What is best AI with least sides?

[brad1986]

Wondering what AI would be best? What specifically is the differance between arimidex /aromisin/letro?
25 yo
5'10
195
13%bf
running sustonon 500mgs/equipoise 600mgs

[ucf465]

letro is a last resort AI if u HAVE gyno and want almost all (98%) of estrogen pulled out of ur system. so dont use while on cycle cause u need estrogen to make gains unless the dreaed gyno rears its ugly head. but even then it can usually be tamed with adex or nolva (nolva is a SERM, not an AI).

between adex and aromasin , aromasin is supposedly better because it bind to SHBG which in turn frees up more testosterone . unfortunately its quite a bit more expensive dose to dose than adex.

someone correct me if im wrong here, but adex pulls out about 80% of estrogen which should more than suffice. its the cheapest too.

[Bonaparte]

Less sides? Definitely Aromasin .

[THE-DET-OAK]

Im not gonna correct you ufc but your thoughts on AI's are def off.

[markiejw]

Im not gonna correct you ufc but your thoughts on AI's are def off.

What's point of this? I too am looking for the answer on AI's. If he's wrong why would you not put out the more correct advice?

[THE-DET-OAK]

i dont want to challenge anyone cause of the bad rap i have at the moment.

adex and letro are type II inhibitors.

aromasin is a type I

type II inhibitors attach to the aromatase enzyme inhibiting it from doing its job, temporarily. it then releases the enzyme, and the enzyme can then go back to doing its job. thats why these 2 can give you a rebound. meaning once you stop them aromatase enzymes can be built high and all the sudden a swarm of estrogen hits your receptors. I do think this is talked about more than it actually happens though.

Type I is a suicidal inhibitor. this means once it attaches the aromatase enzyme it binds permanently. the enzyme gets discarded and never has a chance to do its job again. there is no rebound with aromasin.

letro CAN kill estrogen completely, but that is dose dependent. I always tell guys to at least have some in the cupboard cause its like the nuclear weapon for gyno at the right dose. small doses can effectively control estrogen without killing it, for most.

adex is the weakest.

aromasin is about 12% stronger.

for aromasin people tend to confuse "suicidal" with its potency.

here is a good anaology by my friend Mr. Hummdidly, im sure it will help you understand how it works.

"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 hitmen and as a result more rooms in the house can be entered. Eventuallly with enough hitmen you could kill the entire population of the house and cease drug production."

[THE-DET-OAK]

question for the vets, I saw this on another board a while back and always wondered. since nothing is perfect, what happens when aromasin attempts to bind to an enzyme but for some reason the binding doesnt happen. what doe this enzyme do? is its make up genetically altered? is it possible for it to run around being a bad boy doing things its not suppose to?

[marcus300]

Ive always done well with a-dex or aromasin , if I had to pick one I think i would go with aromasin IMHO, but I hate letro and it doesnt work well with me at all.

[Tlee8769]

Aromasin works fantastic for me and others i know a-dex can have a rebound effect for some and letro is to potent in my opinion for just an AI on cycle without have many sides works great for others that encounter some major estrogen effects. The clear choice for me is Aromasin a bit more expensive but if you cant afford the stuff then i doubt you can afford eating enough to get proper gains from a cycle.

[Granovich]

this is confusing lol
i used Arimidex with test e cycle and there was no rebound of what so ever.
what about a more complicated cycle like test/tren /masteron ?

[Tlee8769]

this is confusing lol
i used Arimidex with test e cycle and there was no rebound of what so ever.
what about a more complicated cycle like test/tren/masteron ?

What is so confusing about it ?

[lovbyts]

i dont want to challenge anyone cause of the bad rap i have at the moment.

adex and letro are type II inhibitors.

aromasin is a type I

type II inhibitors attach to the aromatase enzyme inhibiting it from doing its job, temporarily. it then releases the enzyme, and the enzyme can then go back to doing its job. thats why these 2 can give you a rebound. meaning once you stop them aromatase enzymes can be built high and all the sudden a swarm of estrogen hits your receptors. I do think this is talked about more than it actually happens though.

Type I is a suicidal inhibitor. this means once it attaches the aromatase enzyme it binds permanently. the enzyme gets discarded and never has a chance to do its job again. there is no rebound with aromasin.

letro CAN kill estrogen completely, but that is dose dependent. I always tell guys to at least have some in the cupboard cause its like the nuclear weapon for gyno at the right dose. small doses can effectively control estrogen without killing it, for most.

adex is the weakest.

aromasin is about 12% stronger.

for aromasin people tend to confuse "suicidal" with its potency.

here is a good anaology by my friend Mr. Hummdidly, im sure it will help you understand how it works.

