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: In healthy young adults, the 24-hour profile of plasma growth hormone (GH) levels consists of stable low levels abruptly interrupted by bursts of secretion. In normal women, daytime GH secretory pulses are frequent. However, in normal men, a sleep-onset-associated pulse is generally the major or even the only daily episode of active secretion. Extensive evidence indicates the existence of a consistent relationship between slow-wave (SW) sleep and increased GH secretion. There is a linear relationship between the amount of SW sleep (measured by either visual scoring or spectral analysis of the EEG) and the amount of concomitant GH secretion. During ageing, SW sleep and GH secretion decrease exponentially and with the same chronology. Pharmacological stimulation of SW sleep results in increased GH release, and compounds that increase SW sleep may therefore represent a novel class of GH secretagogues.Growth Hormone & IGF Research 05/2000; 10 Suppl B:S57-62. DOI:10.1016/S1096-6374(00)80011-8 · 1.33 Impact Factor