MESO-Rx
Anabolic Steroids
Bill Roberts: Help on 2 on 4 off cycle
- Thread starter tgfan
- Start date
mac111
New Member
ok so, you dont need any advice then....
I respectfully disagree.
I think we should call it a (anabolic) steroid.
Testosterone is a steroid hormone. It is androgenic. It is anabolic.
It is an "anabolic-androgenic steroids" or simply an "anabolic steroid".
I understand why many people don't want to call testosterone a steroid.
It is a semantics game.
Steroids have been so demonized that it is almost impossible to overcome the stigma associated with them.
However, this is exactly what millions of men who are using testosterone replacement therapy (TRT) must do.
The majority of those men have probably internally demonized steroids and have bought into the steroid hysteria seen in U.S. media.
But at the same time, they themselves are using testosterone and have great (i.e. positive) results.
This creates cognitive dissonance for the new therapeutically-inclined steroid user.
It's easiest to resolve this dissonance by NOT calling testosterone a steroid.
Similarly, pharmaceutical companies who have billions to gain from legal steroid (testosterone) sales don't want to waste time and money trying to change the perception of steroids. The easiest path to riches for bigpharma is to perpetuate the perception that testosterone is completely unrelated to those evil anabolic steroids.
Personally, I find this approach to be incredibly dishonest. It fails to addresses the big problem: steroid demonization.
Steroids are not evil. We should not pretend they are in an effort towards mainstream acceptance of testosterone for TRT.
Accordingly, I think we should proudly and rightly reclaim testosterone as an anabolic steroid. Of all the drugs included in the category of anabolic-androgenic steroids, testosterone is the best. It should be the compound that is representative of the entire class of AAS.
i dont need to read up.
i came here for advice. my first post in the form of a question. and not the only one ive had. ie bros, can you give me some advice. check it out. its a question on an alternate use of steroids. like a 2 week on. 2 or more off. but different. later this idea was relayed to me. a bill roberts idea. and seems to work for some.
right now i dont need advice. not yours anyway. youve never tried a two week cycle. never will. and have no practical experience or advice. it could work you say. if you use a suspension, a short acting steroid, and then expect moderate, or as you say minimal gains. over time these add up. and that type of drug is recomended. the results to be expected. so thanks so much for your "help".
methyl estradiol is more potent. methyl test aromatizes into methyl estradiol. really who uses methyltest. boldenone aromatizes. less than test. methyl boldenone aromatizes into. you guessed it. methyl estradiol. methyl boldenone is aka d-bol. d-bol recomended. works. works well. id like a sample.
so its me. im over analyzing. someone one told me. the first part of analyzing is... anal. its too much. but i like drugs. how they work. i analyze.
but im not alone. why make alterations in steroids. why look for sarms. they are selective. thats why. build muscle. burn fat. forget about sides. dan duchaine did. thioderon? he talked about. not androgenic. not estrogenic. pure. ill have to look that up. just popped into my head. whatever.
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Remember the reason for doing 2 weekers guys. It's NOT to get the most gains. It's only a way to do steroids very safely with little to no sides. In my opinion the worst side of roid use is how all of them totally annihilate good cholesterol levels(hdl) and the 17aa orals(and winny injectable) are the worst in this regard. However, even low dose T does it.
I have not had any hdl reduction while doing a two weeker.
Also, two weekers a re a way to get some gains above what you could do naturally and keep almost all of them since T recovery is very rapid.
Also, it's a way for guys that have been mentally addicted to roid use to use way less roids. After all why cycle 12 weekers several times a year or worse yet stay on roids all the time more or less and use T for HRT while off, unless you plan on making a living as a pro bodybuilder.
Below is a GREAT read from Bill Roberts. Those guys that are paranoid about these two weekers should read this.
The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.
This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the clomid use.
So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.
What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.
Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.
--------------------------------------------------------------------------------
The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones – instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
--------------------------------------------------------------------------------
Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:
Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
Use an amount and kind of AAS that is low enough to avoid much inhibition. primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.
I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the "clock" that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.
--------------------------------------------------------------------------------
Drugs of Use With Regard to Inhibition
Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.
Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.
clomid: After a cycle is over, clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.
Nolvadex: This works in the same manner as clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If clomid is used, there is no need for Nolvadex.
HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.
Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.
Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.
Tribulus: If this is of benefit, I have not been able to observe it myself. I have only tried the Tribestan brand, but this is the brand that earned tribulus its reputation.
Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have seen no evidence that taking melatonin at night speeds recovery. It is useful though for those who have allowed their sleep patterns to be disrupted and who wish to reset their natural clocks.
--------------------------------------------------------------------------------
General Recommendations
Pharmaceutical drugs should of course not be self-prescribed: the following are simply recommendations of what works well, not of what to do without physician’s advice. Enough said.
The best cycle plans are either brief two week cycles with short acting drugs, which allow a very fast recovery (less than one week) or cycle of approximately 6-10 weeks, which usually allow reasonable recovery and allow quite a bit of time to make gains. Cycles in the 3-5 week range are less efficient because they combine the disadvantage of relatively little time gaining with the disadvantage of slower recovery.
If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the cycle if possible, as described above. HCG should not be used during the recovery itself since it will increase androgen and estrogen levels, which will be inhibitory to the hypothalamus and pituitary.
clomid use should begin, if it was not used during the cycle, as soon as androgen levels drop enough that recovery becomes possible. This would be about two weeks after the last injection of long acting steroid esters, assuming reasonable doses such as 500 mg/week. clomid use should start with 300 mg on the first day (50 mg six times) to quickly get blood levels as high as needed, and then maintained with 50 mg/day. This is needed because of the half-life of the drug. It should be continued until one is sure that natural testosterone production is back and testicle size is returned to normal, with the exception that if use has been more than about 6 weeks, one might try dropping it for a few weeks to see what happens. If no further improvement occurs, then clomid would be resumed. It has been studied medically for long-term use and found safe for periods of at least a year. However, a small percentage of users develop vision problems from clomid, which are generally reversible upon discontinuing the drug. So if you have this problem, certainly the drug should be discontinued.
If aromatizable injectables were used, an antiaromatase would be useful for 3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram per week or more.)
Lastly, ephedrine seems to be of some help. The same dose as used for dieting (e.g. 25 mg three times per day) seems quite sufficient.
Long term inhibition can potentially be a serious side-effect of AAS use, and this risk should be minimized by avoiding excessively long cycles. This really does not compromise gains greatly, since the body cannot grow rapidly week in, week out, 52 weeks per year anyway. And even moderate post-cycle inhibition is something we wish to minimize, since it is frustrating to lose much of one’s gains in the first few weeks after a cycle as a result of low natural testosterone and no AAS being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful.
I have not had any hdl reduction while doing a two weeker.
Also, two weekers a re a way to get some gains above what you could do naturally and keep almost all of them since T recovery is very rapid.
Also, it's a way for guys that have been mentally addicted to roid use to use way less roids. After all why cycle 12 weekers several times a year or worse yet stay on roids all the time more or less and use T for HRT while off, unless you plan on making a living as a pro bodybuilder.
Below is a GREAT read from Bill Roberts. Those guys that are paranoid about these two weekers should read this.
The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.
This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the clomid use.
So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.
What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.
Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.
--------------------------------------------------------------------------------
The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones – instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
--------------------------------------------------------------------------------
Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:
Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
Use an amount and kind of AAS that is low enough to avoid much inhibition. primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.
I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the "clock" that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.
--------------------------------------------------------------------------------
Drugs of Use With Regard to Inhibition
Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.
Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.
clomid: After a cycle is over, clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.
Nolvadex: This works in the same manner as clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If clomid is used, there is no need for Nolvadex.
HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.
Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.
Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.
Tribulus: If this is of benefit, I have not been able to observe it myself. I have only tried the Tribestan brand, but this is the brand that earned tribulus its reputation.
Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have seen no evidence that taking melatonin at night speeds recovery. It is useful though for those who have allowed their sleep patterns to be disrupted and who wish to reset their natural clocks.
--------------------------------------------------------------------------------
General Recommendations
Pharmaceutical drugs should of course not be self-prescribed: the following are simply recommendations of what works well, not of what to do without physician’s advice. Enough said.
The best cycle plans are either brief two week cycles with short acting drugs, which allow a very fast recovery (less than one week) or cycle of approximately 6-10 weeks, which usually allow reasonable recovery and allow quite a bit of time to make gains. Cycles in the 3-5 week range are less efficient because they combine the disadvantage of relatively little time gaining with the disadvantage of slower recovery.