"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 hitmen and as a result more rooms in the house can be entered. Eventuallly with enough hitmen you could kill the entire population of the house and cease drug production."

Good information and explanation above in bold and is exactly why I plan on having aromasin on hand from now on.

[xeroxy]

It is a good post and well explained, i'd just like to point out one fact about letro, it does not reduce estrogen by as much as is claimed (98%) it's around 46-68% in males, obviously this is dose dependant but we are of course talking about the normal doses of 2.5mg.
The 98% that is claimed and posted sometimes is from studies done on females.
Regarding the post on estrogen rebound (or lack of it) from adex, well this depends on the dosage/duration and when and what steroids were taken.
As testerone levels decrease so does the amount of aromatase and therefore estrogen, then you need to take into account the dose, duration and half life of adex, when it was used and for how long after cycle it was used and finally the half life of the aromatase enzyme itself and the amount of aromatase enzyme in the individual, which differs significantly from person to person, hence why some people suffer gyno and others do not.

[brad1986]

wow thanks guys. Never had gyno problems before this last cycle i could tell my nipples were getting sensitive by the end of my cycel but with in a few weeks i was on pct and the nolva killed what i had. But now i realize the importance of having it on hand . my bf was higher this last cycle so i think they may have contributed

[Granovich]

What is so confusing about it ?

the confusing thing is which is better to use ?

[bigpapabuff]

everyone is different, I like liquid exemestane, it works better than adex imo. It's my favorite ai to use when on a cycle.

[bigbossofdariver]

so if you were to take adex or aromasin and you took a dosage so they both equally redeuced estrogen would your test levels be the same on both of them? or is aromasin better at increasing test lvels?

[markiejw]

i dont want to challenge anyone cause of the bad rap i have at the moment.

adex and letro are type II inhibitors.

aromasin is a type I

type II inhibitors attach to the aromatase enzyme inhibiting it from doing its job, temporarily. it then releases the enzyme, and the enzyme can then go back to doing its job. thats why these 2 can give you a rebound. meaning once you stop them aromatase enzymes can be built high and all the sudden a swarm of estrogen hits your receptors. I do think this is talked about more than it actually happens though.

Type I is a suicidal inhibitor. this means once it attaches the aromatase enzyme it binds permanently. the enzyme gets discarded and never has a chance to do its job again. there is no rebound with aromasin.

letro CAN kill estrogen completely, but that is dose dependent. I always tell guys to at least have some in the cupboard cause its like the nuclear weapon for gyno at the right dose. small doses can effectively control estrogen without killing it, for most.

adex is the weakest.

aromasin is about 12% stronger.

for aromasin people tend to confuse "suicidal" with its potency.

here is a good anaology by my friend Mr. Hummdidly, im sure it will help you understand how it works.

"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 hitmen and as a result more rooms in the house can be entered. Eventuallly with enough hitmen you could kill the entire population of the house and cease drug production."

Thanks for breaking this down TDO. Great post.

[THE-DET-OAK]

so if you were to take adex or aromasin and you took a dosage so they both equally redeuced estrogen would your test levels be the same on both of them? or is aromasin better at increasing test lvels?

dont worry about which one increases T levels, on a cycle the difference is minimal. besides regardless of what you use to lower estrogen, it will have the same effect, since the increase is due to the reduction in T conversion. so the answer to your 1st question is yes. Aromasin is that best at lowering SHBG though, due to some recent conversation's with Swifto though I am beginning to question how important that really is in most cases.

[AbusedYam]

I use adex at .25, but it kinda made me have low energy the next day

[Ashop]

Wondering what AI would be best? What specifically is the differance between arimidex /aromisin/letro?
25 yo
5'10
195
13%bf
running sustonon 500mgs/equipoise 600mgs

I like ARIMIDEX real well.

[bigbossofdariver]

dont worry about which one increases T levels, on a cycle the difference is minimal. besides regardless of what you use to lower estrogen, it will have the same effect, since the increase is due to the reduction in T conversion. so the answer to your 1st question is yes. Aromasin is that best at lowering SHBG though, due to some recent conversation's with Swifto though I am beginning to question how important that really is in most cases.

thanks man, and im actually wondering becuase my estrogen levels are extremely high and i have never even cycled before. ordered some adex cpl days ago from arr gonna be running half a dose eod. didnt know if there was that big of a difference.

