That’s what I was thinking, maybe like a fast hoping it would have a “re boot” type of reaction on are endocrine system preventing the extra conversion to the unwanted metabolites.
Saw palmetto may lower 3 bdiol. But I have seen some studies of saw palmetto showing it did not reduce DHT in older men. Also saw palmetto could increase estrogen and that would negate any benefits.
THe path of action is to work out how messed up our T-DHT-3bdiol-3adiol levels and ratios are compared to normal men. Once we have that we can determine if this could be the root cause of the anti androgenic symptoms of PFS. Then we need to determine what influences their levels and how they respond to say testosterone administration and determine the source of this hormonal imbalance.
There are many studies showing that estrogens down regulate AR receptor numbers. In fact even soy can do this. Other hormones can also interfere with the transcription of the androgen receptor. I was just reading a study yesterday where in certain cells DHEA blocked the effects of androgens just like an anti androgen. And as I have been saying 3bdiol is a potent estrogen.
If you are in the US and need some help funding this test please send me the message and I will help you out. Thanks
I won’t be there before at least two months, but maybe we can consider it then if you didn’t find enough volunteers.
Hi Vincentv, I tried to email you. I am very keen to help in any study at all for this syndrome…please email me or call me....llewellyn_samuels@hotmail.com 0415 140 917
thank mate…
meridianvalleylab.com/testosterone-metabolites
Who’s getting this test done. You can get this test done for about $200
$200 small price to pay for even the smallest possibility of having info to help figure this out.
Reply here if you can do it.
Im getting the blood drawn monday morning and shipping the test back. It cost me approximately 165. Was pretty easy to order and setup. Hope this sheds more light. Im barely living.
In the Harvard study, they do extensive amounts of blood work in two sessions that they feel are necessary to understand our condition. Please consider participating in the studies. I feel it would be a much better use of your money.
They are testing these at the Baylor study, and I asked if I could have the test results, and the doctor said yes.
That is awesome. It is really great to see others coming from the Baylor study, as Awor had mentioned some time ago that one was slightly behind. Thanks man.
Lets keep it going guys, and get both of these studies finished up.
5-Androstane-3,17-diol (3-diol), an estrogenic
metabolite of 5-dihydrotestosterone, is a potent
modulator of estrogen receptor ERexpression in the
ventral prostrate of adult rats
abstract
Prostate is one of the major targets for dihydrotestosterone (DHT), however this gland is
also recognized as a nonclassical target for estrogen as it expresses both types of estrogen
receptors (ER), especially ER. Nevertheless, the concentrations of aromatase and estradiol
in the prostate are low, indicating that estradiol may not be the only estrogenic molecule
to play a role in the prostate. It is known that DHT can be metabolized to 5-androstane-3,17-diol (3-diol), a hormone that binds to ERbut not to AR. The concentration of 3-diol
in prostate is much higher than that of estradiol. Based on the high concentration of 3-diol
and since this metabolite is a physiological ERligand, we hypothesized that 3-diol would
be involved in the regulation of ERexpression. To test this hypothesis, adult male rats
were submitted to castration followed by estradiol, DHT or 3-diol replacement. ERand
AR protein levels in the prostate were investigated by immunohistochemistry and Western
blotting assays. The results showed that after castration, the structure of the prostate was
dramatically changed and ERand AR protein levels were decreased. Estradiol had just
minor effects on the parameters analyzed. DHT-induced partial recovery of ERwhile it
was the most effective inductor of AR expression. Replacement with 3-diol-induced the
highest levels of ER, but was comparatively less effective in recovering the AR expression
and the gland structure. These results offer evidence that one functional role of 3-diol in
the prostate may be autoregulation of its natural receptor, ER.
© 2007 Elsevie
Some highlights
It is noteworthy that the prostate concentration of 3-diol (10 pmol/g)
is 100-fold higher than estradiol [5], thus corroborating the
hypothesis that it may be the major ligand of ERin this gland
Based on the high concentration
of 3-diol and considering that this metabolite is a physiological ligand of ER, which is the subtype of ER more
widely expressed in the prostate, we hypothesized that 3-diol would be involved in the mechanism of regulation of
the ERexpression.
A key finding from our study was that 3-diol indeed has a potent
effect on the induction of ERexpression in the rat ventral
prostate
Compared with controls, bilateral
castration reduced the ERimmunostaining in the epithelium
by around 37%, as determined by the image analysis (Fig. 3).
