3a-diol / 3b-diol testing

As per the latest study on propecia :
“Patients treated for male pattern hair with finasteride show, after
discontinuation of the drug, altered levels of neuroactive steroids in
cerebrospinal fluid and plasma”

We need to start testing these parameters in ourselves to see if this is present in all of us.

As I have posted before. 3bdiol is a potent estrogen. There is in fact a patent to uses it as an estrogen receptor agonist.

This study seems to clearly demonstrates that we are producing these hormones in excess.



Many of us here see good results on TRT at the start but the results seem to fade quickly. Most non PFS people on TRT would usually find that this is related to increased estradiol. But many of us here have tried many aromotaze inhibitors without luck. So this kind of rules e2 out of the picture. Now the studies show increased 3bdiol it seems very likely that the increase in 3bdiol is negating the affects of TRT.

We really need to do further investigation on this and perhaps some testing as to how 3adiol and 3bdiol respond to different TRT doses.

These hormones can be tested here :

meridianvalleylab.com/testosterone-metabolites

In my experience with various forms of TRT and many AIs I have recovered pretty much all my symptoms but the results just do not last. So this gives me hope.

The study also goes into shows that dyhydroprogesterone aand tetrahydroprogesterone levels are low in post fin cases but I am not sure if these things can stop TRT from working. It would seem in my opinion that something like 3bdiol is in fact something that could stop TRT from working.

Vincentv- can you at all fit this into the context that I have been saying for years, that there is somehow a problem with estrogen/progesterone relationship? Something that has now surfaced after the dermatology journal article, where dermatologists have hinted that the increasing number of male patients on finasteride have shown a condition called melasma generally attributed to women due to estrogen/progesterone imbalance?

We need to start putting all these pieces of the puzzle together

Vincent have you tested for this?

Searching on this topic i found something that i would like to call your attention for:
Please follow tbe threads

allthingsmale.com/forum/show … Diol-LOW-!!

allthingsmale.com/forum/show … %3B-diol-G&p=206687#post206687

This is in line with tbe last study i posted about finasteride reducing 3b hsd!!

xptriado : Which study?

Costa : Would love too but can not find a lab in my country so we need people in the US to test.

Finatruth : As 3bdiols are too high in PFS yes then we have too much estrogenic hormones compared to other hormones.

Please if you are in the US do what you can to get this tested. It looks like this will be a big piece in the PFS puzzle. We can then further see what is happening when on trt by testing these metabolites while on TRT. If you are in the US do this test. Finatruth I believe you are in the US. Please do the test asap.

Guys please do these tests. I do not live in USA.

I feel so strongly that there is something to this. I will do my best to get tests when I can.

Check out this study on men taking finasteride, and the effect on 3adiol. It’s pretty profound, even after 1 month:

ncbi.nlm.nih.gov/pubmed/23474436

Again, connected to what they fou d i thisstudy:
viewtopic.php?f=9&t=9075

But xptriado, the results Vincent posted conflict that study. Or else are unrelated.

The one you posted suggests that 3B-HSD is inhibited while on Propecia, leading to decreased 3B-diol levels.

The Italian study in the initial post shows increased 3B-diol levels in PFS patients.

So even if 3B-HSD activity is lower on the drug, it appears much higher while off it.

A point to consider is - if this metabolite is key to PFS, then it wouldn’t explain those who experienced side-effects while on the drug.

Besides which, I don’t think it’s unusual to find altered 3A-DIOL and 3B-DIOL levels in current Propecia users. These are DHT metabolites, so of course if you almost completely deplete DHT these will similarly be reduced. I’m not sure how the researchers concluded 3A/B-HSD activity was impeded because of that, they simply had less precursors.

A few things led me to these metabolites before I saw the study.

