures deoxypyridinoline [Dpd]) and N-telopeptide (NTx)
The WHO, in an attempt to provide more accurate, reliable, and useful data for determining osteoporosis and fracture risk, has created a model for determining 10-year risk of hip fracture. This model, called FRAX, considers 11 key factors that the Women’s Health Initiative (WHI) study found most helpful in making this determination, along with a couple of other new ones:
- Bone density, age, gender, BMI, weight, height, previous fracture, parent with hip fracture, smoking and alcohol use, rheumatoid arthritis, current glucocorticoid use, and treated diabetes (Brown, 2009; Hudson, 2010, p. 121)
- A FRAX online calculator can be found at http://www.shef.ac.uk/FRAX
The Bone Preservation Diet: Beyond Calcium
A healthy skeletal system with strong bones is essential to overall health and quality of life…. With appropriate nutrition and physical activity throughout life, individuals can significantly reduce the risk of bone disease and fractures. —U.S. Surgeon General
When women are diagnosed with osteoporosis via DEXA scan, the medical profession is often quick to intervene with bisphosphonate drugs, such as Fosamax® and Boniva®. Yet these drugs, which inhibit bone breakdown, have increasingly been shown to increase the risk of necrosis of the jawbone and to increase risk of femur bone breakage (Wilson, 2010; Sedghizadeh et. al., 2009; Ruggiero, Mehrotra, Rosenberg, & Engroff, 2004). They may also be responsible for some cases of heart arrhythmias and esophageal cancers (Wilson, 2010). Interestingly, this immediate response with the prescription pad is in direct contradiction to a pyramid of care developed and promulgated by the Surgeon General (HHS, 2004). This pyramid considers diet and lifestyle the first and foremost means of preventing and treating osteoporosis, with assessment and treatment of underlying causes next, and only as a last resort are drugs to be considered. So, taking the Surgeon General’s office at its word, let’s take a look at diet and lifestyle.
For bone preservation and osteoporosis prevention, the emphasis is on an anti-inflammatory diet, as it is for all degenerative conditions, with special focus on the vitamin- and mineral-rich foods that can provide the nutrients necessary for keeping our skeletal minerals where they belong — in our bones.
Despite all the focus on calcium, many other minerals are required to keep our bones strong and flexible. In fact, it has long been recognized that a diet abundant in potassium- and magnesium-rich fruits and vegetables is crucial in the prevention of bone loss (Zhu, Devine, & Prince, 2008; Muhlbauer & Li, 1999; Tucker et. al., 1999).
Keeping bones healthy throughout life depends on eating mostly organic foods rich in all vitamins, minerals, and accessory and phytonutrients. Emphasizing clean, sustainably raised sources of protein; soaked or sprouted whole grains (not flours or flour products); and a colorful array of vegetables and fruits, especially non-starchy deep green vegetables and low-glycemic fruits, such as berries, will be the best means of ensuring intake of these essential bone nutrients.
Also including kelp and other sea vegetables, rich in many trace minerals, can help provide an additional “insurance policy” of optimum mineral intake and a rich diversity of tasty fare. Mineral broths from vegetables, bones, or both, are a great way to nourish bones, body, and soul. Used alone as a beverage, or as the base of a more complex soup or stew, broths are simple and contain easily utilized nutrients that enhance all aspects of health, not just the bones.
Specific Dietary Components
Optimal amounts of protein, whether of animal or vegetable origin, are an absolute requirement for the health of our bones. Dietary protein provides the substrate for bone matrix [35% of our bones are collagen, a protein (Brown, 2009)] and stimulates the production of insulin-like growth factor- 1 (IGF-1), a factor that promotes bone formation via osteoblast (bone-producing cells) production (Dawson-Hughes, 2003; Dawson-Hughes & Harris, 2002). But think Goldilocks here, because either too much or too little protein can be problematic; you want it just right. And you want this protein accompanied by generous portions of vegetables, not by a plate full of starches.
It has been a long-held misconception that vegetarians always have better bone strength than meat eaters and that the diet of omnivores is too acid producing to preserve our mineral reserves. As previously discussed, this hypothesis has been disproved. Animal proteins also contain phosphorus, another crucial component of bones and also necessary for proper calcium utilization, as long as it is in its whole food form and not as added phosphoric acid, as found in soft drinks, preservatives, and processed meats. Protein of any sort — nuts, seeds, eggs, dairy, flesh, organs meats, beans, grains — causes urinary calcium loss, because all protein increases the net acid load. But protein, whether of vegetable or animal origin, improves bone mineral density as long as dietary intake of calcium is above 540 mg daily (Dawson-Hughes & Harris, 2002). If the diet is rich in replacement mineral foods, especially green vegetables but also fruits, herbs, and spices, this level will be easily obtained.
