Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

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Delfador
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Re: Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

Unread post by Delfador »

Also, for me, microdosing SSRIs triggers full blown mania, which helps with pssd a little, but does not solve it altogether. Manic people canstill have flat affect, and some sort of anhedonia.
arahant
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Re: Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

Unread post by arahant »

Delfador wrote: Wed Oct 21, 2020 12:34 pm But I do not believe that PSSD is a form of BD. If you are ready to believe that, then you are basically saying that people with no windows have unipolar depression.

I do not believe either and I am saying nothing, I just wonder if BD makes it more susceptible to PSSD.
Also, for me, microdosing SSRIs triggers full blown mania, which helps with pssd a little, but does not solve it altogether. Manic people canstill have flat affect, and some sort of anhedonia.


If microdosing SSRIs can trigger full-blown mania, it somehow confirms that psychiatrist claims:

"That SSRIs in people with BD can have severe consequences"

So that's why GPs prescribing SSRis for every "depressive" complaint can be dangerous for the BD population.

In some cases, mania can be dangerous because of reckless behavior, also self-hurting impulses can happen.

(This physician has written a warning post on his social networks, regarding one of his patients quitting BD treatment because of the stigma of "seeing a psychiatrist" in his country, and changed his physician to a GP, which prescribed SSRI/SRNI, I think Venlafaxine, then the patient got manic outbreak followed by severe depression and ended his life).

Since it's unlikely to last forever, it exhausts so that the following depressive phase can be quite severe in terms of blunted affect and anhedonia.
Wellbutrin (2007 - 2018)
Wellbutrin + Sertraline (2015)
Wellbutrin + Ritalin (2016 - 2018)
Wellbutrin + Ritalin + Sertraline (3 months in 2018)
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Delfador
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Re: Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

Unread post by Delfador »

Yes, in 2018 and 2019 BD caused me frequent trouble with law enforcement. I started being "known" to every cop in my town. After a while they just pittied me I guess, and didnt even pull me over or cuff me when im being a dick.

Now I'm managing it way better. I only have the rare occasional asshole vibe at work, and one time with my (very supportive) partner. This cost me my career tho. I can't stay in a company for long before someone realises I'm a fruitcake. And I am currently unemployed since my last fuck up in august.


But hey... BD is nothing compared to pssd.

I don't want to make this thread about BD but since we opened this bracket, I also noticed certain foods (beans, ginger, coke but not coffee, food rich in MSG, food with certain ratios of fat/carb/proteins etc..) and certain medications (fluconazole) help me trigger and sustain hypomania.

When I'm manic, I do not take ANYTHING to lower my mood. Because I don't want my mood to be low. Low mood means 100% pssd.

Triggering and maintaining manic episodes has been my main strategy of pssd management, and I still am at the begining of understanding what's going on.
rmichaelballow
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Re: Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

Unread post by rmichaelballow »

Delfador wrote: Tue Oct 20, 2020 7:10 am I'm just writing this topic to remind us all of some things we tend to forget.

While I somewhat agree with the 5ht1a autoreceptor theiry of pssd ethiology, there is something that bugs me:

If we were as good as 5ht1a K.O (knockouts), then we would indeed have high levels of serotonine in our synapses, all the time.

If this was truly the case, we would all: be very prone to serotonine syndrome. We would get serotonine toxicity while using any serotoninergic drug. From SJW to LSD and MDMA, and we already know this does not happen in PSSD sufferers any more than normal people.

If our sexual dysfunction was due to serotonine building up in the synapses (due to 5ht1a k.o), and activating 5ht2c receptors (those are well known to inhibit dopamine reward pathways), then we would also have suppressed appetite for food. This also does not seem to be the case for PSSD sufferers (it is the case for me personally tho).

But I do not second guess this theory altogether, in fact, I believe some of it is true. One thing that makes me believe in it is : since I got pssd a few years ago, I slowly developped bipolar disorder. Sometimes my cycles are very rapid, I even had hypomanic episodes develop in the course of a day then fade away the next day. And this particular form is often related to downregulated 5ht2b receptors., which makes sense in the context of high serotonine.


I sometimes think that there are high serotonine production and liberation periods in every pssd sufferer, but those periods do not manifest into higher serotonine signaling due to Upregulated MAO. And it is through high MAO that our dopaminergic system is inhibited.

