Study Shows Finasteride Drops Neurohormones in the brain by 876%

[braziliandude]

Ok so this is a web site that a brazilian guy created just to talk about it…
Correiovip also knows him , im going to post it and translate it

riscosdofinasterida.blogspot.com/

This explains the depression, panic attacks, anxiety, mood swings and brain fog caused by post Finasteride Syndrome. The link that we managed to complete the study is on Megaupload, but the site was closed by the U.S. government. Let’s find another source and so available will be posted here.

As soon as he posts something else ill put it up here

[tim1911]

Well there’s your pfs then? Looks like an allopregnanolone deficiency, among others.

I used this thread to suggest that steroids didn’t come back to baseline post finasteride.

viewtopic.php?f=27&t=5733

It then goes into how catastrophic an allopregnanolone deficiency would be ala multiple sclerosis, which has also been recently shown to have a deficiency in allopregnanolone.

I’m really torn now between the high igE results and this study, one of them has to hold the answer.

Doesnt quite explain the brief recoveries so many have before their big crash though, and why we were better off on the drug than off it.

If allopregnanlone is immosuppressive(via study posted by mew about ms) and we are low, and symptoms dont usually hit until 5ar2 regenerates, and we have 4 out of 4 with high igE this looks alot like an auto Immune condition. Time and pending research will tell.

[bluecloud87]

That is terrifying. However, as Tim rightly pointed out, it is very strange how PFS comes about when we quit the drug considering these effects. I took 2.5 mg (5 capsules) of Avodart, which, i am fairly sure would of had devastating effects on my brain and hormones and yet i felt better than most of my days clean and healthy since PFS. So what gives?

Is any of the research going to focus on the possibility of an autoimmune problem?

[Len]

@TIM1911

Like you said before, it is as if we have developed an allergy to androgens. And just like Awor said, it is not that we do not have enough, it is that our cells no longer respond to or accept the androgens as they should, or at least something to that degree. Classifying it as auto immune disorder theoretically seems very realistic. Thank God for Awors research, it is actually all starting to make some sense. We shall see. Nice couple of threads here guys, that was all very interesting. Thank you very much.

[Mew]

it is as if we have developed an allergy to androgens

… it is not that we do not have enough, it is that our cells no longer respond to or accept the androgens as they should, or at least something to that degree. Classifying it as auto immune disorder theoretically seems very realistic.

re: auto-immune disorder – maybe, maybe not.

Androgen Resistance or Androgen Insensitivity are conditions that exist in nature, typically due to genetic mutations at the androgen receptor level. This condition can be CAIS (Complete Androgen Insensitivty Syndrome), PAIS (Partial) or MAIS (Mild).

en.wikipedia.org/wiki/Androgen_insensitivity_syndrome

Note that treatment typically involves supraphyisological dosages of androgen to try and overcome the AR receptor defect:
viewtopic.php?f=5&t=1417

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As it relates to Finasteride, – some posts by Dr. Alan Jacobs, neuroendocrinologist:
blog.alanjacobsmd.com/alan-jacobs-mds-blog/2010/04/a-neuroendocrine-approach-to-finasteride-side-effects-in-men.html

"If high normal levels of testosterone, combined with low estrogen levels, does not relieve the hypogonadal symptoms, then the possibility that the man has some resistance to testosterone must be considered. "

blog.alanjacobsmd.com/alan-jacobs-mds-blog/2010/06/a-proposed-mechanism-for-prolonged-sexual-side-effects-from-finasteride.html

I am wondering whether the propensity of finasteride to cause lasting partial androgen resistance in a subset of men relates to the number of CAG repeats in exon 1 of their androgen receptor genes, perhaps those with the greatest number of repeats are at highest risk.

blog.alanjacobsmd.com/alan-jacobs-mds-blog/2010/10/another-piece-of-the-post-finasteride-hypogonadism-puzzle.html

“This brings up the idea that there is a common epigenetic mechanism that may apply generally to medications that cause persistent sexual dysfunction. It may be the case with finasteride that a common epigenetic effect interacts with a less common variant in the androgen receptor gene CAG repeat profile to cause its syndrome of crippling persistent post-finasteride hypogonadism.”

Dr. Crisler’s insights:

viewtopic.php?f=22&t=2551

… it often takes testosterone levels well above normal range to get these guys feeling right again. Again, I do not know why.

… The notion that [b]some sort of receptor downregulation is occuring is verified by the fact achieving androgen levels as much as 50% above normal range can be necessary[/b] for those who do not find relief using less drastic measures.

… This is the dilemma. Our best thought at this point is, for this subset of men, finasteride induces some epigenetic effect which results in some sort of androgen resistant state. For them, therapy may necessitate androgen administration to above normal range testosterone levels.

… Good T levels, with E in place, yet hypogonadism symptoms means there is some sort of androgen resistance at work.

[tim1911]

It seems mew that testosterone is one of the steroids that is normal on that chart, the one that concerns me is the allopreg.

These doctors say that we have symptoms that resemble hypogondanism, but i have posted a few studies that can very much liken our condition to ms, which looking at that chart both conditions pfs, ms have low levels of allopreg.