Instead, it is excess protein in the absence of plant foods, i.e., nutrient deficient diets, that poses the greatest risk. Vegan diets, because they avoid animal products of any kind, can be deficient in calcium and vitamins D3 and K2, so particular attention needs to be paid to adequate intake of these nutrients. However, when nutrient status is good, BMD in vegans has been shown to be lower than that of omnivores and slightly lower than that of lacto-ovo-vegetarians, but the differences were quite modest, had no statistical significance, and were expected to be of no clinical significance (Ho-Pham, Nguyen, & Nguyen, 2009).
The bottom line appears to be that protein intake should be optimized according to individual need and not restricted in amount and type due to concerns about bone health. Just be certain that there are also optimal amounts of foods rich in all the required bone health cofactors to ensure the right balance of nutrients, and improve digestion, when necessary, to get them absorbed and utilized.
Healthful fats provide a vital role in bone remodeling. Among other functions, they transport the fat-soluble nutrients that support bone health, and they help regulate hormone function. They are best consumed in their unadulterated, whole foods form, or as high quality supplemental fats and oils.
Healthful fats include both polyunsaturated and saturated fatty acids. Long-chain unsaturated fatty acids, such as alpha-linolenic and eicosapentaenoic acids, appear to contribute to strong bones more than other omega-3s (Orchard et al., 2013). However, more important than the type of unsaturated fatty acid is the balance between omega-3 and -6, in other words, the right balance between anti-inflammatory activity and inflammation production. A nested study within the WHI study, found that the highest red blood cell ratios of omega-3:6 predicted one-half the number of hip fractures of those with the highest omega-6:3 ratios (Orchard et al., 2013). Interestingly, there were no correlations with BMD.
Omega-3 fatty acids supplementation, if one is deficient, can lower inflammation, which is an essential element of osteoporosis. A six-month trial of 900 mg daily omega-3 fats demonstrated an increase in serum levels of calcium and vitamin D, and reduced bone resorption (Sharif, Asalforoush, Ameri, Larijani, & Abdollahi, 2010). Include foods rich in essential fatty acids, including cold-water fish such as salmon and sardines, and nuts and seeds, such as flax, pumpkin seeds, and walnuts. Grass-fed beef and pastured eggs will also contain valuable amounts of the beneficial PUFAs.
But high quality saturated fats from foods such as raw dairy, coconuts, and pastured and grass-fed animals are also a necessary component of bone health and optimal bone remodeling (Fallon & Enig, 2000). The butter from grass-fed cows, for instance, contains excellent levels of vitamins A, D, and K2, all necessary for strong bones. It’s always wise to strike a balance with all fat intake to obtain beneficial ratios and thus avoid imbalances in any one direction.
Yes, calcium is definitely an important component of a bone-protective diet, but not in the quantities we ingest it. When calcium is added to everything from orange juice to margarine, and women are supplementing in ever increasing doses, it’s time to rethink this overly simplified approach to strengthening a complex human system. (More on calcium, below.) Good dietary sources of calcium include:
- Moderate intake of organic or raw dairy products (such as milk, yogurt, kefir, and cheese)
- Dairy, once thought to be detrimental to bone health, shown not to impair calcium uptake (Fenton & Lyon, 2011)
- Dark green leafy vegetables (such as broccoli, collard greens, and spinach), which also contain magnesium and potassium
- Canned fish/crustaceans with bones
- Organic tofu (in moderation, sprouted recommended)
- Almonds, sesame seeds
More important than calcium may be magnesium, if only because the over-the-top emphasis on calcium, coupled with depleted magnesium in soil and food, has left many of us deficient in this most important mineral. A recent small study showed strong evidence for both significant magnesium and zinc depletion in women with both osteopenia and osteoporosis, compared to women without these diagnoses (Mutlu, Argun, Kilic, Saraymen, & Yazar, 2007).
Magnesium is a critical cofactor for approximately 400 enzyme reactions in the body. Deficiency due to low intake and soil depletion is thought to be rampant. As it is also easily depleted through stress, eating magnesium-rich foods — greens (vegetables, algae, seaweeds), nuts and seeds, whole grains — is crucial. Supplementing may also be a good idea for many.
- Oral supplementation shown to reduce bone turnover in post-menopausal osteoporotic women (Aydin et al., 2010)
- Stimulates absorption of calcium into bones, so is absolutely necessary
- Increasing magnesium intake while lowering calcium intake to 500 mg daily shown to increase bone density (Nieves, 2005)
Vitamin C is crucial for the formation of collagen and for normal bone development.
- Present in all fruits and vegetables
- Easily broken down in the presence of heat or oxygen, so the fresher the better
- Those who eat primarily processed foods are at greater risk of deficiency
- Low serum vitamin C associated with increased risk of osteoporotic fractures (Martínez-Ramírez et al., 2007); however, 10 g daily, administered orally in menopausal women, did not reduce markers of bone turnover (Talaulikar, Chambers, & Manyonda, 2012).
A hormone more than a vitamin, D is essential for the absorption of calcium from the small intestine, so it’s
absolutely critical for bone health. It also helps us assimilate phosphorus.
