Lets discuss our views on PCT....

[bigrobbie]

About once a year I post a PCT thread covering the basics and watch the claws come out! There are so many different opinions that I understand no one will ever agree. We have the master of Post Cycle Therapy with us here at Meso so I'm not trying to be Meso's authority on PCT by posting this. I just wanted to post a thread outlining a pretty basic PCT and the basics behind why we need this therapy.

Some PCT points of view:

So we agree that, as I mentioned, one of the most debated yet essential process' we as Iron Athletes must endure is the conclusion of a cycle! Saying that, it's no surprise then that we dread post cycle steroid recovery (PCT) not only because of the emotional ride it sends many of us on, but also because...quite simply...our cycle is over.

PCT is often, I'm sad to say, almost an after thought to some newer AAS users. This is who I really wrote this for...the newbie!

I see more and more PCT forums with a few stickies and a question or two on start times or doses. PCT is not a formality unless you have a desire to live out your days on PDE-5 inhibitors and balls like BB's in a rubber thimble!

I worry, I'm guilty too, that time on=time off + a few weeks is becoming a lost method. Guys, cruising won't do you any good and staying on, well...seen Rick Flair topless since 84? Just sayin! To stay healthy you should run shorter (8-12 week) cycles at reasonable doses, running a solid PCT and time off exceeding time on when PCT is complete.

Why do we use gear? Why is it good? How can it harm? The good: treatment of andropause, TA, prevention of muscle wasting in AIDs victims, recovery from burns and injurys. The rec user and athlete gain an increase in lean muscle mass, drop in body fat, and a sense of well being.
The bad: higher LDL, lowered HDL, hypertension, possible enlargement of prostrate and yes...addiction! I did say addiction so flame if you must, I stand by it. The most discussed bad side of AAS is shutdown which brings us to the topic at hand.

PCT's importance:

Gonadatropin releasing hormone (GnRH)is pulsated, which is a fancy way to say, released from the hypothalamus to maintain healthy sexual function between the axis'by the release of (LH) and (FSH). These two hormones work with leydig cells and a healthy hpta is the result due to mens testes actually working to produce sperm and testosterone. When an exogenous hormone such as testosterone is administered on a moderate scale, or dose, hypogonadism from lowered test levels occur (I can't find a mg to shutdown ratio or dose) resulting in a drop in serum production and male estrogen dominance. When the exogenous test administration is moderate the problem can be remedied by dropping the estrogen levels. I do believe, however the longer the cycle and higher the dose recovery can be much more complex than 4 weeks of a SERM.
I've flip-flopped ove the past 2 years on the question "Is shutdown is shutdown end of story?" or "Is shutdown more extreme depending on the cycle and gear you use?" I'm a believer in the ladder these days where I used to think the former (as I said I flip flop). Saying that to say that I feel cycle choice determines the effort you will have to use to fully recover.

PCT method:

I like a 4 compound "proactive" PCT. Since HCG mimics LH I use that on cycle at 250iu twice weekly begining week 3 of the cycle, this is my first step. I now have 3 compounds left to use for PCT only (with exception of estrogen control during cycle).

My preference upon starting PCT is to use 2 SERMs and an AI. I'm older so I still use Clomid, Nolvadex and usually adex (letro sometimes). No 300mg Clomid frontloads for me though. I use Clomid weeks 1-3 of PCT at 50mg/ml. Clomid is a weak estrogen so its only purpose is to block binding and trigger LH and FSH release. It's the grunt clearing up some for the Nolvadex to drop E levels low enough that hpta begins producing again. Oversimplified, yes, but I want a newbie to be able to get the gist of what we are trying to do here. I didn't forget the AI...imagine you have restarted test production naturally again by binding and manipulating estrogens. You are a little above your baseline T level and you drop the Nolvadex after 20mg/e.d. For 4-6 weeks. The excess estrogen made from elevated natural test levels will be able to bind at will. The last 2 weeks after ending all serms dose 1mg adex e.o.d. To keep too much estrogen forming due to aromatase!

