Fucked by Finasteride / calling all expert steroid users

[Shaolin]

Hello there, I am one of the poor unlucky individuals who have been decimated by the use of finasteride for 1 month at 1mg/day.

Side effects after quitting

2 years of no libido whatsoever, no erections, no sexual thoughts, very low ejaculate, no orgasms

3 years of heavy metabolic problems, a.k.a. adrenal and thyroid issues, now partly recovered

last year been facing extreme testicular regression and shutdown for no apparent reason, since the drug is out of my system 7 years now. Yet my last testing shows very low activity of 5-ar II, which converts T to dihydrotestosterone and very high estradiol levels.

My testicles have lost three quarters of their size and keep atrophying in extreme pains every day as we speak.

I have tried many many substances, drugs and herbs to stop this. The problem is that no matter how much i try to raise testosterone it mostly (90%) goes into estradiol and very very little if any goes to dihydrotestosterone which is what is needed for my testicles to survive.

I am thinking lately of running a cycle with high doses of Proviron (50-75 mg/day) and HcG in order to try and boost my androgenicity and give my testicles a chance to recover.

The question is!!!

1. is it possible to run an androgenic cycle in the same logic as an anabolic cycle?? That is instead of reaching high testosterone levels to try to reach high DHT levels and at the same time try to keep testicles alive or recover them with using HcG medium doses + dht??

2. Is it possible that dht acts as an anti-estrogen and brings my very high estradiol levels down in due time??

3. Does anyone know if high levels of DhT express higher 5-ar II levels or the opposite??

 

[solo47]

Have you seen a medical specialist, like an internist or urologist? Obviously, you have serious medical issues that cannot be blamed on running some roid seven years ago.

Solo

 

[Structure]

Hello there, I am one of the poor unlucky individuals who have been decimated by the use of finasteride for 1 month at 1mg/day.

Side effects after quitting

2 years of no libido whatsoever, no erections, no sexual thoughts, very low ejaculate, no orgasms

3 years of heavy metabolic problems, a.k.a. adrenal and thyroid issues, now partly recovered

last year been facing extreme testicular regression and shutdown for no apparent reason, since the drug is out of my system 7 years now. Yet my last testing shows very low activity of 5-ar II, which converts T to dihydrotestosterone and very high estradiol levels.

My testicles have lost three quarters of their size and keep atrophying in extreme pains every day as we speak.

I have tried many many substances, drugs and herbs to stop this. The problem is that no matter how much i try to raise testosterone it mostly (90%) goes into estradiol and very very little if any goes to dihydrotestosterone which is what is needed for my testicles to survive.

I am thinking lately of running a cycle with high doses of Proviron (50-75 mg/day) and HcG in order to try and boost my androgenicity and give my testicles a chance to recover.

The question is!!!

1. is it possible to run an androgenic cycle in the same logic as an anabolic cycle?? That is instead of reaching high testosterone levels to try to reach high DHT levels and at the same time try to keep testicles alive or recover them with using HcG medium doses + dht??

2. Is it possible that dht acts as an anti-estrogen and brings my very high estradiol levels down in due time??

3. Does anyone know if high levels of DhT express higher 5-ar II levels or the opposite??

Hi Shaolin,

I have heard of this before, although I haven't followed the issue closely to see how other people have tried to treat it. I am not a doctor, and I have never used steroids, but I have done quite a bit of endocrine-androgen research. This is how I would go about treating your problem:

• Testicular atrophy is not due to lack of T or even DHT, it is due to lack of LH. Presumably you have had your LH levels checked. What are they? HCG acts in the same way as LH, so you could artificially elevate your LH levels this way. Also, what is your level of FSH?
• T is converted into E by the enzyme aromatase. If for some reason your body is converting all of your T into E, then you might want to look into an aromatase inhibitor. I've never used one, and I hear that some serious side effects can result if you misuse it. Also keep in mind that you will need some E to function normally (libido, bone mineral density, etc.), so you definitely don't want to over-do it.
• If you are deficient in DHT, then you can always supplement with DHT directly. For example, if you search for "Andractim", you are likely to find that this product is sold regularly in a 2.5% gel without prescription in Europe (usually to treat gynecomastia, although this claim is questionable).
• Andractim is a hydroalcoholic gel, and is rapidly absorbed. This can cause problems even in healthy individuals: while DHT does not directly suppress the pituitary, it does have a round-and-about way of suppression. Overusing this gel will cause suppression. Also keep in mind that since it is rapidly absorbed (and perhaps cleared as well) you may need to use it more than once daily. You will have to do some research on this to figure out the dosing, etc.

