The allopregnanalone theory. This could be it.

General Discussion
#1

Many believe that the neurosteroid Allopregnanalone is responsible for our troubles in PFS. I was skeptical at first in reading this however the more research I have done the more I am begining to think that it is indeed the main contributor. Let’s look at what we know.

We know that Allopregnanalone is made from Progesterone via the alpha 5a type 2.
We know that finasteride inhibits this.

I know that 5htp completley rid me of my brain fog. 5htp is the precursor to serotonin and it’s supplementation will significantly increase serotonin levels.

We know that Serotonin can increase levels of Allopgrenanalone int the brain. (ncbi.nlm.nih.gov/pubmed/19593190)
ncbi.nlm.nih.gov/pubmed/11415849

Many of us including myself have found that our libidos are significantly higher after a night of drinking. I found several studies showing that alcohol will increase allo levels significantly but only after sleep. This would explain why my libido only jumped the next day not during the night of drinking. yupb.com/preventing/preventing-1390.html
“They found that rats injected with an intoxicating dose of alcohol compared with control rats injected with saline exhibited ~700% increases of allopregnanolone in the cerebral cortex, a brain region important in the sedative and cognitive effects of alcohol”

So this begs the question… How the hell can someone get a hold of ALLO? They give it to people all the time in studies so it has to be available somewhere and has to be relatively safe.

Thoughts?

yupb.com/preventing/preventing-1390.html

#2

Like to add one thing. Some of you may say well if serotonin increases allo then why didn’t my ssri work to alleviate my brain fog. Good question and I was on Paxil for years and it never touched my fog. The reason i believe is that although SSRI have been shown to incresae allo levels it is only done in certain parts of the brain. SSRI’s do not increase serotonin all they do is prevent it uptake in the synapse region of the brain. 5htp on the other hand will flood your body with more serotonin.

#3

if the above equation is correct then it also describs why women who use progestrone based IUD don’t recover years after removing it. they have side exactly like us including pre-age menupause (in their thirties).As long as IUD is in place synthetic progestrone replaces natural progestrone and when removed body crashes since natural progestron has got to gutter. These women are low in progestrone in their blood tests. The interesting fact is I contacted one lady who was using progestrone cream and she told me that she had to stop it, as it has stopped working.

how long have you been on 5HTP? did your muscles, fatigue ans gunk improve?
is there any withdrawn effect of 5HTP?
if 5 htp increases serotonin so effectively then why we are given paxil why not just 5 htp?

#4

I was on 5htp for two months. The reason I began taking 5htp was to see if it would alleviate my anxiety a bit so I could get off of Paxil. I was blown away when it cleared my brain fog for the first time in 11 years.

There is no withdrawal to 5htp that I am aware of. It’s not like an SSRI.

5htp does increase serotonin however it will increase it everywhere. SSRI only do it in the synapse so I ended up getting nasusea and jitteryness after a while of taking it. However my brain fog never returned to what it was prior even after I got off. I took it for about a month to notice any benefit.

Yes I noticed an increase in libido, morning erections and ejaculation volume while on it however that went away after I got off.
Those who have used 5htp successfully have to cycle it. 3weeks on 1 week off or some use it a few times a week. For me I took 1month of daily use and then my brain was healed it was amazing.

Also carbs would make my brain fog worse but after 5htp that no longer happened.

Interesting about the progesterone, I was wondering what the dangers of supplementing that would be. When I had mine tested it was borderline high.

Have you noticed your libido to be improved after a night of drinking?

#5

Yes I do believe this is the heart of the problem but can we link this to why progesterone might not be sythnthisized at the receptor site. I’m convinced that progesterone has something to do with all of this since our symptoms mimic low progesterone (estrogen dominance) perhaps we need the metabolite progenalone instead? If the receptor site is blocked it won’t matter what levels of progesterone are in our bodies. Take a look at what I posted yesterday in the theory section “what binds us all”

#6

There is subtle difference between us and ladies with IUD. They have low level progesterone where as we have higher level nevertheless the effect is same. I think Finaturth is right thought not sure it is cause or effect just like cortisol.Many are high in blood but low in sliva tests.
I can not say anything about drinking.I never drank in my life, don’t know even the taste, sorry.