- Best obtained from sun exposure
- Fat soluble, so good fats in the diet are important to store D for future use
- Food sources: wild mackerel and salmon, fish eggs, cod liver oil, pastured eggs, leafy greens (contain precursors), and mushrooms
Vitamin K is a family of fat-soluble vitamins: K1 (phylloquinone), K2 (menaquinone [MK]), and K3 (menadione). K1 is primarily involved in providing necessary blood clotting activity. As the “phyllo” in its name implies, phylloquinone is obtained from plant foods, where it is found in the chlorophyll. It is most abundantly available in leafy green vegetables: collard greens, spinach, salad greens, kale, broccoli, Brussels sprouts, cabbage, etc.
K2’s main function is to make sure that calcium gets to where it needs to be — in the bones, not in the arteries. It is found in many different forms – MK1–14, but MK-4 and MK-7 are the two most-studied forms and are critical elements of human health. MK-4 is found in animal tissues, where it has been converted from K1 (also see description of K3, below). MK-7 is formed by bacterial fermentation of plants, as in natto (a fermented soybean product), as well as in the intestines of animals. Menaquinone is found in a few foods: MK-7 in natto; MK-4 in dairy (esp. kefir, hard cheeses, butter), grass-fed organ meats, egg yolks from pastured chickens, and lacto-fermented foods. However, except for natto, there are only small concentrations of K2 in foods.
K3 is an intermediary, catabolized in the digestive tract from the K1 we ingest as food, where a very small amount is converted by commensal bacteria to MK-4, and the rest is delivered to our peripheral tissues, where it is also converted to MK-4 (Hirota, et al., 2013). (You may also see K3 as a synthetic form of K used in supplements.)
There is currently no consensus as to how much vitamin K1 can ultimately be converted to K2. In fact, prior to the 2013 study mentioned above, it was known that K1 converted only minimally to K2 in the digestive tract, leading researchers to speculate that K2 probably had to be consumed in foods. Since K2 is primarily found in animal foods, this led some to believe that vegans, especially, might be sorely lacking in this very important nutrient. It remains unknown whether or not this is true, and there is still much to be learned. However, when clients present with osteoporosis and/or heart disease, they may very well require more of both dietary K1 and K2 (people frequently do NOT consume enough green vegetables, anyway), and this is the important take-away.
Recent research is also revealing the ability of all three forms of vitamin K to inhibit cancerous cell growth both in vitro and in vivo (Lamson & Plaza, 2003), so K truly is Special.
Other Important Bone Nutrients (Colbin, 2009, p. 41)
- Aids synthesis of estrogen and vitamin D
- Dried fruits
- Necessary for utilization of vitamins B and C, synthesis of cartilage, and bone growth and maintenance
- Nuts and seeds
- Whole grains
- Dark leafy greens
- Enhances action of vitamin D
- Seafood, especially oysters
- Pumpkin seeds
- Dried beans
- Essential for formation of collagen
- Nuts and seeds
- Organ meats
- Exercise caution if drinking water from copper pipes or using copper cookware
- Promotes formation of bones, teeth, and collagen
- Whole grains such as wheat, oats, and brown rice, and their products (beer has highest amounts)
- Strengthens collagen
- Meats and fish
- Whole grains
- Sunflower seeds
- Helps regulate homocysteine (along with B6 and B12), which interferes with collagen synthesis
- Leafy greens
- Tuna, salmon
- Brown rice
- Dried beans
And DO rely more on food for all nutrients, especially the minerals. More and more research indicates that minerals are best absorbed through foods, which contain all the cofactors required for utilization by the body (notice I didn’t say absorption*), and not through supplementation. In fact, a recent small-scale study (Napoli, Thompson, Civitelli, & Armenento-Villareal, 2007) found:
… a significant correlation between a higher intake of dietary calcium and increased estrogen metabolism via the 16 α-hydroxyl active pathway, as well as higher BMD in women who consume predominantly dietary calcium versus calcium from supplements.
*Absorption indicates a nutrient has reached the bloodstream from the digestive tract, but not that the cells of the body can fully utilize it.
Herbs and Spices
We tend to set herbs, especially, aside into a separate therapeutic category, to be taken as capsules or tinctures or extracts. Yet for purposes of bone health, using both herbs and spices generously in food preparation will provide us with an extra boost of high-powered nutrients, especially the anti-inflammatory phytonutrients.
