Duly noted MAC hadn't seen that before, especially as a patient complaint.
MESO-Rx
Anabolic Steroids
first cycle help
- Thread starter Chipsam
- Start date
mac111
New Member
yeah its a right royal pain, once i went above 30mgs i just couldnt squat or deadlift or walk any distance. possible it doesnt affect every single person like tht but it is a very common complaint with dbol from what ive gathered from ppl in real life and on boards.
I've read that using HCG while taking either nolva or clomid is counterintuitive (according to Bill Roberts on here). It interferes with LH recovery (what nolva/clomid does basically).
Take the HCG during cycle* or pre-PCT.
Last edited:
mac111
New Member
correct
Utter nonsense, when used as recommended. I do use aromasin now, but neither I nor anyone I've heard ever had impotence problems as the result of properly used arimidex.
Solo
mac111
New Member
dunno solo, ive experienced lack of desire with cycles that included adex, may be something there mate, prob as a consequences of estro levels rather than directly from the adex. its hard to pinpoint due to variances
I suspect you missed the point.
Lower testosterone to estrogen levels are a well documented etiology for male impotence. When a typical cycle ends testosterone DECREASES (precipitiously) and estrogen INCREASES, which is why I use it at that juncture.
Conversely very high ratios because of very low estrogen levels (which is what Amiridex causes) can also cause ED, although less well documented, (yet is also based on lab results from some of my patients whom complain of ED during their cycle; myself included!)
Novaldex incompletely blocks the e receptors unlike amiridex (reason the aromatase inhibitors were initially developed)
I attempt to treat all of my patients based on the literature and most of my commentary is well documented in the heme-onc arena for the treatment of ESTROGEN responsive breast cancer.
Obviously there are some individualistic variations but it's intuitive from my perspective. You just don't need 100% blockade during a cycle. Besides Nolvadex is considerably less expensive at most pharmacies than Amiridex, even when generic is prescribed.
A similar practice may not necessary for you, but is has certainly helped a few of my patients during their cycle.
In case your wondering I manage at least 300 patients monthly whom are on-off cycle.
Lower testosterone to estrogen levels are a well documented etiology for male impotence. When a typical cycle ends testosterone DECREASES (precipitiously) and estrogen INCREASES, which is why I use it at that juncture.
Conversely very high ratios because of very low estrogen levels (which is what Amiridex causes) can also cause ED, although less well documented, (yet is also based on lab results from some of my patients whom complain of ED during their cycle; myself included!)
Novaldex incompletely blocks the e receptors unlike amiridex (reason the aromatase inhibitors were initially developed)
I attempt to treat all of my patients based on the literature and most of my commentary is well documented in the heme-onc arena for the treatment of ESTROGEN responsive breast cancer.
Obviously there are some individualistic variations but it's intuitive from my perspective. You just don't need 100% blockade during a cycle. Besides Nolvadex is considerably less expensive at most pharmacies than Amiridex, even when generic is prescribed.
A similar practice may not necessary for you, but is has certainly helped a few of my patients during their cycle.
In case your wondering I manage at least 300 patients monthly whom are on-off cycle.
Oops
Correction that should read;.......I manage at least THIRTY per week.....
Correction that should read;.......I manage at least THIRTY per week.....
Thanks for the correction, DJ. Arimidex, according to my experience & understanding, blocks a good deal of estrogen, but does not kill all estrogen. So — again, used in smaller amounts like 0.5 mg EOD — it should protect nipples and prevent estro bloat. There has been much adverse publicity in recent years against Nolva, so I don't bother with it any more. Plus it just blocks the reception of estrogen in certain important areas; it does not lower estrogen levels overall, so it could result in estrogen bloating or sexual side effects, even though the nipples are mostly protected. Like many others, I prefer aromasin over arimidex for post-cycle recovery because there apparently is no sudden drop of levels resulting in a sudden backlash (a flood of estrogen) when one stops. Not questioning your assumed professional competence, Doc, but these are pretty well known facts, are they not?
Respectfully,
Solo
Solo
You are obviously well educated and have "been there and done that" personally!
When I registered on Meso several months ago I simply observed quite a few threads curious about the knowledge base of its "veteran members", forbidding rules, censorship, and or "moderation" etc.. Eventually it became apparent, "MESO WAS DIFFERENT", (I was much more involved in 2-3 other forums, one as a paid consultant, yet many of my rebuttals were etched out, deleted or otherwise completely censored) it actually had knowledgeable "partiscipant observers" whose input was based on either fact or experience which was actually CREDIBLE!
It's people like you, MANDS and MAC whom challenge my thought processes, which on occasion, even change my practice patterns.
However before I can respond to your queries we will need to agree (or disagree )
on four hormonal derangements common to most (very much dependent upon cycle DURATION and strength) post cycle protocols, excluding ANY post cycle therapy of course.
They include the following:
Testosterone decreases
Estrogen increases
Luteinizing hormone is very low OR approximates zero (essentially NO pulsitile activity occurs)
Cortisol increases
Without agreeing about these changes any further discussion would be a somewhat fruitless endeavor, so let me know you thoughts.
Regards
Jim
You are obviously well educated and have "been there and done that" personally!
When I registered on Meso several months ago I simply observed quite a few threads curious about the knowledge base of its "veteran members", forbidding rules, censorship, and or "moderation" etc.. Eventually it became apparent, "MESO WAS DIFFERENT", (I was much more involved in 2-3 other forums, one as a paid consultant, yet many of my rebuttals were etched out, deleted or otherwise completely censored) it actually had knowledgeable "partiscipant observers" whose input was based on either fact or experience which was actually CREDIBLE!
