When most people think of bones, the first thing that comes to mind is calcium. Calcium is indeed critical to bone health. However, bones also contain other minerals, connective tissue proteins and living cells. What’s more, the skeleton does not function independently of the rest of the body. Bone health is greatly influenced by a complex web-like interplay of a variety of factors ranging from dietary intake to hormonal levels, from digestive ability to mental-emotional stress. The attainment of optimal bone health necessitates a holistic approach. When the other variables that contribute to bone health are favorable, calcium requirements fall significantly. There are many other facts about calcium in need of discussion. 

According to the National Institute of Health Consensus Development Panel on Optimal Calcium intake, as published in the Journal of the American Medical Association in 1994, "the task for individuals to meet calcium requirements on a continuing basis [without the use of calcium supplements] is a formidable challenge." One study found that for females past age 11, no age group consumed even 75% of the RDA for calcium. Calcium supplementation at 500 mg. per day increased bone density in a group of 12-year-old girls. A study performed on prepubertal identical twins already ingesting the RDA for calcium found calcium supplementation significantly increased bone mineral density. This is of critical importance because of the concept of peak bone mass. Up until about age 25 to 35, bone continues to increase in density and then reaches a peak. After this time, bone density begins to decline as the process of bone resorption exceeds bone formation. The peak bone mass achieved and the subsequent rate of bone loss are the main factors that determine whether osteoporosis will develop or not. If an individual achieves a higher peak bone mass, he or she can withstand greater bone loss before becoming susceptible to fracture. Having higher peak bone mass is like having more money in the bank. Taking steps to build strong bones beginning in childhood can prevent osteoporosis in later life. This is why one researcher has said that osteoporosis is a pediatric disease. Most people should be taking calcium supplements for life. 

Calcium absorption appears to be most efficient in doses of 500 mg. or less. Although calcium absorption is slightly better when taken with food, it may be better to not do so because of its ability to impair absorption of other minerals. Timing of calcium supplementation is of importance. A study found that when calcium supplements were taken at 11 p.m. versus 8 a.m., there was an inhibition of parathyroid hormone release, which translated into reduced bone loss. Calcium should be taken in several doses over the day, with one being late at night. 

The form of calcium used for supplementation is a critical issue. Calcium carbonate, tribasic calcium phosphate, and calcium sulfate are poorly absorbed by individuals with hypochlorhydria. Hypochlorhydria is the very common condition of inadequate production of hydrochloric acid by the stomach. Hydrochloric acid is important for proper absorption of a number of nutrients. It is estimated that half of people over age 65 have hypochlorhydria, although it may occur at any age. In individuals who have no stomach acid production, calcium citrate has been found to be absorbed ten times better than calcium carbonate. Calcium carbonate neutralizes stomach acid. This may result not only in impaired absorption of calcium, but at least 22 other nutrients as well. Unfortunately, many doctors, including so-called "osteoporosis specialists", recommend calcium carbonate for their patients. 

The overall best form of calcium to use for bone health is Microcrystalline Hydroxyapatite Concentrate (MCHC). MCHC is more than calcium. It is bovine-source whole bone concentrate. Not only does it contain calcium and other minerals naturally occurring within bones, but it also contains hydroxyapatite, collagens, non-collagen proteins including the calcium-binding protein osteocalcin, and various growth factors including insulin-like growth factor I and II and transforming growth factor beta. Numerous studies have found MCHC to be effective in slowing or even reversing bone loss in postmenopausal women. When compared to calcium carbonate, MCHC was more than twice as effective in slowing bone loss in postmenopausal women with osteoporosis. In another study with postmenopausal women, while calcium gluconate stopped bone loss, MCHC actually produced an increase in bone mass. An animal study has found that relative to other forms of calcium (including carbonate), MCHC improved the patterns and quality of bone healing after fracture. 