So a basic PCT looks:

This is based on testicular atrophy being minimized due to hcg administration during cycle.

1-3 Clomid-50mg/e.d.
1-5 Nolvadex-20mg/e.d.
5-7 Adex-1mg/3Xwk

Final summary:

I hope this helps someone, I wanted to put the focus of PCT on not just the last weeks after cycle, but as PART of the cycle itself. They (PCT and Cycle) should complement each other by 1) Keeping as many gains as possible from cycle 2) PCT doesn't need to be as tough as I know many of you have had it be (myself included) if we are proactive with and during cycle.

Comments and/or opinions are welcome...I'd like to see the small or large differences between how each person views PCT! I also think it's important for the newbie to view the different perspectives....Thank's guys. opcorn:

 

[etul86]

About once a year I post a PCT thread covering the basics and watch the claws come out! There are so many different opinions that I understand no one will ever agree. We have the master of Post Cycle Therapy with us here at Meso so I'm not trying to be Meso's authority on PCT by posting this. I just wanted to post a thread outlining a pretty basic PCT and the basics behind why we need this therapy.

Some PCT points of view:

So we agree that, as I mentioned, one of the most debated yet essential process' we as Iron Athletes must endure is the conclusion of a cycle! Saying that, it's no surprise then that we dread post cycle steroid recovery (PCT) not only because of the emotional ride it sends many of us on, but also because...quite simply...our cycle is over.

PCT is often, I'm sad to say, almost an after thought to some newer AAS users. This is who I really wrote this for...the newbie!

I see more and more PCT forums with a few stickies and a question or two on start times or doses. PCT is not a formality unless you have a desire to live out your days on PDE-5 inhibitors and balls like BB's in a rubber thimble!

I worry, I'm guilty too, that time on=time off + a few weeks is becoming a lost method. Guys, cruising won't do you any good and staying on, well...seen Rick Flair topless since 84? Just sayin! To stay healthy you should run shorter (8-12 week) cycles at reasonable doses, running a solid PCT and time off exceeding time on when PCT is complete.

Why do we use gear? Why is it good? How can it harm? The good: treatment of andropause, TA, prevention of muscle wasting in AIDs victims, recovery from burns and injurys. The rec user and athlete gain an increase in lean muscle mass, drop in body fat, and a sense of well being.
The bad: higher LDL, lowered HDL, hypertension, possible enlargement of prostrate and yes...addiction! I did say addiction so flame if you must, I stand by it. The most discussed bad side of AAS is shutdown which brings us to the topic at hand.

PCT's importance:

Gonadatropin releasing hormone (GnRH)is pulsated, which is a fancy way to say, released from the hypothalamus to maintain healthy sexual function between the axis'by the release of (LH) and (FSH). These two hormones work with leydig cells and a healthy hpta is the result due to mens testes actually working to produce sperm and testosterone. When an exogenous hormone such as testosterone is administered on a moderate scale, or dose, hypogonadism from lowered test levels occur (I can't find a mg to shutdown ratio or dose) resulting in a drop in serum production and male estrogen dominance. When the exogenous test administration is moderate the problem can be remedied by dropping the estrogen levels. I do believe, however the longer the cycle and higher the dose recovery can be much more complex than 4 weeks of a SERM.
I've flip-flopped ove the past 2 years on the question "Is shutdown is shutdown end of story?" or "Is shutdown more extreme depending on the cycle and gear you use?" I'm a believer in the ladder these days where I used to think the former (as I said I flip flop). Saying that to say that I feel cycle choice determines the effort you will have to use to fully recover.

PCT method:

I like a 4 compound "proactive" PCT. Since HCG mimics LH I use that on cycle at 250iu twice weekly begining week 3 of the cycle, this is my first step. I now have 3 compounds left to use for PCT only (with exception of estrogen control during cycle).

