![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 19 of 19. This is the beginning of the thread.
Posted by Jay2112 on September 11, 2021, at 14:13:18
Hey folks..
I am getting really worried...yet again. My damn meds give me a few weeks of anger, a couple of days of remission, then back again all friggen OVER again!! My anger level is volcanic, and my irritation is horrific.
NO medication seems to help, only a bit of cannabis. (And no, cannabis is NOT the problem..I have independently tested and verified this,)
Damn!!! I just can't seem to put up with people, awaken angry, have horrible dreams, and I get no pleasure out of most things. 30 years on god damn meds, and I still can't control this. "Mood Stabilizers" make me feel like crap...same with all antidepressants. Anti-psychotics make me angry...very angry. Same with beta-blockers, and all of those. Benzo's make me angry. Cannabis is the *only* thing that brings some relief. And very large doses of Lyrica (pregabalin).Now, Effexor really seems to rev up the anger level. After being on it for almost 20 years, shouldn't my friggen serotonin and norepinephrine receptors be majorly downregulated? Every pill still feels like the first time I took this stuff, causing a very irritable mood. But, Tegretol and Depakote/Epival do the same thing!!
And yes, I have tried going without meds, and that makes me suicidal and hopeless. So..I am going to continue using my THC capsules for relief. No, this stuff does not cause me any anger or irritation. It is the only hope I have. (p.s. Taking very, very large doses of Tegretol and Epival, so I feel almost 'stoned' on them, is also the only other things that help. Problem is, I get some really bad side-effects like major dizziness and somnolence.)
Is this the result of taking decades long worth of heavy psych meds? I JUST want a nice, balanced peaceful feeling. I get very, very frustrated...and am hurting the ones I love. My apartment is in shambles, because I get wound up and frustrated trying to organize. I just get p*ssed off, and say f**k it!
I got a beautiful baby kitten, who is rambunctious, and gets into my mess, making it even worse. And, my tolerance level is so damn low, I scream at her constantly. (I have never hit her, no matter what, though..thank christ!!)But, I want to just show her love, tenderness, and empathy. I *used* to be a very relaxed person..with such gentleness and happiness in life. That was part of my disposition.
On a personal note...sorry if this is TMI, but I struggle with impotence. I have well-controlled type 2 diabetes, but from my research, is another major cause of ED. Taking dopamine agonists ALSO enrage me, and don't seem to help. I feel like I am heading down the road to early onset dementia, Parkinson's, or Alzheimer's. Oh, and my sleep is filled with dark, abysmal dreams, replaying horrors from my past over and over again. The only thing good about what Effexor USED to do, is suppress the exhausting REM sleep causing this.
Out of answers...and thinking of using micro-doses
of psilocybin, or MDMA. And, I may try very small dose of Androgel. Just afraid that being over 50, my chances of getting prostate cancer are ever increased.So, ya, I am scare s*itless! Any help would be greatly appreciated. The only thing I actually enjoy is my return to university, and studying intellectual topics. One thing about my social life..I have a brother I love very much..but he, not to sound snobby, does not have an open intellectual understanding of life and the world. The neighbours I do have in my building, are just grumpy, anti-intellectual muscle-heads.
Well, thanks for reading this far.
(A defeated)
Jay
Posted by linkadge on September 11, 2021, at 14:34:59
In reply to Help..severe anger...., posted by Jay2112 on September 11, 2021, at 14:13:18
Yeah, effexor can make me angry too. It tends to make me overly opinionated and argumentative. I had to come off this (but for other reasons).
Some things that help me in this regard are lithium, DHA, magnesium, niacin, periodic fasting, replacing coffee with black tea. Tryptophan may help too. Hormones can sometimes work both ways (reducing anger in some and increasing it in others).
You might also try quercetin.
Linkadge
Posted by Jay2112 on September 11, 2021, at 19:14:32
In reply to Re: Help..severe anger...., posted by linkadge on September 11, 2021, at 14:34:59
> Yeah, effexor can make me angry too. It tends to make me overly opinionated and argumentative. I had to come off this (but for other reasons).
