I do ask because I did not recover after 5 years of taking finasteride. Almost 3 years after I quit DHT inhibitor I still did not regain my DHT natural expression. I feel exactly the same as when I was on the drug regimen.
Is there anyone who did not recover from Fin and is still suffering 5 alfa reductase type II defficiency??
Cheers to everyone…
According to this thread you took Dutasteride for 4 months and are saying that is what caused you these issues… I’m confused, did you take Finasteride BEFORE Dut?
hairlosstalk.com/interact/vi … 46&t=43183
To be able to detect 5AR deficiency would likely require genetic PCR analysis of the 5AR gene/androgen receptor encoding for a chromosomal mutation. So far nobody has had this done.
However, since many guys continue to lose hair after quitting Fin, and experience brief recovery after quitting the drug (as DHT levels come back up within 2 weeks - month, as 5AR enzyme regenerates), it would appear 5AR is working correctly, and is not the issue.
Have you had bloodwork as outlined on this site (Hormones & Bloodtests section)? You may find you have low Testosterone, as for many guys here, that’s when their issues began – after quitting the drug, their T, LH, FSH levels crashed and they were left with major hormone imbalances, often with elevated Estradiol, SHBG, TSH or Prolactin. If you do not have bloodwork, you should get it done.
There are also other topics on your question, do a search for “mutation”.
I took finasteride for 4,5 years. I stopped taking it because it simply stopped working for me and I did recover after quiting it. But then when the hairloss started to occur againg I became interested in dutasteride and bought it. I had a 4 months regimen with Dut and unfortunetely did not return to normality in all sexual and mental way. It’s been 3 years since I stopped taking this poison…
My tests are correct.
I have T in the upper one third. Rest is balanced despite Progesteron and Cortisol which are elevated. HPTA also in a normal range.
I heared that autosomal overproduction of Progesteron can be a potent 5AR inhibitor and maybe downregulating progesteron might cure my symptoms… and idea so far…
HERE I PRESENT MY THEORY:
egy-chams wrote:
Hypo I’m not scientific as most of you here; but I can think of something:
I mean, lets track back the problem again. Finasteride’s supposed problem is inhibiting testosterone natural pathway thru conversion to DHT-which inturn keeps estradiol in check-thus the final result is a supraphysiological concentration of testosterone; which will be detoxified by the increased gene expression of liver aromatase to estradiol; which inturn- inhibit the HPTA via feed back mechanism.the results we have are:
1-increased activity of liver and my be testicular aromatase; hence increased estradiol conc.
2-decreased DHT levels
3-decreased testosterone levels”secondary hypogonadism”
And what happens when someone uses a testosterone ester injection for body building?
He will experience the same effects which are due to supraphysiological conc. Of T with the resultant conversion to estradiol via over-transcripted aromatase.
But why should steroid users recover easily by correcting the HPTA while can’t we?
The answer is that only difference between our secondary hypogonadism and post-steroid secondary hypogonadism is that we have inactive 5 alpha reductase. That is why steroid users will recover by just correcting their T levels, which can then be corrected to the more powerful DHT easily. I think DHT is responsible for full recovery since it is the most powerful androgen in the body.
Now, again, why can’t we recover by correcting T even months after stopping fin? Because even correcting the T can’t restore the DHT to pre-fin values. Why? Because 5 alpha reductase is still inactive even after stopping fin.why? I believe this is because of a powerful deactivation of 5 alpha reductase gene transcription. Only impaired gene transcription will persist even after even stopping fin. You know what? This is hellish.
I believe the FDA must force Merck to do a research to outline this; otherwise we will second guess the reason for the rest of our lives hopelessly.
p.s“sorry for my bad English, I’m not a native English speaker”
btw hypo, we have already ingested what is worse than snake oil, at least there is an antidote for snake oil!
Actually I agree with Egy-chams:
Especialy concerning the latest findings and Dr.Shippen book summary presented in the other subject.
