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    1. #1
      IronpumpedLady's Avatar
      IronpumpedLady is offline Vixen
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      I thought I'd post up some info I had put together for someone that was asking me about PCT~

      Now the following is a list of definitions of Estrogen, Progesterone and Cortisol, as well as the drugs that control them.
      SERM's (Selective Estrogen Receptor Modulator) : These block certain estrogen receptors, depending on the drug, and dont actually lower estrogen in the blood. Estrogen is left to circulate with nowhere to go. Because of this, SERMS have a positive effect on cholesterol levels. They have a negative effect on IGF-1, so if bulking, only take them if totally necessary. They are good at blocking gyno. Commonly used during PCT, and less often used while cycling. A SERM like nolvadex is widely used in PCT to help kickstart the HPTA back to normal function, in conjunction with other beneficial drugs.

      AI's (Aromatase Inhibitors) : There are 2 types of AI's. Type I (suicide inhibitor) attaches to the aromatase enzyme and permanently disables it. Type II compete for the enzyme, but dont destroy it. Both are effective at lowering estrogen substantially. Both are commonly used during both cycling and PCT. Used mainly when low estrogen levels are desired, like contest preparation/cutting. Beware that lowering estrogen with strong AI's can have a negative effect on cholesterol levels and low estrogen levels can lead to sore joints, cause your losing estrogens anti-inflammitory effect. Can also have a negative impact on your libido. Estrogen has an important role in mass building and joint health, as noted below where "estrogen" is explained.

      RI's (Reductase Inhibitors) : These drugs stop the conversion of testosterone into DHT wherever 5-alpha reductase enzymes are present. RI's work by blocking the action of the 5-alpha. There are 2 5a's. Type I 5a and Type II 5a. Different RI's block one or both of these 5a's. The main reason someone uses RI's is to stop hairloss. They are common anti hairloss drugs. The problem is, when you block the dht conversion, there are less androgens available and may reduce your gains. Sometimes people report less strength, aggression and drive to train.

      Estrogen : The first hormone we need to keep an eye on. Many AAS convert to estrogen via the aromatization process. Some AAS are worse than others. Also, estrogen spikes after a cycle. High levels of estrogen leads to gyno, water retention, fat storage etc. Estrogen plays a key role in progesterone related gyno. We either block its receptors with SERMS or reduce its production with AIs. We watch estrogen levels during a cycle and in PCT. Lowering estrogen too much will mess up your blood lipids. Letting it get out of control will cause sides like gyno, water retention etc. Estrogen plays a role in IGF-1 levels, may lower IGF-1 when blocked with a SERM. Estrogen is also beneficial hormone when bulking, promoting higher androgen receptor concentrations (!). It also is beneficial in another way - its supposed to act as an anti-inflammatory - this means blocking or reducing it too much during a heavy bulking cycle can result in injury to joints. Obviously different estrogen levels are desired for different goals, and it is not always good to block its action or its production. Usually, while bulking, estrogen is allowed to rise unless gyno or water retention (leading to high blood pressure) becomes a problem. When cutting and shedding water and lifting a little lighter (contest prep for example) estrogen is usually dropped with an AI. Proper diet and training can help the bad side effects high estrogen can have.

      Progesterone : Its not so much progesterone that we watch, which is actually a healthy hormone, but progestins which may act upon its receptors. Progestins, like Tren or Deca (nor-9's), may act on its receptor or lower progesterone in the blood. Gyno and lactating are more common side effects. Some people use progesterone receptor blockers to combat this, or a prolactin production inhibitor.

      Cortisol : The third hormone, the stress hormone. When elevated to long, it will store fat. Eat muscle. Cause lethargy. Moodiness. You may crave carbs by the boat load. Cortisol spikes after a cycle because AAS blocks it while on cycle, upping cortisol production and receptor sites. IMO not enough attention is payed to this. It has special functions in the body that are absolutely necessary, like its anti-inflamitory ability. However, when elevated for long periods, it turns into a muscle eating beast. The most important time to watch cortisol is after a cycle, when it spikes. There are a couple ways to help control this, explained below.


