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Glucocorticoid Replacement Is Permissive for Rapid Eye Movement Sleep and Sleep Consolidation in Patients with Adrenal Insufficiency¹

Clinical Psychobiology Branch (D.G.B., T.A.W.), National Institute of Mental Health; and Laboratory of Developmental Neurobiology (T.C.F.) and Pediatric and Reproductive Endocrinology Branch (T.C.F., D.H., G.P.C.), National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892; Sleep Disorders Unit, Department of Neurology, Fundacion Jiménez Díaz (D.G.B., O.L.), 28040 Madrid, Spain; Research and Epidemiology Unit (J.J.G.) and Division of Endocrinology, Department of Medicine, Cedars-Sinai Research Institute-University of California School of Medicine (T.C.F.), Los Angeles, California 90048; and Division of Endocrinology, Department of Medicine, Charles R. Drew University of Medicine and Sciences-University of California School of Medicine (T.C.F.), Los Angeles, California 90059

Address all correspondence and requests for reprints to: Theodore C. Friedman, M.D., Ph.D., Division of Endocrinology, Charles R. Drew University of Medicine and Sciences, 1721 East 120th Street, Los Angeles, California 90059. E-mail: friedmant{at}hotmail.com

There is a well described temporal relation between hormonal secretion and sleep phase, with hormones of the hypothalamic-pituitary-adrenal (HPA) axis possibly playing a role in determining entry into and duration of different sleep stages. In this study sleep features were studied in primary Addison’s patients with undetectable levels of cortisol treated in a double blind, randomized, cross-over fashion with either hydrocortisone or placebo supplementation. We found that REM latency was significantly decreased in Addison’s patients when receiving hydrocortisone at bedtime, whereas REM sleep time was increased. There was a trend toward an increase in the percentage of time in REM sleep and the number of REM sleep episodes. Waking time after sleep onset was increased, whereas no differences were observed between the two conditions when total sleep time or specific non-REM sleep parameters were evaluated. Our results suggest that in Addison’s patients, cortisol plays a positive, permissive role in REM sleep regulation and may help to consolidate sleep. These effects may be mediated either directly by the central effects of glucocorticoids and/or indirectly through CRH and/or ACTH.

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