I stopped Propecia years ago. I also had 4 months experience with Dutasteride. Now It’s been 3 years since I do not take any medication for hairloss.
I suffer all the symptoms that you mention here and even something extra, like face redness (maybe somebody mentioned that but did not notice). Plus I do not loose hair any more!!! Can you imagine without any drug, medication… anything, hair stopped falling so as my sex life went away.
I spent 1000 of hours trying to find out what is going on with me and I do finally know the horrible truth. Our problem in most cases is the: DEFFICIENCY OF 5AR/DHT IN THE BRAIN. 5AR gene is distroyed and it is irreversible.
How I got to this knowledge.
When my condition got horrible I did complexed tests. All of them were correct (even Testosteron was high), despite PROGESTERON. Tests were done 3 years from stopping drug rgimen
Now look at Dr.Shippen text summary for the moment:
We can see that while on propecia and when stopping propecia, our brains have a deficiency of DHT in them, which is what propecia does in order to stop hair loss. The deficiency in DHT causes the hormone progesterone not to be converted to allopregnenolone, so brain repair does not take place as it should and there is a deficiency of GABA that can lead to high levels of anxiety. The body then tries to correct this problem of a lack of brain repair. This attempt logically does one of two things to the adrenal glands. Firstly, this attempt could possibly create such stress on the adrenals that they wear out and get fatigued, or else, secondly, the adrenals might know the body needs allopregnenolone and so tries to make the needed allopregnenolone by producing more and more progesterone. This progesterone never gets converted into allopregnenolone, though, because the DHT is blocked. The adrenals may eventually get worn out by contiuing to produce more and more progesterone that never does anything because there is no DHT. The progesterone may even not be converted as it should into testosterone, cortisol, DHEA, etc., in the adrenal cascade, because it is being saved in the attempt to make the crucial allopregnenolone, thereby resulting in deficiencies in other hormones that are normally made from progesterone.
This is exactly what happens in my body. Progesteron is permanently upregulated due to the defficiency in the 5AR/DHT. It cannot convert to 5alfaprogesteron —>Allopregnolon via 5AR!!
This Mental Fog/Brain Fog is directly associated with this phenomenom, because our brains does not support enough Allopregnolon and Gaba. Defficiency of these neurosteroids causes neurological problems that you discuss. There is no doubt it is permanent and associated with a demage of 5AR, because it is 3 years since I finished my hairloss regimen.
I wonder why don’t you discuss your progesteron levels, and I strongly suggest you better start to do so…
Cheers. We are f***ed but should not loose faith at least…
This quote is not taken from Dr. Shippen himself, it is from the user Smithpulitzer who wrote it in a post dated Nov 14, 2006 on the old Yahoo Forum, offering his opinion on how to recover from the drug’s effects.
health.groups.yahoo.com/group/fi … sage/11753
Please do NOT misquote people’s words and claim they are those of a medical professional, it is seriously misleading.
Ok
Sorry to sound harsh, that isn’t my intention – just need to make sure we clearly label all materials and their sources, especially if we are to present such things to doctors ourselves. Your contributions ARE appreciated.
I know you said you have bloodtests and they are all fine, but would you mind posting them in the Hormones & Bloodtests section? Would be interesting to see your results.
Cheers.
Ok. I will do this in a minute. Cheers.
Regarding possible ways to boost 5AR activity, see these studies… some interesting ideas:
propeciahelp.com/forum/viewtopic.php?t=429
propeciahelp.com/forum/viewtopic.php?t=984
You may also want to have a read through this thread, some interesting ideas:
i’m going to have actually agree with this guy that this is permanent. I took it for only three weeks at a very low dose and although i have minimal sexual sides 9 months after quiting compared to most on here all of the other mental and physical symptoms have just gotten worse and worse. also as time goes on while i can still get erections and such it seems my sex drive is fading away. we are all truely f***#$ it’s ashame.