If I was you, I would work with an endocrinologist so that you could closely monitor your blood work as you make changes. Also, I would make changes slowly, one at a time, so you can give your body time to adjust, and also to figure out what is happening --- change too many things at once, and you may not even know what product is responsible for what effect (or worse yet, one product may not be able to do its job due to the side effects of another product).

I would first start with HCG. Then I would look into aromatase inhibitors, if your T is still low and your E is still high. After trying aromatase inhibitors, I would adjust the dosages so that my T and E were both at a normal level. Remember also to look at SHBG and free testosterone to make sure that your T is not being tied up.

After all of that, if your T and E are normal, but your DHT is still low, I would try andractim or an injectable DHT preparation.

Good Luck!

 

[PS LABS FOUNDER]

What the fawk??

This was 7 years ago and you have not corrected the problem yet? Dude it not likely that its the riod from 7 years ago

if it was me but you probly have already done these -
id do clomid/ nolva/ hcg/ tribulious terrious/ maca and whatever other herbs i could do get my natural test as high as i could!!!

Good luck man at dont do riods till u fix this problem

 

[Shaolin]

I started working in a research lab in a medical university now so i have access to a lot of testing. Finasteride has messed me up and a few thousands of other people. It has blocked my 5- ar II for good and all T as i said is converted to estrogen (e2).

LH is normal (4.5). Fsh is low normal (2.8).

The only thing that is high is estradiol e2 and total estrogens. (55 ng/dl with normal <30)

Testosterone is also mid range (460 ng/dl)

Androstenediol Glucuronide is very very low (1.24 normal range is 12-18)

No endocrinologist can help really, i ve been to several countries, several experts have seen me in the field of endocrinology, neuroendocrinology, antiaging, sex medicine specialists what the fuck else to do.

I used arimidex it makes me feel shit and causes more inflammation.
I used andractim and proviron, causes some relaxation and also some more inflammation

I have low SHBG, and using Testosterone gel on my testicles to increase the rate of conversion of T to dht works a bit but causes fatigue.

It seems that finasteride messed with many parameteres apart from the obvious ones, since out of nowhere i started developing fatigue after its use and ended up with serious metabolic issues.

The big question is, will HcG along with arimidex stabilize my testicles and hold on my high aromatase activity?? Or do i need to add some proviron in the mix to give testicles the needed building blocks??

I am also thinking of HMG.

I also have this question. Is it normal for testicles while they shut down to cause great pains and can someone reverse this process or do they shut down without any pains at all??

 

[Shaolin]

Clomid and nolva tried them too, but couldn't handle them my body seems not to tolerate drugs after finasteride. I geat headaches and weakness from the first pill. I am a living wreck. I can't believe that this drug did this to me. Before finasteride i never had issues and had sex like a mad man. Now everything is so messed up

 

[Structure]

I started working in a research lab in a medical university now so i have access to a lot of testing. Finasteride has messed me up and a few thousands of other people. It has blocked my 5- ar II for good and all T as i said is converted to estrogen (e2).

LH is normal (4.5). Fsh is low normal (2.8).

The only thing that is high is estradiol e2 and total estrogens. (55 ng/dl with normal <30)

Testosterone is also mid range (460 ng/dl)

Androstenediol Glucuronide is very very low (1.24 normal range is 12-18)

No endocrinologist can help really, i ve been to several countries, several experts have seen me in the field of endocrinology, neuroendocrinology, antiaging, sex medicine specialists what the fuck else to do.

I used arimidex it makes me feel shit and causes more inflammation.
I used andractim and proviron, causes some relaxation and also some more inflammation

I have low SHBG, and using Testosterone gel on my testicles to increase the rate of conversion of T to dht works a bit but causes fatigue.

It seems that finasteride messed with many parameteres apart from the obvious ones, since out of nowhere i started developing fatigue after its use and ended up with serious metabolic issues.

The big question is, will HcG along with arimidex stabilize my testicles and hold on my high aromatase activity?? Or do i need to add some proviron in the mix to give testicles the needed building blocks??

