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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 9 to 33 of 33. Go back in thread:
Posted by PeterMartin on September 27, 2022, at 10:55:31
In reply to Re: Buspar vivid/terrible nightmares? SLS?, posted by undopaminergic on September 26, 2022, at 11:13:14
Love the discussion, thanks!
Haven't had the nightmares in the past couple days. Hopeful it'll be a helpful medicine for me.
Is anyone familiar with gepirone? Doing research on pubmed for Buspar led me to that drug. It's another 5HT1a agonist - kind of a sister drug to Busper - that is said to have done ok in trials, but never got FDA approval. It seems like there's still some potential it'll go to market as a company has submitted an NDA......but I couldn't find anything conclusive.
There are studies dating back to the 90s that use it for research....so I'm guessing some around here are familiar with it.
Posted by SLS on September 27, 2022, at 11:43:20
In reply to Re: Buspar vivid/terrible nightmares? SLS?, posted by undopaminergic on September 26, 2022, at 11:13:14
Hi, UD.
Great explanations.
I have combined Parnate 120 mg/day with methylphenidate and also with amphetamine. On top of that, came T4 and desipramine. It was of little value if remission was to be my goal.
I think tyramine actually displaces NE from storage vesicles and allows the NE to be released through the terminal button passively.
"Mechanism
The administration of tyramine displaces norepinephrine, epinephrine, and dopamine from pre-synaptic storage vesicles.[19] The release of these neurotransmitters, particularly norepinephrine, is responsible for vasoconstriction, increased heart rate, and a rise in blood pressure. Therefore, tyramine functions as an indirect sympathomimetic by causing the release of presynaptic endogenous neurotransmitters. Tyramine acts as a substrate for monoamine oxidase, further limiting the breakdown of monoamine neurotransmitters.[20]"
https://www.ncbi.nlm.nih.gov/books/NBK563197/
- Scott
> >
> > One combo I have heard of is an MAOI + Buspar + a dopamine agonist. I don't know if any of the dopamine agonists would be safe with Marplan or any MAOI? I have never heard of contraindications between them.
> >
>
> It depends on what you mean by dopamine agonists. Direct agonists like pramipexole and ropinirole should be perfectly safe, because they don't elevate serotonin or noradrenaline. Indirect dopamine agonists that function as reuptake inhibitors, like methylphenidate, are generally safe unless they also inhibit serotonin reuptake. Amphetamines are more risky, because they act like tyramine -- releasing noradrenaline -- and this can potentially lead to hypertensive crises. However, with caution, amphetamines can be a great way to augment a MAOI.
>
> Cocaine is a serotonin reuptake inhibitor, so in theory it should be dangerous to combine with a MAOI. However, I wonder why I've never heard of any problems with this combination. Maybe it's because cocaine has a short half-life, so it wears off before it produces any dangerous serotonin syndrome.
>
> > I guess the only concern would be blood pressure.
>
> And serotonin toxicity. Incidentally, sometimes a little elevation of blood pressure is a good thing, because MAOIs often produce hypotension.
>
> -undopaminergic
>
Posted by undopaminergic on September 27, 2022, at 11:56:29
In reply to Re: Buspar .... [Spinoff] Gepirone?, posted by PeterMartin on September 27, 2022, at 10:55:31
> Love the discussion, thanks!
>
> Haven't had the nightmares in the past couple days. Hopeful it'll be a helpful medicine for me.
>
> Is anyone familiar with gepirone? Doing research on pubmed for Buspar led me to that drug. It's another 5HT1a agonist - kind of a sister drug to Busper - that is said to have done ok in trials, but never got FDA approval. It seems like there's still some potential it'll go to market as a company has submitted an NDA......but I couldn't find anything conclusive.
>
> There are studies dating back to the 90s that use it for research....so I'm guessing some around here are familiar with it.
>Yes, I have known about it for a long time, but never "zoomed in" on it much, so you probably know more about it than I do.
-undopaminergic
Posted by undopaminergic on September 28, 2022, at 7:54:46
In reply to Re: Buspar vivid/terrible nightmares? SLS? » undopaminergic, posted by SLS on September 27, 2022, at 11:43:20
> Hi, UD.
Hi SLS.
> I have combined Parnate 120 mg/day with methylphenidate and also with amphetamine. On top of that, came T4 and desipramine. It was of little value if remission was to be my goal.
>What was the problem with the combination? Did it not elevate your mood enough, or did it have adverse effects?
> I think tyramine actually displaces NE from storage vesicles and allows the NE to be released through the terminal button passively.