- Sea salt
Supplementing with Herbs
Some herbs are specifically recommended for osteoporosis because they have a proven track record for balancing hormones and benefiting bone health):
- Phytoestrogen-containing (require gut bacteria to conversion to usable forms) (Weed, 2002):
- Black cohosh (Actaea racemosa or Cimicifuga racemosa)
- Chasteberry (Vitex agnus-castus)
- Dong quai (Angelica sinensis)
- Green tea (Camellia sinensis)
- Hops (Humulus lupulus)
- Licorice root (Glycyrrhiza glabra)
- Nettle (Urtica dioica) – can also be used as a whole food
- Red clover (Trifolium pratense ): mineral-rich and contains all four of the major types of phytoestrogens (lignans, coumestans, isoflavones, and resorcylic acid lactones)
- Specific bone-supporting herbs (i.e., mineral-rich). Best used as herbal teas or vinegar infusions (Weed, 2001):
- Comfrey leaves (Symphytum uplandica x)
- Nettle (Urtica dioica)
- Oatstraw (Avena sativa)
- Red clover (Trifolium pratense)
The best bone mineral supplement is only as good as the diet it accompanies!
In general, all clients should have individually designed bone support protocols based on their digestive function, levels of intake of protein, nutrient-dense plant foods, and processed, mineral-depleting foods. Not everyone will desire or require extensive supplementation.
If you or a client feels strongly about taking a supplement for long-term general bone health maintenance, it is highly recommended you choose a whole-foods-based combination supplement that provides all of the nutrients and cofactors necessary to maintain and build bone. This type of supplement will avoid the imbalances that may be created by taking high-potency nutrients for long periods of time, especially those containing large amounts of calcium. And, as previously mentioned, the body is adapted to not only absorb but to more fully utilize minerals from food sources. Such a supplement will include calcium, magnesium, phosphorus, zinc, vitamins D and K2, silica, and boron. Supplements may also include other trace minerals, such as strontium and vanadium, as well as a matrix of whole foods cofactors, including those rich in carotenoids, flavonoids, vitamin C, organosulfurs, essential fats, and more. These nutrients will be in far lower potencies than the supplements we’re used to seeing, but evidence suggests that whole foods nutrients of all types are utilized by the body far better than their lab-made surrogates (James Doherty, BioSan Labs, personal communication).
Alternately, higher dose supplements often require taking several capsules daily, so for long-term use, taking a lower dosage is recommended.
If you decide to choose a high-potency supplement, instead of the usual 2:1 ratio of calcium to magnesium, it may be far better to choose either equal amounts or slightly greater amounts of magnesium to calcium (Brown, 2009). Be sure it contains several of the other co-starring nutrients required for bone health and in forms that are easily assimilated.
Also be sure to help your clients enhance their digestive capabilities, since receiving nutrients depends on them getting into the bloodstream and cells. Calcium, magnesium, and zinc, especially, depend upon adequate stomach acid to be fully utilized in the body.
The Calcium Myth
If we believe the common “wisdom,” osteoporosis results from a lack of estrogen and calcium, and though women are no longer urged to consider synthetic hormone replacement (due to the findings of the Women’s Health Initiative study), they are now even more strongly urged to consume dairy products and calcium supplements.
Dairy products, it turns out, have been shown to be good dietary sources of calcium. They neither cause excess calcium excretion, nor do they create metabolic acidosis (Fenton & Lyon, 2011). Calcium supplements haven’t fared nearly as well.
If we had a dime for every client wanting to know what kind of calcium supplement to take, we’d all be rich. But if you give it any consideration at all, it seems a preposterous and simplistic view that taking excessive amounts of one nutrient could solve a complex human health problem: bones are made of calcium; take more calcium. This does not take into account the dynamic process of bone breakdown and remodeling that requires a squadron of nutrients to accomplish and maintain. Excess calcium also has some very serious ramifications:
- Without the necessary cofactors to absorb and utilize it, calcium is just as likely to end up in joints or kidneys or arteries as it is in bones.
- With all the calcium we consume in this country, if calcium was the skeletal health “silver bullet” it’s made out to be, we would be seeing decreasing rates of osteoporosis. We are not seeing this decline and, in fact, the United States has one of the highest rates of osteoporosis in the world (Barron, 2010).
- And to top it all off, a meta-analysis of 16 large studies has found that calcium supplementation, without additional vitamin D, can increase the rate of myocardial infarction (heart attacks) by up to 31% in those taking it (Bolland et. al., 2010).
- In 2008, members of the same research group, in a randomized, placebo-controlled, five-year study, had found the same effect, yet it took two years for this information to make news headlines (Bolland et. al., 2008)
- What is not mentioned in the 2010 news is that the 2008 study found increases in ALL types of cardiovascular disease with use of calcium-only supplements.
The take-away here is pretty straightforward: our bodies are not machines that require simple inputs to effect beneficial changes. We need to think in terms of whole systems that require an array of interdependent nutrients and cofactors. Nutrients, in the form of whole foods, provide these.