Phosphorus is an essential component of bone. The average American diet, however, supplies excess phosphorus by way of meat and soda. This contributes to a secondary hyperparathyroidism, which causes increased bone resorption, as calcium is lost from the body. Excess dietary fat binds to calcium in the intestines, preventing its absorption. Aluminum (which is often found in water, antacids, processed cheese, table salt, aluminum foil, and antiperspirants) weakens bones by increasing urinary and fecal excretion of calcium. The citrate form of calcium may increase aluminum absorption. Excess dietary salt increases the loss of calcium in the urine. Sugar causes calcium and magnesium to be lost in the urine. Caffeine intake increases release of epinephrine or adrenaline, which causes calcium and magnesium to be lost in the urine. Although younger women's bodies seem to compensate for this with increased intestinal absorption of calcium, older women are not as resilient in this regard. Phytates, found in certain grains, decrease the absorption of calcium and other minerals from these grains. Plant enzyme supplements can be used to break down the phytates. Studies on the impact of consumption of cow's milk on bone health have produced mixed results. Cow's milk should not be consumed by those with an allergy to it or with intolerance to the milk sugar lactose. 

Nicotine, antacids, diuretics, corticosteroids, inadequate stomach acid production, malabsorption, heparin, thyroid medication, and various disease states can contribute to osteoporosis. Alcohol may cause osteoblastic (bone building cell) dysfunction, leading to decreased bone formation and increased demineralization. Alcohol also depletes magnesium and other nutrients. 

Excessive intake of animal protein (which contains the amino acid methionine) can lead to increased levels of homocysteine in the body. Homocysteine is a toxic amino acid, which weakens bones and contributes to atherosclerosis and possibly to dementia, arthritis and cancer as well. Postmenopausal women have been found to have higher homocysteine levels than younger women. Homocysteine levels are also elevated by heavy coffee consumption. Homocysteine levels can be reduced by supplementation with folic acid, vitamins B12 and B6, and trimethylglycine. Excessive animal protein, grains, refined carbohydrates, coffee, alcohol and stress all contribute to excessive tissue acidity. One of the ways the body neutralizes excessive acidity is by liberating calcium from bones. The calcium found in rhubarb, spinach, chard and beet greens is poorly absorbed because it is bound to oxalic acid. Eating refined foods not only reduces the amount of vitamins, minerals, essential fatty acids, and phytonutrients consumed, but it actually depletes nutrients the body may have in storage. Cadmium interferes with the incorporation of calcium into bone, while other heavy metals deplete the body of magnesium. Fluoride has a beneficial effect on bone - up to a point. At higher doses, it makes bones brittle. Fluoride supplementation can result in a shift in bone density from appendicular (arms and legs) bone to axial (spinal) bone. Not surprisingly, fluoride has been associated with increased appendicular fractures. Xenoestrogens are foreign estrogen-like compounds. DDT and PCBs are examples of xenoestrogens. These toxic chemicals may contribute to bone loss by blocking binding of estrogen to receptor sites. 

It is possible to get too much calcium. Excess calcium can interfere with attempts to strengthen bone, possibly by impairing magnesium absorption. Calcium is indeed the most plentiful mineral within bone. However, magnesium may be the single mineral we should really be focusing attention on in attempting to improve bone health. Magnesium is necessary for conversion of vitamin D to its active form. Magnesium aids the absorption of calcium from the intestinal tract and regulates its transport into and out of cells. Magnesium reduces phosphorus absorption, plays a role in the proper functioning of the bone related hormones calcitonin and parathyroid, and activates the enzyme alkaline phosphatase which is involved with forming new calcium crystals within bone. One study found sixteen of nineteen osteoporotic women to be deficient in magnesium. All those who were deficient in magnesium had abnormal crystal formation in their bones, which probably weakens the structure, increasing the risk to fracture. The three women with normal magnesium status had normal crystal formation. It is significant that magnesium supplementation increases the density of the weight bearing trabecular bone, whereas calcium primarily increases the non-weight bearing cortical bone. Trabecular bone is mostly found within the spine and the ends of long bones such as the hip. Cortical bone is found within the shafts of long bones. Over a lifetime, women lose, on average, half of their peak trabecular bone mass and about thirty-five percent of cortical bone mass. Most osteoporotic fractures occur within trabecular bone, with the spine being the most common site. In a study of postmenopausal women on hormone replacement therapy, those who were given a multi-vitamin-mineral supplement containing two times the RDA of magnesium experienced an eleven percent increase in trabecular bone mineral density after one year. This increase in bone mass was sixteen times greater than seen in the control group of women who received no supplemental nutrients. Another study found that nearly seventy-five percent of postmenopausal women who took 250-750 mg. of magnesium daily had an increase in bone mass from one to eight percent over two years. The United States Recommended Daily Allowance (U.S.R.D.A.) for magnesium is probably too low. Other countries recommend people consume up to more than four times more magnesium than the U.S.R.D.A. Probably about seventy percent of Americans consume less than the 300 mg. U.S.R.D.A. for magnesium. Magnesium supplements in the form of glycinate, malate, orotate, aspartate, chloride, and citrate are all good choices. 