My preference upon starting PCT is to use 2 SERMs and an AI. I'm older so I still use Clomid, Nolvadex and usually adex (letro sometimes). No 300mg Clomid frontloads for me though. I use Clomid weeks 1-3 of PCT at 50mg/ml. Clomid is a weak estrogen so its only purpose is to block binding and trigger LH and FSH release. It's the grunt clearing up some for the Nolvadex to drop E levels low enough that hpta begins producing again. Oversimplified, yes, but I want a newbie to be able to get the gist of what we are trying to do here. I didn't forget the AI...imagine you have restarted test production naturally again by binding and manipulating estrogens. You are a little above your baseline T level and you drop the Nolvadex after 20mg/e.d. For 4-6 weeks. The excess estrogen made from elevated natural test levels will be able to bind at will. The last 2 weeks after ending all serms dose 1mg adex e.o.d. To keep too much estrogen forming due to aromatase!

So a basic PCT looks:

This is based on testicular atrophy being minimized due to hcg administration during cycle.

1-3 Clomid-50mg/e.d.
1-5 Nolvadex-20mg/e.d.
5-7 Adex-1mg/3Xwk

Final summary:

I hope this helps someone, I wanted to put the focus of PCT on not just the last weeks after cycle, but as PART of the cycle itself. They (PCT and Cycle) should complement each other by 1) Keeping as many gains as possible from cycle 2) PCT doesn't need to be as tough as I know many of you have had it be (myself included) if we are proactive with and during cycle.

Comments and/or opinions are welcome...I'd like to see the small or large differences between how each person views PCT! I also think it's important for the newbie to view the different perspectives....Thank's guys. opcorn:

Sticky? Plz?

 

[Sworder]

Very informative post, thanks for taking your time to do so

 

[para1]

you are the Lion with the Viron !
seriously, excellent post. when you say adex, you mean arimadex at 1 mg every other day? can arimadex permanently depress estrogen though? does the clomid cause any long term vision problems?

 

[Sworder]

The hcg is to keep the testicles from atrophying but nothing is keeping the H(ypothalamus) and the P(ituitary) from down regulation. Has it been a generally known fact that it is the testicles that suffer the most and that it is the testes post cycle that there is an abundance of GnRH and the testes are getting fed tons of LH and FSH but they can't bind(?) to the leydig cells or they have problems responding from being dormant for so long? Or is the hcg mainly to keep the testicles in check at least and make sure that they won't have any problems and they will respond to any LH and FSH when needed.
I would see the hcg being another thing that can mess with the pituitary and keep the pituitary suppressed further or desensitizing the leydig. This is not based on any experience or studies, it is rather how I envision it in my little head. Would be great if somebody could help clarify

 

[bigrobbie]

Hcg simply mimics LH, they keep the testes from atrophy and basically trick them into thinking function is normal.

Hcg does nothing for the H or P. It's action is strictly (to my knowledge) testicular function.

Bill or the Doc can take this even further...as well as many other guys here. Heavyiron, Reinheart, Get Some...the list of guys I'd like to hear from on this is endless...

 

[bigrobbie]

Para1, glad to hear from ya. A 1mg daily dose (of arimidex) has been shown to produce estrogen suppression sometimes greater than 80%. That suppression though I do not believe to be permanent.

 

[para1]

does the question concerning arimadex causing permanent suppression of estrogen warrant further research or am i worrying about nothing?
keep in mind what propecia has done to dht levels that seem to be permanent in some men.

 

[bigrobbie]

I think you can never research too much, never stop, but I don't think you have to worry bro.

 

[BBC3]

Just to add some thoughts as I have always been of the opinion that PCT is not necessary. On the one hand I quickly realized that this is a MONKEY SEE MONKEY DO PHENOMENA which seems retarded. But at the same time I put a lot of stock in "WHAT WORKS" & anecdotal experience. Lately I have been changing my views, but not for the reasons one might think.

