Amphetamine is an instant, but short lasting, cure

[DeGenesis]

for what its worth tizanidine is an alpha 2 agonist used as a muscle relaxer and helps with sleep initiation, only has a short half life so can be useful for people who wake in the middle of the night too?? Im sure many of these meds also affect other adrenergic receptors but to a much lesser degree. One example would be salbutamol for asthmatics which targets beta 2 receptors to relax smooth muscle of the respiratory system, a common side effect is tachycardia as it also has some effect on beta 1 receptors.

Alpha-2 agonists reduce the release of both epinephrine and norepinephrine. That is, they are sympatholytics.

 

[DeGenesis]

I read it differently. It talks about both antagonism of of alpha2 receptors (this would impair the calming and sensory filtering effects of Norepinephrine) and direct stimulation of 5HT (Serotonin) receptors.

It indirectly stimulates 5-HT receptors due to increased release of serotonin.

You are correct that it did not address adrenergic signalling.

 

[heapsreal]

Alpha-2 agonists reduce the release of both epinephrine and norepinephrine. That is, they are sympatholytics.

I mentioned it as it might be effective for people who have sleep problems and feel like its an adrenaline problem. May play a part in treating people with hypertensive pots/oi.

The frontal sinus infections i get increase my blood pressure as they become blocked and i think this is one of the reasons i get bad headaches. I get blood pressure readings like 160/110, although systolic isnt too bad the diastolic is high, my normal bp is 130/80. The tizanidine has lowered my bp when i have been in this situation and this has helped reduce the headches from the sinus infections??

So it does help lower bp, but the short half life means its only a short term solution, may benefit certain situations though??

 

[DeGenesis]

I mentioned it as it might be effective for people who have sleep problems and feel like its an adrenaline problem. May play a part in treating people with hypertensive pots/oi.

The frontal sinus infections i get increase my blood pressure as they become blocked and i think this is one of the reasons i get bad headaches. I get blood pressure readings like 160/110, although systolic isnt too bad the diastolic is high, my normal bp is 130/80. The tizanidine has lowered my bp when i have been in this situation and this has helped reduce the headches from the sinus infections??

So it does help lower bp, but the short half life means its only a short term solution, may benefit certain situations though??

There has been a lot of talk about clonidine in regards to CFS/ME. Clonidine and tizanidine's pharmacology is very similar, but clonidine lasts a lot longer. I use it to treat hyperadrenergic POTS, but I have been told that it can be very detrimental to those with ME. There is a lot of talk about clonidine on the DINET forums, if you are interested. Clonidine also helps me when my blood pressure is too high, but that is just my personal experience.

Good luck.

 

[heapsreal]

There has been a lot of talk about clonidine in regards to CFS/ME. Clonidine and tizanidine's pharmacology is very similar, but clonidine lasts a lot longer. I use it to treat hyperadrenergic POTS, but I have been told that it can be very detrimental to those with ME. There is a lot of talk about clonidine on the DINET forums, if you are interested. Clonidine also helps me when my blood pressure is too high, but that is just my personal experience.

Good luck.

yes i have read about it, i think there is also a rebound effect with clonidine if stopped suddenly, so requires a tapering off of the dose. The short half life of tizanidine could be helpful for those who have intermittent episodes of hypertension from orthostatic issues. Might also help those who cant sleep after amphetamine use or maybe having side effects from amphetamines, maybe good to have on hand if one is going to try amphetamine/stimulants??

 

[Sushi]

There has been a lot of talk about clonidine in regards to CFS/ME. Clonidine and tizanidine's pharmacology is very similar, but clonidine lasts a lot longer. I use it to treat hyperadrenergic POTS, but I have been told that it can be very detrimental to those with ME....

Interesting. Clonidine was awful for me, but then I have ME and OI but not POTS.

Sushi

 

[IreneF]

Hip: Yes, my son has ADHD, inattentive type.

 

[Valentijn]

Also, do you speak for everyone at this forum?

You clearly stalk me and take any chance to attack me. What's up?

You said we're very anti-psychiatry. I corrected you.

And I'm not stalking you - I read or skim every post on the forum, and when someone incorrectly applies stereotypes to forum members I usually feel compelled to reply.

 

[Leopardtail]

True, but I think the mental relaxation induced by stimulants may also play a role in ameliorating ADHD. Perhaps the relaxation is mediated by the effects on the prefrontal cortex?

