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Anyone here have optimal (>5-700 ng/dl) test levels after multiple steroid cycles?

Anyone here have optimal (>5-700 ng/dl) test levels after multiple steroid cycles?

I have not tried using a serm on cycle or seen anyone who has but if you do I recommend NOT running the same serm in PCT

Why is that? Should you not use the same AI in pct as used on cycle ?
 
Why is that?
Desensitization!! After so long the hypothalamus gets desensitized!! That's why frankly I recommend not taking a serm on cycle. Desensitization is not a good think in the hypothalamus and it happens just use some good ol google search on clomid and you'll see the same evidence.

I now people have been flamed in the past for recommending use tbooster on cycle but I don't think it's pointless​ at all. There are good legit supplements that mimic or increase LH and FSH. Tbh I actually think this is a better time then ever. Is is going to prevent shut down? Hell to the no. Might it make recovery easier? I truly believe it will.
 
Desensitization!! After so long the hypothalamus gets desensitized!! That's why frankly I recommend not taking a serm on cycle. Desensitization is not a good think in the hypothalamus and it happens just use some good ol google search on clomid and you'll see the same evidence..

After 19 months, Clomid still effective -- BJU Int. 2012 Aug;110(4):573-8.

Clomid still effective after 3 years -- BJU Int. 2012 Nov;110(10):1524-8.

Try again?
 
Desensitization!! After so long the hypothalamus gets desensitized!! That's why frankly I recommend not taking a serm on cycle. Desensitization is not a good think in the hypothalamus and it happens just use some good ol google search on clomid and you'll see the same evidence.

I now people have been flamed in the past for recommending use tbooster on cycle but I don't think it's pointless​ at all. There are good legit supplements that mimic or increase LH and FSH. Tbh I actually think this is a better time then ever. Is is going to prevent shut down? Hell to the no. Might it make recovery easier? I truly believe it will.

And I have to ask...

Do you really think you have any sort of understanding of pharmacology or physiology? I have yet to see you explain even the most rudimentary physiologic process.

Desensitization? The hypothalamus gets desensitized? How? Where? The entire thing? Which receptors? Through what mechanism(s)? What are the downstream effects?
 
^^^ugh you are a tool!! yes it's the fuking recoptors, not the whole thing. you knew god damn well what I meant. I have no desire to continue this charade with you.

Go and provide half ass studies, that prove nothing, as they are missing fuk ton of information; that would get ripped apart in any medical environment if it wasn't a anti-steriod study. try running hiv, cancer, etc study with as little information provided in those studies. where the participants don't even receive any treatment and say well I guess this cancer is permanent.

People here aren't retarded and what I'm talking about is easily found on Google soooooo I'm out
 
^^^ugh you are a tool!! yes it's the fuking recoptors, not the whole thing. you knew god damn well what I meant. I have no desire to continue this charade with you.

Which receptors, specifically?

People here aren't retarded and what I'm talking about is easily found on Google soooooo I'm out

I wasn't trying to be insulting -- I merely asked a pointed question, because that's what we do in academia and research. If you can't handle this method of inquiry, then don't discuss these topics. I'm allowed to call you out when you offer explanations that are utterly lacking in substance. If this offends you, well, this is your ego's problem, not mine.
 
Which receptors, specifically?



I wasn't trying to be insulting -- I merely asked a pointed question, because that's what we do in academia and research. If you can't handle this method of inquiry, then don't discuss these topics. I'm allowed to call you out when you offer explanations that are utterly lacking in substance. If this offends you, well, this is your ego's problem, not mine.
You see there is a difference between an academic debate and douche baggery! You attempted to do the first but ended up being the second!! If you can't see that review your post look at your wording and I don't have the desire to debate (not using this negatively debates can be positive) with a douchebag so I am out..

Unsubscribed
 
You see there is a difference between an academic debate and douche baggery! You attempted to do the first but ended up being the second!! If you can't see that review your post look at your wording and I don't have the desire to debate (not using this negatively debates can be positive) with a douchebag so I am out..

Unsubscribed

I was a bit condescending in my initial question. I apologize.
 
subbed.
 
