Sleep Deprivation Reduces Circulating Androgens in Healthy Men

Cortés-Gallegos, V.; G, Castañeda; Alonso, R; Sojo, Isaura; Carranco, Armando; Cervantes, C. Escobar; Parra, Adalberto

doi:10.3109/01485018308990167

Cited by 34 publications

(22 citation statements)

References 19 publications

(11 reference statements)

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“…For this reason, the students being tested had free access to meals, fluids, and tobacco. In the present limited series, the data show a reduction in the main circulating androgens as well as that of E, during the first 24-h period in association with acute sleep deprivation; no significant change occurred in the blood concentrations of C or of the pituitary hormones as previously reported [7]. As the period of observation continued to 48 h of restricted sleep, T, A, and DHT tended to return to baseline values; C, FSH, and LH concentrations did not vary significantly as compared to initial estimates of these hormones.…”

Section: Discussionsupporting

confidence: 65%

“…The 24-h periodicity, our most important social time unit, exhibits the well-known behavioral state of sleep, and various physiological as well as clinical aspects of sleep rhythm and sleep disorders have demonstrated a link with the endocrine system [20][21][22]271. A 24-h restless period in a group of healthy men was shown to diminish circulating androgens [7]. This acute form of sleep prevention might be compared to the most common sleep disorder-insomnia.…”

Section: Introductionmentioning

confidence: 99%

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Sleep Deprivation and Adaptive Hormonal Responses of Healthy Men

et al. 1989

Archives of Andrology

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To study the effects of sleep deprivation on the pituitary-testis axis physiology, we measured the circulating levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), testosterone (T), androstanedione (A), dihydrotestosterone (DHT), estradiol (E,), and cortisol (C) in eight healthy men as follows: phase I (control), phase II (24-h restless period), phase JII (48-h restless period), and phase N (24-h recovery period). All samples were taken at 8:OO a.m. There was a significant decrease of T, A, DHT, and E, in phase II but no decrease in FHS, LH, PRL, or C. In phase I11 there was no further decrease in any androgen, although E, decreased along with the increase of PRL. In phase N E, and PRL tended to return to baseline values, and the androgens were very similar to the controls. FHS, LH, and C showed no change under the effects of phase III. These data extend the adaptive androgenic response and the association of the role of E, and PRL to restricted or disturbed sleep in men.

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Section: Discussionsupporting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Sleep Deprivation and Adaptive Hormonal Responses of Healthy Men

et al. 1989

Archives of Andrology

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“…This unexpected discrepancy between the cross-sectional and longitudinal studies could be due to differences in the subject selection procedures for the two studies or the influence of other aspects of sleep staging and quality not measured in this study. For example, in the cross-sectional study men with minimal sleep apnea may have had greater first night sleep disturbance than the chronically somnolent patients with more severe sleep apnea (35). Similarly, despite identifying men with snoring and/or apnea in the larger cross-sectional study, we were unable to distinguish between mixed central and obstructive apnea patterns, and these two variants, although sharing many common pathophysiological and clinical features (36), may result in different androgen responses.…”

Section: Discussionmentioning

confidence: 97%

Neuroendocrine Dysfunction in Sleep Apnea: Reversal by Continuous Positive Airways Pressure Therapy*

Grunstein

Handelsman

Lawrence

et al. 1989

The Journal of Clinical Endocrinology & Metabolism

286

211

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We studied the effects of sleep apnea on neuroendocrine function in a cross-sectional study of 225 consecutive men undergoing sleep studies and in a longitudinal study of 43 men with severe obstructive sleep apnea before and after 3 months of successful treatment with nasal continuous positive airways pressure to eliminate upper airways obstruction. Blood samples were collected at 0600-0630 h on awakening for measurement of plasma insulin-like growth factor I (IGF-I), total and free testosterone, sex hormone-binding globulin (SHBG), LH, FSH, PRL, T4, T4-binding globulin, and cortisol. The plasma hormone levels were analyzed in relation to the severity of sleep apnea, as indicated by the desaturation index (the hourly rate of episodes of arterial oxygen desaturation greater than 4% of the stable baseline) and the mean minimal oxygen saturation during the desaturation episodes. In the cross-sectional study plasma IGF-I, free and total testosterone, and SHBG levels were significantly lower in relation to the severity of sleep apnea, whereas plasma LH, FSH, PRL, T4, T4-binding globulin, and cortisol were not. The decreases in plasma IGF-I and total and free testosterone were independent of the effects of aging and adiposity by covariance analysis. In the longitudinal study plasma IGF-I, total testosterone, and SHBG, but not free testosterone, significantly increased after 3 months of nasal continuous positive airways pressure treatment. We conclude that sleep apnea causes reversible neuroendocrine dysfunction in men, which is manifested by decreased plasma. IGF-I, testosterone, and SHBG levels. This neuroendocrine dysfunction is related to the severity of the sleep apnea, as indicated by the nadir levels of arterial oxygen desaturation and the rate of desaturation episodes. These hormonal measurements may provide biochemical markers for both the severity of sleep apnea and its response to therapeutic intervention. In addition, sleep apnea may be a previously unrecognized confounder of the neuroendocrine correlates of aging.

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“…68 Serum testosterone decreased during a 5-day training course involving sleep loss, hard physical work, and caloric deficiency.1, Testosterone decreased to below 25% of precourse levels after 48 hours of sleep loss. This decrease reflected reduced production of testosterone, not increased metabolism.…”

Section: 250mentioning

confidence: 98%