Thread: Hi Cortisol levels
02-24-2005, 07:33 AM #1
Hi Cortisol levels
According to my 2 last blood tests I have high Cortisol levels...that's not good cos I'm in catabolism phase! Before my cycle it was 21 now 2 months later is 30...Any suggestions? Can I do something for that?
02-25-2005, 04:46 AM #2
No one yet??
02-25-2005, 06:47 AM #3
I'll bump this to keep it up there for you. Wish I could help.
02-25-2005, 12:17 PM #4Member
- Join Date
- Dec 2004
Steroid molekyles block the cortisone reseptors and cause the cortisone level to elevate. When you come off the cycle and the steroids are leaving your body the reseptors are suddenly freed. It can make you very catabolic due to high cortisone level, especially if your test level don't come up fast enough. Cortisone can supress test, but I think test can supress cortisone also.. Do a proper PCT with clomid.
Clenbuterol is a typical drug to fight cortisone and prevent catabolism. I think it blocks the reseptors, and in the meanwhile the cortisone level will go back to normal. I'm not sure how it works but you can do a search on it..
Last edited by ace ventura; 02-25-2005 at 12:24 PM.
02-25-2005, 01:26 PM #5
Get 7oh(lean xtreme) it is what 7oxo dhea converts to in the body it is made by designer suppliments it effectivly reduces cortisol works very well
02-25-2005, 02:24 PM #6
I love Phosphatidylserine! I use it with every PCT... Cytodyne makes a good product called "cytodyne" BUT it costs a pretty penny, cause I use double the rec. dosage.
02-25-2005, 03:48 PM #7
02-25-2005, 03:51 PM #8
General info: http://www.drugs.com/PDR/Remeron_Tablets.html
This study is on depressed patients.
"Mirtazapine Attenuates Hypothalamic-pituitary-adrenocortical Axis Hyperactivity in Depressed Patients"
A DGReview of :"Attenuation of hypothalamic-pituitary-adrenocortical hyperactivity in depressed patients by mirtazapine"
By Anne MacLennan
German clinicians have found that mirtazapine rapidly attenuates the dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) system seen in depressed patients.
They note, however, that this effect of mirtazapine is not necessarily related to clinical improvement.
Previous research suggested that dysregulation of the HPA system might play an important role in the pathophysiology of depression, and that normalization of HPA axis hyperactivity precedes successful treatment with antidepressants, write Dr. Cornelius Schüle and colleagues at the Department of Psychiatry at University of Munich.
Previous studies demonstrated that mirtazapine acts as an antagonist at presynaptic beta 2 receptors and at post-synaptic 5-hydroxytryptamine (5-HT) and histamine H1 receptors. In addition, it has been shown to have an acute inhibiting effect on cortisol secretion in healthy subjects.
Dr. Schüle and colleagues investigated whether mirtazapine might reduce HPA axis hyperactivity in patients with depression, and whether this is related to treatment outcome.
They enrolled 40 patients who met Diagnostic and Statistical Manual - Revision IV criteria for a major depressive episode, and who were treated with mirtazapine 45 mg daily for 5 weeks. The combined dexamethasone suppression/corticotropin releasing hormone stimulation (DEX/CRH) test was carried out 1 week before and 1 week after the start of mirtazapine treatment.
The clinicians found that mirtazapine effectively reduced the overshoot of cortisol and adrenocorticotropin in the DEX/CRH test in the first week among patients who either responded or did not respond to treatment.
Dr. Schüle and colleagues conclude, "Apparently, mirtazapine rapidly attenuates HPA axis hyperactivity in depressed patients via direct pharmaco-endocrinological effects. However, this amelioration of HPA system dysregulation is not necessarily related to clinical improvement."
This is on Healthy ones
Effects of mirtazapine on growth hormone , prolactin, and cortisol secretion in healthy male subjects.
Laakmann G, Schule C, Baghai T, Waldvogel E.
Psychiatrische Klinik, Ludwig Maximilians Universitat, Munchen, Germany. firstname.lastname@example.org
In the present study the effects of acute PO-administration of 15 mg mirtazapine on the growth hormone (GH), prolactin (PRL), and cortisol (COR) secretion were examined in eight physically and mentally healthy male subjects, compared to placebo. Mirtazapine is a new antidepressant agent which does not inhibit the reuptake of norepinephrine or serotonin but is an antagonist of presynaptic and, presumably, postsynaptic alpha 2-receptors as well as an antagonist of postsynaptic 5-HT2 and 5-HT3-receptors. After insertion of an i.v. catheter, blood samples were drawn 1 h prior to the administration of mirtazapine or placebo, at time of application, and during the time of 4 h after application in periods of 30 min. Plasma concentrations of GH, PRL, and COR were determined in each blood sample by double antibody RIA methods. The area under the curve (AUC) value was used as parameter for the GH, PRL, and COR response. With respect to GH and PRL secretion, mirtazapine did not show any effects in comparison with placebo. However, in all subjects, the COR concentrations were remarkably lower after mirtazapine compared to placebo, the difference being obvious in the mean value graphs 60 min after the application up to the end of the measurement period. The t-test for paired samples revealed a highly significant difference (P < 0.01) in COR-AUC-values between the mirtazapine group (mean COR-AUC: 1558.07 micrograms/100 ml x 240 min) and the placebo group (mean COR-AUC: 2698.86 micrograms/100 ml x 240 min). Further studies have to elucidate the question whether the demonstrated inhibition of COR secretion after application of 15 mg mirtazapine is caused by central or peripheral effects of this substance.
Hope this helps.
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