[quote]MODOK wrote:
Or at least tell us what thread you posted the reference in previously; I can’t seem to find it.[/quote]
Here it is.
http://www.T-Nation.com/readTopic.do?id=879199&pageNo=0#881533
[quote]exogenously injected testosterone is indistinguishable to the body from it’s own, as it is the exact same molecule.
As levels of exogenous testosterone fall below what the body normally needs, the body [will via the negative feed-back loop (basic physiology -hello!)] will sence this, and begin producing testosterone to pick up the slack.
As exogenous levels fall further, endogenous levels will continue to rise to a point where exogenous levels fall off altogether, and the hpta takes over as the only source for testoterone again.[/quote]
so, lets speak numbers here to get it more properly as im trying to understand your reasoning.
say you are on a 600mg test/week cycle (lets for simplicity’s sake assume its only test).
1)you have forced your body to work with 600mg of testosterone. As you taper down to say 200mg your body detects a decline to test levels and trys to maintain homeostasis by reaching the previous (600mg) levels, this is a slow prosses but in the end you will have your HPTA up and working again.
2)you taper down to 200mg, then to 100mg, then to 50mg and then to 20mg. So your body will (bellow say 100mg) start figuring out its in the low zone so it starts producing slowly but stedily test again.
if you are saying number 1) you are sugesting that the body has no absolute levels of testosterone value so what it understands is diferentials not amounts.
strange thing, i though that the GnRH pulse was mediated by androgen receptors in the hypothalamus…hmmmm…perhaps i am (unlike you) stupid.
if you are saying number 2)you drop to 200mg, still being supressed and hindering your gains. You drop to 50mg, on average natural T is sometihng like 70mg/week, so probably your body will need to make those 20 extra mg, you drop to 20 your body will need to make 50 extra mg.
again, i was under the impression that the GnRH pulse is mediated by…well you get the picture.
At some point you state that you sould be clean of any non testosterone compound. Why is that? Do they not bind to the androgen receptor? Do they not cause HPTA inhibition? Does not your body infact detects them as androgens?Would 2mg of dianabol shut you down regardless, or do they posses some other form of function in the HPTA other than androgen receptor binding?
regarding the medical field and receptor mediated pharmacology:
my oh my…do you know of ANY medication that is NOT receptor dependant? I dont know much about biology but i though that receptors are the only way the cell has to comunicate with the outside world bar osmosis…hmmm…
so ok, you give a theurapetic dose of anavar…Say what? 5mg ed? After week 4 or what have you you drop to 2.5 ed and then 2.5 eod.
right, yes, i see how that coresponds with the 60+ mg a bodybuilder would take.
btw, no athletes i know (including east germans and russians that where medicaly supervised) did not “taper” doses.
you my friend are ignorant
[quote]epote wrote:
so, lets speak numbers here to get it more properly as im trying to understand your reasoning.
say you are on a 600mg test/week cycle (lets for simplicity’s sake assume its only test).
1)you have forced your body to work with 600mg of testosterone. As you taper down to say 200mg your body detects a decline to test levels and trys to maintain homeostasis by reaching the previous (600mg) levels, this is a slow prosses but in the end you will have your HPTA up and working again.
[/quote]
No, I didn’t say that, your body will do nothing to respond to falling blood levels of testosterone untill it is below your own personal natural ‘norm’. I never said anything about ‘up-regulating’ receptors in the hpta.
[quote]epote wrote:
2)you taper down to 200mg, then to 100mg, then to 50mg and then to 20mg. So your body will (bellow say 100mg) start figuring out its in the low zone so it starts producing slowly but stedily test again.
[/quote]
Yes, at some point during the process your hypothamus will sence low testosterone levels and the pituitary - testicular axis will restart.
[quote]epote wrote:
if you are saying number 1) you are sugesting that the body has no absolute levels of testosterone value so what it understands is diferentials not amounts.
[/quote]
This is not what I said at all. Everyone genetically has a different range of testosterone in which their body naturally resides. It is below 100mg per week, but exactly what it is nobody can say for sure.
