debate on proviron for pct

[ganu]

hi guys have seen a lot of debate on many forums regarding proviron being used for pct..am on 6th week of var/tbol cycle..2 more weeks of var to go

nolva 20 and clomid 50 for 4weeks was my initial idea

but then i was suggested to drop clomid(due to its sides and similar benefits to nolva) and add .25 adex or 50 proviron..

nolva helps in getting Lh back to normal and raise hdl too

which one (clomid/adex/proviron)will help resume the natural test production caused by hpta suppression/shutdown and combat increased cortisol induced catabolism.dont want to lose this hard earned muscles

also have my crown thinning a bit since i started this cycle..

will also use tribulus/niacin/vit e-1000 with pct

[Bad Viking]

Stick with your initial idea

No proviron for pct...it is still an AAS. Try Clenbuterol .

[Mafiusu]

i wont use proviron in pct but ive only seen it have an effect on HPTA at much higher doses than what we run. i still dont chance it.

[Ashop]

Stick with your initial idea

No proviron for pct...it is still an AAS. Try Clenbuterol.

I tend to agree...NO PROVIRON for PCT.

[ganu]

Guys what about increase in cortisol and catabolism..which product to counter it

[Roshambo]

I used proviron in my PCT and worked fine. I used as follows:
Nolva 20mg ED for 2wks
Clomid 50mg ED for 3wks
Provrion 20mg ED until my wood returned which was about 1mo.

This is what worked for me.

[Dancer]

10mg am dbol

[british bulldog 1]

you dont need proviron

[ganu]

10mg am dbol

what does that mean..dbol for pct?

[Dancer]

what does that mean..dbol for pct?

yeap 10mg @ 8 am

[LickAlotOfPuss]

Well personally i'm not a clomid fan, pro as a pct should do fine. I have used it before, but also hang onto the dex. Clomid gives me weird side effects.

[Dancer]

The use of proviron as a pct measure is counter productive.

Basic reasons

over all goal of a given PCT should be the restoration of HPTA in the given time frame that the PCT takes place. Without the restoration of HPTA there is not point what so ever to doing PCT and thus you might as well say F it and go on some good old HRT.

Proviron has a active half life that is 2x as a long as dbol .

let me give a little credit here:


http://www.steroid.com/Dianabol.php

In order to successfully bridge between cycles (and this means using a low dose of AAS, in this case dbol), you need to recover your natural hormonal levels to pre-cycle levels or to within acceptable parameters, and then you start your next cycle. The idea here is that you won´t lose any gains, but rather a low dose of an AAS will help you maintain them. Typically, you´d use around 10mgs/day of dbol and combine it with an aggressive Post-Cycle Therapy (PCT) course of Nolvadex (and/or Clomid) and HCG . This would give you full androgen replacement from the Dbol and a shot at recovering your natural hormonal levels via the other stuff you are taking. Remember, the 100mg/day dose of dbol in the study we looked at earlier did not suppress Test, LH, or FSH to a degree that would make recovery impossible and certainly not with 1/10th that dose in conjunction with an aggressive PCT.

All in all, this is a very good drug, and a potent tool for quick gains or retaining gains...when used properly and safely.


As for The A in the HPTA lets look at that.

It is actually active at night prior to bed. The male body produces the day's test at night

50mg of proviron with a 5 hour half-life in 12 hours will leave over 20mg of AAS in the good old blood stream. So your body detects the extra androgen and either shuts down or produces less natty test.

10mg dbol half life 2.5-3 hours... in 12 hours there is not a detectable amount of dbol left.

vaaaallllaaaahhhhhh

[chuckt12345]

^ id take that dbol on pct advise with a grain of salt because hes using dbol in conjunction with bridging

[Dancer]

^ id take that dbol on pct advise with a grain of salt because hes using dbol in conjunction with bridging

In a mentaly handicapped voice:


Whhhhhyiiie

[chuckt12345]

cause you copy paste bridging advise for dbol for a guy taking about using proviron for a tbol pct.

[Dancer]

I should have stopped his quote when i added my own, this is my add:

As for The A in the HPTA lets look at that.

It is actually active at night prior to bed. The male body produces the day's test at night

50mg of proviron with a 5 hour half-life in 12 hours will leave over 20mg of AAS in the good old blood stream. So your body detects the extra androgen and either shuts down or produces less natty test.

10mg dbol half life 2.5-3 hours... in 12 hours there is not a detectable amount of dbol left.