Vitamin D is critical to bone health and recent studies have found its deficiency to be epidemic - even in those taking multi-vitamins containing vitamin D. Vitamin D is necessary for calcium absorption. It also contributes to bone health by spurring the conversion of the adrenal hormone DHEA to estrone (estrogen) within the bone building cells called osteoblasts. Studies have found supplements of vitamin D to increase bone mass and decrease recurrence of fractures in women with postmenopausal osteoporosis. Most diets are low in vitamin D. Seven out of ten samples of milk were found to contain less than eighty percent of label claims for vitamin D. Skim milk is a poor vehicle for vitamin D which requires dietary fat for absorption. Malabsorption is also a contributor to vitamin D deficiency. Vitamin D can also be manufactured within the body. This occurs when the skin is exposed to sunlight. The ability of the body to produce vitamin D declines with age. Where you live is a consideration as well. Sunlight in Los Angeles is adequate to produce vitamin D year round, whereas in Boston the angle of the sun between November and February prevents synthesis of vitamin D by the body. Use of sunscreen prevents vitamin D production as well. Magnesium and boron are needed to convert vitamin D to the biologically active form, 1,25-dehydroxy-vitamin D3. Supplements of this nutrient should be in the form of D3. 

Manganese plays an important role in the formation of the organic matrix upon which bone mineralization occurs. One study found osteoporotic women to have manganese levels seventy-five percent below normal. Manganese deficient diets fed to rats resulted in smaller, less dense bones with less resistance to fracture. 

Vitamin K is needed for the formation of the bone protein osteocalcin, which helps incorporate calcium into bone. People with osteoporotic fractures have been found to have one-third of the blood vitamin K levels of normal. An animal study found fracture healing rate to triple when extra vitamin K was given. Other animal studies found vitamin K to inhibit steroid-induced bone loss. Vitamin K reduces urinary calcium loss in postmenopausal women. Vitamin K deficiency may result from not eating an adequate amount of vegetables. Also, because intestinal bacteria produce vitamin K, which is used by the body, antibiotic therapy may result in vitamin K deficiency. Vitamin K supplements of 500 to 1000 mcg. can be used safely, except by people taking medication to reduce blood clotting. 

Boron supplementation has been found to help normalize hormone levels in postmenopausal women. Whether this is accomplished through a non-toxic mechanism is questionable. Boron deficiency has been found to decrease calcitonin levels and increase urinary excretion of calcium. If found to be deficient, boron should be supplemented. 

Many other vitamins and minerals, when deficient, may result in osteoporosis. Copper deficiency in rats has resulted in decreased bone mineral content and reduced bone strength. Silica strengthens connective tissue by supporting the process of cross-linking of fibrils. Zinc aids the biochemical activity of vitamin D and acts as a cofactor for several enzymes involved in the synthesis of the organic bone matrix. Vitamin B6 is a cofactor in the enzymatic cross-linking of collagen strands and its deficiency has been found to produce osteoporosis in rats. Vitamin A is needed for osteoblast health. Potassium increases the retention of calcium within the body. Strontium supplementation was found to increase spinal bone mineral density in postmenopausal women with osteoporosis. Vitamin C deficiency can result in osteoporosis, as this vitamin is critical for connective tissue formation. Lysine helps to strengthen bones. Potassium bicarbonate supplemented at 240-480 mg. per day reduced bone loss in postmenopausal hospitalized women. Chromium influences bone health by virtue of its role in carbohydrate metabolism. Insulin resistance impairs magnesium status. Chromium supplementation can improve insulin resistance. Advanced glycation endproducts (which are basically a consequence of high blood sugar levels) appear to speed bone resorption. Chromium, vitamin E, and the extensively researched plant-derived ipriflavone help to counter this process.

