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Complementary and Alternative Medicine Series

Nutritional Influences on Osteoporosis

Tori Hudson, ND

Numerous modifiable and nonmodifiable factors influence the risk and prevention of osteoporosis. This article provides the practitioner with an understanding of the nutritional influences, both dietary and supplementary, on bone density and fracture susceptibility. By educating patients (especially young girls), health care providers may be able to reduce the risk of osteoporosis and associated debilitating fractures. For women who have already been diagnosed with osteoporosis, these nutritional factors can serve as an adjunct to conventional therapies to slow bone loss and, more importantly, decrease the risk of fractures.

Interventions for treating osteoporosis include both antiresorptive agents and agents that enhance bone formation. Antiresorptive agents reduce the imbalance between bone resorption and formation by decreasing excessive osteoclast activity. These agents exert their greatest effect on trabecular bone, stabilizing its structure. They are therefore most effective at the most common site of osteoporotic fracture: the spine. Bone-enhancing agents increase the number of bone-forming units and stimulate the activity of individual osteoblasts.


DIETARY INFLUENCES

Sound nutrition is an essential component of normal growth and tissue development, including bone. Calcium is considered to be the most important nutrient for attaining peak bone mass and preventing osteoporosis. Diets low in dairy products (eg, calcium-rich beverages), fruits, and dark green, leafy vegetables generally do not provide adequate calcium.

Although less critical to bone health than calcium, there are several other dietary factors that affect bone health, and these factors can also be involved in the development of low bone density. For example, a high-sugar diet may reduce the calcium content of bone. Sugar also causes a significant increase in fasting serum cortisol levels. A serving of refined sugar increases the urinary excretion of calcium.¹

In addition, due to their lack of nutrient-rich germ and bran, it is often postulated that refined grains and flours may also play a role in the development of osteoporosis. The refining process produces white flour void of vitamin B₆, folic acid, calcium, magnesium, manganese, copper, and zinc. These minerals all have roles in the health of bones although deficiencies have not been clearly implicated in the development of osteoporosis in humans.

Caffeine

Caffeine consumption may have an effect on calcium loss and bone density. Some studies have shown an increase in calcium excretion in the urine after ingestion of caffeine.^2-4 However, this has not been proved to be consistent in other research. In a study by Lloyd et al,⁵ data were collected in 138 women at two points separated by 2 years. Analyses indicated no association between dietary caffeine intake and total-body or femoral-neck bone density or bone mass. Furthermore, no associations were found between caffeine consumption and longitudinal changes in total-body or femoral-neck bone measurements.⁵

Alcohol

The influence of alcohol consumption on bone density and fractures is confusing. Several studies have shown that chronic alcoholism leads to osteopenia and an increased incidence of skeletal fractures.^6-8 However, the causal mechanism is unclear. Alcohol may have a direct effect on bone cells, plus an indirect effect through mineral regulatory hormones. The effect of alcohol consumption on bone resorption still has not been clearly established. While some studies show higher rates of bone resorption in moderate and heavy drinkers,⁹ others have found no effect.¹⁰ And in a recent 2000 study, moderate alcohol intake (more than 28.6 g/wk) has been associated with higher bone mineral density in postmenopausal women.¹¹ This may be due to a combination of lower parathyroid hormone concentrations and higher serum estradiol levels. Nonetheless, alcohol consumption beyond seven drinks a week is a known risk factor for osteoporosis.¹²

Protein and Phosphorus

Several other dietary factors can influence calcium balance. For example, excessive dietary protein may promote bone loss. In particular, animal protein causes an increase in urinary excretion of calcium, as calcium is mobilized from the bone to buffer the acidic protein breakdown products. In addition, the amino acid methionine is converted to homocysteine, which can also cause bone loss. Also, many high-protein foods contain large amounts of phosphorus, high concentrations of which mobilize calcium from the bones to maintain serum homeostasis. Therefore, high-phosphorus beverages like soft drinks are also implicated in osteoporosis development. A study in children showed that soft drinks can have a significant impact on calcium levels. Fifty-seven children with low serum calcium levels were compared with 171 children who had normal calcium levels.¹³ Of the 57 test subjects, 66.7% drank more than four 12- to 16-oz bottles of soft drinks per week. Only 28% of the 171 control subjects consumed that many soft drinks per week. In all 228 children, there was a strong correlation between the serum calcium level and the amount of soft drinks consumed each week. The more soft drinks consumed, the lower the blood calcium level. High-sodium diets can also cause an increase in urinary excretion of calcium in some individuals.¹⁴

Soy

Growing attention has been focused on soy foods for their potentially positive impact on bone health. Soybeans contain phytoestrogenic isoflavones. The main isoflavone in soy, daidzein, is similar in composition to the compound ipriflavone; this is a semisynthetic version of the isoflavone daidzein, which is used in Europe to treat osteoporosis, and is available over the counter in the United States as a dietary supplement. Soy is the only dietary source of daidzein, which is a nonsteroidal estrogen-like molecule, but is not estrogen. A diet high in soy products can lengthen the menstrual cycle by 1 to 5 days, especially the follicular phase. This may have a positive effect on bone density due to longer exposure to elevated estrogen levels.