>I think that is part of it, but it's more complex than that. There are at least two other actions of tyramine and other trace amines: they reverse the direction of the neurotransmitter (reuptake) transporter, and they bind to trace amine associated receptors (possibly the latter produces the former).
-undopaminergic
Posted by SLS on September 28, 2022, at 11:18:06
In reply to Re: Buspar vivid/terrible nightmares? SLS? » SLS, posted by undopaminergic on September 28, 2022, at 7:54:46
Hi.
> > I have combined Parnate 120 mg/day with methylphenidate and also with amphetamine. On top of that, came T4 and desipramine. It was of little value if remission was to be my goal.
> What was the problem with the combination? Did it not elevate your mood enough, or did it have adverse effects?
In 1987, after 5 years of treatment failures, a doctor put me on a combination of Parnate and desipramine. It was harsh at first, but it eventually brought me close to remission. Functionally, I was very much improved. However, anhedonia remained less improved. I was quite happy with that state of affairs. After 6 months of remission, a delusional mania emerged for the first time as an adverse effect of drug treatment. The doctor discontinued both antidepressants, and I relapsed within 2 months. My doctor had no intentions of giving me a MAOI + TCA combination ever again - which was a monumental mistake. In 1990, I became psychotically manic after *discontinuing* Nardil. I was still responsive to it, though. I entered a psychiatric clinic as an inpatient. They treated me with Thorazine and then Haldol, after which I became absolutely refractory to all treatments. Taking clorgyline, a *specific* and irreversible MAOI was powerful enough to break through the wall of non-response. I became responsive to drugs again, but it would take another 20 years to find the right treatment for me.I am now close to being in full remission.
Current treatment regime - :
Nardil - 90 mg/day
Nortriptyline - 150 mg/day
Lamotrigine - 300 mg/day
Lithium - 300 mg/day
- Scott
Posted by SLS on September 28, 2022, at 13:52:49
In reply to Responsive ) Refractory ) Responsive ) Remission » undopaminergic, posted by SLS on September 28, 2022, at 11:18:06
I left one thing out. Clorgyline is an irreversible monoamine oxidase inhibitor *specific* for MAO-A. It is probably the most potent antidepressant in the world. I was fortunate to be treated with it when I was a research patient at the NIH. It appears that if an MAOI doesn't inhibit MAO-A, it is ineffective in treating depression. However, low dosages of selegiline inhibit MAO-B only, which is sufficient for treating Parkinsons Disease. Parkinsons is a movement disorder caused by the deterioration of dopamine neuron terminal buttons.
MAO-A - Norepinephrine and Serotonin
MAO-B - Norepinephrine and Dopamine
Selegilne becomes effective for depression *only* once the dosage is increased to the point where it begins to inhibit MAO-A along with MAO-B. MAO-A raises serotonin levels. MAO-B does not. However, inhibiting MAO-B exclusively is sufficient to treat Parkinsons Disease. Parkinsons is a disorder in which dopamine activity becomes progressively impaired. At higher dosages, selegiline loses its selectivity for MAO-B and begins to inhibit MAO-A as well. EMSAM is the MAO-B inhibitor product that is approved for depression. If you read the label, the company is clear in describing that EMSAM is effective for treating depression, but only at a patch dosage that inhibits MAO-A.
> > > I have combined Parnate 120 mg/day with methylphenidate and also with amphetamine. On top of that, came T4 and desipramine. It was of little value if remission was to be my goal.> > What was the problem with the combination? Did it not elevate your mood enough, or did it have adverse effects?
---------------------------------------------------------
In 1987, after 5 years of treatment failures, a doctor put me on a combination of Parnate and desipramine. It was harsh at first, but it eventually brought me close to remission. Functionally, I was very much improved. However, anhedonia remained less improved. I was quite happy with that state of affairs. After 6 months of remission, a delusional mania emerged for the first time as an adverse effect of drug treatment. The doctor discontinued both antidepressants, and I relapsed within 2 months. My doctor had no intentions of giving me a MAOI + TCA combination ever again - which was a monumental mistake. In 1990, I became psychotically manic after *discontinuing* Nardil. I was still responsive to it, though. I entered a psychiatric clinic as an inpatient. They treated me with Thorazine and then Haldol, after which I became absolutely refractory to all treatments.Taking clorgyline, a specific and irreversible inhibitor of MAO-A was powerful enough to break through the wall of non-response. I became responsive to drugs again, but it would take another 20 years to find the right treatment for me.