Ipriflavone is a synthetic isoflavone, which has been used for years in other countries for prevention and treatment of osteoporosis. Ipriflavone increases the activity of the bone building osteoblast cells and inhibits the bone-resorbing osteoclast cells. It also increases the calcitonin-releasing activity of estrone. Ipriflavone also appears to be good for the heart. Animal studies have found it to have an oxygen-sparing quality and it has been found to reduce damage to mitochondria. Mitochondria are the parts of cells where aerobic metabolism or energy production takes place. Damage to mitochondria is associated with the aging process. One effect of ipriflavone that causes me some concern is its ability to inhibit cytochrome P450 1A2 and possibly other cytochromes. These are detoxication enzymes, which play a role in the processing, and elimination of toxins and biochemicals from the body. Supressing these enzymes is beneficial when they are overactive but may be counterproductive if they are already sluggish. Laboratory tests are available to measure the activity of cytochrome P450 1A2. Having said that, it should be noted that ipriflavone's safety record is very good. It has been very well tolerated with incidence of side effects being similar to that seen with placebo. Ipriflavone has been found to increase both cortical and trabecular bone. Studies have found ipriflavone to slow or even reverse bone loss in postmenopausal females. One study of 55 postmenopausal women with osteoporosis found ipriflavone to produce an average increase in bone mineral density of the lumbar spine and femur neck of three to five percent after one year. When compared to salmon calcitonin, a drug approved for the treatment of osteoporosis, ipriflavone produced a greater increase in bone mineral density in postmenopausal osteoporotic women. Ipriflavone has been found to increase bone mineral density, reduce the incidence of vertebral fracture, decrease pain, and improve mobility in osteoporotic women. Ipriflavone is recently available in the United States. It is more effective when combined with vitamin D. Ipriflavone has other beneficial effects. It has been found to reduce glucocorticoid (stress hormone) -induced bone loss. Animal studies have found an ipriflavone metabolite to inhibit lipopolysaccharide-induced nitric oxide release from macrophages. What this means is that ipriflavone dampens immune system activation generated by the presence of unfriendly bacteria within the intestinal tract. This is of significance to bone health because of the apparent role of inflammation in bone resorption. The "gut-bone connection" also underscores the importance of a holistic approach to bone health and health in general. 

The etiologic (causative) role of inflammation in cardiovascular disease and dementia is gaining support within the scientific community. There is also mounting evidence that inflammation plays a role in osteoporosis. In fact, the way estrogen may slow bone loss is by blocking the production of pro-inflammatory messenger molecules called cytokines. The specific cytokines involved in this process appear to be tumor necrosis factor, interleukin-1, and interleukin-6. The gastrointestinal tract’s immune system produces a lot of these chemicals in response to toxic chemicals, food antigens, and unfriendly bacteria. These cytokines stimulate bone resorption and inhibit bone formation. Estrogens and, to a lesser extent, progesterone and androgens (e.g. testosterone) appear to inhibit the transcription of the interleukin-6 gene, thereby reducing interleukin-6 production. Vitamin D3 inhibits production of IL-1. Several animal studies have found omega 6 and omega 3 essential fatty acids and their derivatives to inhibit pro-inflammatory cytokines and increase bone mass. EPA (naturally occurring in cold water fish) was found to counter weakening of bone due to calcium deficiency in ovariectomized (having ovaries and, therefore, most estrogen removed) rats. Omega 3 fatty acids have been shown to reduce levels of the pro-inflammatory cytokines IL-1B and TNF. EPA inhibits the conversion of DGLA to arachidonic acid, which is a precursor to PGE2 - a pro-inflammatory eicosonoid (hormone-like compound). Omega 3 fatty acids also raise levels of IGF, a bone-building hormone that decreases with age. IGF-1 counters the effects of IL-1. Rats fed a linoleic acid-rich diet were found to have greater bone density than those fed diets deficient in this essential fatty acid. Animal studies have demonstrated that dietary evening primrose oil and fish oil in a 3 to 1 ratio produced greater bone mass than either a 1 to 1 ratio of these oils or a 3 to 1 ratio of sunflower and linseed oil. Evening primrose oil and fish oil are probably, therefore, the better oils to use. These fatty acids may also contribute to bone metabolism by their role in helping to bind estrogen to bone cell membranes. 

