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5HT2A agonism = fatigue; 5HT2A antagonism = fatigue?

5ht2a

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#1 PeaceAndProsperity

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Posted 02 March 2017 - 09:28 PM


DOES IT EVER STOP? I just began taking inositol again and found out that antagonism (or reduced function) of the 5HT2A receptor seems to also cause fatigue (I've known that inositol causes fatigue for some time).

 

I'm thinking to myself, what the hell am I supposed to do? Can't leave it be because I feel horrible with this increased susceptibility to 5HT2A activation (guess I have one of those mutations that increases risk of schizophrenia by increasing 5HT2A receptor expression). I guess at least antagonism solves some of my issues, will just have to learn to live with fatigue.



#2 Finn

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Posted 14 March 2017 - 10:31 AM

From where did you get information of inositol being 5HT2A antagonist, or did you mean that you were planning to take 2A antagonist to combat inositol's 2A agonism? Ritanserin 5HT2A/2C antagonist destroys inositol caused improvement in some animal models of depression, so inositol mechanism is more likely to include 2A agonism, than antagonism. So inositol isn't likely 2A antagonist, and taking 2A antagonist to combat inositol's 2A agonism is unlikely to work out well.

 

https://www.biopsych...ositol-5ht2.htm

 

 


Edited by Finn, 14 March 2017 - 10:34 AM.


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#3 PeaceAndProsperity

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Posted 14 March 2017 - 10:56 AM

From where did you get information of inositol being 5HT2A antagonist, or did you mean that you were planning to take 2A antagonist to combat inositol's 2A agonism? Ritanserin 5HT2A/2C antagonist destroys inositol caused improvement in some animal models of depression, so inositol mechanism is more likely to include 2A agonism, than antagonism. So inositol isn't likely 2A antagonist, and taking 2A antagonist to combat inositol's 2A agonism is unlikely to work out well.

 

https://www.biopsych...ositol-5ht2.htm

 

Thanks for the post. So inositol is used like an SSRI, it causes downregulation of the 5ht2a receptor? That makes it useless for me. I noticed that when my 5ht2a receptor is extremely overactivated then it improves it for me immediately and this is not something an agonist would do, unless it's a partial agonist.



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#4 jaiho

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Posted 14 March 2017 - 11:13 AM

It's impossible to know the state of our individual receptors unless you had your brain sliced open.

What ailment are you trying to treat?

 

 


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#5 PeaceAndProsperity

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Posted 14 March 2017 - 12:44 PM

It's impossible to know the state of our individual receptors unless you had your brain sliced open.

What ailment are you trying to treat?

You can draw conclusions from your experiences and from testing and there is no shame is drawing these conclusions even if they are simplistic.

 

Extreme fatigue

Extreme ocd

Irritability

Extreme ruminating thoughts and mental hyperactivity, borderline disorganization of thinking

Blunted affect with paradoxical moodiness and a negative perception of everything

Heart beating too forcefully though blood pressure and pulse is relatively normal

And a few other things I forgot

 

I've already made a lot of threads on these issues. Everything I've tried which increases activity at the 5ht2a receptor causes these issues or exacerbates them while things that reduce function seem to alleviate them. Tryptophan and 5htp can cause these issues as can most serotonergics though some serotonin increasing agents like sjw and ginkgo biloba can cause anxiety and other issues without these specific issues.

 

 



#6 jaiho

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Posted 14 March 2017 - 12:51 PM

You should try this.

OCD is linked to low serotonin. Fatigue, blunted affect is depression, also low serotonin.

While the low serotonin theory has been debunked, serotoinergic substances would have a big impact on those symptoms.

 

I'd suggest this algorithm

http://psychotropica...al-ad-algorithm



#7 PeaceAndProsperity

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Posted 14 March 2017 - 01:11 PM

You should try this.

OCD is linked to low serotonin. Fatigue, blunted affect is depression, also low serotonin.

While the low serotonin theory has been debunked, serotoinergic substances would have a big impact on those symptoms.

 

I'd suggest this algorithm

http://psychotropica...al-ad-algorithm

 

It's definitely not low serotonin. I have high serotonin, I am very sensitive to serotonin increasing drugs and I have most of the personality traits strongly associated with increased serotonergic activity.

One disease model for autism is increased serotonin and this explains many of the symptoms of the disease as well as the personality traits associated with autism.

 

I don't understand the point of taking an SSRI when serotonin levels in the blood are presumably already too high and the patient shows signs of increased serotonergic activity. Do we really need to bash someone's skull with a hammer to solve a migraine?

 

We need a serotonin reuptake enhancer...

 

I have noticed something interesting. Reduced nmda activity can cause hypersensitivity of the 5ht2a receptor and possibly explain in part hallucinations from nmda antagonists. On the other hand, things like theanine which acts on glutamate receptors and indirectly gaba by being converted to gaba like glutamate itself is, can sometimes reduce and sometimes potentiate 5ht2a hyperactivity, but trends towards reducing. Also, Acetyl-cysteine practically every single time I take it worsen the serotonin issues I have. I am also sensitive to glutamate, gelatin or gummy bears which contain the glutamate amino acid, or l-glutamine as a supplement, tends to send me into extreme rage like seen in autism.

My thinking is obviously that as glutamate affects dopamine it also affects serotonin, so my sensitivity to serotonin may lie in part in my sensitivity to glutamate. This is after all one of the disease models for autism if I remember correctly.

But my experimentation with magnesium and creatine has not gone too well and I am at a loss.

 

Btw I will read your link and comment on it later. There is a lot to read.


Edited by PeaceAndProsperity, 14 March 2017 - 01:11 PM.


#8 jaiho

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Posted 14 March 2017 - 01:18 PM

You may not need an ssri as monotherapy, but perhaps a combination.

I've given up analysing individual receptors. I find, when it comes to OCD & blunted affected, it needs similar treatment to anhedonia.

Which is triple reuptake inhibition.

Serotonin by itself is not the answer, but a part of it. The only relief i've felt is from broad action, SNRI + DRI and 5HT antagonism, which is the combo i'm promoting.


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#9 PeaceAndProsperity

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Posted 14 March 2017 - 06:42 PM

You may not need an ssri as monotherapy, but perhaps a combination.

I've given up analysing individual receptors. I find, when it comes to OCD & blunted affected, it needs similar treatment to anhedonia.

Which is triple reuptake inhibition.

Serotonin by itself is not the answer, but a part of it. The only relief i've felt is from broad action, SNRI + DRI and 5HT antagonism, which is the combo i'm promoting.

 

I am seriously afraid I will turn full blown psychotic from anything that increases all monoamine neurotransmitters as last time I took coenzyme vitamin b6 for multiple days I couldn't fall asleep and my pseudohallucinations were worsened considerably.


Edited by PeaceAndProsperity, 14 March 2017 - 06:44 PM.


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