  1. Why have I been able to feel good benefits on TRT that fade within a week?
  2. Why does faster acting testosterone work better for providing short term benefits on TRT?
  3. Why are the benefits of TRT lost even when estrogen is kept in check.
  4. Why doesnt T work? We know what T does in the body so why isnt it working as it should in PFS? It does not seem the receptor is blocked in my case because TRT does cause increased body hair in me + hairloss on the head.
  5. WHy do many of us have high levels of binding hormones such as SHBG an in my case CBG. These things are increased with estradiol. But even when I take AIs my CBG does not decrease much at all it seems.
  6. Why does my saliva e2 test not match my blood e2. Blood e2 shows levels which are in range. Siliva is always over range. 1.5 to 2 times the range. I found out that SHBG binds strongly to 3bdiol but not 3adiol. So perhaps my free e2 is high because there is increased competition for SHBG binding. Excess
  7. I have tried almost every AI but they provide some short term benefits in some cases but now I have started using formestane as an AI it is also a 5ar inhibitor + it is a very weak androgen and I feel consistent progress. My DHT has decreased on formestane but yet I get morning wood every day.
  8. Many here report that they do not get the side effects to they quit. There is some convoluted theory about this which seems overly complex. A simple theory would be due to excess DHT metabolites specially 3bdiol which is estrogenic. Which has now been proven with the latest study.
  9. Most of us here have low LH / FSH compared to our free T levels. This indicates that something is having negative feedback on our testosterone production. Again many here fail to explain why this is or otherwise convoluted theories are provided. Now that we know that these DHT metabolites are too high in PFS patients these are going to feedback on LH and FSH.

I did experience loss of libido after a few weeks on propecia and then after the loss of libido I started feeling some depression a week later. But after I quit my side effects seem to transform that is when my digestive system seem to change I got a very dry scalp, fatigue lower appetite etc.

So we need to take a look at just how big a role 3bdiol/3adiol has in the side effects we are feeling now. We need to find out if these metabolites are stopping TRT from working. We must investegate how they are affected by T supplementation. We need to look at things like free T to 3bdiol/3adiol ratios.

Then we need to work out how our 3bdiol/3adiol levels compare to our 3adiolG levels.

What’s 3adiolG in relation to the other two? What is it metabolised from?

I am also confused As to what 3bdiol is and why we think it may be important.

I’m also confused as to why or how are 3bdiol or 3adiolg levels respond when we take TRT is important.

I thought the reasoning behind why we think 3adiolg is important is because it measures are 5 alpha reductase type 2 enzyme or are body’s ability to convert testosterone to DHT?

3bdiol is a potent estrogen. It is well known that in men high estradiol can counteract the positive effects of testosterone. This is why many men take aromotaze inhibitors on TRT if their estradiol is too high. In the study on PFS it shows that PFS cases had at least double the levels of 3bdiol compared with normal men. This would indicate that their cells are being exposed to excess estrogens.

Many report that they feel benefits on TRT but these benefits are lost after days or weeks. This could be explained by T metabolizing into 3bdiol and counteracting increased T. For myself TRT can make me worse after a couple weeks. Many have tried aromotaze inhibitors but few have had any long term success lowering their estrogens.

From all my experementation so far I could say that 3bdiol could be the cause of many of my own symtoms and the study proves that it looks to be an issue. We need to do some more detailed testing. Meridian labs offers this in order to see just how off our 3adiol/3bdiol/DHT/T ratios are.

Can you provide a direct link to the full study in this thread please? Might be helpful to have it posted.

Here it is attached.
The Journal of Steroid Biochemistry and Molecular Biology Volume issue 2014 3bdiol .pdf (689 KB)

I’m glad we are seeing estrogen as the main culprit. I went to the dentitst last week, after a routine cleaning, he commented on how much bleeding I was having. He indicated that he sees this sort of condition in women who are in their second trimester of pregnancy.

Vincentv- have you thought about sharing this information with the Harvard or Baylor study ?

I was um preoccupied when this study came out officially. Even though I had heard of the results prior to it being published. Do you guys know if it got any major attention when it was published? Seems like it shows a pretty clear link between inasteride and persistent side effects.

I believe this was funded by the PFS foundation so I guess they know about it. Seems the PFS foundation are doing a good job.

the above study talks about results of different tests from the 12 PFS people in CFS and plasma

I’m assuming plasma means blood test, is this correct?

Also what does CSF mean?
Is this urine?

It’s clear the results of this study shows common trends from test results of the PfS group which i am still trying to read more about and understand.

But where in the study does it make it clear that high estrogen is one of the common traits seen in the PFS group as a member stated above.

Am I missing it?