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Decreased Pituitary-Gonadal Secretion in Men with Obstructive Sleep Apnea

Endocrine Institute (R.L., A.A.), Haemek Medical Center, Afula 18101, Israel; Unit of Anatomy and Cell Biology (A.H., L.L.), Endocrine Laboratory, Rambam Medical Center, Haifa, Israel; and The Sleep Research Center (P.H., P.L.), Technion, Israel Institute of Technology, Haifa 32000, Israel

Address all correspondence and requests for reprints to: Prof. R. Luboshitzky, Endocrine Institute, Haemek Medical Center, Afula 18101, Israel. E-mail: . luboshitzky-r{at}clalit.org

Abstract

Decreased libido is frequently reported in male patients with obstructive sleep apnea (OSA). The decline in morning serum testosterone levels previously reported in these patients was within the normal adult male range and does not explain the frequent association of OSA and sexual dysfunction. We determined serum LH and testosterone levels every 20 min between 2200–0700 h with simultaneous sleep recordings in 10 men with sleep apnea and in 5 normal men free of any breathing disorder in sleep. The mean levels and area under the curve of LH and testosterone were significantly lower in OSA patients compared with controls [LH, 24.9 ± 10.2 IU/liter·h vs. 43.4 ± 9.5 (P < 0.005); testosterone, 67.2 ± 11.5 nmol/liter·h vs. 113.3 ± 26.8 (P < 0.003)]. Four of 10 patients had hypogonadal morning (0700 h) serum testosterone levels. Analysis of covariance (ANCOVA) revealed that the 2 groups differed significantly in the amount of LH and testosterone secreted at night independent of age or degree of obesity. After partialing out body mass index, there was a significant negative correlation between the amounts of LH and testosterone secreted at night and the respiratory distress index, but not with degree of hypoxia.

Our findings suggest that OSA in men is associated with dysfunction of the pituitary-gonadal axis. The relation between LH-testosterone profiles and the severity of OSA suggests that sleep fragmentation and, to a lesser extent, hypoxia in addition to the degree of obesity and aging may be responsible for the central suppression of testosterone in these patients.

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