Now for you lennon and others interested in auto immune, to my limited knowledge on the subject allopreg is immunosupprisive as per the researcher in the study provided by mew.
Now if this (allopreg) is nailed by finasteride you have got an immune system waiting to run wild, in theory.
In Ms there is a break down at the blood brain barrier and immune cells are allowed to enter the central nervous system.
So what im trying to say here is that potentially it is allopreg which is playing a role in maintaing the bbb or stopping the immune system from crossing it, in theory.

So according to limited info 5ar2 is expressed in the cns and dht is present. So not only having the antibodies in the blood we could have them in cns once the 5ar2/dht comes back, which would make corticosteroids etc not much help for some symptoms as they dont cross the bbb.

[Len]

It is all very confusing to me I guess. I wish I had an understanding of these things like some of you guys do. You seem to really grasp all of this pretty well. Thank you for the info. Any chance these things are being researched specifically in Awors research? If it cannot be spoken about I understand. I just feel personally that this thread and the related info makes sense. The idea that we have more or less developed an allergy or an insensitivity to androgens just makes sense. Well anyways, I will leave these things to you guys who actually have an understanding of it all, I just find this topic very interesting.

[Second_Amendment]

@Lennon

It is all very confusing to me I guess. I wish I had an understanding of these things like some of you guys do. You seem to really grasp all of this pretty well. Thank you for the info. Any chance these things are being researched specifically in Awors research? If it cannot be spoken about I understand. I just feel personally that this thread and the related info makes sense. The idea that we have more or less developed an allergy or an insensitivity to androgens just makes sense. Well anyways, I will leave these things to you guys who actually have an understanding of it all, I just find this topic very interesting.

As of now, unfortunately, the findings are the intellectual property of the scientists. The results are kept secret until they get their paper published thus getting credit for their work. But I wouldn’t worry about awor missing anything. His team seems highly competent. Remember, he said there are abnormalties with the Androgen Receptors and the problem is a complex one. To me, this hints more at some type of epigenetic effect than an autoimmune disorder.

[Oscar]

I have discussed this study in this thread: viewtopic.php?f=1&t=5960.

There is no 5aR2 in the human brain. Therefore neurosteroids shouldnt of been inhibited. The study in this thread only quotes circulating neuroactive steroids in blood - not whats happening in the brain!

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@Mew

Androgen Resistance or Androgen Insensitivity are conditions that exist in nature, typically due to genetic mutations at the androgen receptor level. This condition can be CAIS (Complete Androgen Insensitivty Syndrome), PAIS (Partial) or MAIS (Mild).

Androgen Insensitivty Syndrome is an illness that you are born with. It does not develop later in life! A fault with the androgen receptor that can cause Androgen Insensitivty developing later in life has NEVER been recorded.

Insensitivity to testosterone can be caused by an autoimmune disease directed against testosterone. (and Autoimmune diseases against enzymes can be caused by using enzyme inhibitors). This HAS been recorded.

It really is that simple. So for that reason, objectively speaking, an epigentic change to antibodies is more likely than an epigenetic change to androgen receptors.

[Mew]

A fault with the androgen receptor that can cause Androgen Insensitivty developing later in life has NEVER been recorded.

The problem we are dealing with – PFS – has never been documented either.

5AR inhibitors are relatively new drugs, all the more reason this post-drug adverse reaction of persistent hypogonadal effects needs further investigation. It may lead to novel insights into androgen receptor / 5AR2 / epigenetic function as it relates to androgen metabolism, prostate cancer or other areas.

That said, what you state is also worth consideration. Hopefully in time, through research, we will be able to confirm which areas/mechanisms are or are not playing a role in the condition.

[tim1911]

What i would like to know is how long the after finasteride results were taken. One day, 3 weeks etc makes a big difference in the pfs timeline.

[braziliandude]

hey tim it says right on the top of the image…4 months after starting to take finasteride!

[tim1911]

I take it as 1 test pre fin and one after 4 months of treatment. I am wondering how long after treatment finished was the “after” test done, as i see this as being quite important.

[spstriken]

Mew when you talk of super physiological level of TRT how would you control E2? we already are dealing fast conversion of T to E.
you know when I was on Agel that was my problem. My legs were full with water.
I tell you interesting thing ,recently I visited India and I felt a lot better in the sunshine but soon I got water retention in my legs although not as much as when I was on Agel. I was not taking no med, no TRT.
If you use Arimidex with high level of TRT you will get other set of problems. I have posted here already about sides from Adex. In muscle chatroom there is a thread about Adex and on messo forum, more and more people are now talking about sides from Adex. these are almost same as from fin.
My suggestion is DHT (andractim)+TRT.

[annon]

do we know if this was taken when on fin or off. if off how many months of and has he got pfs?

[tim1911]

Anyone who crashed/got sides on the drug and never recovered (like myself) has to take serious look at this chart.
I wish i could fund testing of all of the above steroids for myself, and compare them against the mean pre finasteride column.

[Enden]

That chart was originally posted by me on HLT. Here’s the document;
Finasteride Treatment and Neuroactive Steroid Formation.rar (145 KB)