[quote]epote wrote:
strange thing, i though that the GnRH pulse was mediated by androgen receptors in the hypothalamus…hmmmm…perhaps i am (unlike you) stupid.
[/quote]
Actually, Estrogen controls to a large part the negative feedback system. It is testosterone aromatising to estrogen and then binding to the ER in the hypothalmus that is thought to regulate testosterone.
That is why administering Arimidex has been seen to artificially increase natural test production however, it is also known that a steroid that binds well to the AR is more suppressive than a steroid than weaker steroids, irregardless of how much said steroid aromatizes. The exact mechanism behind this is unknown however.
This of course is shown by using products such as Adex, or clomid - these drugs do increase testosterone, however their effects are temporary and self-limiting.
[quote]epote wrote:
if you are saying number 2)you drop to 200mg, still being supressed and hindering your gains. You drop to 50mg, on average natural T is sometihng like 70mg/week, so probably your body will need to make those 20 extra mg, you drop to 20 your body will need to make 50 extra mg.
[/quote]
We can’t talk exact numbers, but you get the general idea. Don’t forget of course when using a preparation like Enanthate or Cypionate that you have to calculate the weight of the ester, which tends to take up at least 30%.
[quote]epote wrote:
again, i was under the impression that the GnRH pulse is mediated by…well you get the picture.
At some point you state that you sould be clean of any non testosterone compound. Why is that? Do they not bind to the androgen receptor? Do they not cause HPTA inhibition? Does not your body infact detects them as androgens?Would 2mg of dianabol shut you down regardless, or do they posses some other form of function in the HPTA other than androgen receptor binding?
[/quote]
As I said above, we don’t know exactly how Steroids that bind well to the AR cause suppression, via non-ER means, but they do.
As for other steroids, given time they will clear the body. Steroids with long chained esters hang around longer in the muscle but as soon as they are freed of their ester they are either bound by SHBG, or used, and metabolized, then excreted via the kidneys.
Orals such as dbol have a 4 hour half life, so they are eliminated quite quickly, in fact so fast that you can actually take dbol in the morning, and still keep your hpta active, as it works mainly at night during sleep.
As I said though all non-testosterone steroids need to be eliminated sufficiently to trace amounts before a successfull taper/ recover can occur. This is also rings true, if you were to use Anthony’s protocol.
[quote]epote wrote:
regarding the medical field and receptor mediated pharmacology:
my oh my…do you know of ANY medication that is NOT receptor dependant? I dont know much about biology but i though that receptors are the only way the cell has to comunicate with the outside world bar osmosis…hmmm…
[/quote]
Well yes of course all medications are receptor mediated, however some medications for example antibiotics bind to receptors on bacteria.
As I said before, and i’ll elaborate: for all long term therapy when stopping a medication, and not replacing it with somthing else to compensate, you have to taper. Even antihypertensives need tapering.
If a patient on metoprolol stopped taking their medication for example they would have rebound tachicardia, which could develop into A-fib, causing an eventual MI, or CVA. AAS is no different, there are withdrawal symptoms, and not just related to the hpta
- I am talking deppression, skin disorders, a dramatic drop in AAS levels could lead to a high rate of catabolism due to the ‘crash’ which inturn would elevate creatinine levels, which could put further stress on a BB who already had early stage renal failure which btw is asymptomatic (say a Flex Wheeler)
Btw, I saved a man’s life today, what did you do?
[quote]epote wrote:
so ok, you give a theurapetic dose of anavar…Say what? 5mg ed? After week 4 or what have you you drop to 2.5 ed and then 2.5 eod.
right, yes, i see how that corresponds with the 60+ mg a bodybuilder would take.
[/quote]
Anavar isn’t a good example, as it doesn’t aromatise, and binds very poorly to the AR. Its quite weak, and most of it’s mechanism of action surounds increasing the muscles creatine phospate retention. But yes it would be wise to taper it if you were using it long term.
