Fucked by Finasteride / calling all expert steroid users

[Shaolin]

Im not telling you that you are full of shit, i m just saying that its well known for many many years that the activity of 5-ar II is measured through its metabolic by product quite accurately and this is done in several clinics and universities throughout the world. That's all. Nothing more nothing less.

When i started searching this cascade of finasteride side effects i visited my pediatric endocrinology prof that i linked above, Chrousos and he had his team of several endos around him and i told him ok look i took finasteride and i cant find what's going on. My testo is great, my dht is also quite high, all hormones are in place and i still dont get any libido. He then ordered this 3-adiol-g test and he told me i am hypogonadal and in due time this should correct. The guy sees patients with congenital resistance to androgens and he sais that this test is the most accurate there is at this point, along with some other urine metabolite ratio testing.

Two years later i get another measurement because my testicles are very sore and they regress and i see my 3-adiol-g level gone down 200% and estradiol levels doubles. So i go to another doctor in belgium and he measures this metabolite without even ordering dht. He told me in words DHT levels are USELESS because i kept asking why my DHT is so high and i have no hairloss but also no libido. The guy is supposed to be the director of the anti-aging docs worldwide and has an eight decades old endocrinology clinic. His great grandfather was one of the first docs to deal with hormones. So i guess that two people that has spent their lives dealing with issues like that and seen hundreds of finasteride patients might know more than us. I don't know what else to say.

Just, when my 5-ar activity increases this metabolite also increases. DHT level fluctuates from 50-80 pg/ml always on top of range but it doesnt correlate with my libido or my hairloss or how my testicles feel. I dont know where this dht comes from, probably it should from 5-ar I activity.

Who cares, end point is i need something to drop the estradiol smoothly and recover my hypothalamic-pituitary-gonadal system without side effects

 

[Structure]

If you end up trying letrozole, just make sure to take as little as possible --- that shit is really strong. I've heard it can completely suppress E in doses as small as .1 mg. Also keep in mind that it has a really long half life, so it takes as long as 60 days to reach steady state levels. I'd get some of that ,and shave off a small amount to take each day, and check my E levels closely.

Letrozole kills sex drive when all of your E is gone, so you want to check your E closely to avoid over suppression of E.

And I'd stay away from the permanent (type I, "suicide inhibitor") AIs for now. If you over did it, and permanently suppress your E, that would definitely not be good for your libido.

 

[Shaolin]

I just ingested half a pill of aromasin 25mg today because i couldnt handle the testicular inflammation no longer. I dont know about the letro, but i will give it a try later on. I also ordered inhibit-e(an ATD) whats your opinion about this?? for a more mild but definate (hopefully) estrogen suppression. I am trying to save my testicles at this point and see if really suppressing estrogen will do the trick.

Apart from that i am also thinking that progesterone plays a role in deactivating dht, because i see its level is also increased since its conversion is also catalyzed by 5-ar II.

I will have to find ways to suppress that too. Someone told me that b-6 is good for suppressing progesterone but i am not sure it won't affect dht as well. Who knows

Any info on progesterone suppression??? and any insight on atd's like inhibit-e??

 

[Reginald]

I just ingested half a pill of aromasin 25mg today because i couldnt handle the testicular inflammation no longer. I dont know about the letro, but i will give it a try later on. I also ordered inhibit-e(an ATD) whats your opinion about this?? for a more mild but definate (hopefully) estrogen suppression. I am trying to save my testicles at this point and see if really suppressing estrogen will do the trick.

Apart from that i am also thinking that progesterone plays a role in deactivating dht, because i see its level is also increased since its conversion is also catalyzed by 5-ar II.

I will have to find ways to suppress that too. Someone told me that b-6 is good for suppressing progesterone but i am not sure it won't affect dht as well. Who knows

Any info on progesterone suppression??? and any insight on atd's like inhibit-e??

excuse me if i entrude/(jump in)... always i wondered about progesterone. what it is? is it released at adrenal glands? what medicine should anybody use in order to spike and stimulate his own progesterone release at adrenal? thank u. oh,yes...also the same question about how to stimulate your own adrenaline(epinephrine) ,thanx again

 

[Structure]

Another idea for you: I don't think that testicular atrophy due to hypogonadism is supposed to be painful or associated with inflammation, be it steroid induced or otherwise. Hopefully someone can jump in here and say what their experience has been. From what I understand, the most common cause of testicular pain and inflammation is epididymitis. It's always possible that you have chronic, untreated epididymitis. You definitely want to see a urologist (not an endo) to get your nuts checked out, because that would be a quick fix if that was the problem. There are many causes of epididymitis: bacterial, viral, and "sterile" epididymitis. All three are painful.