>
> Some things that help me in this regard are lithium, DHA, magnesium, niacin, periodic fasting, replacing coffee with black tea. Tryptophan may help too. Hormones can sometimes work both ways (reducing anger in some and increasing it in others).
>
> You might also try quercetin.
>
> Linkadge
>
>Hey Linkadge:
Hope you are doing well. My next shot at med *may*
be moclobemide. My pdoc will not try me on a traditional MAOI, I think at least until I give the moclobemide a shot. Thing is, I don't think I can do without a stimulant. But, moclobemide was a bit stimulating when I took it about 25 years ago. I actually did sorta like it. So...not quite sure. Plus, I was also thinking of Luvox, as it, back then at least, was a smoothing-out kinda med. I did ok on Prozac, but it's norepinephrine-stimulating properties also made me feel like a prisoner.I am spending lots of money on cannabis, but it is worth it. I've tried CBD many times, and I honestly feel worse after ingesting it. I can't tolerate magnesium, as I have early stage kidney disease...that sorta goes for lithium too.
But, I have tried taking the 150mg dose of lithium, fine. But I need the higher dose, usually around six hundred milligrams. Do you know at what dose lithium becomes an NMDA antagonist?I've tried most of the 'natural' route...had a really tough time with B vitamins, as too high doses can majorly mess your mind around. Really, though, serotonin and norepinephrine, raised by drugs, seem to cause more problems than not. I am more attracted to opioids, and anything to calm my horrible anxiety. Oddly, calcium works well for me. Not all the time, though. Amphetamine too...god...I love that stuff. :)
Thanks...
Jay
Posted by linkadge on September 12, 2021, at 17:13:34
In reply to Re: Help..severe anger.... » linkadge, posted by Jay2112 on September 11, 2021, at 19:14:32
Here are a few things that can help stretch your cannabis budget. I use medical cannabis and have found some tricks to help make it more potent / last longer.
Note: I mostly use edibles, so some of the items mentioned below may not apply. Read all 6 below, some you probably know some you may not.
1) Get a good product and don't neglect the CBD. I have found that without CBD, I seem to develop a faster tolerance to weed. Adding CBD (for me) seems to enhance the effect and keep it working more consistently.
2) Try decarbing. Gram for gram, I find well decarbed weed stronger as an edible than vaped (although it takes about an our to start to work). I purchased the 'Ardent' decarboxylator. It is a bit pricy ($220 CAD) however I have easily made my money back. It heats it to the exact temp for the exact amount of time to decarb the product well. Gram for gram, I get much more effect out of edibles when using these methods.
3) Grind *after* decarbing. Otherwise the sticky trichomes just get stuck to your grinder. After it is decarbed it grinds more easily.
4) Supplement with folic acid. Folic acid enhances the biological effect of cannabinoids (see study below) and cannabinoids can reduce the uptake of folic acid (i.e. easy for stoner to become deficient). The supplement methylfolate is a more biologically active form of folic acid and (at least here in Canada) is very cheap.
https://bioteach.ubc.ca/TeachingResources/Biochemistry/fakepapers/Cannabinoidreceptors.pdf
5) Liberally add black pepper to your diet. Black pepper contains piperine which has been shown to significantly increase the bioavailability of CBD (perhaps THC too). In the study below, it increased the bioavailability by 2.5x! I.e. 2.5 times more CBD actually enters your blood stream when piperine is added to the diet. Also black pepper is a bit of an MAOI which can enhance the effects. See study below. Additionally, black pepper contains substances that inhibit anandamide reuptake. I.e. boosting the endocannabinoid system.
https://pubmed.ncbi.nlm.nih.gov/32198013/
6) After decarbing and grinding I measure out the exact amount I want. Stick it in your mouth but before you swallow put a teaspoon of olive oil in your mouth. Then literally chew the weed and olive oil together for a few minutes before swallowing. This mechanically extracts the ingredients and mixes it into the oil. Ingesting with oil also increases the absorbtion as they are fat soluble. Also, olive oil contains oleic acid which converts to oleamide. Oleamide has its own cannabimimetic effects.
