Posted by karaS on September 16, 2004, at 17:58:18
In reply to Re: Staying up all night as AD-raybakes? Larry? any? » karaS, posted by Larry Hoover on September 16, 2004, at 7:35:38
> > What is the science behind the antidepressant effect of staying up all night? Is it cortisol related? Does MAO and reuptake of neurotransmitters have anything to do with it?
> >
> > thanks,
> > K
>
> Hey Kara. My brain went on holiday for a few days. Or, it had some ponderations to conclude. Or, my quitting coffee had something to do with it. Or, I'm just weird. Anyway...
>
> What a coincidence! I was just reading a just-published study on this, last night. If you read the first and second abstracts, here, you might conclude that they show different cortisol responses in the responders. One says increase, the other decrease. But, the third abstract might have the answer. Failure of the the cortisol autoreceptors (I'm invoking the same paradoxical response paradigm as with stimulants, even though I don't even know if there are cortisol autoreceptors), might be the distinguishing factor, as dexamethasone suppression measures cortisol-feedback sensitivity.
>
> The takehome message is that it looks like sleep deprivation kickstarts the growth hormone system which has been suppressed by excess cortisol associated with depression. Simultaneous to that is extra release of TSH, but there are two categories of feedback sensitivity there, too. Our bodies are very complicated systems, but then they'd have to be, to evolve so far from the natural chaos of unregulated systems.
>
> Lar
>
>
> Am J Psychiatry. 2004 Aug;161(8):1404-10.
>
> Impact of sleep deprivation and subsequent recovery sleep on cortisol in unmedicated depressed patients.
>
> Voderholzer U, Hohagen F, Klein T, Jungnickel J, Kirschbaum C, Berger M, Riemann D.
>
> Department of Psychiatry and Psychotherapy, University Hospital of Freiburg, Freiburg, Germany. Ulrich_Voderholzer@psyallg.ukl.uni-freiburg.de
>
> OBJECTIVE: One night of sleep deprivation induces a transient improvement in about 60% of depressed patients. Since depression is associated with abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis, the authors measured cortisol secretion before, during, and after therapeutic sleep deprivation for 1 night. METHOD: Fifteen unmedicated depressed inpatients participated in a combined polysomnographic and endocrine study. Blood was sampled at 30-minute intervals during 3 consecutive nights before, during, and after sleep deprivation. Saliva samples were collected at 30-minute intervals during the daytime before and after the sleep deprivation night. RESULTS: During the night of sleep deprivation, cortisol levels were significantly higher than at baseline. During the daytime, cortisol levels during the first half of the day were higher than at baseline in the patients who responded to sleep deprivation but not in the nonresponders. During recovery sleep, cortisol secretion returned to baseline values. CONCLUSIONS: This study demonstrated a significant stimulatory effect of 1 night of sleep deprivation on the HPA axis in unmedicated depressed patients. The results suggest that the short-term effects of antidepressant treatments on the HPA axis may differ from their long-term effects. A higher cortisol level after sleep deprivation might transiently improve negative feedback to the hypothalamus or interact with other neurotransmitter systems, thus mediating or contributing to the clinical response. The fast return to baseline values coincides with the short clinical effect.
>
> Clin Endocrinol (Oxf). 1999 Aug;51(2):205-15.
>
> Sleep deprivation effects on the activity of the hypothalamic-pituitary-adrenal and growth axes: potential clinical implications.
>
> Vgontzas AN, Mastorakos G, Bixler EO, Kales A, Gold PW, Chrousos GP.
>
> Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University, Hershey, PA 17033, USA.
