Osteoporosis is characterized by abnormally low bone mass, micro-architectural deterioration of bone tissue leading to increased bone fragility, and a consequent increase in fracture risk. (1) The term osteoporosis is widely used clinically to mean generalized loss of bone, or osteopenia, accompanied by relatively atraumatic fractures of the spine, wrist, hips, or ribs. It is manifested clinically as fractures, and, on noninvasive quantitative imaging tests, as low bone density.

Osteoporotic fractures, particularly in aging women, represent a major health problem in industrialized nations. In the United States, approximately 150,000 hip fractures occur annually in women over age 65, with 15 percent to 25 percent of these women experiencing excess mortality or needing long-term nursing home care. (2) Osteoporotic vertebral crush fractures, manifested by back pain, loss of height, and decreased ambulation are present in 5 percent to 10 percent of women by age 60 and 40 percent by age 80. (3)

It is convenient to consider type I and type II osteoporosis: type I is associated with estrogen loss in women and androgen loss in men; (4) type II is the gradual age-related loss of bone mass that occurs in both sexes. (5) Type I osteoporosis is associated with increased bone turnover; resorption exceeds formation, with disproportionate loss of trabecular compared to cortical bone. These individuals are likely to experience fractures of the distal radius, vertebrae, ribs, and pelvic bones, and are usually women between 55 and 70 years of age. Type II osteoporosis is associated with loss of differentiated bone cells from stem cell precursors, resulting in predominant cortical bone loss and predisposition to hip fracture; most of these individuals are over 70 years old, and female predominance is less striking. (6)

Although bone turnover rates decrease progressively with age, bone formation is decreased to a slightly greater degree than is resorption, probably because resorption rates increase, resulting in a gradual net loss of bone. A variety of hypotheses regarding the nature of this pattern have been suggested, including relative osteoblast failure, calcium and vitamin D deficiencies related to dietary change, decreased efficiency of intestinal calcium absorption and renal calcium retention, and falling levels of calcitonin and estrogen in the face of rising levels of PTH. (7) , (8) Thus, physiologic involutional osteopenia has multiple etiologic factors. (9) Pathologic osteopenia has additional etiologies and different phenotypic expressions in different individuals. For example, biopsies from men or women with mid-life symptomatic osteoporosis can contain a spectrum of changes, with some individuals showing inactive bone remodeling and others showing very high turnover rates. (10)

Diminished absorption of calcium by the intestine is a physiologic consequence of aging, although the reasons are unknown. (11) , (12) In some women, this malabsorption becomes severe enough to add a component of hyperparathyroidism to their osteoporosis. Estrogen loss after menopause probably enhances bone resorption; androgenic hormones and some progestins, levels of which also decline with time, may have positive effects on bone mass. Premature menopause, occurring before the age of 45, is associated with rapid bone loss in some women. (13) Early menopause may be caused by the use of cytotoxic drugs in young women. Diminution in physical activity, in sunlight exposure, and dietary intake of calcium and vitamin D probably play important roles in the osteopenia of aging.

Several features of osteoporosis suggest a role for local factors in pathogenesis: (1) no systemic hormone plays an essential role; (2) differential bone loss occurs in different parts of the skeleton; (3) levels of cytokines, prostaglandins, and local growth factors may be altered in osteoporosis. (14) Production of IL-1, TNF alpha, and IL-6 may be increased in estrogen-deficient and osteoporotic patients. (15) The loss of bone after ovariectomy in rats can be blocked by inhibiting the activity of IL-1 and TNF alpha. (16) PGE2 production is increased in bones from oophorectomized animals and decreased by estrogen administration. (17) Nonsteroidal anti-inflammatory drugs that inhibit prostaglandin synthesis can slow bone loss in ovariectomized animals and postmenopausal women, although the effect is limited. (18) , (19) IL-6 levels increase with age in humans, and estrogens and androgens can decrease IL-6 production. (20) , (21) However, there are also negative studies on the role of cytokines in osteoporosis. (22) , (23)