      Now that you brushed up on some defentions, here are some useful compounds :

      SERMS (Selective Estrogen Receptor Modulation)

      Nolvadex (Tamoxifen Citrate) : Nolvadex is a SERM. It selectively binds to certain estrogen receptors, effectively blocking the estrogen and stopping unwanted sides such as gyno. It DOES NOT lower estro levels in the blood, it only blocks it from binding to certain receptors. It also helps your blood fat levels. It does not suppress LH, blocks desired estro receptors and helps stop HCG from desensitizing your testicles to natural LH. Nolva should be used during HCG therapy, at 20 mg a day, for the reason i just mentioned. Can be used during cycle if you see signs of gyno. Its mainly used to block the estrogen spike when you come off cycle, and should be used right through to the end until natural test levels are back. One drawback to consider about Nolva is that it may cause progesterone receptors to become more sensitive. This means that while using progestins such as Deca or Tren, you may become more sensetive to progestin related gyno.

      Faslodex (Fulvestrant) : Approved for use in 2002 for breast cancer research, this drug is unlike most we have seen. It is classified as an estrogen receptor downregulator. It prevents estrogen from exerting its influence on the estrogen receptor. Similar to Nolvadex, but is not selective. It hits all estrogen receptors. It also does this to progesterone receptors to a lesser degree. It is injectable, at 250mg a month. No information on how it affects blood lipids. It is also very expensive.

      Clomid (Clomiphene Citrate) : This drug is also a SERM, almost identicle to Nolva. It is said to be a weaker blocker mg for mg than Nolva. Its common use is in PCT, usually for about a month, used after HCG and all AAS esters have run out of your body. Even though it is weaker than Nolva at blocking, it is believed to be quicker at bringing HPTA back to balance. Both are commonly used during PCT. It binds to different receptors than Nolva. There is a lot of debate on this, but until there is solid proof, it may be prudent to include this in your PCT. Commonly taken at about 100mg a day.

      Fareston (Toremifene Citrate) : This is a second generation SERM. Approved for use in 1997. Chemically very similar to Nolva and Clomid, it is less powerful mg for mg. Fareston may have a stronger posotive effect on your cholesterol levels. For those who find this an important issue, this is a drug of choice. Used every day at around 60mg.

      Evista (raloxifene) : A newer SERM, Evista is shown to be a blocker in breast tissue, but acts as a receptor agonist in bone tissue (unlike Nolvadex). This action promotes bone density. Taken at about 60mg a day. Evista may prove to be very beneficial, as it also helps cholesterol levels (like Nolvadex). Evista is supposed to have a more powerful gyno blocking effect than Nolvadex.

      Cyclofenil : Much like Nolvadex, this is also a SERM. Used at about 600mg a day, it is weaker mg for mg. A good alternative if Nolva is not available, which is usually not the case.

      AI (Aromatase Inhibitors)

      Teslac (Testolactone) : This is a first generation steroidal aromatase inhibitor. Like a suicide, it permanently attaches to the aromatase enzyme. Taked at a maximum of 250mg a day. It is not as strong as the newer AI's, but some people still like to use it. It can lower estrogen about 50%. Streroidal in structure, it has no anabolic effect.

      Aromasin (Exemestane) : This drug is classified as a Type I Suicide AI. It binds to the aromatase enzyme and kills it. It is effective at lowering estrogen up to 85%. Once again, you have to watch out for your cholesterol levels. Used mainly for cutting when low estrogen levels are desired. Aromasin is shown to help bone density. Clinical doses are about 25mg a day, but it has been shown that as little as 2.5mg a day can be as effective.

