I take no credit for this ,i was just wondering what you guys make of it whether its good info or bad ,First of all there are three different types of gyno: estrogen induced, progesterone induced and prolactin induced. Of course you can avoid all three types of gyno by keeping estrogen within the normal range. The precursor to any type of gyno is estrogen! Once you let estro build up you signal to your brain that you have conceived doesn't matter if you are a man or woman keep in mind, your body at this point will have to go through certain processes to prepare you for lactation. Firstly your body will rush to use that estrogen and build up breast tissue (lump) which is mandatory for the lactation process. Once this stage has been completed and you have let estrogen still high your progesterone will increase (estrogen can still remain high) which is an attempt of your body to make the tissue larger and also make your aerolas bigger (puffy and enlarged nipples) again to get them ready for lactation. Last stage of gyno is prolactin/lactation, all previous stages were preparing the body for this moment at this point your progesterone and estrogen will drop and your prolactin will spike, this is when someone starts lactating
Estrogen, estrogen, estrogen!
Most challenging hormone for the steroid user is estrogen by far. Think about it's the cause of any changes in your gyno/pecs, mood, libido, hardness, bloat, skin, prostate, appetite you name it when you feel off 90% of the time is due to low/high estrogen levels.
When you hit your sweet spot you will know you cant miss it, you will feel happy, content, you will fuck like a champ eat like a champ and train like a champ and too top it off everybody around you will be happy as well
Here is an indicator I used since my early days on hormones:
?Too low E2=great erections, difficulty to ejaculate, dull orgasm.
Too high E2=inability to maintain erection, therefore, great difficulty ejaculating, just forget it.
Centered E2=easy erections, able to control ejaculation, stunning orgasm. ?
Low and high estrogen sides are very alike the more experienced you get the easier is to differentiate between them but it will always be tricky, if in doubt get your estradiol checked though bloodwork
High estrogen sides
Acne, loss of libido, water retention (Bloat), pissing less than the water you consume, moon face, very small testicles, scrotum hanging too high, soft testicles, extreme oiliness all over, aggression (roid rage), depression, bitchiness, lethargy, insomnia, soft erections, extreme cravings for sugar/chocolate, high bp, bp spikes, enlarged prostate, pressure in lower abdomen when urinating, thin stream, constipation (from water retention)
Low estrogen sides
Dry skin, dry lips, dehydration, loss of libido, good morning wood no wood when its time for sex, loss of wood while having sex, loss of sensitivity, dry gland (penis), white gland, loss of girth, irritability, mood swings, crying for no reason, dht rage (aggression you take out on others), dull orgasm, hesitation just before urinating, night sweats, loss of appetite, constant fatigue, lethargy, constipation (due to dehydration), diuretic effect (pissing more water than you are consuming), itchy scalp, obsessive thoughts
Of course YMMV, I got each and everyone of those sides the past few years I have been juicing and I am sure I am forgetting some sides. When you get one side effect it is just an indication use this list to make a full picture. So say you have loss of libido, no zits and dry skin/flaking you know your e2 is low. Say you have loss of libido, acne, uncontrollable aggression, and bloat you know your e2 is too high. Never go by one side only, being bloated only means nothing, having dry skin only means nothing again.
AIs
Keep in mind estrogen is good for you in many ways (libido, mood, skin quality, hair, nails etc) BUT most importantly estrogen is good for your liver. I am sure you have heard how arimidex and letrozole are bad for your liver values when aromasin is 'better', in reality all AI?s are as bad as each other for your liver values. The moment you start lowering estrogen the worst your liver values will get doesn?t matter what AI you use all it matters is how much you are lowering your estro. If you lower your estro say by 10nl/dl you wont notice much if you crash your estro down to single digits I guarantee you your hdl/ldl will be completely out of whack no matter what AI you used
Suicidal AI vs Non suicidal/binding AI
Adex and letro are non suicidal AI?s all they do is bind any estrogen you convert directly on your aromataze enzyme. Each AI binds a different percentage of estrogen, letro binds more than adex of course. Problem with biding AI?s is once you seize use all the estro that had accumulated over the weeks/months you were using the AI suddenly gets released this process is called estrogen rebound and I am sure you know it can be far worse than estrogen while on a cycle since normaly when you drop your AI you either cruise with a low dose of test or pct. In both cases you have far less test in you and once all that estrogen is released you got a much higher chance of getting gyno and of course you are going to be bloated like a balloon and feel soft for weeks till your estro comes down to normal levels.