Risk Factors (24) , (25) , (26) , (27) , (28) , (29)

    Aging – reduced intestinal calcium absorption; rise in parathyroid hormone; decline in calcitonin; senescence of bone multicellular units. Genetics – increased susceptibility of certain populations, low peak bone mass, small body build (especially leanness); concordance in monozygotic twins and mothers—daughters. Race – osteoporosis incidence in Caucasians, Asians, Hispanics, and African Americans. Menopause - declining levels of estrogens and progestins; especially severe if decline is sudden, as in oophorectomy. Hypogonadism – occurring in males; low levels of luteinizing hormone or testosterone. Drugs - glucocorticoids, anticonvulsants. Immobilization - any inactivity or weightlessness. Poor nutrition and other health habits - low intake of calcium, little sunlight exposure, cigarette smoking, alcohol abuse and drug abuse, low physical activity. The risk of osteoporosis has been associated with heavy caffeine consumption. One study found that more than two cups of coffee or four cups of tea a day increased the amount of urinary calcium output and the incidence of hip fractures. (30) Excess phosphorus in the body increases the excretion of both calcium and magnesium. Foods containing phosphorus, phosphate, phosphoric acid, and oxalic acid can interfere with adequate calcium absorption. Animal protein, soft drinks, and tea should be consumed in moderation. There is some debate over the benefits of dairy products in the diet. Although most dairy products contain moderate to high levels of calcium, they are also relatively high in animal protein and a significant source of phosphorus. A recent Japanese study demonstrated that supplementing with calcium (200mg oyster shell with seaweed) more effectively suppressed parathyroid hormone than supplementing with milk. (31) Parathyroid hormone increases blood levels of phosphorus and increases calcium excretion in the urine. Sugar also induces calcium excretion and has been implicated in kidney stone formation. (32)


National Institute of Arthritis and Musculoskeletal and Skin disease (NIAMS), 2003.

    10 million Americans are affected with osteoporosis. 18 million people are at risk for developing osteoporosis. Osteoporosis' cost to health care is $15-20 billion a year.

National Osteoporosis Foundation, 2003.

    80% of the population with Osteoporosis are women. 1 in 2 women and 1 in 8 men 50 yrs. and over will have osteoporosis related fractures. Osteoporosis is responsible for more than 1.5 million fractures annually.
      300,000 hip fractures 250,000 vertebrae 250,000 wrists 300,000 other bone fractures

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Osteoporosis is often called the "silent disease" because bone loss occurs without symptoms. People may not know that they have osteoporosis until their bones become so weak that a sudden strain, bump, or fall causes a hip fracture or a vertebra to collapse. Collapsed vertebra may initially be felt or seen in the form of severe back pain, loss of height, or spinal deformities such as kyphosis, or severely stooped posture.

Osteoporosis is characterized by low bone mass, micro-architectural deterioration of bone tissue leading to increased bone fragility, and a consequent increase in fracture risk. (33) It is manifested clinically as fractures, and, on noninvasive quantitative imaging tests, as low bone density.


    Bone loss Decreased bone mass Bone weakness, increase in fractures or vertebral collapse Loss of height Severe back pain Kyphosis

Treatment Options


The goal is to reduce the risk of fracture by reducing the loss of bone mass. Prevention is more effective than treating established disease, but both require attention. Available therapies include estrogen replacement (in combination with progesterone), calcium supplementation, weight-bearing exercise, vitamin D, and bisphosphonates. If a fracture has occurred, symptomatic relief and aggressive therapy to halt further bone loss are indicated.

