AI's

[Mr. Humdiddly]

I don't know if you and I agreeing on things is good for business. lol

No worries this sparse bit of common ground give us somewhere to stand for our altercations on other topics.

 

[jimbo79]

bump

 

[farmgorgon]

Hi. I'm a newbie but have been lurking and reading in various places for a couple of years.

Am doing my first cycle for recreational purposes to gain a bit of LBM before a holiday, using dbol as 'supplement' along the lines of the various articles, 10mg ED with weekends off.

I use 1mg Adex twice a week, which I came to considering the half life, the typical dose recommended and the amount of drug I'm using.

I'm approaching the end of my third week. Gains have been limited and I'm wondering whether am using too much Adex in the circumstances as flagged by the article in the OP. I have (perhaps obviously!) no sides so far.

(Diet/ training is suitable for my goals)

Thanks

 

[RJ]

Hi. I'm a newbie but have been lurking and reading in various places for a couple of years.

Am doing my first cycle for recreational purposes to gain a bit of LBM before a holiday, using dbol as 'supplement' along the lines of the various articles, 10mg ED with weekends off.

I use 1mg Adex twice a week, which I came to considering the half life, the typical dose recommended and the amount of drug I'm using.

I'm approaching the end of my third week. Gains have been limited and I'm wondering whether am using too much Adex in the circumstances as flagged by the article in the OP. I have (perhaps obviously!) no sides so far.

(Diet/ training is suitable for my goals)

Thanks

1. start a new thread. Please don't hijack this one.
2. Dbol only sucks. Dbol @ 10mg/d is fucking retarded.
3. Your gains have been limited because of #2.
4. Obviously reading for a couple of years hasn't helped.
5. Check out the newb stickies about why test only is a great first cycle and the numerous ones about why Dbol only sucks for any cycle.

 

[Mr. Humdiddly]

1. start a new thread. Please don't hijack this one.
2. Dbol only sucks.
3. Your gains have been limited because of #2.
4. Obviously reading for a couple of years hasn't helped.
5. Check out the newb stickies about why test only is a great first cycle and the numerous ones about why Dbol only sucks for any cycle.

Ah nothing like the refreshing sense of brutality emanating from a RJH newb beat down.

 

[Hell]

Good Information...Thanks!!

 

[Furiously Skinny]

First off, that was a great read. I do have a question. Since AIs are to be used during cycle, what would happen if one were to use them for post cycle therapy? Would it just delay the onset of estrogen related effects?

Thanks for the great article!

 

[Mr. Humdiddly]

First off, that was a great read. I do have a question. Since AIs are to be used during cycle, what would happen if one were to use them for post cycle therapy? Would it just delay the onset of estrogen related effects?

Thanks for the great article!

Aromatase inhibitors stop the conversion of testosterone to estrogen. During the start of PCT you have very little endogenous testosterone. So there is not really much to convert. Pretty much a waste of money.

 

[Krazydiamond]

Great read, to the point and not too technical. Always been a adex guy but my training partner doesnt respond to anything but letro, everybodys different just got to experement a bit and find what works for you. Bump!

 

[Dark_Side]

Aromatase inhibitors stop the conversion of testosterone to estrogen. During the start of post cycle therapy (pct) you have very little endogenous testosterone. So there is not really much to convert. Pretty much a waste of money.

What about if you were running Human Chorionic Gonadotropin (HCG) throughout your post cycle therapy (pct)?

 

[RJ]

What about if you were running Human Chorionic Gonadotropin (HCG) throughout your post cycle therapy (pct)?

no good. Human Chorionic Gonadotropin (HCG) is suppressive to the HPTA, so its counter-productive DURING post cycle therapy (pct). During cycle and up to post cycle therapy (pct) is fine.

 

[Dark_Side]

no good. Human Chorionic Gonadotropin (HCG) is suppressive to the HPTA, so its counter-productive DURING post cycle therapy (pct). During cycle and up to post cycle therapy (pct) is fine.

ok. PM sent

 

[Mr. Humdiddly]

What about if you were running Human Chorionic Gonadotropin (HCG) throughout your PCT?

