Preventing Osteoporosis in Menopause
Preventing Osteoporosis in Menopause
By Lennie Martin, RN, FNP, DPH
Maintaining bone health is a major concern for women entering midlife and menopause. In the United States and Canada more than 4,000 women complete the transition of menopause every day.1 Due to increased life expectancy, the average American woman will spend one-third of her life postmenopausal.2 After menopause, women have increased risk of osteoporosis, which can reduce function and quality of life and lead to disability and premature death. Today’s women seek natural approaches to preventing this disease.
Of the 28 million Americans with low bone mass, 80% are women.3 In the five to seven years following menopause, women can lose up to 20% of their bone mass. Annually, some 1.5 million fractures, primarily of the vertebra, hip, and wrist, are attributed to osteoporosis. White women 60 years and older have twice the incidence of fractures as black women. Once hip fractures occur, 15-25% of women who were living independently remain in long-term care, and women have 5-20% greater risk of dying within the first year than age cohorts.4 The cost of osteoporosis-related hospital and nursing home stays has been placed at $15 billion per year by the National Osteoporosis Foundation.5
Pathophysiology of Osteoporosis
Osteoporosis results from dysfunction in the skeletal repair process called bone remodeling. Normal activity causes fatigue cracks in bone architecture.6 If not repaired these small cracks can coalesce to become macroscopic fractures. In the repair process, precursor cells along the adjacent marrow and bone surface increase around the injury site, developing into osteoclasts that eradicate the debris and prepare the bone for formative activity of osteoblasts, which creates new bone cell matrix.7 This process takes about 120 days, mediated by chemicals that are influenced by parathyroid hormone, estrogen, and vitamin D.8 In osteoporosis, increased osteoclastic activity removes too much bone structure, while aberrant osteoblastic function fails to form enough new bone.8 Eventually this results in reduced density in the bone matrix, causing structural deficiency and susceptibility to fractures.
After menopause, accelerated bone loss occurs mainly in trabecular bone (vertebral bones), which is believed to be associated with a decline in endogenous estrogens. Fractures develop earlier in trabecular bone than in cortical bone, because of greater biological activity and stresses on vertebral bones.9 Enhanced osteoclastic activity appears to be the major cause. Osteoporosis of aging, affecting both men and women, is thought to be caused by decreased osteoblastic activity. This mainly affects cortical bone, especially the hips and pelvis. Elevated parathyroid hormone levels, altered vitamin D metabolism, and poor calcium absorption are associated with this type of osteoporosis.9
Self-Care Approaches for Preventing Osteoporosis
About 20-25% of menopausal women in the United States are at risk for osteoporosis, with an estimated lifetime risk of 50%.4 Many risk factors for osteoporosis (see Table 1) are modifiable through nutrition and lifestyle. Since very little bone accrues after the post-pubertal growth spurt, it is important to encourage these practices early. A high-peak bone mass provides protection against osteoporosis to women as they age.
Table 1-Risk factors for osteoporosis | |
Genetics: | Family history of osteoporosis, Caucasian or Asian descent |
Menstrual history: | Late puberty, amenorrhea, early menopause |
Constitution: | Small-boned frame, low body weight |
Lifestyle: | Physical inactivity, low calcium intake, cigarette smoking, excessive intake of alcohol, caffeine, salt, and protein |
Health issues: | Glucocorticoid use, hypothyroidism, diabetes, anorexia/bulimia |
Calcium. The daily calcium requirement for women is 1,000-1,500 mg. The average American diet supplies about 500 mg of calcium daily.4 (See Table 2.) Inadequate calcium intake forces parathyroid hormone and vitamin D to increase bone resorption. Calcium and bone mass studies have demonstrated that supplementing 1,000 mg calcium daily improves bone mass in postmenopausal women.10 Calcium supplements provide differing amounts of elemental calcium: calcium carbonate 40%, tricalcium phosphate 39%, calcium citrate 21%, calcium lactate 13%, and calcium gluconate 9%. Calcium citrate may be preferred for those with digestive problems, as it has high bioavailability. Decreased ability to absorb calcium, often a consequence of aging, increases risk of hip fractures with greatest risk among women who have lower absorption and intake.11 To maximize absorption, calcium supplements should be taken with meals.
Table 2-Dietary sources of calcium | |
Food | Calcium Content |
Plain yogurt, 2%, 1 cup | 415 mg |
Rhubarb, 1 cup | 38 mg |
Milk, skim, 1 cup | 32 mg |
Mozzarella cheese, 1 oz | 27 mg |
Canned salmon, with bones, 3 oz | 181 mg |
Collard/mustard greens, ½ cup | 179 mg |
Cottage cheese, 2%, 1 cup | 155 mg |
Tofu, ½ cup | 130 mg |
Broccoli, cooked, ½ cup | 89 mg |
Soybeans, cooked, ½ cup | 88 mg |
Source:Foundation for Osteoporosis Research and Education. Available at: http://www.FORE.org. Accessed on March 20, 2000. |
Vitamin D. Adding vitamin D and trace minerals improves the effects of calcium on bone density and reduces fracture risk.11 Regular sun exposure for 15-20 min/d usually provides adequate production of vitamin D; otherwise, a supplement of 400 IU should be taken daily.4 Prolonged intake of high doses of vitamin D can lead to hypercalcemia, evidenced by fatigue, muscle weakness, depression, anorexia, nausea, and constipation. Excessive supplementation may increase production of the active metabolite calcitriol or the precursor 25-hydroxyvitamin D, which alters intestinal absorption and mobilizes calcium from bone.12 This "negative calcium balance" actually removes calcium from bone, therefore contributing to osteoporosis. Vitamin D becomes toxic only in relatively large amounts (2,000-50,000 IU daily) over long periods of time.
