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Adrenal insufficiency and insomnia
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James Offline
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Adrenal insufficiency and insomnia
It has been hypothesized that adrenal insufficiency can lead to insomnia through several mechanisms. First that during the early stages of adrenal suppression that elevate cortisol leads to the insomnia since cortisol promotes alertness. And that during severe adrenal dysfunction low cortisol levels during sleep lead to a hypoglycemic reaction leading to a release of epinephrine. Epinephrine being stimulatory would thus wake a person and keep them awake. The cortisol claims though are up to debate.

Some researchers claim that it is high cortisol that keeps us awake at night since it is part of the fight or flight response and helps to keep us alert.


http://jcem.endojournals.org/cgi/content.../86/8/3787

"We conclude that insomnia is associated with an overall increase of ACTH and cortisol secretion, which, however, retains a normal circadian pattern. These findings are consistent with a disorder of central nervous system hyperarousal rather than one of sleep loss, which is usually associated with no change or decrease in cortisol secretion or a circadian disturbance."



On the other hand this study shows no change in cortisol in insomniacs, but rather a drop in melatonin:

http://linkinghub.elsevier.com/retrieve/...8102002494

"Ten drug-free patients (4 males, 6 females) with primary insomnia (mean age±S.D.: 39.2±9.1 years) and 10 age- and gender-matched healthy controls participated in the study. All subjects spent three consecutive nights in the sleep laboratory with polysomnography. Measurement of cortisol and melatonin (from 19:00 h to 09:00 h) was performed prior to and during the last laboratory night. Contrary to expectation, cortisol secretion did not differ between healthy controls and insomniac patients. On the other hand, nocturnal melatonin production was significantly diminished in insomniac patients. Polysomnographically determined sleep patterns, in contrast to subjective ratings of sleep, demonstrated only minor alterations of sleep in the insomniac group. The lack of increased cortisol secretion in the patients with primary insomnia indicates that results from studies on the biological consequences of experimental sleep loss in healthy subjects cannot be applied to primary insomnia in general, especially if there are only minor objective sleep alterations. In spite of the negligible objective sleep disturbances in the present sample, nocturnal melatonin production was reduced, which tentatively suggests a role for this hormone in primary insomniacs."



Here are some more studies on the subject:

http://cat.inist.fr/?aModele=afficheN&cpsidt=17328957

"In adults, the melatonin onset typically occurs during low cortisol secretion. Administration of exogenous melatonin around dusk will shift the phase of the human circadian clock to earlier hours (advance phase shift) leading to phase advances in circadian rhythms (e.g., sleep, endogenous melatonin, cortisol). With aging, the production of melatonin declines and is shifted to later hours while the production of cortisol increases and its peak occurs earlier in the night. In a randomized placebo-controlled crossover study with 8 patients with insomnia aged 55 years and older, a group characterized by low and delayed melatonin production, administration of prolonged-release melatonin in the evening was able to rectify the early onset cortisol production. This delay in nocturnal cortisol onset may explain in part the improvement in sleep quality in elderly patients with insomnia, in schizophrenics, and in depressed patients."



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2128619/

"In the past, few studies have assessed cortisol levels in insomniacs and their results were inconsistent. The majority of these studies reported no difference between “poor” sleepers and normal individuals in the levels of 24-h cortisol and 17-hydorxysteroid excretion.[58]"

"In a following controlled study 24-h serial ACTH and cortisol levels were significantly higher in insomniacs compared to normal sleepers.[31][figure 3] Within the 24-h period the greatest elevations were observed in the evening and during the first half of the night. Furthermore, within the group of insomniacs, the sub-group with high degree of objective sleep disturbance [percent of total sleep time (%TST) <70] had higher amount of cortisol compared to the subgroup with low degree of sleep disturbance.[figure 4] Finally, pulsatile analysis revealed a significantly higher number of ACTH and cortisol pulses in insomniacs compared to normal sleepers, while cosinor analysis indicated a significant circadian rhythm without differences in the temporal pattern of ACTH and cortisol secretion between the two groups. Conclusively, this study suggests that insomnia is associated with an overall 24h increase of the ACTH and cortisol secretion, which however retains a normal circadian pattern. Therefore, insomnia seems to be a disorder of 24-h hyperarousal rather than sleep loss. This approach is further supported by studies investigating the effects of sleep loss on cortisol secretion. Most of the studies have found no change [61-63], or decrease in the secretion of cortisol [39,64] after sleep deprivation, whereas in these studies that reported significant increase of cortisol in the evening following the night of sleep loss[65-66], sleep deprivation was associated with rather stressful experimental conditions, i.e. lying in bed in a dimly lit room and receiving calories through an iv catheter."

"Since insomnia is associated with high cortisol levels, particularly in the evening, it is possible that evening measures of cortisol may be a useful marker of the biological severity of insomnia. Such a marker may affect our treatment strategies in managing an insomnia patient. However, further studies are needed to establish cortisol or other hormones, as biological markers of this chronic condition."

http://www.ajmc.com/supplement/managed-c...pS117-S120

"The HPA axis is involved in the secretion of CRF which, in turn, acts on receptors in the anterior pituitary to cause a release of adrenocorticotropic hormone (ACTH) into the bloodstream. The ACTH then acts on the adrenal cortex to cause the production and release of cortisol.12Patients with chronic insomnia have been shown to have significantly higher levels of ACTH and cortisol than individuals without insomnia. The findings further demonstrate that insomnia is, indeed, a disorder of CNS hyperarousal.13"

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06-18-2012 05:04 AM
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