Aromasin is the new generation of AI its suicidal, the difference being with the other AI?s is Aromasin will actually destroy/kill a certain percentage of your aromataze enzyme so by doing so it also kills any estrogen that was attached to that enzyme. Means when you stop using aromasin you wont rebound at all like you would with the binding AI?s and if anything you will have to wait for a while for your body to start producing more aromataze (very bad if you crashed your estro comparing to the other AI?s). Each person is different in the rate they create new aromataze for me it takes around 2 weeks for someone else it can take one or three weeks. Only way you can speed up the process is by using HGH, you can use all the dbol you want all the test suspension you want if you crashed your estro with aromasin and you don't have aromataze you wont even bloat from those compounds there wont be any estrogen conversion, also you will get 0 results from the dbol at least.
Arimidex/Anastrozole
Adex will lower your estro by about 50-60% of course if you keep taking it that percentage accumulates so you lower 50% by another 50% and so on, you can easily end up with your estradiol in the singles if you take it for long enough at a high enough dose and you aren't converting much estrogen from aromatizing gear (using low dose of test high dose AI). Adex imo is the best suited for trt purposes, reason being the rate of which it lowers estrogen compared to the other AI?s is smaller. For trt purposes you only need 1mg of total adex per week to keep estro in range (e2= 20-25ng/dl=sweet spot)
Why adex is bad for blasting: This small posting has been posted on another forum by a doctor not my words but reflects a lot of my experiences with adex
"Adex is not particularly effective for drugs that tend to be subject to peripheral aromatization, methandrostanolone in particular. Often a full 2mg daily of Adex will still not stop dbol bloat and cramping
Arimidex is best at E1 suppression (tissue affinity, gonadal, adrenal, etc and because its a competitive inhibitor). it suppress e1 at even the lowest of doses, but takes rather high doses to see significant impact on peripheral aromatase"
While cutting with a low test dose and non aromatizing gear is as good as an AI as any but while bulking with compounds that aromatize heavily Adex is the worst AI you can use. No matter how much you use you will still be much more bloated than you would by using aromasin/letro
Common dose while blasting: 0.5mg ed/eod
Trt dosage: 0.25mg eod, 1mg e6-7d
Aromasin/Exemestane
Hands down the best down for blasting but it does have its downsides. I found that the more you use aromasin the more senstitive you become to it. When starting out with aromasin even 25mg per day is a common dose for a mild cycle say 750mg test and 500mg deca. As time goes by the more you use it the less aromasin you will need, you will end up needing 12.5mg eod if not less for a mild cycle. It doesn't happen in a few days though it takes months. Another drawback of aromasin is hairloss, comparing to the other AI?s I found it makes me shed a lot more. Once side effect of aromasin is Alopecia, the other two AI?s have hairloss/hair thinning as a side effect but not full blown Alopecia.
Like mentioned earlier the biggest fear with aromasin is crashing estro to low. At this point all you can do is wait or up your hgh dose. Give it at least 10days before you start taking any more AI even if you are switching to say Adex.
The best write up about aromasin which reflects my experience with it 100% is here:
Ahhhhh-romasin?! The king of anti-estrogens.
This post is kind of long, but take the time to read it, it's probably the most important thing you'll ever read if you're a BB'er (haha well maybe not, but there's some gold in here)
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
the good:
-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
-increases IGF-1
-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
the bad:
-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 don't 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.
