Is CED59 being stupid...? TRT/Bridge Discussion

[kwyckemynd00]

Great sex between whom? I'm out if you think you're getting anywhere near me with that thing.

YOu think I can't get near you with it?

Look next to your left foot....

 

[natedogg]

YOu think I can't get near you with it?

Look next to your left foot....

Ahhh...what the...damn that thing is about as thick as a pencil.

 

[kwyckemynd00]

Ahhh...what the...damn that thing is about as thick as a pencil.

Yeah, yeah.....but it sure is long isn't it? *smooch*

 

[milwood]

Yeah, yeah.....but it sure is long isn't it? *smooch*

okay, I guess this one IS getting away from us.

On topic, however, aside from having amusing dialogue, I appreciate CED's call for advice and the people who have advised. Really brings home the great advantage of having this forum and such conversations. Props to all...

 

[natedogg]

okay, I guess this one IS getting away from us.

On topic, however, aside from having amusing dialogue, I appreciate CED's call for advice and the people who have advised. Really brings home the great advantage of having this forum and such conversations. Props to all...

Humor and good advice. You can't beat that.

 

[Ubiquitous]

Discussion, Good advice, no burning, and capping it off with good old mansex talk.

=perfect thread:clap2:

 

[rhinochaser48]

Don't know where you got that from but research suggests otherwise. Testosterone administration actually upregulates the AR for a very long time. Doses given to men showed upregulation of up to 6 months before any type opf down regulation ocurred and even then it never went below baseline.

You have to look at other genetic factors on why people stop responding (probably diet anyway).


I don't understand the point of cruising in a normal healthy man. You are only going to increase the chances of lower test production in the long run.

I don't remember where I read it. Someone had theorized this and I read it as convincing.

It would seem logical that the human body would adapt in some manner to establish a homeostasis at some point.

A quick search pulls up something Nandi claims:

http://www.wannabebig.com/printarticle.php?articleid=225

In long term studies in humans we get yet a different picture. In work conducted by Sheffield-Moore et. al., (16) older men were supplemented with testosterone so as to bring their testosterone levels into the mid to high physiological range. Androgen receptor expression had more than doubled after one month of treatment, yet by 6 months had returned to baseline. If this downregulation occurs when supraphysiological doses of testosterone are used, it could very well explain why gains tend to slow during a long cycle.

Here is the study he cited:


Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ. Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

Testosterone administration to older men improves muscle function: molecular and physiological mechanisms.

Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.

Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77550, USA. [email protected]

We investigated the effects of 6 mo of near-physiological testosterone administration to older men on skeletal muscle function and muscle protein metabolism. Twelve older men (> or =60 yr) with serum total testosterone concentrations <17 nmol/l (480 ng/dl) were randomly assigned in double-blind manner to receive either placebo (n = 5) or testosterone enanthate (TE; n = 7) injections. Weekly intramuscular injections were given for the 1st mo to establish increased blood testosterone concentrations at 1 mo and then changed to biweekly injections until the 6-mo time point. TE doses were adjusted to maintain nadir serum testosterone concentrations between 17 and 28 nmol/l. Lean body mass (LBM), muscle volume, prostate size, and urinary flow were measured at baseline and at 6 mo. Protein expression of androgen receptor (AR) and insulin-like growth factor I, along with muscle strength and muscle protein metabolism, were measured at baseline and at 1 and 6 mo of treatment. Hematological parameters were followed monthly throughout the study. Older men receiving testosterone increased total and leg LBM, muscle volume, and leg and arm muscle strength after 6 mo. LBM accretion resulted from an increase in muscle protein net balance, due to a decrease in muscle protein breakdown. TE treatment increased expression of AR protein at 1 mo, but expression returned to pre-TE treatment levels by 6 mo. IGF-I protein expression increased at 1 mo and remained increased throughout TE administration. We conclude that physiological and near-physiological increases of testosterone in older men will increase muscle protein anabolism and muscle strength.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 11832363 [PubMed - indexed for MEDLINE]

I couldn't find anything like this that may say whether or not exercise has an influence on the AR.

Bobo - Comments?

 

[Nullifidian]

First off, no recovery is possible during a bridge obviously. The way I see it there is only 1 reason to ever bridge. That reason is, if the way your cycles turned out, you have another cycle beginning less than 6 weeks from the end of the last one. In which case, PCT is pretty pointless since by the time PCT is just ending, you're going right back on.