Using these 6, I have cut my spending to about $100 (Canadian) every 3 months.
Linkadge
Posted by SLS on September 12, 2021, at 21:43:51
In reply to Help..severe anger...., posted by Jay2112 on September 11, 2021, at 14:13:18
Hi, Jay.
Is your symptom more of aggression or one of anger withoug aggression?
carbamazepine (Tegretol) has been used for years to treat non-epilepsy aggression and child conduct disorders? It has a sister drug called oxcarbazepine (Trileptal). Its advantage over carbamazepine is that it is without the liability to produce agranulocytosis - no biweekly or monthly blood tests are required. Oxcarbazepine might also affect the metabolism of other drugs less than does carbamazepine, but I'm not sure. The only thing to watch for with oxcarbazepine is hyponatremia - low blood sodium. I doubt it is a common occurrence, though.
- Scott
Posted by SLS on September 14, 2021, at 13:58:37
In reply to Re: Help..severe anger.... » linkadge, posted by Jay2112 on September 11, 2021, at 19:14:32
Jay,
My recommendation is that you take a pass on moclobemide. It can produce remarkably quick results for depression, and possibly anxiety. People often begin at 300 mg/day and improve remarkably, but usually only briefly. However, dosage escalation is all but inevitable, and usually results in a failure to remain well at 1200 mg/day. For me, I experienced a noticeable and clean improvement within a couple of days, but I relapsed within 2 days. My reaction became foul quickly, and left me tortured, curled up in a fetal position on the couch, and audibly whimpering.
Personally, I think MAO-A is essential for an MAOI to work for depression, particularly one where anhedonia or anxiety is present. After watching a bunch of RIMAs appear and then disappear, moclobemide is the last one to stand. It has a remarkably short half-life, and is sometimes considered partially irreversible. A low-tyramine diet is still necessary, but the daily intake can be as high as 50 mg. Irreversibility seems all but essential for MAOIs to be effective. Brofaromine and the others that were developed were never approved anywhere in the world with the exception of one of the Balkins, I can't remember which one.
In my early research, I came upon an MAOI called clorgyline. It is a remarkably potent and specific inhibitor of MAO-A. Unlike moclobemide, it is irreversible. It was never developed for marketing. However, it was (and probably still is) the gold standard for manipulating and tagging the MAO-A enzyme. I caught wind that the NIH was using it on their most treatment-resistant cases. My doctor there called it their "ace-in-the-hole". At a time when I was totally unresponsive to all treatments, including Nardil and Parnate, clorgyline kicked a few bricks out of the wall that allowed me to regain some responsivity to future treatments. I was on it for awhile, but the improvement was at best moderate, and very episodic. Before leaving the NIH, asked the head of the department, William Z. Potter, if he would add desipramine. He said yes, but only 10 mg/day. I didn't bother. Perhaps I made a mistake, but ultimately, it wouldn't have made a difference. Unfortunately, there were some reports that among the very, very few people who were taking clorgyline, cardiac side effects emerged in a few of them. They withdrew clorgyline from their patient population. Clorgyline had been considered the most efficacious antidepressant on Earth.
It is important to know that selegiline / l-deprenyl / EMSAM does not produce an antidepressant response until the dosage has reached high enough for it to inhibit MAO-A in addition to the selective inhibition of MAO-B at lower dosages. Therefore, selegiline is selective for MAO-B at the low dosages used to treat Parkinson's, but not at high dosages. If selegiline were specific for MAO-B rather than specific, it would never work to treat depression.
- Scott
Posted by SLS on September 14, 2021, at 15:42:31
In reply to Re: Help..severe anger...., posted by SLS on September 14, 2021, at 13:58:37
Should be:
It is important to know that selegiline / L-deprenyl / EMSAM does not produce an antidepressant response until the dosage is high enough to inhibit MAO-A in addition to the inhibition of MAO-B at lower dosages. Selegiline is selective for MAO-B at the low dosages used to treat Parkinson's, but not at the higher dosages necessary to produce an antidepressant effect. If selegiline were *specific* for MAO-B rather than *selective*, I doubt that it would work to treat depression.