Treatment with estradiol, DHT, as well as 3-diol, was able
to increase the ERlevels. Although significant, the effect of
estradiol on ERlevels was comparatively smaller than the
other hormones.
As found for the immunohistochemistry, recovery of ERpromoted by the 3-diol greatly
exceeded that of control animals
Treatment with estradiol, DHT, as well as 3-diol, was able
to increase the ERlevels. Although significant, the effect of
estradiol on ERlevels was comparatively smaller than the
other hormones. Higher recovery was observed after 3-diol
resupplementation, when the ERlevel was above controls.
Greater recovery
of epithelial AR occurred after replacement with DHT and 3-diol. Nevertheless, while DHT increased the AR protein to levels significantly higher than controls, the recovery promoted
by 3-diol did not reach control levels (Fig. 4). DHT but not 3-diol was able to induce AR expression in stromal cells as well
as in smooth muscle cells.
We compared the effects of estrogen, DHT and its metabolite
3-diol, in modulating the expression of estrogen receptor ER
and androgen receptor in the ventral prostate of adult rats.
The data obtained provided evidence that treatment with 3-diol was the most potent in inducing ERlevels.
On the other
hand, DHT induced the highest levels of AR protein and was
the most effective in maintaining the structure of the gland.
These results offer evidence that
one functional role of 3-diol may be the autoregulation of its
natural receptor, ER. To our knowledge, this is the first report
to show ERmodulation by 3-diol in the prostate.
ERlevels was significantly reduced after castration, which
is consistent with previous findings [3,39,44]. In contrast to
the prostate, castration had no effect on ERand ERexpression in the efferent ductules of the reproductive tract[45].
Replacement with DHT and 3-diol recovered ERexpression to levels comparable to those of control prostate. Others
have also demonstrated androgen (DHT) upregulation of ER
mRNA and/or protein in the rat ventral prostate or prostate
cancer cell lines
However, in the present study, 3-diol increased ERlevels significantly more than did DHT. It
is known that 3-diol does not accumulate in the prostate,
since it is rapidly and irreversibly converted to triols, which
are eliminated via the circulation for final excretion
Besides prostate,
evidence that 3-diol may act as a hormone has also been
found in other tissues, such as testis [47], efferent ductules
[22] and brain[19,21]. Therefore, it is becoming clear that
to discriminate the direct from indirect estrogenic effects of
androgens through aromatization to estradiol or reduction to
DHT is necessary, considering that the nonaromatizable DHT
may actually act as a source of a potent estrogenic compound
Resembling the
DHT effects, the content of androgen receptor was greatly
increased by 3-diol, but not by estradiol. Modulation of androgen receptor by 3-diol was previously investigated in ER
knockout mice (ERKO)[
In conclusion, the present data demonstrated that 3-diol,
a metabolite of DHT, is a potent inductor of ERexpression in
the prostate.
Thanks Vincent. While researching 3bdiol, I found something interesting.
genecards.org/cgi-bin/carddi … ene=AKR1C2
UniProtKB/Swiss-Prot Summary: AK1C2_HUMAN, P52895
Function: Works in concert with the 5-alpha/5-beta-steroid reductases to convert steroid hormones into the
3-alpha/5-alpha and 3-alpha/5-beta-tetrahydrosteroids. Catalyzes the inactivation of the most potent androgen
5-alpha-dihydrotestosterone (5-alpha-DHT) to 5-alpha-androstane-3-alpha,17-beta-diol (3-alpha-diol). Has a high
bile-binding ability
Catalytic activity: Trans-1,2-dihydrobenzene-1,2-diol + NADP(+) = catechol + NADPH
Catalytic activity: A 3-alpha-hydroxysteroid + NAD§(+) = a 3-oxosteroid + NAD§H
Enzyme regulation: Inhibited by hexestrol with an IC(50) of 2.8 uM, 1,10-phenanthroline with an IC(50) of 2100 uM,
1,7-phenanthroline with an IC(50) of 1500 uM, flufenamic acid with an IC(50) of 0.9 uM, indomethacin with an
IC(50) of 75 uM, ibuprofen with an IC(50) of 6.9 uM, lithocholic acid with an IC(50) of 0.07 uM, ursodeoxycholic
acid with an IC(50) of 0.08 uM and chenodeoxycholic acid with an IC(50) of 0.13 uM
Biophysicochemical properties: Kinetic parameters: KM=260 uM for (s)-tetralol; KM=520 uM for (s)-indan-1-ol;
KM=5000 uM for benzene dihydrodiol; KM=1 uM for 5-beta-pregnane-3-alpha,20-alpha-diol; KM=208 uM for
9-alpha,11-beta-PGF2; KM=0.3 uM for 5-beta-androstane-3,17-dione; KM=79 uM for PGD2;
Genatlas biochemistry entry for AKR1C2:
aldo-keto reductase family 1,member C2 (3-alpha hydroxysteroid dehydrogenase,type III),mainly expressed in
liver,also in other tissues,with high affinity binding for bile acids,also catalyzing detoxification of
polycyclic aromatic hydrocarbons
I think we may have found the reason why Ibuprofen gave relief to some PFS victims.