In that situation, bridging could be good. Why? Because replacement levels of androgens aren't going to kick the crap out of your system (blood pressure, etc.). Thus, while your HPTA cannot recover in that time, the rest of your body can.

 

[kwyckemynd00]

Nullifidian: See...this is where I"m confused.

SWALE treats many of his patients in an attempt to RESTART their HPTA with 125mg/wk of Test + 250 x 2 IU hCG.

Therefore, I'm left confused This, to me, implies that HPTA recovery is possible to some degree during this time period.

 

[DR.D]

You can do it successfully, but I think you may be disappointed with the results after the long cycle with all that gear. Honestly, I would do an ActivaTe bridge at this point. I started gaining better on that during my PCT than I had been at the end of my cycle! I'd still add it even if you do the TRT, and go with 500u twice a wk on the hCG rather than 250 if you decide to do it, or 100u/day works well if you are injecting another water base anyway like IGF, suspension or whatever. If you try it, you will learn from it at least, but I don't do it anymore. I might if I was 5 or 10 years younger, but PCT's are very versatile now and don't have to slow you down as much (even if they can get expense).

 

[CEDeoudes59]

Thanks Dr. D for coming over - im going the PCT route but i'll ponder the future

 

[supersoldier]

So you were on for 19 weeks, eh? :yawn: :yawn: :yawn:

Steroid abuse is bad, mmmmkay? :nutkick: :lol:

 

[CEDeoudes59]

look who's talking

 

[Dwight Schrute]

I don't remember where I read it. Someone had theorized this and I read it as convincing.

It would seem logical that the human body would adapt in some manner to establish a homeostasis at some point.

A quick search pulls up something Nandi claims:

http://www.wannabebig.com/printarticle.php?articleid=225




Here is the study he cited:


Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ. Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7




I couldn't find anything like this that may say whether or not exercise has an influence on the AR.

Bobo - Comments?

Yes, so in other words downrugaultion doens't occur to the point it never goes below baseline. IOW, its not really a factor at all. Even Dr. Crisler doens't believe there isn't any downregulation at all from his HRT trials. Plus you forgot to boldface this line:

"IGF-I protein expression increased at 1 mo and remained increased throughout TE administration."


Exercise downregulates the AR right after exercise with a rise in testosterone and cortisol then upregulates several hours after that. Plus looking at these factors is a waste IMO anyway. These condiotions change constantly just based on exercise and diet alone.

 

[exnihilo]

Dose / Before / After / Change / p-value
25 mg / 593 ± 48 / 253 ± 66 / 340 ± 85 / 0.0029
50 mg / 566 ± 78 / 306 ± 58 / 260 ± 64 / 0.0037
125 mg / 553 ± 53 / 570 ± 75 / 57 ± 75 / 0.7425
300 mg / 653 ± 50 / 1,345 ± 139 / 691 ± 143 / 0.0005
600 mg / 632 ± 63 / 2,370 ± 150 / 1,737 ± 156 / 0.0001


Taken From:

Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81.

Testosterone dose-response relationships in healthy young men.

Bhasin S, Woodhouse L, Casaburi R, Singh AB, Bhasin D, Berman N, Chen X, Yarasheski KE, Magliano L, Dzekov C, Dzekov J, Bross R, Phillips J, Sinha-Hikim I, Shen R, Storer TW.

Maybe shutdown is not so dose dependent? Hmmm...........well...........I dunno......ALR told me otherwise, now I"m confused again........... *bah* i hate learning ****.

Helps to actually read the article Kwycke

Testosterone dose-response relationships in healthy young men.

Bhasin S, Woodhouse L, Casaburi R, Singh AB, Bhasin D, Berman N, Chen X, Yarasheski KE, Magliano L, Dzekov C, Dzekov J, Bross R, Phillips J, Sinha-Hikim I, Shen R, Storer TW.

Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA. [email protected]

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.



If the GnRH agonist were not used, I'd bet that people receiving less than their natural production of test would still have normal testosterone levels, as the body would "pick up the slack". LH and FSH would be lower in a dose dependant manner, but that's why you wean off.

I am thoroughly convinced at this point that a cruising period lasting 8-10 weeks at the end of a cycle with tapering doses from 100-25mg or so in conjunction with low dose SERM usage is the right way to go. Now I just need test subjects to validate my hypothesis

 

[kwyckemynd00]

Helps to actually read the article Kwycke ....