Info on progesterone: progesterone is the second hormone in the adrenal steroidogenesis path (the first is pregnenolone, which itself is made from cholesterol). If you have elevated progesterone, it is likely due to an enzyme deficiency in the adrenal path (the most common is 21 hydroxylase deficiency). Regardless of which adrenal enzyme is deficient, they are all treated the same way: with catabolic steroids (i.e. prednisone or dexamethasone). If you find that your progesterone is too high, then you treat it with one of these drugs. Keep in mind, this is serious stuff. If you have an adrenal problem like this, it is really important that you get your steroids dosed correctly. I imagine you would want to take less than .5 mg of dexamethasone per day (about 3 mg of prednisone), but talk to an endo about this. Both too little or too much cortisol can cause serious health problems. You don't want to fuck around with this.

Progesterone also appears in the gonadal steroidogenesis path, but not as much in men as women.

I've heard of people inhibiting cortisol release to try to prevent catabolism, but I haven't looked into this very closely, and thus don't know what drugs are used to do it. I imagine it is pretty dangerous, as an addisonian crisis can result (i.e. electrolyte imbalance, ventricular fibrillation, and death). I've never looked into how people would stimulate progesterone production. (Reginald: Why would you want to?)

I have heard that ATD can block the androgen receptor from binding to androgen, so you may not want to go that route (see Effects of ATD on male sexual behavior and androge... [Horm Behav. 1989] - PubMed result).

 

[Shaolin]

Man its from finasteride this atrophy and its painful because it is inflammatory in nature. Too low intratesticular dht and too high of e2 and progesterone causes that. I also have sore nipples and very sensitive ones. Maybe i should try some thing to bring down progesterone too.

I dont know im too tired, maybe i just do my self out of this shit. Its been too long, 7 years and no solution. 3 years i lasted in bed thinking that one day i will have the strength to walk again properly, i couldnt stand and breath from the exhaustion, i couldn't concentrate, couldn't recognise objects at some point. And all due to this shit, one day before i took it i was so strong and active, played hours and hours of sports study medicine did so much per day now only hope is i die rapidly and suddenly. Maybe thats the best thing i can do for my self right now

 

[Fulano]

Man its from finasteride

You can't know that for sure. Check all of the other possibilities. What if it is an inflamatory or infectious contition of the testicles, like the other poster said?

You've had zero luck pursuing other options up until now. What do you have to lose from investigating some other possibility?

 

[Structure]

Fulano is right. I hope we have convinced you to see a urologist. In any case, good luck, and hang in there. Let me know how it goes.

 

[Shaolin]

Been to urologists a few dozen times too. Nothing that they find weird. Its all written in finasteride studies that it causes apoptosis of testicular tissue, shut's down all proteins needed for maintentance of testicles and surrounding glands. Its a f fucked up drug. I can go on and on telling you what i have tried till today to get better, its a 7 year continuous battle, i just can't accept that nothing in this world can fucking increase endogenous 5-ar activity

There has to be a way.

I am thinking if i take some anti-prolactin like dostinex and some anti-aromatase together, what the fuck would that do?? It should drive estrogen really down logically. But i have this stupid feeling that anti-aromatases also block t to dht conversion a bit too, i have seen this happen in my body and some others state its possible through some cross linking of residual drug substrate in similar receptors. I mean this game is so hard to play what the fuck

 

[Bill Roberts]

If it's "all written in finasteride studies" that it causes apoptosis in the testes and testicular atrophy lasting for years after discontinuation of brief use, or maybe even that it causes painful testes for years, is it too much to ask for you to be specific on where we can see this for ourselves?

 

[Shaolin]

Finasteride Studies • PROPECIAHELP: Unresolved Finasteride Propecia Proscar side effects info & discussion forum

you will find a lot of research there regarding this. Does it change anything with me or anyone else? I have normal LH levels yet testicles are suffering from atrophy and its not the kind you get from exogenous steroids.

Been to the university hospital today they made me do an utrasound to find out where this burning feeling was from on my testis and dick, everything is clean, as i told them it would be, i ve done my 4th ultrsaound this last 6month. It is so weird that noone believes that hormonal imbalances may cause testicular inflammation.

Anyways, why wouldn't someone believe this drug atrophies testicles/seminal vesicles prostate etc etc?? It's used to combat prostate cancer, bring down PSA and downregulate the AR. Offcourse this was not written on the drug leaflet that it is used for as a chemotherapeutic steroid. Nothing like that was written there.

 

[Shaolin]

By the way, Bill do you have any idea why this happens after stopping a drug like that?? Why do we get locked in this state of high e2, high progesterone, low conversion of T to dht ??

