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by Tori Hudson, N.D.

Osteoporosis is defined as a skeletal disease characterized by low bone mass and a deterioration in bone microarchitecture leading to bone fragility and susceptibility to fracture. The World Health Organization has defined osteoporosis as a bone mineral density (T-score) that is 2.5 standard deviations below the mean peak value in young adults. This definition is useful because it provides objective criteria, but it has limitations because it ignores the importance of other determinants of bone strength. In addition, it also ignores other risk factors for fractures in elderly women such as a maternal history of hip fracture.

Osteoporosis-related fractures will develop in half of all women and one-fifth of all men older than 65 years. Within the first year following a hip fracture, the mortality rate is increased by up to 20 percent, and as many as 25 percent of the survivors will be confined to long-term care facilities one year after the fracture.

Osteoporosis is far easier to prevent than to treat. Osteoporosis prevention strategies need to start in the teenage years. Education should include several key areas: 1) medical problems early in life that can lead to osteoporosis; 2) medications that can interfere with calcium metabolism; 3) the role of nutrition and exercise early in life and their necessity in achieving peak bone density; 4) awareness of the long-term consequences for bone health, if anorexic.

Several approaches are available to prevent osteoporosis and to treat both those who are at high risk and those who have developed the condition. Natural medicines are especially key in prevention. Once osteoporosis has been diagnosed, many of the natural interventions such as diet, exercise, nutritional supplementation and herbal medicines could be used aggressively in milder cases to slow bone loss, reduce fracture rates and possibly have a small impact on increasing bone density. In more serious osteoporosis cases, the natural intervention will become adjunct to a primary antiresorptive therapy. Natural hormone replacement therapy may be considered as a substitute for conventional hormone replacement therapy in selected individuals with monitoring. Natural interventions for osteoporosis include dietary and lifestyle factors, exercise, nutritional supplementation, soy phytoestrogens and natural hormone replacement therapy. Each of these areas deserves special attention. The purpose of this article is to provide an overview of the dietary and nutritional supplementation strategies.


Several dietary factors affect bone health and are involved in the development of osteoporosis: insufficient calcium intake, vitamin d deficiency, low calcium, high phosphorus intake, high animal protein diets, excess salt intake and other mineral deficiencies.

Studies have shown that excessive dietary animal promote may promote bone loss. Animal protein particularly causes an increase in urinary excretion of calcium. Raising daily protein intake from 47-142 grams doubles the excretion of calcium in the urine. Calcium is mobilized from the bone to buffer the acidic breakdown products of protein. In addition, the amino acid methionine, found highest in meat, dairy products, and eggs is converted to homocysteine, which in high amounts may also cause bone loss.

A vegetarian diet, on the other had, is associated with a lower risk of osteoporosis, even though vegetarians do not have greater bone mass in their twenties, thirties, and forties. Several studies have shown that vegetarians do have significantly higher bone mass later in life which would indicate that vegetarians lose bone more slowly than nonvegetarians. Many high protein animal foods also contain high amounts of phosphorus, which mobilized calcium from the bones in order to maintain homeostasis in the bloodstream.

Numerous other factors are implicated in osteoporosis development: high phosphorus beverages (associated with low blood calcium levels), refined sugar (increases the loss of calcium by causing an increase in the fasting serum cortisol levels), high sodium intake (causes an increase in urinary excretion of calcium) and refined grains( lack of nutrient-rich germ and bran and deficiencies of vitamin B6, folic acid, calcium magnesium, manganese, copper and zinc).

One of the best general dietary preventive habits to acquire is to eat a lot of dark green leafy vegetables. These dark greens are a rich source of vitamins and minerals including calcium, vitamin K, and boron. Soybean products containing soy isoflavones may also slow bone loss. Soy diets have been studied in animal models where it has shown an ability to inhibit bone loss although not to the extent of estradiol. A study conducted at the University of Illinois found that menopausal women had an increase in mineral levels and density in their lumbar spines after taking 55-90 mg of isoflavones for six months. The placebo group showed the lowest bone density and the greatest bone loss, while the estrogen group showed the highest bone density and the slowest bone loss. What was surprising was that the soybean protein diet was effective in preventing bone loss in the fourth lumbar vertebra and, although less so, in the right hip as well. Soybean protein seems to have more of an effect on trabecular bone than on cortical bone.

Foods high in calcium include kelp, Swiss and cheddar cheese, carob flour, dulse, collard greens, turnip greens, molasses, almonds, brewer’s yeast, parsley, corn tortillas, dandelion greens, sunflower seeds, Brazil nuts, tofu, calcium fortified soy milk, Goat’s milk, whole milk, sesame seeds, buckwheat, broccoli, walnuts, cottage cheese, spinach and sardines.

Alcohol and smoking

Consumption of alcohol appears to promote bone loss. Scientific evidence links excessive alcohol (seven ounces or more per week) with lower bone mass, increased bone loss, and a higher incidence of fracture. However, in another study, moderate alcohol intake, less than seven drinks per week, was found to be associated with a lower risk of hip fractures compared to women who did not drink. The results of most studies show that smokers lose bone more rapidly and have a lower bone mass than nonsmokers. In female smokers, the risk of hip fracture is increased by 1.5-2.5 fold. Smoking tobacco increases estrogen metabolism by the liver and consequently increases bone loss in women taking estrogen replacement therapy.