Why is that? Should you not use the same AI in pct as used on cycle ?
I've never seen this. Curious to his source for that info
 
If receptors got desensitized then we'd all be screwed as the body is always using hormones.
This specific topic is discussed by Patrick Arnold who explains it better than I.
Ultimately it is other factors that causes the use of exogenous hormones to become less effective thereby requiring the use of more.
But it isn't because of receptors getting desensitized to the binding of (insert hormone)
Better terminology might be building up a tolerance. Not receptor desensitization
 
I was a bit condescending in my initial question. I apologize.
If you had joined two years ago you would of been met with the same condescending tone, and had a good discussion. But the snowflakes have come of age, and cannot handle confrontation even if for intelligent discussion. I've had to learn to change how I respond in the last couple years to post. I've been a member here since 08. This'll be my 3rd username.
 
I've never seen this. Curious to his source for that info

If receptors got desensitized then we'd all be screwed as the body is always using hormones.
This specific topic is discussed by Patrick Arnold who explains it better than I.
Ultimately it is other factors that causes the use of exogenous hormones to become less effective thereby requiring the use of more.
But it isn't because of receptors getting desensitized to the binding of (insert hormone)
Better terminology might be building up a tolerance. Not receptor desensitization
Wasn't talking ais or hormones here Im talking serms. Desensitization also may not have been that best choice of words here but the point is still valid. Will happen during an 8 week cycle through pct??? We don't know the length of time here is not really the issue. Things like clomid have been ran for longer safely. Though this is untested Waters we have no idea how the body will react, there is just to many variables to account for. It's why i think if you are gonna use a serm on cycle, I think you should use a different serm pct. Why risk the serm loosing efficiency of up regulating GNRH production.
 
What's the harm in giving it a try? Bodybuilders will eat all sorts of drugs that have never been tested in humans, but you tell them to try something that is basically harmless, but that happens to go against conventional "bro science" even though the pharmacologic basis is solid, and they completely flip out and tell you that you're totally wrong.

I know that Torem (and Nolva, and Clomid) works on cycle to maintain HPG-axis functionality and any or all of you are welcome to find out the way I did -- through experimentation. I'm done playing "dad"



Nope, but everything that a study demonstrated as true, was already true before the study existed. Studies are nice, but in the absence, sometimes you just have to look at the underlying physiology and pharmacology and do your own N=1 study.

No I should have been more clear. I have a ton of studies however this was circa 2000-02 when the discussion was more prevalent. At this point I do not know where the hard drive is that I had all of my studies on (former chem major). I pulled up an old post of mine from here on toremifene. So its nothing to do with my belief. It has more to do with sharing knowledge to those less fortunate to have access to people with years of experience in the field I.e. patrick and william.
I thought you may have had mores full studies. This is why I asked.
 
I thought you may have had mores full studies. This is why I asked.

I have but a few studies using a SERM to prevent HPG-axis shutdown during exogenous androgen administration. None of these studies used toremifene, so even if I post them, people will complain loudly about that fact.

That SERMs prevent HPG-axis shutdown on cycle shouldn't surprise anyone who understands their pharmacology: SERMs are not hypothalmic ER-alpha antagonists. An antagonist merely blocks the receptor from binding the active ligand. They are inverse agonists -- they bind to the receptor and then produce the opposite effect of an agonist, in this case, estradiol. So, it matters not if circulating androgens are high, since SERMs aren't merely blocking the effects of E2 on ER-alpha, they are initiating the downstream actions that are the exact opposite as what happens when E2 binds to ER-alpha.

Is this all starting to make more sense now, to everyone?
 
So by "modulating" estrogen, do SERMS cause a downregulation of E2?

Explain what you mean by "downregulation."

Do you mean a reduction in ER-alpha receptor density? (probably not) An overall decrease in downstream estrogen signalling in ER-a pathways? (absolutely) A reduction (ER-a) or increase (ER-b) in E2 mediated transcription at certain tissue sites? (absolutely) An overall reduction in the levels of circulating E2? (possibly, due to effects on SHBG)

The thing you have to remember when you run a SERM, is that you're essentially granting that chemical permission to manage your HPG/HPA-axes, and all associated downstream effects. For tamoxifen, this means potential liver problems, reduced IGF-1, elevated prolactin levels and an increased cancer risk. For clomiphene, this means potential cholestasis, sharply elevated SHBG and potential occular toxicity. For toremifene, this means... A reduction in prostate cancer risk and a risk of cardiac arrest if you have a pre-existing cardiac arrhythmia. This is why I like toremifene so much -- it's basically the perfect SERM for regulating the hypothalamus. It's not quite as potent as tamoxifen or clomiphene, but it doesn't need to be. The potency of those drugs are what causes problems with them.