    Hormone Replacement Therapy
    Hormone replacement therapy is the treatment of choice for postmenopausal osteoporosis. (34) Estrogen may stops bone loss and may even produce a modest degree of skeletal accretion in those with established disease. (35) , (36) Observational studies have consistently noted a 35 percent to 50 percent reduction in hip, wrist, and vertebral fractures in women who have used estrogen for at least 5 years after menopause, in addition to improving the lipid profile (HDL cholesterol rises, LDL cholesterol falls) and overall cardiovascular risk declines. (37)
    Natural estrogens (estradiol, conjugated estrogens) are preferred for replacement therapy over the synthetic ones (ethinyl estradiol), because they are shorter acting and less likely to cause adverse effects. Estradiol is the principal estrogen secreted by the ovary. It is available as 17-beta estradiol by transdermal patch or in a micronized oral preparation. The other natural oral formulation is conjugated equine estrogens. Oral preparations undergo first-pass metabolism by the liver, converting about half of estradiol to estrone. Transdermal 17-beta estradiol does not undergo hepatic first-pass metabolism; although this prolongs duration of action, it reduces the beneficial effect on hepatic lipid. Treatment should be at the onset of menopause if maximum prevention of bone loss is to be achieved. Estrogen therapy may need to be continued indefinitely, because skeletal loss will resume if treatment is halted and, after several years, the beneficial effects of estrogen will be lost. Patients over the age of 75 show little or no benefit from as much as 10 to 12 years of estrogen therapy started at the time of menopause.
    For the woman with a uterus, the most serious adverse effect when using estrogen replacement therapy is a marked increase in the risk of endometrial cancer. (38) It was once thought that the risk can be eliminated by the concurrent use of progesterone, which prevents unopposed endometrial stimulation. (39) However, in July of 2002 a study was published greatly questioning not only the benefits of HRT but also the now confirmed risks of using HRT. (40) This study was part of The Women's Health Initiative (WHI) and involved greater than 16,000 women. The trial was stopped early when routine data analysis revealed that women taking a combination of estrogen and progestin had an increased risk of breast cancer and cardiovascular events among others. Other large trials have raised similar concerns as the WHI trial, (41) , (42) but the WHI was the first to confirm this increase breast cancer risk in healthy women with a uterus. The conundrum for patients with osteoporosis is that the trial showed a reduced risk of hip fracture with this hormone combination.

    Estrogen alone may also increase the occurrence of breast cancer, with postmenopausal women with breast cancer possibly experiencing marked stimulation of tumor growth from initiation of estrogen therapy. (43) Other adverse effects, more commonly seen with use of synthetic estrogens, include migraine headache, cholelithiasis, worsening of endometriosis or fibroid tumors, and acute thrombosis. The woman being considered for estrogen therapy needs careful breast and pelvic examinations, Pap test, and mammogram before onset of hormone replacement. Transient bloating, nausea, and breast tenderness may be noted after initiation of hormone replacement therapy.

    Drugs that have these tissue-specific effects have been termed selective estrogen receptor modulators (SERMs). Potentially, the benefits of estrogen can be derived without the accompanying risks. This tissue selectivity is biologically possible because the conformation of a drug-estradiol receptor complex determines the particular DNA response elements to which it can bind. Raloxifene, a benzothiophene that binds to the estrogen receptor is a selective estrogen receptor modulator. (44) The raloxifene-estrogen receptor complex does not bind to the estrogen-response element. Instead, it binds to a unique area of DNA, the raloxifene response element, to have estrogen-antagonist effects on breast and endometrium and estrogen-agonist effects on bone and cholesterol. (45)
    Biphosphonates are synthetic compounds that bind avidly to bone mineral and can inhibit its resorption. (46) Administration of the bisphosphonate etidronate increases spinal bone mineral density and decreases the rate of spinal fractures, making it a very useful treatment for patients with vertebral compression fracture. Benefits are greatest in those with low bone density and after 2 years of therapy. Because continuous use of etidronate can inhibit bone mineralization, it must be used cyclically in patients with osteoporosis. Newer, more potent bisphosphonates (pamidronate, alendronate) have shown promise in the prevention of bone loss associated with early menopause, corticosteroid use, and immobilization. Long-term effects and optimal dosing for bisphosphonate therapy remain to be determined. (47)
    Daily subcutaneous injections of 100 units of salmon calcitonin in combination with oral calcium of 1000 mg daily will increase total body calcium in postmenopausal women by several percent, presumably reflecting an increase in skeletal mass. (48) Changes in specific bones have been too small to measure. After a year, there is no further increase in total body calcium, and it declines in parallel to untreated control patients. The high cost and minimal benefit of calcitonin make it a poor choice for treatment of osteoporosis.
    Sodium fluoride
    Sodium fluoride therapy leads to a striking increase in trabecular bone density if given in doses ranging from 40 to 60 mg/d, but cortical bone density decreases, increasing skeletal fragility. (49) The dense fluorotic bone is abnormal both chemically and crystallographically and has undesirable mechanical properties in vitro. Fluoride is not FDA approved for use in osteoporosis.
    Parathyroid hormone
    Parathyroid hormone stimulates new bone formation, increases trabecular bone, and improves calcium balance while producing chemically and histologically normal bone without hypercalcemia. (50) , (51)
    Thiazide diuretics
    Thiazide diuretics may prevent osteoporosis because they reduce the urinary excretion of calcium. (52) Whether thiazides should be used to prevent bone loss must take into account their potentially deleterious effects: increased plasma cholesterol, triglyceride, glucose, and uric acid levels; decreased high-density lipoprotein levels; and potassium depletion, which may predispose to arrhythmia. If the efficacy of thiazide diuretics in preventing fractures is confirmed by clinical trials and this benefit outweighs the risks inherent in thiazide use, then thiazides may be particularly beneficial in the medical treatment of postmenopausal women with hypertension. (53)

