ive been reeding that the nolva will cause more receptors to pop up causing and even greater production of estrogen, but i bet its because they dosed it wrong and didnt do it right.
This was taken from another board, credit to basskiller
PCT and Cycle Recomendations: Estrogen, Progesterone and Cortisol control
I am starting this thread after tons of reading, and taking advice from the more prominent members from various boards. I just wanted to summarize a bunch of useful threads here, bringing it together in one post and simplifying the popular substances used to control estrogen/progesterone/cortisol and restore natural test levels. Ill go over the compounds briefly, and summarize at the end of the post. I'd like to thank Hooker for his input on this thread. A few defenitions before you start :
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 posotive 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, and are commonly used while cycling and in PCT.
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.
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.
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. 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.
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, 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.
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%. Once again, watch out for you 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.
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.
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, or in the last couple weeks of your cycle at a higher dose, like 1000iu EOD. This is done before PCT starts with Clomid, as it is no good to mix the two. Always include Nolva with your HCG, they work together well. My suggested doses are not concrete, and you should be careful not to overdose and 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 Hooker 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.
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.
SUMMARY
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. I hope this post helps out, as i wrote it for beginners who are having a hard time searching through the massive amount of info... this thread will be updated as often as i learn something new... enjoy!
Hope this helps Luch