Wow...I didin't have access to the entire article.

So, ALR was probably right on when he said that shutdown is dose-dependent. Makes sense since some ppl don't shut down easily--based on that info, I asked him if that's b/c of higher natty T levels, he said yes (one of a few possible factors).

Thx for the article....now, if only I could find a study where endogenous test was not supressed :twisted:

I've noticed that orals can shut me down, but when I'm on the test solo, at 500mg/wk, i hardly feel it and my nutz dont' shrink for jack, even if I lay off the hcg.

thx exnihilo

 

[exnihilo]

Wow...I didin't have access to the entire article.

So, ALR was probably right on when he said that shutdown is dose-dependent. Makes sense since some ppl don't shut down easily--based on that info, I asked him if that's b/c of higher natty T levels, he said yes (one of a few possible factors).

Thx for the article....now, if only I could find a study where endogenous test was not supressed :twisted:

I've noticed that orals can shut me down, but when I'm on the test solo, at 500mg/wk, i hardly feel it and my nutz dont' shrink for jack, even if I lay off the hcg.

thx exnihilo

Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.

Matsumoto AM.

Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Seattle, Washington 98108.

In normal men, chronic testosterone (T) administration results in negative feedback suppression of gonadotropin and sperm production. However, azoospermia is achieved in only 50-70% of men treated with high dosages of T. Furthermore, the relative sensitivity of LH and FSH secretion to chronic administration of more physiological dosages of T is unclear. We determined whether a T dosage higher than those previously given would be more or less effective in suppressing spermatogenesis and whether, within the physiological range, T would exert a more selective effect on LH than on FSH secretion. After a 4- to 6-month control period, 51 normal men were randomly assigned to treatment groups (n = 9-12/group) receiving either sesame oil (1 mL) or T enanthate (25, 50, 100, or 300 mg, im) weekly for 6 months. Monthly LH and FSH levels by RIA and twice monthly sperm counts were determined. During treatment, T levels were measured daily between two weekly injections. Chronic T administration in physiological to moderately supraphysiological dosages resulted in parallel dose-dependent suppression of LH, FSH, and sperm production. T enanthate (50 mg/week) suppressed LH and FSH levels and sperm counts to 50% of those in placebo-treated men (ED50). T enanthate (300 mg/week), was no more effective than 100 mg/week in suppressing LH, FSH, and sperm production. Serum T levels in men who received 100 and 300 mg/week T enanthate were 1.5- and 3-fold higher than those in placebo-treated men, respectively. Except for mild truncal acne, weight gain, and increases in hematocrit, we detected no significant adverse health effects of chronic high dosage T administration. We conclude that 1) LH and FSH secretion are equally sensitive to the long term negative feedback effects of T administration; 2) sperm production is suppressed in parallel with the LH and FSH reductions induced by chronic T administration; and 3) even at the clearly supraphysiological dosage of 300 mg/week, T enanthate does not reliably induce azoospermia in normal men. However, there was also no evidence of a stimulatory effect of this T dosage on spermatogenesis. Furthermore, we found no evidence of major adverse health effects of T administered chronically even at the highest dosage.

PIP: In Seattle, Washington, health workers randomly assigned 51 healthy men (mean age, 29 years) to a group that was to receive either 1 ml sesame oil or testosterone enanthate (T enanthate) at various doses once a week for 6 months so an investigator could determine the safety and efficacy of long-term administration of T enanthate in suppressing spermatogenesis and whether it would bring about a more selective feedback effect on luteinizing hormone (LH) than on follicle stimulating hormone (FSH) secretion. 4-6 months prior to treatment, observations and measurements were performed with no administration of hormones. T enanthate effected a significant dose-dependent suppression of both serum LH and FSH levels. At 50 mg of T enanthate per week, the LH level was 65% and the FSH level was 62% of control values; at 100 mg/week, the levels were at 32% and 34% of control values, respectively. T enanthate also contributed to a significant dose-dependent suppression of both sperm counts and concentrations. At 50 mg/week, the sperm count was 36% of control values; at 100 mg/week, it was 0.8% of control values. T enanthate at a dose of 300 mg/week was no more effective than 100 mg/week. The dose-dependent suppression curves were parallel for the hormones, sperm counts, and sperm concentrations. Men who received 100 mg and 300 mg T enanthate per week had higher T levels than the men treated with sesame oil. These levels were at and above the upper limits of the normal range. The men suffered from no significant adverse health effects. There were cases of mild truncal acne, weight gain, and increases in hematocrit. These findings show that LH and FSH secretion are sensitive to long-term negative feedback effects of T administration as well as is spermatogenesis. T enanthate may prove to be a useful male contraceptive agent.