[quote]epote wrote:
btw, no athletes i know (including east germans and russians that where medicaly supervised) did not “taper” doses.
you my friend are ignorant
[/quote]
O.k I really don’t know what you are trying to say here, as it doesn’t make sense other than this entire post by yourself being a failed attempt to flame me. I hope however that you did learn something
ok, so your point is this:
provide a tapered HRT dose untill hpta is restored. Thus you have no “low test” sympoms. Ok, i can see the reasoning in that, BUT, you assume we do nothing in pct to compesate (or accelarate) that procedure. Nolva does increase natural T, and then there is hCG etc.
point is, tapering while (probably) les harsh in terms of withdowall would probably be better (although you could argue that the decreased motivtion to work out could work benificialy from a performance standpoint) but it would difenetly take longer forcing you to be “on drugs” for far longer
[quote]
Btw, I saved a man’s life today, what did you do? [/quote]
and then you braged about it on the internet?
excuse me i mistated, you are not ignorant, you are a jack ass.
[quote]Prisoner#22 wrote:
I saved a man’s life today, what did you do?
[/quote]
I killed a man in Reno just to watch him die…
[quote]epote wrote:
ok, so your point is this:
provide a tapered HRT dose untill hpta is restored. Thus you have no “low test” sympoms. Ok, i can see the reasoning in that, BUT, you assume we do nothing in pct to compesate (or accelarate) that procedure. Nolva does increase natural T, and then there is hCG etc.
point is, tapering while (probably) les harsh in terms of withdowall would probably be better (although you could argue that the decreased motivtion to work out could work benificialy from a performance standpoint) but it would difenetly take longer forcing you to be “on drugs” for far longer
Btw, I saved a man’s life today, what did you do?
and then you braged about it on the internet?
excuse me i mistated, you are not ignorant, you are a jack ass.[/quote]
O.k, Nolva can be used, but it won’t do sh!t untill hormone levels are lower than adequate in your body. I advocate using an AI like arimidex, to ensure estrogen levels are kept at normal amounts, as estrogen can prolong recovery. Many users of nolva figure this out when they go off it, and experience the ‘rebound’ effect as elevated estrogen that was kept from binding in their body is freed to bind at the ER. Using arimidex throughout the cycle eliminates the real need for nolva post cycle.
As for the longer time ‘on’ two points: first off pm me and I will give you a link to a pct calculator, and you will see actually just how long it takes for longer acting esters used in a cycle to sufficiently clear the body for pct to begin. (Anyone else who is interested feel free to pm me as I can’t post this link on the main board).
Secondly, As soon as hormone levels fall below your norm, the body systems return to normal, you don’t even feel that you are steroids, from a health point of view, the negative effects of high test levels such as changes in blood lipid profiles will return to normal.
As for the training comment, I have tried it both ways - i.e. not training after a cycle, and training hard after a cycle, and gains were kept way better with the training hard.
Finally, the only reason I made the ‘I saved a man’s life’ comment, is that you were calling me ignorant, and that pissed me off.
As I said before, I got no hidden agenda here, just sharing experience and info that I have learned with other bro’s.
The proof of all I have outlined in this thread, is demonstrated in this study.
