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looks like your one thats going to have to learn the hard way... have fun
Sent from my Samsung Galaxy
Test E/Tren E/Eq
- Thread starter dirxx
- Start date
looks like your one thats going to have to learn the hard way... have fun
Sent from my Samsung Galaxy
Reverend, you're saying I'm gonna have no balls after this, but you're not telling me why. Like, really.. why? Scientifically speaking.
Just to be clear, I will NOT be taking nolva with tren. I cut tren in week ten, and I'm taking nolva AFTER week 12. Yes, there may be some tren left in the system, like 70mg's left when I begin nolva, but that will be irrelevant, seeing as it will clear up quickly, not enough time for gyno to form.
And also, don't forget the letrozole, anti estrogen and anti prolactin to some extent .. (here is the AI you've been talking about)
Regarding gyno I think the chances of me developing it with 200mgs of tren, 500mg of test weekly AND letrozole are pretty damn slim.
What about cortisol? What does the stress hormone have to do with this particular cycle set-up?
Blood pressure is elevated with every steroid to some extent. If it rises, I'll take some captopril for the duration.
Liver? Winstrol is pretty safe at these dosages, plus I'm taking liv 52, so no problem there.
Kidneys? They aren't affected directly by aas in any major way, the most dangerous thing for the kidneys is high bp, but I've got that covered.
Sit tight, I've done my homework.
Just to be clear, I will NOT be taking nolva with tren. I cut tren in week ten, and I'm taking nolva AFTER week 12. Yes, there may be some tren left in the system, like 70mg's left when I begin nolva, but that will be irrelevant, seeing as it will clear up quickly, not enough time for gyno to form.
And also, don't forget the letrozole, anti estrogen and anti prolactin to some extent .. (here is the AI you've been talking about)
Regarding gyno I think the chances of me developing it with 200mgs of tren, 500mg of test weekly AND letrozole are pretty damn slim.
What about cortisol? What does the stress hormone have to do with this particular cycle set-up?
Blood pressure is elevated with every steroid to some extent. If it rises, I'll take some captopril for the duration.
Liver? Winstrol is pretty safe at these dosages, plus I'm taking liv 52, so no problem there.
Kidneys? They aren't affected directly by aas in any major way, the most dangerous thing for the kidneys is high bp, but I've got that covered.
Sit tight, I've done my homework.
nelson_303
New member
Yo dirxx. Listen to these dudes. You have not done enough reading. No fucking nova. And your cycle timeline blows. Eq 16 weeks or not worth it. How many cycles have you ran before. Please rethink your cycle. Or you will have no balls and some nice DD's to shake at the bar.
nelson_303
New member
Sorry for the disrespect. How old are you dog??
nelson_303
New member
Do the test/tren run 1st. Then plan a huge cycle around EQ. And EQ is for people with real patience. It takes weeks to kick in. It's a long as hell cycle. But hella worth it.
TheRippedReverend
Banned
You have not done your homework! I have experiance with AAS since you were a little sperm sack in mommys tummy!
NOLVA it shit period!!! You want some scienctific writing! I was the experiment!
What does AAS have to do with the stress hormone? Your fucking kidding rite!?
Aas doesnt mess with bp!? Liver!? Your an idiot really bro. Hey have fun u realky have no clue no clue at all. Tren will not be outra your system in 2 weeks lmfao even if its aceate.
Letro is not for Prolactin!!!! For estrogen!
Progesterone its a different fucking hormone!
Kidneys are not affected sigh watch your piss turn dark brown. How do you think everything gets broken down by your heart and blood only!?
Clussless bro tried to help
SERM's (Selective Estrogen Receptor Modulator) : These block certain estrogen receptors, ***ending 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. To learn how this works, please refer to Anthony Roberts PCT in the PCT section.
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.
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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.http://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 cocktail 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 Replacement 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.
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 and RECOMMENDATIONS
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.
What Is Nolvadex/Tamoxifen?
Tamoxifen is considered as the antagonist of the estrogen receptor which again is primarily present in the breast tissue of the human body. It is interesting to note that certain breast cancer cells require that the estrogen levels need to grow with passing time. Ideally, Tamoxifen has been used as the standard endocrine for the treatment of early breast cancer patients. It is therefore used as an anti estrogen therapy and it is mainly given to postmenopausal women. The role of an estrogen is to bind as well as activate the estrogen receptors that are present in the breast cells of a human body. The role of Tamoxifen is to stop estrogen to bind with the receptor. Although it is metabolized into compounds that aid in the binding of estrogen receptors, Tamoxifen does not allow the estrogen receptors to get activated in the breast cells of the human body. Hence, the growth of breast cancer cells can be stopped by making use of this compound. Nonetheless, results vary from person to person and the use of Tamoxifen cannot be deduced as a permanent cure for breast cancer patients.