Perhaps Finasteride useage, via messing with C19, C21 and 5AR liver metabolism, left us with altered hormone ratios that resemble those of a pseudohermaphrodite/person with genetic 5AR deficiency… however, I don’t know if anyone has gotten the below tests done yet. I know I certainly will be on my next round of bloodtests, and pushing for genetic analysis for 5AR chromosomal mutation.
One ray of hope that this may not be truely irreversible: anecdotal reports of Dr Shippen/Crisler helping some guys recover, and my own brief semi-recovery for 2 days, during an episode of norwalk virus 1.5 yrs ago, after 1 yr off the drug: propeciahelp.com/forum/viewtopic.php?t=789
If my body could spontaneously recover on its own, it IS possible – just need to find out what changed. I have a feeling liver 5AR metabolism is somehow linked to all of this.
propeciahelp.com/forum/viewtopic.php?t=568
"… decreases of the ratios between 5a-and 5ß steroids:
propeciahelp.com/forum/viewtopic.php?t=658
"The steroid profile was compared to male pseudohermaphrodites with inherited 5 alpha-reductase deficiency who have a global defect in C19 and C21 5 alpha-metabolism. Mean plasma DHT levels were decreased at all doses, resulting in elevated T/DHT ratios.
The mean urinary:
… ratios were elevated compared to pretreatment levels and placebo control values.
The results indicate that finasteride has a broad steroid spectrum inhibiting C19 and C21 5 alpha-steroid metabolism and affecting hepatic [liver] and peripheral 5 alpha-metabolism.
These results suggest that a single gene codes for a single 5 alpha-reductase enzyme with affinity for multiple steroid substrates. The steroid profile is strikingly similar to that of male pseudohermaphrodites with inherited 5 alpha-reductase deficiency."
propeciahelp.com/forum/viewtopic.php?t=1082
“…showed markedly elevated T/5DHT ratios”
“…analyses of steroid hormone metabolites for random urine samples by a gas chromatograph-mass spectrometry revealed markedly increased ratios of 5ß to 5a metabolites, especially for tetrahydrocortisol (THF) derived from cortisol”
… “Although this would primarily be due to defective 5-reductase-2 activity in the liver, which would mainly catalyze adrenal rather than testicular steroid hormones (6, 10, 30), urinary steroid hormone profile analysis is a highly sensitive and noninvasive test and, therefore, appears to be more advantageous than serum androgen measurement for the diagnosis of 5-reductase-2 deficiency.”
Screenshot from below link:
books.google.com/books?hl=en&lr= … #PPA122,M1
Mew thanks for your assistance in finding the possibilities to boost 5AR.
Actually from my experience the best way of boosting the remaining 5AR/DHT is when you take most antibiotics when you are sick or for prostatis reason. Most antibiotics are progestins antagonists and they also exaggerate androgen expression. That’s why many people report improvement while taking antibiotics but this is very well understood and logical. Usually improvement persist for the time of the treatment and some weeks or maximum months after.
I really wonder where are you planing to directly test 5AR genetic expression. Such tests costs houndred of thousand dolars/euro.
Please tell me what is your plan for that cause I just can’t believe you got it established.
Mew, would you like me to write my onw story in the proper section? Do you really believe any doctors would be interested in our devastating problems… I rather believe in Jerry McGuire words… “show me the money…” Are we showing money… more preferably to the lawers department then medical.
I’m going to ask the doc and see what he says, I’m going to find out how its done and the costs involved.
That would be great, as well please put a link to your hormones (as posted the other day) in your story.
I would encourage you to speak to some law firms to see what they say. Most of the negative evidence about this drug’s effects are contained in the Finasteride Studies section.
Offtopic, but did you perhaps take an antibiotic for your norwalk virus? Just asking as I am feeling much better when on a mild antibiotic…
edit: did not see majkellos’ post about antibiotics, but did definitely notice a similar thing
No, I did not. The only thing I was given when I went to the hospital was an IV with saline injection.