The body's response to chronic inflammation can contribute to osteoporosis by way of elevated cortisol levels. Cortisol is an anti-inflammatory stress hormone secreted by the adrenal or stress glands. Actually, cortisol and DHEA are the body's two main long-acting stress hormones. Cortisol is a catabolic hormone, meaning it breaks complex living tissue into smaller components. DHEA has anabolic or tissue-building effects and helps to balance the metabolic influences of cortisol. For good health, cortisol and DHEA levels must be properly balanced. These hormones are secreted on a continual basis and influence virtually all body tissues and functions. 

Under stress, production of cortisol and DHEA increases and results in changes within the body which allow for better adaptation to the stressor. Once the stress is gone, the output of these hormones returns to baseline levels. This is a healthy response - the body is designed to respond to episodic stress. However, prolonged stress results in breakdown of the body's stress response system; cortisol levels rise while DHEA levels fall. This hormonal imbalance shifts the body into a catabolic state - everything begins to deteriorate - including the bones. High levels of cortisol decrease bone formation and accelerate bone resorption. This is accomplished through reduction in: osteoblast (cells that make bone) proliferation, type I collagen production, levels of osteocalcin - the protein which incorporates calcium into bone, and the bone-building hormone IGF-1. DHEA, on the other hand, increases levels of IGF-1. In fact, in a study of postmenopausal women, DHEA supplementation increased bone mineral density and improved vaginal health without producing the potentially harmful changes within the endometrium of the uterus, which is often an effect of estrogen. Many different things stress the body and can result in elevations of cortisol and reductions in DHEA levels. The three most common stressors are mental-emotional stress, inflammation, and dysglycemia (swings in blood sugar levels). Cortisol and DHEA levels are best measured from saliva samples. When these hormones are found to be imbalanced, treatment involves first identifying the causative stressors. Dietary changes, natural supplements, exercise, stress reduction techniques, designer music, and light therapy are some of the techniques that are useful in reducing chronic stress. Supplementation of DHEA and the cortisol-lowering compound phosphorylated serine are also usually necessary. Medical doctors often prescribe synthetic cortisol, such as Prednisone, to reduce inflammation. The bone-thinning effects of this therapy can be countered by restriction of dietary phosphorous (found in high concentration in meat and soda); by supplementation of DHEA, vitamins D and K, microcrystalline hydroxyapatite concentrate and ipriflavone; and by exercise. 

Exercise is important throughout life. However, its greatest value with regard to bone is probably its ability to increase peak bone mass in early life. Exercise before puberty can produce gains in bone mass which last into adulthood. The greater the peak bone mass achieved, the more bone can be lost before the fracture threshold is reached. Increases in bone mass from exercise during the post-menopausal period are minimal and only maintained as long as the exercise is continued. The benefits of exercise appear to be greatest for those individuals who have lower initial bone mass. Exercise has benefits beyond increasing bone density. Activity during growth appears to improve the trabecular architecture of bone, enhancing its strength. This is an important concept. Two bones can have the same density but their ability to resist fracture can vary quite a bit depending on their internal architecture. Exercise can also prevent osteoporotic fracture by improving muscle strength and balance, thereby preventing falls. Weight-bearing exercises such as tennis and high impact aerobics have been shown to increase bone mass. Walking may be preferable to jogging because the heel strike that is associated with walking results in transmission of shock up the lower extremity to the hip, where it stimulates bone growth. In addition to weight-bearing exercises and balance enhancing exercises such as Tai Chi, muscle strengthening exercises should also be performed. Muscular contraction increases bone mass at the site where it attaches to bone. There is a correlation between muscle strength and bone mineral density. Frequent vigorous exercise is great for the skeleton but care should be taken not to overtrain as cortisol elevations and reductions in DHEA and estrogen can result. 