- Scott
Posted by undopaminergic on September 15, 2021, at 4:05:42
In reply to Re: Help..severe anger...., posted by SLS on September 14, 2021, at 13:58:37
>
> Personally, I think MAO-A is essential for an MAOI to work for depression,
>I agree.
>
> In my early research, I came upon an MAOI called clorgyline. It is a remarkably potent and specific inhibitor of MAO-A. Unlike moclobemide, it is irreversible. It was never developed for marketing. However, it was (and probably still is) the gold standard for manipulating and tagging the MAO-A enzyme. I caught wind that the NIH was using it on their most treatment-resistant cases. My doctor there called it their "ace-in-the-hole". At a time when I was totally unresponsive to all treatments, including Nardil and Parnate, clorgyline kicked a few bricks out of the wall that allowed me to regain some responsivity to future treatments. I was on it for awhile, but the improvement was at best moderate, and very episodic. Before leaving the NIH, asked the head of the department, William Z. Potter, if he would add desipramine. He said yes, but only 10 mg/day. I didn't bother. Perhaps I made a mistake, but ultimately, it wouldn't have made a difference. Unfortunately, there were some reports that among the very, very few people who were taking clorgyline, cardiac side effects emerged in a few of them. They withdrew clorgyline from their patient population. Clorgyline had been considered the most efficacious antidepressant on Earth.
>Why would clorgyline be more effective than the non-selective MAOIs? Is MAO-B inhibition harmful to the treatment of depression?
-undopaminergic
Posted by SLS on September 16, 2021, at 12:26:00
In reply to Re: Help..severe anger.... » SLS, posted by undopaminergic on September 15, 2021, at 4:05:42
> >
> > Personally, I think MAO-A is essential for an MAOI to work for depression,
> >
>
> I agree.
>
> >
> > In my early research, I came upon an MAOI called clorgyline. It is a remarkably potent and specific inhibitor of MAO-A. Unlike moclobemide, it is irreversible. It was never developed for marketing. However, it was (and probably still is) the gold standard for manipulating and tagging the MAO-A enzyme. I caught wind that the NIH was using it on their most treatment-resistant cases. My doctor there called it their "ace-in-the-hole". At a time when I was totally unresponsive to all treatments, including Nardil and Parnate, clorgyline kicked a few bricks out of the wall that allowed me to regain some responsivity to future treatments. I was on it for awhile, but the improvement was at best moderate, and very episodic. Before leaving the NIH, asked the head of the department, William Z. Potter, if he would add desipramine. He said yes, but only 10 mg/day. I didn't bother. Perhaps I made a mistake, but ultimately, it wouldn't have made a difference. Unfortunately, there were some reports that among the very, very few people who were taking clorgyline, cardiac side effects emerged in a few of them. They withdrew clorgyline from their patient population. Clorgyline had been considered the most efficacious antidepressant on Earth.
> >
>
> Why would clorgyline be more effective than the non-selective MAOIs? Is MAO-B inhibition harmful to the treatment of depression?That's a really good question. I don't know the answer to it. I'm guessing that you are referring to a scenario similar to that of citalopram and escitalopram?
A long time ago, I read that Parnate (tranylcypromine) is actually partially reversible.
I found this, but one has to assume that the pharmacological effect being referred to is MAO inhibition. I imagine it is, but I don't see how this would be of consequence.
"However, recent research has demonstrated that tranylcypromine can produce direct and reversible pharmacologic effects"
https://pubmed.ncbi.nlm.nih.gov/1813896/
- Scott
Posted by undopaminergic on September 16, 2021, at 13:08:18
In reply to Re: Help..severe anger.... » undopaminergic, posted by SLS on September 16, 2021, at 12:26:00
> >
> > Why would clorgyline be more effective than the non-selective MAOIs? Is MAO-B inhibition harmful to the treatment of depression?