>
> OBJECTIVES: Although several studies have shown that sleep deprivation is associated with increased slow wave sleep during the recovery night, the effects of sleep deprivation on cortisol and growth hormone (GH) secretion the next day and recovery night have not been assessed systematically. We hypothesized that increased slow wave sleep postsleep deprivation is associated with decreased cortisol levels and that the enhanced GH secretion is driven by the decreased activity of the HPA axis. DESIGN AND SUBJECTS: After four consecutive nights in the Sleep Laboratory, 10 healthy young men were totally deprived of sleep during the fifth night, and then allowed to sleep again on nights six and seven. Twenty-four hour blood sampling was performed serially every 30 minutes on the fourth day, immediately following the previous night of sleep and on the sixth day, immediately after sleep deprivation. MEASUREMENT: Eight-hour sleep laboratory recording, including electroencephologram, electro-oculogram and electromyogram. Plasma cortisol and GH levels using specific immunoassay techniques. RESULTS: Mean plasma and time-integrated (AUC) cortisol levels were lower during the postdeprivation nighttime period than on the fourth night (P < 0.05). Pulsatile analysis showed significant reduction of both the 24 h and daytime peak area (P < 0.05) and of the pulse amplitude (P < 0.01), but not of the pulse frequency. Also, the amount of time-integrated GH was significantly higher for the first 4 h of the postdeprivation night compared to the predeprivation night (P < 0.05). Cross-correlation analyses between the absolute values of the time-series of each hormone value and percentage of each sleep stage per half hour revealed that slow wave sleep was negatively correlated with cortisol and positively correlated with GH with slow wave sleep preceding the secretion of these hormones. In contrast, indices of sleep disturbance, i.e. wake and stage 1 sleep, were positively correlated with cortisol and negatively correlated with GH. CONCLUSION: We conclude that sleep deprivation results in a significant reduction of cortisol secretion the next day and this reduction appears to be, to a large extent, driven by the increase of slow wave sleep during the recovery night. We propose that reduction of CRH and cortisol secretion may be the mechanism through which sleep deprivation relieves depression temporarily. Furthermore, deep sleep has an inhibitory effect on the HPA axis while it enhances the activity of the GH axis. In contrast, sleep disturbance has a stimulatory effect on the HPA axis and a suppressive effect on the GH axis. These results are consistent with the observed hypocortisolism in idiopathic hypersomnia and HPA axis relative activation in chronic insomnia. Finally, our findings support previous hypotheses about the restitution and immunoenhancement role of slow wave (deep) sleep.
>
> J Psychiatr Res. 2001 Jul-Aug;35(4):239-47.
>
> Sleep deprivation and hypothalamic-pituitary-adrenal (HPA) axis activity in depressed patients.
>
> Schule C, Baghai T, Zwanzger P, Minov C, Padberg F, Rupprecht R.
>
> Department of Psychiatry, Ludwig-Maximilian-University, Nussbaumstr. 7, 80336 Munich, Germany. cornelius.schuele@psy.med.uni-muenchen.de
>
> In the present study we investigated HPA axis activity in depressed patients treated with partial sleep deprivation (PSD) in order to identify endocrinological characteristics related to PSD responsiveness. Thirty-three drug-free patients (14 men, 19 women) suffering from major depression according to DSM-IV criteria were treated with PSD. Response to PSD was defined as a reduction of at least 30% according to the 6-item version of the Hamilton Depression Scale (6-HAMD). Subsequently, the combined dexamethasone-suppression/CRH-stimulation test (DEX/CRH test) was performed. Patients were pretreated with 1.5 mg dexamethasone (DEX) at 23:00 h and challenged with 100 microg corticotropin-releasing hormone (CRH) the following day. Postdexamethasone cortisol concentrations (before CRH administration) served as parameters for the DST status (dexamethasone suppression test). The cortisol stimulation after CRH was used as measurement for the DEX/CRH test status. Of the depressive patients, 54.5% (18 out of 33) responded to PSD. DST suppressors (postdexamethasone cortisol levels < 15 ng/ml) showed a significantly greater reduction in 6-HAMD scores after PSD than DST nonsuppressors. Furthermore, a significant negative correlation between postdexamethasone cortisol levels and reduction in 6-HAMD scores after PSD could be established. However, there was no relationship between the cortisol stimulation following CRH challenge and response to PSD. Although the combined DEX/CRH challenge test is a more sensitive marker for HPA axis dysregulation in depression than the standard DST, the negative feedback of the HPA system reflected by the DST status is apparently more closely associated with response to partial sleep deprivation in major depressive disorder.
>
No worries. (I just thought that your alter ego, Harry Loover, had taken over!) Anyway, how ironic that you were just reading about this very thing.P.S. I got that book by Dr. Perlmutter. It's much more general and geared towards the masses as you might imagine. I doubt you'd enjoy it as much as the article he wrote.
Thanks!
K
poster:karaS
thread:391316
URL: http://www.dr-bob.org/babble/alter/20040901/msgs/391652.html