The COMPLETE AI list... or is it?

Which AI is your favorite in your PCT arsenal?

  • ATD

    Votes: 20 15.6%
  • 6 oxo

    Votes: 34 26.6%
  • 6 bromo

    Votes: 18 14.1%
  • Formestane

    Votes: 19 14.8%
  • Research Chem Steroidal

    Votes: 18 14.1%
  • Research Chem NON-steroidal

    Votes: 19 14.8%

  • Total voters
    128
celc5

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Which AI do you prefer in your post cycle therapy arsenal?

I'm not really asking about serms, test booster, or cort control... UNLESS these choices affect which AI you use :head:

Let's get the opinions... pros and cons will generate discussion!!! :study:
 
TripDog

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armidex....easiest on lipids,and cheaper that overhyped marketing bullsh*t supplements
 
Rodja

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I though Aromasin was easiest on the liver and lipids?:think:
 
TripDog

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I though Aromasin was easiest on the liver and lipids?:think:
i think they're both rather easy.....compared to say..letro
 
bpmartyr

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Arimidex (Anastrozole) is a non-steroidal AI. I was under the impression that it is suppressive and should not be used in post cycle therapy.

Exemestane (Aromasin) is steroidal and would be better suited to PCT - again, from my limited understanding.

That being said, I don't use AI's in PCT. SERM only camp here. Didn't see a poll option for: "none of the above". :)
 
celc5

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Fellas, are 6brom/6oxo/ATD hard on liver and lipids? I've never heard this mentioned with typical AI chatter (of course I'm less familiar with the research chems so I may just be ignorant).

BP, how do I add to the poll list? I wasn't thinking about actually not using an AI in post cycle therapy. I'd like hear your logic if you don't mind... or if you've discussed this already, a link would also rock :head:
 
bpmartyr

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Fellas, are 6brom/6oxo/ATD hard on liver and lipids? I've never heard this mentioned with typical AI chatter (of course I'm less familiar with the research chems so I may just be ignorant).

BP, how do I add to the poll list? I wasn't thinking about actually not using an AI in post cycle therapy. I'd like hear your logic if you don't mind... or if you've discussed this already, a link would also rock :head:
Don't know on the poll editing question.

AI' are typically harder on the lipids while SERMs stress the liver and generally improve lipids.

There have been many discussions here debating the topic of AI use in PCT. There are intelligent people and arguments on both sides. My side, in short, feels dropping estrogen too low is unhealthy and believe a SERM alone is enough to jumpstart the HPTA. The compounds cycled can alter the composition of hormone levels present at the inception of PCT. Generally, the majority of the people on these boards are running short oral cycles with no aromatizing compounds. Since your already shut down and have no testosterone for your body to convert to estrogen, and your steroid is not converting, you have low estrogen to begin with. Now your pumping yourself full of an AI and putting a damper on your bodies ability to produce any estrogen from the testosterone you start to produce somewhere in the PCT. I would assume, with our bodies being as efficient as they are, that aromatase would be increased in an attempt to get the estrogen you need and still have not been getting. So now your PCT is finished and your pumping out higher than normal aromatase which acts on your rejuvenated test levels.

Estrogen should be controlled not eliminated. It is necessary and helpful at normal levels.


Quote:
Originally Posted by Dr. John
Using an AI during post cycle therapy, as many advocate, lowers E too much, thereby extending the time of Lipid Profile damage, endothelial dysfunction, and lowered estrogen in neurological tissues (dangerous to cognitive function--permanently). IMPO, estrogen antagonism should be the first line therapy.
 
celc5

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I like your point about the short oral cycles. I'd guess that they cause some SUPRESSION but rarely shut down. Problem is, most post cycle philosophy is aimed at combating complete shutdown.

Also, I wonder if estrogen actually rebounds as intensely and quickly as it seems. I've seen AI philosophies with no serm where the AI is ramped down (ie 75,50,50,25 ATD). So this philosophy says estrogen rebounds HARD and FAST :think: Overkill on the AI?

In the popular AI inverse to serm theory, I see a more intelligent plan. But it seems that mild gyno sometimes pops up AFTER even a seemingly solid post cycle plan... hence a delayed estrogen rebound. Some taper after the ramp to avoid the rebound. Looks good IMO.

