Thank you for this @Raphael3636 !
Exemestane, sold under the name Aromasin? by Pfizer, is an orally available suicidal aromatase inhibitor. <This sentence describes exactly why exemestane is the king of Anti-E’s for bodybuilding purposes.
Because exemestane is steroidal this gives it a favorable estrogen suppression profile and confers a few really awesome benefits over other anti-estrogens both on paper and in real experience. Steroidal anti-estrogens have the benefit of being lipid-friendly and they all lower SHBG which increases the ratio of free to bound testosterone, which as many experienced BB’ers know can have a relatively profound positive impact on gains.
I think it is important to understand how drugs work in order to properly dose them, exemestane is a suicidal aromatase inhibitor, this means that it binds with aromatase enzymes and as it does so permanently disables the enzyme and destroys it. Hence the “suicidal” this chemical is like a kamikaze pilot out to destroy your aromatase enzymes which is what makes it so special.
Exemestane’s half life in the male body is actually very short (~9 hours) and it is quickly eliminated, however, since as soon as it enters your bloodstream it quickly destroys 80-90% of the aromatase enzymes present in your body, it is effective in maintaining significant reductions in estrogen for up to 72 hours after a single 25mg dose. Estrogen levels only begin to rise again after your body has begun to make new aromatase enzymes to replace the ones destro by exemestane.
There is a great study on the pharmacokinetics of exemestane in men which found the following:
-24 hours after one 25mg dose estrogen levels are reduced by 70-80%
-72 hours later estrogen levels are still 40% below baseline even though the drug itself is almost completely eliminated
-120 hours after initial dose estrogen levels return to baseline (without rebounding)
this means that you can find the timing and dosage that works for you, i’ve seen some guys recommend between 25mg ED and 12.5mg e4d, and you can see why both are effective while providing different levels of estrogen suppression, and it is this flexibility that makes exemestane such a versatile Anti-E.
BUT WAIT, there’s more. Aromasin is also a badass PCT drug! In males exemestane was found to increase total testosterone by ~60% after 10 days @ 25mg/day, however the same study found that while it increased total testosterone by 60% free testosterone was increased by over 100 percent! that’s right, it DOUBLES bio-available testosterone (natty of course).
I can tell you this much, when I take aromasin for PCT the results are dramatic, honestly my Libido is never absent at any point during PCT and I absolutely feel great within a matter of days, and this is taking 12.5mg ED, the only side effect i notice is stiff joints and other stiff areas
-powerful aromatase inhibitor capable of stopping gynecomastia completely on its own (for aromatizing compounds)
-has powerful bloat-reduction effects
-lowers SHBG, increasing free test & makes all other anabolic steroids more bio-available (read: more gains)
-can actually boost Libido on and off cycle
-NO adverse changes in lipid profiles for men (granted if you are using it on cycle this may be different)
-is NOT liver toxic
-no estrogen rebound
-typical aromatase inhibitor issues here include stiff joints and possibly lethargy
-more difficult to come by than a-dex or letro
Appropriate uses for Exemestane:
#1) on cycle estrogen control - that’s right, any and all estrogen related problems can and should be corrected with this compound, from gynecomastia to acne to bloat exemestane is a panacea, run it at 12.5mg e4d for gynecomastia protection and bloat control, or run it at 25mg ED for pre-contest or for gynecomastia sensitive individuals or moon face. the beauty of aromasin is it’s okay to use preventatively and not just as spot treatment for gynecomastia as it doesn’t hurt gains nearly to the degree that other Anti-E’s do, i’d still recommend using Anti-E’s only if you need them, but if you must use one throughout your cycle, you couldn’t pick a better compound to use.
#2) PCT. Aromasin is the premier PCT drug in my experience… honestly PCT is kind of fun with aromasin (maybe that’s a stretch) but it’s a breeze compared to clomid/nolva and significantly better than a-dex (more powerful and fewer sides) it works excellently with HCG - human chorionic gonadotropin - and keeps the extra aromatization from the HCG - human chorionic gonadotropin - injects at bay (you can even run higher dosages of HCG - human chorionic gonadotropin - above 500iu/inject) and another bonus is since it’s safe and comfortable to run for longer periods of time, you can stretch your PCT out to 6 or 8 weeks for suppressive cycles to make sure you get everything back in full working order
#3) gynecomastia reversal - in conjunction with a selective estrogen receptor modulator (raloxifene or tamoxifen) and/or a dihydrotestosterone derived compound aromasin can be effective in reversing/reducing existing gynecomastia
#4) off cycle testosterone boost - sometimes if i dont feel like running a cycle but still want a little extra kick i’ll take 25mg EOD for 4-6 weeks, gains aren’t improved all that greatly but significantly, but i do it more for the Libido/mental effects anyways.