Other Possible Supplementation
Vitamin D, as previously mentioned, plays a major role in calcium absorption and bone health. Vitamin D supplements or exposure to the sun (about 20 minutes a day in summer), in combination with calcium, can help heal bone fractures and decrease the risk of future bone breaks. Recommended intakes of vitamin D for the prevention or treatment of osteoporosis will depend upon blood levels of 25-OHD3. When low (<20 ng/ml) it is important to take high doses until levels are brought to 40 – 50 ng/ml:
- Older adults: During the winter, or in the case of a bone fracture, 5,000 IU daily may be required. Once blood levels have optimized, maintaining at around 2,000–4,000 IU daily is advised. Individual requirements will vary, so keep tabs on levels by testing at least yearly.
Preliminary studies also suggest that the following nutrients show promise in the prevention or treatment of osteoporosis:
- Dehydroepiandrosterone (DHEA): promotes osteoblast activity, inhibits osteoblast apoptosis (Wang et al., 2012)
- 3-5 g of a 10% DHEA cream for 12 months significantly increased bone density in post-menopausal study subjects (LaBrie et al., 1997)
- Therapeutic dosage: 10-25 mg, oral, daily for women; up to 50 mg for men
- Best to start with 5 mg and titrate upward
- NOTE: Use caution if choosing DHEA supplementation. This is a hormone and may exert strong effects. To be used only in those with very low levels and with medical supervision. Some studies suggest increased risk of breast cancer in those with elevated levels (Raven & Hinson, 2007).
- Melatonin: reduced peak melatonin levels occur with age and may contribute to development of osteoporosis. Bone remodeling has circadian rhythm, and melatonin affects both osteoblast and osteoclast activity (Maria & Witt-Enderby, 2014). Information is still sparse, but more should be coming out in the years to come. Melatonin can also help with age-related sleep issues, and is a powerful antioxidant.
- 0.1–5 mg daily [3 mg used in one successful study (Kotlarczyk et al., 2012)
- Because melatonin, too, is a hormone, the best approach is to begin with very low doses.
Exercise is number one:
- Physical activity is THE main determinant of bone health (Murray, 2005, p. 754; Pizzorno, 2008, p. 573)
- Improves bone density, geometry, and neuromuscular competency:
- Reduces risk of fracture in a fall AND reduces likelihood of falling (Teta & Teta, 2010)
The best way to exercise to preserve and build bone mass (Teta & Teta, 2010):
- High-intensity and high-velocity weight training to build power and agility, with
- Functional exercise, which targets strengthening the core and building balance, with
- Jumping exercises, which build bone
- Ten to 15 minutes of heel drops, hopping, or jumping 3 days a week to increase bone density and strength (Brown, 2010)
- Working with a trainer or physical therapist can ensure doing the right exercises the right way for each individual
- Chronic stress creates elevations of cortisol; destructive to bones
- Chronic stress depletes magnesium, which is necessary for bone health; often lacking in our diets
- Also depletes other critical nutrients for health, bone, or otherwise, including vitamins B and C
Prevent bad falls
- Eliminate obstacles in the home such as:
- Throw rugs
- Loose cords
- Low pieces of furniture
- Keep rooms well-lit
- Use hip pads
- Get regular eye exams
Bones as metaphor (areas to explore with clients when appropriate):
- Does your client lack backbone?
- Does her life lack structure?
- What kind of love and support does (s)he have?
- Is life falling apart?
If these seem strange or funny to you at first glance, consider the long-term stress produced by any of these and try to understand them in light of the bone-thinning actions of cortisol and the depletion of bone-support nutrients, such as magnesium and vitamin C. Allowing your client to explore some of these issues may allow her/him to find motivation to make beneficial changes beyond just the obvious.
The deterioration of the aging human skeletal system must be viewed in the context of overall health and degeneration. Our bones are simply one manifestation of the care we do or do not take of ourselves through our food and lifestyle choices. Certainly, as with any condition, there will be genetic factors to consider, but if we see our bones as vital living organs, we can nourish their activity, maintaining a strong framework to support our bodies and our lives. We can choose to eat whole, organic, local, and sustainably raised foods, and we can include supplements and lifestyle options that will enhance our bones in order to preserve the strength of this body system. By choosing to support our skeletal system through Eating for Health, we are concurrently supporting other systems, too, creating a whole that is far greater than the mere sum of its parts.
Interested in taking your nutrition education to the next level? Check out our programs!
Online Nutrition Consultant
- Many articles on bone metabolism, testing, osteoporosis
- The Whole-Food Guide to Strong Bones by Anne Marie Colbin, 2009, New Harbinger
- Vitamin K2 and the Calcium Paradox by Kate Rhéaume-Bleue, 2012, Wiley.
- Weston A. Price Foundation: Dem bones: Do high protein diets cause osteoporosis?
Arthritis Foundation. (2008, Mar-Apr). Rate of bone loss during menopause [PDF]. Research Update. Retrieved from http://www.arthritis.org/files/images/research/March-April%2008.pdf
Aydin, H., Deyneli, O., Yavuz, D., Gözü, H., Mutlu, N., Kaygusuz, I., & Akalin, S. (2010, Feb). Short-term oral magnesium supplementation suppresses bone turnover in postmenopausal osteoporotic women [Abstract]. Biol Trace Elem Res, 133(2): 136-43. doi:10.1007/s12011-009-8416-8.