      Lentaron (Formestane) : A Type I Suicide AI. Lentaron is not classified as a drug, and can be sold over the counter as a suppliment. Not as strong as the third generation AIs (arimidex, femera). Can lower estrogen by about 60%. Used as an injectable, it is dosed at about 250mg every 2 weeks. Due to poor bioavailability, daily doses of oral Lentaron are about 250mg.

      Arimidex (Anastrozole) : This is a widely used type II AI. It competes with estrogen for the aromatase enzyme. This effectively lowers estrogen up to 80% in the blood. Approved for use in 1995 to fight breast cancer. At doses up to 1mg a day, it has been shown to be very effective at controlling estrogen while on cycle or in PCT. It is usefull for curbing the effects that come with aromatizing AAS's while in cycle, and can be used in PCT. Nolvadex is shown to decrease the effectiveness of Arimidex when used together. In this case a suicide inhibitor may be more well suited, like in PCT. It is also called L-dex, in its liquid form.

      Femera (Letrozole) : Letro is a competative Type II AI also. Also farely new compared to other compounds, it is shown to be effective at lowering estrogen by blocking the aromatase enzyme. Doses up to 2.5mg a day are used, but usually as low as .5mg a day can be just as effective. Clinical studies show Femera to lower estrogen by 75-78%, sometimes up to 95%. Once again, watch out for your blood lipids (cholesterol) to get out of whack. There may a noted rebound effect of estrogen levels that goes along with Letro use.

      Cortisol Control

      Cytadren (aminoglutethimide) : This drug has the ability to reduce cortisol at higher doses (1000mg a day), and act as an AI at lower doses (250mg a day). The cortisol effect is shortlived if taken for a number of consecutive days. Can lower estrogen a lot, anbout 90%. The higher dose has a long list of sides. More effective as an AI.

      Mirtazapine :This is used to lower cortisol. Even though it may be effective in cortisol control, Johan has pointed out that it may cause some phycological side effects, like making you feel like a zombie. Here is a pubmed abstract for is effects on cortisol levels, among other things.https://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract

      Cytodyne (Phosphatidylserine) : This is also used to lower cortisol, but is only effective in lowering about 30%. There are other ingredients in Cytodyne than Phosphatidylserine. Phosphatidylserine is the only real proven ingredient to lower cortisol, or so ive gathered so far. Effective at 800mg a day of PS as an ingredient.

      Relacore : This over the counter ****tail of herbs and vitamins and minerals is supposed to reduce the amount of cortisol in your blood. I find it chills me out a little, however i read some places that it may raise estrogen. I used it for a bit, however I dont bother any more.

      Vitamin C: At doses of about 1.5 grams a day, can have a lowering effect on elevated cortisol, not to mention its other healthy effects.

      LH Repalacement Therapy - Testosterone Stimulating Drugs

      HCG (Human Chorionic Gonadotropin) : HCG is a replacement for your natural LH (luteinizing hormone). LH is what your body produces to tell your testicles to produce natural testosterone. LH levels drop when using AAS (HPTA suppression). Using HCG while on cycle prevents testicular shrinkage, speeding PCT when the time comes. Using Nolva while using HCG helps stop HCG from de-sensitizing your testicles to natural LH. In my opinion, any decent cycle/PCT should include HCG. It has been suggested to me that HCG can be used throughout a cycle at 500iu E4D, but im unsure of this from practical experience. The most favorable way is to use it in the last couple weeks of your cycle at a higher dose, like 500iu ED. The trick is to end the use of HCG just as the last AAS is running out of your system. So, 3 weeks before the the last ester leaves your blood, you would start the HCG/nolva combo. HCG at about 500iu ED and Nolva 20mg ED. This is done before Nolva/aromasin (for example) PCT starts, and runs about a few weeks longer than the end of the HCG. Always include Nolva with your HCG, they work together well. Be careful not to overdose on HCG and permanently desenstize your testicles to LH. HCG has an active life of about 3 days. Vitamin E is a booster, read the next one :

      Vitamin E : As Anthony Roberts pointed out to me, vitamin E increases the response to HCG. This may be useful in making the low doses of HCG we use more effective at growing back shrunken testicles. Doses can be generally 1000iu a day while using HCG.