It is ideally a drug which is taken orally in the form of an edible tablet and it is known to interfere with the activity of the estrogen levels present in the breast tissue. It has been studied that unless the estrogen levels in the human body are kept under strict control, they can lead to breast cancer. Tamoxifen has primarily been used for the past 30 years for treating patients suffering from breast cancer. It has also been administered to patients who are in their early stages of breast cancer. Even patients whose breast cancer has spread to various parts of the body have been known to use Tamoxifen on a regular basis. It has been stated that this drug has the ability to stop cancer cells from spreading within the human body but ironically there is no substantial study which clearly backs this statement with the help of substantial proof. Nonetheless, owing to the hype that it has received via media, people who are having breast cancer or those women who run the risk of developing breast cancer have been known to take this medicine on a regular basis. Interestingly, it has also been seen that women who are suffering from ductul carcinoma in stu, which in turn is similar to invasive breast cancer, have also been known to administer this medicine on a regular basis.
In the past 20 years steroid users have been using nolvadex for a number of reasons. To ether help reduce bloat or gyno problems during a cycle or after a cycle to help recovery natural test production. In men, tamoxifen "nolvaldex" is sometimes used by steroid-taking, weight-training athletes.An alternative and highly similar compound is clomiphene citrate "clomid". These drugs are used as anti-estrogen therapy. In this regard, the drug is used for three purposes. The first purpose, is to reduce the effect of circulating estrogens even if Tamoxifen itself increase the circulating level of estrogens since they are not bound to the estrogen receptors. Abnormally high levels of estrogen in men, can be caused by taking highly aromatizing anabolic steroids e.g. Dianabol, Anadrol or Testosterone. In dosing with a dosing with 20 mg of Novaldex (Tamoxifen) for the duration of a steroid cycle, a reduction in water retention can be achieved. This prevents large fluctuations in water weight within the muscle.
Using Tamoxifen for the duration of a steroid cycle may or may not promote a preferable outcome for a weight training athlete, as the temporary increase in water weight within the muscle increases strength and allows larger weights to be used for the duration of the steroid cycle. Said water will dissipate once usage of steroids has ceased, and a dramatic loss in weight can be observed. Tamoxifen is also used to prevent estrogen related gynecomastia, resulting from elevated estrogenic levels. It can be taken as a preventative measure in small doses, or used at the onset of any symptoms e.g. nipple soreness/sensitivity. In the latter case, dosing reverses the affliction
However it Is now well known that well taking nolvadex serum level estrogen raises and yet another drug must be taken with it during cycle,during pct,or after pct to prevent estrogen rebound. (how retarded). Studies have of course shown the its use can cause a rise in lh and test production but at what cost? Many other factors must be taken into account.
All this is happening in complete ignorance as they are not aware that this medicine has certain side effects that can prove fatal in the longer run. At the same time robbing ones self of a better pct and cycle from using drugs like this.
Though I do feel its "ok" to use them "if you must" but use as little as you can and use support/pct sups to help alleviate the side effects and bad feelings one gets from these harsh drugs.
Where Was This drug Discovered?
Interestingly, this drug was discovered by AstraZeneca Pharmaceuticals which were earliest known as ICI pharmaceuticals. It is now sold under various trade names such as Nolvadex, Valodex and Istubal. Although it is sold under various names, it is primarily known and popularly termed as Tamoxifen. Although this drug is widely used in treating breast cancer patients, it also has adverse side effects which very few people are actually aware off.
Once praised for its benefits in preventing breast cancer recurrence, the lucrative pharmaceutical drug tamoxifen is now implicated in causing dangerous side-effects, including other types of cancers.
In the early 1970's, a shameful chapter closed on the widespread use of a known carcinogenic and endocrine-disrupting drug called DES (diethylstilboestrol), the first synthetic, non-steroidal estrogen drug. Against the advice of its creator, Sir Charles Dodd, between four and six million American and European women and 10,000 Australian women innocently used DES for the prevention of miscarriage and pregnancy complications.
In addition, DES became a popular though unproven drug for a variety of other conditions. It was used for the suppression of lactation, the treatment of acne, the treatment of certain types of breast and prostatic cancer, and as an inhibitor of growth in young girls, an estrogen replacement in menopause and a "morning after" pill.
It would take 30 years to accept what laboratory tests had indicated as early as 1938 — that DES was a highly dangerous and harmful drug. It was reported that, 20 years after taking DES, mothers had a 40 to 50 per cent greater risk of breast cancer than non-exposed mothers. In addition, the children of DES mothers showed a high incidence of reproductive abnormalities, miscarriages, vaginal cancer, testicular cancer, sterility and immune dysfunction. In fact, it is feared that repercussions of this drug will be felt for generations to come.
The irony of this entire debacle is that the medical establishment finally acknowledged that DES was useless in preventing miscarriages. Thus, DES, another disastrous experiment on women, was added to the long list of major medical blunders.