[THE-DET-OAK]

how old are you? have you ever done PH's?

[bigbossofdariver]

how old are you? have you ever done PH's?

no nothing, alrdy been to a doctor and he refered me to an endo. i made a thread asking for advice on the hrt section. im pretty sure i got this under control. but im 19 and my estrodial was 90.

[THE-DET-OAK]

thats crazy man, just so you know the AI will not work forever, eventually the negative feedback loop will catch up with you and your body will just produce more aromatase enzymes.

its prolly lifestyle choices, poor diet or just bad luck.

you should read the warrior diet, there are alot of estrogenic foods. meaning they can cause your E to get high. not too mention alot of plastics can do the same thing. conversely there are alot of antiestrogenic foods. if you could fix your E without an AI it would be beneficial in the long run and raise your total test.

[bigbossofdariver]

had no idea that AI's could make your body produce more estrogen, still learning been reading as much as i can the last couple months. but i have been changing my diet and losing the body fat. will probably get tested again once i get to around 10 percent bodyfat.

[THE-DET-OAK]

had no idea that AI's could make your body produce more estrogen, still learning been reading as much as i can the last couple months. but i have been changing my diet and losing the body fat. will probably get tested again once i get to around 10 percent bodyfat.

its not really that it will make you produce more, its just that over a long time they will not continue to increase T levels, this is after continued use. what im saying is that an AI is not a treatment for hypogonadism.

[bigbossofdariver]

its not really that it will make you produce more, its just that over a long time they will not continue to increase T levels, this is after continued use. what im saying is that an AI is not a treatment for hypogonadism.

im pretty sure my test levels are just fine, but i will def keep that in mind.will be getting blood test done every 6 months or so to keep things regulated.

[THE-DET-OAK]

i doubt your T levels are fine if your E is triple what it is suppose to be. the normal male should convert about 3%. your doing 9% where do you think your body is getting the the other 6% from????? I could be wrong but i doubt it. do you have a high BF%?

here is some info you need read up on.

This case illustrates the challenges in diagnosing and treating infertility in the setting of obesity. Given the unique physiologic connections between adiposity, increased conversion of testosterone to estradiol, and the effect this increase has on suppressing gonadotropin release and spermatogenesis, treatment of infertility in this population differs from that of most men with infertility. The off-label use of aromatase inhibitors to decrease peripheral conversion of testosterone to estradiol provides a unique method of manipulating the normal regulatory mechanisms of the hypothalamic–pituitary–gonadal axis to promote endogenous normalization of testosterone levels and to enhance spermatogenesis and fertility. This case suggests that aromatase inhibition could be an effective treatment for infertility in the setting of obesity-related hypogonadotropic hypogonadism. Data concerning the safety and efficacy of long-term use of aromatase inhibitors for the treatment of hypogonadism is, however, currently lacking and placebo-controlled trials are needed; therefore, even if semen parameters improve with aromatase inhibitor therapy, once fertility is achieved we recommend conventional testosterone therapy with close follow-up for long-term treatment of hypogonadism.

http://www.nature.com/nrendo/journal...ndmet0844.html

[bigbossofdariver]

yes my body fat is quite high, thanks for the article good read. so you think my endo will prescribe trt?

[Bullseye Forever]

I really like the Aromasin myself better

[slimshady01]

thanks man, and im actually wondering becuase my estrogen levels are extremely high and i have never even cycled before. ordered some adex cpl days ago from arr gonna be running half a dose eod. didnt know if there was that big of a difference.

Your not taking propecia are you ?

[THE-DET-OAK]

yes my body fat is quite high, thanks for the article good read. so you think my endo will prescribe trt?

even if he does i dont think he should do it. like i said I think there is a good chance you can fix a lot of this with diet

[Swifto]

It is a good post and well explained, i'd just like to point out one fact about letro, it does not reduce estrogen by as much as is claimed (98%) it's around 46-68% in males, obviously this is dose dependant but we are of course talking about the normal doses of 2.5mg.
The 98% that is claimed and posted sometimes is from studies done on females.
Regarding the post on estrogen rebound (or lack of it) from adex, well this depends on the dosage/duration and when and what steroids were taken.
As testerone levels decrease so does the amount of aromatase and therefore estrogen, then you need to take into account the dose, duration and half life of adex, when it was used and for how long after cycle it was used and finally the half life of the aromatase enzyme itself and the amount of aromatase enzyme in the individual, which differs significantly from person to person, hence why some people suffer gyno and others do not.