Something interesting to ponder: Finasteride inhibits 5AR-II enzyme. After quitting the drug, many guys here find their dicks “shrinking” and retreating into a kind of “pre-pubertal” state… which seems eerily similar (though not to the same degree) to those boys/men that are born with hypospadias/micropenis due to 5AR deficiency, partial/complete androgen insensitivity syndrome, or maybe 17b-Hydroxysteroid Dehydrogenase 3 Deficiency…
I dunno, just thought, more stuff one can test for.
captura.uchile.cl/dspace/bitstre … /Rey_R.pdf
To identify steroidogenic pathway defects, and because the first steroidogenic steps are the same in the testis and the adrenal, serum levels of 17OH-pregnenolone (17OH-P5), dehydroepiandrosterone (DHEA),
17OH-progesterone (17OH-P4), 4-androstenedione (4-A), and cortisol
were measured in basal conditions and after a standard ACTH
stimulation test (0.25 mg iv) as previously described (23).
The post-ACTH/basal cortisol levels ratio was used to evaluate overall adrenal steroidogenic response. The functional activities of P450c17 and 3-
hydroxysteroid dehydrogenase (3-HSD) were assessed comparing the
results of 17OH-P5, DHEA, 17OH-P4, and 4-A measurements in our
patients with the normative values for glucocorticoids and sex steroids
in healthy pediatric population published by Lashansky et al. (24).
Furthermore, a molecular study of the 3-HSD type 2 gene (HSD3B2) was
performed, as already reported (23). The activity of testicular 17-HSD
was assessed with the testosterone/4-A ratio after hCG stimulation.
[b]The association of a lack of testosterone increase after the hCG test and a testosterone/4-A ratio less than 0.5 was considered as highly predictive of 17-HSD deficiency /b.
Finally, the activity of 5a-reductase was evaluated by using the testosterone/DHT ratio after hCG stimulation. [b]A testosterone/DHT ratio higher than 35 was considered as highly predictive of 5a-reductase deficiency /b.
A testosterone hCG/basal ratio of at least 2 associated with AMH SDS of at least 2 was considered as highly predictive of partial androgen insensitivity.
rarediseasesnetwork.epi.usf.edu/ … x.htm#nomo
17b-Hydroxysteroid Dehydrogenase 3 Deficiency
17b-Hydroxysteroid dehydrogenase 3 deficiency is a very rare autosomal recessive form of male pseudohermaphroditism. Affected (46,XY) individuals are insufficiently virilized at birth to be raised as boys, and hence most are raised as girls. At the time of expected puberty, plasma testosterone levels increase, and considerable virilization occurs, similar to steroid 5a-reductase 2 deficiency. Thus, these patients, who are raised as girls initially, often request reassignment to male gender during puberty.
Diagnosis
Plasma androstenedione levels are elevated 10-fold or more, whereas testosterone and dihydrotestosterone levels are in the low or low normal range for normal males. The diagnosis can be made at birth due to genital ambiguity based on the high androstenedione/testosterone ratio (basal or after hCG stimulation). Otherwise, the diagnosis is made at puberty when virilization occurs. Molecular genetic diagnosis is often required to distinguish PAIS, steroid 5a-reductase 2 deficiency, and 17b-Hydroxysteroid dehydrogenase 3 deficiency, due to the similarities and difficulties in establishing these diagnoses.
3b-Hydroxysteroid Dehydrogenase Deficiency
Classical (severe) and nonclassical (mild) forms of 3b-hydroxysteroid dehydrogenase deficiency (3b-HSD) CAH are known. In the classical form, steroid synthesis in both the adrenal cortex and the gonads (testes, ovary) is affected.
Circulating androgen precursor steroids are converted outside the adrenal to androgens. Virilization of affected females can occur. In males, prenatal differentiation of the external genitalia is incomplete because of the gonadal defect.
Thus, in this disorder genital ambiguity can affect individuals of both sexes. Only in the severe form has a gene for 3b-HSD been identified. The nonclassical form has no demonstrated genetic mutation and seems to wax and wane hormonally.