Out of this early research, a new drug appeared on the horizon which would be soon be heralded as a shining star in the war against the growing epidemic of breast cancer. In the late 1960's the pharmaceutical industry developed a drug called "tamoxifen". As a synthetic, non-steroidal compound with hormone-like effects (many of which are poorly understood), tamoxifen has a similar structure to DES. In fact, it was observed that tamoxifen caused the same abnormal changes seen in cells of women taking estradiol and DES. This similarity raised alarm bells for some.
Pierre Blais, well known as a drug researcher who was ejected from Canada's health protection bureaucracy when he spoke out about silicone breast implants, describes the story of tamoxifen as "the story of modern drug design which produces garbage drugs". He says, "Good drug design ceased, unfortunately, in the 1930s." Tamoxifen, Blais asserts, "...is a garbage drug that made it to the top of the scrap heap. It is a DES in the making."
Blais's dire predictions were ignored with the promise of a potential drug treatment for breast cancer. Tamoxifen was first approved by the US Food and Drug Administration (FDA) for use as a birth-control pill; however, it proved to induce rather than inhibit ovulation.(just goes to show how retarded they truly are) Although tamoxifen didn't work as a contraceptive, it was found to lower mammary cancer rates in animals. Animal studies showed that tamoxifen prevented estrogen from binding to receptor sites on breast tissue cells. Tamoxifen also reduced the incidence of breast cancer in rodents after administration of a breast-carcinogenic substance. This discovery provided the impetus to study its effects in treating human breast cancer.
Estrogen is the common link between most breast cancer risk factors, i.e., genetic, reproductive, dietary, lifestyle and environmental. It both stimulates the division of breast cells (healthy as well as cancerous) and, especially in its 'bad' form, increases the risk of breast cancer. Thus, hormonal drugs such as tamoxifen that block the effects of estrogen on the breast were expected to reduce the risk of breast cancer recurring in women treated for breast cancer.
Tamoxifen acts as a weak estrogen by competing for estrogen receptors much as phyto-estrogens do(I want you to keep this word PHYTO ESTROGENS IN MIND WE WILL COVER IT AGAIN LATER). Like phyto-estrogens, tamoxifen has mild estrogenic properties but is considered an anti-estrogen since it inhibits the activity of regular estrogens. More accurately, tamoxifen is an estrogen-blocker(Not a estrogen reducer)
HORMONAL EFFECTS OF TAMOXIFEN IN OLIGOSPERMIC MEN -- WILLIS et al. 73 (1): 171 -- Journal of Endocrinology
Yes the test shows over time that both lh and androgins were raised, but at the same time (serum level estrogen was tripled)and thus the reason many experence rebound gyno after its use. ANd its why when you come off of the nolvadex and or clomid its very very likely you will then get ( re shut down) because high levels of estrogen can cause a shut down to the hpta and at the very least prevent recovery. Though studies show well on them lh is raised. Big deal what about after!!!!!!! the studies all of the studies clearly show that well on them serum level estrogen is raised. When you come off of them and estrogen is high then whats going to happen!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Tamoxifen fights breast cancer by competing with estrogen for space on estrogen receptors in the tumor tissue. Every tamoxifen molecule that hooks onto an estrogen receptor prevents an estrogen molecule from linking up at the same site. Without a steady supply of estrogen, cells in an estrogen-receptor-positive (ER+) tumor do not thrive and the tumor's ability to spread is reduced.
However, tamoxifen exhibited two conflicting characteristics. It could act either as an anti-estrogen or as an estrogen. Therefore, while tamoxifen is anti-estrogenic to the breast, it also acts as an estrogen to the uterus and, to a lesser extent, the heart, blood vessels and bone. Moreover tamoxifen also acts as an estrogen in the liver thus causing the lowering of IGF-1
In This Issue -- 82 (21): 1661 -- JNCI Journal of the National Cancer Institute
http://cancerres.aacrjournals.org/cg.../49/7/1882.pdf
Effect of low dose tamoxifen on the insulin-like growth factor system in healthy women
Comparison of Tamoxifen and Testosterone Propionate in Male Rats: Differential Prevention of Orchidectomy Effects on Sex Organs, Bone Mass, Growth, and the Growth Hormone-IGF-I Axis -- Fitts et al. 25 (4): 523 -- Journal of Andrology
For people suffering from breast cancer I guess this would be a good thing. Since Lowering IGF would reduce the growth of everything. However this is not one any of the people using nolva for pct or on cycle use want now is it?
So, although it initially showed the tendency to counter breast cancer recurrence, it would soon be revealed that it also promoted particularly aggressive uterine and liver cancers, caused fatal blood clots and interfered with many other functions.
Doctors, however, were quick to jump on the tamoxifen bandwagon, turning a blind eye to its more injurious tendencies. Starting in the 1970's oncologists began using tamoxifen to treat women with cancer, often in combination with other drugs, radiation or surgery such as lumpectomy and mastectomy, with modest success. Like DES, tamoxifen's benefits were then extended for use as a preventive against osteoporosis and heart disease.