The human body is astute at finding stasis, AND REGARDLESS of factors even like TIME ON and INTENSITY or AMOUNT OF STEROID GIVEN - I THINK....

First you have to understand my views on SERUM COUNTS, which I will not go into here. But they can easily be found in posts search. Of course all of my ramblings are poppycock as far as current medical practice. But first I belive the body hones production surplus as we age, and steroid use expedites this condition. Second, I am thinking a poor estrogen demand profile is what causes failure to NORMALIZE after hormone administrations.

My recent change of thought is this. While I think PCT has no relevance with the BODY'S ABILITY TO RESUME PRODUCTION (Physically at the testes or brain) . HOWEVER, I am starting to wonder if PCT is not CRITICAL to RESETTING THE BODY'S DEMAND PROFILE at the receptor site its self.. SO to speak.. Meaning lately I am starting to wonder about receptor site control by precendence of population of the hormones. And perhaps it becomes necessary to block estrogen related hormone activity at the SITE in order to restore POPULATION BALANCE, thus creating a more CORRECT DEMAND PROFILE.

Remember that we measure the need for PCT based on SERUM COUNT, which I have descibed in other how I feel is a complete misnomer. Further you have to consider, and I have not confirmed anywhere, but I suspect that testicular shutdown is much more severe in bodies with higher preponderances of androgen receptors. I have NEVER experienced 'peanut' tyhpe shinkage while only reaping high levels of estrogens on SynT. Perhaps softness, or minor diminishment in size that has persisted for extended durations though. So how does that apply above.? A body that has lost control of receptor sites to estrogens in excess may have conditions that will remain in place contributing to the continued "Softness", or perhaps even "low SERUM COUNTS". So then you have a condition of continued shut down. BUT NOT BECAUSE THE BODY CAN'T RESUME PRODUCTION, BUT BECAUSE IT DOES NOT WANT TO as protection from excess E metabolism that is continuing due to control by preexisting population OR Excess estrogen receptor growth as a result. I am not sure my thoughts as to which yet.....

This of course all runs along the premise I broadcast - that hormone production is NEVER a function of sensing directly at the brain, but actually a result of RECEPTOR END ACTION thus transmitting demands to the brain throught the CNS.. I wonder.

About once a year I post a PCT thread covering the basics and watch the claws come out! There are so many different opinions that I understand no one will ever agree. We have the master of Post Cycle Therapy with us here at Meso so I'm not trying to be Meso's authority on PCT by posting this. I just wanted to post a thread outlining a pretty basic PCT and the basics behind why we need this therapy.

Some PCT points of view:

So we agree that, as I mentioned, one of the most debated yet essential process' we as Iron Athletes must endure is the conclusion of a cycle! Saying that, it's no surprise then that we dread post cycle steroid recovery (PCT) not only because of the emotional ride it sends many of us on, but also because...quite simply...our cycle is over.

PCT is often, I'm sad to say, almost an after thought to some newer AAS users. This is who I really wrote this for...the newbie!

I see more and more PCT forums with a few stickies and a question or two on start times or doses. PCT is not a formality unless you have a desire to live out your days on PDE-5 inhibitors and balls like BB's in a rubber thimble!

I worry, I'm guilty too, that time on=time off + a few weeks is becoming a lost method. Guys, cruising won't do you any good and staying on, well...seen Rick Flair topless since 84? Just sayin! To stay healthy you should run shorter (8-12 week) cycles at reasonable doses, running a solid PCT and time off exceeding time on when PCT is complete.

Why do we use gear? Why is it good? How can it harm? The good: treatment of andropause, TA, prevention of muscle wasting in AIDs victims, recovery from burns and injurys. The rec user and athlete gain an increase in lean muscle mass, drop in body fat, and a sense of well being.
The bad: higher LDL, lowered HDL, hypertension, possible enlargement of prostrate and yes...addiction! I did say addiction so flame if you must, I stand by it. The most discussed bad side of AAS is shutdown which brings us to the topic at hand.