Am J Physiol Endocrinol Metab 281: E1172-E1181, 2001;
0193-18
Vol. 281, Issue 6, E1172-E1181, December 2001
Testosterone dose-response relationships in healthy young men
Shalender Bhasin1, Linda Woodhouse1, Richard Casaburi3, Atam B. Singh1, Dimple Bhasin3, Nancy Berman3, Xianghong Chen4, Kevin E. Yarasheski4, Lynne Magliano2, Connie Dzekov1, Jeanne Dzekov1, Rachelle Bross3, Jeffrey Phillips3, Indrani Sinha-Hikim1, Ruoquing Shen1, and Thomas W. Storer2
1 Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles 90059; 2 Laboratory for Exercise Sciences, El Camino College, and 3 Harbor-University of California Los Angeles Medical Center, Torrance, California 90502; and 4 Biomedical Mass Spectrometric Research Resource, Department of Internal Medicine, Washington University, School of Medicine, St. Louis, Missouri 63110
Abstract:
Testosterone increases muscle mass and strength and regulates other physiological processes, but we do not know whether testosterone effects are dose dependent and whether dose requirements for maintaining various androgen-dependent processes are similar. To determine the effects of graded doses of testosterone on body composition, muscle size, strength, power, sexual and cognitive functions, prostate-specific antigen (PSA), plasma lipids, hemoglobin, and insulin-like growth factor I (IGF-I) levels, 61 eugonadal men, 18-35 yr, were randomized to one of five groups to receive monthly injections of a long-acting gonadotropin-releasing hormone (GnRH) agonist, to suppress endogenous testosterone secretion, and weekly injections of 25, 50, 125, 300, or 600 mg of testosterone enanthate for 20 wk. Energy and protein intakes were standardized. The administration of the GnRH agonist plus graded doses of testosterone resulted in mean nadir testosterone concentrations of 253, 306, 542, 1,345, and 2,370 ng/dl at the 25-, 50-, 125-, 300-, and 600-mg doses, respectively. Fat-free mass increased dose dependently in men receiving 125, 300, or 600 mg of testosterone weekly (change +3.4, 5.2, and 7.9 kg, respectively). The changes in fat-free mass were highly dependent on testosterone dose (P = 0.0001) and correlated with log testosterone concentrations (r = 0.73, P = 0.0001). Changes in leg press strength, leg power, thigh and quadriceps muscle volumes, hemoglobin, and IGF-I were positively correlated with testosterone concentrations, whereas changes in fat mass and plasma high-density lipoprotein (HDL) cholesterol were negatively correlated. Sexual function, visual-spatial cognition and mood, and PSA levels did not change significantly at any dose. We conclude that changes in circulating testosterone concentrations, induced by GnRH agonist and testosterone administration, are associated with testosterone dose- and concentration-dependent changes in fat-free mass, muscle size, strength and power, fat mass, hemoglobin, HDL cholesterol, and IGF-I levels, in conformity with a single linear dose-response relationship. However, different androgen-dependent processes have different testosterone dose-response relationships.
sexual function; testosterone effects on muscle; cognitive function; plasma lipids; prostate-specific antigen; testosterone effects on insulin-like growth factor I; testosterone and hemoglobin
I have more respect for Prisoner than probably anyone on this website, however I just so happen to have the exact products that are layed out in Anthony Robert’s “BS” protocol.
I am a fan of clomid because it works really well for me in restoring testicular size.
However, I have heard that the more you use it, the more desensitized the testes become. I have already used it once this year and was thinking about trying something different (Anthony Robert’s protocol).
I have had bad luck with Nolva because the first time I used it, it was 10 - 20mg/ED on cycle with test/tren/dbol and I got a gyno lump in my left nipple. Nolva has left a bad taste in my mouth, but I have the a bottle of the stuff and might as well use it before it expires.
The cycle I am starting is this:
Date: April 2011
Substance: Test Cypionate, Primobol (Methenolone Enanthate), and Masteron (Dromastanolone Dipropionate)
Dose: 250mg/week test, 400mg/week primo, 100mg/E3D masteron (last 30 days)
Length: 10 weeks (12 weeks active)
Side Effects: I plan to use Arimidex .5-1mg ED and will keep letro on hand
Gains: Mostly dry
I know the test is really low dose, but I am very sensitive to test than any other substance. It’s a lower dose than a normal cycle so is the taper protocol the best one?
Three PCT options:
Option 1: I could do HCG 250iu twice weekly on cycle, and proceed with clomid for three weeks post cycle. I guess I could use the Aromasin too, but how?
Option 2: I could do Anthony Robert’s protocol to use the products I have on hand:
Week 1 - 3
Nolva: 20mgs/day
HCG: 500iu/day
Aromasin: 20mgs/day
Vitamin E: 1,000iu/day
Week 4
Nolva: 20mgs/day
HCG: none
Aromasin: 20mgs/day
Vitamin E: none
Nolva: 20mgs/day
HCG: none
Aromasin: none
Vitamin E: none
Nolva: 20mgs/day
HCG: none
Aromasin: none
Vitamin E: none
Option 3: I could do the Prisoner test taper and throw away the nolva and aromasin because they will expire.
I have another forum asking this exact same question about the PCT Protocol. Check it out:
Hmmm, what should I do?