RJH nailed it. Human chorionic gonadotropin or Human Chorionic Gonadotropin (HCG) for short is a heterodimeric glycoprotein. Therefore it is composed of both alpha and a unique beta subunit. The alpha subunit is a biologically identical match to luteinizing hormone, thyroid stimulating hormone and follicle stimulating hormone.

Sound familiar? LH, FSH, and TSH are all glycoproteins stimulated by the HPTA. So while Human Chorionic Gonadotropin (HCG) itself is not exogenous testosterone it's results still cause a glycoprotein abundance resulting in HPTA shutdown in attempt to achieve homeostasis.

 

[Dark_Side]

RJH nailed it. Human chorionic gonadotropin or Human Chorionic Gonadotropin (HCG) for short is a heterodimeric glycoprotein. Therefore it is composed of both alpha and a unique beta subunit. The alpha subunit is a biologically identical match to luteinizing hormone, thyroid stimulating hormone and follicle stimulating hormone.

Sound familiar? LH, FSH, and TSH are all glycoproteins stimulated by the HPTA. So while Human Chorionic Gonadotropin (HCG) itself is not exogenous testosterone it's results still cause a glycoprotein abundance resulting in HPTA shutdown in attempt to achieve homeostasis.

Thanks Mr H.!
Last time I took Human Chorionic Gonadotropin (HCG), I took it coming off a 8 week PH cycle. I ended up getting it because my balls were the size of raisons. So for a post cycle therapy (pct) I took Human Chorionic Gonadotropin (HCG) with clomid.
Balls dropped an inch and I kept all my gains, so it worked well!
Now that I've joined here, for my cycle I'll take it during and up to a week before post cycle therapy (pct).
Thanks guys!

 

[CenturionHRT]

Great thread Hum.

Rated 5 stars...

 

[roidedsurfbum]

Mr. Hum...great workup on AI's! You mentioned that you use Letro yourself...which dosing pattern do you follow? Also, how counter-productive, if at all, is Letro do any gains? I ask only because a fair number of the "anti-AI crowd" like to claim that Letro will kill your cycle. Being a noob myself, and very partial to your well-educated opinion, I'd like to hear what your thoughts are on the subject.

Thanks again man

 

[Mr. Humdiddly]

Mr. Hum...great workup on AI's! You mentioned that you use Letro yourself...which dosing pattern do you follow? Also, how counter-productive, if at all, is Letro do any gains? I ask only because a fair number of the "anti-AI crowd" like to claim that Letro will kill your cycle. Being a noob myself, and very partial to your well-educated opinion, I'd like to hear what your thoughts are on the subject.

Thanks again man

I implement a .1mg dose daily approximately 1 hour prior to my TNE and Prop injects. This is to decrease aromatase prior to TNE injection. Works wonders even at 1.4g test per week. As for AI's killing gains I think my before and after picks in my steroid cycle can serve as anecdotal evidence.

 

[gorillaglue]

Nice post Humdiddly; repped as requested (scratch that-I need to spread some rep around to others first apparently). Good luck with getting newbs to use the search engine.

But there is one thing you posted that confuses me slightly; perhaps you can clarify:

Originally Posted by Mr. Humdiddly
Due to the "suicide" aromatase inhibition pertaining to exemestane misunderstandings regarding dosing have arisen. The pfizer drug trial relayed information that a 25mg dose of aromatase decreased estrogen for 3 days. However, the during that time frame estrogen was tapering back up. The cyclic life of aromatase reproduction increases during exogenous testosterone implementation. The half-life of exemestane is well documented at 9-12 hours. So daily dosing is required.

Some believe the daily use of aromatase will dip estrogen levels too low. The decreased lipid cell penetration levels of type 1 AI's such as exemestane ensure that not all aromatase can be permanently disabled.

Perhaps an analogy can help. Pretend you (exemestane) are a hitman in a drug house. However you only have the keys to certain doors in the house. Periodically new people (aromatase) spawn in the rooms. The first run you go through and kill everything and there is lots of killing. The second run through there are less people in the rooms you have access to so the people killed is less.