I need to go to the university library and read this article, it's like half an hour away though so I'm procrastinating. I think this article will have graphs with testosterone concentrations based on dosage of testosterone. Since they didn't mention that people on less than 100mg of T/week had lower testosterone levels than people on sesame oil, I assume that they didn't (which makes sense if you think about it).

As far as orals shutting you down:

Figure 3. Total androgen concentration. Total serum T (hatched portion) and OX (black portion) concentrations in five young men on days 0, 3, and 5. *, T decreased significantly from days 0 and 3 to day 5 (P < 0.05).

So yeah, it appears that oral steroids can shut you down really hard

 

[CEDeoudes59]

mighty good info, when i get my head right I read it again
thanks EX

 

[DR.D]

...I am thoroughly convinced at this point that a cruising period lasting 8-10 weeks at the end of a cycle with tapering doses from 100-25mg or so in conjunction with low dose SERM usage is the right way to go. Now I just need test subjects to validate my hypothesis

You are very right, if you have the patience to do it, but an AI could sub for the SERM on such a long cruise I bet.

 

[ss01]

This might lead one to also hypothesize that maybe the reason why orals have a reputation of generating gains that are difficult to keep is because of the much greater shutdown, and we all know that PCT isn't everyone's priority... OTOH now with the new generation of PCT products, that reputation just might become quite false.

Just thinking out loud here... Put me in my place if I'm deluded...

 

[Dwight Schrute]

Wow...I didin't have access to the entire article.

So, ALR was probably right on when he said that shutdown is dose-dependent. Makes sense since some ppl don't shut down easily--based on that info, I asked him if that's b/c of higher natty T levels, he said yes (one of a few possible factors).



thx exnihilo

No, not really.


From SWALE:

"Clomid does not cause an increase in LH (and therefore endogenous T production) in an environment of androgenic suppression. IOW, the "Clomid burst" is a myth.

Well, complete suppression is complete suppression. I regularly see this at dosages of just 100mg per week. At whatever weekly dose that happens, beyond that, the LH production is flatlined at <0.1. We do know (experientially), though, that testicular atrophy becomes more and more evident as time goes on, and it seems to me this may have something to do with--in fact, may be the most important part of--recovery. The HP begins to produce LH rather quickly (as serum androgen concentration drops below whatever threshold each man possesses). I believe recovery is moreso a matter of getting the testes to respond to LH stimulation."


In other words, the length of time seems more important than any dose.

Your LH bottoms out with very little endogenous administration and I take Dr. Crislers word over anyone the "feels" it anyday. At least his conditions are controlled.

 

[size]

Hey size, do you have any children because you would make a great father. If only you could get your alcoholism under control. Just kidding.

No children. However, I truly do try to help individuals from making short term mistakes that could effect one's long term well being. BBing/training/fitness should be about health, well being, and looking/feeling good, and not only aobut getting big.
If I did not think I could help anyone, then I would no longer participate in message boards. Message boards are a great asset today that could have helped many in the past.

My drinking is b/c I like beer.

 

[Dwight Schrute]

I've noticed that orals can shut me down, but when I'm on the test solo, at 500mg/wk, i hardly feel it and my nutz dont' shrink for jack, even if I lay off the hcg.

thx exnihilo

Atrophy is caused by a lack of sperm production (since the bulk is made up of sertoli cells, not leydig cells) than testosterone production. IOW you could be shut down and have no atrophy but the longer time goes on more chance sperm production is hindered causing more atrophy.

 

[size]

Atrophy is caused by a lack of sperm production (since the bulk is made up of sertoli cells, not leydig cells) than testosterone production. IOW you could be shut down and have no atrophy but the longer time goes on more chance sperm production is hindered causing more atrophy.

Keep time on short and they stay "plump"
:lol:
To me, I read people using these extended cycles, and it makes me ask why? Measuring the (+) vs (-), in my opinion, the (-) are too great. Many of these negatives could be avoided with reduced cycle lengths.

