Higher plasma IGF-1 levels are associated with increased delta sleep in healthy older men.
ABSTRACT Sleep quality declines with age, with less time in deep or slow wave sleep (SWS) and reduced amplitude of the delta waves that characterize it. Age-related declines also occur in lean body mass, growth hormone (GH), and insulin-like growth factor 1 (IGF-1). These changes in sleep quality and anabolic status may be related, as administration of GH or growth hormone releasing hormone (GHRH) can enhance SWS and decrease awakenings in young men. Here we examine the relationship between plasma IGF levels and delta sleep quality in older men.
The sleep EEG of 30 healthy elderly men (64 +/- 6 yrs; range 50-75) was recorded on the second of 2 consecutive nights. Plasma samples were drawn within 3 weeks of EEG recording, and IGF levels were assayed by RIA after acid extraction.
IGF explained 28% (semi-partial correlation coefficient r = .53; p = .003) of the variance in average delta energy per epoch of SWS, after age-related variance was removed. Higher IGF was associated with higher average delta energy. Similar results were obtained for total delta energy during SWS (r = .37, p = .04) 4nd time spent in SWS (r = .42, p = .02). Other measures of sleep quality (e.g., wakefulness, REM sleep) were not correlated with IGF. The IGF delta relationship was minimally influenced by moderator variables such as thyroxine (T3, T4), and/or body mass index (BMI).
We conclude that age-adjusted IGF levels in healthy senior men co-vary significantly with SWS and the delta energy that characterizes it.
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ABSTRACT: Changes in sleep were studied during 6 hours after intracerebroventricular (ICV) administration of Insulin-like growth factor-1 (IGF-1) or the structurally related insulin. IGF-1 was injected either at dark onset (0.05 or 0.5 microgram) or 6 hours after light onset (0.05, 0.5, or 5.0 microgram). The small dose of IGF-1 consistently, albeit modestly, enhanced NREMS over the 6 hour postinjection period in both the dark and the light cycles (REMS increased only at night). The NREMS-promoting activity vanished when the dose was increased to 0.5 microgram, and 5.0 microgram IGF-1 elicited a marked and prompt suppression in NREMS. Heat-inactivated IGF-1 (0.05 microgram) did not alter sleep. On a molar base, the NREMS-promoting dose of insulin was higher than that of IGF-1. Late (hours 7-17 postinjection) enhancements in EEG slow wave activity during NREMS were observed after 5.0 microgram IGF-1. The results indicate that IGF-1 can promote NREMS and may contribute to the mediation of the effects of GH on sleep. The acute sleep-suppressive activity of the high dose of IGF-1 is attributed to an inhibition of endogenous growth hormone-releasing hormone (GHRH).Sleep research online: SRO 02/1998; 1(2):87-91.
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ABSTRACT: When alcohol is a large proportion of daily nutrient energy, the network of signals for energy homeostasis appears to adapt with abnormal patterns of sleep and growth hormone (GH) release along with gradual acquisition of an addictive physical dependency on alcohol. Early relapse during treatment of alcoholism is associated with a lower GH response to challenge, perhaps reflecting an altered balance of somatostatin (SS) to somatropin releasing hormone (GHRH) that also affects slow wave sleep (SWS) in dependent patients. Normal patterns of sleep have progressively shorter SWS episodes and longer rapid eye movement (REM) episodes during the overall sleep period, but the early sleep cycles of alcoholics have truncated or non-existent SWS episodes, and the longer REM episodes occur in early cycles. During SWS delta wave activity, the hypothalamus releases GHRH, which causes the pituitary to release GH. Alcohol-dependent patients have lower levels of SWS power and GH release than normal subjects, and efforts to understand the molecular basis for this maladaptation and its relation to continued alcohol dependence merit encouragement. More needs to be learned about the possibility of decreasing alcohol dependency by increasing SWS or enhancing GHRH action.Alcohol 06/1999; 18(2-3):109-22. DOI:10.1016/S0741-8329(98)00073-1 · 2.04 Impact Factor
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ABSTRACT: We observed the new onset of severe obstructive sleep apnoea syndrome (OSAS) in an adult male patient during human growth hormone (hGH) replacement therapy. This prompted us to evaluate the potential influence of hGH substitution therapy on sleep in middle-aged men. A longitudinal study. Five male patients (aged 44-56 years, median age 54 years) with postoperative pituitary insufficiency given hGH replacement therapy for 1-2 years (median dose 2.0 U/day; median IGF-I serum concentration 351 microg/l) and 6 months after cessation of hGH treatment (median IGF-I level 77 microg/l - 1 microg/l = 0.131 nmol/l). Polysomnographic studies were performed, and the following parameters were determined: time in bed (TIB), sleep period time (SPT), total sleep time (TST), sleep efficiency (SE = TST/TIB), sleep stage 1 onset latency (SL), different sleep stages [W (wake), S1, S2, SWS (slow wave sleep = S3 + S4) and REM; % of SPT], stage shifts per hour of SPT (SS/h), stage shifts to W/h of SPT [A/h (awakening)], index of apnoea and hypopnoea events per hour of TST (AH/h), arousals from apnoea and hypopnoea per hour of TST (Ar/h), index of obstructive (OAH/h), central (CAH/h) and mixed (MAH/h) events of apnoea and hypopnoea per hour of TST and minimal desaturation (MD). Median baseline results were: TIB, 479 min; SPT, 465 min; TST, 405 min; SE, 77%; SL, 8.5 min; W, 18.9%; S1, 8.2%; S2, 52.7%; REM, 13.5%; SS/h, 17.7; A/h, 2.8; AH/h, 11.9; Ar/h, 4.4; MD, 80%. These parameters did not change significantly after cessation of hGH treatment. In contrast, median SWS decreased significantly from 33 min (7.1%) to 7.5 min (1.8%; P = 0.03). Median OAH/h decreased significantly from 4.4 to 0.1 (P = 0.03) whereas CAH/h increased from 6.3 to 14.6 (P = 0.03) after cessation of hGH. Correspondingly, one patient with OSAS improved markedly whereas another patient developed new and asymptomatic central SAS after cessation of hGH. This study showed that hGH replacement therapy influenced sleep reaction in a complex way in middle-aged men; cessation of treatment was associated with a significant decrease in slow wave sleep and a shift from obstructive to central apnoea and hypopnoea.Clinical Endocrinology 07/2002; 56(6):805-10. DOI:10.1046/j.1365-2265.2002.01531.x · 3.35 Impact Factor