I am thinking lately about my sore nipples and wondering is it just the E2 or the progesterone that is increased too?? Maybe i should try some dostinex on top of an anti-aromatase. But still wondering if any of these will eventually lead T into DhT

 

[Bill Roberts]

I looked at the site and went through the threads that seemed (at first glance anyway) to be most promising for perhaps backing up the claim of causing apoptosis in the testes and perhaps even chronically shrunken testes for years after discontinuance or painful testes but didn't find it. That doesn't mean it may not be there, but I didn't see it. Can you provide a specific example?

I agree completely with regard to the effect *while* it is reducing DHT levels but as to ongoing effect for years afterwards I don't have any ideas as to how it could and I have not seen one shown to be true. That doesn't mean that it may not have been or that, even if not yet shown, there couldn't be some way.

In a way it may be that focusing on finasteride use 7 years ago may be distracting from the issues that are important or very important.

My preferred order of dealing with hormonal imbalance is first to address estrogen levels. It isn't always the case that brining E2 to low-normal will improve T but it very often is the case and very often is completely satisfactory in this. Additionally, though this doesn't prove that for an individual that his changing his E2 levels may change his outcomes, it's been shown recently that E2 levels are very strongly correlated with cardiovascular risk, with low-normal being the most favorable part of the range.

If I understand correctly your DHT levels are normal. I appreciate that you have evidence suggesting (but I think, just as it seems to me as there are alternate explanations not proving) low peripheral production of DHT.

For whatever reason either for any amount of androstanediol in the blood is not glucuronidated as much as is typical and instead is generally converted to androsterone before being glucuronidated; or there may not be as much conversion of DHT to androstanediol peripeherally regardless of there being normally-increased levels of DHT in those tissues; or lastly it might be the theory you are saying that maybe peripheral conversion to DHT is decreased. The test cannot establish which of these it is.

But correcting your symptoms makes sense as being the main concern.

As mentioned I'd get estradiol low-normal; I prefer letrozole with blood testing to establish correct dosing; unfortunately on the testicles problem if a urologist does not know I'm in much less position to know but it does not make sense to me that low testicular DHT is to blame; HCG could be an interesting experiment at say 500 IU 3x/week; but really I have no idea on the pain and doubt that atrophy is the cause of the pain.

There are times when a person has to see an unreasonably large number of doctors before finding one who immediately or quickly knows exactly what it is and one is then left wondering how on earth the others never figured it out. Hopefully that will be the case for you before too many doctors. Of all your issues, the pain one is what strikes me as the most serious.

Did you have progesterone levels tested? (I missed it if so.) As with his comments generally, Structure has given good advice. I don't have any experience in dealing with elevated progesterone levels, if that is the case, and would definitely seek an endocrinologist if there is a problem there.

 

[Shaolin]

Well progesterone levels are a bit high too, and i think they work in combination with high e2 levels to do this to me.

The research about apoptosis of testicles/seminal vesicles etc etc is there i ve read it a dozen times just don't remember the exact title, i will ask the administrator to provide again. Its logical because dht singals production of several proteins needed for testicular integrity, i remember i checked every single one of them in the net to see what the fuck they do and i was surprised.

The big question is why, when i take an anti-estrogen i feel like my situation is worse ?? Is it maybe that it brings down 5-ar II slightly as well as bringing down aromatase?? Some times the whole HPG works very strange and i ve read anecdotal evidence that anti-estrogens may have some residual or cross linking anti-dht activity too. Well that could be a case but offcourse another would be that once e2 levels are brought down fairly enough this potential cross linking bond between 5-ar II and aromatase could be broken and 5-ar II activity will stabilize or even increase. We are talking about a drug that has reseted our homeostasis and possibly mRNA synthesis of this specific receptor who knows how the fuck our body recognises its function nowdays.

Yet, when i take transdermal liposomal testo i feel my balls relax and not inflammed any more, but i can't take this now, i want to leave it as my last resort (plus i cannot tolerate it properly because of wasted adrenals after finasteride, and those testo megadoses needed to channel into dht are hard on my HPA system)

The other deal would be to take lower transdermal T and HcG shots as you say so that there is a balanced exogenous input and endogenous output of T plus use an anti-aromatase. I am also saving this for last action.

My main goal now is to find something that will definately bring down e2 levels and at the same time boost T to such an extend that there will be a great channeling via this downregulated enzyme into dht. Once this happens i think recover or at least resetting the system to a new point is achievable.