Today, doctors are treating about one million American breast cancer patients with tamoxifen, about 20 per cent of them for more than five years. As studies published in the New England Journal of Medicine in 1989 and the Journal of the National Cancer Institute in 1992 showed, women with breast cancer who took tamoxifen reduced their chances of developing cancer in the other breast (contralateral cancer) by about 30 to 50 per cent. These findings would later be challenged.
Tamoxifen is now recommended for all pre-menopausal women with hormone-positive cancers, as well as for most postmenopausal women with breast cancer and/or a growing number of women with hormone-negative cancers. Tamoxifen is currently used by more women with breast cancer than any other drug.
Tamoxifen (brand name Nolvadex) is now the most widely prescribed cancer medication in the world. It generated revenues of US $265 million in 1992. By 1995, worldwide sales of Nolvadex reached $400 million. (7) And at AUD $90 for one month's supply, it doesn't come cheap (the Australian Pharmaceutical Benefits Scheme covers $70).
Global sales of tamoxifen in 2001 were $1,024 million.[54] Since the expiration of the patent in 2002, it is now widely available as a generic drug around the world. Barr Labs Inc had challenged the patent (which in 1992 was ruled unenforcable) but later came to an agreement with Zeneca to licence the patent and sell tamoxifen at close to Zeneca's price.[55] As of 2004, tamoxifen was the world's largest selling hormonal drug on record and off record may be the number 1 selling drug in word of all time to date. So we are truly talking about billions in revenue world wide for drug companies,sources,ug's and more. Money is at the root of this drug and why its so heavily pushed on all forums by everyone. Its cheap to make and it brings in billions plain and simple.
These numbers are nothing compared to what this drug now makes for the drug companies,sources.ug's selling it. So you can bet your life they will make sure every test and study in the world is published to make sure its seen in a good light. This not even including its "off label use" Ie all us men using it for on cycle and pct. The use of the drug for this reason triples its sales and you can just emagen the amount of money its making. You do the math my friends!. At this very moment 500000000 sources and people with monitary ties to this drug are out there pushing like crazy to make sure you and everyone else keeps its use for pct alive. This is the #1 reason why we have not given up on this years ago.
Tamoxifen was developed by UK-based Imperial Chemical Industries (ICI), one of the world's largest multinational chemical corporations. Zeneca, an ICI subsidiary, is responsible for manufacturing and marketing the hormone and is now the world's largest cancer-drug company.
CARCINOGENENIC EFFECTS
It wasn't long before laboratory studies showed that tamoxifen acted as a carcinogen. It has been found that tamoxifen binds tightly and irreversibly to DNA, the genetic blueprint of a cell, causing a cancerous mutation to take place. Even Australia's conservative National Health and Medical Research Council (NHMRC) warned that no amount of tamoxifen is safe when it comes to carcinogenic effects.
In California there is a law called "Proposition 65" that requires the state to publish and maintain a list of all known carcinogens. In May 1995, the state's Carcinogen Identification Committee voted unanimously to add tamoxifen to its list.
When research is done on anti-cancer drugs (such as SERMs), the aim is to find a drug that prolongs life, with the least amount of acute side-effects. In other words, the goal isn’t so much about finding a cure, as it is finding something that can alleviate the symptoms and/or prolong life.
When it comes to steroid users so many are willing to forgo any and everything to get the one simple effect they desire (recovery). The popularity of these drugs stems from the popular advice to use these drugs for everything from testosterone recovery.bitch tits,make your **** grow bigger, increase the amount of jiz you drop on a girls face, and everything in between. Advice on its use is handed out like candy and everyones got a sweat tooth for quick advice. Of course many "vets and so called know it alls" defend it to the death and it can do no wrong. Mainly do to not wanting to be wrong,habit,they got money involved with it, or just for the sake of argument.
“Its FDA approved for cancer treatment. It must be safe!”
It’s wrong to assume that an “FDA approved” drug has a proven safety profile. The FDA has continually issued stronger health warnings for tamoxifen over the years. For instance, in 1994 the FDA demanded that the tamoxifen manufacturer Zeneca (an ICI sub-division), issue warning letters to health care practitioners about the increased risk of endometrial and gastro-intestinal cancers with tamoxifen use. Zeneca also reported adverse effects similar to those seen with DES, such as reproductive abnormalities in the animals whose mothers received tamoxifen. (remember, DES was the original synthetic estrogen, and also an analog to tamoxifen)
A number of cancer researchers have pointed out the health risks too, such as Elwood et al (6) -
“[Tamoxifen], therefore, is not appropriate for use in the general population because of the known increased risk of endometrial cancer”
What Are Side Effects Of Temoxifen
You Can Get Blood Clots!
