(Study) Neurosteroid Levels in PFS patients

[Oscar]

[xptriado]

why would they feel worse after an exam?!
maybe because they have now less csf??
how is this exam made?!

[IthinkFingotmetoo]

@xptriado

why would they feel worse after an exam?!
maybe because they have now less csf??
how is this exam made?!

The wording on that chart is confusing.

I think it means that they polled these individuals at the time of the sampling. They asked them how their symptoms were before taking Finasteride, during use, the worst the symptoms got after discontinuation of the drug, and what their current rating of the symptoms was at the time of the poll.

[moonman1]

@Oscar

@Second Amendment

These findings perfectly corroborate the over expressed AR hypothesis.

No they don’t. Did Prof Melcangi once mention androgen receptors as being the cause of this?

Now we have this study and rumours of increases AR levels in NUMB genital skin. How do we put it together?

Well, there is zero evidence that upregulated ARs can reduce DHT, 5aR, increase estrogen or inhibit Neurosteroid synthesis.

However, we know that inhibiting 5aR upregulates Androgen Receptors[1] AND reduces DHT, increases estrogen and inhibits neurosteroid synthesis.

Therefore the problem lies with 5aR. Occams razor and all that!

[1] ehrs.org/conferenceabstracts … sawaya.htm

According to these findings, Oscar is correct. The issue would be with the 5ar enzyme, especially in the CFS. This could explain why another study found high levels of AR, but it doesnt seem (according to this) that the issue is with the AR or post-AR proccess.

The study used a small number of patients (6 or so), so the follow up study will use more and also looke for genetic susceptablility as to why our 5ar enzymes are stuck/broke.

I personally would like to see if CFS 5ar metabolites stay low even when we are able to get plasma levels normal…

If this IS the case then you would think that synthetic DHT and allopreg. would be our treatment. We should know a lot more when the next Italian study is published.

[sanane]

detected nothing or under limit of DiHydroProg and TetraHidroProg in CNS, that was fanstastic on all PFS…

[bens]

Anyone know why 3-alpha-diol is so high in plasma?

3-alpha-diol is (from wikipedia):

• a weak antiandrogen (greaaaaaaat…)
• a major metabolite of DHT
• a potent positive allosteric modulator of the GABAA receptor
• is known to have rewarding , anxiolytic, prosexual, and anticonvulsant effects

The last two sound a lot like allopregnanolone and THDOC. Could it be upregulated due to the absence of those two?

It is formed by the same enzyme as allo and THDOC… 3aHSD. Increased activity of the 3aHSD enzyme? Or because 3aHSD isn’t being used to form allo and THDOC… there is much more floating around to form 3adiol.

[bens]

@xptriado

with such a small sample it’s very difficult to understand. basically i was thinking, by looking at the MEAN that in plasma DHT was being excessively converted into something else because there is a much higher than usual value of 3alpha diol, which is a metabolite of some DHT metabolisation into something else (if i udnerstood properly).

but then i realised they are making MEANs with only 3 people…of which subject 2 seems to be an outlayer for DHEA and subject 3 an outlayer for 3alpha diol…

they probably should have taken a few more people on board?

by the way, how do you test the CSF? Is it painful??

Subject 3 has no 3adiol in plasma because he has no DHT to convert to 3adiol. Same reason no one has any allopreg… absence of its precursor so 3aHSD can’t do its job.

[weaksides]

@moonman1

5α-androstane-3α

Does it cross the blood brain barrier? Otherwise 5α-androstane-3α in plasma isn’t the same as in the brain.

[Tomas]

That is why it makes no sense to do blood test and check blood levels of Testosterone, DHT, etc.
Our problem is not in the blood, but in the CFS.
We should check and control the neuroactive steroids, and try to fix them.

[Tud50316]

Hi Oscar, could you please drop a link to this study when you get a chance?