Inappropriate uses for exemestane:
#1) giving your gf hot flashes
Common dosages: 12.5mg ed/eod, 25mg ed/eod
Trt dosages: 6.25mg ed, 12.5mg 2-3 times per week
Letrozole
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 ton 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
Serms
Keep in mind all 3 serms will work in favor 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
Nolvadex/Tamoxifene
Agonist: Liver, uterus (female)
Antagonist: Breast/nipple
As I am sure you heard nolvadex reduces IGF-1 levels 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
Raloxifene/Evista
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
Agonist: Liver
Antagonist: Brest/nipple
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% (That's 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 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 some say it can substitute hcg but I haven't tried that route way to many mental sides to use it on cycle imo
Prolactin support
Caber/Cabergoline/Dostinex/Cabaser
Caber will lower both progesterone and will inhibit prolactin/lactation. It's a dopamine agonist means it wont allow your body to lactate since it will occupy your dopamine receptors which are responsible for lactation. Caber is the perfect prolactin support when running any 19nor imo since the side effects are minimal, no drowsiness, doesn't affect sleeping patterns and in general as far as dosing goes is far more flexible than pramipexole or bromo. Also there is no withdrawl when ceasing use of caber like with pramipexole
Caber is a regognised ed med, it reduces downtime (not to be confused with multiple orgasm) so if you need 24h recovery between sessions two weeks after taking caber you will see a significant decrease in downtime you will need 12-16h to be ready for the next session, if you need 2h you will need 1h with caber etc
Also its known for the multiple orgasm effect, so when you ejaculate you will feel as if you are releasing two or three loads at the same time. This needs some input for the user though its not instant, the more you hold it in the more orgasms you will have in the end. Also without caber say you are having sex and you let some cum slip through you got a big chance to loose your hardon, with caber even if you let quite a bit slip through your hardon will become stronger and stronger and your climax will be insane. In this sense you can actually have 4-5 small orgasms coupled with a huge orgasm in the end that will feel as two more orgasms put together. Again it needs practice and self control from the user
Common dose on cycle: 0.25-0.50mg e3d
Common does to stop lactation: 1-1.5mg e3-5d
Pramipexole/Mirapex
Prami like caber will decrease progesterone and will inhibit prolactin/lactation. It's a dopamine agonist like caber so it will occupy dopamine receptors which are responsible for lactation
prami is a very peculiar drug! You need to taper up really slowly to get to the desired dose and also taper down really slowly to avoid the mild withdrawal effect it will cause. Prami is an addictive substance I wouldn't recommend it for any cycle over 8 weeks the more you use it the harder it will be to come off it, also you will find you will want to increase the dose to maintain the ed effect. Prami's ed effect is nowhere near as good as Caber. It does reduce downtime like caber does but that's about it there is not enhancement in your orgasm or your libido contrary to caber. Only advantage of prami over caber is that if taken at the right time (2-3h) before bedtime it can work as good as a benzo to knock you out to sleep. Which when running tren is a bonus. If however you dose it wrong (unwillingly ofc) say 30-1h before bed time you will find that after 2-3h of sleep you will be wide awake and probably sweating since the dopamine you suppressed 4h ago rebounds and you feel as if you just had a hit of coke in your sleep, not a good feeling. Also every time you up the dose it takes some adjusting even if you are used to the substance. I found that overtime I would up the dose for the first few nights I would sleep very light almost like sleeping awake that's how it felt.
Sleep sides like vivid dreams and waking up mid night can be avoided by taking prami at the right time so you got to experiment with this (the earlier you take it the better). Make sure you never take prami in the morning or too early in the evening you are going to feel drained, dizzy, nauseous and like a zombie all you will think its when the time comes to go to sleep
The worst part with prami starts when you quit, for the first few days after you quit, you will wake up in your sleep many times as if you were quitting cigarettes or weed even, then you will have the lightest sleep ever as if you were sleeping with your eyes open and the dreams will be negative and intense. Basically you get all the prami sides you had earlier only they cant be avoided since you don't take prami anymore. This will subside completely after 5-7days
Common dose on cycle: taper up from 0.125mg to 0.25mg-0.50mg (the high dose only if you are stacking two 19nors or high dose of tren). After you are done with your cycle taper down even slower from 0.50mg to 0.125mg and stay one week on each increment then quit. No matter what you do expect some discomfort the first 3-5 days after you quit
Dose to stop lactation: You would probably need 1-2mg per day to stop lactation but I wouldn't recommend it, it would take ages to rump up to that dose, if you are already lactating use caber worse thing that could happen when jumping to a high dose of caber would be to get a flush face that lasts 12-14h (annoying but much better than puking your guts of for hours)
The purpose of this article is too look at the effects of estrogen both good and bad, and how we can properly manage them while on cycle using the various compounds available to us. The relevance of Estrogen management is more important than ever now in my opinion. This is due to several factors. First of all the knowledge of Estrogen and its effects in males has grown substantially in the last few years. Also a more basic but very real reason is the trend we have seen in cycles over the last several years. It used to be cycles were 6 - 8 weeks in length. In the past it was common that short ester cycles were run 6 weeks and long estered ones 8 weeks. Now cycle lengths of 12-16 weeks+ have become the norm. This added time and exposure to the deleterious effects of unmanaged or improperly managed estrogen makes the topic more important than ever.