I am now close to being in full remission.
Current treatment regime:
Nardil - 90 mg/day
Nortriptyline - 150 mg/day
Lamotrigine - 300 mg/day
Lithium - 300 mg/day
- Scott
Posted by undopaminergic on September 29, 2022, at 6:13:35
In reply to Clorgyline is a MAOI specific for MAO-A., posted by SLS on September 28, 2022, at 13:52:49
> However, low dosages of selegiline inhibit MAO-B only, which is sufficient for treating Parkinsons Disease. Parkinsons
>In the case of selegiline amphetamine metabolites are also involved to an extent. This does not apply to rasagiline.
> is a movement disorder caused by the deterioration of dopamine neuron terminal buttons.
>I'm pretty sure the whole cells are affected. They go through apoptosis.
> MAO-A - Norepinephrine and Serotonin
> MAO-B - Norepinephrine and Dopamine
>MAO-A metabolises dopamine, and is indeed more involved in that process than MAO-B. I don't think MAO-B breaks down norepinephrine; its preferred substrate seems to be phenylethylamine (PEA).
-undopaminergic
Posted by SLS on September 29, 2022, at 11:02:40
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » SLS, posted by undopaminergic on September 29, 2022, at 6:13:35
> > However, low dosages of selegiline inhibit MAO-B only, which is sufficient for treating Parkinsons Disease. Parkinsons
> >
>
> In the case of selegiline amphetamine metabolites are also involved to an extent. This does not apply to rasagiline.Interesting. I didn't know that.
Thanks.
- Scott
Posted by linkadge on September 29, 2022, at 16:14:46
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » SLS, posted by undopaminergic on September 29, 2022, at 6:13:35
To add to the conversation:
New research suggests that MAO-B doesn't break down dopamine as previously thought (at least not to any appreciable extent). However, as mentioned, it does metabolize PEA and it seems to be involved in the formation of GABA. Inhibiting MAO-B reduces the synthesis of GABA which may have motor improving effects. Also, alpha-synuclein clumping is reduced by inhibiting MAO-B and this may produce some of the therapeutic effects in Parkinsons.
A recent study showed that MAO-B was elevated in the prefrontal cortex of depressed patients. Hence, some degree of MAO-B inhibition may be therapeutic in depression (even if it doesn't produce an immediate mood boost). There is also some evidence that COVID may increase MAO-B levels which may contribute to some of the brain fog / loss of energy in long COVID.
Linkadge
Posted by undopaminergic on September 29, 2022, at 16:58:25
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » undopaminergic, posted by linkadge on September 29, 2022, at 16:14:46
> To add to the conversation:
>
> New research suggests that MAO-B doesn't break down dopamine as previously thought (at least not to any appreciable extent).
>I recall reading some research that's not so new any more, suggesting that in rodents, MAO-B is not involved in dopamine metabolism under normal physiological conditions, but in humans it is more involved (not sure how much).
-undopaminergic
Posted by SLS on September 29, 2022, at 17:48:52
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » undopaminergic, posted by linkadge on September 29, 2022, at 16:14:46
* Great post, Linkadge. I wish my hippocampus was as big as yours. Your posts are always a wealth of information and understanding (critical thinking).
* UD, your information regarding MAOIs is certainly more current than mine.
> To add to the conversation:
>
> New research suggests that MAO-B doesn't break down dopamine as previously thought (at least not to any appreciable extent). However, as mentioned, it does metabolize PEA and it seems to be involved in the formation of GABA. Inhibiting MAO-B reduces the synthesis of GABA which may have motor improving effects. Also, alpha-synuclein clumping is reduced by inhibiting MAO-B and this may produce some of the therapeutic effects in Parkinsons.
>
> A recent study showed that MAO-B was elevated in the prefrontal cortex of depressed patients. Hence, some degree of MAO-B inhibition may be therapeutic in depression (even if it doesn't produce an immediate mood boost). There is also some evidence that COVID may increase MAO-B levels which may contribute to some of the brain fog / loss of energy in long COVID.
>
> Linkadge
As far as the necessity to block both MAO subtypes to treat depression, I haven't come across anything that would lead me to believe that an antidepressant response requires that MAO-B be inhibited. In fact, selegiline and clorgyline demonstrate the reverse. I like to mention clorgyline because it is specific for MAO-A. It doesn't affect MAO-B at all. So, for a bunch of treatment resistant cases of depression, the NIH provided clorgyline for people who responded to nothing else. Many of these patients went home happy for the first time. As the doctors at NIH liked to say, "Clorgyline is our ace-in-the-hole." As for selegiline, an antidepressant response occurs only when the dosage is high enough to inhibit MAO-A as well as MAO-B. The manufacturer's package label is explicit regarding this.It seems that heterogeneity in mood disorders is more the rule than the exception. I would not reject research demonstrating that a subset of patients need MAO-B to inhibited in order to achieve remission.