The benefits of estrogen replacement therapy at menopause are well known. Estrogen can slow bone loss, improve mental-emotional health, prevent dementia, reduce risk to heart disease, and more. The bone-building benefits of progesterone are less well known. Whereas estrogen inhibits bone resorption, progesterone stimulates bone formation. Progesterone has been found to increase bone mass in postmenopausal women. Testosterone is another sex hormone with positive effects on bone. A study found greater increase in bone mineral density in women given estrogen and testosterone compared to those only given estrogen replacement. When considering hormone replacement therapy, several facts should be considered. It is true that hormone replacement therapy is associated with an increased risk of uterine and breast cancer. However, it should be noted that osteoporosis causes more deaths (largely due to complications from hip fracture) than cancers of the breast and cervix combined. What's more, the number of deaths due to cardiovascular disease that are prevented with estrogen replacement therapy are many times greater than the number produced through increased cancer incidence. Looking at overall mortality, estrogen replacement therapy prevents many, many more deaths than it causes. Of course, each individual is unique and if a woman is at high risk to breast cancer, that is an important consideration. 

Using more precise customized hormone replacement can minimize this risk. Many women are being overdosed with these hormones. Dr. Ilias Ilyia, director of Diagnos-Techs™ laboratory, has found that seventy percent of women given supplemental estrogen did not need it in the first place. Diagnos-Techs™ has developed a very accurate way to assess levels of these hormones. Multiple saliva samples collected over the course of a month are used to measure the cyclical fluctuations of estrogen and progesterone. Saliva is actually superior to blood for evaluating these hormones because it accurately reflects the concentrations of "free" hormones in circulation. Hormones in the bloodstream are mostly protein-bound which makes them inactive. It is only the free or unbound hormone that is able to pass into the cells and exert activity. For premenopausal women and for those women less than five years past menopause, this test gives extremely valuable information regarding not only the absolute levels, but also the cyclical relationships of these hormones - something that is unique to each woman. Testosterone and DHEA levels are also measured with this test. This information allows for greater customization of hormone replacement with regard to which hormones to supplement, the quantities to use, and the days during the month that they should be taken. By comparison, a single blood sample gives very limited insight into the cycling of these hormones. Repeat testing, after using the hormones for several months, allows for fine-tuning of therapy. In women more than five years past menopause, the hormones are no longer secreted in a cyclical fashion. In this situation, a single saliva specimen is all that is required to measure levels of these hormones. 

When hormone replacement is indicated, it can be accomplished in several forms including capsule, sublingual, and transdermal patch. These hormones should not be used in the form of a cream that is applied to the skin. "Natural" progesterone and Mexican wild yam creams are particularly popular. First of all, any hormones these creams contain are synthesized in a laboratory. The body does not convert wild yam into hormones as is claimed. Diosgenin from wild yam can only be converted to progesterone in a laboratory. These creams often contain hormones that are not listed on the label. Another drawback is that even if the amount of hormone is listed on the label, one cannot know how much she is taking because the hormones oxidize and degrade with time. There is, however, a more dangerous problem with hormonal creams, which has to do with overdosing. Some of the hormone in these creams passes quickly into the bloodstream upon application to the skin. Once in the blood, it circulates throughout the body, influencing metabolism. A percentage of the hormone in these creams does not pass directly into the bloodstream but instead gets deposited in the subcutaneous fat, which acts as a reservoir. The hormone stored within the fat slowly leaks into the bloodstream. With continued application of hormone cream to the skin, day after day, hormone levels in the blood rise in an exponential fashion due to the contribution of the hormone from the fat stores. This very easily leads to excessive levels of the hormone in circulation. I routinely see patients who have used natural progesterone and other creams whose salivary hormone levels are so high they are beyond values the laboratory even tests for! Not only does an excessive concentration of a given hormone produce toxicity in and of itself, but it leads to further damage by imbalancing other hormones with which it shares complex relationships. 