If I were a physician, I would be prescribing toremifene to all of my secondary hypogonadal patients in lieu of TRT. With a small dose of a DHT-derived compound for a little extra "push", toremifene is simply amazing as a "standalone" TRT for secondary. I maintain total T levels around 850-950, my lipids are perfect, my ACTH and salivary cortisol are now in range (I suffered from "adrenal fatigue" for years), my liver values are perfect, my libido is great, my skin looks better than it ever has (thank you ER-b agonism), and when I cycle I don't have to worry about shutdown, acne, AIs, or any other nonsense. At 40, I can honestly say I look and feel better than I did when I was 30.
 
Haven't read through every post, but the main reason everyone thinks they've "fully recovered" post cycle is due to when everyone does blood work.

Most individuals get bloods within a few weeks of ending PCT when realistically the test stimulating hormones are still active.

Then people tend to jump into their next cycle within a couple months without re-testing.

It's not until you stay off gear, serms, test-boosters etc... that you realize your junk is messed.

Most people aren't willing to go off everything hormonal for 6-months to even test the theory.
 
So this stuff has been around for a long time and somehow no one made the connection that no ones test levels return to normal? I find that very hard to believe. I don't know **** about PH but this looks like next level bro-science being developed before my eyes. That's not to say people here aren't very knowledgeable but it looks like some a few people saying that the risk might be higher than what people lead to believe and other people are chiming in like "yea bro you do PH and you'll never return to normal levels again".
 
Who knows any ex AAS users who have established a baseline average through periodic blood tests to compare post cycle levels after long term cessation of use? I personally have not met one user. At best I know a few guys who have had bloods prior to their first cycle.
 
Interesting. What`s your Toremifene dosage/ range of dosage?
By DHT compound you mean Proviron/ Andractim / Anavar ?
 
I prefer raloxifene as my serm in pct. off topic.
 
Anyone here have optimal (>5-700 ng/dl) test levels after multiple steroid cy...

So this stuff has been around for a long time and somehow no one made the connection that no ones test levels return to normal? I find that very hard to believe. I don't know **** about PH but this looks like next level bro-science being developed before my eyes. That's not to say people here aren't very knowledgeable but it looks like some a few people saying that the risk might be higher than what people lead to believe and other people are chiming in like "yea bro you do PH and you'll never return to normal levels again".

My understanding was we were talking about more moderate/long term use, not a one time thing.

And returning normal range and a persons actual "normal" are two different things. I agree with you though that it's not a blanket statement... and everyone is different, along with there use.
 
Anyone here have optimal (>5-700 ng/dl) test levels after multiple steroid cycles?

My understanding was we were talking about more long term use, not a one time thing.

And returning normal range and a persons actual "normal" are two different things. I agree with you though that it's not a blanket statement... and everyone is different, along with there use.

Data shows a different story, which is what this thread is about. The bottom line is that a single steroid cycle can (and most likely will) cause testosterone levels to be permanently lower than baseline levels after the typical PCT protocol.

As OP and Spurfy have pointed out, the extent of damage is related to the type of AAS used, with compounds in the 19nor family being the most volatile on the HPTA. Cycle length is also a factor
 
Data shows a different story, which is what this thread is about. The bottom line is that a single steroid cycle can (and most likely will) cause testosterone levels to be permanently lower than baseline levels after the typical PCT protocol.

As OP and Spurfy have pointed out, the extent of damage is related to the type of AAS used, with compounds in the 19nor family being the most volatile on the HPTA.

I haven't read the studies but would agree from personal experience and experience a friends.
 