>
> That's a really good question. I don't know the answer to it. I'm guessing that you are referring to a scenario similar to that of citalopram and escitalopram?
>I hadn't thought of it like that, but I guess there is an analogy. Just to clarify, I'm wondering why specific MAO-A inhibition with clorgyline would be better than dual MAO-A and MAO-B inhibition with classic MAOIs. MAO-B contributes to dopamine breakdown, so one would think that inhibiting it in addition to MAO-A would be beneficial, rather than the opposite, that is MAO-B inhibition being detrimental.
> A long time ago, I read that Parnate (tranylcypromine) is actually partially reversible.
>I seem to recall that it is *slowly* reversible. So slowly that it is negligible in practice. Also, I've read that tranylcypromine is slightly selective for MAO-B.
> I found this, but one has to assume that the pharmacological effect being referred to is MAO inhibition. I imagine it is, but I don't see how this would be of consequence.
>
> "However, recent research has demonstrated that tranylcypromine can produce direct and reversible pharmacologic effects"
>
> https://pubmed.ncbi.nlm.nih.gov/1813896/No, at least as I understand it, they are speaking specifically about non-MAOI actions of tranylcypromine -- that would be, for example, the amphetaminergic action. MAO inhibition, because it is so slowly reversible, does not require tranylcypromine to be continuously present in tissues. Other pharmacodynamical actions, that are readily reversible, do require certain concentrations of the drug. Therefore, the pharmacokinetics (ie. clearance) of the MAOI compound itself are of interest even though it is irrelevant to the maintenance of MAO inhibition.
-undopaminergic
Posted by SLS on September 17, 2021, at 3:45:40
In reply to Re: Help..severe anger.... » SLS, posted by undopaminergic on September 16, 2021, at 13:08:18
> > >
> > > Why would clorgyline be more effective than the non-selective MAOIs? Is MAO-B inhibition harmful to the treatment of depression?
> >
> > That's a really good question. I don't know the answer to it. I'm guessing that you are referring to a scenario similar to that of citalopram and escitalopram?
> >
>
> I hadn't thought of it like that, but I guess there is an analogy. Just to clarify, I'm wondering why specific MAO-A inhibition with clorgyline would be better than dual MAO-A and MAO-B inhibition with classic MAOIs. MAO-B contributes to dopamine breakdown, so one would think that inhibiting it in addition to MAO-A would be beneficial, rather than the opposite, that is MAO-B inhibition being detrimental.
I'm sure there is a biological reason for why we see this. I just don't know what it is. Selegiline (including EMSAM) does not exert antidepressant effects until the dosage is high enough to lose its selectivity. Both MAO-A and MAO-B become inhibited, yet this drug sucks as an antidepressant. By comparison, the reversible inhibitor of MAO-A (RIMA), moclobemide, produces an antidepressant far more robust than selegiline. Unfortunately, the improvement is farily brief. My guess is that reversibility is a liability. Moclobemide yields a progressive dosage escalation and ultimate failure. In my experience, moclobemide is more anhedonic and motivating than tranylcypromine while it lasts. I was always under the impression that Nardil inhibits more MAO-A than tranylcycpromine does. Maybe you can look into that. I'm a little short on time.Psychiatry: So many questions. So few answers.
- Scott
Posted by undopaminergic on September 17, 2021, at 8:22:53
In reply to Re: Help..severe anger.... » undopaminergic, posted by SLS on September 17, 2021, at 3:45:40
> >
> > Just to clarify, I'm wondering why specific MAO-A inhibition with clorgyline would be better than dual MAO-A and MAO-B inhibition with classic MAOIs. MAO-B contributes to dopamine breakdown, so one would think that inhibiting it in addition to MAO-A would be beneficial, rather than the opposite, that is MAO-B inhibition being detrimental.
>
>
> I'm sure there is a biological reason for why we see this.