If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the cycle if possible, as described above. HCG should not be used during the recovery itself since it will increase androgen and estrogen levels, which will be inhibitory to the hypothalamus and pituitary.
clomid use should begin, if it was not used during the cycle, as soon as androgen levels drop enough that recovery becomes possible. This would be about two weeks after the last injection of long acting steroid esters, assuming reasonable doses such as 500 mg/week. clomid use should start with 300 mg on the first day (50 mg six times) to quickly get blood levels as high as needed, and then maintained with 50 mg/day. This is needed because of the half-life of the drug. It should be continued until one is sure that natural testosterone production is back and testicle size is returned to normal, with the exception that if use has been more than about 6 weeks, one might try dropping it for a few weeks to see what happens. If no further improvement occurs, then clomid would be resumed. It has been studied medically for long-term use and found safe for periods of at least a year. However, a small percentage of users develop vision problems from clomid, which are generally reversible upon discontinuing the drug. So if you have this problem, certainly the drug should be discontinued.
If aromatizable injectables were used, an antiaromatase would be useful for 3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram per week or more.)
Lastly, ephedrine seems to be of some help. The same dose as used for dieting (e.g. 25 mg three times per day) seems quite sufficient.
Long term inhibition can potentially be a serious side-effect of AAS use, and this risk should be minimized by avoiding excessively long cycles. This really does not compromise gains greatly, since the body cannot grow rapidly week in, week out, 52 weeks per year anyway. And even moderate post-cycle inhibition is something we wish to minimize, since it is frustrating to lose much of one’s gains in the first few weeks after a cycle as a result of low natural testosterone and no AAS being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful.
No use in getting into a pissing match with you. You seem to be generally quite argumentative anyway. For your information I have been in general practice for 20 years and have been a trainer of pro athletes, including pro bodybuilders for 20 years.
You said ....--"blocker? so you only use tamoxifen as an estrogen receptor antagonist, thus no hpta stimulation from clomifen. got it."
What on earth are you talking about. Are you saying that Clomid actually stimulates the hypothalamus? Nolva and clomid do exactly the same thing...they block the estrogen receptor. Both work.
"While it has been claimed that Clomid “stimulates” production of luteinizing hormone (LH) and therefore of testosterone, in fact Clomid’s activity is achieved not by stimulation of the hypothalamus and pituitary, but by blocking their inhibition by estrogen." Bill Roberts
You said this ..."***High estrogen, low test, delayed physiological homeostasis; Sounds Like A Crash To Me LOL
Crash is the time in which you await natural hormonal physiological levels to normalize"
Bro, a crash is a big drop in T and for a long time. Yes, the hypothalamus will sense after you stop the blocker(T levels are higher than your normal from proper PCT.) but the drug goes way gradually and thus estrogen blockade goes away gradually....there is no crash. Things just normalize(to your own physiological levels) over a period of time and it's gradual. Ie: 3 days after you stop a Nolva you still have half the drug in your system....so there is still some blockade but it's less....thus T levels drop a bit as the hypothalamus senses more estrogen. it's a slow gradual return to your normal T levels bro....no crash.
The trouble is some guys stay on roids too long or repeat them too soon and get testicular shrinkage , and don't use HCH during a cycle to help keep the testis working and sizable. The pituitary also gets inhibited. So PCT with a blocker and or an AI doesn't work as well. It will eventually work but it can take a long time and guys can loose most of their gains waiting.
So for the non competitive bodybuilder 2 weeks "on" and 4 weeks off, done with the right roids, and training, eating and sleeping right, really is the way to go.
No crash and little to no sides. Bill Roberts is truly a steroid guru to have figured this out years ago.
RG
Let me add this regarding PCT and recovery of normal T production.
BY FAR the most important thing in recovery of the HPTA axis is getting the testes up to size so they can respond well to LH. This is a non issue with two weekers because there is no testicular shrinkage(or very very little at most).
As Bill Roberts said, LH production is even greater after a two weeker because the pituitary has not gone to sleep and is hyper-sensitive to GnRH from the hypothalamus.
ESTROGEN BLOCKERS or AI's POST CYCLE.