I am also thinking of HMG.

I also have this question. Is it normal for testicles while they shut down to cause great pains and can someone reverse this process or do they shut down without any pains at all??

If SHBG is low, then free T is high. Free T is all that matters, not total T; total T is a measurement of free T, plus whatever T is bound up by SHBG. Also, what is your DHT measured at? These two numbers (free T and DHT) are important in figuring out what needs to be treated.

Before I answer your other questions, I need to know what these numbers are. After all, if you start using HCG, you will suppress your production of LH...

 

[PS LABS FOUNDER]

Clomid and nolva tried them too, but couldn't handle them my body seems not to tolerate drugs after finasteride. I geat headaches and weakness from the first pill. I am a living wreck. I can't believe that this drug did this to me. Before finasteride i never had issues and had sex like a mad man. Now everything is so messed up

50 mg clomid should not give any adverse effects and should make ur balls bigger / more hormey and sexual - you should give clomid - JUST CLOMIOD ANOTHER TRY ALONE

ALSO DID YOU EVER DO MACA OR TRIBULIOUS LIKE I SAID ? U TRIED THOSE

I KNOW UR LH IS NORMAL LEVELS BUT TRY THEM ANYWAY

 

[Shaolin]

Well dht doesn't matter because i have low 5-ar II activity as shown by its metabolite (3-adiol-g or androstanediol glucuronide). Total dht is a useless value.

LH is also pretty useless because it fluctuates with great inconsistency so doctors tell me to go after FSH values which mine are constantly around 2.8-3.2 since all them years.

I started HcG just for the heck of it yesterday at 500 IU but am considering HmG for better results just don't know where to obtain it yet.

The major issue however remains the deactivated or suppresed activity of 5-ar II, so even if i manage to handle clomid, which i can't i tried, i can't even manage arimidex at 1/4 dose i get awfull headaches that last 2 days, nothing will change unless clomid supresses estradiol which i don't think it does.

I am looking for a potent herbal anti-aromatase or if proviron could do the trick and lower my aromatase activity i could run this for as long as need and then see if i can run some clomid if i feel better in a few months. But the major issue here is, does proviron improve 5-ar II activity or does it surpress it ?? Research sais at least in anterior prostate it rebuilds it, and increases the enzymes expression, which is quite anecdotal since every metabolic byproduct you use normally feedsback on the enzyme that catalyses its production and slows it down.

Very complex shit i guess

I am also thinking of running GnRH shots once in a while to see response.

There has to be a way to reactivate this 5-ar II for fuck sake

 

[Structure]

Well dht doesn't matter because i have low 5-ar II activity as shown by its metabolite (3-adiol-g or androstanediol glucuronide). Total dht is a useless value.

LH is also pretty useless because it fluctuates with great inconsistency so doctors tell me to go after FSH values which mine are constantly around 2.8-3.2 since all them years.

I started HcG just for the heck of it yesterday at 500 IU but am considering HmG for better results just don't know where to obtain it yet.

The major issue however remains the deactivated or suppresed activity of 5-ar II, so even if i manage to handle clomid, which i can't i tried, i can't even manage arimidex at 1/4 dose i get awfull headaches that last 2 days, nothing will change unless clomid supresses estradiol which i don't think it does.

I am looking for a potent herbal anti-aromatase or if proviron could do the trick and lower my aromatase activity i could run this for as long as need and then see if i can run some clomid if i feel better in a few months. But the major issue here is, does proviron improve 5-ar II activity or does it surpress it ?? Research sais at least in anterior prostate it rebuilds it, and increases the enzymes expression, which is quite anecdotal since every metabolic byproduct you use normally feedsback on the enzyme that catalyses its production and slows it down.

Very complex shit i guess

I am also thinking of running GnRH shots once in a while to see response.

There has to be a way to reactivate this 5-ar II for fuck sake

T is converted into DHT by 5a-reductase. DHT is converted into 3a-diol by 3a-oxioreductase. If you are concerned about your 5a-reductase activity, then you should be concerned about your DHT levels, because you can't make it without 5a-reductase.

As you have mentioned yourself, this is complex. If you want to figure out what is going wrong, you are going to have to look at each step in the process, not just your 3a-diol. How you treat the problem should be based on where the process is going wrong. For example, you know what the end result is (your symptoms), and you suspect that Finasteride started the problem, so you need to look at every step in the chain of androgen metabolism.