BP what about compromising and running a low dose non steroidal AI starting about 3 weeks into post cycle and running it for 3 or 4 weeks. I'm not advocating, just trying to understand as I'm new to "underground world" of cycling. :cheers:
 
bpmartyr

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BP what about compromising and running a low dose non steroidal AI starting about 3 weeks into post cycle and running it for 3 or 4 weeks. :
Did you mean steroidal? 6-Oxo, 6bromo and ATD are steroidal.

I actually really like running the NHA stack right after PCT.
 
celc5

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Did you mean steroidal? 6-Oxo, 6bromo and ATD are steroidal.

I actually really like running the NHA stack right after post cycle therapy.
yup. nha immediately AFTER post cycle therapy (rather than during) is along the lines of what I was getting at :thumbsup:

any thoughts on suppression vs. shutdown per my blabbering in post #8?

any thoughts on how intensely and/or how quickly estrogen rebounds?
 
bpmartyr

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6-oxo affect lipids ? are you sure ?
I am not certain, no. According to Ergo, it does not effect them much.

From a writeup by PA:

No evidence of acute toxicity

A complete metabolic analysis was done examining changes in blood cells and lipids, liver function, kidney function, and immune function. No adverse changes were observed in any of these areas over the course of the three weeks. In fact, indications are that liver function actually improved slightly, and average cholesterol level dropped by about 26 points. That is an 11.6% reduction in cholesterol in 3 weeks! The explanation for this dramatic improvement is not known at this time.

I don't know what ratio of LDL/HDL that 26 point drop was. If my HDL dropped 26 points I would not be too happy. Likely it was mostly HDL however knowing Patrick.

In other news;
A little pubmed info on the "big 3" non-steroidal:

South Manchester University Hospital, Academic Surgery, Education and Research Centre, Southmoor Road, Manchester M23 9LT, UK. [email protected]

Oestrogen is known to influence blood lipid levels and though its cardioprotective effects are less clear than once thought, there remains concern that reduction of oestrogen levels during hormonal treatment for breast cancer may have an adverse effect on cardiovascular risk. While tamoxifen has been shown to improve lipid profiles, the aromatase inhibitors have a very different mode of action and do not possess the oestrogen-agonistic effects of tamoxifen. At present, there are few data on the effects of these agents on lipid profiles. Available data are mixed, but suggest that the different aromatase inhibitors have different effects on lipid profiles. Some studies show anastrozole as generally having little effect on lipids, while others have indicated adverse effects on lipid profiles/increased hypercholesterolaemia. Letrozole has been associated with adverse effects on lipid profiles in some studies, including BIG 1-98, but short-term data from randomised trials do not show increased cardiovascular morbidity. By contrast, exemestane, which has been studied in slightly more detail, may either have little effect or may be associated with slightly improved lipid profiles. In general, the changes have been small and are likely to be of little relevance in women with advanced breast cancer, but if these agents come to be used in early breast cancer, their impact on lipid profiles may become more important. Many studies are currently underway with the aromatase inhibitors, with safety assessments including monitoring lipid levels. The results of these studies are keenly awaited.

PMID: 16100522 [PubMed - indexed for MEDLINE]
 
celc5

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BP AWESOME posts my friend :cheers:

Does anyone know why 6oxo/trione is not that popular anymore? It seems like a solid AI to me :think:
 
matthew76

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My thoughts are that 6 OXO IS popular - ATD is not because of it's "libido" concerns.

SERM here - but also add 6 OXO

Following PH cycle, my supplement intake is consist of (After PCT) - IGF-2 / RPM / X-Lean
 
Last edited:
pistonpump

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im with 6oxo based on what i have used for PCT. I believe 6oxo actually boosts LH by some mechanism. ATD can go to hell. Id like to use Aromasin but cost kinda held me back, i will someday. Aromasin would be better with a SERM from what i have read in the past. Arimidex has a negative influence on IGF levels btw and aromasin does not and is better on the lipids.
 
celc5

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piston, you mentioned that you like 6oxo. Why do you think aromasin would be better with a serm? So you would use 6oxo if you didn't use a serm but would prefer aromasin if serm were used... UNconfuse me bud :lol:
 
pistonpump

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i like 6oxo yeah but i would take aromasin over it. I have read studies on aromasin. I have also read posts from experienced guys explaining why they think its better. It works in conjuction with a serm...im sorry i cant remember exact reasons lol but yeah thats what i go by. I have yet to try it tho so its hard to say. IMO there might be a reason its so expensive. I have a cheap source for it so itll probably be in my arsenal soon. 12.5mg eod.