They don't do a great deal actually, UNTIL AFTER NATURAL T PRODUCTION is at least getting close to normal....to a point that estrogen(from the aromatization of this T to e) is starting to become inhibitory at the hypothalamus.
HCG is KEY.
Keep your nuts from shrinking during a cycle like Bill Roberts says, so that they can respond well with good T production once androgen levels drop post cycle to what the hypothalmus considers below normal(so it will release GnRH).
William Llewellyn is another guy that knows his shit, like Bill Roberts. Bill may be highly higher on the gura list though lol.
Llewellyn doesn't like even small doses of HCG DURING cycles because he thinks it can desensitize the Pituitary to natural LH(as Bill mentions above).
So.....he starts his dose late is a cycle(post cycle but when androgen levels from aromatizing steroids are still elevated).
Here's a quote from him.
"An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2) , which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of clomid would typically be added ( my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.
Sample Post-cycle Plan:
Week 3: 5000IU HCG total + 20mg Nolvadex daily
Week 4: 5000IU HCG total + 20mg Nolvadex daily
Week 5: 2500IU HCG total + 20mg Nolvadex daily
Week 6: 20mg Nolvadex daily
Week 7: 20mg Nolvadex daily
Week 8: 20mg Nolvadex daily "
HCT will increase androgen production post cycle(testosterone) and that's what we are trying to do. However, you have to be careful with this stuff because it can increase T level well above your normal level once the testes are back to normal size....so there is "some" risk in HCG being inhibitory in and of itself post cycle once testicular volume has returned to normal.
The blockers Nolva or Clomid(or an AI at a decent dose) will take care of the inhibition from raising estrogen from the raising T levels above though.
For the record I prefer Bill Roberts plan of preventing testicular atrophy in the first place by taking HCG at low dose during the cycle or at least half way through. This way you are not guessing about when testicular volume is back to normal size , and thus when to stop the HCG, post cycle....thus no chance of androgen inhibition post cycle with the HCG use itself.
RG
BY FAR the most important thing in recovery of the HPTA axis is getting the testes up to size so they can respond well to LH. This is a non issue with two weekers because there is no testicular shrinkage(or very very little at most).
As Bill Roberts said, LH production is even greater after a two weeker because the pituitary has not gone to sleep and is hyper-sensitive to GnRH from the hypothalamus.
ESTROGEN BLOCKERS or AI's POST CYCLE.
They don't do a great deal actually, UNTIL AFTER NATURAL T PRODUCTION is at least getting close to normal....to a point that estrogen(from the aromatization of this T to e) is starting to become inhibitory at the hypothalamus.
HCG is KEY.
Keep your nuts from shrinking during a cycle like Bill Roberts says, so that they can respond well with good T production once androgen levels drop post cycle to what the hypothalmus considers below normal(so it will release GnRH).
William Llewellyn is another guy that knows his shit, like Bill Roberts. Bill may be highly higher on the gura list though lol.
Llewellyn doesn't like even small doses of HCG DURING cycles because he thinks it can desensitize the Pituitary to natural LH(as Bill mentions above).
So.....he starts his dose late is a cycle(post cycle but when androgen levels from aromatizing steroids are still elevated).
Here's a quote from him.
"An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2) , which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of clomid would typically be added ( my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.
Sample Post-cycle Plan:
Week 3: 5000IU HCG total + 20mg Nolvadex daily
Week 4: 5000IU HCG total + 20mg Nolvadex daily
Week 5: 2500IU HCG total + 20mg Nolvadex daily
Week 6: 20mg Nolvadex daily
Week 7: 20mg Nolvadex daily
Week 8: 20mg Nolvadex daily "
HCT will increase androgen production post cycle(testosterone) and that's what we are trying to do. However, you have to be careful with this stuff because it can increase T level well above your normal level once the testes are back to normal size....so there is "some" risk in HCG being inhibitory in and of itself post cycle once testicular volume has returned to normal.
The blockers Nolva or Clomid(or an AI at a decent dose) will take care of the inhibition from raising estrogen from the raising T levels above though.
For the record I prefer Bill Roberts plan of preventing testicular atrophy in the first place by taking HCG at low dose during the cycle or at least half way through. This way you are not guessing about when testicular volume is back to normal size , and thus when to stop the HCG, post cycle....thus no chance of androgen inhibition post cycle with the HCG use itself.