So far, you have established that your LH and FSH are normal, although your FSH is in the low normal range. This is a known result of high E, and yours is high (high E results in less GnRH, which results in less FSH). You've also mentioned that you have low total T, but as I've mentioned before, total T is not significant, free T is.

If your free T is normal, then move to the next step, DHT. If your DHT is normal, then your 5a reductase is working fine. I'm guessing that your free T and your DHT are normal, otherwise you would have mentioned what they are by now.

If I was you, I'd be more concerned about that high E than I would about 5a reductase, especially if your DHT is normal. You've been taking a lot of different steroids, many of which can cause high E. What is the longest you have gone without taking any supplements? Was your E elevated during this time as well?

Also, you specifically mention headaches, dysphoria and mood instability. These can result from high progestins. Have you had your progesterone / pregnenolone levels checked? Progestins are often high when you have adrenal issues (CAH, 21-OH deficiency, etc.), and you mentioned that you had adrenal issues. You'll notice that these three symptoms are known side effects of the birth control pill, which contain progestins and estrogens.

I don't know if testicular atrophy is painful, hopefully someone else will say something about that. But I do know that if you start taking HCG, then you will eventually suppress your natural production of LH, which will be a problem when you discontinue HCG. I would try to find a way to tolerate one of the aromatase inhibitors out there and take it concurrently, if I was going to take HCG at all. And for God's sake, see a doctor and monitor your blood work closely so you don't throw anything else out of balance.

 

[KBD]

Id rather lose all my hair and go bald than resort to propecia.

Its caused way to many problems like this. I dont understand why people even use it. If you want your hair back, take some biotin and rogain of all things. Just not finasteride, cause once your sex drive is gone on that, its gone!

 

[Stretch]

5ar activity is increased by supraphysiological levels of testosterone...

But I doubt you won't want to use any exogenous T... at least not until you find a way to control the conversion to E2
Posted from my Android device

 

[Stretch]

***But I doubt you would want...
Posted from my Android device

 

[Reginald]

Hello there, I am one of the poor unlucky individuals who have been decimated by the use of finasteride for 1 month at 1mg/day.

Side effects after quitting

2 years of no libido whatsoever, no erections, no sexual thoughts, very low ejaculate, no orgasms

3 years of heavy metabolic problems, a.k.a. adrenal and thyroid issues, now partly recovered

last year been facing extreme testicular regression and shutdown for no apparent reason, since the drug is out of my system 7 years now. Yet my last testing shows very low activity of 5-ar II, which converts T to dihydrotestosterone and very high estradiol levels.

My testicles have lost three quarters of their size and keep atrophying in extreme pains every day as we speak.

I have tried many many substances, drugs and herbs to stop this. The problem is that no matter how much i try to raise testosterone it mostly (90%) goes into estradiol and very very little if any goes to dihydrotestosterone which is what is needed for my testicles to survive.

I am thinking lately of running a cycle with high doses of Proviron (50-75 mg/day) and HcG in order to try and boost my androgenicity and give my testicles a chance to recover.

The question is!!!

1. is it possible to run an androgenic cycle in the same logic as an anabolic cycle?? That is instead of reaching high testosterone levels to try to reach high DHT levels and at the same time try to keep testicles alive or recover them with using HcG medium doses + dht??

2. Is it possible that dht acts as an anti-estrogen and brings my very high estradiol levels down in due time??

3. Does anyone know if high levels of DhT express higher 5-ar II levels or the opposite??

no,no. i don't think your problem is/has relate on finasteride/proscar. i assume u need Clomid only,or Tormifene.

 

[Shaolin]

Thanks for the info. Yet blood DHT is still not a valid measurement, since T gets transformed into DHT by 5-ar I as well as 5-ar II. The problem is that 5-ar II is the main problem with us taking finasteride. And this enzyme is located in our prostate, testicles, and surrounding glands mostly and its lack of function provides low amouts of dht in those tissues. So the 3-adiol-g is the enzyme that shows what is going on regarding your androgenicity.

5-Alpha Reductase Over-Inhibition

I have adrenal issues meaning low cortisol, all this shit started after fin as well. I never did any other steroids, just finasteride, one month, and since then all hell broke loose. I tried nolvadex for two days, couldnt tolerate it, clomid for one day, same shit, arimidex twice also same problems. All those drugs that affect my T and estrogen levels seem to cause similar symptoms which are toxicity or low adrenal function symptoms. Yet even taking cortisol doesn't make me better.