>My best theory is as follows: MAO-B has been called phenylethylaminase, because its primary substrate is phenylethylamine (PEA), which at higher concentrations works like amphetamine. Thus PEA releases dopamine (and noradrenaline and maybe serotonin) from dopaminergic nerve terminals. This may result in a sensitation of dopamine autoreceptors, reducing dopamine synthesis and release. This may result in a functional depressive (apathetic, etc.) effect. So I wonder whether adding sulpiride or amisulpride would help.
But: PEA administered during MAO-B inhibition in sufficient quantities yields a powerful antidepressant (or stimulant) effect.
> Selegiline (including EMSAM) does not exert antidepressant effects until the dosage is high enough to lose its selectivity. Both MAO-A and MAO-B become inhibited, yet this drug sucks as an antidepressant. By comparison, the reversible inhibitor of MAO-A (RIMA), moclobemide, produces an antidepressant far more robust than selegiline. Unfortunately, the improvement is farily brief. My guess is that reversibility is a liability. Moclobemide yields a progressive dosage escalation and ultimate failure. In my experience, moclobemide is more anhedonic and motivating than tranylcypromine while it lasts. I was always under the impression that Nardil inhibits more MAO-A than tranylcycpromine does. Maybe you can look into that. I'm a little short on time.
>I don't feel this is important enough to spend much time investigating. It is an interesting curiosity. I wouldn't say moclobemide is necessarily a better antidepressant than EMSAM, but I don't have experience with this. You could be right.
> Psychiatry: So many questions. So few answers.
Yeah.
-undopaminergic
Posted by undopaminergic on September 17, 2021, at 12:10:28
In reply to Re: Help..severe anger.... » SLS, posted by undopaminergic on September 17, 2021, at 8:22:53
> > >
> > > Just to clarify, I'm wondering why specific MAO-A inhibition with clorgyline would be better than dual MAO-A and MAO-B inhibition with classic MAOIs. MAO-B contributes to dopamine breakdown, so one would think that inhibiting it in addition to MAO-A would be beneficial, rather than the opposite, that is MAO-B inhibition being detrimental.
> >
> >
> > I'm sure there is a biological reason for why we see this.
> >
>
> My best theory is as follows: MAO-B has been called phenylethylaminase, because its primary substrate is phenylethylamine (PEA), which at higher concentrations works like amphetamine. Thus PEA releases dopamine (and noradrenaline and maybe serotonin) from dopaminergic nerve terminals. This may result in a sensitation of dopamine autoreceptors, reducing dopamine synthesis and release. This may result in a functional depressive (apathetic, etc.) effect. So I wonder whether adding sulpiride or amisulpride would help.
>
> But: PEA administered during MAO-B inhibition in sufficient quantities yields a powerful antidepressant (or stimulant) effect.
>Alternative theory: there could be a MAO-B substrate that is depressogenic. It may be hitherto unidentified as a MAO-B target.
MPTP is a neurotoxin that produces Parkinson's disease. It is actually a precursor to the actual toxin; MAO-B converts MPTP to the MPP+ ion. There could be some other toxin that produces depression rather than Parkinson's, and which is *inactivated* by MAO-B, so that if you inhibit MAO-B, this substance is let loose on the CNS.
-undopaminergic
Posted by SLS on September 17, 2021, at 15:24:36
In reply to Re: Help..severe anger.... » SLS, posted by undopaminergic on September 17, 2021, at 8:22:53
Hi.
> I don't feel this is important enough to spend much time investigating. It is an interesting curiosity. I wouldn't say moclobemide is necessarily a better antidepressant than EMSAM, but I don't have experience with this. You could be right.What I said was that, by comparison, the reversible inhibitor of MAO-A (RIMA), moclobemide, produces an antidepressant far more robust than selegiline. Unfortunately, the improvement is fairly brief.
It is very common for people to feel *great* on moclobemide within a week or two. Sometimes, they experience a marked improvement within a few days. The problem is, most people do not stay improved. Despite increasing the dosage from the 300 mg/day that they had initially responded to, increasing the dosage up to the maximum dosage of 1200 mg/day still allows for a relapse shortly afterwards. That was my experience, too, but the improvement didn't last for even one week.
