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Test Taper Protocol
 

seekonk
Level

Join date: Apr 2009
Posts: 623

Prisoner wrote:

the research showed no hpta suppression while using a serm and low dose testosterone - 100mg per week



I am trying to understand what this means. Is it from a published study?

Did someone measure endogenous T production during treatment and determine that it was unaffected? This would require some way to distinguish between T from exogenous and endogenous source, maybe by some calculation. Or does it just mean that endogenous T returned to baseline immediately after cessation of treatment?

What dose of SERM are we talking about?

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elnino57
Level 1

Join date: Jun 2003
Posts: 11

Is this really effective? Just planning my future cycle.

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cybercom8
Level

Join date: Aug 2010
Posts: 111

hi Guys,

I recently followed the test taper protocol. What i noticed is this. I kept like 95% of my gains up until taking 80mg of test weekly. The minute I tapered to 60mg, most of my gains start going. Any advice regarding this? Ive also noticed the steroid acne die down then suddenly flare up again.

Also my testicles have shrunken again. I did use HCG during my cycle and it worked. But now on the taper things seem to be going wrong. Its ever since i shot the 60mg of Test E. Im also on clomid post cycle...moving onto half a tab as i have been tapering it as well.

any advice.

Also something that could add to the loss of my results is i have recently be rather stressed with some work related issues as well as not eating as much as i used to. So this is possibly also why I have lost some results but the other part i think is linked to something im doing wrong in the test taper.

any help would be great

thanks

Nick

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t-minotaur
Level 4

Join date: May 2009
Posts: 126

Hey guys,

I have some questions regarding the Test Taper Protocol as I am ending my cycle and would like to try this approach.

Here is my 16 week cycle:
Weeks 1 - 10, 200mg/week test cyptionate
Weeks 1 - 10, 400mg/week Primobolan enanthate
Weeks 11 - 15, 250mg/week test cypionate
Week 16, 200mg/week test cypionate

On-Cycle Therapy:
Weeks 1 - 16, 250iu HCG 2x weekly
Weeks 1 - 16, 2iu HGH 5x weekly
Weeks 1 - 10, .5 - 1mg Arimidex daily
Weeks 11 - 16, .75mg Letrozole daily

I was considering doing the test/masteron approach. I have test cypionate and masteron prop.

Test Taper Protocol PCT:

Week 1 - 4, 25mg test cyp (Mon and Fri)
16-17mg mast prop (Tues, Thurs, Sat)
Taper off Letro by week 3

Week 5, 20mg test cyp (Mon and Fri)
13-14mg mast prop (Tues, Thurs, Sat)

Week 6, 15mg test cyp (Mon and Fri)
10mg mast prop (Tues, Thurs, Sat)

Week 7, 12-13mg test cyp (Mon and Fri)
8-9mg mast prop (Tues, Thurs, Sat)

Week 8, 10mg test cyp (Mon and Fri)
6-7mg mast prop (Tues, Thurs, Sat)

Week 9, 7-8mg test cyp (Mon and Fri)
5mg mast prop (Tues, Thurs, Sat)

Week 10, 5mg test cyp (Mon and Fri)
3-4mg mast prop (Tues, Thurs, Sat)

My only concern is that these doses seem ridiculously low. I read the forum and it said to backload a 1 inch slim pin. I guess that is an insulin pin and I should use the shoulder as the injection site? Any thoughts on this PCT?

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Singhbuilder
Level 1

Join date: Apr 2008
Posts: 1119

Might as well chuck this into here aswell.
Im planning a cycle and this is how it looks, how does the waiting and taper periods look?
Anything need changing?

Wk 1-10 Test 400 - 1200mg/wk
Wk 1-4 Dbol - 40mg/d
Wk 8-12 Winstrol - 60mg/d
Wk 10-12 Test Prop - 350mg/wk
Wk 1-12 hCG - 250iu 2x/wk
Wk 1-16 adex - .5mg E3D (tapering down from wk 12-16)

Wk 12-16 Test prop/Mast prop - 50mg/50mg wk (waiting period)
Wk 17 Test prop/Mast prop - 40mg/40mg
Wk 18 Test prop/Mast prop - 30mg/30mg
Wk 19 Test prop/Mast prop - 20mg/20mg
Wk 20 Test prop/Mast prop - 10mg/10mg
Wk 16-20 Nolva - 20/20/20/10

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seekonk
Level

Join date: Apr 2009
Posts: 623

Schwarzenegger wrote:
Given that using a SERM with 100mg of test does not impact HPTA function, ...