#7

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#8

Wow, wow, wow…hold on to your seats. Ok, while I was on finasteride I developed TMJ (predominately women), I also developed a very rare disorder called mdds also named mal de debarquement syndrome. Very little is known of this syndrome. Basically I took a cruise for 7 days back in 2008. When I got off the cruise, I felt the rocking of the boat for months!! It was horrible and only slowes down after many months. So what’s the connection? Researchers in this little known disorder (which also affects 90% women) have recently moved away from beliefs of inner ear disorder and now believe it could be hormonally related to levels of progesterone and estrogen!!! As I wrote in my theory, I believe everyone is affected from the first pill but other hormones keep it in check. Perhaps those effected had more or less sensitive progesterone receptors. I believe this is an enormous piece of this puzzle

ncbi.nlm.nih.gov/m/pubmed/9918575/

#9

Airborne, of course it’s the root cause. Its not a secondary effect, its a primary effect!! It is something we actually know finasteride does!! Everyone is searching for things finasteride doesn’t do or hasn’t proven in tests to affect. Old saying in the medical profession…when diagnosing, look for horses not zebras.

#10

You’re losing me here. Which are you saying is the issue? Low Progesterone? High Progesterone? Progesterone receptor issue? Histamine? Cortisol? Estrogen? Allopregnenolone???

#11

Finatruth
you should go for blood and sliva progestrone levle tests first.I think it is just the effect not the cause. I already wrote women with IUD got low progestrone but we have higher than normal progestrone. how would you treat it? if you look the forum some chaps have tried progestrone creame already in the past but then gave up. if you think it is the piece of the puzzle then please go for both sliva and blood progestrone tests and then apply your treatment and then again go for the same tests to see the difference. But again it is just like cortisol, higher in blood but lower in sliva and we show symptoms of lower cortisol.

#12

This lab in Paris has a “urinary pansteroid” test that measures allopregnanelolone.

It also measures 5ar activity, testosterone, and dht, 3a Diol G.

labbio.net/index.php?page=order

119 Avenue Philippe Auguste
75011 Paris
Tel : (33)1 43 67 57 00
Fax : (33)1.43.79.00.27
contact@labbio.net

#13

Low progesterone (or the effects of it because of blocked receptor, possibly because of the inhibited progesterone to Allopregenalone conversion) that would lead to estrogen dominance (progesterone is a calming anti-inflamatory hormone) this would give rise to estrogen dominance which is an inflamatory affect. Estrogen dominance gives rise to high histsmine being released by cells. What is your body’s only response to such inflamation? Cortisol! We both the vasodilation and vasoconstriction effects from this. Upswings and downswings. The histsmine, all though harmfull to cell tissue is probably where we get the libido and sexual urge from…then the vasoconstricting effects of cortisol. I know when I have any sexual function my penis is actually red and flushed. When I have zero sexual function I have construction, pelvic inflamation etc and zero libido. This actually all makes sense and incorporates both the neurological/neurosteriodal effect as well as the endocrine affect such as low testosterone etc

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#14

Spstriken, it could be a ratio problem or as I believe a receptor issue. If it walks and talks like a dog it is. I have every single symptom of someone who is estrogen dominant from the itching ears, dry skin, tremor, eustahian tube dysfunction etc to low thyroid function and low testosterone. We actually know what finasteride does. Check out the latest study I posted about serotonin and finasteride. Cells were pretreated with progesterone and once finasteride was applied it completely abolished the protective affects of progesterone!!! And thus lowered the serotonin affect on the treated cells! Completely abolished!!! That’s instantaneous!! I believe this drug did that to all of us, even the person like me who took it for years!!!

#15

Spstriken, ahhh do most people have higher levels of progesterone? I will have mine checked too. That is interesting, perhaps it is not get metabolized? Perhaps cortisol is blocking the progesterone receptor site (which I read can happen). If we all have higher to normal levels that is telling in and of itself

#16

Is this place legit? I thought allopreg could not be meausured?

#17

When I was tested in 04 my Progesterone was high normal. It was barely within reference range, almost high.

#18

So I still have the outstanding question of… Where can we get allopregnanlone??? It seems they give it to people in studies all the time. Why is this not available commercially?

#19

Take a look at this study. Down regulated biosynthesis of Allopregenalone induced by testosterone in the brain was reversed using S-fluxoretine. SSRI that doesn’t seemed to be marketed.

m.pnas.org/content/102/6/2135.abstract

#20

It seems to be set in stone that we have a problem with neurosteroids. Does anyone have any more information regarding this? If we have such a problem, what are our options? Is Dr. Traish now focusing on neurosteroids because he thinks this is the source of our sexual problems? Does anyone know how or what we can do to get diagnosed with this neurosteroid problem? I am trying to get into a neural stem cell treatment (I’ve been contacting universities on the east coast and west coast) but I need a proper neurological diagnosis first. There are many clinical trials going on right now. Any advice, help?

Also, are Dr. Irwig and Dr. Traish the doctors in the US who know most about PFS and are up to date on the research?