RG
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very true. most people have no interest in looking like a competitive bodybuilder. so no reason why they should use cycle designed for competitive bodybuilder. just use most effective cycle to get results they want with fewest side effects and nothing more. that's this. all the good stuff with none of the bad.
mac111
New Member
you're a very strange guy, you do realise you quote yourself quite alot? but then, what is it they say about madness and talking to oneself?
and your 'knowledge on these compounds is very skewed and inaccurate. get back to us when you actually have some practical experience......
Is it as good as a 8-12 weeker at lower doses ...NO....but 2 weekers are NOT about getting the best gains possible. They are about reducing sides, and increasing T recovery speed and KEEPING your smaller gains.
RG
Wow I've seen you on the cycling forums and your knowledge is intimidating. So I have a question for you.
The 2 week on 4 off cycle intrigues me. I have a small stockpile of epistane and superdrol I've been itching to use. I've also got Tamoxifen citrate.
Would a 2 week on 4 off cycle be useful with a oral like epistane @ 40-50mg ish? If so, what would I dose the Nolvadex at?
you're a very strange guy, you do realise you quote yourself quite alot? but then, what is it they say about madness and talking to oneself?
and your 'knowledge on these compounds is very skewed and inaccurate. get back to us when you actually have some practical experience......
My mommy says I'm "special".
My knowledge isnt skewed or inaccurate. I'm just asking questions on alternate uses of drugs whos most popular applications are well documented. Information on these drugs isn't in short supply. I can also always reference the books I own on steroids. Two by Bill Llewelyn, one by Seth Roberts (why all the Roberts?), this site, About the Anabolics Book, the great info here at Meso, and countless others.
Speaking of practical experience. Do you have any regarding two week cycles? There's a lot of good information above.
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Not a good choice...too weak. But you could throw it in with the below.....
The best combo for the typical guy is d-bol 50mg a day and tren ace 100mg/day for ten days(then stop, test suspension 100mg a day. Letrozole at least .5mg/day and start that a week before the cycle starts due to it's long half life(slowly builds up and slowly goes away).
If you don't have suspension you can use prop but do a 300mg front load on day one, then 100mg a day, then stop at day 10.
The dbol goes all the way through day 14.
Post cycle there is no estrogen issues due to the very short half life of suspension and dbol so PCT with a blocker or continuing on with an AI like letro doesn't do anything to restore HPTA. As Bill Roberts has said, you get no measurable testicular shrinkage so the nuts ca respond rapidly to LH. The pituitary is also hyper-sensitive to GnRH from the hypothamalus.
However, T levels will be restored very rapidly, like in days or even within a day of the dbol and and estrogen clearing....so you should take an e blocker like clomid or nolva, or an AI like letrozole. This will allow T levels to climb well above normal and help keep the gains as long as you continue to train , eat and sleep properly. In fact you can easily continue to gain.
Yes, all blockers and AI's will reduce IGF-1 levels but the resultant high T levels they give more than make up for that in the muscle building department.
You may not have a sex drive on more than .25mg of letro and some guys get a crappy sex drive from Clomid and nolva(not me).
Then after a few weeks you an stop the blocker or AI. Estrogen levels will rise if the AI is stopped, or estrogen levels will be sensed by the hypothalamus if a blocker is stopped......then a slow gradual return to your normal T output will occur over a few weeks time since these drugs have long half lives and especially letro.
I would not take Nolva or clomid long term...longer then a 3 month cycle. Too many potential sides. I would not use letrozole at a dose greater then .25 per day for any length of time. I do think low dose letro is safer to use long term than clomid or nolva but you should get your lipid profile checked after a few months "on" even .25mg of letro.
RG
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mac111
New Member
yeah, and mr realgains also believes that synthetic test is not a steroid
and if you believe him on keeping gains, you're being very much mistaken, the only way to ever keep any decent gains from AAS is by staying on them (not advised) unless you are in the 1% with crazy genetics.
hint, beware internet warriors [
)]I've had decent results with Tren A, Dbol & Test P, but I'm looking to run a few 2-weekers without Tren A due the the issue of reduced aerobic performance. Thus, I'm looking for an alternative protocol. I was thinking about just dropping the Tren A and increasing the Test P, but to what levels... ?