EDIT: SERMs lower IGF levels while Aromasin has a postive effect on them, thats one reason.
 
neoborn

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armidex....easiest on lipids,and cheaper that overhyped marketing bullsh*t supplements
Hey! You wouldn't be directing that "bullsh!t " etc towards Formestane would you? hmmmm?

When Forms in the house everyone :box: :box: :box:

:D

Much Love,

Neoborn

P.S I love Form
 

pudzian2

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im with 6oxo based on what i have used for post cycle therapy. I believe 6oxo actually boosts LH by some mechanism. ATD can go to hell. Id like to use Aromasin but cost kinda held me back, i will someday. Aromasin would be better with a SERM from what i have read in the past. Arimidex has a negative influence on IGF levels btw and aromasin does not and is better on the lipids.
what is your 6oxo dosing protocol if using with a SERM in PCT
 
pistonpump

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hard to say i cant quite remember how i used it last time. probably 600 then tapered down. Im experimenting every cycle now to find out what works best for me, just winging it so to speak. Thing is you dont want to eradicate estrogen so when using a SERM 600mg might not be a good idea when the SERM dose is high. Maybe when the serm starts to drop down (week3) add maybe 400mg and taper down from there for 4 weeks, if i were to use it in PCT with a SERM again that is.
 

pudzian2

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hard to say i cant quite remember how i used it last time. probably 600 then tapered down. Im experimenting every cycle now to find out what works best for me, just winging it so to speak. Thing is you dont want to eradicate estrogen so when using a SERM 600mg might not be a good idea when the SERM dose is high. Maybe when the serm starts to drop down (week3) add maybe 400mg and taper down from there for 4 weeks, if i were to use it in post cycle therapy with a SERM again that is.
Yea I suppose it will take trial and error for every individual to find what PCT works best for them
 
pistonpump

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Yea I suppose it will take trial and error for every individual to find what post cycle therapy works best for them
even with cycling...this cycle i have been taking different approaches and it has worked well. Ill be doing a new PCT approach as well.
 
celc5

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what is your 6oxo dosing protocol if using with a SERM in post cycle therapy
I was throwing around some ideas for using 6oxo inverse to torem in my next post cycle plan. I'll start low and ramp up week to week. I'm guessing that I'll peak my 6oxo dosage around 500 or 600 in week 3 and 4 before tapering. My joints are particularly sensitive to 6oxo though so I may never get the dosage as high as I would like.
 

pudzian2

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I was throwing around some ideas for using 6oxo inverse to torem in my next post cycle plan. I'll start low and ramp up week to week. I'm guessing that I'll peak my 6oxo dosage around 500 or 600 in week 3 and 4 before tapering. My joints are particularly sensitive to 6oxo though so I may never get the dosage as high as I would like.
Yea i hear you. My joints are sensitive without any hormonal influence. I have to be careful with AI's
 
Force of Green

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Hey! You wouldn't be directing that "bullsh!t " etc towards Formestane would you? hmmmm?

When Forms in the house everyone :box: :box: :box:

:D

Much Love,

Neoborn

P.S I love Form
I personally think formestane works for PCT. It doesn't erradicate estrogen and it slightly raises IGF-1 levels. Many studies show that it DOES raise LH levels at proper doses. The pharmaceutical injectible version has been discontinued because of the better options for treating breast cancer, but IMO it holds a VERY special place in the body building realm.

Also, many users who make injectible concoctions of formestane say that the results they get are better than what primobolan's profile promises.
 