I developed pretty severe ADHD after getting ME/CFS, and also from an episode of viral meningitis. On some days I could not even read a simple one paragraph email. I just could not input the text info on the computer screen into my brain.

It subjectively felt to me that my brain had too much internal tension to function properly, and that this tension was the cause of the ADHD. I was taking a cocktail of supplements to try to treat the ADHD; and I also found long hot baths worked wonders for my ADHD (probably due to the fever effect); whenever these supplements and hot baths succeeded in relaxing this internal tension, then my ADHD would diminish, and my brain would then function properly — at least enough to enable me to read my emails.

So I find it interesting that: (a) not only me, but many ADHD people complain of the inability to calm their mind; (b) that when I was able to calm my mind, my ADHD would melt away, and I would function properly for a while.

I have yet to try stimulants for ADHD, but generally my ADHD is now much better than it was. It is a pity that you cannot buy stimulants like Ritalin online, as they are controlled drugs. I am not sure what my doctor would say I asked for some Ritalin from him. He's not that sympathetic to the idea that I have ME/CFS, so he may not be sympathetic to me saying that I have ADHD either.

I am still getting my head around this stuff @Hip. While all the stimulants 'turn things on'. Some of those stimuli can in fact be calming. NE for example at correct levels gives the clam watchfull alertness that allows one to remain on guard duty through the night, but far too much of it produces day dreaming.

Dopamine by contrast produce complete in ability to focus on anything sensory at very low levels, produce calm drive at correct levels and produces acute concentration on all of the sense that is very distracting along with high agitation with too much of it.

One 'stimulant' however can suppress another, e.g. too much Dopamine suppresses NE production. There is a complex inter-relationship between the receptors for Catechols. Similar issues occur across the Catechol and Indol axes, but I don't yet understand those well.

 

[MeSci]

I guess psychiatry are trying to make out they are neurologists as they prescribe drugs that can help neurological symptoms?

A lot of them do indeed seem to pretend to be neurologists.

 

[Leopardtail]

A lot of them do indeed seem to pretend to be neurologists.

I wish I could like that comment a thousand times.

One things that blows a massive hole in their 'psychosomatic' hypotheses is that they do not understand the brain stem. Essentially with all actions short of deliberate suicide it provides a filter between cognition and bodily function. It will not allow you to 'stop breathing yourself to death' the minute you fall unconscious, it takes over, when you are conscious it fights with cognition producing that constant urge to breath, ultimately forcing breathing like it or lump it. In similar fashion it will not allow what they call their 'unconscious mind' (effectively the limbic system) to induce serious bodily harm (e.g. Sophia Merca).

I have given one simple example, but it performs a wide range of bodily control functions according to its own agenda.

 

[xchocoholic]

Hi. I gave up on trying to follow this but figured I'd add my experience anyways.

I'm taking low doses of modafinil and caffeine pills.

As a pwme with oh and pots I haven't found either of these helps my dysautonomia / hypoperfusion. I still get a huge blood rush in my upper body when I lay down. So much that I feel best if I go from standing to sitting then laying down. My heart pounds if I lay down too quickly.

Modafinil helps me think more clearly and with less straining. But I still have memory problems and trouble finding the right word at times. I'm taking appr 10 mg once in the am and later if needed. I let it dissolve in my mouth for better absorbancy.

Caffeine speeds up my thinking process but it isn't clear like it is on modafinil. Caffeine definitely makes me feel more awake. Modafinil doesn't. So I need both. Neither has returned me to my pre-me state, 1990, but the improvement is notable to me. Menopause fried my brain. Lol.

We need to consider how pem interfers with the effects of stimulants too. My pem is very clear now but wasn't for years. I would assume some mostly functional pwcs, esp those who work, have what I call chronic pem. So determining a reaction may be more difficult for them.

If I rest for a few days I have the energy to function for several hours on the 3rd or 4th day. Pem sets in within 24-48 hrs typically. I suspect my OI keeps me in this vicious circle. OI => hypoperfusion => pem.

If I have severe pem, increasing the amount of caffeine or modafinil
I normally take has no effect. I'm still couchbound and can't follow tv or a conversation.

Sometimes when I have pem I nap off and on all day and sleep 10-12 hours that night. Neither caffeine or modafinil change that now. Caffeine worked for a few glorious months tho. Lol. Because of my history with seizures I'm too chicken to increase my dosages too much.