Barron, J. (2006, Dec 18). Osteoporosis. Natural Health Newsletter. Retrieved from http://www.jonbarron.org/anti-aging-program/12-18-2006.php
_______ (2010, Aug 9). Killer calcium? Natural Health Newsletter. Retrieved from http://www.jonbarron.org/heart-health-program/nl100809/killer-calcium.php
Bolland, M. J., Barber, P. A., Doughty, R. N., Mason, B., Horne, A., Ames, R., … Reid, I. R. (2008). Vascular events in healthy older
women receiving calcium supplementation: Randomized controlled trial [Full text]. BMJ, 336(7638):262-6.
Bolland, M. J., Avenell, A., Baron, J. A., Grey, A., MacLennan, G. S., Gamble, G. D., & Reid, I. R. (2010). Effect of calcium supplements
on risk of myocardial infarction and cardiovascular events: Meta-analysis. BMJ, 341:c3691. DOI:10.1136/bmj.c3691
Bonjour, J-P. (2013, Oct 14). Nutritional disturbance in acid–base balance and osteoporosis: A hypothesis that disregards the essential
homeostatic role of the kidney [Full text]. Br J Nutr, 110(7): 1168–1177. doi:10.1017/S0007114513000962
Brown, S. E. (2013, Oct 24 Review). Rethinking “primary” osteoporosis: Isn’t all osteoporosis really just “secondary” osteoporosis?
Retrieved from http://www.betterbones.com/osteoporosis/secondaryosteoporosis.aspx
____ (2010, Oct 26). Bone density testing biased: Thin, small women take note. Retrieved from
—– (2009, Jan 1). Rethinking the nature of osteoporosis and osteopenia. Retrieved from
Colbin, A.M. (2009). The whole-food guide to strong bones. Oakland, CA: New Harbinger
Dawson-Hughes, B. (2003, Mar). Interaction of dietary calcium and protein in bone health in humans [Abstract]. J. Nutr.
133:852S–854S. Retrieved from http://jn.nutrition.org/cgi/content/abstract/133/3/852S
Dawson-Hughes, B. & Harris, S.S. (2002, Apr). Calcium intake influences the association of protein intake with rates of bone loss
in elderly men and women [PDF]. Am J Clin Nutr, 75(4):773-9. PMID: 11916767
Fallon, S. & Enig, M. (2000, Jan 1). Dem bones: Do high protein diets cause osteoporosis? Weston A. Price Foundation. Retrieved
Fan, B., Lu, Y., Genant, H., Fuerst, T., & Shepherd, J. (2010, Jul). Does standardized BMD still remove differences between Hologic
and GE-Lunar state-of-the-art DXA systems? [Full text]. Osteoporos Int, 21(7):1227-36. doi: 10.1007/s00198-009-1062-3
Fenton, T.R. & Lyon, A.W. (2011, Oct). Milk and acid-base balance: Proposed hypothesis versus scientific evidence [Abstract]. J
Am Coll Nutr, 30(5 Suppl 1):471S-5S. PMID: 22081694
Fenton, T.R., Tough, S.C. , Lyon, A.W., Eliasziw, M., & Hanley, D.A. (2011). Causal assessment of dietary acid load and bone disease:
A systematic review & meta-analysis applying Hill’s epidemiologic criteria for causality [Full text]. Nutr J, 10:41.
Fenton, T. R., Lyon, A. W., Eliasziw, M., Tough, S. C. & Hanley, D. A. (2009, Sep 15). Phosphate decreases urine calcium and increases
calcium balance: A meta-analysis of the osteoporosis acid-ash diet hypothesis [Electronic version]. Nutrition Journal,
Finkelstein, J.S., Brockwell, S.E., Mehta, V., Greendale, G.A., Sowers, MF.R., Ettinger, B., … Neer, R.M. (2008, Mar). Bone mineral
density changes during the menopause transition in a multiethnic cohort of women [Full text]. J Clin Endocrinol Metab,
93(3): 861–8. doi:10.1210/jc.2007-1876
Hirota, Y., Tsugawa, N., Nakagawa, K., Suhara, Y., Tanaka, K., Uchino, Y., …Okano, T. (2013, Nov 15). Menadione (vitamin K3) is a
catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4
(vitamin K2) in rats [Abstract]. J Biol Chem, 288(46):33071–80. doi:10.1074/jbc.M113.477356
Ho-Pham, L.T., Nguyen, N.D., & Nguyen, T.V. (2009, Oct). Effect of vegetarian diets on bone mineral density: A Bayesian meta-
analysis [Full text]. Am J Clin Nutr, 90(4): 943-50. doi:10.3945/ajcn.2009.27521.