[Mafiusu]

why would you want to take anything that would have any negative effect of HPTA when trying to recover. 10mg dbol is not a good idea dont care when you take it. am/pm whatever

[The Deuce]

I should have stopped his quote when i added my own, this is my add:

As for The A in the HPTA lets look at that.

It is actually active at night prior to bed. The male body produces the day's test at night

50mg of proviron with a 5 hour half-life in 12 hours will leave over 20mg of AAS in the good old blood stream. So your body detects the extra androgen and either shuts down or produces less natty test.

10mg dbol half life 2.5-3 hours... in 12 hours there is not a detectable amount of dbol left.

Dude why the DBOL ?? especially such a low dose once a day... I am curious as to hear what the benefits of such a thing would be... please tell me.. I am eager to hear this...

[Dancer]

why would you want to take anything that would have any negative effect of HPTA when trying to recover. 10mg dbol is not a good idea dont care when you take it. am/pm whatever

Cause it didn't I have had kidney/liver...blah blah blah... every 6-12 months...

I did have ablood test prior to cycle and post.... And the restoration did happen...

Negative feedback on HPTA how?

"Am/pm whatever"... well if I am wrong about it, post when hypothalamic-pituitary activity happens!

[Dancer]

Dude why the DBOL?? especially such a low dose once a day... I am curious as to hear what the benefits of such a thing would be... please tell me.. I am eager to hear this...

Its all about the half life and the natty ability of your body to produce test.

10mg am will be outta your body by the time your hypothalamic response feedback would take place.

[ganu]

Its all about the half life and the natty ability of your body to produce test.

10mg am will be outta your body by the time your hypothalamic response feedback would take place.

bro do you have anything that supports this theory

the var combined with tbol for 8weeks has already leading to my hpta shut down..my 4th week blood report shows my lh and fsh crashing down,,

for pct nolva would resurrect my lh while improving the hdl..

correct me if i am wrong..but any aas,for eg dbol would only cause the same effect as var or tbol(maybe on a weaker level @10mg) if used for pct.. how would natty test come back to normal if the body is still being conveniently provided from outside source..true its out of the system but tbol too is out of the system by the time you sleep even if you split it 3 times a day..so does a tbol user not use anything for pct..

i know proviron is dht derived and very good during cycle,binds to the shbg and frees up test..but what i am worried about is the strong androgenic property it has which makes me think if its really good for therapy and how

[Dancer]

bro do you have anything that supports this theory

the var combined with tbol for 8weeks has already leading to my hpta shut down..my 4th week blood report shows my lh and fsh crashing down,,

for pct nolva would resurrect my lh while improving the hdl..

correct me if i am wrong..but any aas,for eg dbol would only cause the same effect as var or tbol(maybe on a weaker level @10mg) if used for pct.. how would natty test come back to normal if the body is still being conveniently provided from outside source..true its out of the system but tbol too is out of the system by the time you sleep even if you split it 3 times a day..so does a tbol user not use anything for pct..

i know proviron is dht derived and very good during cycle,binds to the shbg and frees up test..but what i am worried about is the strong androgenic property it has which makes me think if its really good for therapy and how

There are no legal studies done on BBer or PLer that conduct PCT.

Thats for even PCT with respect to use of HCG used by BBers or PLers.

HPTA is well documented.

Dbol half-life is also public knowlegde.

As is nolv as you pointed out. But the studies you ref to are not done as a controlled PCT involving PCT for BBers or PLers.

[Dancer]

bro do you have anything that supports this theory

the var combined with tbol for 8weeks has already leading to my hpta shut down..my 4th week blood report shows my lh and fsh crashing down,,

for pct nolva would resurrect my lh while improving the hdl..

correct me if i am wrong..but any aas,for eg dbol would only cause the same effect as var or tbol(maybe on a weaker level @10mg) if used for pct.. how would natty test come back to normal if the body is still being conveniently provided from outside source..true its out of the system but tbol too is out of the system by the time you sleep even if you split it 3 times a day..so does a tbol user not use anything for pct..

i know proviron is dht derived and very good during cycle,binds to the shbg and frees up test..but what i am worried about is the strong androgenic property it has which makes me think if its really good for therapy and how

I am sorry I did not answer the var issue... Oxan has a half life of 9 hours.

The HPTA is a mechanisim that becomes active at night in males. The process is well documeneted. I can list all the studies but there is no point.

[alpmaster]

But what does having dbol in your system for 3 hours accomplish?

