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I have tried many prozac, lexapro, effexor, buspar, and trazadone. All seemed to have
worse side effects then benefits.Anyways, what is everyones experience with this drug?
Im thinking of giving it a shot.
Its said to have anxiolytic, anti depressive, anti nausea, pro libido, pro appetite and sleep enhancing effects.
Almost sounds too good to be true.
I dont eat much at all. Im always too nauseated (from stress? anxiety?) with a lack of appetite. Im surprised if i get 1500 calories a day yet im moderately active.
I was going to try this a few months back but my psyc said it was a trash drug and that trazadone was many times better.
Well your doctor might be thinking that Trazodone is a better sleep pill than Remeron (but I’m not feeling the same way, I was sleeping better on Remeron and it far less sedating to me). 15 minutes after a Trazodone pill, it feels like getting hit by a truck.
Otherwise, I don’t think Trazodone can be consider a cleaner antidepressant than Remeron, quite the contrary, I think it’s a pretty poor antidepressant.
I’m glad I’m off all those AD now, addressing hormones imbalance was the thing I had to do to, not taking AD, I’m sure of it now.
Have you checked other possible physical cause of your anxiety?
@The450Man 669 wrote:
I have tried many prozac, lexapro, effexor, buspar, and trazadone. All seemed to have
worse side effects then benefits.Anyways, what is everyones experience with this drug?
Im thinking of giving it a shot.
Its said to have anxiolytic, anti depressive, anti nausea, pro libido, pro appetite and sleep enhancing effects.
Almost sounds too good to be true.
I dont eat much at all. Im always too nauseated (from stress? anxiety?) with a lack of appetite. Im surprised if i get 1500 calories a day yet im moderately active.
I was going to try this a few months back but my psyc said it was a trash drug and that trazadone was many times better.
@The450Man 669 wrote:
I have tried many prozac, lexapro, effexor, buspar, and trazadone. All seemed to have
worse side effects then benefits.Anyways, what is everyones experience with this drug?
Im thinking of giving it a shot.
Its said to have anxiolytic, anti depressive, anti nausea, pro libido, pro appetite and sleep enhancing effects.
Almost sounds too good to be true.
I dont eat much at all. Im always too nauseated (from stress? anxiety?) with a lack of appetite. Im surprised if i get 1500 calories a day yet im moderately active.
I was going to try this a few months back but my psyc said it was a trash drug and that trazadone was many times better.
TRAZODONE:
I generally would not give Trazodone to any man who isn’t over 45 years-old, who doesn’t have a Total Testosterone under 300. Any other combination has too high a risk of developing priapism requiring emergency surgery. And it can happen with as little as 25 mg of Trazodone.
Trazodone does work well for sleep. It is a mild antidepressant, thus higher doses are necessary. It usually does not cause agitation or restlessness. At higher doses, however, it can cause irregular heart beats and lightheadedness – thus one has to watch out for falling. It is a mild aphrodisiac for women, helping improve vaginal secretions when aroused.
—
REMERON (MIRTAZAPINE):
Mirtazapine does the following:
- Blocks presynaptic alpha-2 adrenergic receptors, resulting in an increase in norepinephrine signaling. Presynaptic alpha-2 receptors on serotonin neurons also inhibit serotonin signaling. Blocking such alpha-2 receptors results in an increase in serotonin signaling.
- Blocks serotonin 2 (a) receptors, which may result in increased dopamine signaling in the frontal cortex.
- Blocks serotonin 3 receptors (helps reduce nausea).
- Blocks histamine 1 receptors, which may cause sedation, increased appetite.
- Blocks alpha-1 adrenergic receptors (mild – may reduce blood pressure).
- Blocks acetylcholine muscarinic receptors (mild) – may cause dry mouth, blurred vision, constipation, forgetfulness. This may also increase dopamine signaling
.
The overall indirect increase in dopamine signaling helps support libido.
Weight gain can be significant. The lower the dose (down to 15 mg a day), the larger the weight gain and the more sedation one gets. Past 30 mg a day, weight gain is reduced since the increase in norepinephrine signaling that results helps outweigh the block in histamine, thus reducing the increase in appetite.