#5) hypogonadism - so you’re getting older, you’ve been cycling since you were 21 and your natty test levels just never get back in the good range, but you don’t wanna go HRT??? aromasin will get you back in the game without having to take the plunge for HRT.
This is an AI you can do without its by far the harshest of all AI?s not necessarily cause your estrogen will be too low, letrozole as a compound/active ingredient is really harsh
Ever climb up the stairs and felt as if you were dying same as a 500lb man would after taking two steps? That?s what letro can do to you. My view on this is that it affects ones triglycerides, if you use letro long enough at max dose your triglycerides will be so high that even after climbing ten steps you will be struggling to breath
Only application of letro (which can be avoided/substituted with aromasin) is for contest prep, I would never use it for either bulk, cut or gyno reversal too many side effects for very little gain
Also ever took letro and still had nipple sentivity? Wonder why? Letro lowers shgb dramatically this allows free testosterone to spike and as a result free estrogen, this is the reason the letro gyno reversal protocol doesn?t work (esp when its suggested to use it for one week only). In order to have low free estrogen (Which AI?s cant lower) you need to drop your total estrogen low. However everyone trying to reverse gyno already have high estrogen and the moment you add letro you have a tonne of free estrogen in your blood stream, which can make your gyno worse… To protect against free estrogen you need a serm, that?s why you cant have gyno reversal without a serm since all AI?s lower shgb.
Keep in mind you cant use nolva with adex or letro you minimize their efficiency by 40% that doesn?t work vice versa though nolvadex efficiency stays at 100%.
Common dosage: 0.62mg ed/eod, 1.25mg ed/eod
Keep in mind all 3 serms will work in favour of your liver (Agonists) since they are mild estrogens, like said earlier estrogen is good for your liver so adding a serm will always improve your hdl/ldl. All serms don?t lower estrogen in fact they will increase your total estrogen. They also block your estro in the nipple area, but similar to the binding AI?s once that estro gets released you rebound and you end up with even higher estro than before
Agonist: Liver, uterus (female)
As I am sure you heard nolvadex reduces IGF-1 leves by 25% now that might seem like the biggest disadvantage ever but if you take into account that your liver is going to be healthier while you use it, it balances out the deduction of your igf-1 levels.
Nolvadex is more suited for pct purposes not on cycle therapy (oct) since it increases natural test levels by 60% and decreases igf-1 levels
Dosage on cycle: 20-40mg
Agonist: Liver, bone (increases bone density like deca and is a recognised treatment for osteoporosis)
Antagonist: Breast/nipple (stronger than nolva for gyno)
Raloxifene doesn?t affect igf-1 levels whatsoever, also it increases bone density but does nothing for your tendons like deca does, so it might be a double edge sword if you are not using deca along side it since by having stronger bones and muscles chance for tendon injury is higher.
Raloxifene is the ideal AI for oct since its an agonist for your bones, doesn?t affect igf-1 levels and is perfectly safe to run with a 19nor. Raloxifene shouldn?t be used in pct since it raises natural test levels by 40% only, 20% less than nolvadex
Dosage on cycle: 60mg-120mg
Nolva vs Raloxifene for HGH/IGF-1
Objective: The aim was to compare the impact of raloxifene and tamoxifen on GH-IGF-I and gonadal axes in healthy men.
Design: We conducted a randomized, open-label crossover study.
Patients and Intervention: Ten healthy men were randomized to 2-wk sequential treatment with tamoxifen (10 and 20 mg/d) and raloxifene (60 and 120 mg/d), with a 2-wk intervening washout period.
Main Outcome Measures: We measured the GH response to arginine and circulating levels of IGF-I, LH, FSH, testosterone, and SHBG.