Taking low dose liposomal testosterone applied on my testicles decreases the inflammation over there but also causes fatigue.

So what is left to do?? I took one dose of HcG at 500 mIU and what happened?? More testicular atrophy and pain.

No matter what i do this happens, its going on for years since taking finasteride, just this year it has speed up. Like your hair loss speeds up when 5-ar II activity is very high.

Doctors told me not to take arimidex on its own, i never understood why. If i could just block the high E2 and this could improve the rate of conversion of T to dht then hurray !!! problems solved. But apart from the effect arimidex has on my body (fatigue, weakness, headaches) there is no improvement rather more problems with testicles.

Its not only me, there's like a few thousands of us affected with finasteride and noone seems to find anything working.

The only thing that relaxes me a bit and makes me feel better is a bit of proviron. Yet second dose always causes more inflammation in testicles and shrinkage.

It seems that my body has locked at this level of average T, high estradiol and intratesticular conversion of T to dht and anything and i mean anything i use messes my balance even more.

I recently bought some quercetin dim and chrysin. These substances are said to control E2 or metabolize it better but also cause some 5-ar II inhibition.

Any feedback on them???

 

[Structure]

Thanks for the info. Yet blood DHT is still not a valid measurement, since T gets transformed into DHT by 5-ar I as well as 5-ar II. The problem is that 5-ar II is the main problem with us taking finasteride. And this enzyme is located in our prostate, testicles, and surrounding glands mostly and its lack of function provides low amouts of dht in those tissues. So the 3-adiol-g is the enzyme that shows what is going on regarding your androgenicity.

5-Alpha Reductase Over-Inhibition

I have adrenal issues meaning low cortisol, all this shit started after fin as well. I never did any other steroids, just finasteride, one month, and since then all hell broke loose. I tried nolvadex for two days, couldnt tolerate it, clomid for one day, same shit, arimidex twice also same problems. All those drugs that affect my T and estrogen levels seem to cause similar symptoms which are toxicity or low adrenal function symptoms. Yet even taking cortisol doesn't make me better.

Taking low dose liposomal testosterone applied on my testicles decreases the inflammation over there but also causes fatigue.

So what is left to do?? I took one dose of HcG at 500 mIU and what happened?? More testicular atrophy and pain.

No matter what i do this happens, its going on for years since taking finasteride, just this year it has speed up. Like your hair loss speeds up when 5-ar II activity is very high.

Doctors told me not to take arimidex on its own, i never understood why. If i could just block the high E2 and this could improve the rate of conversion of T to dht then hurray !!! problems solved. But apart from the effect arimidex has on my body (fatigue, weakness, headaches) there is no improvement rather more problems with testicles.

Its not only me, there's like a few thousands of us affected with finasteride and noone seems to find anything working.

The only thing that relaxes me a bit and makes me feel better is a bit of proviron. Yet second dose always causes more inflammation in testicles and shrinkage.

It seems that my body has locked at this level of average T, high estradiol and intratesticular conversion of T to dht and anything and i mean anything i use messes my balance even more.

I recently bought some quercetin dim and chrysin. These substances are said to control E2 or metabolize it better but also cause some 5-ar II inhibition.

Any feedback on them???

Both 5ar1 and 5ar2 convert T to 5a-DHT, and a portion of that 5a-DHT is converted into 3a-adiol by 3a-oxioreductase. In other words, your 3a-adiol measurement doesn't care which 5ar enzyme converted the T into 5a-DHT; 3a-adiol only measures how much of that 5a-DHT has been converted by 3a-oxioreductase.

That link you posted corroborates what I am saying: they note that 3a-adiol can be converted back into 5a-DHT, and thus 3a-adiol functions as a store of potential DHT. It is similar to T that is bound up by SHBG: a store of unused T.

Maybe you are thinking of 5b-DHT? 5b-DHT is created from T by 5b-reductase. 5b-DHT is not androgenic and does not bind to AR. I doubt that your lab includes this in your DHT measurements, but if you want to know for sure, you can always just call them and ask. They will know.