Soy appears to have an estogenic effect on bone in some experimental evaluations. The bone density of ovariectomized rats was evaluated when soy was used to replace casein in the diet, compared with rats that received estrogen. The addition of soy inhibited bone loss, although not to the same extent achieved with estrogen.¹⁵ Another study of ovariectomized rats reported a positive effect of the soy phytoestrogen genistein in maintaining bone density.¹⁶ These authors also reported that genistein suppressed the osteoclast activity, both in vitro and in vivo.

Several human studies have provided further insight into the beneficial role of soy in promoting bone health. Research conducted at the University of Illinois found that menopausal women had an increase in bone mineral levels and density in the lumbar spine after taking 55 to 90 mg/d of isoflavones for 6 months.¹⁷ 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. Notably, the diet containing soy proteins was effective in preventing bone loss in the fourth lumbar vertebra and, to a lesser extent, in the right hip as well. Soy protein seems to have more of an effect on trabecular bone, which is more prominent in the spine, than on cortical bone, which is more prominent in the hip. Although soy protein did not prevent bone loss to the same degree as estrogen, the positive effect was undeniable.

Research on the relation between soy isoflavone intake and bone mineral density was conducted in the Study of Women’s Health Across the Nation, a US cohort study of women aged 42 to 52 years.¹⁸ For white and black women, median intakes of genistein were too low to analyze. In Chinese American women, no association between genistein and bone mineral density was found. Japanese American women who were premenopausal (but not perimenopausal) had a higher soy isoflavone intake than the other groups, and were also found to have a higher bone density of the spine and femoral neck—7.7% and 12% greater than that of the lowest group, respectively.

Soy products are also a good source of calcium. A diet that includes high amounts of soy can provide meaningful amounts of calcium, and some soy foods contain as much or more calcium than a serving of dairy products (Table).

View this table

Table. Content of Calcium in Dietary Soy Products

NUTRITIONAL SUPPLEMENTATION

Calcium

In postmenopausal women, calcium supplementation has been shown to decrease bone loss by as much as 50% at nonvertebral sites. The effects were greatest in women whose baseline calcium intake was low, in older women, and in women with established osteoporosis.¹⁹ In a study by Elders et al,²⁰ a significant decrease in vertebral bone loss was observed with supplementation of 1,000 to 2,000 mg/d of calcium. After 1 year of this regimen, however, this benefit was lost.

Although dietary calcium is essential throughout a woman’s life, it is not effective in preventing the accelerated bone loss associated with menopause. Ten years postmenopausally, calcium supplementation again becomes effective in reducing age-related bone loss.²¹

Calcium salts differ in their actual calcium content. Calcium carbonate contains 40% of calcium in elemental forms; calcium citrate, 24%; tribasic calcium phosphate, 39%; calcium lactate, 13%; and calcium gluconate, 9%. Some studies demonstrate that calcium citrate is generally thought to be more bioavailable than calcium carbonate and more beneficial at the bone level.²² However, most of the comparison studies were performed in individuals who were fasting, and calcium citrate is better absorbed in a fasting state than is calcium carbonate. Hydrochloric acid is secreted in the stomach during eating, and under those circumstances, when taken with meals, there appears to be no difference between the absorption of calcium carbonate and calcium citrate.²³

Nonetheless, this point may be important in older patients, as hydrochloric acid production decreases with age, making calcium citrate a more appropriate form of supplementation. Also, women who take calcium at bedtime on an empty stomach may benefit from calcium citrate. It is unclear whether calcium citrate is preferable to calcium carbonate for those on antacids and proton pump inhibitors.

Vitamin D

Vitamin D enhances intestinal calcium absorption, thereby contributing to a favorable calcium balance in the system. Increased calcium absorption also reduces parathyroid hormone-mediated bone resorption. In the United States, most infants and young children have adequate vitamin D consumption from fortified milk. During adolescence, however, the consumption of dairy products drops off, and inadequate vitamin D intake is more likely to adversely affect calcium absorption.