Other Nutrients. Vitamin C, magnesium, vitamin B6, vitamin B12, boron, manganese, zinc, and folic acid help maintain healthy bone dynamics.13,14 Adequate protein is needed (90 g in an 1,800 calorie diet), but excessive protein intake results in chronic acid load, which must be buffered by drawing calcium from the skeleton. Too much protein can cause hypercalciuria and a negative calcium balance,15 and can reduce bone mineral density.16
Isoflavones. Bioflavonoids are a large family of plant compounds that have estrogenic activity, contributing to healthy lipid profiles, decreased bone turnover, and calcitonin secretion.17 Isoflavones are found mainly in one subfamily of legumes. The principle isoflavones in soy are genistein, daidzein, and metabolites. Soy isoflavones enhance bone density in rat models,18 and diets high in soy appear to protect women against osteoporosis.17
Ipriflavone (IP), synthesized from daidzein, has been examined in more than 60 human studies. IP was found to be effective for inhibiting bone resorption and enhancing bone formation, resulting in increased bone density and decreased fracture rates in osteoporotic women.19 It lacks direct estrogenic effect, interacting instead with unique binding sites in preosteoclastic cells.20 This selective effect on bone rather than reproductive tissue makes it behave similarly to selective estrogen receptor modulators, such as raloxifene, but without the potential harmful effects of these drugs.21 Ipriflavone does appear to potentiate estrogen’s effect.
Clinical trials of IP vs. placebo have found slightly increased or stable bone mineral density (BMD) in IP groups while placebo groups had decline in BMD.22,23 IP appears particularly effective in older women (over age 65), resulting in 6% increase in BMD after one year,24 and decrease in fracture rates.25 The usual dosage of IP is 600 mg/d, which appears safe and well tolerated. Minor side effects include GI upset, skin rashes, headaches, and drowsiness.19
Essential Fatty Acids (EFAs). EFAs such as omega-3 and omega-6 help maintain bone health by enhancing synthesis of bone collagen and increasing calcium absorption from the gut, leading to reduced urinary excretion of calcium and increased calcium deposition in bone. In osteoporosis of the elderly, loss of bone calcium is associated with ectopic calcification, especially of the arteries and kidneys. Ectopic calcification may be much more dangerous than osteoporosis itself, since the majority of deaths in women with osteoporosis are from vascular causes, and not directly due to fractures.26 Supplementing with EFAs increases bone density in the lumbar spine and hip with reduced risk of fracture, compared to bone density declines in placebo group.27
Exercise. Physical activity that exerts moderate stress on bones, such as walking, jogging, and racquet sports, can help prevent osteoporosis. Walking 1½ miles or exercising for one hour three times a week can retain bone mass.28 Lumbar spine bone density increased in older postmenopausal women participating in a nine-month weight-bearing exercise program.29 Other studies have shown that exercise increases calcium retention, prevents bone loss, and retards osteoporosis.30
Lifestyle. Excessive alcohol, caffeine, and salt intake, as well as cigarette smoking, has adverse effects on bone health and can promote osteoporosis. Alcohol directly impedes osteoblastic function,31 and may increase osteoclastic activity and bone loss.32 Caffeine in excess increases urinary calcium excretion and ultimately drains off skeletal calcium.33 One to two cups of coffee daily is thought to be safe,34 but drinking a liter (34 oz) daily causes excessive calcium loss. High dietary salt intake has been shown to increase urinary calcium excretion and lead to bone loss in rats.35 Cigarette smoking increases the metabolism of sex hormones and decreases dietary calcium absorption.36
Conclusion
While previous generations often suffered in silence, today’s women actively seek self-care solutions during the menopause transition. These women want a partner in their health care provider to help them understand their options, the risks and benefits, and the wide range of alternatives for their unique situation.
Dr. Martin is Emeritus Professor of Nursing at Sonoma State University and has a women’s health practice at Sierra Family Medical Clinic in Nevada City, CA.
References
1. North American Menopause Society. Available at: http//www.menopause.org. Accessed March 1, 2000.
2. Greendale GA, Judd HL. The menopause: Health implications and clinical management. J Am Geriatr Soc 1993;41:426-436.
3. National Osteoporosis Foundation. 1996 and 2015 osteoporosis prevalence figures: State-by-state report. Washington, DC; 1997.