Have you any idea that a regular dosage of Tamoxifen can actually increase the chances of blood clots? Well, this is a true fact and can be fatal for those who are using this drug to get rid or avoid the chance of getting Gyno on cycle and or for pct. According to recent medical studies, it has been noticed that people who have been using Tamoxifen on a regular basis have had a substantial increase in terms of their blood clots. Hence, as compared to those people who are not using this drug, their chances of getting blood clots is relatively higher.
A blood clot can be defined as an internal body mechanism by which the cut can be stopped from bleeding excessively. The proteins present in your blood work along with the platelets and in a bid to form a clot. This is also termed as coagulation. In the event of an injury, this can prove to be really very effective as it would stop the flow of blood from your wound and thus save your life. Nonetheless, if the blood clots while it is moving through your body, it can prove fatal. This is also termed as hyper coagulation and it can prove very dangerous for the concerned individual. Tamoxifen has been known to cause hyper coagulation and hence, it needs to be taken under strict medical supervision.
When the study was conducted, it was ascertained that a relatively large number of people developed this conditions and although not many people using this drug were actually studied, those that were using it regularly, were in a shock to find out that it also led to blood clots.
Hence, although this drug is helpful to a certain extent, we need to also see that the extent of damage it can do to our body in terms of hazardous blood clots are much more and hence, you as a steroid user need to exercise caution and spend some quality time researching on this so called ‘wonder-drug’ before making it an eminent part of your daily routine and or pct.
One of the main reasons why a blood clot is considered dangerous is because this drug causes a clot inside the blood vessel which in turn is known as thrombus. What happens is that at times this blood clot can travel through your blood streams and get pushed into your lungs. When this happens, you can be rest assured that your life is in acute danger as this condition is life threatening. This condition is also known as pulmonary embolus. Similarly, a clot this clot can also block the blood vessels in the brain and this in turn may lead to a stroke. When this blood clot clocks the blood vessels of your heart, it stops the blood from rushing to your heart area thereby reducing the oxygen supply to that area. This in turn leads to cardiac arrest.
All the above mentioned conditions arising from blood clots, which in turn are caused from a regular intake of Tamoxifen, can prove to be life threatening for the concerned individual. Hence, even before you decide to take this medication on a regular basis, you need to exercise caution and be prepared to face the ill effects of this so called ‘wonder-drug’.
Increased susceptibility to gyno -
Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.
This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developing gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting upon the progesterone receptor).
It is interesting to speculate. Is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?
You Can Develop Cataract!
Cataract can be defined as a thin white layer of membrane which blocks the passing light to the retina thereby clouding your vision. Although it is relatively painless, it does cloud your vision and can even blind you if it is not removed through the means of a surgical procedure. The retina is ideally a nerve layer which is located at the back of the eye socket and its main purpose is to direct the light which is entering the eye via the means of electromagnetic signals to the brain. Once the brain receives these nerve signals, it is passed on to the nervous system, after which you can transform your vision into clear moving pictures. If this thin layer of membrane is blocked owing to any reason, you would have problems with your vision.
While aging is looked on as the major cause behind cataract, it has recently been noticed that patients using Tamoxifen have been identified as ones susceptible to cataract on a regular basis. people who are aging and using this drug on a regular basis are on a higher risk of contracting cataract as compared to those who are not using Tamoxifen. The other eye problems that can be faced by individuals include scarring of the corneal area and abrupt retinal changes.
In case you are using this drug regularly and you have a cloudy, fuzzy or foggy vision, you need to get your eyesight checked with immediate effect. In case you are unable to withstand the glare of lamps and are unable to catch a glimpse of the morning sun, then again you need to get your eyes checked. This is so because, Temoxifen has a natural tendency to obstruct the normal eye vision and if you do suffer from this symptom, you may not be able to drive at night as the headlamps of the opposing vehicle may blind you momentarily.
In order to get rid of cataract that has been developed owing to a continuous intake of Temoxifen, you may need to undergo a corrective surgery. In case you want to delay a surgical procedure, you may want to light up your room with plenty of tubes and bulbs and keep your eyeglass up to date with the latest prescription. Ideally, the only known cure for cataract that has been a resultant of Temoxifen is a surgical procedure.
If you would like to avoid this problem, you would have to seek an alternative to Temoxifen at the earliest given opportunity.
Libido reduction & erectile dysfunction
Erectile dysfunction ow libido, and general impotence are typical complaints from men recently discontinuing steroids or HRT therapy, which is often combated by Clomid or Nolvadex, paradoxically so.
Regardless of any positive effects on fertility or testosterone levels, Clomid and Nolvadex use is highly correlated with erectile dysfunction, libido suppression, and even emotional disorders Research with male breast cancer patients has also reported decreased libido, and thrombosis associated with tamoxifen use. he thrombotic effect (blood vessel clogging) could explain the mechanism by which SERMs may inhibit erectile function, by reducing circulation to erectile tissue (as discussed before)
Nolva/clomid both raise shbg.
This is something I do not see a lot of people disusing so I I wanted to make it well know. Just do a web search on TAMOXIFEN,clomid or nolva raises shbg or any variation and you will get all the studies and prof you need.