Nutritional Supplementation


Calcium is the most abundant mineral in the human body, of which 99 percent is present in the bones and teeth. Obviously calcium is intimately related to bone health but studies on the relationship between calcium intake and osteoporosis have produced conflicting results. While calcium deficiency is undoubtedly one cause of osteoporosis, it is becoming apparent that calcium intake alone will not reverse osteoporosis, and may only partially prevent its incidence. A deficiency of other nutrients is now being recognized as a probable contributing factor. We do women a great injustice by just recommending calcium for the prevention of osteoporosis. In two studies, when calcium was administered with a broad spectrum of vitamins and minerals, women demonstrated greater bone improvement than in any studies with calcium alone or calcium with hormones. (54) , (55)

Although calcium alone is not the answer to preventing osteoporosis, not getting adequate dietary calcium is definitely a major risk factor to this disease. Unfortunately, many Americans are eating diets that do not supply adequate levels of the minerals necessary for skeletal health. For example, results from the U.S. Department of Agriculture’s Nationwide Food Consumption Survey revealed that a majority of people in the United States consume less than the RDA of calcium. (56) The survey also reported that approximately 60 percent of infants between the ages of 0 to 5 years old and 40 percent of children between the ages of 6 to 11 had average daily calcium intakes of less than 800mg. Also, 60 percent of male adolescents and 85 percent female adolescents had calcium intakes below the recommended level of 1,200mg/day. Large percentages of male and female adults were also found to have average daily calcium intakes below recommended levels.

However, taking large amounts of calcium alone may actually interfere with the absorption of other nutrients such as iron, zinc, and magnesium. Traditionally, calcium and magnesium have been recommended in a 2:1 ratio. Some health professionals are now recommending a 1:1 ratio of these minerals.

Mounting evidence suggests that calcium deficiency may be a result not only of inadequate intake, but also because of the calcium-wasting effects of our diets. People in many countries consume fewer dairy products and less calcium than people in the U.S., and they have much less osteoporosis and can maintain healthy bones on intakes of 200-475mg/day. (57) A high intake of caffeine, alcohol, and salt all increase urinary calcium excretion and are associated with an increased risk of osteoporosis. (58) , (59)

High phosphorus-containing foods can be another big cause of calcium loss. Excess phosphorus consumption can cause increased calcium excretion, which displaces calcium from bones. Animal protein and cola soft drinks are both high in phosphorus, and American’s high consumption of these items tends to leach calcium from the body, contributing to osteoporosis. (60) , (61)

Dairy products are the primary source of calcium for most Americans. However, many people have problems digesting milk and dairy products due to lactose intolerance and milk is also a frequent cause of food allergies. Many people who are concerned about dietary cholesterol and fat have switched to low fat milk and dairy products. Other excellent sources of calcium are dark leafy green vegetables, broccoli, legumes, nuts, whole grains, and fortified soymilk. Suggested dietary intakes for calcium vary with different age groups and between men and women. Although there are many types of calcium supplements, the following calcium products are reported to be better absorbed than some of the inorganic calcium salts: calcium citrate, calcium malate, calcium aspartate, and microcrystalline hydroxyapatite compound (MCHC).