Posted by undopaminergic on September 30, 2022, at 6:28:50
In reply to Re: Clorgyline is a MAOI specific for MAO-A., posted by SLS on September 29, 2022, at 17:48:52
>
> As far as the necessity to block both MAO subtypes to treat depression, I haven't come across anything that would lead me to believe that an antidepressant response requires that MAO-B be inhibited. In fact, selegiline and clorgyline demonstrate the reverse. I like to mention clorgyline because it is specific for MAO-A. It doesn't affect MAO-B at all. So, for a bunch of treatment resistant cases of depression, the NIH provided clorgyline for people who responded to nothing else. Many of these patients went home happy for the first time. As the doctors at NIH liked to say, "Clorgyline is our ace-in-the-hole."
>But why is clorgyline more effective than nonselective MAOIs? Does it have other mechanisms of action in addition to MAO-A inhibition, or is inhibiting MAO-B a negative thing when treating depression?
Why did you stop using it?
-undopaminergic
Posted by linkadge on September 30, 2022, at 15:41:54
In reply to Re: Clorgyline is a MAOI specific for MAO-A., posted by SLS on September 29, 2022, at 17:48:52
It's not that MAO-B is necessary for the antidepressant effect, but that it might provide additional (perhaps complementary) effects on energy and cognition. Also, on a theoretical basis, the MAO-B inhibition may exert some neuroprotective and anti-inflammatory effects.
Linkadge
Posted by linkadge on September 30, 2022, at 15:46:14
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » SLS, posted by undopaminergic on September 30, 2022, at 6:28:50
In addition to its effects on MAO, Clorgyline is a potent agonist at the imidazoline receptors. Imidazoline receptors are only partially characterized, but agonists at this receptor system appear to have significant antidepressant effects. Imidazoline receptors modulate the alpha-2 receptors and may also have an ability to regulate MAO levels (independent of the direct effects of clorgyline). Rapid acting antidepressants (like agmatine) are imidazoline agonists. It is entirely possible that this effects contributes to the antidepressant effects of clorgyline (and separates it from other MAOIs).
Linakdge
Posted by linkadge on September 30, 2022, at 17:11:44
In reply to Re: Clorgyline is a imidazoline agonist, posted by linkadge on September 30, 2022, at 15:46:14
Clorgyline is a potent sigma agonist and an extremely potent imidazoline receptor agonist.
https://en.wikipedia.org/wiki/Clorgiline
"It has been found to bind with high affinity to the sigma 1 receptor (Ki = 3.2 nM)[3][5] and with very high affinity to the I2 imidazoline receptor (Ki = 40 pM).[6]"
Posted by undopaminergic on September 30, 2022, at 17:44:50
In reply to Re: Clorgyline is a imidazoline agonist, posted by linkadge on September 30, 2022, at 17:11:44
> Clorgyline is a potent sigma agonist and an extremely potent imidazoline receptor agonist.
>
> https://en.wikipedia.org/wiki/Clorgiline
>
> "It has been found to bind with high affinity to the sigma 1 receptor (Ki = 3.2 nM)[3][5] and with very high affinity to the I2 imidazoline receptor (Ki = 40 pM).[6]"
>Interesting findings!
-undopaminergic
Posted by SLS on October 1, 2022, at 20:12:13
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » SLS, posted by undopaminergic on September 30, 2022, at 6:28:50
> >
> > As far as the necessity to block both MAO subtypes to treat depression, I haven't come across anything that would lead me to believe that an antidepressant response requires that MAO-B be inhibited. In fact, selegiline and clorgyline demonstrate the reverse. I like to mention clorgyline because it is specific for MAO-A. It doesn't affect MAO-B at all. So, for a bunch of treatment resistant cases of depression, the NIH provided clorgyline for people who responded to nothing else. Many of these patients went home happy for the first time. As the doctors at NIH liked to say, "Clorgyline is our ace-in-the-hole."
> >
>
> But why is clorgyline more effective than nonselective MAOIs? Does it have other mechanisms of action in addition to MAO-A inhibition, or is inhibiting MAO-B a negative thing when treating depression?I don't know. Your guess is as good as mine. Sometimes, I just pay attention to what works without worrying about how it works. That's what doctors have been doing since 1957 (unfortunately).