Tc .. x

 

[misskatniss]

@Leopardtail And I wish I could like YOUR post a thousand times. THANK YOU for putting it in such a sharp, precise form what I was trying to capture in words: Why I am so sure that their the-unconscious/tricky-soul-blah-blah is nonsense. How you describe it is excellently put. Thanks!

As a humble psychologist I am a little aware of brain stem etc. I was really shocked about how early psychiatrists wouldn´t consider anything but a "psychosomatic" reason for such a devastating physical condition without ever investigating on neurological, adrenal or similar issues... How they just thought about Sero and Dopa as simple monocausal buttons to push and then the "depressed-yet-she-doesn´t-know it-and therefore-wants-no-cure"-young woman would (have to) get up again, healed of course. And how quickly they would blame the unconscious of the patient if this doesn´t occur: "You don´t do this (=not healing) on purpose, but..."

How many times have they really measured the "low Sero / too high Dopa" which they manipulated with various drugs in high doses? Zero times. And even if they had done so, our brain is much too complex to simply deduce "let´s raise this and lower that and all trouble´s gone". That´s not only antiscience or ignorance. That´s arrogance.

I truly forgot that psychiatrists are GPs as well, because they didn´t seem to be. Not even did they claim it were only in my mind. They also stated that there were no physical reasons without having checked out anything but a simple blood test. As if e.g. broken legs were visible in the blood. Broken mitochondria and many other things are not visible in a common blood test, yet they would state my conviction as psychotic fixation. And like this make sure no doc will ever in depth investigate on the reasons as it is so cozy to have the "explanation" right there. As soon as a doc asks what is going on and I tell him everything and that I was in a mental institution, I am already labelled.

How can you guys figure out all that alpha-etc.-detail? You are geniusses Wished all docs had that kind of approach.

 

[Leopardtail]

Basically we figure out the body the way we would figure a broken car engine out. If somebody says this drug had this effect.... we look up how it works,, and in the case of alpha-2 receptors, then look up the action of the receptors. Most of us have been at this for years. My special interests are mitochondria and hormone issues, because they are my primary problems. My previous job used to involved working out how systems were interacting and why stuff was suddenly going wrong (e.g. when web server worked perfectly for 6 days then suddenly failed very seven days). I use the same kind of analytic techniques to figure out what's happening in ME.

Other than that is a lifetime of interest in health and two years of very targeted use of medical textbooks. Rather than studying in a way that's system focussed (psychiatry, neurology, hormones) we study in a way that's problem focussed and examines the interaction between systems. We also have some real specialists on here who we can ask when we 'don't get it'.

Alex is a biochemsitry ace, I do endocrinology and energy generation, hip does neurology and associated chemistry, MeSci does leaky gut.... Phoenix is a real team effort and because we are all patients, bad ideas get corrected very fast..... I get more criticism if I haven't got it quite right here than I would at a university.

 

[MeSci]

I still get a huge blood rush in my upper body when I lay down. So much that I feel best if I go from standing to sitting then laying down. My heart pounds if I lay down too quickly.

Have you seen this thread? I'm sure your contributions would be welcome there!

 

[misskatniss]

@Leopardtail I admire your work and the community spirit. And as a nerd girl with a lot of sympathy for pattern recognition I like the problem-solving-based approach which is what I do or started with. In an interactive system like the body quite demanding, but so interesting!!

If only I were able to contribute. There´s so much precious info being created here!! I learned so much in few weeks here, and a few things already helped me a little but with big impact on my life quality, e.g. discovering the histamine link, the gut stuff etc.

So grateful, guys!!

 

[xchocoholic]

Have you seen this thread? I'm sure your contributions would be welcome there!

Hi. I'm enjoying doing laundry today (sarcasm) so I only read a few posts on that thread but I typically don't notice my heart pounding when I lay on either side. Maybe once in awhile but never enough to give it any thought.

I only lay on my back when I'm trying to recover from pots/hypoperfusion tho. It feels like my whole upper body needs to unwind from effects of the hypoperfusion. I can't imagine any other position allowing my muscles to fully recover. Full recovery typically takes 60-75 minutes. And I feel GREAT at that point.

Back to having fun. Lol. X

 

[Hip]

I am still getting my head around this stuff @Hip. While all the stimulants 'turn things on'. Some of those stimuli can in fact be calming. NE for example at correct levels gives the clam watchfull alertness that allows one to remain on guard duty through the night, but far too much of it produces day dreaming.