It seems most ex AAS users end up on TRT
Yes but so much missing info. Also when were the studies conducted? Look how old the participants were. Also look at when the last cycle was. Based on all that info we can definitely make an assumption (may be false) that these guys are cycle with improper pct or didn't even have pct. Heck people used 6oxo for pct only no serm, then trib based product for pct again no serm. That's for the area that actually used pct for the most part people weren't using serm pct. In the 70s and 80s used cycled on then just came off it happened a ton. As I said those studies tell us almost nothing. We have zero clue what the long term impact of a proper cycle and pct will be.
 
Data shows a different story, which is what this thread is about. The bottom line is that a single steroid cycle can (and most likely will) cause testosterone levels to be permanently lower than baseline levels after the typical PCT protocol. well saying most don't know their baseline we can't make this conclusion. Also as mentioned before that data we have is so incomplete that we don't know how it would be we using proper pct

As OP and Spurfy have pointed out, the extent of damage is related to the type of AAS used, with compounds in the 19nor family being the most volatile on the HPTA. Cycle length is also a factor totally agree with everything here for sure
Read bold also love you brother :)
 
Data shows a different story, which is what this thread is about. The bottom line is that a single steroid cycle can (and most likely will) cause testosterone levels to be permanently lower than baseline levels after the typical PCT protocol.

As OP and Spurfy have pointed out, the extent of damage is related to the type of AAS used, with compounds in the 19nor family being the most volatile on the HPTA. Cycle length is also a factor

I am willing to accept "a single steroid cycle can cause testosterone levels to be permanently lower" but I cann't accept "and most likely will" because suddenly it becomes a blanket statement. I think Movin_weight's response was pretty spot on.

How old is the user? What PH did they take, what dosage, and how long was the cycle? I don't know what the least "damaging" PH is but a 4 week cycle of that at a low dosage for a 40 year old male cannot be lumped in the same category as a 19 year old that takes the harshest PH for max duration with poor support and PCT. They just can't be lumped together.

What we need is a test of subjects in a certain age group, using a specific dosage of a specific PH and witness that the test levels never return to the expected range of test for their age, activity, diet, sleep etc etc. We'd have to witness that none of them returned to expected levels. Once we have someone that DOES return to expected levels it no longer is an absolute blanket statement. There are factors that prevent a person from returning to normal levels and there are factors that allow someone to return to normal levels.

Don't get me wrong, I'm not saying that a single cycle of a PH, any PH, cannot permanently impact test levels. I don't know enough to say anything on that subject, but once you start throwing blanket statements across such a huge spectrum of scenarios (age, PH, duration, dosage) then you HAVE to throw out the whole argument.

Personally, I agree it sounds like there is a lot more risk of permanent test levels being impacted than the general consensus BUT there are people that also report their test levels return to their baseline after a cycle (some say multiple cycles) so we cannot just say "run a cycle and your test is permanently suppressed".
 
I would love to post his full blood work but he hasn't given me the okay yet soo ill just a picture of a text he sent me. Note that me and him work as pharmacist technician together (I don't any more he still does) and there is a bi-yearly bloodwork that's required due to medication we make. I'll still try to get him to let me post his bloodwork. Last thing before I post the text I will say his cycles.

Age 19 epistane 30/30/40/40/60(yes he dumb as fuk for cycling early and I called him on it and he agrees now) and was even dumber and only used recycle and dpol as pct.

Age 21 test 12weeks with dbol kicker 500mg test 40dbol for 4weeks pct 8weeks pct of 25mg clomid and first 4 weeks 20nolva

Age 23(last year) 8 weeks test 500mg and 80 mg var (he gained so much on this) pct 8weeks 25mg clomid with TEST1FY pro I gave him

Year later texted me this and I have the bloodwork now but not approval to the bloodwork YET

Invalid Link Removed



note the text happened well before this thread happened, I only blurred name and number, and changed nothing!
 
Well then, case closed!
Not saying cases closed. Far from it. Matter of fact I'm more on your side that damage does occur. However, we cannot make such conclusion based of the information we have!!!! All the data is lacking way to much info.
 
I am wanting to sort of re do PCT, I was at 516 test at 21 but mid high free test. I hadn't cycled in a year and I have been breaking out badly on my back ever since. It was a 15 week cycle of test with tren ace for 4 weeks. A solid PCT of Clomid and Nolva for 5-6 weeks and I used Aromasin at a low dose. My back acne cleared up that next summer but has been back in full force since the summer ended.