Maybe you don't need any MAO-B inhibition at all to treat depression. There is evidence that you can effectively treat depression with compounds that are specific to MAO-A. The two examples I have in mind are clorgyline (irreversible) and moclobemide (reversible). I can' think of a single selective inhibitor of MAO-B that is effective in depression. Pargyline is selective for MAO-B, but not specific. It disappeared decades ago.
https://www.nature.com/articles/s12276-021-00646-3
> Why did you stop using it?
I was supplied with clorgyline by the NIH. That was part of the bargain. Clorgyline was discovered and manufactured for many years as a biological probe for neuroscience investigations. It was never approved. Perhaps no one became interested because the patent had expired. I don't know. The NIH had been using clorgyline for quite a few years before I got there. Having been aware of clorgyline for 10 years, I was quick to sign up for their research patient program. Clorgyline was what the NIH used to treat patients who responded to nothing else. I received my supply through the mail, I think. It worked for me more than any other single drug had. The problem was, the head of research department wouldn't let me add a tricyclic to it. I absolutely must have both in order to respond.
The reason I stopped taking clorgyline was because the partial improvement without a tricyclic was not sufficient for me. A few years passed when I found out that the NIH were no longer using clorgyline, and required that all of their former patients, most of whom were in remission, stop taking it. They became concerned when a number of adverse cardiac events were reported. My only thought is that clorgyline might be capable of producing cardiac valvulopathy. This was the case with fenfluramine, which is a potent serotonin (5-HT) releaser. Remember Fen-Phen?
- Scott
Posted by SLS on October 1, 2022, at 20:15:34
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » undopaminergic, posted by linkadge on September 29, 2022, at 16:14:46
> To add to the conversation:
>
> New research suggests that MAO-B doesn't break down dopamine as previously thought (at least not to any appreciable extent). However, as mentioned, it does metabolize PEA and it seems to be involved in the formation of GABA. Inhibiting MAO-B reduces the synthesis of GABA which may have motor improving effects. Also, alpha-synuclein clumping is reduced by inhibiting MAO-B and this may produce some of the therapeutic effects in Parkinsons.
>
> A recent study showed that MAO-B was elevated in the prefrontal cortex of depressed patients. Hence, some degree of MAO-B inhibition may be therapeutic in depression (even if it doesn't produce an immediate mood boost). There is also some evidence that COVID may increase MAO-B levels which may contribute to some of the brain fog / loss of energy in long COVID.
>
> Linkadge
>I found this earlier today:
"MAO-A and MAO-B, with different substrate specificities4. In particular, epinephrine, norepinephrine, melatonin, and serotonin are mainly metabolized by MAO-A, whereas phenylethylamine and benzylamine are mainly degraded by MAO-B."
https://www.nature.com/articles/s12276-021-00646-3
- Scott
Posted by SLS on October 2, 2022, at 13:03:05
In reply to Re: Clorgyline is a imidazoline agonist, posted by linkadge on September 30, 2022, at 17:11:44
> Clorgyline is a potent sigma agonist and an extremely potent imidazoline receptor agonist.
>
> https://en.wikipedia.org/wiki/Clorgiline
>
> "It has been found to bind with high affinity to the sigma 1 receptor (Ki = 3.2 nM)[3][5] and with very high affinity to the I2 imidazoline receptor (Ki = 40 pM).[6]"I didn't know clorgyline had those additional effects. The neuroscientists of the past didn't have the technology being used today to have determined these things. It makes you want to throw your hands in the air. So much data, so little understanding.
Moclobemide has a stunning antidepressant effect during the first two weeks of treatment. It is what is called a RIMA - a reversible inhibitor of MAO-A. In the long-term, however, it is usually a dead-end. People get well, but don't stay well. My guess is that this is related to its reversibility. It would be interesting to know if moclobemide has some of the same additional properties you cited for clorgyline
- Scott
Posted by linkadge on October 2, 2022, at 15:38:53
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » linkadge, posted by SLS on October 1, 2022, at 20:15:34
Yes. I believe that was one of the studies I read. Apparently in Alzheimer's there is an abnormal accumulation of gaba in certain brain regions that impairs synaptic function / plasticity. MAO-B inhibitors have some ability to counteract this. MAO-B tends to increase with age as well. So, some degree of MAO-B inhibition may have anti-aging properties.