Diagnosis
3b-HSD is diagnosed following an ACTH stimulation test showing elevation of serum D5-17-hydroxypregnenolone, dehydroepiandrostenedione, and ratios of D5-17 hydroxypregnenolone/17-hydroxyprogesterone and D5-17-hydroxypregnenolone/cortisol. The disorder has an autosomal recessive inheritance. Some 40 mutations in 3ß-HSD type II gene already have been described.
Mew I do not wat to make any false assumption but to be honest I define my situation mental/sexual following my personal intuition.
It says that some of our 5 alpha reductase cells has been cut out for unknown reasons. I focus on the mental/sexual personal feelings because what you can see, even if most of guys here go for the labolatory tests, they get semi-low DHT results, but still kept within the range scale.
How do I define my personal feellings about that? The impression of myself makes me realize that I am a one third of a man I used to be. I mean that my senses in terms of vitality, mentality, sexuality are turned to one third of my personal pre-treatment baseline.
I can realy feel following my senses what kind of biochemistry stands befind all our mental and sexual sides.
I can see how porgesteron can cause anxienty when it cannot be turned via 5AR into its metablites, a potent neurosteroids. I can feel how the whole testosteron cannot be converted to DHT on the right level.
I realy understand how such a weak boichemstry, rapped by those nasty chemicals can react to even a little influance targeted on further 5AR activity. Remember that you only have got maybe a one third of the cells you had before.
Guys write about this hypersensivity to any weak dht supressors…
Why most of us are alergic to most antioxidants, cigarets, caffeine… why it makes a problem to go and eat sushi… hah? why some other foods makes you feel strange or allergic? Finaly why it is possible so easly to stop the rest of your hairloss, even if it still occurs. Any logical and simple answers?
It makes a total sense to me… The brain is really 5AR deficient now… so what else could actually happen then…
There will be some people maybe trying to make a further discusions or saying… hey do not make a false assumptions… etc… I am not doing any… Consider it as my senses voice. Thay are telling me this and I only translate it. On the other hand peolple who still does not believe it, have to seach some theory because I did found a medical backround to my senses words.
Glaxo/Merck are save then anyway. We won’t prove in any court that a few years ago Propecia/Dutasteride had taken our libido away irreversibly. Remember that it propably will still remain within the range.
The problem is that ranges and human senses are something different, might be even opposit as you can see.
Shame.
I just spoke to my Endo (here in Canada) and he said that 5AR, Allopregnenalone, 3HO, 5-dihydrodexoxycorticosterone, and allotetrahydrodexoxycorticosterone are not available for testing and these are only done in research labs. I didn’t get to ask about genetic tests but no doubt they’ll be the same as the others. I asked about the Adiol-G test and he said that it wouldn’t reveal anything about 5AR. He told me the test has to do with stuff released by the adrenal glands and he lost me after that. Basically, if we here in Canada and most likely in the US want to test any of these we’ll have to track down a research lab or doctors/schools doing research into this.
This what you said relates to my feeling that we might have a problem with some local disfunctions of adrenal glands, not the whole systemic conversion of 5AR. It also might connect 5AR deficiency with andrenal fatigue explaining that it is basicly the same issue.
My Endo ran a bunch of adrenal tests (cortisol, 24hr urine to test adrenaline and dopamine, etc.) last month and he said that all the tests show absolute normal adrenal function with no outliers. He said that there are no other tests to to do with regard to adrenals causing mental/sexual problems and that “adrenal fatigue” is a nonspecific term and isn’t something you’ll hear a doctor diagnose you as having. Basically, if you think you have something wrong with your adrenals then get your Endo to run tests to see if this is the case but don’t diagnose yourself and start treating it with dodgy supplements. One guy on here did that and got himself into some trouble.
However, I do believe that 5AR could have caused or be a cause of our problems by either being down regulated, mutated, “turned off”, caused hormone imbalances, or altered other enzymes. But as I stated before, 5AR and enzymes are not available for testing.