4. Lindsay R, et al. Osteoporosis: What’s new in prevention and treatment. Patient Care 1996;30:24-53.
5. Ray NF, et al. Medical expenditures for the treatment of osteoporotic fractures in the Unites States in 1995: Report from the National Osteoporosis Foundation. J Bone Miner Res 1997;12:24-35.
6. Schaffler MB, et al. Aging and matrix microdamage accumulation in human compact bone. Bone 1995;17:521-525.
7. Burr DB, et al. Bone remodeling in response to in vivo fatigue microdamage. J Biomech 1985;18:189-200.
8. Riggs BL, et al. A unitary model for involutional osteoporosis: Estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men. J Bone Miner Res 1998;13:763-773.
9. Licata AA. Update on osteoporosis: Strategies for prevention and treatment. Women’s Health Prim Care 1999;2:229-244.
10. Dawson-Hughes B, et al. A controlled trial of the effect of calcium supplementation on bone density in post-menopausal women. N Engl J Med 1990;323:878-883.
11. Ensrud KE, et al. Low fractional calcium absorption increases the risk for hip fracture in women with low calcium intake. Study of Osteoporotic Fractures Research Group. Ann Intern Med 2000;132:345-353.
12. Schwartzman MS, Franck WA. Vitamin D toxicity complicating the treatment of senile, postmenopausal, and glucocorticoid-induced osteoporosis. Four case reports and a critical commentary on the use of vitamin D in these disorders. Am J Med 1987;82:224-230.
13. Weber P. The role of vitamins in the prevention of osteoporosis—a brief status report. Int J Vitam Res 1999;69:194-197.
14. Bunker VW. The role of nutrition in osteoporosis. Br J Biomed Sci 1994;51:228-240.
15. Licata AA, et al. Acute effects of dietary protein on calcium metabolism in patients with osteoporosis. J Geront 1981;36:14-19.
16. Tesar R, et al. Axial and peripheral bone density and nutrient intakes of postmenopausal vegetarian and omnivorous women. Am J Clin Nutr 1992;56:699-704.
17. Barnes S. Evolution of the health benefits of soy isoflavones. Proc Soc Exp Biol Med 1998;217:386-392.
18. Arjmandi BH, et al. Dietary soybean protein prevents bone loss in ovariectomized rat model of osteoporosis. J Nutr 1996;126:161-167.
19. Ohta H, et al. Effects of one-year ipriflavone treatment on lumbar bone mineral density and bone markers in postmenopausal women with low bone mass. Horm Res 1999;51:178-183.
20. Petilli M, et al. Interactions between ipriflavone and the estrogen receptor. Calcif Tissue Int 1995;56: 160-165.
21. Yamazaki I. Effect of ipriflavone on the response of uterus and thyroid to estrogen. Life Sci 1986;38: 757-764.
22. Adami S, et al. Ipriflavone prevents radial bone loss in postmenopausal women with low bone mass over two years. Osteoporos Int 1997;7:119-125.
23. Agnusdei D, et al. A double blind, placebo-controlled trial of ipriflavone for prevention of postmenopausal spinal bone loss. Calcif Tissue Int 1997;61:142-147.
24. Passeri M, et al. Effect of ipriflavone on bone mass in elderly osteoporotic women. Bone Miner 1992;19 (suppl 1):S57-S62.
25. Agnusdei D, Bufalino L. Efficacy of ipriflavone in established osteoporosis and long-term safety. Calcif Tissue Int 1997;61:S23-S27.
26. Kruger MC, Horrobin DF. Calcium metabolism, osteoporosis and essential fatty acids: A review. Prog Lipid Res 1997;36:131-151.
27. Kruger MC, et al. Calcium, gamma-linolenic acid (GLA) and eicosapentaenoic acid (EPA) supplementation in osteoporosis. Osteoporos Int 1996;6 (suppl 1):250.
28. Krolner B, et al. Physical exercise as a prophylaxis against involutional vertebral bone loss: A controlled trial. Clin Sci (Colch) 1983;64:541-546.
29. Dalsky GP, et al. Weight bearing exercise training and lumbar bone mineral content in postmenopausal women. Ann Intern Med 1988;101:824-828.
30. Sinaki M. Exercise and osteoporosis. Arch Phys Med Rehabil 1989;70:220-229.
31. Diamond T, et al. Ethanol reduces bone formation and may cause osteoporosis. Am J Med 1989;86:282-288.
32. Kimble RB. Alcohol, cytokines, and estrogen in the control of bone remodeling. Alcohol Clin Exp Res 1997;21:285-391.
33. Hasling C, et al. Calcium metabolism in postmenopausal osteoporotic women is determined by dietary calcium and coffee intake. J Nutr 1992;122:1119-1126.
34. Barger-Lux MJ, et al. Effects of moderate caffeine intake on the calcium economy of premenopausal women. Am J Clin Nutr 1990;52:722-725.
35. Goulding A, Campbell DR. Effects of oral loads of sodium chloride on bone composition in growing rats consuming ample dietary calcium. Miner Electrolyte Metab 1984;10:58-62.
36. Krall EA, Dawson-Hughes B. Smoking and bone loss among postmenopausal women. J Bone Miner Res 1991;6:331-338.
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