I've seen 3a-diol used in some articles as an indirect measure of androgenicity in hirsute women, but I've never seen anyone try to say that even if your free T and DHT are normal, 3a-adiol levels can supercede this information and contrarily indicate a deficiency of 5ar function, nor have I seen anything that shows that 3a-adiol is selectively converted from DHT that was made only using the 5ar1 enzyme. If you have a link to an article on either of these subjects, I'd be interested to read about it, just in case I am missing something. Everything that I've read in the past indicates that 5AR activity is directly reflected in the ratio of free T to DHT, since again, the only way that conversion is possible is through 5ar.

I think the reason your doctor told you not to take an aromatase inhibitor by itself is because in normal people, taking it without any added T will result in very low E levels, and that causes problems. Whatever treatment you decide on, don't expect to see any improvement overnight. Testicular atrophy doesn't reverse itself that quickly.

I still think that if your E levels are too high, and you didn't artificially create that high E by supplementing with androgens, then you should try to find a way to tolerate an aromatase inhibitor, in small amounts. Have you tried letrozole? I don't have any firsthand experience with an AI, but maybe someone else on this forum can say what their experience has been like.

Also, keep in mind that the group you are in is small, and the mechanism by which Finasteride has caused these problems is not well understood, so the mechanism that is going wrong may not be where you expect. I wouldn't fixate on any one parameter like 5ar, especially if it is coming back normal. Instead, look at each step in the metabolic chain, and focus on irregularities. The biggest irregularity you have with adrogenicity is your high E. This is why I would fix that, and see how everything balances out afterward.

I would also take a look at the different steps in the cortisol synthesis chain. If you have low cortisol, it is useful to figure out where the block in the synthesis chain is: ACTH -> Pregnenolone -> 17OH-pregnenolone -> 17OH-progesterone -> 11-deoxycortisol -> cortisol. Also, check your progesterone values. If there is an enzymatic deficiency in this chain, you will see an abundance of prohormones leading up to that enzymatic step, and a deficiency of prohormones after it. People with 21-OH deficiency see this as a buildup of all prohormones up to and including 17-OH progesterone, and a deficiency of 11-deoxycortisol and cortisol. You want to check this out since a buildup of adrenal prohormones can cause headaches, mood instability, depression, etc.

 

[Structure]

After responding earlier this afternoon (see above), I looked up 3a-diol-G, just for the fuck of it. This is what I've found:

• A paper written in 1982 (3 alpha, 17 beta-androstanediol glucuronide in plasma. A marker of androgen action in idiopathic hirsutism.) laid the foundation for using 3a-diol-G to measure peripheral androgen action in hirsute women.
• The reason why these scientists were looking at it was because a group of bearded ladies was stumping everyone with their seemingly normal levels of androgens (i.e. women with "idiopathic" hirsutism). Although their free T was a bit high, and their DHT was even higher, it just didn't add up when you considered just how hairy these women were. Some of them even had normal free T and DHT.
• They first looked at 3a-diol (which is distinct from 3a-diol-G), and that wasn't particularly impressive.
• However, every last one of them had hugely increased levels of 3a-diol-G.

The conclusion was that this was the "end of the line" for that metabolic pathway. You could clear out all of the previous steps by just converting excess hormone to the next step in the chain. 3a-diol-G was the one that would actually show some build-up, and revealed that there was a lot of androgen pushing through that metabolic pathway to get these women hairy.

3a-diol-G is good for distinguishing people with elevated peripheral androgenic activity from those who do not have this elevated activity, given that both groups of people seem to have normal levels of free T and DHT. The converse of this is not true: low 3a-diol-G does not show an impairment of 5ar activity; the step that converts free T to DHT can be working just fine, but the body may not have such a need to convert much of the resultant DHT into 3a-diol.

The way to check for a deficiency in 5ar activity is just to look at the ratio of free T to DHT, much in the same way that to check for any other enzyme deficiency, you check the ratio of the hormones on either side of the conversion (e.g. for 21-OH deficiency, check the ratio of 17OH-progesterone to 11-deoxycortisol).

 

[PS LABS FOUNDER]

no,no. I don't think your problem is/has relate on finasteride/proscar. I assume u need clomid only,or tormifene.

clomid low dose 50mg's a day alone - try it it should help!!!!!!!!