Premarin should not be used either. Premarin is estrogen derived from horse urine. It appears to carry a strong potential to cause DNA damage, which can initiate cancer. Other safer forms of estrogen should be used. Likewise, progestins should not be used. These are synthetic forms of progesterone that may be unnecessarily dangerous. The motivation for drug companies to produce such compounds was that these are patentable, whereas the natural hormone is not. 

A safer option to consider before estrogen replacement therapy is the enhancement of the body's own estrogen levels. This can be accomplished to varying degrees depending on a variety of factors. Assuring adequate intake of fat promotes higher levels of biologically active estrogen. Animal fat is apparently most effective in this regard. Underweight individuals can increase estrogen levels by attaining normal bodyweight. Since conversion of DHEA to estrogen is spurred by cortisol, assuring adequate levels of these adrenal hormones is important. The fact that DHEA levels fall with prolonged stress has been described. It was also previously mentioned that with prolonged stress, cortisol levels remain elevated. However, if this process continues long enough, the adrenal glands become exhausted and their production of cortisol falls below normal levels. Inflammation increases when cortisol levels are low. Recall that inflammation can contribute to bone loss. Excess cortisol levels are not good for bone health but neither are subnormal levels. Since estrogen is eliminated from the body after processing in the liver, its detoxication is another area of concern. If the body's mechanisms of detoxifying estrogen are operating too rapidly, less estrogen remains in circulation. Laboratory tests are available to measure these detoxication pathways. When detoxication is found to be abnormal, treatment to correct this is needed. Licorice, P.A.B.A., and naringinin (found in grapefruits) are supplements that can slow the body's elimination of estrogen and thus increase its retention. Caution needs to be exercised with this approach, as other hormones and chemicals are also retained in circulation. Boron has also been found to elevate estrogen levels in postmenopausal women. 

Although an excess of dietary protein is associated with bone loss, inadequate protein also can contribute to osteoporosis. Animal source protein helps raise estrogen levels. Research has specifically looked at red meat in this regard. American vegetarian women have been found to excrete two to three times more estrogen in their feces, and have 20% to 40% lower levels of estrogen circulating in blood, than American omnivores (those who eat plant and animal foods). My own observation has been that women who are vegetarian have a greater incidence of amenorrhea (cessation of the menstrual cycle) and lower bone density. A 1997 study of 258 postmenopausal Taiwanese vegans (those who eat no animal products at all) found increased incidence of bone loss of the lumbar spine and femoral neck. Another study comparing vegetarians and omnivores found vegetarians to have lower bone mineral density at the hip, but not the spine. Adequate dietary protein, whether from animal or plant sources, is necessary to form the connective tissue framework of bone. One study concluded that adequate dietary protein might be a determinant of the peak bone mass attained by premenopausal white women. Vegan diets often are deficient in protein, calcium, iron, vitamins B12 and D, and overall calories. Whey protein has been found, in a study of ovariectomized rats, to strengthen bone. Another study of elderly patients with osteoporotic hip fractures found daily protein supplements increased IGF-1 levels, slowed bone loss at the hip, and allowed for earlier release from the hospital. 

Soybeans may offer a viable alternative to estrogen replacement therapy. The power of soybeans is due to chemical compounds called isoflavones. The two most biologically active isoflavones in human tissues are genistein and daidzein. Isoflavones are structurally similar to estrogen and weakly bind to estrogen receptors in the body. Isoflavones produce many of the same effects as estrogen but cannot substitute for the hormone in all its capacities. Isoflavones, like estrogen, have beneficial effects on bone, the cardiovascular system, the brain, and also reduce symptoms of menopause such as hot flashes. Besides estrogenic activity, isoflavones exert many other beneficial actions in the body, including anti-cancer effects. This is why while estrogen is associated with an increased risk to breast cancer, isoflavones inhibit breast cancer cell growth. 