Perhaps, not dig up 5 year old threads on Anthony Conner’s PCT methods?
Just to start with, why would one choose to – quite unnecessarily – lose testicular function during the cycle and thus have to regain it concurrently with regaining LH production?
Wouldn’t it make a lot more sense to maintain testicular function during the cycle, and then discontinue a week prior to the last injection so that it does not inhibit LH production in recovery, which it will do when present in substantial amounts?
With regard to this PCT method, as Robert Downey Jr’s character said in Tropic Thunder, “Never go full retard.”
[quote]Bill Roberts wrote:
Perhaps, not dig up 5 year old threads on Anthony Conner’s PCT methods?
Just to start with, why would one choose to – quite unnecessarily – lose testicular function during the cycle and thus have to regain it concurrently with regaining LH production?
Wouldn’t it make a lot more sense to maintain testicular function during the cycle, and then discontinue a week prior to the last injection so that it does not inhibit LH production in recovery, which it will do when present in substantial amounts?
With regard to this PCT method, as Robert Downey Jr’s character said in Tropic Thunder, “Never go full retard.”[/quote]
I posted in this forum after I looked at the date and it said 2006. Oops!
It was such a good forum though, I thought, well maybe now there’s some new insight, but apparently it’s the same old story.
I agree with you on what you said above, but I have a question about when to discontinue the HCG on-cycle. Why would you discontinue a week before the last injection if you are using long esters that will be present in the system up to two weeks after the last injection? Wouldn’t it be better to cease the HCG a week after the last injection?
Depending on the particular dosages and choices of steroid, it can be the case that HCG could be pushed somewhat longer than above – for example to coincide with the last injection if longer-acting esters are used – with the HCG still falling to a minimally-suppressing level before or at the same time that androgen level falls enough to allow recovery.
One week will cover all cases except where exclusively very short acting compounds such as orals or acetate esters are used. In those instances, depending on HCG dosage, I’d prefer for the last HCG injection to be a little more than week before the last oral dose or 5 days or so before the last injection.
In those instances where because the steroid dosage is more substantial and the esters are longer acting, it’s true that the HCG could be run somewhat longer than the above, but if testicular function was maintained during the cycle with HCG, the time difference won’t be important. Testicular function won’t be impaired in that brief period.
But yes in many instances it could be continued somewhat longer. The above was written to include cases such as simple 500 mg/week testosterone enanthate cycles or cycles using exclusively short-acting compounds, as well as cycles using more ambitious doses of longer acting compounds. You are right that it can be the case that this is an earlier discontinuance than what could be chosen if having the specific details of the cycle.
Very interesting read. Would like to see if Prisoner is still advocating the taper for PCT. I just looked at a recent thread he was in where the person proposed the standard Nolva 40/40/20/20 PCT and he said “…cycle looks good”
[quote]Toby Queef wrote:
Very interesting read. Would like to see if Prisoner is still advocating the taper for PCT. I just looked at a recent thread he was in where the person proposed the standard Nolva 40/40/20/20 PCT and he said “…cycle looks good”[/quote]
He sort of designed the ‘stasis-taper’ that’s outlined in the sticky. Im pretty sure this thread predates his ‘stasis-taper’ theory.
If I remember correctly Prisoner used to recommend a Taper when coming off of longer cycles, and a standard SERM PCT for shorter standard cycles.
[quote]BONEZ217 wrote:
[quote]Toby Queef wrote:
Very interesting read. Would like to see if Prisoner is still advocating the taper for PCT. I just looked at a recent thread he was in where the person proposed the standard Nolva 40/40/20/20 PCT and he said “…cycle looks good”[/quote]
He sort of designed the ‘stasis-taper’ that’s outlined in the sticky. Im pretty sure this thread predates his ‘stasis-taper’ theory. [/quote]
It does, by at least a year. I’m reading through all of it now. Thinking I might give the stasis-taper a go this time around. I didn’t have any problems recovering with a SERM-only PCT so part of me thinks don’t fix what isn’t broken…but the other part of me wants to see if another way can be even better.