 

[Dwight Schrute]

Well people read into studies and see only LH levels are reduced by 65% and think that testosteron suppression is therfore only reduced by 65% and it doens't work like that. Several hormone sactually raise LH levels for a period of time (Dbol for example) but testosterone is still 0. You can have LH levels that aren't effected but its the response of the leydig cells TO LH that determine testosterone production.

 

[Dwight Schrute]

So yeah, it appears that oral steroids can shut you down really hard

Has nothing to do with orals. Deca and Tren will do the same.

 

[CEDeoudes59]

so bobo, a bit off subject, does HCG maintain sperm count as well as maintaining 'size' of the testis?

i always get a maybe or depends on that one...
i'd perfer a 'probably' or 'usually'..

 

[Dwight Schrute]

Yes. It has been used to treat azoospermia but I'm not sure how much ebcause the dosages used were rather high and also was used with HMG. So actually, that should be a maybe.

:lol:

 

[CEDeoudes59]

it's a probably then
swale seems to think so too.
I couldn't imagine doing HRT without HCG, let alone I couldn't imagine doing a cycle without either...

 

[exnihilo]

I have never disputed the idea of using HCG to maintain testicular sensitivity to LH.

I never said that 65% LH levels = 65% of natural testosterone production, though if the testes are functioning properly and there are no other negative feedback mechanisms in play that is what I would expect.

I never argued against androgenic supression.

I never stated that orals were they only things that were extremely supressive.

SWALE stated that in his experience, the androgenic supression effects of testosterone were sufficient to obviate any effect SERMs would have @ 200+ mg/week.

Of course swale has seen some people shut down completely at 100mg of testosterone a week. Everyone is different, ask him if that is the predominant norm in his experience (the way he mentions it, it doesn't sound like it is). Also, if you look at the study I posted they mention that 100mg of testosterone is sufficient to raise plasta T concentrations to 1.5 times above baseline. The study that showed 100mg of testosterone a week was only sufficient to maintain baseline testosterone levels also utilized a GnRH agonist to completely supress endogenous T production, so the fact that 100mg of testosterone is enough to supress some people isn't THAT suprising is it? I'm advocating a protocol that does seem to have some scientific grounding (though of course I'm missing the full texts of a couple articles and thus there may be some nuances that have escaped me - I'm sure you can relate). I have stated repeatedly that the final determinant of the efficacy of the protocol would be determined by direct experimentation, and I'm willing to put my time and money where my mouth is on that score.

Also, could you please reference books or articles written by Dr. Crisler that you are constantly paraphrasing?

 

[Dwight Schrute]

I have never disputed the idea of using HCG to maintain testicular sensitivity to LH.

I never said that 65% LH levels = 65% of natural testosterone production, though if the testes are functioning properly and there are no other negative feedback mechanisms in play that is what I would expect.

I never argued against androgenic supression.

I never stated that orals were they only things that were extremely supressive.

SWALE stated that in his experience, the androgenic supression effects of testosterone were sufficient to obviate any effect SERMs would have @ 200+ mg/week.

Of course swale has seen some people shut down completely at 100mg of testosterone a week. Everyone is different, ask him if that is the predominant norm in his experience (the way he mentions it, it doesn't sound like it is). Also, if you look at the study I posted they mention that 100mg of testosterone is sufficient to raise plasta T concentrations to 1.5 times above baseline. The study that showed 100mg of testosterone a week was only sufficient to maintain baseline testosterone levels also utilized a GnRH agonist to completely supress endogenous T production, so the fact that 100mg of testosterone is enough to supress some people isn't THAT suprising is it? I'm advocating a protocol that does seem to have some scientific grounding (though of course I'm missing the full texts of a couple articles and thus there may be some nuances that have escaped me - I'm sure you can relate). I have stated repeatedly that the final determinant of the efficacy of the protocol would be determined by direct experimentation, and I'm willing to put my time and money where my mouth is on that score.

Also, could you please reference books or articles written by Dr. Crisler that you are constantly paraphrasing?

I never said you did x2.

LH, FSH, TEST production are not dose dependent with different drugs.

You said orals could suppress you hard. It has nothing to do with the drug being oral at all.

Swale stated that time is more important than that dose because LH levels are nil at a SMALL dosage of test. Ask him if prolonging a cycle with small of test is beneficial or using HCG during PCT is wise. He will tell you no.

"The suppression is surely produced by the induced T. I am not aware that LH directly suppresses at the hypothalamus or pituitary. However, we are finding more and more sites where LH is bioactive, and this is also a good reason to use HCG throughout the steroid cycle in cases where LH production is reduced.