Trait Anxiety and Tamoxifen Effects on Bone Mineral Density and Sex Hormone- Binding Globulin -- Cameron et al. 64 (4): 612 -- Psychosomatic Medicine
iHOP - Information Hyperlinked over Proteins [ SHBG ]
Sex Hormone Binding Globulin in Clinical Perspective; Acta Obstetricia et Gynecologica Scandinavica - 66(3)
ages 255-262 - Informa HealthcareWiley InterScience :: Session Cookies
2. Nolva lowers Igf-1 Again just a simple search on (TAMOXIFEN or nolva lowers IGF 1 and walla you got all the prof you need.
In This Issue -- 82 (21): 1661 -- JNCI Journal of the National Cancer Institute
http://cancerres.aacrjournals.org/cg.../49/7/1882.pdf
Effect of low dose tamoxifen on the insulin-like growth factor system in healthy women
Comparison of Tamoxifen and Testosterone Propionate in Male Rats: Differential Prevention of Orchidectomy Effects on Sex Organs, Bone Mass, Growth, and the Growth Hormone-IGF-I Axis -- Fitts et al. 25 (4): 523 -- Journal of Andrology
They can cause Major triglyceride and glucose problems and even to the point of Severe hypertriglyceridemia or also Pancreatitis
Severe hypertriglyceridemia caused by tamoxifen-tr... [Endocr J. 1997] - PubMed result
Tamoxifen-induced hypertriglyceridemia in association with diabetes mellitus - EM|consulte
SpringerLink - Journal Article
Capecitabine-Induced Severe Hypertriglyceridemia: Report of Two Cases -- Kurt et al. 40 (2): 328 -- The Annals of Pharmacotherapy
Elsevier: Article Locator
Estrogen and Triglycerides
http://annonc.oxfordjournals.org/cgi.../11/8/1067.pdf
WikiGenes - Hypertriglyceridemia
A word on clomiphene (Clomid) –
Clomiphene (Clomid) consists of two stereoisomers which possess radically different pharmacodynamics. Zuclomiphene has predominantly estrogenic effects and slow clearance while the enclomiphene isomer has predominately anti-estrogenic effects and quick clearance. his creates a divergent effects between estrogen blockage and estrogen stimulation and an acute imbalance once Clomid administration is discontinued. Bodybuilders will often complain of “estrogenic rebound” after stopping Clomid, which could be attributed to the lingering estrogenic isomer zuclomiphene as the anti-estrogenic enclomiphene has long cleared the system. (Recently, enclomiphene has been isolated by the pharmaceutical company Repros, for use in Androxal™.)
For all intents and purposes, tamoxifen is a superior SERM, simply for the fact that tamoxifen provides a purely anti-estrogenic isomer, whereas Clomid provides a mix of anti and pro estrogenic effects.
In regards to the health consequences about to be listed, it can be safely assumed that Clomid will share similar detrimental effects as tamoxifen, since it shares the same triphenylethylene backbone and carcinogenic tendencies.
One of the main reasons why people make use of Clomid is for the purpose of recovering their bodies after a steroid cycle In simple words, this drug is mainly used in the form of post cycle therapy. Clomid has the actual potential to stimulate the production of hypothalamus which in turn would release a particular kind of hormone called gonadotrophic hormones. This hormone has the natural ability to allow the human testicles to secrete testosterone, which in turn would bring the depleting levels of testosterone in the body to its permissible levels. When this is achieved, the human body would stop losing its muscle mass in a natural way. Reacovery of test production is the gaols at any cost is the common thought.
Its a known fact that both clomid and nolvadex cause some really messed up mood swings.
Clomid/nolva have been known to cause severe mood swings in users and it has apparently been noticed that anyone who has been making use of Clomid/nolva have suffered from such side effects on a regular basis. Many users have categorically complained that the use of Clomid has been considered as the worst side effect that they have suffered so far. A few features of mood swings may include a change in the usual behaviour, tearful behaviour, excessive depression, anxiety and extremely sensitive in nature. Stop acting like you don't know what I am talking about. We all know its true.
Liver cancer -
Originally, tamoxifen was accepted as being non-toxic to the human liver upon finding that tamoxifen did not cause noticeable liver damage (DNA adducts) during short-term test tube studies with human liver cells.
However, it became apparent that test tube research was largely flawed due to the low rate of metabolism in such a superficial environment. It was soon discovered that the hepatotoxic effects from tamoxifen stem from the metabolism and buildup of the a-hydroxytamoxifen and N-desmethyltamoxifen metabolites, which would only appear in an in vivo environment. Surely enough, the results from the original rat studies showing dramatic carcinogenic effects on the liver, soon correlated with human data when researchers found the same type of liver DNA adducts in tamoxifen patients.
