*The Ross Protocols: Beginner, Intermediate, and Advanced Cycles!*

[bigslimfitting]

....wow this is like mom and dads house. lol So if I'm doing dbol at the beginging 5 of 8 weeks now of my cycle of about 12 weeks, i should stop taking it after 8 weeks, wait till I take my last shot of test e/ EQ and then start taking it again for 4 weeks and then start clomid? Also this is my first cycle,...but money aint an issue. So can i just take an ass load of clomid? For a longer time frame i mean.

 

[Ross]

how can you say everyone? some people maybe but that would be a minority, but myself and many many others have not crashed using the traditional pct regime which has been used for years.

edit: so in other words you dont have studies done to show this exceeds a traditional pct regime??

So you are saying that you maintain ALL of your gains using just an AI and some SERMS??


NOT ALL ANDROGENS CAUSE SHUTDOWN*

"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.

SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)

Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.

The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier PCT.
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Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links

Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.

Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS

 

[Mavafanculo]

let me rephrase this for some of the more illiterate readers

ross, why do you recommend waiting 4 weeks from your last shot of testosterone to start pct in this cycle?

X please stop the uncivil belligerence .

and the same applies to everyone else.

I bulk deleted a string of posts once the bullshit started flying. If anyone feels their post shouldnt have been deleted and was a valid civil question or refutation re-post it.

we're determined to maintain a civil mature atmosphere here on the anabolics board. members are returning because the flame wars have ended.

let's get back to positive helping mode, and get with the program

 

[Tatyana]

X please stop the uncivil belligerence .

and the same applies to everyone else.

I bulk deleted a string of posts once the bullshit started flying. If anyone feels their post shouldnt have been deleted and was a valid civil question or refutation re-post it.

we're determined to maintain a civil mature atmosphere here on the anabolics board. members are returning because the flame wars have ended.

let's get back to positive helping mode, and get with the program

I am with Mava on this one, I think that presenting arguments and discussing things are great, but attacking the individual is not an argument and it is faulty logic.

People ususally do this when they can't explain their point.

 

[Tatyana]

So you are saying that you maintain ALL of your gains using just an AI and some SERMS??


NOT ALL ANDROGENS CAUSE SHUTDOWN*

"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.

SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)

Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.

The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier PCT.
-------------------------------------------------------------------------

Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links

Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.

Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure.


All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS

I still don't get how this paper is evidence of what you say.

The subjects were already in primary testicular failure.

They were given LH to get their testicles going again, and it says that they still had suppressed testosterone levels.

It is demonstrating that the administration of steroids, one I have never heard of any of the lads using, I forget its common name now, does suppress the HPTA.



It shows that it is supppressing testosterone, even with giving them a leutenising hormone releasing factor/hormone. That in itself is meant to get test going again. They did this at the beginning and the end of this study.


Also, with regard to endocrinology research, this paper is really really old.

 

[xrsist]

I am with Mava on this one, I think that presenting arguments and discussing things are great, but attacking the individual is not an argument and it is faulty logic.

People ususally do this when they can't explain their point.

do you mind telling me which point i couldnt explain to "the good sun" tatyana?

i asked a simple question to ROSS, not anyone else

 

[Tatyana]

do you mind telling me which point i couldnt explain to "the good sun" tatyana?

i asked a simple question to ROSS, not anyone else

I haven't read the entire thread yet.

I will have a look later and see if I can get what everyone is saying

 

[digger]

do you mind telling me which point i couldnt explain to "the good sun" tatyana?

i asked a simple question to ROSS, not anyone else

Simple questions don't usually involve labeling someone "illiterate."

Instead of saying (in effect) "You're full of crap," try saying "I don't understand this part."

• You don't embarrass yourself when it turns out you're wrong
• You might actually learn something
• If it turns out you were right and the other guy was wrong (it could happen...) he's more likely to admit it.

It's called being "civil." It's called "being a grownup."

 

[*Swifto*]

Ross claims to have started endogenous testosterone whilst using "inhibitive" compounds AFTER compounds that cause complete shutdown have been used.

Most disagree with this statement, I know of people who have tried it and it doesnt work (with BW).

There are also no stuides to back this claim that I have seen or heard of.

Its a great idea, but there isnt much, if anything, to back it up.

 

[Tatyana]

No matter what the body will not produce more gains even when swapping and mixing compounds,

I would like to know more about this.

There are only two isoforms of the testosterone receptor, and really, when you see the structure of testosterone (and oestrogen, progesterone and all their various forms), they are not that different, but the subtle differences do make a BIG difference.

Obviously there is a differential binding capacity with testosterone and dihydrotestosterone, and from what I have read, the modifications on steroids is basically adding an extra long chain to the 5-ring molecule so it will either

1. Not be cleared from the body as rapidly

2. Stay in the receptor site longer????

So my question is, really, is testosterone just testosterone?


As soon as your put androgens in the blood stream the body attempts to reach homeostatis and slows your gains down even if your pumping loads in or swapping compounds,

Very true, your receptor sites will become saturated quite quickly, and once they are full, adding more will not do anything.

Sort of like trying to squeeze 20 eggs into a standard dozen egg box.

There is some suggestion that there may be some other mechanism of action at supraphysiological doses, but I haven't found anything solid about this yet.

If this was true we would all be doing this and be 500lbs+, come on for gods sake,

I haven't got the paper, but from what I can remember reading it, people can have a very different response to steroids, up to 4x a different response, probably due to a different number or polymorphisms (natural variations) on the androgen receptors.


The body grows very fast at the begining of any cycle depending on compounds then it reacts to the growth by shutting it down, staying on for what ever reason results in more sides,

Has anyone got a link/paper about the differential binding of various exogenous steroids?