It also lowers estrogen to "undetecable levels in males", as shown in this study.

I do not have the full paper, but would be very interested if you were able to find it, then tell me the dose used and how much estrogen was suppressed.

thats crazy man, just so you know the AI will not work forever, eventually the negative feedback loop will catch up with you and your body will just produce more aromatase enzymes.

its prolly lifestyle choices, poor diet or just bad luck.

you should read the warrior diet, there are alot of estrogenic foods. meaning they can cause your E to get high. not too mention alot of plastics can do the same thing. conversely there are alot of antiestrogenic foods. if you could fix your E without an AI it would be beneficial in the long run and raise your total test.

The poxy search function isnt working right now, but when I can locate my post on anti-aromotase foods and the attached comparable study, I will post it here.

its not really that it will make you produce more, its just that over a long time they will not continue to increase T levels, this is after continued use. what im saying is that an AI is not a treatment for hypogonadism.

AI's have been used to treat hypogonadism by changing the androgen:estrogen ratio.

Here one study in the "Therapeutic Uses of AI's in males".

Here's another on obese men quadrupling their endogenous T levels. Thats 1 2.5mg tab, 1x week.

There are plenty more on AI's treating hypogonadism and this is a treatment many Endo's suggest, after or before SERM treatment for T normalization.

[Swifto]

My choice:

Aromasin 10mg/ED or EOD. Even though the half life is 27 hours, yes.

Letro and Tamox should always be kept on hand.

[THE-DET-OAK]

Hey Swifto, do you think the AI will work for long periods? I am surprised endo's would hand out an AI for hypo. no studies are longer than about 12 weeks. if you look at the study i posted, they did treat obese mean with arimadex, TT levels rose and so did spermatogenesis. They also go on to say that treatment effects are different in non-obese patients.

they go on to say long term treatment has not yet been studied long enough. and they do not suggest it. the study is recent.

if you look at the study of long term treatment in male monkeys, sperm and TT drops off at about day 85. and is not as effective in the long run.

so IMO i think it will eventually catch up with you, and long term aromatase inhibition may be bad for you as well.

[Swifto]

Hey Swifto, do you think the AI will work for long periods? no studies are longer than about 12 weeks. if you look what at the study i posted, they did treat obese mean with arimadex, TT levels rose and so did spermatogenesis.

they go on to say long term treatment has not yet been studied long enough.

if you look at the study of long term treatment in male monkeys, sperm and TT drops off at about day 85. and is not as effective in the long run.

so IMO i think it will eventually catch up with you, and long term aromatase inhibition may be bad for you as well.

I havent seen the full papaer, but there is a study done using Arimidex over 24 months.

http://clinicaltrials.gov/ct2/show/NCT00136695

If you, or some one with access can get hold of it, it would almost certainly shed some light on the long term effects AI's posses on endo. T.

Here's one on Arimidex over 12 weeks.

J Clin Endocrinol Metab. 2004 Mar;89(3):1174-80.

Effects of aromatase inhibition in elderly men with low or borderline-low serum testosterone levels.

Leder BZ, Rohrer JL, Rubin SD, Gallo J, Longcope C.
Source
Endocrine Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.

Abstract

As men age, serum testosterone levels decrease, a factor that may contribute to some aspects of age-related physiological deterioration. Although androgen replacement has been shown to have beneficial effects in frankly hypogonadal men, its use in elderly men with borderline hypogonadism is controversial. Furthermore, current testosterone replacement methods have important limitations. We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62-74 yr) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14). Hormone levels, quality of life (MOS Short-Form Health Survey), sexual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups. Mean +/- SD bioavailable testosterone increased from 99 +/- 31 to 207 +/- 65 ng/dl in group 1 and from 115 +/- 37 to 178 +/- 55 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.054 group 1 vs. group 2). Total testosterone levels increased from 343 +/- 61 to 572 +/- 139 ng/dl in group 1 and from 397 +/- 106 to 520 +/- 91 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.012 group 1 vs. group 2). Serum estradiol levels decreased from 26 +/- 8 to 17 +/- 6 pg/ml in group 1 and from 27 +/- 8 to 17 +/- 5 pg/ml in group 2 (P < 0.001 vs. placebo for both groups and P = NS group 1 vs. group 2). Serum LH levels increased from 5.1 +/- 4.8 to 7.9 +/- 6.5 U/liter and from 4.1 +/- 1.6 to 7.2 +/- 2.8 U/liter in groups 1 and 2, respectively (P = 0.007 group 1 vs. placebo, P = 0.003 group 2 vs. placebo, and P = NS group 1 vs. group 2). Scores for hematocrit, MOS Short-Form Health Survey, International Index of Erectile Function, and American Urological Association Symptom Index Score did not change. Serum prostate-specific antigen levels increased in group 2 only (1.7 +/- 1.0 to 2.2 +/- 1.5 ng/ml, P = 0.031, compared with placebo). These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined.