Dopamine by contrast produce complete in ability to focus on anything sensory at very low levels, produce calm drive at correct levels and produces acute concentration on all of the sense that is very distracting along with high agitation with too much of it.

One 'stimulant' however can suppress another, e.g. too much Dopamine suppresses NE production. There is a complex inter-relationship between the receptors for Catechols. Similar issues occur across the Catechol and Indol axes, but I don't yet understand those well.

If you do gain a good understanding of how stimulants work and how neurotransmitters interact, especially in the context of ME/CFS, please share it with us in new thread. I don't much much in this area, and would like to learn more.


Wellbutrin (Bupropion) and Near Complete Remission from ME/CFS

This is particularly because I recently had an extraordinary experience with taking Wellbutrin (bupropion), an antidepressant that also has stimulant effects. At a low dose of just 60 mg per day of Werllbutrin (the "SR" extended release version), my ME/CFS fatigue and brain fog were almost completely eliminated, and I found my ADHD and anhedonic depression suddenly in remission too.

My mind became so sharp and capable from Wellbutrin that I started doing some complex computer programming — something I have not been able to do since getting ME/CFS. In fact my mind felt so competent that I even began rapidly learning and using new computer languages that I had no prior knowledge of (such as the web language PHP).

So not only was my brain fog abolished by Wellbutrin, but I actually found my mind more competent and capable that it was even before getting ME/CFS. The only major cognitive symptom that Wellbutrin did not fix was my medium term memory difficulties, but this was only a minor problem. With my new cognitive powers, I embarked on an ambitious and interesting new web software project. And my depression was gone too; I felt in a really good, productive and highly motivated mood.

I was ecstatic, because I really thought I had found my personal cure for ME/CFS, especially as I found this paper that details a couple of cases of great improvements in ME/CFS from Wellbutrin. However, all good things it seems come to an end, and after around two weeks of this incredibly good cognition and intelligence that Wellbutrin had bestowed on me, my razor sharp mind just suddenly disappeared, and although I kept taking the same daily dose of Wellbutrin, I just descended back into my regular zombie-like ME/CFS brain fog. Infuriating.

Though at least my experience proved to me that as soon as you get the brain chemistry right, ME/CFS pretty much disappears. But I wanted to know why all these very significant benefits I obtained from Wellbutrin just evaporated after a few weeks.

Looking around online, a found several commenters talking about the Wellbutrin two week "honeymoon period," during which you feel really fantastic, but after around two weeks, all the benefits quickly taper off and disappear.

I thought this loss of the benefits from Wellbutrin might might just be a simple tolerance effect to this stimulant drug. So I decided to stop taking Wellbutrin, and wait three weeks before taking it again, so that any tolerance my brain had developed to Wellbutrin would dissipate. However, when I tried Wellbutrin again after this three week break, I could not replicate almost complete remission from brain fog and fatigue that this drug had given me before.

So something very strange is happening here.

It's possible that one or more supplements I was taking during the original two weeks of Wellbutrin were somehow acting in concert with Wellbutrin in order to provide this remission from ME/CFS. This is something I am looking into (I keep full records of all the drugs and supplements I take each day).

I'd really like to get some handle on the neurochemistry Wellbutrin, and how it was able to put my ME/CFS into near remission for two weeks. If I can figure out how Wellbutrin might be working in the ME/CFS brain, I might be able to come up with a workaround that extends the Wellbutrin two week honeymoon period indefintely. This would then provide me, and I hope others here too, with a treatment that can effectively put the fatigue and cognitive symptoms of ME/CFS into near remission.


Some Notes on Wellbutrin (Bupropion)

Wellbutrin is a norepinephrine-dopamine reuptake inhibitor (NDRI); though Wellbutrin's dopamine reuptake inhibition is very weak, so it is more of just a norepinephrine reuptake inhibitor (NRI). I read that Wellbutrin is converted into hydroxybupropion relatively quickly, and the dopamine reuptake inhibition is done primarily through Wellbutrin, so once it’s converted into the metabolite it becomes mostly focused around norepinephrine.

Wellbutrin also antagonizes the nicotinic acetylcholine receptor.†

Wellbutrin downregulates beta adrenergic receptors.

