3B-Adiol activates estrogen receptor?

5 alpha

Well-Known Member
Messages
226
I just stumbled upon something that looked interesting. Meridian valley lab is a lab that offers hormone metabolite tests. Meridian valley promotes the particular test that I had done back in 2014 as a screener for prostate cancer risk. In a nutshell it's saying that higher 3B-Adiol levels reduces your chances of getting prostate cancer. Here is the link to read about it in more detail:

3β-Adiol, a Testosterone Metabolite, May Prevent and Reverse Prostate Cancer | Meridian Valley Lab

Well anyway what caught my eye is the fact that it's saying 3B-Adiol activates estrogen receptors....

What I noticed from my Metabolite test back in 2014 I had low as in flagged low 3B-Adiol levels which is short for (5a-Androstane-3B,17B-diol)

My 3b-Adiol levels tested in at 3.7 on a reference range of 4.0-20.2 NG/ML

Seeing that 3b-Adiol activates estrogen receptors and I got much worse from inhibiting testosterone-estrogen conversion like others have as well this struck me as being interesting.

I wonder if anyone else (especially PFS people that get worse from inhibiting estrogen) also have low 3B-Adiol. If they do this hints towards problem with estrogen receptors correct?

also,

17B-HSD makes 3B-Adiol. DHT is converted to 3B-Adiol via 17B-HSD. The same meridian valley lab test had my DHT levels right in the middle of the labs reference range. So despite my DHT levels being normal my 3B-Adiol levels are low so this probable means that my 5AR is working fine but my 17B-HSD is not.

For some reason I am not getting an easy answer on quick google searches and I cant remember the answer to this question. Does Saw P, Fin and Dut inhibit 17B-HSD as well?
 
Last edited:

Helen

Well-Known Member
Staff member
Messages
5,415
I just stumbled upon something that looked interesting. Meridian valley lab is a lab that offers hormone metabolite tests. Meridian valley promotes the particular test that I had done back in 2014 as a screener for prostate cancer risk. In a nutshell it's saying that higher 3B-Adiol levels reduces your chances of getting prostate cancer. Here is the link to read about it in more detail:

3β-Adiol, a Testosterone Metabolite, May Prevent and Reverse Prostate Cancer | Meridian Valley Lab

Well anyway what caught my eye is the fact that it's saying 3B-Adiol activates estrogen receptors....

What I noticed from my Metabolite test back in 2014 I had low as in flagged low 3B-Adiol levels which is short for (5a-Androstane-3B,17B-diol)

My 3b-Adiol levels tested in at 3.7 on a reference range of 4.0-20.2 NG/ML

Seeing that 3b-Adiol activates estrogen receptors and I got much worse from inhibiting testosterone-estrogen conversion like others have as well this struck me as being interesting.

I wonder if anyone else (especially PFS people that get worse from inhibiting estrogen) also have low 3B-Adiol. If they do this hints towards problem with estrogen receptors correct?

also,

17B-HSD makes 3B-Adiol. DHT is converted to 3B-Adiol via 17B-HSD. The same meridian valley lab test had my DHT levels right in the middle of the labs reference range. So despite my DHT levels being normal my 3B-Adiol levels are low so this probable means that my 5AR is working fine but my 17B-HSD is not.

For some reason I am not getting an easy answer on quick google searches and I cant remember the answer to this question. Does Saw P, Fin and Dut inhibit 17B-HSD as well?


Others dont do bad on inhibiting aromatase, 50% of people feel cured doing that.

DHT is not converted to 3b - adiol via 17b- hsd. It is converted to 3b-adiol from DHT via 3 beta hsd.

since the body is retaning too much calcium, estrogen and all estrogen agonists will be switched off


calcium retention is happening either from overexpressed gaba receptor. or from high copper in the brain. which then increases 3 beta hsd to the right side. which increases progesterone and lowers 3b adiol which is an estrogen .




infection for intance, can also lead to calcium activation. since calcium is needed for phospholipase A2, to produce immune response.

This happens because of SIBO.

Small intestine overgrowth happen in small intestine. this causes leaky gut., and indigested protein enters the blood, this causes immune response,

which increases phospholipase. A2. basically increases calcium absorption. this immune response activates converson of vitamin D to active vitamin D 1.25/ test is in your blood , it will be sky high .

this high calcium decreases potassium and thyroid ability to enter the cell.

Body fight this, by raising progesterone, and retaining potassium.

with 3 beta hsd. 3 beta hsd goes in both directions, if going to the left, it increases 3b adiol= estrogen. if goes to the right it increases progesterone.


This is why activation of phospholipase a2, causes high calcium.

and this high calcium stops - turns off estrogen, since estrogen would increase calcium also.


So as I said

possibilities for a slow oxidizer.


1) high copper in the brain.

2) overexpressed gaba receptor

3) immune system overactivation, by SIBO ( fungal bacterial or viral infection)






|But of course I am not sure about if you are slow or fast oxidizer, did you do a hairtest?



,
 
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5 alpha

Well-Known Member
Messages
226
Others dont do bad on inhibiting aromatase, 50% of people feel cured doing that.

