Jagger, to clarify, I will no longer comment on ANY of your posts. Should any one else have a question I'd be delighted to reply.
MESO-Rx
Anabolic Steroids
first cycle help
- Thread starter Chipsam
- Start date
Agree with what? Your conclusion that PCT is a good idea? Of course I agree with that. As for the rest, you go on into such unrelated detail I kind of lose your trend.
You're not claiming to be a medical doctor, are you Jim? You say you have experience working with "patients" and you can quote a lot of chemistry, but let's just say you don't write like a medical doctor.
Anyway, background knowledge such as yours is welcome here.
Solo
Last edited:
I'll stand with the idea that arimidex is not known (when used properly) for causing male impotence. In fact, the contrary is more likely. But everyone is different, so it's not impossible that some guys react unexpectedly. It's a bit tough to understand how an increase in testosterone (without blocking all estrogen) should result in impotence. Could it be someone is making correlations and confusing it with causation?
Solo
That seems to be his M.O.--talk in circles, spew some nonsense, then conclude that what YOU said is wrong. He has not put forth anything remotely resembling a coherent argument to anything I've had to say to him so far, and as you can see he has chosen to ignore my posts.
The guy is clueless. I feel sorry for his "patients" (though they are likely just paid by actors on TV cause there's no way this guy is a doctor in real life)
SOLO with deference, our back!
I only posted your "utter nonsense" reply to entice you to do return and complete this discussion because you know what your talking about and you asked me to explain my earlier posting.
I was not attempting to be sarcastic or antagonistic, I just wanted to finish this thread with you.
First I am a licensed PRACTICING PHYSICIAN in the state of TEXAS.
Second, am BOARD CERTIFIED In emergency-trauma and subspecialty certified in sports medicine. (I have no reason to lie and certainly have no desire to impress ANY ONE especially because of my educational credentials).
Third, you should see my cursive hand writing it's quite unimpressive.
Fourth, I stated Amiridex COULD cause impotence because of the lowered E-2 levels (estrogen is an modest veno-dilator via the nitric oxide pathway, and it's actually used in catheterization labs occasionally for that purpose) I believe I mentioned the the data was less well substantiated however.
Fifth; Two recently (2011 and 2012) released studies with a combined total of approximately 200 male patients with breast cancer revealed impotence was considerably more common in the TAMOXIFEN subset.
SO WERE RIGHT AND I WAS WRONG and the evidence is convincing!
Sixth; Amiridex does result in approximately 95% reduction of aromatase activity in females but apparently this does not result in a proportional depression of E-2 levels, especially in males.
Seven; Exemestane was approved by the FDA 2005-6 which means many studies clarifying its use and safety profile are now approaching completion (some of course already have). Additionally it is classified as a steroidal A-I which binds aromatase IRREVERSIBLY. I don't believe we know what that means clinically, but a study released this month demonstrated that it will attach to the ANDROGEN RECEPTOR as well!
Eight: Since Tamoxifen has agonistic and antagonistic estrogen receptor activity with a adverse side effect profile, necessitating discontinuation in MALES, that approximates 25%, (based on recent studies) I will no longer recommend its use in patients prone to gynecomastia; because their WAF ("white animal fat") aromatase concentration is also higher predisposing them more peripheral "swelling". I also suspect adipose aromatase activity would be higher in those whose body fat exceeds 15-20%. We know aromatase is increased in "obese patients" so much so that it's use is a relatively common practice treating the hypogonadal infertility occasionally associated with the condition. Ergo, I now recommend treatment in this SUBSET of patients with a non-steroidal AI, as YOU ORIGINALLY SUGGESTED!
Ninth: I am unaware of any evidence which demonstrates a rebound phenomena occurs upon the discontinuation of AIs. Subsequent to their completion estrogen will increase gradually but should not "overshoot" previous baseline levels, especially when considering, the Armidex half life of roughly forty eight hours should ensure elimination of the active compound in about ten days. Consequently I see no benefit of tapering the dosage over time.