PCT's importance:

Gonadatropin releasing hormone (GnRH)is pulsated, which is a fancy way to say, released from the hypothalamus to maintain healthy sexual function between the axis'by the release of (LH) and (FSH). These two hormones work with leydig cells and a healthy hpta is the result due to mens testes actually working to produce sperm and testosterone. When an exogenous hormone such as testosterone is administered on a moderate scale, or dose, hypogonadism from lowered test levels occur (I can't find a mg to shutdown ratio or dose) resulting in a drop in serum production and male estrogen dominance. When the exogenous test administration is moderate the problem can be remedied by dropping the estrogen levels. I do believe, however the longer the cycle and higher the dose recovery can be much more complex than 4 weeks of a SERM.
I've flip-flopped ove the past 2 years on the question "Is shutdown is shutdown end of story?" or "Is shutdown more extreme depending on the cycle and gear you use?" I'm a believer in the ladder these days where I used to think the former (as I said I flip flop). Saying that to say that I feel cycle choice determines the effort you will have to use to fully recover.

PCT method:

I like a 4 compound "proactive" PCT. Since HCG mimics LH I use that on cycle at 250iu twice weekly begining week 3 of the cycle, this is my first step. I now have 3 compounds left to use for PCT only (with exception of estrogen control during cycle).

My preference upon starting PCT is to use 2 SERMs and an AI. I'm older so I still use Clomid, Nolvadex and usually adex (letro sometimes). No 300mg Clomid frontloads for me though. I use Clomid weeks 1-3 of PCT at 50mg/ml. Clomid is a weak estrogen so its only purpose is to block binding and trigger LH and FSH release. It's the grunt clearing up some for the Nolvadex to drop E levels low enough that hpta begins producing again. Oversimplified, yes, but I want a newbie to be able to get the gist of what we are trying to do here. I didn't forget the AI...imagine you have restarted test production naturally again by binding and manipulating estrogens. You are a little above your baseline T level and you drop the Nolvadex after 20mg/e.d. For 4-6 weeks. The excess estrogen made from elevated natural test levels will be able to bind at will. The last 2 weeks after ending all serms dose 1mg adex e.o.d. To keep too much estrogen forming due to aromatase!

So a basic PCT looks:

This is based on testicular atrophy being minimized due to hcg administration during cycle.

1-3 Clomid-50mg/e.d.
1-5 Nolvadex-20mg/e.d.
5-7 Adex-1mg/3Xwk

Final summary:

I hope this helps someone, I wanted to put the focus of PCT on not just the last weeks after cycle, but as PART of the cycle itself. They (PCT and Cycle) should complement each other by 1) Keeping as many gains as possible from cycle 2) PCT doesn't need to be as tough as I know many of you have had it be (myself included) if we are proactive with and during cycle.

Comments and/or opinions are welcome...I'd like to see the small or large differences between how each person views PCT! I also think it's important for the newbie to view the different perspectives....Thank's guys. opcorn:

 

[Fulano]

All I know about PCT is first-hand experience. No blood tests. No theories about the specific mechanism of action. Here is my first-hand experience with two different cycles, one with PCT, one without it:

On one occassion I did a 2 week cycle with no hCG and no PCT just to see what would happen. After 2 weeks of Dianabol, Tren, and Winny, I was exhausted and had no sexual desire. My penis and scrotum were flaccid and deflated. I was capable of getting and maintaining an erection, but I had ZERO interest in sex. Over the next 14 days after discontinuing the drugs I remained exhausted. I slept 10 hours a day and still felt like I needed to nap all day long. I gained 8 lbs on the cycle, and then I lost 11 pounds over the next 14 days after discontinuing steroids, even with normal workouts and eating. On the morning of the 15th day... BAM, everything was back to normal. i woke up with a morning erection. I had normal turgidity in the penis and scrotum, and my energy levels felt normal. Over the course of the next two weeks, I gained back all the weight I had lost and even went up a little in strength. So, the 2 week cycle with no hCG or PCT resulted in a net gain of muscle mass and strength, but it was a roller coaster of side effects.