      Progesterone Control

      Lilopristone, Onapristone: These are progesterone blockers also, said to be safer and possibly more effective than RU-486 when it comes to progesterone blocking. They were developed after RU-486 in an attempt to make more effective, less harsh drugs to block progesterone.

      Dostinex (Cabergoline), Bromo (Bromocriptine), B-6 : These are used for Deca/Tren gyno sides. This type of gyno is related to progesterone and its receptors. Tren/Deca may act on the progesterone receptor, as they are progestins, and may increase prolactin in the blood (causing lactating). These drugs stop production of prolactin at the pituitary gland. Controlling estrogen levels with an AI also helps here, as progestins themsleves haven't been proven to cause gyno.

      RU-486 (Mifepristone - abortion pill) : This drug has the ability to block estrogen, progesterone AND cortisol. It may or may not be very well tolerated, but I would like to find out more about it, as it is used in the bodybuilding world. In PCT it is used to block cortisol and progesterone. A powerful drug that may turn out to be a good choice, but i need more evidence and feedback from experience useing RU-486. Check out this thread i have going if you would like to learn more about it :

      RI's (5a Reductase Inhibitors)

      Proscar (Finasteride) : This is primarily a Type II 5-alpha blocker. This means that when you are taking a high dose of testosterone, the resulting conversion of test to DHT in certain parts of the body become to high for ones own comfort, mainly hairloss and prostate enlargement. This is where the type II 5a enzymes are mainly found. This will not work against AAS that are already highly androgenic by design, without conversion. AAS like Tren will still exhibit high androgenic properties. Used at doses up to 5mg a day.

      Avodart (Dutasteride) : Like Proscar but newer and more effective at blocking the effects of DHT in not only the scalp and prostate (which are Proscar's main strengths) but also in the skin, effectively reducing acne. This is because Avodart will block both Type I and Type II 5-alpha enzymes, covering more of the problem areas due to DHT. Available in .5mg softgels, this is an effective dose. Approved for use in 2002.

      Fat Burning, Anti-Catabolic

      Clen (Clenbuterol) : Clenbuterol is a bronchodilator. Everyone knows clen is used to burn fat. Why am I listing it here in a PCT thread? Well, for its anti-catabolic properties. Clen may lower the effect of AAS while on cycle, so I personally dont use it while cycling. It does, however, have an effect on cortisol levels. While on cycle, cortisol is not to much of a problem if you eat right. AAS use increases cortisol production, and increases receptor sites. This means that when you finish a cycle, cortisol spikes along with estrogen. This is a part of the "crash" that is often overlooked. People have reported that blocking cortisol in PCT speeds along fat loss. Clen is supposed to have a blocking effect on cortisol. So, along side of its ability to burn fat, it is anti catabolic in it ability to block cortisol until desired hormone levels are achieved in PCT. For me, it makes sense to use clen in PCT until desired hormone levels are achieved, as it also burns away fat in the process.


      All AAS can supress the HPTA, even in small doses, thus lowering natural LH. Factors that affect ones ability to recover quickly are genetics, cycle length or steroid type. Some AAS will shut you down hard and fast, some not so bad. Some lucky people can rebound quickly without medications, but many need it to avoid a crash and losing muscle/gaining fat. It is in our best interest to use the appropriate medications in the CORRECT doses to keep sides down (like bloat), grow quickly and keep quality mass when we are done our cycles. Most of us can get away with using 2 or 3 compounds to keep sides to a minimum, rebound quickly, and keep gains we worked hard for. Higher levels of AAS (and therefore higher estrogen/progestins) may require more intense hormone control and heavier PCT. Remember, we are aiming to level out estrogen, progesterone, cortisol and testosterone. In PCT, we are trying to achieve equilibrium of the HPTA, getting FSH (follicle stimulating hormone) and LH (luteinizing hormone) back to normal. Keeping our hard earned gains is obviously our first priority.