Lastly, you asked if estrogen would preferentially increase over testosterone POST CYCLE, my last post was an explanation as to why this may very well be the case. I apologize of any misunderstanding and look forward to discussing the complex pathophysiological issues exclusive to anabolics with you again soon.
I will post those referenced articles as promised earlier (gotta figure out how to do that I'm certainly no computer wizard).
P.S. I do this (and enjoy doing so) because I find it's a welcomed break from my hectic practice.
Best Wishes
JIM
I only posted your "utter nonsense" reply to entice you to do return and complete this discussion because you know what your talking about and you asked me to explain my earlier posting.
I was not attempting to be sarcastic or antagonistic, I just wanted to finish this thread with you.
First I am a licensed PRACTICING PHYSICIAN in the state of TEXAS.
Second, am BOARD CERTIFIED In emergency-trauma and subspecialty certified in sports medicine. (I have no reason to lie and certainly have no desire to impress ANY ONE especially because of my educational credentials).
Third, you should see my cursive hand writing it's quite unimpressive.
Fourth, I stated Amiridex COULD cause impotence because of the lowered E-2 levels (estrogen is an modest veno-dilator via the nitric oxide pathway, and it's actually used in catheterization labs occasionally for that purpose) I believe I mentioned the the data was less well substantiated however.
Fifth; Two recently (2011 and 2012) released studies with a combined total of approximately 200 male patients with breast cancer revealed impotence was considerably more common in the TAMOXIFEN subset.
SO WERE RIGHT AND I WAS WRONG and the evidence is convincing!
Sixth; Amiridex does result in approximately 95% reduction of aromatase activity in females but apparently this does not result in a proportional depression of E-2 levels, especially in males.
Seven; Exemestane was approved by the FDA 2005-6 which means many studies clarifying its use and safety profile are now approaching completion (some of course already have). Additionally it is classified as a steroidal A-I which binds aromatase IRREVERSIBLY. I don't believe we know what that means clinically, but a study released this month demonstrated that it will attach to the ANDROGEN RECEPTOR as well!
Eight: Since Tamoxifen has agonistic and antagonistic estrogen receptor activity with a adverse side effect profile, necessitating discontinuation in MALES, that approximates 25%, (based on recent studies) I will no longer recommend its use in patients prone to gynecomastia; because their WAF ("white animal fat") aromatase concentration is also higher predisposing them more peripheral "swelling". I also suspect adipose aromatase activity would be higher in those whose body fat exceeds 15-20%. We know aromatase is increased in "obese patients" so much so that it's use is a relatively common practice treating the hypogonadal infertility occasionally associated with the condition. Ergo, I now recommend treatment in this SUBSET of patients with a non-steroidal AI, as YOU ORIGINALLY SUGGESTED!
Ninth: I am unaware of any evidence which demonstrates a rebound phenomena occurs upon the discontinuation of AIs. Subsequent to their completion estrogen will increase gradually but should not "overshoot" previous baseline levels, especially when considering, the Armidex half life of roughly forty eight hours should ensure elimination of the active compound in about ten days. Consequently I see no benefit of tapering the dosage over time.
Lastly, you asked if estrogen would preferentially increase over testosterone POST CYCLE, my last post was an explanation as to why this may very well be the case. I apologize of any misunderstanding and look forward to discussing the complex pathophysiological issues exclusive to anabolics with you again soon.
I will post those referenced articles as promised earlier (gotta figure out how to do that I'm certainly no computer wizard).
P.S. I do this (and enjoy doing so) because I find it's a welcomed break from my hectic practice.
Best Wishes
JIM
Nolvadex (tamoxifen citrate) NOLVADEX (TAMOXIFEN CITRATE) TABLET [ASTRAZENECA PHARMACEUTICALS LP]
See: https://thinksteroids.com/community/posts/789022
[P3-206] Hypogonadism with Estrogen Removal (HER): Effects of Androgens and Estrogens on Sexual Desire in Young Adult Men https://thinksteroids.com/community/posts/765178
The Relationships between Sex Hormones and Sexual Function in Middle-Aged and Older European Men https://thinksteroids.com/community/posts/777169
I was waiting for the full-text article before posting, but this seems like an opportune time.