HCG is "to suppressive' only when itr is being administered while we are trying to recover the HPTA. Then it is, just as Androgel or 100mg pf test cyp per week would be. IOW, you cannot "hide" androgens from the HP."



If you want to put you time and money on a protocl that really makes no sense IMO considering the alternatives and results, go for it. You are basically trying to do something that can already be achieved DURING your cycle. This discussion has been beaten to death at CEM and other baords in which Dr. Crisler posts so its nothing new at all and I'm sure can find those discussions at various boards.

As for references, its was he stated on several boards. If you want to ask him go for it. Maybe you could attend one of the seminars he gives to the various HRT and medical orginizations.

http://www.allthingsmale.com/


"Dr. John before 3,000 fellow physicians at an American Academy of Anti-Aging Medicine International Convention"

IF you want your questions answered, go to the source but you seem inclined to do this regardless of what is stated. I mean he has already performed your "experiement" so maybe you can save some time and money. If you just want to do for your own curiosity, knock your socks off.


:clap2:

 

[CEDeoudes59]

okay good, i thought Ex was talking to me... :run:

Okay, so no light dose (250ius x 2x a week) of HCG during PCT...

 

[Dwight Schrute]

Not if you use it throughout your cycle....

 

[DR.D]

Some of you guys are making this issue more black and white than it really is. I will agree that desensitization to HP stimulation over long periods of exogenous hormone use seems to be the biggest factor, but dose and the specific steroid do play a role too. It is shown that hCG response is greater when FSH levels are high. FSH levels are higher when estradiol is low. Estradiol is low when an AI is administered in conjunction with hCG or test (as I suggested before on the cruising). Estrogen suppresses Leydig function at doses so low that LH is not even affected first! Even Sertoli cells are capable of estrogen secretion. Also when prolactin levels are higher, there is synergism with LH in stimulating Leydig cells to produce test. There is a latency period with prolactin spikes and test production, as seen with dopamine antagonists like haloperidol. LH/hCG spikes don't directly correspond to increased test production really. When GNRH is administered with LH, plasma test concentrations are more reliably increased without this latency phenomenon. I have advocated use of halotestin as a "bridge" option during PCT based on this research. In real life, I have found it to be effective in that recovery proceeds without delay and spermatogenesis is augmented. LH spikes are reduced in number, but not their magnitude. In this case, LH spikes do seem to correlate more closely with test secretion! So it is a complicated issue and everyone must experiment to find their own limitations. Some will find "tricks" that work, while other will not be able to break the rules.

 

[lifted]

Bridging with Halo...that's a new one...lol.

 

[exnihilo]

Actually halotestin has one of the lowest affinities for the androgen receptor of just about any steroid. Not really an attractive compound to me though.

 

[Dwight Schrute]

Some of you guys are making this issue more black and white than it really is. I will agree that desensitization to HP stimulation over long periods of exogenous hormone use seems to be the biggest factor, but dose and the specific steroid do play a role too. It is shown that hCG response is greater when FSH levels are high. FSH levels are higher when estradiol is low. Estradiol is low when an AI is administered in conjunction with hCG or test (as I suggested before on the cruising). Estrogen suppresses Leydig function at doses so low that LH is not even affected first! Even Sertoli cells are capable of estrogen secretion. Also when prolactin levels are higher, there is synergism with LH in stimulating Leydig cells to produce test. There is a latency period with prolactin spikes and test production, as seen with dopamine antagonists like haloperidol. LH/hCG spikes don't directly correspond to increased test production really. When GNRH is administered with LH, plasma test concentrations are more reliably increased without this latency phenomenon. I have advocated use of halotestin as a "bridge" option during PCT based on this research. In real life, I have found it to be effective in that recovery proceeds without delay and spermatogenesis is augmented. LH spikes are reduced in number, but not their magnitude. In this case, LH spikes do seem to correlate more closely with test secretion! So it is a complicated issue and everyone must experiment to find their own limitations. Some will find "tricks" that work, while other will not be able to break the rules.

:frustrate

 

[Dwight Schrute]

Bridging with Halo...that's a new one...lol.

The effects of fluoxymesterone administration on testicular function.

Jones TM, Fang VS, Landau RL, Rosenfield RL.

