Higher Plasma IGF-1 Levels Are Associated With Increased Delta Sleep in Healthy Older Men
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.
Available from: Enrico Bellato
- "Patients with fibromyalgia often complain of sleep disorders  and these are probably involved in its pathogenesis . As revealed by electroencephalographic examinations, the fourth phase of sleep is the most disturbed and a direct consequence should be a deficit of GH and insulin-like growth factor 1 (IGF-1) [84, 85]. Given that these hormones are involved in muscle microtrauma repair, the healing of this tissue could be affected by sleep disturbances . "
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ABSTRACT: Fibromyalgia syndrome is mainly characterized by pain, fatigue, and sleep disruption. The etiology of fibromyalgia is still unclear: if central sensitization is considered to be the main mechanism involved, then many other factors, genetic, immunological, and hormonal, may play an important role. The diagnosis is typically clinical (there are no laboratory abnormalities) and the physician must concentrate on pain and on its features. Additional symptoms (e.g., Raynaud's phenomenon, irritable bowel disease, and heat and cold intolerance) can be associated with this condition. A careful differential diagnosis is mandatory: fibromyalgia is not a diagnosis of exclusion. Since 1990, diagnosis has been principally based on the two major diagnostic criteria defined by the ACR. Recently, new criteria have been proposed. The main goals of the treatment are to alleviate pain, increase restorative sleep, and improve physical function. A multidisciplinary approach is optimal. While most nonsteroidal anti-inflammatory drugs and opioids have limited benefit, an important role is played by antidepressants and neuromodulating antiepileptics: currently duloxetine (NNT for a 30% pain reduction 7.2), milnacipran (NNT 19), and pregabalin (NNT 8.6) are the only drugs approved by the US Food and Drug Administration for the treatment of fibromyalgia. In addition, nonpharmacological treatments should be associated with drug therapy.
Pain Research and Treatment 11/2012; 2012(6):426130. DOI:10.1155/2012/426130
Available from: James m Krueger
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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: The hypothalamic growth hormone (GH)-releasing hormone (GHRH) promotes non-rapid eye movement sleep (NREMS). Insulin-like growth factor-1 (IGF-1) acts as a negative feedback in the somatotropic axis inhibiting GHRH and stimulating somatostatin. To determine whether this feedback alters sleep, rats and rabbits were injected intracerebroventricularly (i.c.v.) with IGF-1 (5.0 and 0.25 microgram, respectively) and the sleep-wake activity was studied. Compared to baseline (i.c.v. injection of physiological saline), IGF-1 elicited prompt suppressions in both NREMS and rapid eye movement sleep (REMS) in postinjection hour 1 in rats and rabbits. The intensity of NREMS (characterized by the slow wave activity of the EEG by means of fast-Fourier analysis) was significantly enhanced 7 to 11 h postinjection in rats. Plasma GH concentrations were measured in 30-min samples after i.c.v. IGF-1 injection in rats and a significant suppression of GH secretion was observed 30 min postinjection. The simultaneous inhibition of the somatotropic axis and sleep raises the possibility that the sleep alterations also result from an IGF-1-induced suppression of GHRH. The late increases in NREMS intensity are attributed to metabolic actions of IGF-1 or to a release of GHRH from the IGF-1-induced inhibition.
Brain Research 03/1999; 818(2):267-74. DOI:10.1016/S0006-8993(98)01286-4 · 2.84 Impact Factor
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