Finally Found a Treatment...Can Anyone Please Explain This?

Hip

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I’m still wondering about interactions with alpha receptors and/or effects on microglia or other cells.
Do we know if cabergoline is an agonist or antagonist at the alpha-adrenergic receptor? Agonists cause vasoconstriction, so antagonists may cause vasodilation. So maybe cabergoline affects blood flow, and in turn tissue oxygenation.
 

Hip

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One of my theories at this point is that Cabergoline acts as an alpha 2 antagonist which would cause a decrease in vascular resistance and increase dilation.
We posted the same idea at the same time! Yeah, that's what I was thinking.
 
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Treeman

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While they’re clearly very synergistic and do both overlap, ITPP seems to be better at improving physical energy and metabolism which is expected and caber improves mood and psychological symptoms more. Fucked my girlfriend like a champ last night after having almost no sex drive or function for months
Cabergoline

"It has at times been used as an adjunct to SSRI antidepressants as there is some evidence that it counteracts certain side effects of those drugs, such as reduced libido and anorgasmia. It also has been suggested that it has a possible recreational use in reducing or eliminating the male refractory period, thereby allowing men to experience multiple ejaculatory orgasms in rapid succession, and at least two scientific studies support those speculations" https://en.wikipedia.org/wiki/Cabergoline#Medical_uses My ME/CFS seesm to be on a similar level as yours, however if I took the above and had the same benefit as you, I think me wife would leave my within the week................
 

Swim15

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^Wife would leave? Wasn’t sure if that was a typo haha.

I just wanna vent for one second cause I am/was supposed to start medical school in 19 days...I just decided to postpone a year two days ago and then I replicate this treatment. Scared as fuck to start knowing I have CFS though...I legitimately can’t even believe this situation lol.

I’d feel a tiny bit better if I could compare to an alpha blocker and see if that has the same effect and could understand the pathophysiology a little more.

Eye rolls at the absurdity and prayers for everyone with CFS
 

Judee

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I don't understand the mechanism exactly but I have to think it has something to do with dopamine. My reasoning is because I took a bunch of things to raise dopamine three days ago and had the best day I've had in years.

The bad part is that I'm in a crash today even though I skipped those supplements yesterday to cycle them and even rested but taking them again today isn't working.
 

mitoMAN

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I don't understand the mechanism exactly but I have to think it has something to do with dopamine. My reasoning is because I took a bunch of things to raise dopamine three days ago and had the best day I've had in years.

The bad part is that I'm in a crash today even though I skipped those supplements yesterday to cycle them and even rested but taking them again today isn't working.
I had the same. I am suffering from ADD and when taking Amphetamine and Methylphenidate (Ritalin) perscribed for my ADD for the first time, I was doing 100% good, like pre-CFS- HOLY SHIT. I never felt so good in my past 16 years. So I actually thought ADD might be my personal CFS...
But after 2 months, my crash got so hard, I've been bedridden for almost a year now :)

Now if I take any dopamine medication, I just a get a crash straight away, no boost no more.
 

Treeman

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I’m not as gifted as many on here when it comes to understanding biochemistry etc. I think I could grow my knowledge, but then I thought there are many very educated, experienced and knowledgeable individuals working on ME/CFS and they can’t work it, why would I think I could? I’m not going to try, just read, listen and hopefully have a stroke of luck and find some kind of solution through that. I admire those who do though, and hope someone stumbles across answers daily.

https://www.alldaychemist.com/cabgolin-0-25mg-tablet.html
 

sb4

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Do we know if cabergoline is an agonist or antagonist at the alpha-adrenergic receptor? Agonists cause vasoconstriction, so antagonists may cause vasodilation. So maybe cabergoline affects blood flow, and in turn tissue oxygenation.
Maybe I'm wrong here but for the alpha adrenergic 2 receptor, if you block it, that increases adrenaline as it is a feedback receptor, so if cabergoline is an agonist there it should decrease adrenaline.
I think this is how mirtazapine works.
 

Hip

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Maybe I'm wrong here but for the alpha adrenergic 2 receptor, if you block it, that increases adrenaline as it is a feedback receptor, so if cabergoline is an agonist there it should decrease adrenaline.
There does seem to be some unpredictable or paradoxical effects from cabergoline, as I came across this article which states that in cases of high blood pressure:
High blood pressure of pregnancy, or history of—Cabergoline usually decreases blood pressure but at times it may increase blood pressure and worsen these conditions.
 

mitoMAN

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Maybe I'm wrong here but for the alpha adrenergic 2 receptor, if you block it, that increases adrenaline as it is a feedback receptor, so if cabergoline is an agonist there it should decrease adrenaline.
I think this is how mirtazapine works.
I just asked my coach who uses caber in athletes to counter the Trenbolone prolactin sides.
He actually said that most guys get TIRED when adding caber. So he also doesn't a understand why they work so well for swim
 

junkcrap50

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How long have you been on this combo? How long have you been in remission due to it? Before trying other drugs to test the mechanism, wouldn't it be better to stay on both for a while to see if it has lasting effects?
 

Wishful

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we are much more certain about hypoxia,
Hypoxia doesn't seem to match my observations of my ME. My ME doesn't change with situations that would change oxygen intake, and it has changed with things that wouldn't obviously change oxygenation levels, so I don't see it as a likely factor. Do you have any arguments to convince me otherwise?
 

bread.

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Hypoxia doesn't seem to match my observations of my ME. My ME doesn't change with situations that would change oxygen intake, and it has changed with things that wouldn't obviously change oxygenation levels, so I don't see it as a likely factor. Do you have any arguments to convince me otherwise?
with all due respect, your me does not resemble the me that seems to affect the vast majority of patients. the vast makority of patients get physical PEM. I am definitely not trying to convince you of anything about your ME.
 

Wishful

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the vast makority of patients get physical PEM.
Yes, and I did get physically-induced PEM, but that seemed to be from muscle damage (which triggers immune activation), rather than from non-damaging muscle usage. If it was oxygen-related, I should have triggered on long walks or bike rides, but not triggered on a minute or so of window-washing.

Having a majority of PWME share a symptom doesn't mean that the symptom is directly due to the core dysfunction of ME; it could just indicate a common downstream effect. If a significant percentage of PWME don't show that symptom, then it's most likely a downstream effect. Treating that effect probably won't treat the rest of ME.
 

ruben

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Hello everyone. What symptoms are we talking about this helping? Does it help with gut problems too. Things like nausea, bloatedness, poor appetite stuff I mean.