As an antidepressant, it tends to be milder than the serotonin-reuptake inhibitors or the serotonin-norepinephrine reuptake inhibitors. The overall effect on signaling systems is relatively mild except for its block of histamine receptors. It generally is not adequately effective for reducing anxiety.
@gu3vara 670 wrote:
Well your doctor might be thinking that Trazodone is a better sleep pill than Remeron (but I’m not feeling the same way, I was sleeping better on Remeron and it far less sedating to me). 15 minutes after a Trazodone pill, it feels like getting hit by a truck.
Otherwise, I don’t think Trazodone can be consider a cleaner antidepressant than Remeron, quite the contrary, I think it’s a pretty poor antidepressant.
I’m glad I’m off all those AD now, addressing hormones imbalance was the thing I had to do to, not taking AD, I’m sure of it now.
Have you checked other possible physical cause of your anxiety?
yea im slowly getting there. Im doing it mostly by myself so its a long process. Plus convincing my doctors to run tests is a hassle in its own.
I think i just need a 24 hour cortisol test. Im almost positive i have some form of adrenal issues.
Never knew Remeron had activity with norepinephrine. Wouldnt that be worse for anxiety/depression in that it would increase stress signaling?In addition..
does anyone know a way to stimulate my appetite? I really need to get some more food into me. Force feeding dosnt work, i just end up in dry heaves and vomit it up.
Most psychiatric medications increase appetite. This is a problem in the long run, once people improve in function.
The antidepressants – by and large – increase appetite. Remeron is useful in this regard. I often use it when using stimulants to treat attention deficit/hyperactivity disorder since the stimulants reduce appetite and risk impaired growth. The tricyclics, such as Amitriptyline, stimulate appetite significantly. The serotonin-reuptake inhibitors gradually increase appetite and weight.
The atypical antipsychotic medications generally increase appetite. Zyprexa is used, for example, in cancer treatment, to improve appetite.
The mood stabilizing medications such as Lithium, Depakote, can increase appetite.
I can second what Dr. M says about Remeron when I was on this before finding out I am not depressed but have low testosterone. Remeron put 50 lbs. on me and I slept like a baby. I keep telling my wife she should try this she had knee replacement sugary and now can’t sleep something changed in her she us to fall a sleep at the drop of a hat now she is up all night falls to sleep then wakes up take my Xanax a low does falls back to sleep only to wake in an hour and fall back to sleep and wake every hour on the hour. So she does not take anything tried every kind of sleep med out there and nothing works. I know if she tried Remeron she would sleep. Her Dr. tested her hormones and they are all good she did a 4x’s in day Cortisol Saliva test and this was dam good. I feel so sorry for her I know this not sleeping would drive me nuts.
PhilIt is interesting how desperate people become when they cannot sleep.
But “desperation” and “insomnia” are interrelated.
Insomnia occurs when excessive norepinephrine signaling (with or without excessive histamine signaling) occurs, unbalanced by control signals for norepinephrine (including cortisol, serotonin, dopamine, GABA, progesterone, allopregnenolone, DHEA, estradiol, testosterone, dihydrotestosterone, melatonin, etc.). It many signals to knock down norepinephrine – the primary distress signal in the body.
When a person feels “desperate”, the same thing occurs – excessive norepinephrine and not enough of its control signals.
Norepinephrine has multiple functions – including improving metabolism, energy production, thermogenesis, alertness, wakefulness, maintaining blood pressure, heart rate, improving lung function, etc. etc. Thus a reason excessive norepinephrine production can happen is in an attempt to compensate for problems in these areas – aside from signaling stress, distress, etc. It can be very difficult to knock down norepinephrine if it is compensating for metabolic problems since the mind in this state is in survival mode.
Remeron is the most sedating drug I’ve tried. It does induce sleep, but at only 7.5mg I felt tired until the next evening!
Remeron is said to decrease cortisol/ regulate HPA function. Many people benefit from increaseing cortisol…… this has me confused..Would this be negative or possitive?