Anybody has some insight on this? Especially why most of us dont have suppressed appetite and serotonine syndrome?
Important thinking right here. Generally - no, a post SSRI brain does not have high net serotonin. Without precursors, that would actually be nearly impossible, considering the SSRI induced tissue depletion of Serotonin, and deranged production/synthesis. Transporter molecules' continuous function is critical in Serotonin releasable pool repletion, and the SSRI state is a SERT knockout state.
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Re: Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

Unread post by lepardglass »

Delfador wrote: Tue Oct 20, 2020 7:10 am I'm just writing this topic to remind us all of some things we tend to forget.

While I somewhat agree with the 5ht1a autoreceptor theiry of pssd ethiology, there is something that bugs me:

If we were as good as 5ht1a K.O (knockouts), then we would indeed have high levels of serotonine in our synapses, all the time.

If this was truly the case, we would all: be very prone to serotonine syndrome. We would get serotonine toxicity while using any serotoninergic drug. From SJW to LSD and MDMA, and we already know this does not happen in PSSD sufferers any more than normal people.

If our sexual dysfunction was due to serotonine building up in the synapses (due to 5ht1a k.o), and activating 5ht2c receptors (those are well known to inhibit dopamine reward pathways), then we would also have suppressed appetite for food. This also does not seem to be the case for PSSD sufferers (it is the case for me personally tho).

But I do not second guess this theory altogether, in fact, I believe some of it is true. One thing that makes me believe in it is : since I got pssd a few years ago, I slowly developped bipolar disorder. Sometimes my cycles are very rapid, I even had hypomanic episodes develop in the course of a day then fade away the next day. And this particular form is often related to downregulated 5ht2b receptors., which makes sense in the context of high serotonine.


I sometimes think that there are high serotonine production and liberation periods in every pssd sufferer, but those periods do not manifest into higher serotonine signaling due to Upregulated MAO. And it is through high MAO that our dopaminergic system is inhibited.

Anybody has some insight on this? Especially why most of us dont have suppressed appetite and serotonine syndrome?
I'm in the process of sourcing Fenclonine, I will answer this question once and for all.
Tree
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Re: Do we really have high serotonine, or do we just have incorrect 5ht signaling? (Delfador questions)

Unread post by Tree »

rmichaelballow wrote: Fri Oct 23, 2020 6:25 am
Delfador wrote: Tue Oct 20, 2020 7:10 am I'm just writing this topic to remind us all of some things we tend to forget.

While I somewhat agree with the 5ht1a autoreceptor theiry of pssd ethiology, there is something that bugs me:

If we were as good as 5ht1a K.O (knockouts), then we would indeed have high levels of serotonine in our synapses, all the time.

If this was truly the case, we would all: be very prone to serotonine syndrome. We would get serotonine toxicity while using any serotoninergic drug. From SJW to LSD and MDMA, and we already know this does not happen in PSSD sufferers any more than normal people.

If our sexual dysfunction was due to serotonine building up in the synapses (due to 5ht1a k.o), and activating 5ht2c receptors (those are well known to inhibit dopamine reward pathways), then we would also have suppressed appetite for food. This also does not seem to be the case for PSSD sufferers (it is the case for me personally tho).

But I do not second guess this theory altogether, in fact, I believe some of it is true. One thing that makes me believe in it is : since I got pssd a few years ago, I slowly developped bipolar disorder. Sometimes my cycles are very rapid, I even had hypomanic episodes develop in the course of a day then fade away the next day. And this particular form is often related to downregulated 5ht2b receptors., which makes sense in the context of high serotonine.


I sometimes think that there are high serotonine production and liberation periods in every pssd sufferer, but those periods do not manifest into higher serotonine signaling due to Upregulated MAO. And it is through high MAO that our dopaminergic system is inhibited.

Anybody has some insight on this? Especially why most of us dont have suppressed appetite and serotonine syndrome?
It all has to do with the degree of 5ht1a desensitization. Genetics, length of ssri use, or drugs/supplements used post pssd play a role in the degree of desensitization. This is why people have different degrees of shared symptoms.

I have extreme complex pssd. Both cognitive and sexual functioning is severely impaired. This wasn't the case until I crashed from ginger, a 5ht1a agonist, a couple years ago. I had severe fatigue and emotional bluntness and mild sexual function before crash. After crash cognitive and sexual functioning is extreme and permanent. Presently, my appetite is suppressed to the point where I forget to eat sometimes and very prone to serotonin syndrome. This is why I believe in the 5ht1a/desensitization theory.
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