What dosage of which SERM with 100 mg of test does not impact HPTA function?

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enchilnada
Level

Join date: Aug 2009
Posts: 31

seekonk wrote:
Prisoner wrote:

the research showed no hpta suppression while using a serm and low dose testosterone - 100mg per week



I am trying to understand what this means. Is it from a published study?

Did someone measure endogenous T production during treatment and determine that it was unaffected? This would require some way to distinguish between T from exogenous and endogenous source, maybe by some calculation. Or does it just mean that endogenous T returned to baseline immediately after cessation of treatment?

What dose of SERM are we talking about?



There are studies which are supportive of different aspects. For example, Winters et al., found that if subjects are administered 100 mg of clomiphene twice daily, LH levels are unable to be decreased (and in fact continue to rise) even when serum testosterone levels are elevated up to over 2,000 ng/dl (i.e., the equivalent of the peak concentration reached after a 200 mg dose of testosterone enanthate). Naftolin et al., also had similar results.

http://www.ncbi.nlm.nih.gov/pu...
http://www.ncbi.nlm.nih.gov/.../pubmed/4683184

So, the assumption is that if LH is not suppressed and in fact, increased well beyond baseline, endogenous testosterone production will continue. This has not been tested directly, but could be by administering radio-tagged testosterone. This allows one to determine the amount of endogenous and exogenous testosterone and their levels over time.

If the increase in LH (and increase and/or maintenance of amplitude and frequency) is accepted to be able to still stimulate the testicles to produce testosterone, then one can assume it will do so. hCG has been shown indirectly to do so in one study, with total testosterone levels greater than either the exogenous dose alone or the hCG alone could produce. With that in mind, LH and hCG are indistinguishable to the G protein-coupled receptor to which they bind so one can expect the same result.

http://www.ncbi.nlm.nih.gov/...pubmed/15713727

Last, there is a stronger piece of indirect evidence in a separate study by Finkelstein et al. They found that after administering testolactone (and older aromatase inhibitor), that once again, LH levels could be maintained and even increased, despite exogenous testosterone administration. However, more interestingly, when they compared serum testosterone levels after administration of either testolactone by itself, testosterone by itself, or testosterone combined with testolactone, the serum testosterone level with the combination was significantly higher than those seen after administration of either testolactone or testosterone. It can reasonably be concluded that the additional testosterone seen beyond that already seen after exogenous testosterone administration must have been the endogenous testosterone. Otherwise, if endogenous testosterone were suppressed, this would have not been seen.

http://www.ncbi.nlm.nih.gov/.../pubmed/1908484

There are limitations to this notion which would be helped by further research, but this type of work hasn't been a focus of many research groups.

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seekonk
Level

Join date: Apr 2009
Posts: 623

enchilnada wrote:
There are studies which are supportive of different aspects. For example, Winters et al., found that if subjects are administered 100 mg of clomiphene twice daily, LH levels are unable to be decreased (and in fact continue to rise) even when serum testosterone levels are elevated up to over 2,000 ng/dl (i.e., the equivalent of the peak concentration reached after a 200 mg dose of testosterone enanthate). Naftolin et al., also had similar results.

http://www.ncbi.nlm.nih.gov/pu...
http://www.ncbi.nlm.nih.gov/.../pubmed/4683184

So, the assumption is that if LH is not suppressed and in fact, increased well beyond baseline, endogenous testosterone production will continue. This has not been tested directly, but could be by administering radio-tagged testosterone. This allows one to determine the amount of endogenous and exogenous testosterone and their levels over time.