Results: Tamoxifen, but not raloxifene, significantly reduced IGF-I levels by 25 ? 6% (P < 0.01) and increased SHBG levels by 20 ? 7% (P < 0.05) at the higher therapeutic dose. There was a nonstatistically significant trend toward a reduction in the GH response to arginine with both SERMs. Both drugs significantly increased LH, FSH, and testosterone concentrations. The mean increase in testosterone (40 vs. 25%; P < 0.05) and LH (70 vs. 30%; P < 0.01) was significantly greater with tamoxifen than with raloxifene treatment.
Conclusions: Tamoxifen, but not raloxifene, reduces IGF-I levels. Both SERMs stimulate the gonadal axis, with tamoxifen imparting a greater effect. We conclude that in therapeutic doses, raloxifene perturbs the GH and gonadal axes to a lesser degree than tamoxifen.
Nolva vs Raloxifene for gyno
OBJECTIVES: To assess the efficacy of the anti-estrogens tamoxifen and raloxifen in the medical management of persistent pubertal gynecomastia. STUDY DESIGN: Retrospective chart review of 38 consecutive patients with persistent pubertal gynecomastia who presented to a pediatric endocrinology clinic. Patients received reassurance alone or a 3- to 9-month course of an estrogen receptor modifier (tamoxifen or raloxifene).
RESULTS: Mean (SD) age of treated subjects was 14.6 (1.5) years with gynecomastia duration of 28.3 (16.4) months. Mean reduction in breast nodule diameter was 2.1 cm (95% CI 1.7, 2.7, P <.0001) after treatment with tamoxifen and 2.5 cm (95% CI 1.7, 3.3, P <.0001) with raloxifene. Some improvement was seen in 86% of patients receiving tamoxifen and in 91% receiving raloxifene, but a greater proportion had a significant decrease (>50%) with raloxifene (86%) than tamoxifen (41%). No side effects were seen in any patients.
CONCLUSION: Inhibition of estrogen receptor action in the breast appears to be safe and effective in reducing persistent pubertal gynecomastia, with a better response to raloxifene than to tamoxifen. Further study is required to determine that this is truly a treatment effect.
Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen
Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin
Some good info on clomid:
?Clomiphene is a mixed agonist/antagonist. This is due o the fact that clomiphene is composed of two isomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene). Enclomiphene is an estradiol receptor antagonist. Zuclomiphene is an estradiol receptor agonist. In all likelihood, the net antagonist effect might be due to the composition being 70% trans (enclomiphene) and 30% cis (zuclomiphene). Tamoxifen is more of a strict antiestrogen, decreases the effect of estrogen in the body, and potentiates the action of clomiphene. This combination came about after 100s of clinical experience. - Michael Scally MD
So Tamoxifen is more of an antagonist, than Clomid is. Its better at blocking the ER than Clomid is. Clomid also seems to exert agonistic effects in parts of the brain that control emotion. That would explain why some turn into women on periods during there experiences with Clomid.
Tamoxifen is also made of slightly more isomers, the cis isomer of tamoxifen (inactive one) trans-tamoxifen and trans-4-OHT isomer.
Clomid will double LH at 100mg/ED in 5-7 days and increase FSH by 20-50%. LH rises quickly post cycle, but not that quick.
Clomid will raise enodgenous testosterone (total) by 146% after 3 months at 25mg/ED.
Clomid at 100mg/ED will raise endogenous testosterone (total) by 268% after 8 weeks and free testosterone by 1,410% (Thats not a typo).
-Tamoxifen increased serum testosterone to 142% of baseline in only 10 days. It took 150mg/ED of Clomid to get the same 142% increase. After 6 weeks it raised testosterone and LH levels to an average of 183% and 172% of starting values.
Another thing to note after the above study is how sensitive the pituitary become to GnRH. The more sensitive the pituitary is to GnRH, the more LH it will produce. Tamoxifen increase pituitary sensitivity to GnRH and Clomid seemed to decrease it.
Estrogen will decrease sensitivity to GnRH. It will not increase it. If estrogen were to increase the pituitary to GnRH it calleds “estrogen priming”. Priming the pituitary to become more sensitive to GnRH. This happens in females, but not males. There is no evidence to suggest there is E priming in males.
Tamoxifen is more an an antiestrogen than Clomid is. Both are SERM’s and selective with agonistic/antagonistic effects in “selective” tissues. Both will block the ER in breast tissue. Both are agonists in the liver, which would explain the increase in IGF binding proteins and decrease in plasma IGF?
Dose while on cycle: 50mg eod