However the people in the locked rooms (dense lipid cells) go on making drugs (estrogen). The house's overall drug production is decreased but since you don't have the keys you can not completely halt the drug production.

Now lets apply that analogy to dosing. When you increase the dosing it is like increasing the number of hit-men and as a result more rooms in the house can be entered. Eventually with enough hit-men you could kill the entire population of the house and cease drug production.

I hope that explains why low dose usage (12.5md ED) is fine but, higher doses can cause issues.

If I am reading your comments and analogy correctly, you seem to suggest that given a large enough Aromasin dose (# of hit-men), you could eventually halt drug production completely (~100% suppression of estrogen).

New aromatase enzyme would spawn, but they would be slaughtered on the spot by the army of hit-men, so you would still be near 100% suppression of estrogen (given enough hit-men/a-sin). Hmm, but I think you are saying that the respawning of aromatase enzyme on a cycle would still outpace the slaughter rate of the now resident platoon of hit-men.

Which of the above comments are correct or incorrect?

 

[Mr. Humdiddly]

Nice post Humdiddly; repped as requested (scratch that-I need to spread some rep around to others first apparently). Good luck with getting newbs to use the search engine.

But there is one thing you posted that confuses me slightly; perhaps you can clarify:



If I am reading your comments and analogy correctly, you seem to suggest that given a large enough Aromasin dose (# of hit-men), you could eventually halt drug production completely (~100% suppression of estrogen).

New aromatase enzyme would spawn, but they would be slaughtered on the spot by the army of hit-men, so you would still be near 100% suppression of estrogen (given enough hit-men/a-sin). Hmm, but I think you are saying that the respawning of aromatase enzyme on a cycle would still outpace the slaughter rate of the now resident platoon of hit-men.

Which of the above comments are correct or incorrect?

Lol this hitman analogy has gotten a lot of response. To be honest I did it on a lark.

To answer your question though. Everyone has a different level of aromatase cyclical production. Mine tends to be very high. Now a massive dose of aromasin would render ALMOST all aromatase inactive. There are some denser adipose tissues that only letro can penetrate. This has to do with the permeability of the C20H24O2 formula for aromasin. Obviously the forced catenation of the 24 hydrogen molecules plays a role in this. If you want to know how exactly PM me it gets pretty in depth.

Unfortunately aromasin from clinicals I have read does not have a long term reservoir effect. So ED dosing would render new aromatase inert but, E3D dosing for SOME may cause estrogen levels to increase as aromatase levels increase. Some people only secrete very small amounts or aromatase or release it very sporadically.

So to answer your question dosing ED at high levels would render new aromatase inert approximately 1-2 hours after your dose for everyone but, would not be necessary for SOME people(RJH).

Still your question is purely hypothetical I am hoping because 96% reduction in aromatase over an extended period of time would lead to severe side effects associated with lack of estrones in the body.

 

[gorillaglue]

Lol this hitman analogy has gotten a lot of response. To be honest I did it on a lark.

To answer your question though. Everyone has a different level of aromatase cyclical production. Mine tends to be very high. Now a massive dose of aromasin would render ALMOST all aromatase inactive. There are some denser adipose tissues that only letro can penetrate. This has to do with the permeability of the C20H24O2 formula for aromasin. Obviously the forced catenation of the 24 hydrogen molecules plays a role in this. If you want to know how exactly PM me it gets pretty in depth.

Unfortunately aromasin from clinicals I have read does not have a long term reservoir effect. So ED dosing would render new aromatase inert but, E3D dosing for SOME may cause estrogen levels to increase as aromatase levels increase. Some people only secrete very small amounts or aromatase or release it very sporadically.

So to answer your question dosing ED at high levels would render new aromatase inert approximately 1-2 hours after your dose for everyone but, would not be necessary for SOME people(RJH).

Still your question is purely hypothetical I am hoping because 96% reduction in aromatase over an extended period of time would lead to severe side effects associated with lack of estrones in the body.

Thanks. It was definitely hypothetical. But it could explain why some people have used Aromasin successfully to treat preexisting gyno (anecdotal reports of course) after the letro "pyramid" didn't work for them.