“RATIONALE: It has been suggested that hypothalamic-pituitary-adrenocortical (HPA) system dysregulation plays an important role in the pathophysiology of depression and that normalization of HPA axis hyperactivity precedes successful treatment with antidepressants. Mirtazapine acts as an antagonist at presynaptic alpha(2)-receptors and at postsynaptic 5-hydroxytryptamine (5-HT)(2), 5-HT(3) and histamine H(1) receptors. It has been shown acutely to inhibit cortisol secretion in healthy subjects. OBJECTIVE: In this study, we investigated whether mirtazapine may downtune HPA axis hyperactivity in depressed patients and whether this is related to treatment outcome. METHODS: Forty patients suffering from a major depressive episode (DSM-IV criteria) were treated with mirtazapine for 5 weeks. The combined dexamethasone suppression/CRH stimulation test (DEX/CRH test) was performed before and after 1 week of mirtazapine treatment (45 mg daily). RESULTS: Mirtazapine effectively reduced the overshoot of cortisol and ACTH during the DEX/CRH test both in treatment responders and non-responders within 1 week. CONCLUSIONS: Apparently, mirtazapine rapidly attenuates HPA axis hyperactivity in depressed patients via direct pharmacoendocrinological effects. However, this amelioration of HPA system dysregulation is not necessarily related to clinical improvement.”
Effects of mirtazapine on growth hormone, prolactin, and cortisol secretion in healthy male subjects.
Psychoneuroendocrinology 1999 Oct;24(7):769-84
“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."Some other interesting points”
“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.”
The influence of mirtazapine on anterior pituitary hormone secretion in healthy male subjects.
Psychopharmacology (Berl) 2002 Aug;163(1):95-101
“The area under the curve (AUC) 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 application of placebo or mirtazapine) up to 8:00 a.m. the day after. RESULTS. Multivariate analyses of variance revealed significantly lower COR AUC, ACTH AUC, and UFC values after 15 mg mirtazapine compared to placebo, whereas no differences were found with respect to GH and PRL stimulation, MAP, and heart rate.”Prevention of the stress-induced increase in the concentration of neuroactive steroids in rat brain by long-term administration of mirtazapine but not of fluoxetine.
J Psychopharmacol 2002 Jun;16(2):133-8
“In contrast, chronic treatment with mirtazapine prevented or significantly reduced the stress-induced increases in neurosteroid concentrations in the cerebral cortex and plasma, respectively. These results show that mirtazapine, similar to fluoxetine, initially increases the cortical concentration of neuroactive steroids; however, chronic administration of this drug modulates the plasma and brain availability of these hormones in a manner distinct from that of fluoxetine.”@The450Man 1122 wrote:
Remeron is said to decrease cortisol/ regulate HPA function. Many people benefit from increaseing cortisol…… this has me confused..Would this be negative or possitive?
Remeron can decrease cortisol by causing sedation. Reduction in norepinephrine signaling by blocking histamine causes a decrease in CRH production, which then results in a reduction in ACTH then cortisol.
Realize that this occurs primarily at night, when the histamine blocking effect of Remeron is the strongest in causing a person to sleep.
In the long run, through its effects on the nervous system and its reduction in norepinephrine signaling at night (in at least the low to mid-range doses), Remeron reduces the severity of depression (after all, it is an antidepressant). This results in a restoration of cortisol signaling in response to stress (i.e. an increase in cortisol signaling, or in other words, a restoration of HPA Axis regulation, which was dysregulated in depression). Then cortisol levels go up.
The articles cited are under the myth that clinical depression (e.g. major depressive disorder) has high cortisol levels as one of the causes of depression. I do not see this in real life. I measure nearly every patient’s cortisol levels – men, women, children, young, adult, and aged, everyone. And when I do, I very rarely see a high cortisol level. Nearly everyone is LOW. This includes bipolar disorder, depression, anxiety disorders, PTSD, ADHD, and even schizophrenia. When I saw this trend, I realized that the psychiatric literature on mood disorders and cortisol is simply wrong and does not correspond to real life. Also, the Hans Selye General Adaptive Syndrome curve is completely misinterpreted. Hans Selye is famous for studying stress and the adaptations to stress. From his perspective, it is only when one reaches adrenal exhaustion that one becomes ill. I totally agree. When people have high cortisol levels, they are adapting to their stress – and fairly successfully. It is when cortisol output becomes low in the face of stress does illness occur.