So lets take a look at the effects of Estrogen in Males both positive and negative. While we will see Estrogen plays a key role in several vital functions in males, as well as several functions specifically important to our goals, more is definitely not better when it comes to this Hormone.
On the positive side:
* Estrogen plays a key role in immune system function and inflammatory response.
* It has a positive impact on cholesterol.
* Estrogen is essential for GH and IGF synthesis.
*It plays a role in maintaining proper '"fluid balance" within the body.
*Essential for bone density
*Assists in glucose uptake
The Negatives:
*Increased Risk of Heart Disease
*Increased risk of Prostate cancer
*Increased blood clotting
*Increased risk of Hypertension (high blood pressure)
* Increased risk of cardiovascular event or stroke.
*Gynecomastia
* Improper Fluid Balance (or water retention)
*Estrogens relationship with other hormones. For example, Estrogen has a proportional
relationship with the hormone Prolactin. An increase in Estrogen results in an increase
in Prolactin.
As you can see there are numerous serious positives and negatives when it comes to the effect''s of Estrogen in males. Some of these effects are dependent upon the levels of Estrogen present. For example proper estrogen levels result in improved lipid profiles and cardiovascular health. However elevated estrogen levels result in adverse effects on cardiovascular health and increased risk of heart attack or stroke. Based on this it becomes very clear the optimal situation when it comes to Estrogen while on cycle is to MANAGE it properly. Not eliminate it, not ignore it, but manage it.
To further clarify and specify what I would consider proper Estrogen Management, especially in light of the fact that many positive effects of Estrogen become negative when it is elevated too much, I would define estrogen management as maintaining Estrogen levels in the clinically normal range even while on cycle. In other words keep our E2 levels the same on or off cycle. To take it a step further if Estrogen levels can be kept between 25-30 while on cycle, we can reap the positive effects of Estrogen while virtually eliminating the negative ones.
Lets take a look at Estrogen management while on AAS cycle and how it has evolved over the years, what compounds are available to assist us, and the effects and interactions of these compounds.
Years ago the first attempts at managing Estrogen really didn''t manage it at all;they just eliminated some undesirable side effects while having no impact on Estrogen levels at all. These early attempts were made using serms such as clomid or tamoxifen while on cycle. The specific side effect of elevated estrogen that the use of serms would address is the one of gynecomastia. Serms bind to the Estrogen receptor in breast tissue, blocking estrogen from exerting its effect there and preventing undesired breast tissue growth. As you can see this was an improvement over using nothing at all, however serm use does nothing to address the other negative effects of elevated Estrogen. Some of these negative effects are very serious, much more serious than Gyno from a medical (as well as common sense) not aesthetic perspective. While serms do not address the majority of negative issues of elevated Estrogen it does not mean they do not have a place in this discussion or in treating of addressing this issue. I will get into that more later.
The next progression in Estrogen management is the use of Aromatase Inhibitors to control overall Estrogen levels. This has been a huge advancement in the management of estrogen. Aromatase Inhibitors act upon the Aromatase enzyme. This is the enzyme responsible for the conversion of testosterone to estrogen within the body. Aromatase Inhibitors prevent the binding of Aromatase to testosterone so the process of Aromatozation of test to Estrogen cannot take place. This sounds like the ultimate solution to the problem of Estrogen Management on cycle and too a large degree it is. However there are different Aromatase Inhibitors that may make one a more prudent choice than the other for certain situations or individuals. Also the value of Serms and their role in estrogen management cannot be dismissed just yet.
So we see we have 2 categories of compounds that can be of use to us in properly managing Estrogen or its side effects, Serms and AIs. Let''s take a look at our options in categories, their differences and potential interactions with one another, and how they might be used together to accomplish our goal.
