Background: Sleep-disordered breathing (SDB), such as obstructive sleep apnea (OSA), is more common in men than in women. However, menopause increases the risk for development of OSA. Administration of estrogen and progesterone to postmenopausal women with OSA decreases apnea and hypopnea during sleep.
Objective: Because beneficial changes can be observed soon after administration of a short course of hormones, we hypothesized that suppression of these hormones would rapidly result in the development of SDB.
Methods: Production of sex hormones was suppressed with daily administration of leuprolide acetate (LA), a gonadotropin-releasing hormone analogue, for 5 weeks in women who were participating in a study on pharmacologically induced menopause and physiology. The subjects underwent polysomnographic evaluation at baseline and after 5 weeks of LA administration.
Results: In the 12 healthy women aged 18 to 34 years who participated in the study, sleep architecture and respiration were normal at baseline. After LA administration, the subjects stopped their menses, and their plasma concentrations of l7beta-estradiol (preadministration, mean [SD] 33.9 [9.0] pg/mL; post administration, 10.2 [3.4] pg/mL) and progesterone (preadministration, 0.48 [0.05] ng/mL; post administration, 0.40 [0.06] ng/mL) reached menopausal levels. Sex hormone deficiency was associated with climacteric vasomotor symptoms such as hot flashes and sweating. Sleep latencies and architecture did not change significantly with LA administration. The participants subjectively noticed some increased snoring that was not confirmed by polysomnogram. Specifically, there was no change in arousal index and no evidence for sleep fragmentation to suggest the presence of increased upper-airway resistance during sleep. The apnea-hypopnea index, 0.07 (0.02) to 0.22 (0.11) events per hour of sleep, did not change with sex hormone deficiency.
Conclusions: In this study, sex hormone deficiency in young women resulted in climacteric symptoms and cessation of menses, and was not associated with sleep fragmentation or clinically significant SDB.