 

[Shaolin]

Why does the pain by the way strike you as the most important finding??
the pain is inflammatory in nature and it is directly linked to high e2/low dht. This is typical for finasteride users, the ones that have sides report this sort of pain and also report shrinking of the testicles and change in their shape irrespective of lh levels. Its just that for some once they quit their system rebalances somewhat and this pain goes away. For others it is on and off or continuous as is the atrophy (plus its not atrophy its testicular apoptosis/tissue death). If it was atrophy i would suspect some returning back of the size. My hope is that it is not solely primary damage to the testicles but in the end i don't think i will be able to escape this

The only thing that i guess could be slightly soothing and worth discussing is how come when one's testicles on AAS shut down they manage to get back. I would expect that the low to zero LH FSH signaling is similar to very very little dht being present in the testicles as well. These people don't have pain do they?? Or is it because their estrogen levels are also very low after AAS and concomitant anti-e use??

 

[Shaolin]

Estrogen too high - Help me! • PROPECIAHELP: Unresolved Finasteride Propecia Proscar side effects info & discussion forum

same findings - same estradiol levels same problems for this post-fin user (testicular pains and atrophy)

and look at this

https://thinksteroids.com/community/threads/134296089

AAS users that had testicular pain and jumped on TRT to get better. They also feel its from high e2

I just hope that this toxic estradiol damaged my testicles only to be reversed some time to their original size or at least to a better than this one. Is this however possible???

 

[Shaolin]

Ok i cannot take arimidex to bring down e2. I want to try some other drug again though. I also have aromasin. What would be a good dosage of aromasin?? I dont want to take it every day though is it possible??

Also what about letro?? Is that any good?? the say it helps with progesterone as well and gyno

 

[Bill Roberts]

Aromasin could be used but I don't see a reason to prefer it to Arimidex or letrozole.

Did your adverse response to letrozole occur while estrogen levels were measured to be as desired and not below the normal range? Generally speaking complaints about Arimidex, or any AI, are in fact caused not by a side effect of the drug but by a dosage resulting in excessive therapeutic effect, namely excessive reduction of estradiol. The answer is less drug rather than to switch aromatase inhibitors.

No, testicular atrophy from long periods of low LH or even both low LH and low DHT -- which can happen for example with Deca plus Dianabol -- is a thing that has occurred very very many times with steroid users and does not result in pain.

Something different is going on in your case than simply atrophy from long-ago 5AR inhibition. I am very sorry to say that I have no evidence as to what it could be. If the cause is finasteride, I would place a bet on a toxicity that is not from the 5AR inhibition but which is an independent side effect. Not because I have evidence to show the toxicity, but because so far as I know no mechanism has been proposed by which short-term 5AR inhibition could cause your long term problems.

The inhibition is simply a matter of occupying the receptor site on the enzyme a large percentage of the time while the drug is in the system. No damage is done to the enzyme, and besides this the enzyme is entirely replaced with new enzyme after no great period of time in any case. And having low DHT for a period of time such as yours is not shown to cause problems such as yours. For example, I have spent a very considerable amount of time with practically no DHT at all, due to trenbolone/Dianabol cycles and so have very many others. Testicular pain is not a risk from it.

In terms of things that could be positive -- the above is, much as I wish it were not, somewhat bleak sounding -- things may be better with lower estrogen, and there could be a reasonable chance that the testes would do better with more LH resulting from lower but still normal estradiol, or from effect of HCG. But also possibly not. I cannot explain the pain issue. Inflammation may well be the case, but the cause would almost certainly seem a current abnormality, not a lasting echo (other than a lasting abnormalilty that was caused) from one month of drug use 7 years ago. So what is needed is a doctor who has an answer. I truly hope there is one and your search for him is short and quick.

 

[liftermo]

Hey, its all in your mind brotha

i am sure you got a psychological thing goin on dude. Just look at some porn or something. he he

 

[Shaolin]

Bill I have found at least twenty reports regarding pain and atrophy from fin use. If its not dht as you say, which i also think its not solely due to dht, but due to the overwhelming action of aromatase and estradiol on my testicles and inability of dht to counteract that.

Why on earth would my nipples sore as well and be so sensitive?? Something is triggering this painfull effect on these tissues and gonads. Moreover i reckon that high levels of estrogen upregulate immune reponses and this can manifest as autoimmunity when there is no counteracting action.
The inflammation is very easy to discern i just grab my balls and they are so hot. The doctors in Belgium noticed it from start. They said we need to bring down your inflammation. They prescribed testosterone megadoses and arimidex.

Yesterday i started using aromasin after doc told me to switch see if i can tolerate. He also told me not to take an AI without Testo again. I dont understand the reason. I feel that if i can bring E2 down i should at least show some improvement. I don't want to be on Testo for long run because my levels seem to be ok. I just want this atrophy to stpo.

Anyways today Merck gave me a call asking too many questions.


Bill when u used those AAS and had zero dht as you say, how much estrogen did you have at the time?? Or you used an AI as well. And how do those AAS bring down dht so much?? Did they increase progesterone too?? How did you get better, what sort of pct did you do??