[Dancer]

Interactions of the Hypothalamus, Pituitary, and Testes (HPTA)

During a cycle of AAS, natural production of testosterone decreases, often times to zero. In many cases, the diminished natural testosterone production causes a cessation of sperm production (spermatogenesis), and the male becomes sterile. After the cycle, the body's ability to make testosterone may take months to start again. Aside from the undesirable sterility and loss of strength, other hormone levels get out of whack because of the low testosterone , and cause other problems such as increased body fat and depression. The body produces many hormones, and the levels of most hormones are interrelated. This article will examine the factors involved in regulating the production of certain hormones in the body, particularly by the Hypothalamic-Pituitary-Testicular Axis. As always, the author does not condone the use of steroids by persons not under the care and guidance of a qualified physician.

Endogenous Testosterone

Where is testosterone made in the body? Well, about 95% is produced in the testicles, in special cells called "interstitial cells" or Leydig cells. These cells surround cells in the seminiferous tubules, called Sertoli cells, whose function is to produce sperm. Spermatogenesis in the Sertoli cells requires testosterone, and when endogenous testosterone diminishes, then sperm production stops (and you end up with raisins). Bear in mind that Leydig cells and Sertoli cells are in close proximity to each other. Therefore, the testosterone concentration is high, relative to the concentration in the bloodstream. Sertoli cells require high testosterone concentration for the sperm cells to begin the maturation process. So, even though you might have "a lot" of exogenous testosterone when on-cycle, the concentration is not high enough at the Sertoli cells to promote spermatogenesis because the Leydig cells have shut down. This, combined with a lack of Follicle Stimulating Hormone (FSH), renders many men sterile during a cycle.

The "Axis"
Hang on a minute, the Leydig cells shut down? Why? How?

Well, the short answer is, "hormones". Hormones are the body's way of sending signals, or information from one part of the body to another. In a computer, electrons (electricity) act as the signal; in the body (which doesn't have wires!), the signals must be sent with chemicals, and that is the role of hormones. The term "HPT Axis" refers to the interaction of the hypothalamus, pituitary, and testes (there are other axes as well). For the Leydig cells, Luteinizing hormone (LH) is released from the pituitary and it signals the Leydig cells to produce testosterone. Similarly, the pituitary releases FSH, and it tells the Sertoli cells to make sperm (as well as androgen-binding-protein). The pituitary is a gland that produces and stores a number of hormones, under the control of the hypothalamus. The hypothalamus might be considered to be the General (as in military), and the pituitary would be a Colonel under the General's command. The hypothalamus decides how the body's organs should operate, and the pituitary gives the actual "orders" to the target organs. Some of the "signaling" hormones made or stored in the pituitary are:

Growth Hormone
IGF-I and IGF-II
Thyroid Stimulating Hormone (TSH)
Vasopressin (or Antidiuretic hormone)
Luteininzing Hormone (LH)
Follicle Stimulating Hormone (FSH)
Adrenocorticotropic Hormone (ACTH)

The hypothalamus and the pituitary are very close together, and are located at the base of the brain. Just as the pituitary uses hormones to signal the target organ (testes, thyroid, etc) to do something, the hypothalamus uses other hormones to signal the pituitary to do its job. Some of these "Hypothalamic Releasing Factors" are (along with the pituitary hormones affected):

Hypothalamic Hormone: Regulates:
Gonadotropin Releasing Hormone LH, FSH
Growth Hormone Releasing Hormone GH
Thyrotropin Releasing Hormone TSH
Corticotropin Releasing Hormone ACTH

But how does the hypothalamus know when its commands have been carried out? By what's called a "feedback loop". Just as a General relies on reports from the field, the hypothalamus must monitor the results of its commands. The hypothalamus has sensors (receptors) to determine the levels of the chemicals (hormones) produced by the target organs. For our purposes, we will examine only one feedback loop, the one involving the testes.

The hypothalamus has both androgen receptors and estrogen receptors. When the level of either hormone gets too high, the receptors become more highly activated, and the hypothalamus stops sending Gonadotropin Releasing Hormone to the pituitary. The pituitary, in turn, stops sending LH and FSH to the testes. Thus, the signal is, "stop producing testosterone (and sperm)". We know that androgens (and NOT just estrogen) stop the action of the testes because exogenous DHT by itself (which cannot convert to estrogen) is very effective at shutting down the testes. A schematic of the HPTA (and other glands) is shown below. Note that the other glands are involved in feedback mechanism also.