I don't do 2 week cycles like this anymore. I just did it this way to see how much a 2 week cycle shut me down and how long it would take to recover. This was a personal experiment.

On the other hand, I did an 8 week cycle of Test Cyp and Tren wherein I used hCG for the last several weeks of the cycle and then Clomid and Nolvadex for a couple weeks afterward. I had some minor shrinkage of the testicles before starting the hCG, but they returned to normal on hCG. Other than that I had ZERO other symptoms of shut down, either during the cycle or afterward. In fact, sexual desire and performance and energy levels were higher than normal throughout the cycle and for several months afterward.

Now, obviously there are many factors to consider here. 1) The specific steroids I used during the two cycles were different. I didn't use any testosterone on the one, while testosterone was the foundation of the other. Clearly that could make a very large difference in how I felt. 2) The duration of action of the steroids was different. Test Cyp takes weeks for levels to taper off after a cycle, while the orals and Tren disappeared from my system in a couple days (or sooner) after discontinuing, giving a "cold turkey" effect. 3) The duration of the cycles was different. 4) And there are probably more things I'm not considering.

So, how much of a difference did PCT make? Hard to say. There were so many confounding factors that it may be hard to separate those effects that can be confidently attributed to PCT. Nevertheless, when I used hCG, Clomid, and Nolvadex as recommended I had a very good experience with an easy transition from on-cycle to off-cycle. When I didn't use hCG or PCT, even though it was only a two-week cycle, it was a roller coaster of shut-down and side effects.

 

[bigrobbie]

Now that's what I was looking for!! A+++ post bro!

I won't cycle without hcg if it can be helped anymore.

I didn't put this in my thread, but I've actually found 50mg wk of Clomid on cycle along with hcg to be comparable (for me) to adex/hcg. I prefer adex though as it seems not to mess with my emotional state as Clomid does.

Great reply my friend, thank you!!!!

 

[Reinheart]

I have figured that the best pct regimen is:

20mgs Nolvadex for 4-6 weeks
25mgs Aromasin Daily for 4-6 weeks
80mgs Restandol for the first two weeks
0,5mgs Dostinex twice per week for 4-6 weeks
2-3 grams of L-Carnitine

and a shitload of supplements.

HCG is used throughout the entire cycle, staring from week 3. For HCG i follow the 6 weeks on/2 weeks off protocol while on cycle and it seems to work like a charm. I am currently 14 weeks into my cycle (i am currently using 600mgs test e and 400mgs NPP) and I have ZERO atrophy.

 

[bigrobbie]

Nice...I think I remember a few years ago when you were perfecting that PCT...am I remembering right?

Thanks for the post, NOW WE'RE ROLLIN'!

Keep that good info comin guys!

Thanks Reinie

 

[Sworder]

Does testicular atrophy really reflect upon the functionality of the testicles or rather merely reflect upon the LH/FSH levels provided by the pituitary?

Nice post BBC3

 

[BBC3]

Thank you for the response. I am glad to see at least someone reads my rambles from time to time.

So I will give you my view here too... For the most part the only TRUE MEASURE of testicular physical condition, is a physical GRAB, And there are TWO ASPECTS to testicular Atrophe to consider:
1. The kind a shrinkage we are talking in BodyBuilding, we are talking PEANUT POTENTIAL SMALL.
2. Shrinkage related to SPERM PRODUCTION. This is real. There is a large compostion of sperm hangin on the exterior rear of those boys!

Usually where you have one type you will have the other. But what most dont understand is that the steroid induced shrinkage will reverse LONG BEFORE sperm diminishment shrinkage does.

