Yes, I think he uses google translator and means stem cells.
Really though? Cured of what? PFS? Source? No one has been cured of PFS by any treatment, and certainly not by injecting their own adipose derived stem cells back into their blood stream. It doesn’t help making these completely incorrect statements at a time when we’re under the figurative and literal microscope of the research community.
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!
But you said the problem was Phantom DHT antibodies of a neurological basis.
Seriously Oscar, go away. Your Phantom DHT theory didn’t exactly rattle the scientific community. Now yield this forum to those who come to work.
If all 3 subjects were suffering low testosterone it could explain a lot of things, as hormones can alter the levels of neurosteroids. A similar study with subjects with normal hormone levels and still experiencing pfs symptome along with abnormal ones would be interesting.
[quote=“Costa”]
If all 3 subjects were suffering low testosterone it could explain a lot of things, as hormones can alter the levels of neurosteroids. A similar study with subjects with normal hormone levels and still experiencing pfs symptome along with abnormal ones would be interesting.
you have here people with good hormones values and still suffer from pfs.
I know man. I am one of those. That is why i think that people with good hormonal levels along with people with low hormone levels, all with pfs symptoma should be examined. This would rule out the possibility that the neurosteroids are altered due to low hormones rather than pfs itself.
I know it’s been a while, but my current protocol of Progesterone and DIM is similar to Progesterone and an AI, though maybe an AI needs to be used instead.
Low 5ar activity in the csf?
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??
One take away I see, and yes I know small sample size so it can’t be generalizable to the entire PFS population, is the CFS levels of Tetraprogesterone and Isoprogesterone in the control group is detectable in the control group and undetectable in the PFS patients, addtionally PFS patients have Estrogen metabolites in their CFS fluid and the control group does not. What does this mean, I’m not sure but all 4 of those markers are made from Progesterone according to steroidgenesis.
Indeed that’s a very good point, and I think we can try to conclude more through that.
Another thing I think it’s concludable is that this PFS thing has different profiles.
That subject number 3 has clearly a different profile from the other 2.
Maybe we should start separating the symptoms and doing a statistical distribution of symptoms vs. blood exams, and try to see if profiles show up…
could we know in that study which were the symptoms of each subject?
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.
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.
detected nothing or under limit of DiHydroProg and TetraHidroProg in CNS, that was fanstastic on all PFS…
Anyone know why 3-alpha-diol is so high in plasma?
3-alpha-diol is (from wikipedia):
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.
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.