DHT is not converted to 3b - adiol via 17b- hsd. It is converted to 3b-adiol from DHT via 3 beta hsd.

since the body is retaning too much calcium, estrogen and all estrogen agonists will be switched off


calcium retention is happening either from overexpressed gaba receptor. or from high copper in the brain. which then increases 3 beta hsd to the right side. which increases progesterone and lowers 3b adiol which is an estrogen .




infection for intance, can also lead to calcium activation. since calcium is needed for phospholipase A2, to produce immune response.

This happens because of SIBO.

Small intestine overgrowth happen in small intestine. this causes leaky gut., and indigested protein enters the blood, this causes immune response,

which increases phospholipase. A2. basically increases calcium absorption. this immune response activates converson of vitamin D to active vitamin D 1.25/ test is in your blood , it will be sky high .

this high calcium decreases potassium and thyroid ability to enter the cell.

Body fight this, by raising progesterone, and retaining potassium.

with 3 beta hsd. 3 beta hsd goes in both directions, if going to the left, it increases 3b adiol= estrogen. if goes to the right it increases progesterone.


This is why activation of phospholipase a2, causes high calcium.

and this high calcium stops - turns off estrogen, since estrogen would increase calcium also.


So as I said

possibilities for a slow oxidizer.


1) high copper in the brain.

2) overexpressed gaba receptor

3) immune system overactivation, by SIBO ( fungal bacterial or viral infection)






|But of course I am not sure about if you are slow or fast oxidizer, did you do a hairtest?



,

Interesting...

I have not but I will be soon and I will post my results.

How many PFS people have you seen with low 3b-adiol? Or is it not something people usually get tested perhaps I’m the first . I know several others have tested 3a- diol on the PH forum with no consistent or significant findings
 
Last edited:

Aflac94

Well-Known Member
Messages
381
Others dont do bad on inhibiting aromatase, 50% of people feel cured doing that.

DHT is not converted to 3b - adiol via 17b- hsd. It is converted to 3b-adiol from DHT via 3 beta hsd.

since the body is retaning too much calcium, estrogen and all estrogen agonists will be switched off


calcium retention is happening either from overexpressed gaba receptor. or from high copper in the brain. which then increases 3 beta hsd to the right side. which increases progesterone and lowers 3b adiol which is an estrogen .




infection for intance, can also lead to calcium activation. since calcium is needed for phospholipase A2, to produce immune response.

This happens because of SIBO.

Small intestine overgrowth happen in small intestine. this causes leaky gut., and indigested protein enters the blood, this causes immune response,

which increases phospholipase. A2. basically increases calcium absorption. this immune response activates converson of vitamin D to active vitamin D 1.25/ test is in your blood , it will be sky high .

this high calcium decreases potassium and thyroid ability to enter the cell.

Body fight this, by raising progesterone, and retaining potassium.

with 3 beta hsd. 3 beta hsd goes in both directions, if going to the left, it increases 3b adiol= estrogen. if goes to the right it increases progesterone.


This is why activation of phospholipase a2, causes high calcium.

and this high calcium stops - turns off estrogen, since estrogen would increase calcium also.


So as I said

possibilities for a slow oxidizer.


1) high copper in the brain.

2) overexpressed gaba receptor

3) immune system overactivation, by SIBO ( fungal bacterial or viral infection)






|But of course I am not sure about if you are slow or fast oxidizer, did you do a hairtest?



,

So for case of overexpressed gaba receptor , gaba antagonists would be a stilt (feel better only on them)?

And gaba itself or gaba agonist (benzo, alcohol) would down regulate receptor ?
 

Nina

Well-Known Member
Messages
960
So for case of overexpressed gaba receptor , gaba antagonists would be a stilt (feel better only on them)?

And gaba itself or gaba agonist (benzo, alcohol) would down regulate receptor ?

If you have overexpressed GABA, GABA acts too strong thus you feel too much GABA action. Yes, GABA antagonists would be a STILT.

If you want to cure it longterm and downregulate GABA receptor, then yes GABA agonists would be the way to go. They increase GABA levels thus body downregulates receptors. Wont feel good on them.
 

5 alpha

Well-Known Member
Messages
226
If you have overexpressed GABA, GABA acts too strong thus you feel too much GABA action. Yes, GABA antagonists would be a STILT.

If you want to cure it longterm and downregulate GABA receptor, then yes GABA agonists would be the way to go. They increase GABA levels thus body downregulates receptors. Wont feel good on them.

What can you take to increase GABA levels ?
 

Nina

Well-Known Member
Messages
960
What can you take to increase GABA levels ?

I mean, benzos are the easiest probably. I wouldn't screw around with GABA though. Are you low or high GABA?
 

5 alpha

Well-Known Member
Messages
226
I mean, benzos are the easiest probably. I wouldn't screw around with GABA though. Are you low or high GABA?

I actually don’t know. It’s a path I have never researched. I do like benzos though as in like I feel an awesome sense of calmness and anxiety free especially with “social anxiety” while on them. But after only a short time of taking them and coming off I feel worse than I did before taking them. I have only tried them on a couple of different occasions for about two weeks at a time. Most of the things they helped with I kinda looked at like they are just normal things that I can deal with without the help of Benezos and ultimately they do more harm then good. I never really knew they were “activating” gaba.