I hate Clomid, it gives me horrible headaches.
 
I am wanting to sort of re do PCT, I was at 516 test at 21 but mid high free test. I hadn't cycled in a year and I have been breaking out badly on my back ever since. It was a 15 week cycle of test with tren ace for 4 weeks. A solid PCT of Clomid and Nolva for 5-6 weeks and I used Aromasin at a low dose. My back acne cleared up that next summer but has been back in full force since the summer ended.

I hate Clomid, it gives me horrible headaches.
Try torem
 
I have but a few studies using a SERM to prevent HPG-axis shutdown during exogenous androgen administration. None of these studies used toremifene, so even if I post them, people will complain loudly about that fact.

That SERMs prevent HPG-axis shutdown on cycle shouldn't surprise anyone who understands their pharmacology: SERMs are not hypothalmic ER-alpha antagonists. An antagonist merely blocks the receptor from binding the active ligand. They are inverse agonists -- they bind to the receptor and then produce the opposite effect of an agonist, in this case, estradiol. So, it matters not if circulating androgens are high, since SERMs aren't merely blocking the effects of E2 on ER-alpha, they are initiating the downstream actions that are the exact opposite as what happens when E2 binds to ER-alpha.

Is this all starting to make more sense now, to everyone?

Yes and no. And the reason being is exactly what I was referring to. We have already discussed exactly what you just talked about. This subject was discussed over and over yet there were literally 15 or 20 people whom posted bloodwork showing it did not help to mitigate disruption. HOWEVER there were another 10 or so that posted bloodwork showing it did help (this was over a course of several years across multiple sites). Thats the main reason why I asked about any other studies because I figured there was something new that I had yet to read since I no longer held a serious interest in the matter. I thought maybe something new was out there.
 
It comes down to whether or not you are willing to except the risks, which is quite substantial as current data indicates, of having permanently lowered testosterone levels.

I'd venture to say that OP is like many people who join steroid forums and subscribe to the belief that running cycles with the proper ancillaries and pct protocols in place will mitigate most sides and result in a full recovery, but experience the opposite when all was said and done.

Let's not lie to ourselves. Steroid use is not healthy. Period. Accept that and understand that you are making a decision with life altering consequences when you use anabolics.

If you accept that then cycle; if not cycling may not be for you. Don't be in denial though
 
What would people rank as the most likely to permanently suppress natural test production and what would be the least likely? Where does Halodrol fall into place?
 
I would love to post his full blood work but he hasn't given me the okay yet soo ill just a picture of a text he sent me. Note that me and him work as pharmacist technician together (I don't any more he still does) and there is a bi-yearly bloodwork that's required due to medication we make. I'll still try to get him to let me post his bloodwork. Last thing before I post the text I will say his cycles.

Age 19 epistane 30/30/40/40/60(yes he dumb as fuk for cycling early and I called him on it and he agrees now) and was even dumber and only used recycle and dpol as pct.

Age 21 test 12weeks with dbol kicker 500mg test 40dbol for 4weeks pct 8weeks pct of 25mg clomid and first 4 weeks 20nolva

Age 23(last year) 8 weeks test 500mg and 80 mg var (he gained so much on this) pct 8weeks 25mg clomid with TEST1FY pro I gave him

Year later texted me this and I have the bloodwork now but not approval to the bloodwork YET

Invalid Link Removed



note the text happened well before this thread happened, I only blurred name and number, and changed nothing!

Curious if he was off everything hormonal for a long period of time, serms test boosters etc...

If so good for him! I remember after running a 4 week cycle of trenedrol and pct with toremifene I was at like 400.... levels dropped from there bc I started losing strength and adding fat over the next few months.

19-nor like posted before is a different animal.... test and dht based hormones not nearly as much effect on HPTA
 
Curious if he was off everything hormonal for a long period of time, serms test boosters etc...

If so good for him! I remember after running a 4 week cycle of trenedrol and pct with toremifene I was at like 400.... levels dropped from there bc I started losing strength and adding fat over the next few months.