First we will look at AIs as in my opinion they are the core of our Estrogen Management program. We essentially have 2 types of AI''s to choose from. Type 1 AIs like Exemestane and Type 2 AI''s such as letrozole or Anastrozole (arimidex). The difference in these types is as follows. A Type 1 AI like Exemestane binds permanently to the site on the Aromatase Enzyme where it binds to testosterone allowing its conversion to Estrogen. This permanent binding renders the Aromatase totally and permanently inactive. In contrast Type 2 AIs temporarily bind to this site on the Aromatase Enzyme rendering it inactive as long as the AI is being used. Onçe use of type 2 AI stops the aromatase will reactivate. So whats the difference in these Ai types for our purposes? Well Due to the '"reactivation" if you will of existing Aromatase with a Type 2 AI, when you stop using it a spike in Estrogen (often referred to as rebound) will occur due to the sudden increase availability of Aromatase Enzyme. Another important distinction when it comes to Type 1 and Type 2 AI''s. A Type 1 AI like Exemestane remains unaffected by the introduction of a serm into your Estrogen management program. Type 2 AIs like letrozole and Arimidex suffer a reduced in blood levels and effectiveness with the introduction of some serms. I will touch more on why we may need to introduce a serm a little farther on in this article.
When it comes to the strength of these AI''s letrozole would be the strongest followed by Arimidex and then by Exemestane. Now people might be up in arms saying Exemestane is stronger than Arimidex however when one looks and compare data from studies done on MALES the order of strength is exactly as I stated it, quite often much confusion comes in to play when people recite data on AI's taken from studies on women. The fact is AI's behave differently in males, they are less effective in males, and for our purposes it is only prudent to compare data gathered from studies on males to portray an accurate picture.
The next aspect to be considered when looking at AIs are the effects they indirectly illicit in other areas. We stated the positive effects of Estrogen, we must realize by lowering Estrogen via Ai use some of these positive effects may be compromised. It is important to look at the various AI options available and possibly use the data to help pick which AI we use. letrozole is an extremely potent AI and its effects demonstrate this as would be expected. letrozole has an adverse effect on lipid profile and somewhat on IGF levels. On the other hand Arimdex has a small impact in the area of IGF and depending upon which studies you cite a small adverse impact on lipids to no adverse impact on lipids. Exemestane seems to have no clinical impact on either IGF or lipids.
It is important to realize that it may seem like Exemestane shines as a clear cut winner when it comes to choice of AI, however I do not necessarily believe this to be the case for everyone. In some cases or maybe better said in some people, an extremely powerful AI like letrozole must be used to manage Estrogen properly. Some may respond better to Arimidex than Exemestane. I believe there is a place for all 3 of these. That being said, if possible my personal first choice of AI is Exemestane due to its lack of interaction with other compounds we may need to introduce such as certain serms, its positive effects on IGF and Lipids over other options, and also its lack of potential "rebound"(although I think that is an overstated issue quite often).
Regardless of which AI you choose for the vast majority of us our goal can be accomplished of maintaining Estrogen levels in the normal range while on cycle. It might seem like the discussion is over. Why do we even need to look at Serms? Read on:
So we have our Estrogen levels managed, all should be good. Well yes in most cases it will be but what if it isn't? What if you start to get sensitive, itchy or painful nipples? What if you get a lump around your nipple area? What if you are so predisposed to gyno you still get symptoms using an AI? It shouldnt happen but if it does your immediate solution should be a serm.
So we know what serms do. As stated above they bind to the Estrogen receptor in breast tissue, preventing Estrogen from eliciting its effects, which in this case is undesired breast development and tissue growth. However all serms are not created equal for this purpose. I am of the opinion that Raloxifene and Tamoxifen are the 2 best suited serms for this purpose.
Raloxifene is the serm with the highest binding affinity to the Estrogen receptor in breast tissue. Tamoxifen would be second. This means Raloxifene is the most effective serm available for gyno treatment and or prevention. Another point that bears mentioning, when using a Type 2 AI like Arimidex or letrozole, Tamoxifen reduces blood levels of both of these AI's. Raloxifene on the other hand has no effect on blood levels of these AI's, allowing them to be run in conjunction with Raloxifene with no decrease in AI effectiveness. As was mentioned above any serm can be run with Exemestane (a Type 1 AI) with no impact on Exemestane's effectiveness.