Microcrystalline calcium hydroxyapatite compound (MCHC) is a well-absorbed form of calcium derived from bovine whole bone meal and processed under specific guidelines to eliminate contaminants sometimes found in bone meal. The manufacturing process supplies the exact mineral complex that normally exists in bone in a highly absorbable form. Laboratories making MCHC should assay each batch for lead content. MCHC has been reported in human studies to increase trabecular bone mass and decrease cortical thinning. (62) Preliminary studies also suggest that supplementing with MCHC relieves back pain associated with osteoporosis, reduces parathyroid overactivity, and may prevent or restore bone loss. (63) , (64)


It is estimated that 50 percent of all the magnesium in the body is found in the bones. (65) Magnesium is involved in calcium metabolism, the synthesis of vitamin D, and the formation of bone. Magnesium deficiency was shown to be associated with abnormal calcification of bone in one study of osteoporotic women. (66) In another trial, postmenopausal women who took a high magnesium supplement along with hormones achieved an 11 percent increase in bone mass while women only taking hormones showed a 0.7 percent increase. The supplement also included a range of other nutrients known to be important in bone health. This study is important because it documents the greater effectiveness in treating osteoporosis with a broad range of nutrients rather than with just calcium. (67)

Magnesium is another essential nutrient that is frequently deficient in the diet of Americans. Data from the USDA’s Nationwide Food Consumption Survey, which evaluated 12 age/sex groups of the U.S. population for intake of dietary magnesium, revealed that with the exception of children ages infant to 5 years, the average daily magnesium intakes of all age/sex classes were below the Recommended Dietary Allowance (RDA). Magnesium consumption was particularly low among adolescent females (85 percent), adult females (80-85 percent), and elderly men (75 percent) of the population groups having average magnesium intakes below their respective RDA. (68)

Vitamin K

Vitamin K is essential for bone formation because it is required for the production of osteocalcin, the key calcium-binding matrix protein, which attracts calcium to crystallization sites. New research is making a good case that vitamin K deficiency is a factor contributing to osteoporosis and that supplementation may prevent or reverse bone loss. A study of osteoporotic patients showed that they had 74 percent less vitamin K than controls. (69)

In a study of postmenopausal women, it was shown that low levels of vitamin K reduced the capacity of osteocalcin to attract calcium by 50 percent. This was normalized after women were given vitamin K supplementation. (70) The primary dietary source of vitamin K is dark green leafy vegetables.


Manganese is essential for mucopolysaccharide biosynthesis, which provides a structure upon which calcification takes place. (71) Research indicates that deficient dietary manganese can be a factor in the development of osteoporosis. A recent study showed that women with osteoporosis had blood levels of this trace element 75 percent lower than women of the same age without osteoporosis. (72)

Consumption of refined grains (white breads, flours, and pastas) and other processed foods, where over 50 percent of the manganese has been lost, contribute to deficiencies of this nutrient. (73)


Boron is a trace mineral that has been recently recognized as an essential nutrient for humans. Studies suggest that boron influences the metabolism of calcium, magnesium, vitamin D, (74) estrogen, and testosterone. Boron supplementation significantly reduced urinary excretion of calcium and increased levels of estrogen and testosterone in a group of postmenopausal women. (75) Another study suggests that boron supplementation may be helpful in preventing osteoporosis in postmenopausal women not taking estrogen. Boron raised serum calcium to levels comparable with a control group of women receiving estrogen replacement. (76)