I think this is evidence that MAO-A inhibition is sufficient for a robust antidepressant effect, and that reversibility leaves moclobemide impotent, and it is usually incapable of producing a long-term answer for depression.
- Scott
Posted by SLS on September 17, 2021, at 15:27:06
In reply to Re: Help..severe anger...., posted by undopaminergic on September 17, 2021, at 12:10:28
> > But: PEA administered during MAO-B inhibition in sufficient quantities yields a powerful antidepressant (or stimulant) effect.
> >
>
> Alternative theory: there could be a MAO-B substrate that is depressogenic. It may be hitherto unidentified as a MAO-B target.
>
> MPTP is a neurotoxin that produces Parkinson's disease. It is actually a precursor to the actual toxin; MAO-B converts MPTP to the MPP+ ion. There could be some other toxin that produces depression rather than Parkinson's, and which is *inactivated* by MAO-B, so that if you inhibit MAO-B, this substance is let loose on the CNS.This is an excellent thought. However, I'll need a few more years to understand it.
:-)- Scott
Posted by Jay2112 on September 24, 2021, at 4:55:36
In reply to * Correction regarding selegiline / EMSAM, posted by SLS on September 14, 2021, at 15:42:31
> Should be:
>
> It is important to know that selegiline / L-deprenyl / EMSAM does not produce an antidepressant response until the dosage is high enough to inhibit MAO-A in addition to the inhibition of MAO-B at lower dosages. Selegiline is selective for MAO-B at the low dosages used to treat Parkinson's, but not at the higher dosages necessary to produce an antidepressant effect. If selegiline were *specific* for MAO-B rather than *selective*, I doubt that it would work to treat depression.
>
>
> - Scott
>
>Hey Scott:
Great synopsis of experience/research and experimentation. I read of a few quite solid research studies on the use of a very effective combination of low dose selegiline and 5HTP in tackling dementia in Alzheimer's and Parkinson's.
I have experience with moclobemide from the past, when it first came out here in Canada. I actually did not have to modify my diet *at all*. I don't quite know why, but I (knock on wood) have never had issues with high blood pressure, and in particular, with adrenergic issues. I read that people with a particular adrenergic metabolic gene set have some difficulties with tolerating MAOIs.
But,yeah I had that on/off again effect with moclobemide. I really don't think it is good for people with major anxiety, nor bipolar.
Because I have diabetes, and problems with stomach food motility, I have been looking into some 'hacks' regarding Vagus nerve stimulation. I know it is an old issue, but there is quite a bit of research involving damage to the VN, and how that can really mess us both the brain and the rest of the body.
Thnx,
Jay
Posted by Jay2112 on September 24, 2021, at 5:11:31
In reply to Re: Help..severe anger.... » undopaminergic, posted by SLS on September 17, 2021, at 15:27:06
Just an interesting note...amphetamine (Dexedrine/Vyvanse) has been my only saviour. It MAJORLY reduces anger in me, and I think it is in part due to the sluggishness my diabetes (type II) has ravished on my brain and body. Antidepressants just, mostly, irritate me. Amphetamine has continuously produced a positive effect on me for over 15 years of daily use.
After further reading of the literature, I also think my diabetes has majorly damaged my Vagus nerve system. I have huge problems with food motility in my stomach, never mind major problems with irritability, lack of contentment, and just feeling so damn sluggish.
Jay
Posted by Lamdage22 on October 20, 2021, at 11:44:41
In reply to Re: Help..severe anger....All, posted by Jay2112 on September 24, 2021, at 5:11:31
Does it also reduce anger when you come off?
Posted by Lamdage22 on October 21, 2021, at 2:27:51
In reply to Re: Help..severe anger....All, posted by Lamdage22 on October 20, 2021, at 11:44:41
What I am asking is, do your drug habits worsen the baseline anger? If you ask successful people about their secrets, few will say its amphetamines and marihuana.
This is the end of the thread.
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