More recent human research has reported tamoxifen treated women to have 3x the risk of developing fatty liver disease, which occurs as soon as 3 months into therapy at only 20mg/day. In some cases, the disease lasts up to 3 years, despite cessation of tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy show cases of deadly hepatocellular carcinoma.
In 2002, a bizarre study examined the use of tamoxifen for hepatocellular carcinoma treatment in humans. It was assumed that since tamoxifen could inhibit proliferation of breast cancer, it could offer the same benefit for liver cancer. The devastating results could not have been more indicative of tamoxifen’s hepatotoxic nature, as the tamoxifen treatment significantly increased the rate of death, compared to the group not receiving tamoxifen.
F
Finally, in a case study reviewing tamoxifen induced liver disease; D.F Moffat et al made a profound statement –
“Hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast.” In other words, it appears that liver carcinomas from a large number of breast cancer patients on tamoxifen therapy have been misdiagnosed as an infection from the breast cancer itself.
TheRippedReverend
Banned
Here u go mr scientific
Cortisol is the stress hormone . It plays vital roles in our bodies. It is a powerful anti-inflamitory. Cortisol is secreted when we feel stress, both emotional and physical. It helps us cope. It is a response to fight or flight. When elevated for short periods of time like it is supposed to, it is harmless. Cortisol may suppress testosterone , and vice versa.
Short-term cortisol exposure (seconds to minutes, as you might experience from moderate levels of exercise) causes :
* glycogen breakdown
* increased blood sugar
* fat tissue breakdown
* elevated blood pressure
* improved cardiovascular dynamics (i.e., stronger heart contractions, etc.).
Each of the above factors is a "good" thing while you are exercising--but you want these metabolic parameters to return to baseline levels after exercising.
Chronic cortisol exposure (hours to days to weeks, as you might experience from overtraining, psychological stressors, excessive dieting or too little sleep) causes:
* increase appetite, especially carb craving
* increased blood sugar
* accelerated muscle tissue breakdown
* accelerated connective tissue breakdown (bones, tendons, ligaments, cartilage, skin)
* suppressed immune system function
* increased fat storage, especially trunkal fat (associated with diabetes, heart disease, cancer)
The "moral" of the story is that cortisol is neither "bad" nor "good"--the length of your exposure is what matters. During chronic cortisol exposure, we "shift" or "up" from cortisol being a fat-loss stimulus to it being a signal for fat-gain and muscle loss. Furthermore, it can disrupt numerous body systems.
***thnx RonnietheBull***
Cortisol : Why would your levels be elevated?
People who dont sleep enough, dont eat a balanced diet (cortisol will break down muscle if you dont feed yourself enough protiens) or are experiencing stressfull situations on a daily basis may have prolonged elevated cortisol levels. If your natural, workouts that go to long at high intesity will raise levels. Keeping wrkouts to about an hour helps. More specifically to us, using AAS blocks the effects of cortisol. This in turn ups the production of cortisol and increases receptor sites. Thus, when a cycle is ended, the receptors are freed, and boom, your instantly catabolic, and very much so. It is MOST important to us to control cortisol levels in PCT , right at the end of a cycle. It is not to much of a worry while cycling. This alone should be enough to get your attention. A cortisol spike may make you restless, sleepless and anxious.
Cortisol : What we can do to control it.
The simplist way to control cortisol levels are a balanced diet, moderate excerisize and good sleeping patterns. If you are working out natural, be sure not to overtrain.
On cycle, it is not much a problem. Just eat right, train hard and rest. Like I mentioned above, cortisol is greatly affected by AAS use. It is a major part of the post cycle crash. This is where we should be most concerned.
I will be sure to use some type of cortisol remedy in my next PCT. It should be started as your last ester runs out of your body. One testimony from DemirSteel is he uses RU-486 to fight cortisol in PCT. Some bros have told me cutting cortisol in PCT really helped keep gains. Clenbuterol is said to help, with its anti-catabolic properties, and is a popular choice because of its fat burning ability. It is what i will use in PCT along with my anti-e's.
Cortisol : Remedies we can use.
Here are some meds or natural suppliments that ive found :
-Mirtazapine (http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract)
--May make you feel like a zombie, reported to me that messes with mood.
-Clenbuterol (http://forums./showthread.php?t=148950)
-Relacore (natural suppliment) (http://<br /> http://www.fitnessone...roducts_id/410)
-Relacore is also in Lean Xtreme by designersupps.com (http://designersupps.com/static_site/leanxtreme.php)
-- this one was reported to me to work really well, and i think its natural.
-Phosphatidylserine (Cytodyne) (http://www.nicemuscle.com/cytodyne-82088.htm)
-- an ingredient in some suppliments i have never used. reported to me to work well from a female member.
-RU-486 (http://www.feminist.org/action/action120f.htm)
--do research if you plan on using this drug. It is the abortion pill, and i have limited knowledge on it.