Kacker R, Traish AM, Morgentaler A. Estrogens in Men: Clinical Implications for Sexual Function and the Treatment of Testosterone Deficiency. J Sex Med. Estrogens in Men: Clinical Implications for Sexual Function and the Treatment of Testosterone Deficiency - Kacker - 2012 - The Journal of Sexual Medicine - Wiley Online Library
Introduction. The role of estrogens in male sexual function and the pathogenesis of testosterone deficiency remain controversial and poorly understood.
Aims. To review the distribution of estrogens in normal and testosterone deficient men, their potential role in sexual function, and the clinical implications of elevated estrogens during testosterone therapy.
Methods. A comprehensive, broad-based literature review was conducted on the role of estrogens in male sexual function and testosterone deficiency.
Results. Estrogens elicit a variety of physiological responses in men and may contribute to modulation of sexual function. In the absence of testosterone deficiency, elevations in estrogens do not appear to be harmful and estrogens may help maintain some, but not all, sexual function in castrated men. While the therapeutic use of estrogens at pharmacologic doses has been used to suppress serum testosterone, naturally occurring elevations of estrogens do not appear to be a cause of low testosterone. During testosterone replacement, estrogens may rise and occasionally reach elevated levels. There is a lack of evidence that treatment of elevated estrogen levels during testosterone replacement has benefit in terms of male sexuality.
Conclusion. Further research on the importance of estrogens in male sexual function is needed. Current evidence does not support a role of naturally occurring estrogen elevations in testosterone deficiency or the treatment of elevated estrogens during testosterone therapy.
BTW: I will re-post the abstract as a thread in Men's Health.
See: https://thinksteroids.com/community/posts/789022
[P3-206] Hypogonadism with Estrogen Removal (HER): Effects of Androgens and Estrogens on Sexual Desire in Young Adult Men https://thinksteroids.com/community/posts/765178
The Relationships between Sex Hormones and Sexual Function in Middle-Aged and Older European Men https://thinksteroids.com/community/posts/777169
I was waiting for the full-text article before posting, but this seems like an opportune time.
Kacker R, Traish AM, Morgentaler A. Estrogens in Men: Clinical Implications for Sexual Function and the Treatment of Testosterone Deficiency. J Sex Med. Estrogens in Men: Clinical Implications for Sexual Function and the Treatment of Testosterone Deficiency - Kacker - 2012 - The Journal of Sexual Medicine - Wiley Online Library
Introduction. The role of estrogens in male sexual function and the pathogenesis of testosterone deficiency remain controversial and poorly understood.
Aims. To review the distribution of estrogens in normal and testosterone deficient men, their potential role in sexual function, and the clinical implications of elevated estrogens during testosterone therapy.
Methods. A comprehensive, broad-based literature review was conducted on the role of estrogens in male sexual function and testosterone deficiency.
Results. Estrogens elicit a variety of physiological responses in men and may contribute to modulation of sexual function. In the absence of testosterone deficiency, elevations in estrogens do not appear to be harmful and estrogens may help maintain some, but not all, sexual function in castrated men. While the therapeutic use of estrogens at pharmacologic doses has been used to suppress serum testosterone, naturally occurring elevations of estrogens do not appear to be a cause of low testosterone. During testosterone replacement, estrogens may rise and occasionally reach elevated levels. There is a lack of evidence that treatment of elevated estrogen levels during testosterone replacement has benefit in terms of male sexuality.
Conclusion. Further research on the importance of estrogens in male sexual function is needed. Current evidence does not support a role of naturally occurring estrogen elevations in testosterone deficiency or the treatment of elevated estrogens during testosterone therapy.
BTW: I will re-post the abstract as a thread in Men's Health.