What does the estrogen/androgen feedback loop mean to bodybuilders? It means that, when using exogenous androgens, the hypothalamus is very effectively signaled (by binding to the AR's on the hypothalamus) that there is plenty of androgen, and that the testes should be shut down. As long as the level of exogenous androgen is high enough, no reasonable amount of Clomid (or other estrogen-blocker) will be able to keep the testes functioning. So, the only reason to take Clomid during a cycle is if you are susceptible to gyno, or want to try to reduce the bloating associated with elevated estrogens. Both of these actions take place at sites other than at the hypothalamus.

How does hCG work and what does it do? This hormone (produced by pregnant females) acts very much like LH, and it even closely resembles LH (and FSH) in chemical structure. So, administration of hCG sends a signal to the testes to start production of testosterone (thus, hCG can help prevent testicular atrophy during a long cycle). However, remember that the testosterone produced can signal the hypothalamus to stop sending the signals to turn on the testes. So, hCG can be somewhat inhibiting to the natural process of hormone release. That is why many believe that hCG should not be used at the end of a cycle, when the desire is to stimulate natural production of hormones.

It has become standard practice to use Clomid at the end of a cycle; because it is felt that blockage of the estrogen receptors on the hypothalamus will cause it to start signalling for the production of testosterone by releasing Gonadotropin-releasing hormone. While this sounds very good in theory and works in many cases, it does not always work, particularly in older men. For some, the use of clomid does not help "jump-start" the gonads at the end of a cycle, and some believe that only time will allow the hypothalamus to begin action again. Doctors still rely on the combination of clomid and hCG (yes, even after a cycle), and there appear to be indications that this combination therapy is a little more successful than clomid by itself. To be absolutely sure, a man who uses exogenous steroids should have blood work done after being off-cycle for a while, in order to ensure that the hormone levels have come into normal ranges.

Finally, many men who use steroids get high blood pressure very early in a cycle. While many have attributed this to erythropoiesis (production of too many red blood cells and thickening of the blood), I believe that the increase in BP is due to a direct action of androgens on the hypothalamus, altering the release of Vasopressin. Doctors who prescribe hormone-replacement therapy often monitor the hematocrit (% of red blood cells), and recommend that the patient donate blood if the hematocrit exceeds 50. I am not certain, however, that this helps the elevated blood pressure that much

Good Article on Understanding HPTA Inhibition and Recovery from AS 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

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 .

[Dancer]

Found it:

http://www.uk-muscle.co.uk/steroid-t...-6th-june.html

From memory taking the DBol about 7am worked best.

[Dancer]

But what does having dbol in your system for 3 hours accomplish?

10mg taken at once will increase your average testosterone level by five times and decrease your endogeneous cosrtisone by 50-70%. This, along with the short active life of the drug, would suggest that by using a small dose first thing upon waking is thought by some to help to combat the problems asscociated with coming off of anabolic steroids .

http://www.canadabodybuilding.com/fo...ead.php?t=6110

[ninesecz]

10mg taken at once will increase your average testosterone level by five times and decrease your endogeneous cosrtisone by 50-70%. This, along with the short active life of the drug, would suggest that by using a small dose first thing upon waking is thought by some to help to combat the problems asscociated with coming off of anabolic steroids .

http://www.canadabodybuilding.com/fo...ead.php?t=6110

yes but it does nothing to help kick start natty production! only gets used for bridging cycles!!! what happens when he comes off the d-bol? his levels will still bottom out!

Just get some nolvadex and run it 40/40/20/20 should be fine!

[Dancer]

yes but it does nothing to help kick start natty production! only gets used for bridging cycles!!! what happens when he comes off the d-bol? his levels will still bottom out!

Just get some nolvadex and run it 40/40/20/20 should be fine!

Nine,

I never suggested using it alone.

[alpmaster]

10mg taken at once will increase your average testosterone level by five times and decrease your endogeneous cosrtisone by 50-70%. This, along with the short active life of the drug, would suggest that by using a small dose first thing upon waking is thought by some to help to combat the problems asscociated with coming off of anabolic steroids .

http://www.canadabodybuilding.com/fo...ead.php?t=6110

And in that same link it reads:

Despite appearances, this theory has very little evidence to back itself up with no real scientific evidence to suggest that a bridge is even possible, although granted that the majority of our working knowlege comes through trial and error. However, even the propnents of a "d-bol bridge" admit that complete restoration of LH fucntion will not be acheived until one is completely off of all compounds. With that said, it is unlikely that a "bridge" will help to maintain muscle mass while you are able to recover both HPTA and LH function. The only solution is to come completely off all substances and run a proper post-cycle therapy.