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Couple of questions about AI:

1. Which AI is the best to eliminate gyno? Arimidex, Femara, Aromasin?

2. When using Aromasin for post cycle therapy, is using half a tablet enough? or is one whole tablet required?

3. Is it necessary to taper down Aromasin to prevent estrogen rebound? I know that Aromasin is a suicide inhibitor type, but since I read that post by celc5 on the other thread http://anabolicminds.com/forum/post-cycle-therapy/76880-otc-ais-pros.html stating that he has even seen ATD (which is supposed to be a suicide type) causing an estrogen rebound, that raises some question whether or not aromasin is also needed to be tapered down or not?
 

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Arimidex (Anastrozole) is a non-steroidal AI. I was under the impression that it is suppressive and should not be used in post cycle therapy.
Hmm... my impression was that adex, like formestane, is a 3rd gen AI, which means it's selective, and does not inhibit adrenocorticosteroid synthesis like 1st gen AIs (such as aminoglutethimide). i don't know about ATD and 6-OXO, though, maybe some sides attributed to those are because of that?

as on being suppressive... i wouldn't know about that, some studies i've seen do not seem to support this effect in vivo. see:

Effect of chronic administration of an aromatase i...[J Endocrinol. 2000] - PubMed Result (but see the comment on estrogen)

Estrogen suppression in males: metabolic effects. [J Clin Endocrinol Metab. 2000] - PubMed Result

E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T, sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change.
if it were suppressive, shouldn't LH/FSH decrease?

also: The effect of aromatase inhibition on sex steroids...[J Clin Endocrinol Metab. 2001] - PubMed Result

After 9 weeks of treatment, there were significant decreases in estradiol, estrone, and sex hormone-binding globulin levels by 29%, 73%, and 16%, respectively, and total testosterone increased significantly by 56%.
Effects of aromatase inhibition in elderly men wit...[J Clin Endocrinol Metab. 2004] - PubMed Result

Mean bioavailable testosterone increased from 99 to 207 in group 1 and from 115 to 178 ng/dl in group 2. Total testosterone levels increased from 343 to 572 ng/dl in group 1 and from 397 to 520 ng/dl in group 2. Serum estradiol levels decreased from 26 to 17 pg/ml in group 1 and from 27 to 17 pg/ml in group 2. Serum LH levels increased from 5.1 to 7.9 U/liter and from 4.1 to 7.2 U/liter in groups 1 and 2, respectively. <...>. Serum estradiol levels decrease modestly but remain within the normal male range.
also pretty interesting: Short-term aromatase-enzyme blockade unmasks impai...[J Clin Endocrinol Metab. 2005] - PubMed Result

Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% and elevated mean LH concentrations by 2.1-fold in both the young and older cohorts. <...> In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men.
in the light of those documented LH improvements even with short-term administration at recommended dose, do you have any link/study which shows in which way it would be suppressive? woudn't suppression indicate activity on the HPTA, which seems simple to imagine for a steroidal AI or its metabolites, but not that simple for a non-steroidal AI (how does that bind to the AR, for example?).

Also, I wonder if estrogen actually rebounds as intensely and quickly as it seems. I've seen AI philosophies with no serm where the AI is ramped down (ie 75,50,50,25 ATD). So this philosophy says estrogen rebounds HARD and FAST :think: Overkill on the AI?
maybe i can provide some input in this:

1. depending on the AI, this does not necessarily completely destroy/eliminate estrogen. if you look at many of the available studies (see above), one does find that estrogen is decresed by certain amount, depending on the actual AI applied and the dosing scheme used. if applied carefully, AIs can be helpful in actually controlling (not erasing) estrogen while helping to raise LH, FSH and Test.

2. the idea behind the tapered-down aproach (which was mainly intended for those who don't want or can't use a SERM)is as follows: after a cycle of a non-aromatizing compound, there is very little estrogen in the system. bot testh and e are low. however, aromatase and estrogen activity may (and this is the big question mark) be upgraded. i.e. what little test you produce initially is immediately/to a large amount converted to e (and DHT, obviously). with the short half-life of orals, this would indicate a phase where the anabolic effects of the oral is quickly vanishing, whereas the test is still to low (if its converted "away" to e) to excert an anabolic effect, thusly making it difficult to hang unto gains made on-cycle.

the AI is added to prevent/reduce conversion of test to e, to help the t to remain unconverted and to maintain gains. the ramp-down of the AI in the following phase is then intended to allow the body to slowly normalize aromatase and e levels over time, while minimizing the risk of rebound. i.e. the idea is not to recover from total shutdown as quickly as possible, but to help maintains gains and normalize aromatase and e levels in a controlled and consistent manner over time.