Last edited:
hey guys im an athlete thinking about cyling on sublingual test prop 20mg 2 befor morning sprint drills and 2 before powerlifts at night , i train twice a day 6 days a week track workouts in the morning powerlifting style training at night, as u can emagine its fucking hard and recovery is an issue my main goal is RECOVERY!!!!! i love to train hard i love to push it i want to take sumthing to recover faster and push it harder but not shure waht to take i am tested ive looked up detection times and steroid profiles sounds like only orals, WINDSTROL,TURINABOL,ANAVAR, SUBLINGUAL TEST PROP, those all clear the system and sound like what i should b taking but not sure how to do it witch PCT and stuff like that EX can i run oral windstrol with sub test prop and take arimadex for pct after??? do i need to run hcg during?? please help any info would b great i know injecting is the way to go for real gains but i am a sprinter not a body builder
So, doc, about your assertion that arimidex blocks the estrogen receptors...
At times, we all type/write many thoughts into a general concept. I had no problem understanding that an AI will decrease E2 resulting in less ER activity. I believe you have the same understanding, so any further argument on your behalf is fruitless and meaningless. Why not try to clarify rather than flame.
mac111
New Member
man, dont hijack threads, you've already asked this in another thread....
I have asked the doc for clarification a couple of times, respectfully actually. He has chosen to ignore me in all future debates. That is an interesting definition of flaming you are invoking here. His statement was very specific: "Arimidex completely blocks the estrogen receptor while Nolvadex does not". This is a VERY specific statement and is not really open to any other interpretation. That a medical doctor could have such a fundamental misunderstanding of the difference between the activity of a SERM and an AI is scary, so I was giving the good doctor an opportunity to clarify. He has chosen not to do so. He does't need a support group.
Where does the purported quote, "Arimidex completely blocks the estrogen receptor while Nolvadex does not" appear?
The only statement I am able to locate states, "Novaldex incompletely blocks the e receptors unlike amiridex [sic] (reason the aromatase inhibitors were initially developed)."
That in combination with this comment later in the same paragraph:
Again implying that Arimidex 100% blocks the estrogen receptor.
That is why I have asked him to clarify. He does not wish to do so. That is fine. I hope you're right and it was just a brain fart/typo, but from other posts of his I have seen, that is not likely the case.
What he wrote just does not say that. I know you are not meaning to do it, but you are reading into what he wrote and that is what is leading to the misunderstanding, as I see it.
He said that Nolvadex works one particular way which is not complete; Arimidex was developed so as to work differently.
Not, so as to work in the same way but to a greater degree.
He said that Nolvadex works one particular way which is not complete; Arimidex was developed so as to work differently.
Not, so as to work in the same way but to a greater degree.
As Dr. Scally stated he is writing two thoughts together I believe. Stating that while on cycle it is good to have some estrogen present. I was just going to write this and Millard beat me to it.
mands
Dr S, B.R., and MANDS interesting how you understood the CONCEPT I was attempting to make, which was obviously
ineffective for ONE individual whose apparent primary objective was to develop some deranged contentious
arguement often observed in those are in need of either attention or medication.
He will argue with even YOU until you are blue in the face!
Regards
JIM
ineffective for ONE individual whose apparent primary objective was to develop some deranged contentious
arguement often observed in those are in need of either attention or medication.
He will argue with even YOU until you are blue in the face!
Regards
JIM
lol ok Big Chief. Your concept was correct, but your process of reaching the conclusion was based on poor understanding of the drug's mechanisms of actions. You were lucky to arrive at the conclusion that you did based on faulty reasoning. Hopefully your patients are just as lucky.
But that is all I am going to say on this piece. I only want to help people on this forum--side tracking ends now.
mac111
New Member
:banghead:
im guessing your some teen armed with forum broscience?
lulz what? You have an (alleged) medical doctor on this forum stating that arimidex blocks an estrogen receptor, and its ME that is armed with bro science? My sides are hurting I'm laughing so hard. Are you really that stupid? You seem to be in good company.