Isoflavones have been found to be as effective as estrogen in maintaining bone in ovariectomized rats. A six month study of postmenopausal women found soy isoflavones to increase lumbar spine bone mineral density. Although few human studies have been done to this point, soy isoflavones may turn out to be very important agents in the prevention and treatment of osteoporosis. According to Acharan Narula, Ph.D., an authority in this area, isoflavones should prove to be more powerful than ipriflavone in managing osteoporosis because ipriflavone is converted to daidzein before exerting biologic activity. 

Eating soybeans is one way to obtain isoflavones, but soybeans contain starches that can produce gas and bloating. Texturized vegetable protein, soy milk and tofu are poor sources of isoflavones. A good way to assure adequate intake of these health-promoting compounds is to take supplements of isoflavone-fortified soy protein powder or pills containing isoflavones. "Nutra-Soy" is the brand I recommend most. To benefit from isoflavones, they must first be enzymatically transformed by bacteria within the intestinal tract and possibly by digestive enzymes as well. Imbalanced bacterial flora (which can result from, among other things, overuse of antibiotics) needs to be addressed before supplementing with isoflavones. 

Gastrointestinal function is important to bone health for other reasons as well. If digestion or absorption are malfunctioning, the best of nutrition will not be able to nourish the bones. Again and again I see people who take numerous potent nutritional supplements but are deficient in multiple nutrients because of maldigestion and malabsorption. Special laboratory tests can identify maldigestion and malabsorption and contributing causes such as parasites, bacterial and yeast overgrowth, rapid or prolonged transit time, and gluten intolerance. 

At this point, it may seem reasonable to ask, "What doesn't contribute to osteoporosis?" There are, indeed, many factors to consider. As with any chronic degenerative condition, we must take a holistic approach and correct any dysfunction found in any area of the body. 

An action plan for osteoporosis prevention and treatment follows: 

1. Measurement of bone density at about age 30 in women to determine peak bone mass attained is a good idea. This can be done with DEXA (dual energy x-ray absorptiometry). New technology that utilizes ultrasound appears to be a viable alternative, does not involve x-ray exposure, and may give additional information about bone quality. If a woman has low peak bone mass, she needs to be that much more aggressive about preventing further bone loss. Additional measurements of bone density should be performed at periodic intervals depending on the circumstances. 

2. Monitor progress with a urine test for biochemical markers of bone loss. As bone is broken down, small chemical components of the bone are excreted in the urine. Rate of bone loss can be gauged by measuring these compounds in urine specimens. It is possible to have normal bone density but to be rapidly losing bone. This, too, necessitates aggressive intervention and periodic re-evaluation. 

3. Identify (and correct) vitamin and mineral deficiencies by way of blood and urine tests and hair analysis. These tests can also identify heavy metal toxicity, which may negatively impact bone health. 

4. Assess body acid-base balance via measurements of first-morning urinary pH. Correct any imbalance by use of diet, nutritional supplements (especially potassium bicarbonate), aerobic exercise and stress reduction. 

5. Assure adequate, balanced intake of good quality, unrefined proteins, fats and carbohydrates. Include fish and evening primrose oil supplements. 

6. Modify any lifestyle factors that contribute to bone loss. 

7. Identify and eliminate any sources of inflammation. 

8. Have an Adrenal Stress Index test to measure the body's output of cortisol and DHEA. Take steps to correct any imbalance. 

9. Perform weight-bearing and resistive exercises on a regular basis. Elderly people should also consider exercises to improve balance and take measures to reduce likelihood of falls. 

10. Consider estrogen, progesterone, and testosterone (testosterone alone for men) replacement therapy. Use a test of saliva specimens to most accurately measure these hormones. 

11. Consider regular consumption of soy isoflavones and ipriflavone. 

12. Assess gastrointestinal function and correct any abnormality found. 

In summary, osteoporosis prevention and treatment should address a lot more than calcium, estrogen and exercise, which are the usual focus. Full implementation of this program obviously requires the guidance of a knowledgeable holistic practitioner.