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How Do Oral Contraceptives Affect Bone’s Response to Exercise and Disuse and the Risk for Osteoporosis?

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How Do Oral Contraceptives Affect Bone’s Response to Exercise and Disuse and the Risk for Osteoporosis?

Anita Mantri, B.S.


Osteoporosis afflicts roughly 8 million American women (13). Exercise is often prescribed as a measure of preventing osteoporosis due to its ability to increase bone formation. This eventually increases bone mineral density thus providing a reserve of bone to protect against losses due to estrogen deficiency from menopause. According to CDC reports, from 2011-2013, roughly 26% of American women between the ages of 15 and 44 used oral contraceptives (OCs) as their primary form of birth control (2). 

While the effects of these medications on female reproduction have been examined extensively, less is known about the effects of OCs on other tissues. In particular, while estrogen is well-known to have protective effects on bone in postmenopausal women, the results of studies investigating the effects of the estrogen in OCs on bone in premenopausal women have been mixed (5-8, 12). In 2000, studies conducted by David Burr and Connie Weaver found that OC use was associated with blunting exercise-induced gains in bone (1, 11). This effect appears to be caused by OC-induced suppression of both bone formation and bone breakdown rates. 

While OC use may be thus be less desirable for bones in exercising women, their use during situations of skeletal disuse (e.g. injury, bed rest, spaceflight) may have beneficial effects on bone. OC-induced suppression of bone breakdown rates may lessen losses that normally occur when bones are not mechanically stimulated. Most rodent studies examining the effects of estrogen treatments on bone have assessed estrogen replacements’ effects on bone after menopause by using rats that have had their ovaries removed, making them estrogen-deficient (3, 4, 9, 10, 14). While valuable work, these studies do not provide appropriate models for the effects of estrogen on bone in ovary-intact, premenopausal women. 

Our study aims to further clarify the effect of OC use and mechanical loading on bone health in premenopausal women using a combination of estrogen treatment simulating OC use in rat models of exercise and disuse. The objectives of this study use a novel estrogen-treated rat model in which dietary estrogen treatment simulates OC use. We aim to combine simulated OC use with either exercise or disuse to determine the combined impact of OCs and mechanical loading on bone. Based on the suppressive effects OCs have on bone formation and breakdown rates, we hypothesize that simulated OC use will blunt the beneficial impact of exercise as well as blunt the detrimental effects of disuse on bone. This study will be critical in assessing how OC use may affect bone health and later osteoporosis risk in premenopausal women.

References

1. Burr D, Yoshikawa Y, Teegarden D, Lyle R, McCabe G, McCabe L, and Weaver C. Exercise and oral contraceptive use suppress the normal age-related increase in bone mass and strength of the femoral neck in women 18-31 years of age. Bone 27: 855-863, 2000.

2. Daniels K, Daugherty J, and Jones J. Current contraceptive status among women aged 15-14: United States, 2011-2013. National Health Statistics Reports 173: 1-15, 2015.

3. Danielsen C, Mosekilde L, and Svenstrup B. Cortical Bone Mass, Composition, and Mechanical Properties in Female Rats in Relation to Age, Long-Term Ovariectomy, and Estrogen Substitution. Calcif Tissue Int 52: 26-33, 1993.

4. Fonseca H, Moreira-Goncalves D, Vaz M, Fernandes M, Ferreira R, Amado F, Mota M, and Duarte J. Changes in proximal femur bone properties following ovariectomy and their association with resistance to fracture. J Bone Miner Metab 30: 281-292, 2012.

5. Gargano V, Massaro M, Morra I, Formisano C, Di Carlo C, and Nappi C. Effects of two low-dose combined oral contraceptives containing drospirenone on bone turnover and bone mineral density in young fertile women: a prospective controlled randomized study. Contraception 78: 10-15, 2008.

6. Pasco J, Kotowicz M, Henry M, Panahi S, Seeman E, and Nicholson G. Oral contraceptives and bone mineral density: A population-based study. Am J Obstet Gynecol 182: 265-269, 2000.

7. Prior J, Kirkland S, Joseph L, Kreiger N, Murray T, Hanley D, Adachi J, Vigna Y, Berger C, Blondeau L, Jackson S, and Tenenhouse A. Oral contraceptive use and bone mineral density in premenopausal women: cross-sectional, population-based data from the Canadian Multicentre Osteoporosis Study. CMAJ 165: 1023-1029, 2001.

8. Scholes D, Hubbard R, Ichikawa L, LaCroix A, Spangler L, Beasley J, Reed S, and Ott S. Oral contraceptive use and bone density change in adolescent and young adult women: a prospective study of age, hormone dose, and discontinuation. J Clin Endocrinol Metab 96: E1380-1387, 2011.

9. Sorensen M, Henriksen K, Schaller S, and Karsdal M. Biochemical markers in preclinical models of osteoporosis. Biomarkers 12: 266-286, 2007.

10. Tromp A, Bravenboer N, Tanck E, Oostlander A, Holzmann P, Kostense P, Roos J, Burger E, Huiskes R, and Lips P. Additional weight bearing during exercise and estrogen in the rat: the effect on bone mass, turnover, and structure. Calcif Tissue Int 79: 404-415, 2006.

11. Weaver C, Teegarden D, Lyle R, McCabe G, McCabe L, Proulx W, Kern M, Sedlock D, Anderson D, Hillberry B, Peacock M, and Johnston C. Impact of exercise on bone health and contraindication of oral contraceptive use in young women. Med Sci Sports Exerc 33: 873-880, 2001.

12. Wei S, Jones G, Thomson R, Dwyer T, and Venn A. Oral contraceptive use and bone mass in women aged 26-36 years. Osteoporos Int 22: 351-355, 2011.

13. Wright N, Looker A, Saag K, Curtis J, Delzell E, Randall S, and Dawson-Hughes B. The recent prevalence of osteoporosis and low bone mass in the United States based on bone mineral density at the femoral neck or lumbar spine. J Bone Miner Res 29: 2520-2526, 2014.

14. Yarrow J, McCoy S, Ferreira J, Pingel J, Conrad B, Wronski T, Williams A, Borst S, and Brown M. A rehabilitation exercise program induces severe bone mineral deficits in estrogen-deficient rats after extended disuse. Menopause 19: 1267-1276, 2012.

 

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