It's people like you, MANDS and MAC whom challenge my thought processes, which on occasion, even change my practice patterns.
However before I can respond to your queries we will need to agree (or disagree )
on four hormonal derangements common to most (very much dependent upon cycle DURATION and strength) post cycle protocols, excluding ANY post cycle therapy of course.
They include the following:
Testosterone decreases
Estrogen increases
Luteinizing hormone is very low OR approximates zero (essentially NO pulsitile activity occurs)
Cortisol increases
Without agreeing about these changes any further discussion would be a somewhat fruitless endeavor, so let me know you thoughts.
Regards
Jim
That is correct and here"s why. Remember the proviso was NO post cycle therapy!
The eventual decline of post cycle testosterone levels correlate directly with the half life of the drugs used. The shorter the half life the more precipitous the decline. More importantly any viable moderate to high dose cycle will markedly diminish gonadotropin output thereby markedly lowering endogenous testosterone. ABSENT GONADOTROPIN STIMULATION THE TESTICLES ATROPHY, (pathologically what that means is the Lyedig cells shrunk into near oblivion).
Once the f-Testosterone level reaches 200-300, (much lower in some circumstances) pulsitile gonadotropin production begins to recur. Yet since atrophy has occurred minimal testosterone production will ensue. However male GONADOTROPIN also induces the aromatase enzyme found in the adrenals (which DO NOT atrophy) and since 80% of male estrogen is derived from "adrenal aromatase activity" estrogen RISES in spite of a low testosterone level.
The change is also relative in that a declining testosterone level with a fixed
estrogen level will obviously result in a REDUCED fT-E2 ratio.
THIS IS ONE REASON BOARD "MODERATORS" RANT AND RAVE ABOUT THE NEED FOR PCT, WITHOUT IT YOU'LL FEEL LIKE A WOMEN WITH POST PARTUM DEPRESSION AND LOOK IT TO!
Would you agree SOLO?
JIM
The eventual decline of post cycle testosterone levels correlate directly with the half life of the drugs used. The shorter the half life the more precipitous the decline. More importantly any viable moderate to high dose cycle will markedly diminish gonadotropin output thereby markedly lowering endogenous testosterone. ABSENT GONADOTROPIN STIMULATION THE TESTICLES ATROPHY, (pathologically what that means is the Lyedig cells shrunk into near oblivion).
Once the f-Testosterone level reaches 200-300, (much lower in some circumstances) pulsitile gonadotropin production begins to recur. Yet since atrophy has occurred minimal testosterone production will ensue. However male GONADOTROPIN also induces the aromatase enzyme found in the adrenals (which DO NOT atrophy) and since 80% of male estrogen is derived from "adrenal aromatase activity" estrogen RISES in spite of a low testosterone level.
The change is also relative in that a declining testosterone level with a fixed
estrogen level will obviously result in a REDUCED fT-E2 ratio.
THIS IS ONE REASON BOARD "MODERATORS" RANT AND RAVE ABOUT THE NEED FOR PCT, WITHOUT IT YOU'LL FEEL LIKE A WOMEN WITH POST PARTUM DEPRESSION AND LOOK IT TO!
Would you agree SOLO?
JIM
mac111
New Member
what?! he is just an augmentative so and so!!! [
)]
Thanks MAC, but come on Solo, I need your reply to finish this thread!. I have every intention of including several articles (this time) which support my assertions that are "utter nonsense".
Jim
Jim
I may be misunderstanding you here, but are you saying that arimidex completely blocks E-Receptors, or that arimidex does not act in any way similar to Nolvadex?
I would be interested in your reference material that indicates estradiol will increase by the mechanisms you describe.
Are you saying the gonadotropin itself aromatizes into estradiol? Or that the aromatase enzyme (from the adrenals) acts on another hormone to produce estradiol? If so, what other hormone are we talking about here?
Arimidex is an AI(aromatase inhibitor) as you know and Nolvadex is a SERM(selective estrogen receptor modulator).
With this being said an AI basically destroys/inhibits against the conversion of androgens to estrogen. While a SERM like Nolvadex binds to receptor sites like your breast and other tissues(this means more estrogen is present in theory). Now SERM's can be a little different and act a little different as well. Each SERM is usually specific to a particular tissue or area. Like Nolvadex is agonist at breast and Clomid is an agonist at the Hypothalamus.
Not sure if this helps or not.
mands
I understand the processes well. But it was not clear from the post I quoted that he does, since he stated that Nolva "incompletely" blocks the estrogen recepotrs "unlike arimidex". This could be misinterpreted to represent that adex actually blocks the estrogen receptors, which obviously is not at all true.
This is further evidenced by the statement further down in the paragraph:
Giving further indication that Dr Jim thinks that somehow Armidex results in a "total blockade" of the estrogen receptors. If I interpret this post correctly (and I see no other way it really could be interpreted) then this represents a very fundamental misunderstanding of AI's and SERMs, the difference between the two, and their efficacy in hormone treatment. I would be very scared if my doctor did not know the difference.
Arimidex acts by binding to the aromatase enzymes and rendering them inactive. But the degree to which this occurs is dose dependent. A 0.25 mg dose of Adex will not go nuclear and multiply to cover every aromatase enzyme in the body. You can easily adjust your doses to dial in estrogen levels
I await his reply.
No. Adex lowers the production of estrogen. Nolva does not. Nolva blocks e-receptors at certain sites (like breast tissue). So, in a way the result is similar – protection, but the effect on the body is very different. I hate estro bloat, and adex helps with that, too.
Solo
I know what you said to be true. Obviously the good doctor does not. Looking forward to his reply though.
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