Nutritional Supplements

When women think about what they can do to prevent osteoporosis, most women think of calcium supplementation. Indeed, calcium supplementation has been shown to decrease bone loss in postmenopausal women. The effects have been greatest in women whose baseline calcium intake was low, in older women, and in women with osteoporosis. Many studies have been done to better understand the effect of calcium and vitamin D supplementation both as a preventive measure and as an additional treatment intervention. In a study of 3,270 institutionalized women in France who were treated with calcium (1,200mg per day) and vitamin D (800 IU per day) for three years, the risk of hip fractures was 30 percent lower than in the placebo group. A more recent study demonstrated that 389 men and women over age 63, who were treated with 500 mg calcium per day and 700 IU vitamin D per day, had a decrease in the rate of nonvertebral fractures. This study stands out because, although the fracture rate was decreased, the bone mineral density of the femoral neck increased only 1.2 percent and the total body, 1.2 percent. This is considered a very small increase. Although calcium alone or vitamin alone appear to be beneficial to bone health, better results are achieved with a combination of both nutrients.

There is a great deal of confusion and controversy about which form of calcium is best. I discourage women from using either oyster shell or bone meal calcium. These calcium supplements may contain substantial amounts of lead. Other sources of calcium from various chelates may also contain lead. A study of lead content in 70 brands of calcium supplements was conducted in 1993. Lead was the highest in bone meal, unrefined calcium carbonate, and dolomite. Lead was the lowest in calcium chelate supplements and refined calcium carbonate. Calcium chelates are bound to citrate, fumarate, malate, succinate, and aspartate. These forms of calcium are often better absorbed in most individuals than calcium carbonate.

The Institute of Medicine of the National Academy of Sciences released new calcium recommendation in 1997. These new guidelines call for increased intakes for most age groups. The new calcium recommendations were set at levels associated with maximum retention of body calcium, because bones that are calcium-rich are known to be less susceptible to fractures.

Remember that these numbers have to do with total calcium intake. Estimate the amount that is being taken in the diet, and then supplement the difference to bring it up to the desired recommended levels. This issue is important because higher doses of calcium may interfere with the absorption of other nutrients, especially zinc.

If using calcium citrate or citrate with malate, comparable doses may be anywhere from 20 percent less to one-fourth the dose of calcium carbonate that is required. The variation may be influenced by the individual’s digestion and intestinal absorption. I estimate and prescribe less calcium citrate than the recommendations for carbonate.

Even though calcium has received the most attention, alternative medicine views the importance of magnesium in skeletal metabolism and calcium regulation in a little bit different and perhaps broader context. Magnesium influences both matrix and mineral metabolism in bone. Magnesium depletion causes cessation of bone growth, decreased osteoblastic and osteoclastic activity, osteopenia, and bone fragility. Adequate serum magnesium levels are necessary for proper calcium metabolism; however, adequate calcium intake may not ensure proper bone health if magnesium status is abnormal. Magnesium deficiency has been shown more than once to be related to osteoporosis. Magnesium status appears to have a major influence on the type of calcium crystals present in the bones, and therefore its deficiency is associated with abnormal calcification of the bone. In order to assess the effects of magnesium on bone density, a group of osteoporotic postmenopausal women were given magnesium over a period of two years. At the end of the study, magnesium therapy appeared to have prevented fractures and resulted in a significant percent in crease in bone mass density after the first year of treatment. There was, however, no change in density from then on to the end of the study.

Manganese may be one of the most important trace nutrients related to osteoporosis. Manganese deficiency causes a reduction in the amount of calcium laid down in the bone and thereby an increased susceptibility to fracture. Manganese stimulates the production of mucopolysaccharides that provide a structure on which calcification takes place.

Boron appears to also have an effect on bone loss in postmenopausal women. Boron supplementation has been shown to reduce the urinary excretion of calcium by 44 percent, reduce urinary magnesium excretion and markedly increase the serum concentration of 17 beta-estradiol and testosterone.

Zinc is essential for normal bone formation, enhances the biochemical actions of vitamin D, and is required for the formation of osteoblasts and osteoclasts and for the synthesis of various proteins found in bone tissue. Zinc levels have been found low in the serum and bone of elderly people with osteoporosis.

Copper deficiency may be a related cause of osteoporosis. Copper deficiency is known to produce abnormal bone growth in growing children. Copper supplementation has been shown in laboratory studies to inhibit bone resorption. Its supplementation is deemed necessary in women at risk or with diagnosed osteoporosis.

Accelerated bone loss in menopausal women may in part be due to the increased levels of homocysteine, a breakdown product of methionine. Homocysteine has the potential to promote osteoporosis if it is not eliminated adequately. Since folic acid is involved in the breakdown of homocysteine, supplementing postmenopausal women with this nutrient results in significant reductions in homocysteine levels.

Vitamin K is a strong contributing factor in the prevention of osteoporosis. It is required for the production of osteocalcin, the protein matrix on which mineralization occurs. Osteocalcin attracts calcium to bone tissue, enabling calcium crystal formation to occur. Vitamin K plays a key role in the formation, remodeling, and repair of bone by helping the calcium adhere to the site of this protein matrix.

A synthetic derivative of isoflavones, ipriflavone, is now available over the counter in natural food stores or from alternative practitioners. Two multicenter, two-year clinical trials evaluated the efficacy and bioavailability of ipriflavone in postmenopausal women with low bone mass. Study A showed a bone-sparing effect of 1.6 percent in the spine, and study B, 3.5 percent in the wrist after two years. A significant difference was found between the treatment groups and the placebo groups in both studies. It seems as though ipriflavone has a direct ability to inhibit the osteoclastic cell activity, but how it does this is unknown. Although the effect on the spine and wrist is encouraging, these small increases in bone density do not necessarily mean there is a reduced fracture rate, the true test of an effective treatment for the prevention and treatment of osteoporosis.

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