In general, calcium intake alone may have only a slight protective effect on bone mass and fracture risk, although a recent study in people aged 65 years or older showed that both calcium and vitamin D consumption can significantly reduce the incidence of nonvertebral fractures.²⁴ Another study of postmenopausal women undergoing hip replacement surgery showed that women with hip fractures were more likely to have a vitamin D deficiency than those undergoing elective joint replacement.²⁵ The most unique calcium/vitamin D study demonstrated that in elderly women (mean age, 85.3 years) who lived in a geriatric facility, those who were given calcium, 1,200 mg/d, plus vitamin D, 800 IU/d, had a 49% reduction in the incidence of falls compared with calcium alone.²⁶

Magnesium

Magnesium deficiency has been shown to be related to osteoporosis. Magnesium status appears to have a major influence on the type of calcium crystals present in bone, such that a magnesium deficiency is associated with abnormal bone calcification.²⁷ Some women with reduced bone mineral density do not have an increased fracture rate because they have excellent structural calcification, due in part to high levels of magnesium. It has been demonstrated that women who were given dietary counseling, hormone therapy, 500 mg/d of calcium citrate, and 600 mg/d magnesium oxide had an 11% increase in bone density versus an average increase of 0.7% in women receiving dietary advice and hormones but no supplementation.²⁸

Trace Minerals

Most of the studies on the role of trace minerals in bone metabolism—particularly copper, manganese, and zinc—have been conducted in animals. A few prospective human studies in postmenopausal women on dietary intake and serum levels have begun to shed some light on the possible importance of trace minerals for bone density in women.²⁹

Manganese.—A deficiency of manganese may be one of the more important nutritional factors related to osteoporosis. Manganese deficiency causes a reduction in calcium deposition in bone. Manganese also stimulates mucopolysaccharide production, which provides a framework for the calcification process.³⁰

Boron.—Boron supplementation reduces urinary excretion of calcium and magnesium and increases serum levels of 17ß-estradiol and testosterone.³¹ The benefits of boron supplementation for calcium, magnesium, and hormonal metabolism as reported in the literature would seem to favor its use to help prevent bone loss.

Zinc.—Zinc is essential for the formation of osteoblasts and osteoclasts, and it enhances the biochemical action of vitamin D. It is also necessary for the synthesis of various proteins found in bone. Low zinc levels have been confirmed in the serum and bone of elderly people with osteoporosis.³²

Copper.—A deficiency of copper is known to produce abnormal bone development in growing children, and may be a contributing cause of osteoporosis. In vitro studies have shown that copper supplementation inhibits bone resorption.^33,34

Silicon.—Silicon is concentrated at the calcification sites in growing bone, and therefore, may be involved in the early stages of bone calcification. In animals, silicon-deficient diets have produced abnormal skull development and growth retardation.


OTHER NUTRITIONAL FACTORS

Folic Acid

Folic acid is involved in the breakdown of homocysteine. The increased rate of bone loss seen in postmenopausal women may be due in part to heightened levels of homocysteine, which is a breakdown product of methionine. If homocysteine is not eliminated adequately, it has the potential to promote osteoporosis.³⁵ Postmenopausal women who take folic acid supplements show significant reductions in homocysteine levels.³⁵

Vitamin B₆

Vitamin B₆ also plays a role in homocysteine metabolism. In genetic homocystinuria, B₆ supplementation reverses the elevated levels of homocysteine. Animal studies have shown that vitamin B₆ deficiencies can prolong fracture healing time,³⁶ impair cartilage growth, cause defective bone formation,³⁷ and promote osteoporosis.³⁸ Vitamin B₆ may also influence progesterone production and exert a synergistic effect on estrogen-sensitive tissue.

Vitamin C

Vitamin C promotes the formation and crosslinking of some of the structural proteins in bone. Animal studies have shown that vitamin C deficiency can cause osteoporosis.³⁹ Indeed, it has been known for decades that scurvy, a disease caused by vitamin C deficiency, is also associated with abnormalities of bone.

Vitamin K

Vitamin K is required for the production of osteocalcin. Osteocalcin draws calcium to bone tissue, enabling calcium crystal formation. Osteocalcin provides the protein matrix for mineralization and is thought to act as a regulator of bone mineralization.⁴⁰ Vitamin K plays a key role in the formation, remodeling, and repair of bone by attracting the calcium to the site of this protein matrix.⁴¹ A low dietary intake of vitamin K seems to increase the risk of osteoporotic hip fractures in women, according to data from the Nurses’ Health Study.⁴²


CONCLUSION

Calcium and vitamin D intake are the most influential nutritional factors in preventing osteoporosis. The risk of osteoporosis can be reduced by increasing peak bone mass and minimizing subsequent bone loss. To maximize peak bone mass, even in the context of hereditary and nonmodifiable risk factors, proper nutrition, moderate exercise, and avoidance of smoking and excessive alcohol consumption should begin during childhood and adolescence, and continue throughout life. The physician must encourage dietary habits that promote bone health, and should consider nutritional supplementation that may favorably alter patients’ risk, optimize bone density, and reduce the risk of fractures later in life.

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