Summary
Well, to sum up, cortisol is bad for us when elevated, and coming off a cycle does this. While on cycle, no biggie, as its actions are blocked by AAS. When going natural, eat right, sleep right, DONT overtrain (like 1 hour is the most in a day). I will most certainly be using a cortisol rememdy when i come off cycle. As usual, this thread is open to suggestions, other remedies, and real life experiences fighting cortisol, especially in PCT. Feel free to add your knowledge! Later bro's, im friggen worn out...
Cortisol is the stress hormone . It plays vital roles in our bodies. It is a powerful anti-inflamitory. Cortisol is secreted when we feel stress, both emotional and physical. It helps us cope. It is a response to fight or flight. When elevated for short periods of time like it is supposed to, it is harmless. Cortisol may suppress testosterone , and vice versa.
Short-term cortisol exposure (seconds to minutes, as you might experience from moderate levels of exercise) causes :
* glycogen breakdown
* increased blood sugar
* fat tissue breakdown
* elevated blood pressure
* improved cardiovascular dynamics (i.e., stronger heart contractions, etc.).
Each of the above factors is a "good" thing while you are exercising--but you want these metabolic parameters to return to baseline levels after exercising.
Chronic cortisol exposure (hours to days to weeks, as you might experience from overtraining, psychological stressors, excessive dieting or too little sleep) causes:
* increase appetite, especially carb craving
* increased blood sugar
* accelerated muscle tissue breakdown
* accelerated connective tissue breakdown (bones, tendons, ligaments, cartilage, skin)
* suppressed immune system function
* increased fat storage, especially trunkal fat (associated with diabetes, heart disease, cancer)
The "moral" of the story is that cortisol is neither "bad" nor "good"--the length of your exposure is what matters. During chronic cortisol exposure, we "shift" or "up" from cortisol being a fat-loss stimulus to it being a signal for fat-gain and muscle loss. Furthermore, it can disrupt numerous body systems.
***thnx RonnietheBull***
Cortisol : Why would your levels be elevated?
People who dont sleep enough, dont eat a balanced diet (cortisol will break down muscle if you dont feed yourself enough protiens) or are experiencing stressfull situations on a daily basis may have prolonged elevated cortisol levels. If your natural, workouts that go to long at high intesity will raise levels. Keeping wrkouts to about an hour helps. More specifically to us, using AAS blocks the effects of cortisol. This in turn ups the production of cortisol and increases receptor sites. Thus, when a cycle is ended, the receptors are freed, and boom, your instantly catabolic, and very much so. It is MOST important to us to control cortisol levels in PCT , right at the end of a cycle. It is not to much of a worry while cycling. This alone should be enough to get your attention. A cortisol spike may make you restless, sleepless and anxious.
Cortisol : What we can do to control it.
The simplist way to control cortisol levels are a balanced diet, moderate excerisize and good sleeping patterns. If you are working out natural, be sure not to overtrain.
On cycle, it is not much a problem. Just eat right, train hard and rest. Like I mentioned above, cortisol is greatly affected by AAS use. It is a major part of the post cycle crash. This is where we should be most concerned.
I will be sure to use some type of cortisol remedy in my next PCT. It should be started as your last ester runs out of your body. One testimony from DemirSteel is he uses RU-486 to fight cortisol in PCT. Some bros have told me cutting cortisol in PCT really helped keep gains. Clenbuterol is said to help, with its anti-catabolic properties, and is a popular choice because of its fat burning ability. It is what i will use in PCT along with my anti-e's.
Cortisol : Remedies we can use.
Here are some meds or natural suppliments that ive found :
-Mirtazapine (http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract)
--May make you feel like a zombie, reported to me that messes with mood.
-Clenbuterol (http://forums./showthread.php?t=148950)
-Relacore (natural suppliment) (http://<br /> http://www.fitnessone...roducts_id/410)
-Relacore is also in Lean Xtreme by designersupps.com (http://designersupps.com/static_site/leanxtreme.php)
-- this one was reported to me to work really well, and i think its natural.
-Phosphatidylserine (Cytodyne) (http://www.nicemuscle.com/cytodyne-82088.htm)
-- an ingredient in some suppliments i have never used. reported to me to work well from a female member.
-RU-486 (http://www.feminist.org/action/action120f.htm)
--do research if you plan on using this drug. It is the abortion pill, and i have limited knowledge on it.
Summary
Well, to sum up, cortisol is bad for us when elevated, and coming off a cycle does this. While on cycle, no biggie, as its actions are blocked by AAS. When going natural, eat right, sleep right, DONT overtrain (like 1 hour is the most in a day). I will most certainly be using a cortisol rememdy when i come off cycle. As usual, this thread is open to suggestions, other remedies, and real life experiences fighting cortisol, especially in PCT. Feel free to add your knowledge! Later bro's, im friggen worn out...
TheRippedReverend
Banned
Lol tnx bro
He wanted to play!!! Game on
You know not tryin to be a dick but I wish someone would had told me!
Jus trying to help