Full: http://jcem.endojournals.org/cgi/content/full/89/3/1174)



Interesting to note there isnt much difference between the 1mg/ED and 1mg/wk oral protocol's.


I dont see why longer term protocol's would prove inferior, or suddenly stop after 12 weeks.

Estrogen is a carcinogen and needs to be kept in normal or just below normal ranges. Not zero.

[THE-DET-OAK]

i will look into getting that for sure. the only thing I have been able to go off up until now was the one on male monkeys, and it just seemed like results tapered down. that is where i came up with it wont work for long-term. I know male monkeys can not be directly correlated, so im def open to the new one you pointed out on males, but sometimes they can give you an idea.

Abstract
The role/need for estrogen in regulating testicular function of adult male bonnet monkeys (M. radiata) has been investigated by dosing orally a group of five normal males 2.5 mgs of CGP 47645, a long-acting nonsteroidal aromatase inhibitor (AI), once every 5 days for over 150 days. Such treatment resulted in a 10-fold increment in nocturnal serum testosterone (T) levels, which were sustained for 85 days of treatment, and a twofold increment in basal serum T levels was present throughout the 150 days of treatment. Analysis of ejaculated semen showed a marked reduction (90%) in sperm counts in four out of five monkeys between Days 55–85 of treatment. During this period, the motility score also was markedly reduced from a normal score of 3-5 to 0-2. Flow cytometric analysis of testicular germ cells obtained from biopsy tissue taken on Days 63 and 120 indicated a marked reduction only in elongating/elongated spermatid population (compared to Day 0 values), suggesting inhibition in spermiogenic process. Epididymal sperm maturation also seemed effected as sperm chromatin, on flow cytometric analysis for decondensability following exposure to 5 mM dithiotreitol, showed to be in a hypercondensed state. This study thus indicates that estrogen has an important role in providing normal testicular and sperm function in the primate.

[Swifto]

See what you can find, but that study may actually be ongoing, hence the reason there is no abstract at present.

i will look into getting that for sure. the only thing I have been able to go off up until now was the one on male monkeys, and it just seemed like results tapered down. that is where i came up with it wont work for long-term. I know male monkeys can not be directly correlated, so im def open to the new one you pointed out on males, but sometimes they can give you an idea.

Abstract
The role/need for estrogen in regulating testicular function of adult male bonnet monkeys (M. radiata) has been investigated by dosing orally a group of five normal males 2.5 mgs of CGP 47645, a long-acting nonsteroidal aromatase inhibitor (AI), once every 5 days for over 150 days. Such treatment resulted in a 10-fold increment in nocturnal serum testosterone (T) levels, which were sustained for 85 days of treatment, and a twofold increment in basal serum T levels was present throughout the 150 days of treatment. Analysis of ejaculated semen showed a marked reduction (90%) in sperm counts in four out of five monkeys between Days 55–85 of treatment. During this period, the motility score also was markedly reduced from a normal score of 3-5 to 0-2. Flow cytometric analysis of testicular germ cells obtained from biopsy tissue taken on Days 63 and 120 indicated a marked reduction only in elongating/elongated spermatid population (compared to Day 0 values), suggesting inhibition in spermiogenic process. Epididymal sperm maturation also seemed effected as sperm chromatin, on flow cytometric analysis for decondensability following exposure to 5 mM dithiotreitol, showed to be in a hypercondensed state. This study thus indicates that estrogen has an important role in providing normal testicular and sperm function in the primate.

[Swifto]

Study is still on going...

So when its published we will know more...