If the increase in LH (and increase and/or maintenance of amplitude and frequency) is accepted to be able to still stimulate the testicles to produce testosterone, then one can assume it will do so. hCG has been shown indirectly to do so in one study, with total testosterone levels greater than either the exogenous dose alone or the hCG alone could produce. With that in mind, LH and hCG are indistinguishable to the G protein-coupled receptor to which they bind so one can expect the same result.

http://www.ncbi.nlm.nih.gov/...pubmed/15713727

Last, there is a stronger piece of indirect evidence in a separate study by Finkelstein et al. They found that after administering testolactone (and older aromatase inhibitor), that once again, LH levels could be maintained and even increased, despite exogenous testosterone administration. However, more interestingly, when they compared serum testosterone levels after administration of either testolactone by itself, testosterone by itself, or testosterone combined with testolactone, the serum testosterone level with the combination was significantly higher than those seen after administration of either testolactone or testosterone. It can reasonably be concluded that the additional testosterone seen beyond that already seen after exogenous testosterone administration must have been the endogenous testosterone. Otherwise, if endogenous testosterone were suppressed, this would have not been seen.

http://www.ncbi.nlm.nih.gov/.../pubmed/1908484

There are limitations to this notion which would be helped by further research, but this type of work hasn't been a focus of many research groups.


Great answer! Thank you.

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Viking69
Level 1

Join date: Jun 2005
Posts: 1128

bushidobadboy wrote:
I can never remember the physiological reason for post cycle acne. Something to do with pH of sebaceous secretions being more favourable to bacterial growth.

Personally I would tackle it with some sort of facial wash, rather than an AI.

I don't think it has much to do with Estrogen anyway.

www.proactiv.com apparently offers an effective treatment.

Bushy



For all the guys with backne problems whats works best for me is Palmolive dish soap. I use the blue colored one that says "oxy" something on the bottle. It will also kill warts that develop on your hand by just applying it daily. I have seen this work wonders for several people, better than any acid wash.

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cycobushmaster
Level 1

Join date: Sep 2004
Posts: 2476

tpepper88 wrote:
2thepain wrote:
I am not up on my proviron studies, are there any available that show a negative effect on the HPTA at any dose?


http://www.ncbi.nlm.nih.gov/...2?dopt=Abstract

"In a double-blind placebo controlled study, the clinical effects of 300-450 mg daily mesterolone were investigated in 52 relatively young ..... Mesterolone treatment significantly decreased both plasma testosterone and protein bound testosterone levels."

Granted thats a shit ton of proviron, but theres your study.


another study:

http://www.ncbi.nlm.nih.gov/.../pubmed/2892728

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cycobushmaster
Level 1

Join date: Sep 2004
Posts: 2476

enchilnada wrote:
seekonk wrote:
Prisoner wrote:

the research showed no hpta suppression while using a serm and low dose testosterone - 100mg per week



I am trying to understand what this means. Is it from a published study?

Did someone measure endogenous T production during treatment and determine that it was unaffected? This would require some way to distinguish between T from exogenous and endogenous source, maybe by some calculation. Or does it just mean that endogenous T returned to baseline immediately after cessation of treatment?

What dose of SERM are we talking about?



There are studies which are supportive of different aspects. For example, Winters et al., found that if subjects are administered 100 mg of clomiphene twice daily, LH levels are unable to be decreased (and in fact continue to rise) even when serum testosterone levels are elevated up to over 2,000 ng/dl (i.e., the equivalent of the peak concentration reached after a 200 mg dose of testosterone enanthate). Naftolin et al., also had similar results.

http://www.ncbi.nlm.nih.gov/pu...
http://www.ncbi.nlm.nih.gov/.../pubmed/4683184



interesting stuff...

if this is accurate, why don't we use Clomid on cycle to prevent shutdown altogether?

presumably, this would be due to a limited time-frame, and it no longer works? i'm curious if that's why the TRT folks don't use this....



IMHO, these are interesting studies, but using them here is a tad flawed in logic, as we're not talking about someone having a normal HPTA system, but one fully suppressed from a cycle.


EDIT: as far as Teslac, well, it was awesome... basically the first AI, as it had close to a 90% suppression of estrogen, while bumping testosterone up by 47%...

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