So once I was at the urologist (and a damn good one). Whilst holding the jewels, he said, "I hope you are done having all the children you planned on". So I said well at least someone in the medical profession will own up to the fact the testosterone supping is actually valid male birth control... We later discussed my TRT dosing (from other doc), and I advised him that I had been up on the high side experimenting "briefly" @ 1000mgs for last few weeks. His eyes narrowed and he just said thats WAY too much...

One point I am conveying is that this was a FAT period with some workout combined, but I knew I was pretty estrogenic at the time. The testicles were only soft and slighly dimenished. I could not even imagine what he would say if he saw them the time I had "peanutized" them.[)] The point is they were not even all that affected and he was pretty sure I had hit them hard. Back to the answer.
1. I am not sure how LH & FSH relate as I am not sure about these in SERUM COUNT. I speculate measurements may be somewhat worthless here too, and significantly worthless as a this is a PRODUCTION POINT we are measuring. NOT Conversion like estrogen or DHT. I think there IS A CURVE that does start to mean something as we approach 1.5 and lower on both FSH and LH. As an adjunct I forgot earlier. I also suspec that HCG is more of an agonist, rather than a mimicer, and requires LH present to be effective (Yea, I got a LOAD of it).
2. I speculate they work just fine soft, spongy, and kinda small. At least to whatever degree the body is demanding. I also think there are general age factors affecting physically as a general. I do not think ANYONE will ever regain a plump brazin set like 19 years old. Dont think they had em to start. But who knows cause no one checks first. HOWEVER, it would be safe to say that for most of the new "Low-T" men out there, you will find soft spongies. THIS IS because the brain is throttling down production to stop the estrogen onslaught in progress, and should also be seen in LH&FSH.
3. Consider too a lot of the shrinkage guys feel is the lack of the presence of sperm in the rear "Baggies". This IS substantial in area volume. Poor sperm count can come from Estrogen induced Low-T, or cycling. It takes 100days to breed a batch of sperm in the tanks, EVEN AFTER PRODUCTION IS FULLY TRIGGERED (PCT TIME + RECOVERY TIME + 100 DAYS)

BUT NOW I SEE I MAY HAVE MISSED THE QUESTION. You would be referring to type I or II hypogonadism. Yes as LH & FSH reads lower, there is no doubt that it is reflected in the testicles. And then there is the potential of the actual physical failure of the testicles (I think I is is physical in the testes, always get mixed up). This is possible too. My above thoughts touch on both of that a little bit.

Oh, back to the URO trip. I agreed with him my body fat was too high. He agreed with me that I was probably generating a hell of a lot of estrogen. The purpose of my visit was also to get an AI, and he kept offering AVODART!?!?!? We even discussed new research into SERMS a possible valid prostate protection. He still kept harping on DHT BLOCKERS. I dont even exhibit high DHT symptoms...... It was like a page fell out of the book somewhere....

Does testicular atrophy really reflect upon the functionality of the testicles or rather merely reflect upon the LH/FSH levels provided by the pituitary?

Nice post BBC3

 

[bigrobbie]

Sworder, I think as part of a negative loop, the drop in LH and FSH cause loss of testicular functionality, which leads to TA.

The rub is this, TA is a direct result of failure of GnRH stimulation...

BBC, were you talking about serum lipids? AAS use causes reduction in serum HDLC, but I always thought levels began to raise again approx 1 month after all exogenous steroids had been discontinued and eliminated from activity? I'm not following you 100% bro...help me see your view on serum levels and recovery of hpta. Thanks my friend!

 

[Michael Scally MD]

After treating over 1000+ AAS users, I have found the best method with guaranteed success to be:

 

[bigrobbie]

Lol! Probably the most neglected step too!

 

[Sworder]

Ok think I got a better understanding of it now. Thanks. Had to read through everything again to fully grasp it.

Bigrobbie you explain how you start some adex after completing all SERMs the purpose of this would be to kill off the estradiol getting blocked? I was wondering how long does the estradiol that is getting blocked linger in your body until it "dies" without the use of a AI? I thought AIs would merely inhibit further aromatase activity but it knocks estradiol off too right?