Vitamin D

Vitamin D is one of the primary regulators of calcium absorption. Although deficiencies are frequently found in postmenopausal women with osteoporosis, there also a deficiency on a global level. (77) In a study 539 midwestern women were screened for vitamin D deficiency by the levels of circulating 25-hydroxyvitamin (250HD). The results were 49 subjects (aged 57-77 yr) had low 250HD with reduced vertebral bone density and increased PTH concentrations, suggesting secondary hyperparathyroidism. (78) Inadequate sunlight and dietary intake are largely responsible for reduced vitamin D levels. The most common sources are vitamin D-fortified dairy products, fish, eggs, and liver. Supplementation is recommended for women who do not get regular exposure to sunlight and do not have adequate dietary intake. People who live above the Boston equatorial line may need supplementation because of a lack of sufficient sunlight. (79) Vitamin D supplementation may prevent fractures. (80)

Soy Isoflavones

In cultures where soy products are consumed in abundance, women’s health problems, certain cancers, and cardiovascular disease are reported to be less prevalent. (81) Increasing the dietary intake of soy products increases the intake of phytoestrogens, which weakly mimic the effects of endogenous estrogens. Soy isoflavones (genistein and daidzein) are rich in phytoestrogens and are thought to reduce menopausal symptoms, support bone mineralization, and decrease the risk of certain cancers. (82) , (83) , (84) , (85)

There has been recent interest in the reported use of soy isoflavones in women for decreasing bone loss caused by estrogen deficiency. (86) , (87) , (88) Results indicate that genistein may exhibit estrogenic action in bone and bone marrow, possibly aiding in the regulation of B-lymphopoiesis in the prevention of bone loss, without exhibiting estrogenic action in the uterus. Benefits have been shown at approximately 80 mg a day. (89)

Ipriflavone is a synthetic isoflavone. Numerous studies have evaluated ipriflavone and its impact on the maintenance of bone density. Various sample sizes and study designs have supported the use of this isoflavone for the maintenance of bone density. (90) , (91) , (92) , (93) Opposing results have been noted when ipriflavone was evaluated in postmenopausal osteoporotic women. An extensive prospective, randomized, double-blind, placebo-controlled study involved 474 women and lasted 4 years. Two hundred milligrams of ipriflavone three times a day was compared to placebo, with both groups receiving a calcium supplement. This study demonstrated that ipriflavone did not prevent bone loss. (94)

Herbal Supplementation


Currently, horsetail is used in strengthening and supporting connective tissues including bones, as a mild diuretic, and externally in skin care preparations. (95) Horsetail contains silicic acid, of which a portion is elemental silicon, a vital element for the health tissues and organs of the body including the skin, hair, nails, teeth, bones, tendons, and ligaments.

Horsetail has a reported effect on bone and connective tissue, strengthening and aiding in regeneration due to the silicic acid content (including elemental silicon). (96) Silicon performs an important role in connective tissue, especially in bone and cartilage. (97) Silicon's primary effect in bone and cartilage appears to be on formation of the organic matrix. Bone and cartilage abnormalities are associated with a reduction in matrix components, resulting in the establishment of a requirement for silicon in collagen and glycosaminoglycan formation. Additional support for silicon's metabolic role in connective tissue is provided by the finding that silicon is a major ion of osteogenic cells, especially high in the metabolically active state of the cell. Further studies also indicate that silicon participates in the biochemistry of subcellular enzyme-containing structures. (98) Silicon also forms important relationships with other elements. Although it is clear from the body of recent work that silicon performs a specific metabolic function, a structural role has been proposed for silicon in connective tissue. A relationship established between silicon and aging probably relates to glycosaminoglycan changes. (99) In a laboratory study, a greater amount of glycosaminoglycans was reported to be found in the articular cartilage and connective tissue of silicon-supplemented laboratory animals. (100)