Hey how are ya. I have the results. I got crazy busy with work and have had zero time to got on here. So I guess the good news is the hormone levels all look good but the bad news is based on what my understanding of what you had in mind with the itilian study I think these results conflict that. But here they are.
Androstenedione: 0.6. (Ref range 0.5-2.2)
Testosterone (Te). 6.1 (ref range 2.6-8.9)
DHT. 0.77. (Ref range 0.24-0.84)
Te/DHT ratio 8.0. (7.9-15.2)
5a-Androstane-3B, 17B-DIOL (3B-Adiol) 3.7 low. (Ref range 4.0-20.2)
5a-Androstane-3a,17B-DIOL (3a-Adiol) 3.3 (Ref range 2.3-10.5)
3B-Adiol (DHT-3a-Adiol) ratio 0.9. (Ref range 0.8-6.5)
My hormone levels just don’t match up with how I feel.
No wonder why the medical community thinks we are all fucking insane
Interesing that these do not match up at all with the Italian study. The italian study showed very elevated levels of 3adiol and 3bdiol compared to the controls. 5 alpha victim is showing low levels of both. Very strange. 5 alpha victim took dusteride if that makes any difference.
Still waiting for one more result from a fin user.
We need to get a study that consists of 30 guys.
15 who never took DHT inhibiters and who are healthy and measure the their prostates.
15 people from this website and measure their prostates.
I honestly think shrunken prostate is what’s causing all of the ED, less semen, wattery semen, loss of sensation and eD.
It’s the only logical explanation for a person getting these symptoms but has normal
Hormone levels
I disagree.
After taking Vit D3 my semen has increased from 1 -2 drops to almost a teaspoonful but I still have all the symptoms like shrinkage, loss of appetite, numbness, muscle loss etc etc. When I stop VitD3 all of my symptoms like brain fog, headache, muscle weakness, appetite loss etc come back and yes the volume drops back to 1-2 drops only. Then I start vit d3 again and within few hours (4- 5 ) I start feeling better and symptoms disappear, volume returns normal. It is so unbelievable that only one day VitD3 administration brings volume back to normal (it is not my old normal but new low normal though) although over time sometimes I feel VitD3 is losing its effectiveness. My point here is that shrunken prostate is not the cause just an effect. I don’t know if any has noticed shrinkage in other parts of the body. I have got shrinkage in many parts not just genetialia. I have shrinkage in my feet, toes etc.Big toes look baggy and fluffy, skin is loose around toes, in normal people toes are full and healthy. The difference is so obvious that even a child can tell you the difference easily. Also my hands and fingers are shrunken too, especially back of my hands. Skin is much thinner all over body. Face look much smaller. I think this is all because of collagen and elastin loss.
Hypothalamus controls apettite thats why i think pfs is hypothalamus damage.
How are your hormone levels looking these days. Would you consider having the above mentioned test done to try to compare your results to vins itilian study?
Some of these symptoms you mention sound insane! Before this i would think u r crazy but after living the long term symptoms I get I now believe anything is possible.
Even with that said have u ever considered the possibility of any of those symptoms not being releated to Pfs? Before u get mad in just asking…
The brain is a very powerful thing. Trust me I am by no means questioning if pfs is real with that question
Bones shrinking that fast in result of a endocrin system issue just feels unlikely 2 me but like I said after this anything is possible in my mind now…
Also have u attempted to make a connection between your vit d intake with increased LH or FSH,
In other words do you see higher FSH and or LH levels wile u r on vit d compared to when u r not.
I think u should look into that if u have not to understand more about whst the vit d is doing in your body to make u feel better
Any idea when u r going to have your results?