Serotonin Regulates Prostate Growth Through Androgen Receptor Modulation

TubZy

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Thought this was interesting for the SSRI guys especially how PFS and post SSRI are similar

Serotonin regulates prostate growth through androgen receptor modulation

5-HT inhibits rat prostate branching through down-regulation of androgen receptor (AR). This 5-HT’s inhibitory mechanism is also present in human cells of normal prostate and BPH, namely in cell lines expressing AR when treated with testosterone
 

barbaar

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I wonder if the receptors stay downregulated after quitting. I have low T, probably low DHT too (results not in yet). That would mean upregulated receptors if I'm not mistaken. Or maybe a problem synthesizing hormones somewhere.

Maybe we have two cases here like in PFS. Serotonin stays high -> receptors stay downregulated , or serotonin crashes after quitting and stays low -> upregulated receptors.

Like you said, def a connection here. Fin is used for BPH, 5-HT is proposed as a potential treatment for BPH (I only read the abstract, correct me if I'm wrong). Maybe this explains why some people were cured by low dose SSRI. Maybe their AR was upregulated and they succesfully downregulated it again to normal levels.
 

Helen

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I wonder if the receptors stay downregulated after quitting. I have low T, probably low DHT too (results not in yet). That would mean upregulated receptors if I'm not mistaken. Or maybe a problem synthesizing hormones somewhere.

Maybe we have two cases here like in PFS. Serotonin stays high -> receptors stay downregulated , or serotonin crashes after quitting and stays low -> upregulated receptors.

Like you said, def a connection here. Fin is used for BPH, 5-HT is proposed as a potential treatment for BPH (I only read the abstract, correct me if I'm wrong). Maybe this explains why some people were cured by low dose SSRI. Maybe their AR was upregulated and they succesfully downregulated it again to normal levels.


Receptors are not static. Receptors are constantly either expressed or not. this is done with methylation. there are either overexpressed or underexpressed, this depends on methylation.

in the tests that I saw, there is zero cortisol in PSSD, in talkingant tests. And low b2. and other b vitamins. this tells me that they person is overmethylating. spending B vitamins like crazy.

Meaning the body is trying to express more receptors to support GR and AR. Those 2 are like twins. they go up and down together.

Same tests we got from the Italian study in PFS, which also showed that AR was highly overexpressed in PFS. This also shows that the body it spending folinic acid like crazy to express the receptors.



This is why serotonin downregulates methylation. since serotonin increases cortisol and increases MAO a, which takes a lot of copper from methylation enzymes.


This is why lithium helped some people with since lithium increases serotonin. which increases ACTH. and cortisol secretion.
This then lowers the need for methylation. and for overexpression of AR or GR and b vitamins go back up raising metabolism.

this is why there is a lack of b1 and b2, since the body using those for overmethylating AR. and GR.




I assume in both cases AR is overexpressed( since in Italian study everyone had overexpressed AR ) , only in one case it is the cause of a problem and in second case it is the outcome of the problem , a stilt

it does makes sense. if a person in slow metabolism takes a progestin. that progestin will not make progesterone insensitive. but will kill 5AR and make AR supersensitive.

And if person in higher metabolism takes progestin , that person will get insensitive progesterone and overexpressed AR will be a slilt since if progesterone is not allowed to convert anywhere, this stops 5AR. and this has to upregulate AR experssion which is methylation.
 
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barbaar

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Ah so in PSSD, the (somewhat indirect) reason for the upregulated AR is actually low cortisol, which in turn is caused by low serotonin, and low androgens are just a side effect of the overexpressed AR? IIRC you said serotonin can be low because of low metabolism. I wonder if slow oxidizers are more prone to PSSD then. That would certainly fit my case.

I always love it when you write informative posts like these. I won't pretend I understand everything 100% but still!

Also I just got a message from my doc. I'm finally getting the results of my cortisol + dht tests tomorrow. My guess is both will be low.