      In short, we generally use :

      AI's - While on cycle to "dry up" or lower estrogen because of a persons sensetivity to it (if needed). Used in PCT for the same reason and to help get back to homeostasis. Usually used with a SERM in PCT.

      SERM's - to block estrogen while on cycle (if needed) or to help kickstart the HPTA during PCT (most common use). Usually used with an AI in PCT.

      HCG - To prevent testicular shrinkage during a cycle, or to encourage them to grow back more quickly. Usually used with an AI and SERM in PCT as the last AAS run out of your body, and stopped a few weeks before your SERM and AI.
      Now after reading this, youre probably thinking, "What does the best PCT consist of?". Well that is matter if opinion. For the most part, the census is the following.


      Now newbies are starting to ask, "Arent Nolva and Clomid both SERMS? Why do i need both?". Well im glad you guys asked that.

      There has been far more research on Clomid for male hypogonadism and infertility, than Tamoxifen.
      Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (35)It can also block a bit of estrogen in the pituitary, which is a great benefit when used with HCG (more on that later) (36)(37). The increase in testosterone Nolvadex can give someone with a dysfunctional is basically that 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Why don’t we use Clomid, another SERM? Well, basically because it takes much more to do the same thing. In comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but Nolvadex also has the added benefit of significantly increasing the LH
      (Leutenizing Hormone) response to LHRH (LH-releasing hormone) (6). This most likely indicates some kind of upregulation of the LH-receptors due to the anti-estrogenic effect Nolvadex has at the pituitary. Although both Nolvadex and Clomid are both SERMs, they are actually quite different. As you already know, Nolvadex is highly anti-estrogenic at the hypothalamus and pituitary, while Clomid exhibits weak estrogenic activity at the pituitary (7), which as you can guess, is less than ideal. It should be avoided for the PCT I’m suggesting…and in fact, avoided in general…it’s simply not as good as Nolvadex.

      Need I even add that the 150mgs of Clomid you need to get the hormonal increase experienced with 20mgs of Nolvadex is much more expensive? So lets dump the Clomid…and no, using it along with Nolvadex will provide no “synergy” that I’ve ever seen in any relevant study."

      "Now IMO, selective estrogen receptor modulators(SERMs) such as Clomiphine and Tamoxifen are selective to which tissues they bind too. Clomid being selective to the suprapituitary, while Tamox is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur. With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual PCT duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

      1. Nolva acts as the preventive measure to the estrogen flux occured PC while clomid is the primary LH stimulator(Even more so in the case an AI is not used).
      2. If your running a longer PCT, clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary...

      Follow thus far?

      Here is yet another case and point.

      In just 7 days of Clomid use at 100mgs ED is enough to raise LH and FSH by as much as 50%. You will need nolva also, as the point of these serms is to block estrogen receptors in the HPTA to fool it, and to tell the pituitary to start producing it's own LH and FSH.

      Now ive also been from the school of thought that suggests the use of an AI during PCT for some time now. Like many reading this, i was unsure as to why, but just did as i was told. Well after researching the use of AI's a little, ive uncovered the following. I now see that the point in using AI's during PCT is skewed. It is not worth it because youre lowering estrogen levels to subphysiological levels (unhealthy levels too) which in turn can cause a nasty rebound when all Anti-E's are stopped. SWALE advocates NEVER to use them post cycle for a host of reasons.

