Mirtazapine as Anticortisol - Good Choice?

Mirtazapine as Anticortisol - Good Choice? Mirtazapine as Anticortisol - Good Choice?

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The mechanism of action of mirtazapine, as with other drugs effective in the treatment of major depressive disorder, is unknown.

Evidence gathered in preclinical studies suggests that Mirtazapine enhances central noradrenergic and serotonergic activity. These studies have shown that Mirtazapine acts as an antagonist at central presynaptic α2 adrenergic inhibitory autoreceptors and heteroreceptors, an action that is postulated to result in an increase in central noradrenergic and serotonergic activity.

Mirtazapine is a potent antagonist of 5-HT2 and 5-Ht3 receptors. Mirtazapine has no significant affinity for the 5-HT1A and 5-HT1B receptors.

Mirtazapine is a potent antagonist of histamine (H1) receptors, a property that may explain its prominent sedative effects.

Mirtazapine is a moderate peripheral α1 adrenergic antagonist, a property that may explain the occasional orthostatic hypotension reported in association with its use.

Mirtazapine is a moderate antagonist at muscarinic receptors, a property that may explain the relatively low incidence of anticholinergic side effects associated with its use.

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Endocrinological effects of mirtazapine in healthy volunteers.
Schüle C, Baghai T, Bidlingmaier M, Strasburger C, Laakmann G.

Psychiatric Hospital, University of Munich, Munich, Germany. [email protected]

OBJECTIVE: Unlike other antidepressants, mirtazapine does not inhibit the reuptake of norepinephrine or serotonin (5-HT) but acts as an antagonist at presynaptic alpha2-receptors and at postsynaptic 5-HT2, 5-HT3 and histamine H1-receptors. In the present investigation, the influence of acute oral administration of 15-mg mirtazapine on the cortisol (COR), adrenocorticotropin (ACTH), growth hormone (GH) and prolactin (PRL) secretion was examined in 12 healthy male subjects, compared to placebo. METHODS: After insertion of an intravenous catheter, both the mean arterial blood pressure (MAP) and the heart rate were recorded and blood samples were drawn 1 h prior to the administration of mirtazapine or placebo (7:00 a.m.), at time of administration (8:00 a.m.) and during 5 h thereafter in periods of 30 min. Concentrations of COR, ACTH, GH and PRL were measured in each blood sample by double antibody radioimmunoassay and chemiluminescence immunoassay methods. The area under the curve (AUC; 0-300 min after mirtazapine or placebo administration) was used as parameter for the COR, ACTH, GH and PRL response. Furthermore, the urinary free cortisol excretion (UFC) was determined beginning at 8:00 a.m. (time of administration of placebo or mirtazapine) up to 8:00 a.m. the day after. RESULTS: Two-sided t-tests for paired samples revealed significantly lower COR AUC, ACTH AUC, UFC and PRL AUC values after 15-mg mirtazapine compared to placebo, whereas no significant differences were found with respect to GH AUC, MAP and heart rate. CONCLUSIONS: Since the acute inhibition of COR secretion in the healthy volunteers was paralleled by a simultaneous decrease of ACTH release, central mechanisms (e.g., inhibition of hypothalamic corticotropin releasing hormone (CRH) output) are suggested to be responsible for the inhibitory effects of mirtazapine on COR secretion. Our results are of particular interest in the light of the hypercortisolism observed in depressed patients and new pharmacological approaches such as CRH1 receptor antagonists.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1250201 1" target="_blank" rel="noopener"> http://www.ncbi.nlm.nih.gov/sites/e...Search=12502011
PMID: 12502011 [PubMed - indexed for MEDLINE]

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Time course of hypothalamic-pituitary-adrenocortical axis activity during treatment with reboxetine and mirtazapine in depressed patients.
Schüle C, Baghai TC, Eser D, Zwanzger P, Jordan M, Buechs R, Rupprecht R.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilian University of Munich, Nussbaumstr 7, Munich, 80336, Germany. [email protected]

RATIONALE: In healthy subjects, cortisol and ACTH secretion are acutely stimulated by reboxetine and inhibited by mirtazapine. However, it was not investigated so far whether reboxetine and mirtazapine may also differ in their impact on hypothalamic-pituitary-adrenocortical (HPA) axis activity in depressed patients and whether these effects are related to clinical outcome. OBJECTIVES: In the present study, we investigated the impact of 5-week treatment with reboxetine or mirtazapine on the combined dexamethasone suppression/corticotropin releasing hormone (DEX/CRH) test results in depressed patients. METHODS: Forty drug-free patients suffering from a major depressive episode (Diagnostic and Statistical Manual of Mental Disorders-IV criteria) were treated with either reboxetine (8 mg/day; n=20) or mirtazapine (45 mg/day; n=20) for 5 weeks. Before, after 1 and 5 weeks of therapy, the DEX/CRH test was performed and cortisol and ACTH concentrations were measured. RESULTS: During reboxetine treatment, a gradual and significant reduction in HPA axis activity as measured by the DEX/CRH test was seen, which was most pronounced after 5 weeks of treatment. In contrast, mirtazapine significantly reduced the cortisol and ACTH concentrations during the DEX/CRH test within 1 week. However, after 5 weeks of mirtazapine treatment, the cortisol and ACTH responses to the DEX/CRH test partially increased again both in responders and nonresponders. CONCLUSIONS: This is the first study demonstrating differential effects of various antidepressants on the time course of serial DEX/CRH test results in depressed patients.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1675824 3" target="_blank" rel="noopener"> http://www.ncbi.nlm.nih.gov/sites/e...Search=16758243
PMID: 16758243 [PubMed - indexed for MEDLINE]

The Side Effects

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Doses: 5mg/day to 60mg/day

Mirtazapine(n=453) Placebo(n=361)

Body as a Whole
Asthenia 8% 5%
Flu Syndrome 5% 3%
Back Pain 2% 1%
Digestive System
Dry Mouth 25% 15%
Increased Appetite 17% 2%
Constipation 13% 7%
Metabolic and Nutritional Disorders
Weight Gain 12% 2%
Peripheral Edema 2% 1%
Edema 1% 0%
Musculoskeletal System
Myalgia 2% 1%
Nervous System
Somnolence 54% 18%
Dizziness 7% 3%
Abnormal Dreams 4% 1%
Thinking Abnormal 3% 1%
Tremor 2% 1%
Confusion 2% 0%
Respiratory System
Dyspnea 1% 0%
Urogenital System
Urinary Frequency 2% 1%

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Visit for more information:
http://www.dr-bob.org/tips/split/Mirtazapine-side-effects.htm l" target="_blank" rel="noopener"> http://www.dr-bob.org/tips/split/Mi...de-effects.html

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Physical and Psychological Dependence

Mirtazapine has not been systematically studied in animals or humans for its potential for abuse, tolerance or physical dependence. While the clinical trials did not reveal any tendency for any drug-seeking behavior, these observations were not systematic and it is not possible to predict on the basis of this limited experience the extent to which a CNS-active drug will be misused, diverted and/or abused once marketed. Consequently, patients should be evaluated carefully for history of drug abuse, and such patients should be observed closely for signs of mirtazapine misuse or abuse (e.g., development of tolerance, incrementations of dose, drug-seeking behavior).

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What do you think about MIRTAZAPINE for the ppct and pct? (ppct = pre post cicle terapy)

L. Rea use mirtazapine in somes pct´s (mirtazapine 15mg/day x 4weeks)

i think 15mg/day for 2 week or less are meaby good idea for control of cortisol

PD: Hi everybody , i´m from argentina, sorry if my english isn´t good