 

[Shaolin]

After responding earlier this afternoon (see above), I looked up 3a-diol-G, just for the fuck of it. This is what I've found:

• A paper written in 1982 (3 alpha, 17 beta-androstanediol glucuronide in plasma. A marker of androgen action in idiopathic hirsutism.) laid the foundation for using 3a-diol-G to measure peripheral androgen action in hirsute women.
• The reason why these scientists were looking at it was because a group of bearded ladies was stumping everyone with their seemingly normal levels of androgens (i.e. women with "idiopathic" hirsutism). Although their free T was a bit high, and their DHT was even higher, it just didn't add up when you considered just how hairy these women were. Some of them even had normal free T and DHT.
• They first looked at 3a-diol (which is distinct from 3a-diol-G), and that wasn't particularly impressive.
• However, every last one of them had hugely increased levels of 3a-diol-G.

The conclusion was that this was the "end of the line" for that metabolic pathway. You could clear out all of the previous steps by just converting excess hormone to the next step in the chain. 3a-diol-G was the one that would actually show some build-up, and revealed that there was a lot of androgen pushing through that metabolic pathway to get these women hairy.

3a-diol-G is good for distinguishing people with elevated peripheral androgenic activity from those who do not have this elevated activity, given that both groups of people seem to have normal levels of free T and DHT. The converse of this is not true: low 3a-diol-G does not show an impairment of 5ar activity; the step that converts free T to DHT can be working just fine, but the body may not have such a need to convert much of the resultant DHT into 3a-diol.

The way to check for a deficiency in 5ar activity is just to look at the ratio of free T to DHT, much in the same way that to check for any other enzyme deficiency, you check the ratio of the hormones on either side of the conversion (e.g. for 21-OH deficiency, check the ratio of 17OH-progesterone to 11-deoxycortisol).

Man why are you wasting your time and mine??

5-ar II activity is read by androstenediol-glucuronide better known as 3-adiol-g. I ve done both pathobiochem and endocrinology in med school. Unless you think you have better knoweledge than my prof. George P. Chrousos - Wikipedia, the free encyclopedia
and you want to point that years of testing and screening is useless and i should look at the T/DHT ratio.

Or ask Thierry Hertoghe, who signed my medica diagnoses as hypogonadism, low 5-ar II activity and in the tests he ordered he never even bothered running DhT, just 3-adiol-g.

If them two are wrong then what the heck i have another five or six endo's who have ordered the same test before them in the past in 3 different countries. So around ten endocrinologists (some well known around the world) are ordering the same test, noone bothers looking at DhT values, and you are telling me that T/DhT is still the way to go??


Anyways, the point is that when 3-adiol-g increases i feel way better. The only thing is i cant increase it and hold it there because aromatase is super-active.

Apart from that im looking for 6-OXO as it seems that a suicide inhibitor might be the best choice for my condition. I wonder if i can use that as well, but at least it wont be so harsh on my system as nolva+arimidex.

 

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Instead of just telling me that I'm full of shit, why don't you just go read up on it yourself. Here's a link that talks about the metabolic pathways that clear out DHT: Steroid Analysis - Google Books. Check out pages 466, and 467 (esp. figs 6.3 and 6.4). You'll see that I'm not making this shit up. 3a-diol-G has plenty of uses, but a low value is ambiguous in regards to whether or not you have defective / deficient 5ar.

I'm not a doctor, but I'm not spewing bullshit to you. I'm suggesting that you look at every step in the chain to see where things are going wrong. It sounds like your doctors have not done this in the past, so it is definitely something you could do now.

Doctors aren't Gods, you know. I had to diagnose myself, and I went to plenty of endos (6 in total), including a few at the Mayo Clinic. They have other patients to see, and they don't always have the time to bother researching a zebra diagnosis, especially if your condition isn't what they consider to be serious. My diagnosis came after I did a few years of research, and forced one of my doctors to give me a genetic test. You don't have to be a doctor to research your own health problems and get some good out of it.

You've tried arimidex, but you haven't tried letrozole, and there are other aromatase inhibitors out there to try as well. Not all of them will feel the same way. And Nolva is notorious for making men feel like shit and killing libido (see: Tamoxifen adminstration is associated with a high rate of treatment-limiting symptoms in male breast cancer patients - Moredo Anelli - 2006 - Cancer - Wiley Online Library), so you probably want to try the aromatase inhibitor without a SERM, at least until you can find an aromatase inhibitor that you can tolerate.