Long term daily administration of fluoxymesterone (9alpha-fluoro-17alpha-methyl-11beta, 17beta-dihydroxyandrost-4-en-3-one) was associated with a modest suppression of sperm production and a profound suppression of testosterone levels in the absence of significant effects on plasma gonadotropin levels. Nine normal male volunteers took either 10, 20, or 30 mg of fluoxymesterone daily for twelve weeks. Plasma samples were obtained for testosterone, estrogen, LH and FSH levels at biweekly intervals before, during and for up to 12 weeks after fluoxymesterone treatment. Samples were obtained for dehydroepiandrosterone sulfate, testosterone binding globulin and free testosterone assays at representative times before, during and after treatment. Although lower sperm counts were observed at several points during both the treatment and follow up periods, significant consistent suppression of spermatogenesis could not be demonstrated. Reduced plasma testosterone levels were seen within 24 h after beginning fluoxymesterone, and further reductions were noted throughout the treatment period. Changes in plasma estrogen levels did not correlate with fluoxymesterone administration. Neither plasma LH nor plasma FSH levels were significantly altered by fluoxymesterone. A short term study utilizing a single dose of fluoxymesterone yielded similar findings. It is proposed that fluoxymesterone has a local effect on the Leydig cell which is not mediated by gonadotropins.

 

[CEDeoudes59]

I pulled this one from deep in the board... found it interesting and somewhat relevent to the earlier discussion.

Here's the link, it mainly people praising YJ for a cut and paste, but if you're interested here it is:
http://www.anabolicminds.com/forum/showthread.php?t=1661

Testosterone
Real-World Data
by Tim Ziegenfuss

If you've so much as picked up a newspaper in the last couple of weeks, or even a Time, Newsweek, Sports Illustrated, People, or friggin' Weekly Reader, you've no doubt been force fed yet another article about the horrors of steroids. Yep, steroids are no doubt what the terrorists are planning on dropping into our drinking water, thus creating a horrible epidemic of exploding livers and diminutive testicles that drop out of our pants like tiny popcorn kernels left over from last night's viewing of "The Secret Ya-Ya Sisterhood."

Thankfully, there's some real world research going on about steroid hormones (not much, mind you, but some). Recently, researachers Shalender Bhasin, Linda Woodhouse, Richard Casaburi et al. (of Charles R. Drew University of Medicine and Science, Harbor-University of California Los Angeles Medical Center, Washington University School of Medicine) did a pretty tidy little study on our beloved Testosterone (in this case, the hormone, not the magazine).

The title of the study is, "Testosterone dose-response relationships in healthy young men." As you might guess, they didn't study any 300 lb ripped-to-the-bone bodybuilders claiming to be drug free (yeah right). Instead, they focused on "normal" men and their responses to graded doses of this macho hormone.


Subjects

The subjects in this study consisted of 61 healthy men between the ages of 18-35 years. All had prior weightlifting experience, normal Tstosterone levels, and hadn't used any anabolic agents in the preceding year. All received monthly injections of a long-acting GnRH agonist to suppress endogenous Testosterone production (now that's gotta hurt). Depending on which group they were randomized to, subjects received one of five different weekly doses of Testosterone enanthate for five months (note: there were no significant differences between groups for any variable at the start of the study).

Remember, these are the test subject's values at the time the study began.

Group
Dose
Body weight (kg)
Age (yr)
FFM (kg)
Basal T (ng/dL)
Leg press strength (kg)

1
25 mg
68.0
28
59.1
593
355.5

2
50 mg
77.0
29
65.1
566
407.8

3
125 mg
78.9
28
66.0
553
419.2

4
300 mg
78.4
24
67.3
654
439.8

5
600 mg
74.8
25
64.2
632
431.6



Diet Control

Two weeks before their first intramuscular injection, subjects began following a standardized diet consisting of 36 kcal/kg body weight per day (16.4 kcals/lb) and 1.2 grams protein per kilogram body weight per day (0.55 grams/lb). To put these values in perspective, a 176-pound male would have to ingest 2880 kcals/day and 96 grams of protein/day. To make sure subjects didn't change their dietary habits during the study, they were asked to complete 3-day food records and 24-hr food recalls every four weeks.