Horcajada, M.N. & Offord, E. (2012, Jun). Naturally plant-derived compounds: Role in bone anabolism [Abstract]. Curr Mol
Pharmacol, 5(2):205–18. PMID:21787284
Hudson, T. (2009, Apr). Women’s health update: Essential concepts and updates in HRT, breast cancer, and osteoporosis. Townsend
International Osteoporosis Foundation (IOF). (2014 copyright). Who’s at risk? Retrieved from
Kotlarczyk, M.P., Lassila, H.C., O’Neil, C.K., D’Amico, F., Enderby, L.T., Witt-Enderby, P.A., & Balk, J.L. (2012, May). Melatonin osteoporosis
prevention study (MOPS): A randomized, double-blind, placebo-controlled study examining the effects of melatonin
on bone health and quality of life in perimenopausal women [Abstract]. J Pineal Res, 52(4):414-26.
Krueger, D., Vallarta-Ast, N., Libber, J., Checovich, M., Gangnon, R., & Binkley, N. (2013, Apr). Positioner and clothing artifact can
affect one-third radius bone mineral density measurement [Abstract]. J Clin Densitom, 16(2): 154–9.
LaBrie, F., Diamond, P., Cusan, L., Gomez, J-L., Langer, A.B., & Candas, B. (1997, Oct). Effect of 12-month dehydroepiandrosterone
replacement therapy on bone, vagina, and endometrium in postmenopausal women [PDF]. J Clin Endocrinol Metab, 82(10):
3498 –3505. PMID: 9329392
Lee, J. & Vasikaran, S. (2012, Mar). Current recommendations for laboratory testing and use of bone turnover markers in management
of osteoporosis [Full text]. Ann Lab Med, 32(2): 105–12. doi:10.3343/alm.2012.32.2.105
Maria, S. & Witt-Enderby, P.A.. (2014, Jan 15). Melatonin effects on bone: Potential use for the prevention and treatment for
osteopenia, osteoporosis, and periodontal disease and for use in bone-grafting procedures [Full text]. Jour Pineal Resear.
Advance online publication. doi:10.1111/jpi.12116
Martínez-Ramírez, M.J., Palma Pérez, S., Delgado-Martínez, A.D., Martínez-González, M.A., De la Fuente Arrillaga, C., & Delgado-
Rodríguez, M. (2007, Nov). Vitamin C, vitamin B12, folate and the risk of osteoporotic fractures. A case-control study
[Abstract]. Int J Vitam Nutr Res, 77(6): 359-68. doi:10.1024/0300-98126.96.36.1999.
Mata-Granados, J.M., Cuenca-Acevedo, J.R., Luque de Castro, M.D., Holick, M.F., & Quesada-Gómez, J.M. (2013, Feb). Vitamin D
insufficiency together with high serum levels of vitamin A increases the risk for osteoporosis in postmenopausal women
[Abstract]. Arch Osteoporos, 8(1–2):124. doi:10.1007/s11657-013-0124-5
Meta-eHealth, Ehrlich, S. D., reviewer (2008, Dec 11). Osteoporosis. Retrieved from
Moayyeri, A., Adams, J. E., Adler, R. A., Krieg, M-A., Hans, D., Compston, J., & Lewiecki, E. M. (2012, Jan). Quantitative ultrasound
of the heel and fracture risk assessment: An updated meta-analysis [Abstract]. Osteoporos Int, 23(1): 143-53.
Mutlu, M., Argun, M., Kilic, E., Saraymen, R., & Yazar, S. (2007). Magnesium, zinc and copper status in osteoporotic, osteopenic
and normal post-menopausal women [Full text]. The Journal of International Medical Research, 35:692–695
(2007, May). Effects of dietary calcium compared with calcium supplements on estrogen metabolism and bone mineral density
[PDF]. Am J Clin Nutr, 85(5):1428-33. PMID: 17490982
National Institute of Health (NIH). (2013, Mar [reviewed]). What is osteoporosis? Retrieved from
—– (2011, Oct [update]). Osteoporosis handout on health. Retrieved from
National Osteoporosis Foundation (NOF). (n.d.). What women need to know. Retrieved from http://nof.org/articles/235
Nieves, J. W. (2005, May). Osteoporosis: The role of micronutrients [Abstract]. American Journal of Clinical Nutrition,
81(5):1232S–1239S. Retrieved from http://www.ajcn.org/cgi/content/abstract/81/5/1232S
Orchard, T.S., Ing, S.W., Lu, B., Belury, M.A.., Johnson, K., Wactawski-Wende, J., & Jackson, R.D. (2013, Mar). The association of red
blood cell n-3 and n-6 fatty acids with bone mineral density and hip fracture risk in the women’s health initiative [Abstract].
J Bone Miner Res, 28(3):505–15. doi:10.1002/jbmr.1772
Ostertag, A., Cohen-Solal, M., Audran, M., Legrand, E., Marty, C., Chappard, D., & de Vernejou,l M.C. (2009, Mar). Vertebral fractures
are associated with increased cortical porosity in iliac crest bone biopsy of men with idiopathic osteoporosis [Abstract].
