High Serum Cortisol Levels in Exercise-Associated Amenorrhea
- JU-HONG DING, M.S., M.D.;
- CAROL B. SHECKTER, M.D.;
- BARBARA L. DRINKWATER, Ph.D.;
- MICHAEL R. SOULES, M.D.; and
- WILLIAM J. BREMNER, M.D., Ph.D.
Abstract
Objective: To determine whether basal Cortisol levels are elevated in exercise-associated amenorrhea.
Design: Survey, with hormone levels measured weekly for 1 month and patients followed clinically for 6 months.
Setting: Volunteers were recruited through media advertisements and fliers.
Participants: Ninety-two women were enrolled; 71 (77%) completed the study. Subjects were grouped by menstrual and activity histories reported by a self-administered questionnaire. After 6 months, final groups were assigned: amenorrhea athletes, 19; eumenorrheic athletes, 35; a transition group of amenorrheic athletes who had resumed menses after entering the study, 7; and normal cyclic nonathletes, 10.
Interventions: Four weekly resting blood samples (0800 to 1000 hours) were obtained and measured for Cortisol, estradiol, progesterone, and prolactin levels. Lumbar bone mineral density was measured by dual-photon densitometry.
Measurements and Main Results: Mean (±SE) Cortisol levels were higher in amenorrheic athletes (585±33 nmol/L) than in eumenorrheic athletes (411±14 nmol/L), transition athletes (378±33 nmol/L), or nonathletic women (397±30 nmol/L) (P <0.01). Of nine women with abnormally high Cortisol levels (greater than 579 nmol/L), eight were amenorrheic athletes, and one was a eumenorrheic athlete. Bone mineral density was lower in amenorrheic athletes than in the other three groups (P <0.01).
Conclusions: Increased glucocorticoid levels may be an etiologic factor in exercise-associated amenorrhea. High Cortisol levels could also contribute to decreased bone density. The failure of amenorrheic athletes with hypercortisolemia to regain menses within 6 months suggests that they are at risk for a prolonged acyclic state.
Article and Author Information
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▸From the Division of Endocrinology, Department of Medicine, and the Department of Obstetrics and Gynecology, University of Washington School of Medicine; Medical Service, Veterans Administration Medical Center; and Pacific Medical Center; Seattle, Washington.
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Grant support: in part by the National Institutes of Health grants P50-HD-12629 and R01 HD18967; Clinical Research Center Grant RR-37; the Veterans Administration and the National Dairy Board, Arlington, Virginia, and administered in cooperation with the National Dairy Council, Rosemont, Illinois; and a World Health Organization Research Training Grant.
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▸Requests for reprints should be addressed to Carol B. Sheckter, M.D.; Endocrinology Section (111), Veterans Administration Medical Center, 1660 S. Columbian Way; Seattle, WA 98108.
- © 1988 American College of Physicians
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