DR M,
Interesting information. I recently went off of Pristiq because it was causing me to feel very very unfocused, also it made me sweat worse then I already was.
You have indicated in a previous posting that you almost always saw children that came from extremely violent childhoods suffer from HPA Axis disregulation.( which is my history) , As most antidepressants have done nothing for me, is this a possibility for me.
I saw it do amazing things for my husband. He has low testosterone and I am convinced has ADHD. He doesn’t sleep well at night and is very sensitive to critisim. I saw a different person when he was on this drug. However, he said it did nothing for him.
My husband is 58 years old, hypothryoid, fatigued adrenals and also low testosterone. His level was 10. He is now taking 50 mg bio-identical prescription cream daily.@DrMariano 1126 wrote:
Remeron can decrease cortisol by causing sedation. Reduction in norepinephrine signaling by blocking histamine causes a decrease in CRH production, which then results in a reduction in ACTH then cortisol.
Realize that this occurs primarily at night, when the histamine blocking effect of Remeron is the strongest in causing a person to sleep.
In the long run, through its effects on the nervous system and its reduction in norepinephrine signaling at night (in at least the low to mid-range doses), Remeron reduces the severity of depression (after all, it is an antidepressant). This results in a restoration of cortisol signaling in response to stress (i.e. an increase in cortisol signaling, or in other words, a restoration of HPA Axis regulation, which was dysregulated in depression). Then cortisol levels go up.
The articles cited are under the myth that clinical depression (e.g. major depressive disorder) has high cortisol levels as one of the causes of depression. I do not see this in real life. I measure nearly every patient’s cortisol levels – men, women, children, young, adult, and aged, everyone. And when I do, I very rarely see a high cortisol level. Nearly everyone is LOW. This includes bipolar disorder, depression, anxiety disorders, PTSD, ADHD, and even schizophrenia. When I saw this trend, I realized that the psychiatric literature on mood disorders and cortisol is simply wrong and does not correspond to real life. Also, the Hans Selye General Adaptive Syndrome curve is completely misinterpreted. Hans Selye is famous for studying stress and the adaptations to stress. From his perspective, it is only when one reaches adrenal exhaustion that one becomes ill. I totally agree. When people have high cortisol levels, they are adapting to their stress – and fairly successfully. It is when cortisol output becomes low in the face of stress does illness occur.
@pmgamer18 689 wrote:
I can second what Dr. M says about Remeron when I was on this before finding out I am not depressed but have low testosterone. Remeron put 50 lbs. on me and I slept like a baby. I keep telling my wife she should try this she had knee replacement sugary and now can’t sleep something changed in her she us to fall a sleep at the drop of a hat now she is up all night falls to sleep then wakes up take my Xanax a low does falls back to sleep only to wake in an hour and fall back to sleep and wake every hour on the hour. So she does not take anything tried every kind of sleep med out there and nothing works. I know if she tried Remeron she would sleep. Her Dr. tested her hormones and they are all good she did a 4x’s in day Cortisol Saliva test and this was dam good. I feel so sorry for her I know this not sleeping would drive me nuts.
PhilHey buddy Phil,
Awww, I’m so sorry your wifes not sleeping. My husband has the same problem. He’ll wake up up several times in the night and be bright eyed and bushy tailed. He actually went on Remeron at one time and he was like a new person. I saw signigicant changes in him. He was less sensitive to criticism, not so dingy and more able to focus. (I guess that’s what happens when you get a good nights sleep).
Our step-son ( my husbands son) was murdered in March 2002 at the age of 21. He was shot in the back. . My husband crashed big time after that. He didn’t care about anything. When I finally got him to go for counselling and a Dr started him on Remerron he did better. He decided about 2 years ago that he didn’t need this drug anymore. I disagreed.
Dog gone it, wish you wife could give it a try.Hope you’re feeling better Phil,
well i have been on remeron for about a month. I have gained a few lbs and am feeling better probably because i am actually eating… I have decided to up my dose to 30, bad move?? would the increase in norepinephrine signaling do much to aggravate my anxiety? Worsen what i assume i have.. mild adrenal fatigue??
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