Abstracts of Articles to Be Presented at Conference in Italy

[clampdown33]

I came across the attached .pdf file on the website for the International Meeting on Steroids and the Nervous System, the conference in Italy that’s hosting the roundtable discussion on finasteride in a few days. The file contains all of the abstracts from the articles being presented at the conference, including four abstracts of articles on finasteride. I don’t know if this information is new to anyone or has been posted elsewhere, but I haven’t seen it before, so I thought I’d share it. The finasteride-related content begins on page 92. (If for some reason you can’t open the file, you can follow this link, dafml.unito.it/anatomy/panzi … S13/RT.htm, scroll to the bottom of the page, and click on “Abstracts’ Book Is Here.”

Personally, I found the second and third abstracts most interesting – particularly with the second stating that 5-alpha-derived metabolites of progesterone were reduced not only in plasma but in cerebral spinal fluid measurements, and the third stating that finasteride may have profound dopamine-reducing effects. I don’t pretend to be anywhere close to the most scientifically informed person on this board, though, so if anyone else has any thoughts, feel free to discuss.
SNS13AbstractBook.pdf (2.57 MB)

[tim1911]

To this aim, neuroactive steroids levels were evaluated in paired plasma and
CSF samples obtained from 3 male patients who received finasteride for the treatment of
androgenic alopecia and that after drug discontinuation still show long-term sexual side
effects as well as anxious/depressive symptomatology. Data obtained by liquid
chromatography-tandem mass spectrometry show a general decrease of neuroactive steroid
levels, and particularly of 5a-reduced metabolites of PROG and T in CSF and plasma of
post-finasteride patients. The present results confirm that an impairment of neuroactive
steroid levels, associated to depression symptoms, is present in androgenic alopecia
patients despite the discontinuation of the finasteride treatment

Solve this, solve pfs?

[Finatruth]

Ahhhhhhhhhhh progesterone.

[BP7667]

Look forward to seeing more of this information be released during/after the conferance.

[Finatruth]

Ummm why aren’t more people getting excited!! This is the root problem people!! Isolated!! Come on throw your hands up

[ihatefin]

very interesting to read. some members have reported improvement from prozac. prozac is known to increase certain neuroactive steroid levels. hmmm…

[tim1911]

@Finatruth

Ummm why aren’t more people getting excited!! This is the root problem people!! Isolated!! Come on throw your hands up

I agree. Next step is figuring out why they have remained low in certain individuals (us).

[sonder]

yes and some members have reported improvement from remeron

[Jonson]

What can we do according to this?

[moonman1]

@Finatruth

Ahhhhhhhhhhh progesterone.

Not progesterone, but 5a reduced metabolites of progesterone. Just another way of saying nuerosteroids Allopregnenolone and THDOC. We pretty much already knew that they were low, but the question was always why are they STILL low after quitting 5ar inhibitors.

The dopamine bit is interesting and a new light, but then again it could be as simple at low neurosteroids “frying/over stimulating” our neurons, creating an exhausted environment and low dopamine…

I like the following quote from the abstracts…

[b]

In the quest to shed light on the
mechanisms of finasteride, we have studied the proteomic effects of acute and prolonged
administration of this drug in the brain of male rats. The results of these studies point to
changes in a number of key proteins implicated in steroidogenic metabolism, synaptic
plasticity and GABAergic neurotransmission. Based on these and other results, we are
currently testing a number of novel therapeutic approaches to counter finasteride-induced
depressive effects and explain its antidopaminergic actions.

[/b]

[Finatruth]

Umm, progesterone is the precursor to the endogenous production of Allo.

The biosynthesis of allopregnanolone starts with the converting of progesterone into 5α-dihydroprogesterone by 5α-reductase type I. After that, 3α-hydroxysteroid oxidoreductase isoenzymes (also referred to as 3α-hydroxysteroid dehydrogenase) converts this intermediate into allopregnanolone

[tab]

That thing on dopamine may explain why I ended up with very high prolactin, along with the use of the antidepressant.
Interesting from what I read and from what I heard, is that researchers are not only focusing on the theory of why fin did this to us, but they are also considering therapeutic approaches. I really do appreciate this and the idea that it will require tens of years to cure this condition loses some wheight.

[moonman1]

@Finatruth

Umm, progesterone is the precursor to the endogenous production of Allo.

The biosynthesis of allopregnanolone starts with the converting of progesterone into 5α-dihydroprogesterone by 5α-reductase type I. After that, 3α-hydroxysteroid oxidoreductase isoenzymes (also referred to as 3α-hydroxysteroid dehydrogenase) converts this intermediate into allopregnanolone

No shit. But progesterone is not the issue. Its 5ar metabolites are.

[tab]

He doesn’t say that progesterone is the issue. He means that by supplementing with progesterone you can increase it’s metabolites and maybe jumpstart the system. At least this is what I read in the thing of progesterone.

[moonman1]

@tab

He doesn’t say that progesterone is the issue. He means that by supplementing with progesterone you can increase it’s metabolites and maybe jumpstart the system. At least this is what I read in the thing of progesterone.

If it were that simple then we wouldn’t all still be here.

[Finatruth]

Yes defintely not that easy, they are using progsterone intravenously and intranasaly to help traumatic brain injury patients. They are certainly not rubbing a little of the Pharamacy bought cream on the wrists. However we do have anectodal evidence of people recovering with progesterone cream, and even better someone who reversed the estrogen dominant effect with progesterone and selegeline combo (Dopamine boosting).

What I would like to do is talked to the researchers who did the studies that I previously posted about the protective affects of progesterone on the brain and ask them why they use Finastreide to completely abolish those protective affects. It seem logical that if that potentially happened then the pathway is compromised.

Anyways, lets celebrate that at least it appears science is moving in the right direction and I never have to read another gut flora or candida post again.

If you have a moment take a look at the below study. I noticed in the first 9 months dealing with this (I have actually improved in this area) I had an exagerated response to noise. Like I would be easily startled or even jump a little from some seemingly normal sounds.

news-medical.net/news/2005/02/09/7697.aspx

[Mark2012]

Hi finatruth,

How safe do you believe progesterone is ? It says on the label of the progesterone I have that it is known to cause cancer.

[Finatruth]

Mark2012, I am not currently taking progesterone. I am not a dr. so I would not give any advice with regards to this. I tried 2 different times and had downward swings but rebound from both. If, and I say if because it is what I beleive and what I have always believed, that finasteride somehow changed the estrogen/progesterone ratio and accordingly reduced levels of allopregenalone, then it may take much more complicated treatment protocols to treat it.

The exciting news seems to be that this would fit the “single bullet” theory and could actually explain our condition. Lets all pray more comes from this meeting in Italy.

[tim1911]

A 5ar2 antibody has to be an option. I say this because the symptoms of being on finasteride and having post finasteride syndrome are different, yet the reduction in 5a reduced metabolites of PROG and T remain the same.

[Tlecum]

@Finatruth

Ummm why aren’t more people getting excited!!

Sadly, we are the mice that quit swimming.