I mean, I'm not trying to shut down you're theory. In principle it would seem promising, but I just don't see the evidence that it would work, without getting to the surmounting evidence that it wouldn't.

[The Deuce]

Its all about the half life and the natty ability of your body to produce test.

10mg am will be outta your body by the time your hypothalamic response feedback would take place.

So in turn.. what does that do for you or anyone as far as muscle response, gains, I am confused... educate me

[Dancer]

And in that same link it reads:

Despite appearances, this theory has very little evidence to back itself up with no real scientific evidence to suggest that a bridge is even possible, although granted that the majority of our working knowlege comes through trial and error. However, even the propnents of a "d-bol bridge" admit that complete restoration of LH fucntion will not be acheived until one is completely off of all compounds. With that said, it is unlikely that a "bridge" will help to maintain muscle mass while you are able to recover both HPTA and LH function. The only solution is to come completely off all substances and run a proper post-cycle therapy.

I mean, I'm not trying to shut down you're theory. In principle it would seem promising, but I just don't see the evidence that it would work, without getting to the surmounting evidence that it wouldn't.

There are no legal studies done on BBer or PLer that conduct PCT.

Thats for even PCT with respect to use of HCG used by BBers or PLers.

HPTA is well documented.

Dbol half-life is also public knowlegde.

As is nolv as you pointed out. But the studies you ref to are not done as a controlled PCT involving PCT for BBers or PLers.

[Dancer]

And in that same link it reads:

Despite appearances, this theory has very little evidence to back itself up with no real scientific evidence to suggest that a bridge is even possible, although granted that the majority of our working knowlege comes through trial and error. However, even the propnents of a "d-bol bridge" admit that complete restoration of LH fucntion will not be acheived until one is completely off of all compounds. With that said, it is unlikely that a "bridge" will help to maintain muscle mass while you are able to recover both HPTA and LH function. The only solution is to come completely off all substances and run a proper post-cycle therapy.

I mean, I'm not trying to shut down you're theory. In principle it would seem promising, but I just don't see the evidence that it would work, without getting to the surmounting evidence that it wouldn't.

There are ZERO I MEAN ZERO legal studies that PCT works on our control groups... BBers and PLers

[Dancer]

So in turn.. what does that do for you or anyone as far as muscle response, gains, I am confused... educate me

I suggested a PCT course for you on your thread... ahem... you and serious get done fighting read it and respond back

[ganu]

wow..that was like world war 4..dancer what is bbers and plers..also wheres proviron in all this much much..by the way your name suggest you dance,do you

[Dancer]

wow..that was like world war 4..dancer what is bbers and plers..also wheres proviron in all this much much..by the way your name suggest you dance,do you<<< when i was younger

BBera is bodybuilders and plers is powerlifters.

LOL

ok on the proviron look a few posts up and see the half life take your 50mg ED dosage and you can see that there is going to always be some proviron in your system... thus leading to hpta shut down.

[jimmyinkedup]

proviron @ 50mg/day will have NO adverse effect on hpta recuperation (doses up to 100-150mg/day resulted in no changes in LH and FSH) and will have benefits re SHBG , slight igf increase (via upregualtion of receptors) and sex drive benefits. JMO.....Would i drop clomid - no ...would i still consider throwing in low dose proviron...yes.

[ganu]

proviron @ 50mg/day will have NO adverse effect on hpta recuperation (doses up to 100-150mg/day resulted in no changes in LH and FSH) and will have benefits re SHBG , slight igf increase (via upregualtion of receptors) and sex drive benefits. JMO.....Would i drop clomid - no ...would i still consider throwing in low dose proviron...yes.

so jimmy you saying to put proviron at 50 for 4weeks and retain clomid 50 and nolva 20 for 4 weeks..wont that be too much for not such a harsh 8week var and tbol cycle..also how harsh is provi on the hairline

[chuckt12345]

There are ZERO I MEAN ZERO legal studies that PCT works on our control groups... BBers and PLers

where the legal studys about HPTA and dbol ????

[Dancer]

where the legal studys about HPTA and dbol ????

There are no legal studies done on BBer or PLer that conduct PCT.

Thats for even PCT with respect to use of HCG used by BBers or PLers.

HPTA is well documented.

Dbol half-life is also public knowlegde.

As is nolv as you pointed out. But the studies you ref to are not done as a controlled PCT involving PCT for BBers or PLers.

I posted that a few posts back on this threa, Since no one is reading prior posts I am outty from this thread.....