3. SERMs notoriousy have very long half-lifes (between 5 and 9 days, depending on the exact compound). while you have peak levels a few hours after ingestion, stable serum levels are only reached after prolonged ingestion. the idea to start high on the AI in AI/SERM combined PCT protocols is to allow the SERM a few days to build up to effective serum levels, while preventing conversion of test (little as it may be) to e, at a time when estrogen receptor activity may be upgraded and against which no sufficient protection may be initially available.

In the popular AI inverse to serm theory, I see a more intelligent plan. But it seems that mild gyno sometimes pops up AFTER even a seemingly solid post cycle plan... hence a delayed estrogen rebound. Some taper after the ramp to avoid the rebound. Looks good IMO.
i'm always a strong proponent for tapering down AIs, regardless if used standalone, starting from high-point, or after slow ramp-up. the issue i have with ramp-up/taper-down is that this makes for an excessively long AI phase - if you consider a 4 week cycle of a non-aromatizing anti-estrogenic compound such as SD or Havoc as being part of this. then you'll have cycle time + ramp up time + taper down time... possibly pretty long toi be low on e.

finally, if you ramp up the ai while tapering down the SERM, do you not delay the increase in estrogen (against which the serm is supposed to protect you, breast- and hpta-wise) into the phase where you already have low or no serum levels of the SERM left in the system? why then have a SERM in the first place, if you delay estrogen production until the SERM is gone?

personally, and i am in no way advocating this as the best solution, nor am i actually convinced that it is, i currently believe that if you want to combine SERM and AI it's best to start the AI moderately high (see above for the reasoning), and to taper it down such as to allow estrogen production to reoccur/increase while the SERM is still in full effect to protect the HPTA and breast tissue from its effects. one also has to take into consideration the long half-life of SERMs here, and the build-up of serum levels of the SERM over time.

T.I.
 
celc5

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Wow, now THAT is the info that we're looking for!

Must spread some reps before giving to Interlocutor again.

:goodpost:
 
Kevf

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Language-barrier I guess (dutch ):

What do AI and Serm stand for?
 

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Arimidex (Anastrozole) is a non-steroidal AI. I was under the impression that it is suppressive and should not be used in post cycle therapy.

Exemestane (Aromasin) is steroidal and would be better suited to PCT - again, from my limited understanding.

That being said, I don't use AI's in PCT. SERM only camp here. Didn't see a poll option for: "none of the above". :)
Why no AI's in PCT?
 
Force of Green

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Why no AI's in PCT?
Estrogen is present in the male body for certain reasons. AIs don't assist in the body's ability to regain homeostasis like the SERMs. Simply erradicating estrogen is not a good idea IMO.
 

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could anyone tell me if liquid torem is any good and if so how would you dose it in ml's and should I taper down 6-oxo after or during the torem?
Does this also mean that after 4 week sd cycle that the serm is really a (just in case) some of the test I might have could be coverting into E? If it dosen't aromatize, and test and e are low what purpose does the serm have? sorry if this sounds dumb!
 
swankinrosco

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bump so bow i'm confused, to AI or not to AI after my 3 week SD cycle?
 
celc5

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bump so bow i'm confused, to AI or not to AI after my 3 week SD cycle?
Just something to consider, I just bridged Havoc into SD. The superdrol shut me down HARD in only about a 10 or 12 day period.

For pct, I ran a typical torem taper and added in a low dose of 6oxo around day 7 or 8. I "felt" as though I recovered VERY quickly in terms of eliminating all ON cycle sides within 2-3 days (including a fast bounce back of testicular mass).