Red Clover

There has been a great deal of research and reviews on the effects of phytoestrogens (or plants that contain chemical entities that have estrogenic activities in the body) as they relate to menopausal symptoms. (101) Research has focused on the red clover extract, which contains four principle phytoestrogens (biochanin A, fomonontein, genistein, and daidzein), all with reported levels of estrogen-like activity. (102) A proprietary extract of red clover (Promensil™), standardized to the phytoestrogen content, has gained a great deal of attention in the management of menopause and related symptoms. Studies involving this extract have demonstrated a range of response from no advantage over placebo to a statistically significant improvement in certain menopausal symptoms. (103) , (104) In addition to red clover’s benefit in managing the symptoms of menopause, research has also reported that isoflavones from red clover selectively increased cortical bone density of the proximal radius and ulna in human subjects. (105)


Calcarea carbonica

Typical Dosage: 6X or 6C, 30X or 30CWeak ankles and swollen joints; Sensitive to cold

Calcarea fluorica

Typical Dosage: 6X or 6C, 30X or 30CTendency to bony knots; Induration of the bones

Calcarea phosphorica

Typical Dosage: 6X or 6C, 30X or 30CRheumatic pains with weakness in the hips; Fragile bones; White spots on the nails

Hekla lava

Typical Dosage: 6X or 6C, 30X or 30CSupports calcium metabolism

Traditional Chinese Medicine


Extensive information regarding the treatment of this health condition using Traditional Chinese Medicine is available through the link above.

Diet & Lifestyle

Dietary Considerations: The risk of osteoporosis has been associated with heavy caffeine consumption. One study found that more than two cups of coffee or four cups of tea a day increased the amount of urinary calcium output and the incidence of hip fractures. (106) Another study found that older women with low serum vitamin B12 levels had greater bone mineral loss. (107) Excess phosphorus in the body increases the excretion of both calcium and magnesium. Foods containing phosphorus, phosphate, phosphoric acid, and oxalic acid can interfere with adequate calcium absorption. Animal protein, soft drinks, and tea should be consumed in moderation. There is some debate over the benefits of dairy products in the diet. Although most dairy products contain moderate to high levels of calcium, they are also relatively high in animal protein and a significant source of phosphorus. A recent Japanese study demonstrated that supplementing with calcium (200mg oyster shell with seaweed) more effectively suppressed parathyroid hormone than supplementing with milk. (108) Parathyroid hormone increases blood levels of phosphorus and increases calcium excretion in the urine. Sugar also induces calcium excretion and has been implicated in kidney stone formation. (109)

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for the diagnosis and treatment of osteoporosis. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Chemistry Profile (Blood)

Inherent homeostatic mechanisms will maintain serum calcium levels even at the cost of bone loss. Generally, serum calcium will only move out of reference range in response to parathyroid abnormalities. Liver and kidney function values are important in any evaluation of potential bone disease. Inorganic phosphorus is important for bone formation and urinary acid-base buffering.

Adrenal Function Profiles

Cortisol (110) and DHEA (111) deficiencies have been correlated to osteoporosis.

Bone resorption

Pyrinoline (PYD) Deoxypyrinoline (DPD) Procollagen type I C-terminal telopeptide (ICTP)


The role of estrogen in osteoporosis has been investigated at length and correlations have been postulated. It is possible that assessment of estrogen may be useful in the monitoring of osteoporosis risk. It should be noted, however, that osteoporosis is a disease of multifactorial origin and estrogen assessment should only be a part of a complex evaluation and intervention program. (112)


It is suggested that progesterone levels have a direct bearing on mineral absorption in bone. (113) Progesterone replacement therapy may increase IGF-1 concentration in bone and result in bone density increase. (114)

Pyridinium Crosslinks

Pyridinium crosslinks are products of a unique series of reactions during the maturation of collagen fibrils, leading to the formation of pyridinium (Pyd), and deoxypyridinium (D-Pyd). This assay measures bone resorption, a dynamic marker of the pathogenesis of bone disease and the rate of bone turnover. It is has also demonstrated greater accuracy and sensitivity than hydroxylysine. (115)


This androgen functions primarily as a reproductive hormone, however evidence suggests it plays a significant role in bone health through its influence on maintaining a positive balance of potassium of sodium, potassium, calcium, and phosphorus.


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