19-nor like posted before is a different animal.... test and dht based hormones not nearly as much effect on HPTA
Yes off of everything
 
Who knows any ex AAS users who have established a baseline average through periodic blood tests to compare post cycle levels after long term cessation of use? I personally have not met one user. At best I know a few guys who have had bloods prior to their first cycle.
The only ones are famous millionaires that I have only met for like 10 seconds for a handshake and photo op. And, that isn't going to tell me much of shiiiit!
 
Data shows a different story, which is what this thread is about. The bottom line is that a single steroid cycle can (and most likely will) cause testosterone levels to be permanently lower than baseline levels after the typical PCT protocol.

As OP and Spurfy have pointed out, the extent of damage is related to the type of AAS used, with compounds in the 19nor family being the most volatile on the HPTA. Cycle length is also a factor
You are very correct; however, you know what is so sad about all of this. SOME UGLs have created many Ph's unequal meaning created something that wasn't exactly what it has been claimed to be. I would be willing to bet that many of us have taken something within the past 10-20 years and thought we were using x when in reality it had a bit of a, b, c and z in there.
 
Yes off of everything

That's awesome, he must have been very responsible and did everything right.

Unfortunately most people push the envelope with dosage, cycle length, time off, pct etc....which may be the main contributor to the literature posted.

Research doesn't prove anything... only supports a theory. I feel you simply have to analyze the credible data available and make your own educated decision. There are always other influencing factors even in published research.
 
I am willing to accept "a single steroid cycle can cause testosterone levels to be permanently lower" but I cann't accept "and most likely will" because suddenly it becomes a blanket statement. I think Movin_weight's response was pretty spot on.

How old is the user? What PH did they take, what dosage, and how long was the cycle? I don't know what the least "damaging" PH is but a 4 week cycle of that at a low dosage for a 40 year old male cannot be lumped in the same category as a 19 year old that takes the harshest PH for max duration with poor support and PCT. They just can't be lumped together.

What we need is a test of subjects in a certain age group, using a specific dosage of a specific PH and witness that the test levels never return to the expected range of test for their age, activity, diet, sleep etc etc. We'd have to witness that none of them returned to expected levels. Once we have someone that DOES return to expected levels it no longer is an absolute blanket statement. There are factors that prevent a person from returning to normal levels and there are factors that allow someone to return to normal levels.

Don't get me wrong, I'm not saying that a single cycle of a PH, any PH, cannot permanently impact test levels. I don't know enough to say anything on that subject, but once you start throwing blanket statements across such a huge spectrum of scenarios (age, PH, duration, dosage) then you HAVE to throw out the whole argument.

Personally, I agree it sounds like there is a lot more risk of permanent test levels being impacted than the general consensus BUT there are people that also report their test levels return to their baseline after a cycle (some say multiple cycles) so we cannot just say "run a cycle and your test is permanently suppressed".

In theory this would be a 100% perfect approach but in actual life there are way to many factors to track each person over the course of say 1-2 years. And, as you said, there are many more factors to why someone's testosterone level may differ at various times. Oh how I wish that type of study could actually be visible.
 
I would love to post his full blood work but he hasn't given me the okay yet soo ill just a picture of a text he sent me. Note that me and him work as pharmacist technician together (I don't any more he still does) and there is a bi-yearly bloodwork that's required due to medication we make. I'll still try to get him to let me post his bloodwork. Last thing before I post the text I will say his cycles.

Age 19 epistane 30/30/40/40/60(yes he dumb as fuk for cycling early and I called him on it and he agrees now) and was even dumber and only used recycle and dpol as pct.

Age 21 test 12weeks with dbol kicker 500mg test 40dbol for 4weeks pct 8weeks pct of 25mg clomid and first 4 weeks 20nolva

Age 23(last year) 8 weeks test 500mg and 80 mg var (he gained so much on this) pct 8weeks 25mg clomid with TEST1FY pro I gave him

Year later texted me this and I have the bloodwork now but not approval to the bloodwork YET

Invalid Link Removed



note the text happened well before this thread happened, I only blurred name and number, and changed nothing!

He did 8 weeks of clomid @ 25mg per day and test1fy? This was all that he did? Can you ask him what his free test was?
 
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