For the first 2-3 weeks of pct, libido was absolutely FLATLINED with no response to Paravol, Ejaculoid, or various trib based libido enhancers (all of which I typically would respond very well to). Luckily I had stock piled some Aspire "just in case" a scenario like this ever happened :run:

In regards to your question and relavent to this thread, I suspect that my AX Superdrol simply squashed estrogen. In addition I suspect that, opposite of what the consensus is, Torem also squashes my libido (again, maybe eradicating estrogen???). On the flipside, the nut size returned quickly so I'd say the Torem probably played a role in that.

Again relavent to this thread, I'd say with your SD plan, I would follow BPMarty's philsophy (posted on page 1). Taper your SERM and throw in a low dose of AI around week 3 or 4 of pct and taper for a few weeks.

SD is a decieving beast, use it cautiously. I won't be running it ever again as the explosiveness isn't necessary for me. I think I can almost as good of gains on Halo and epithios with less consequence in the future.
 
BigMfer

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Arimidex (Anastrozole) is a non-steroidal AI. I was under the impression that it is suppressive and should not be used in post cycle therapy.

Exemestane (Aromasin) is steroidal and would be better suited to PCT - again, from my limited understanding.
BUMP
 
crazyfool405

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Don't know on the poll editing question.

AI' are typically harder on the lipids while SERMs stress the liver and generally improve lipids.

There have been many discussions here debating the topic of AI use in PCT. There are intelligent people and arguments on both sides. My side, in short, feels dropping estrogen too low is unhealthy and believe a SERM alone is enough to jumpstart the HPTA. The compounds cycled can alter the composition of hormone levels present at the inception of PCT. Generally, the majority of the people on these boards are running short oral cycles with no aromatizing compounds. Since your already shut down and have no testosterone for your body to convert to estrogen, and your steroid is not converting, you have low estrogen to begin with. Now your pumping yourself full of an AI and putting a damper on your bodies ability to produce any estrogen from the testosterone you start to produce somewhere in the PCT. I would assume, with our bodies being as efficient as they are, that aromatase would be increased in an attempt to get the estrogen you need and still have not been getting. So now your PCT is finished and your pumping out higher than normal aromatase which acts on your rejuvenated test levels.
while what you say makes sense, steroids decrease SHBG and estradiol increases as SHBG decreases. so that sensitized the hypothamus and causes the negative feedback, control estrogen,, and SERMs have mixed agonist and antagonist sides. so a AI will only help
Estrogen should be controlled not eliminated. It is necessary and helpful at normal levels.


Quote:
Originally Posted by Dr. John
Using an AI during post cycle therapy, as many advocate, lowers E too much, thereby extending the time of Lipid Profile damage, endothelial dysfunction, and lowered estrogen in neurological tissues (dangerous to cognitive function--permanently). IMPO, estrogen antagonism should be the first line therapy.
.... bolded
 
crazyfool405

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i think i brought this back from the dead but heres a study
Pharmacology and Pharmacokinetics of the Newer Generation Aromatase Inhibitors1
Aman U. Buzdar2

The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

The newer generation aromatase inhibitors (AIs) as a class show efficacy and tolerability benefits over previously established treatments inpostmenopausal women with advanced breast cancer. At clinically administered doses, the plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) are 41–48 h, 2–4 days, and 27 h, respectively. Time to steady-state plasma levels is 7 days for both anastrozole and exemestane and 60 days for letrozole. Androgenic side effects have only been reported with exemestane. Anastrozole treatment has no impact on plasma lipid levels, whereas both letrozole and exemestane have an unfavorable effect. From indirect comparisons, anastrozole shows the highest degree of selectivity compared with letrozole and exemestane, in terms of a lack of effect on adrenosteroidogenesis. To date, there are no data suggesting any major differences in clinical efficacy between the newer generation AIs anastrozole and letrozole. Based on the observed pharmacological profiles, however, it cannot be assumed that the AIs will display the same tolerability and safety profiles when given for extended periods of time in the adjuvant setting. The effects of anastrozole, letrozole, and exemestane are being investigated in the adjuvant setting, and these data will elucidate the possible long-term consequences of the pharmacological effects reported after short-term exposure.
 
celc5

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Die thread die! :numbered:
Good info keeps popping up. I don't know how people keep finding it since you can't search for just 2 characters as "AI"

Btw, avatar copycat :nutkick: ...j/p bro :)
 

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