Bone, 44(3):413-7. doi:10.1016/j.bone.2008.11.004.
Ozdemir, A. & Uçar, M. (2007, Jun). Standardization of spine and hip BMD measurements in different DXA devices [Abstract]. Eur
J Radiol, 62(3):423-6. PMID:17289322
Pick, M. (2005, Sep 17). Bone density, osteoporosis and the risk of bone fracture. Women to Women. Retrieved from
Raven, P.W. & Hinson, J.P. (2007, Jun). Dehydroepiandrosterone (DHEA) and the menopause: An update [Abstract]. Menopause
Int, 13(2):75-8. PMID:17540138
Ruggiero, S. L., Mehrotra, B., Rosenberg, T. J., & Engroff, S. L. (2004). Osteonecrosis of the jaws associated with the use of
bisphosphonates: A review of 63 cases. J Oral Maxillofac Surg 62:527–534. Retrieved from
Sanson, G. (n.d.). Osteoporosis: Blowing the whistle on the epidemic. Gillian Sanson. Retrieved from
Sedghizadeh, P. P., Stanley, K., Caligiuri, M., Hofkes, S., Lowry, B. & Shuler, C. F. (2009). Oral bisphosphonate use and the prevalence
of osteonecrosis of the jaw. [Abstract]. J Am Dent Assoc, 140(1):61–66. Retrieved from
Sharif, P.S., Asalforoush, M., Ameri, F., Larijani, B., & Abdollahi, M. (2010, Jun). The effect of n-3 fatty acids on bone biomarkers in
Iranian postmenopausal osteoporotic women: A randomized clinical trial [Abstract]. AGE, 32(2): 179-186. doi:
Sornay-Rendu, E., Cabrera-Bravo, J.L., Boutroy, S., Munoz, F., & Delmas, P.D. (2009, Apr). Severity of vertebral fractures is associated
with alterations of cortical architecture in postmenopausal women [Absract]. J Bone Miner Res, 24(4):737-43.
Stone, K.L., Seeley, D.G., Li-Yung Lui, L-Y., Cauley, J.A., Ensrud, K., Browner, W.S., … Cummings, S.R. (2003, Nov). BMD at multiple
sites and risk of fracture of multiple types: Long-term results from the study of osteoporotic fractures [Full text]. Journal of
Bone and Mineral Research, 18(11): 1947–1954. doi:10.1359/jbmr.2003.18.11.1947
Talaulikar, V.S., Chambers, T., & Manyonda, I. (2012, Jan). Exploiting the antioxidant potential of a common vitamin: Could vitamin
C prevent postmenopausal osteoporosis? [Abstract]. Journal of Obstetrics and Gynaecology Research, 38(1): 253–257.
Teta, J. & Teta, K. (2010, Apr). Exercise is medicine: Building bone and plyometrics. Townsend Letter, (321):112–113
Tothill, P., Weir, N., & Loveland, J. (2014, Jan-Mar). Errors in dual-energy x-ray scanning of the hip because of nonuniform fat
distribution [Abstract]. J Clin Densitom, 17(1): 91-6. doi:10.1016/j.jocd.2013.02.008
University of Maryland Medical Center (UMM) (2013). Osteoporosis. Retrieved from
U.S. Department of Health and Human Services (HHS). (2004). Bone health and osteoporosis. A report of the Surgeon General
[PDF]. Retrieved from http://www.surgeongeneral.gov/library/reports/bonehealth/full_report.pdf
Wang, Y.D., Tao, M.F., Cheng, W.W., Liu, X.H., Wan, X.P., & Cui, K. (2012, Apr). Dehydroepiandrosterone indirectly inhibits human
osteoclastic resorption via activating osteoblastic viability by the MAPK pathway [Full text]. Chin Med J (Engl), 125(7):
Weed, S.S. (2002). Phytoestrogens — Friends or foes? Can plant hormones help women in menopause? Do they affect breast
cancer? Retrieved from http://www.menopause-metamorphosis.com/An_Article-phytoestrogens.htm
—- (2001). Healthy bones the wise woman way. Retrieved from http://www.susunweed.com/Article_Bone_Health.htm
World Health Organization (WHO). (2007). WHO scientific group on the assessment of osteoporosis at primary health care level.
Summary meeting report Brussels, Belgium, 5-7 May 2004 [PDF]. Retrieved from
Wilson, D. (2010, Oct 13). FDA issues warning on bone drugs. The New York Times. Retrieved from
Zhu, K., Devine, A., & Prince, R. L. (2008, Jun 25). The effects of high potassium consumption on bone mineral density in a prospective
cohort study of elderly postmenopausal women [Electronic version]. Osteoporos Int, 20:335–340.
DOI:10.1007/s00198-008-0666-3. Retrieved from http://www.springerlink.com/content/d6667l870p6qt5v3