      (Here is the exception. Its advisable to use an AI if you did not use one while on cycle to control estrogen. From Swifto- *AI's are not always needed, especially if one has been used to control estrogen (aromatse activity) during the cycle. There is a high risk of lowering estrogen too low and that can bring its own side effects; Lowered labido, aching joints, poor cholesterol and can negatively effect the immune system. We need some estrogen, not alot, not zero, but one cannot afford a too low an estrogen level at this time of PCT.* I will go into AI's and why not to use them below. In short, Femara is too strong & Adex will likely lead to strong rebound effect when it is stopped. So that leads me to believe suggestion of using Aromasin (25 mgs ED) during PCT is a good one in particular cases, since it does not block all estrogen (a bad thing) nor does it cause a rebound effect. But i will go into detail below.)

      First off, Anastrozole (L-dex, A-dex) doesn't stimulate the HPTA. Thats enough reason right there to void its use in PCT. Now the other main point, is that Tamoxifien reducess the effectiveness of Adex. Clinical endo studies generally show a 28-30% reduction in the efficancy when using both.
      (Feel free to do some research and not take my word for it.)

      Now onto Femera (Letrozole). First off. Letro and your sex drive; Letrozole can and likely will suppress your sex drive. Making it not such a great drug when on PCT for Mr. Happy reasons. The Estrogen Rebound Effect will be the biggest reason why you shouldnt use it in PCT. We've all heard of it. Its quite severe when coming off a dose of Letro. When using Letro, youre lowering estrogen to a point that is below normal. Recovery from a suppressed state can take much longer and Test levels can drop drastically when use is discontinued. The inverse is true also. Estrogen levels will go above normal then slowly fall back to normal after discontinued use.

      With your estrogen being completely inhibited there is a definite estrogen rebound as your body tries to re-stabilize the testosterone:estrogen balance. We can prevent this rebound effect by supplementing further with another AI or SERM. So, I suggest that when you are coming to the end of your cycle you will more than likely be using Nolva in your PCT so just make sure that you begin taking nolva the last day you are going to take your letro and then continue on as you would with regular PCT.

      The IGF-1 levels that are raised with Letro are really of no signifigance because they don't seem to have an effect on localized IGF-1 (most important for growth). So to me, its a waste and won't help in raising testosterone any faster. Its the response of the testes to LH pulses which will signal natural production to occur, and Letro will not have an positrive effect on this. In this area more is not better as the body will only repsond so fast. Stacking Anti-e's won't have much of an effect. I thought it would a year ago until I tried it, then read SWALES recommendations. TO me, recovery wasn't any faster. I have better recovery with blunting cortisol with the addition of Nolva than anything out there (didn't need HCG though).
      Now with AI's in PCT covered, lets move onto the topic of a "Standard PCT". Personally think that the whole 'standard' 4 week PCT needs to be trashed. The idea that 3-4 weeks is the standard of PCT retarts your natural test production, as many people who get bloodwork done on a regular basis can attest to, is not accurate. It can take months after PCT (or even years before full HPTA function is restored) and only in part in some cases. The idea of time on + PCT = time off is a sound one, but in truth, even that amount of time off is insufficient in many cases to restore full HPTA function. With that said, its important to remember to get blood tests done before you begin the cycle, during the cycle, and after PCT.
      (These are all, mgs, per day, per week.)


      *Tamox - 40/40/20/20 --(Until Blood Results have confirmed the HPTA has indeed began to recover.)
      *Clomid - 100/100/50/50 --(Above)
      *Tormifene - 60/40/40/40 -- (Above)
      **Aromasin - 20/20/20/20 --(Above)

      *Use 2 SERMs, not all 3. I prefer Tamox and Clomid, but only because im yet to use Tormifene. From what i hear, Tormifene has recently been reported to be the best SERM at restarting an inhibited HPTA.

      Stay Strong~~!!!

    2. #2
      daved150's Avatar
      daved150 is offline Platinum
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      very good ipl....i think we shouls stick this


      "Actually for once your actually starting sound quite logical!"-djdiggler 07/10/2007


    3. #3
      Klash's Avatar
      Klash is offline Elite FG Resident
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      I second that dave.... Nice compilation IPL

    4. #4
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      nice post - Dave you have the power to sticky this Bro

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