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Stimulatory Effects of Stress on Gonadotropin Secretion in Estrogen-Treated Women¹

Departments of Medicine (J.J.P., P.U.F., R.S.G., S.L.W.) and Obstetrics and Gynecology (M.F.), Columbia University College of Physicians and Surgeons, New York, New York 10032

Address correspondence and requests for reprints to: Dr. Sharon L. Wardlaw, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032. E-mail: sw22{at}columbia.edu

Although stress is known to inhibit the hypothalamic-pituitary-gonadal axis, recent studies in the monkey show that, under certain conditions, in the presence of estrogen, stress may actually stimulate LH release. We investigated the effects of a mild inflammatory stress (2.0–3.0 ng/kg endotoxin) on LH release in five postmenopausal women with and without transdermal estradiol (E2, 0.1 mg) replacement. In another five E2-treated women, LH release was studied when the adrenal was stimulated directly by a 3-h ACTH infusion (Cortrosyn, 50 µg/h ). Mean E2 levels were less than 12 pg/mL in the unreplaced subjects and were 86 ± 10 pg/mL and 102 ± 18 pg/mL in the two groups of E2-replaced subjects. Blood was sampled every 15–20 min for 2 h before and for 7 h after endotoxin or ACTH injection. Mean cortisol and progesterone levels increased in all three groups over time (P < 0.001). In the women without E2 replacement, basal LH was 26.8 ± 5.3 mIU/mL and did not change significantly, over time, after endotoxin (P = 0.58). In the same women on E2, however, a significant increase in LH occurred after endotoxin (P = 0.02), from a mean hourly baseline of 15.3 ± 5.4 mIU/mL to a peak of 50.0 ± 25.2 mIU/mL. During the ACTH infusion, there was a significant stimulation of LH release in the E2-replaced subjects (P < 0.001), from a mean hourly baseline of 13.3 ± 3.0 mIU/mL to a peak of 44.1 ± 11.7 mIU/mL. In both groups, this increase occurred 2–4 h after the initial rise in progesterone and persisted to the end. We conclude that, in the presence of sufficient estrogen, activation of the hypothalamic-pituitary-adrenal axis leads to a stimulation of LH release. This is likely related to a rise in adrenal progesterone and its known stimulatory effect on LH release in the presence of E2. These studies provide a potential mechanism in the human by which an acute stress during the follicular phase of the menstrual cycle might lead to a premature LH surge and thereby interfere with follicular maturation and ovulation.

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