Good article on Wellbutrin: Chemically Correct: Bupropion by Andrew Novick | Mind And Muscle

 

[Leopardtail]

If you do gain a good understanding of how stimulants work and how neurotransmitters interact, especially in the context of ME/CFS, please share it with us in new thread. I don't much much in this area, and would like to learn more.


Wellbutrin (Bupropion) and Near Complete Remission from ME/CFS

This is particularly because I recently had an extraordinary experience with taking Wellbutrin (bupropion), an antidepressant that also has stimulant effects. At a low dose of just 60 mg per day of Werllbutrin (extended release version), my ME/CFS fatigue and brain fog were almost completely eliminated, and I found my ADHD and anhedonic depression suddenly in remission too.

My mind became so sharp and capable from Wellbutrin that I started doing some complex computer programming — something I have not been able to do since getting ME/CFS. In fact my mind felt so competent that I even began rapidly learning and using new computer languages that I had no prior knowledge of (such as the web language PHP).

So not only was my brain fog abolished by Wellbutrin, but I actually found my mind more competent and capable that it was even before getting ME/CFS. The only major cognitive symptom that Wellbutrin did not fix was my medium term memory difficulties, but this was only a minor problem. With my new cognitive powers, I embarked on an ambitious and interesting new web software project. And my depression was gone too; I felt in a really good, productive and highly motivated mood.

I was ecstatic, because I really thought I had found my personal cure for ME/CFS, especially as I found this paper that details a couple of cases of great improvements in ME/CFS from Wellbutrin. However, all good things it seems come to an end, and after around two weeks of this incredibly good cognition and intelligence that Wellbutrin had bestowed on me, my razor sharp mind just suddenly disappeared, and although I kept taking the same daily dose of Wellbutrin, I just descended back into my regular zombie-like ME/CFS brain fog. Infuriating.

Though at least my experience proved to me that as soon as you get the brain chemistry right, ME/CFS pretty much disappears. But I wanted to know why all these very significant benefits I obtained from Wellbutrin just evaporated after a few weeks.

Looking around online, a found several commenters talking about the Wellbutrin two week "honeymoon period," during which you feel really fantastic, but after around two weeks, all the benefits quickly taper off and disappear.

I thought this loss of the benefits from Wellbutrin might might just be a simple tolerance effect to this stimulant drug. So I decided to stop taking Wellbutrin, and wait three weeks before taking it again, so that any tolerance my brain had developed to Wellbutrin would dissipate. However, when I tried Wellbutrin again after this three week break, I could not replicate almost complete remission from brain fog and fatigue that this drug had given me before.

So something very strange is happening here.

It's possible that one or more supplements I was taking during the original two weeks of Wellbutrin were somehow acting in concert with Wellbutrin in order to provide this remission from ME/CFS. This is something I am looking into (I keep full records of all the drugs and supplements I take each day).

I'd really like to get some handle on the neurochemistry Wellbutrin, and how it was able to put my ME/CFS into near remission for two weeks. If I can figure out how Wellbutrin might be working in the ME/CFS brain, I might be able to come up with a workaround that extends the Wellbutrin two week honeymoon period indefintely. This would then provide me, and I hope others here too, with a treatment that can effectively put the fatigue and cognitive symptoms of ME/CFS into near remission.


Some Notes on Wellbutrin (Bupropion)

Wellbutrin is a norepinephrine-dopamine reuptake inhibitor (NDRI); though Wellbutrin's dopamine reuptake inhibition is very weak, so it is more of just a norepinephrine reuptake inhibitor (NRI). I read that Wellbutrin is converted into hydroxybupropion relatively quickly, and the dopamine reuptake inhibition is done primarily through Wellbutrin, so once it’s converted into the metabolite it becomes mostly focused around norepinephrine.

Wellbutrin also antagonizes the nicotinic acetylcholine receptor.†

Wellbutrin downregulates beta adrenergic receptors.

Good article on Wellbutrin: Chemically Correct: Bupropion by Andrew Novick | Mind And Muscle

From what I already understand of this stuff, I am near certain I need a pure NE agonist or re-uptake inhibitor. So that was kinda interesting.

 

[lansbergen]

Wellbutrin also antagonizes the nicotinic acetylcholine receptor.†

Hip that could be a clue. Doing so much and put the nicotine receptors out of order is not a good idea in my opion. The a7 receptor is also important in the immune system.