Certain forms of depression apparently respond to stimulants (at least as adjunctives). I have wondered if MAO-B might be overactive in such forms of depression, leading to a deficit of the endogenous phenylethylamine (PEA). There have been some studies on selegiline (in combination with PEA) for treatment resistant depression. A few studies have found PEA deficits in depression and/or ADHD.
Linkadge
Posted by undopaminergic on October 2, 2022, at 15:47:33
In reply to Re: Clorgyline is a MAOI specific for MAO-A. » SLS, posted by linkadge on October 2, 2022, at 15:38:53
I recall some articles on PEA and selegiline by a Dr. Hector Sabelli. It was based on his writings that I came to use-abuse the combination for a somewhat prolonged period.
-undopaminergic
Posted by linkadge on October 2, 2022, at 15:51:26
In reply to Re: Clorgyline is a imidazoline agonist » linkadge, posted by SLS on October 2, 2022, at 13:03:05
I am going to see a psychiatrist later this month and may ask about an MAOI. I wouldn't mind trying moclobemide, but (as you mention) there have been some issues of efficacy.
I watched a video by Dr. Gillman (the Australian psychiatrist who is a proponent of MAOIS) on Moclobemide. He mentioned the fact that moclobemide seemed to plateau in its ability to inhibit MAO-A. According to some of the studies he was associated with, moclobemide could be displaced from MAO-A by serotonin itself. This, of course, would limit the degree to which it could inhibit MAO-A.
Still, I do know some people who do well on it (especially in combination with lithium). There is a biological mechanism that would support MAO-A as a target in bipolar depression. Apparently, mood stabilizers work to regulate PER2 (which controls circadian rhythm). But, by regulating PER2, there is an upregulation of MAO-A. I hypothesize that MAO-A might become overly active in the depressive phase via PER2.
To be honest, the only benefit I am getting right now is from rhodiola. According to my calculations (translating from animal data) 500mg of rhodiola could inhibit ~30% of MAO-A. I seem to get a noticeable benefit from about 1000mg. I also take amur corktree bark (which is purportedly one of the most potent herbal MAO-B inhibitors). It helps energy. Of course, I'd like to connect with a doctor that is willing try try more than reuptake inhibitors.
https://pubmed.ncbi.nlm.nih.gov/18439826/
Linkadge
Posted by Jay2112 on October 2, 2022, at 19:09:06
In reply to Re: Clorgyline is a imidazoline agonist, posted by linkadge on October 2, 2022, at 15:51:26
Hey Linkadge:
My experience with moclobomide was probably the most interesting of all antidepressants. My problem was, I think a result of my bipolar dx, is I couldn't do too high of a dose. To be honest, a small half 150 dose was an awesome 'lift' out of depression, but I think I needed a mood stabalizer like lithium and esp carbamazapine. When I get too much serotonin stimulation, my Asperger's symptoms take over.
I am finding 'some' interesting results with bromocriptine at bedtime. It apparently, slightly, agonizes serotonin receptors too. However, I may try pramipexole and/or rotigotine (which I have not tried yet.)
Results to follow...
Jay
Posted by linkadge on October 21, 2022, at 17:58:03
In reply to Re: Clorgyline is a imidazoline agonist » linkadge, posted by Jay2112 on October 2, 2022, at 19:09:06
>When I get too much serotonin stimulation, my >Asperger's symptoms take over.
That is a very interesting statement. I don't think I have autism, but when I am on SSRIs (or effexor) I definately present differently to the world. Certainly, I appear colder and more disconnected and I like to ramble on about this fact or that fact. I seem to hold on stronger to my 'interest domains'.
Linkadge
Posted by SLS on November 19, 2022, at 21:52:37
In reply to Re: Clorgyline is a imidazoline agonist » linkadge, posted by Jay2112 on October 2, 2022, at 19:09:06
> Hey Linkadge:
>
> My experience with moclobomide was probably the most interesting of all antidepressants. My problem was, I think a result of my bipolar dx, is I couldn't do too high of a dose. To be honest, a small half 150 dose was an awesome 'lift' out of depression, but I think I needed a mood stabalizer like lithium and esp carbamazapine. When I get too much serotonin stimulation, my Asperger's symptoms take over.
>
> I am finding 'some' interesting results with bromocriptine at bedtime. It apparently, slightly, agonizes serotonin receptors too. However, I may try pramipexole and/or rotigotine (which I have not tried yet.)
>
> Results to follow...
>
> JayAre you still taking moclobemide?
How are you feeling on it?
- Scott
This is the end of the thread.
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