Tamoxifen is the serm with probably the most clinical data supporting its use for gyno prevention and treatment, in all likelihood due to the age of the drug. It is very effective for this purpose and very versatile as it is equally if not more effective in the area of PCT as well, meaning often it is likely on hand so it is readily available for most to use in the case of gyno symptoms.
So let's begin to put this all together. An AI should be the core of your Estrogen management program; the goal should be Estrogen levels in the clinically normal range even while on cycle. Id say between 25-30. I cannot emphasize enough the importance of blood work as a management tool. It really is the only effective means of proper Estrogen management (hormone profile management for that matter).
All AI''s can effectively manage Estrogen. My preference in order for this purpose would be Exemestane , then Arimidex , then letrozole however as stated earlier they all have their place. If Exemestane works well for you you have the luxury of the least amount of undesirable side effects and the most versatility as far as combining with a serm should the need arise for gyno prevention and treatment.
The logical question is why do even need to worry about a serm if I mange Estrogen with an Ai? Well hopefully you don't however in some cases it may become necessary due to predisposition, preexisting gyno , very high dosages of aromatizing steroids and so on. For this purpose Raloxifene is in my opinion the top choice offering no reduction in effectiveness of any AI you are running and the most powerful protection against gyno due to its binding affinity to the E receptor in brest tissue. Tamoxifen is also a very solid option especially if running Exemestane as your Ai. If you are running letrozole or arimidex a corresponding increase in the dosage of Ai may be required due to tamoxifen reducing blood levels and effectiveness of these 2 AIs.
Bringng it to theReal World:
1- Manage Estrogen levels with an AI: Exemestane offers the most versatility with fewest adverse effects.
2- Have a Serm on hand in case of Gyno flare up. Raloxifene is most effective and has no adverse interactions with any AIs.
Run a low dose AI with your cycle to try to keep estrogen in the clinically normal range so you can reap the benefits and reduce the deleterious effects. Have a serm on hand just in case gyno rears its head. If it does start a serm immediately. At this point you NEED blood work so you can properly assess your situation and possibly adjust AI dosage up which may allow discontinuation of serm. It may not. You may need to run a serm and AI in conjunction on cycle but it is very unlikely. An Ai should be able to manage Estrogen properly for the vast majority of us. If you do need to run a serm and AI together I cannot emphasize enough that you need to reevaluate your situation. Elevated estrogen has some serious effects as I mentioned above. You should consider this option as I would encourage many too do anyway. Reduce the amount of aromatizing steroids in your cycle and replace them with non-aromatizing compounds. I cannot emphasize this enough. For example a lower test dose will allow for easier estrogen management. This is probably the single biggest thing any of us can do to help ensure proper estrogen management (besides blood work', which again is essential).
One more topic I want to touch on is Gyno. Gyno is considered the worst side effect of elevated estrogen but the fact is it is far from it. There are many much more serious issues going on inside of you if you start growing breasts. That being said when it does occur or start to occur we want to stop it. So often I see people recommend letrozole to treat gyno. This is a horrible idea in my opinion. letrozole works to treat gyno by lowering overall Estrogen levels so much there is no circulating Estrogen to bind to the Estrogen receptor in breast tissue. If you paid attention above you saw the beneficial effects of Estrogen. Some aren''t even beneficial, they are essential. I think to eliminate estrogen to this point throughout your entire body is foolish. Introduce a serm such as raloxifene, block the Estrogen receptor in the breast. The gyno then cannot grow. Then again using blood work adjust your AI dose to MANAGE estrogen levels while taking the serm to prevent the continuation of the gyno.
You are using an out of date browser. It may not display this or other websites correctly.
You should upgrade or use an alternative browser.
You should upgrade or use an alternative browser.
ai's and more
- Thread starter jonathan
- Start date
D
dolfanshan
Guest
Good read. I posted something similar. I got gyno my last cycle and used nolva with adex and had great success. Nolva will lessen the effectiveness of adex, so I did bump my adex dose up a bit. Nolva does not lessen the effectiveness of aromasin though. From personal experience I would recommend 20mg nolva ed along with your ai for active gyno problems.