Activity Control

Here's the only part of the study that surprised me, at least initially � subjects were asked NOT to perform any type of strength training or endurance exercise during the entire study. This was done to avoid the potentially confounding influence that intense physical activity might have on the dependent variables. The more I thought about it, teasing out the effects that exercise might have on responses to Testosterone would have required an additional five groups (of men that did strength train). And as anyone who's done a research study will tell you, getting a sample size of 61 men is hard enough, but 120 men for a 20-week study? Yet another clear example of how time and monetary constraints influence research design.


Outcome (dependent) Variables

To underscore the comprehensive nature of this study, take a look at this list of outcome variables:

� Fat-free mass (via underwater weighing and DEXA)

� Fat mass (via underwater weighing and DEXA)

� Thigh muscle volume (via MRI)

� Quadriceps muscle volume (via MRI)

� Total body water (via deuterium dilution)

� Leg press strength (via 1-rep max)

� Sexual function and desire (via daily logs)

� Spatial cognition (via checkerboard test)

� Mood (via Hamilton depression and Young manic scales)

� Blood counts and clinical chemistries (too many analytes to list)

� Prostate specific antigen (PSA)

� Total cholesterol and various subfractions

� Total and free Tstosterone

� Luteinizing hormone (LH)

� Sex hormone binding globulin (SHBH)

� Insulin-like growth factor 1 (IGF-1)


Statistical Gymnastics (oops, I mean analyses)

This is where some very good studies sometimes go sour� incorrect analyses of the data (can anyone say repeated T-tests and type-II error?). Luckily, these researchers did their homework and used ANOVA to compare the changes from baseline among the five groups. They even examined all variables for their distribution characteristics and log-transformed those variables that didn't meet the assumptions of a normal distribution prior to analysis.


Results

Okay, here's what you've been waiting for. Let's start with hormone changes. Remember, weekly shots of GnRH assured that each subject's endogenous Testosterone production was at a minimum. Not surprisingly, 25 and 50 mg of Testosterone per week didn't "replace" what the GnRH had shut down. 125 mg/week seemed to keep total and free Testosterone at an even keel, while 300 mg and 600 mg/week doses led to roughly a doubling and quadrupling of Testosterone levels. LH was suppressed at all doses while SHBG increased only with the highest two doses.

Relative to changes in body composition, the lowest two doses of Testosterone led to a significant increase in fat mass (eeew!) while the middle dose (125 mg) once again led to no change. Fat-free mass (aka lean body mass) increased by 5.3 kg (11.7 lb) in the 300 mg group and 8.5 kg (18.7 lb) in the 600 mg group. The ratio of total body water to fat-free mass didn't change in any of the groups, indicating that the increases in fat-free mass were not a result of water retention.

On to muscle size and performance. Following suit, the lowest two doses had basically no effect on thigh or quadriceps muscle volume, leg press strength, or leg power. The 300 mg and 600 mg doses however led to significant increases in all of these parameters. Rather than confuse you with comma spices and annoyingly long sentences, here's what the data look like in table form (note: the % increases represent the change from baseline to week 20).


Dose
Thigh muscle volume
Quad muscle volume
Leg strength
Leg power

300 mg
+9.9%
+8.7%
+16.4%
+16.5%

600 mg
+15.7%
+14.4%
+17.7%
+22.6%


Sexual function, visual-spatial cognition, mood and PSA levels didn't change in any of the groups. None of the blood chemistry or organ toxicity values (e.g., creatinine, bilirubin, ALT, AST, etc.) were altered, with the exception of dose-dependent decreases in HDL-C that ranged from 10-20% (5-8 mg/dL), and a 9.9% increase in hemoglobin in the 600 mg group (the absolute value of 155.7 g/L was still within normal clinical limits, though).


Conclusions

Back in 1985, a researcher named GB Forbes speculated that there was a linear relationship between Tstosterone dose and lean mass accretion. For years, athletes and scientists have nonetheless disagreed about the effect of anabolic steroids on strength, muscle mass, and health status. The data from this thorough study support Forbes' assertion: weekly injections of Testosterone enanthate result in dose-dependent increases in muscle mass, muscle size, strength, and power. The downside is that HDL-C tends to take a nasty dip and at higher doses hemoglobin levels rise a smidgeon.

On a final note, the researchers were quick to point out that there were considerable differences in the response to Testosterone administration within each group. Why? The most likely explanation is that Testosterone might differentially affect some (or all) of the many factors that are thought to control muscle growth, including: nutritional status, physical activity level, glucocorticoid, thyroid, and growth hormone levels, polymorphisms of the androgen receptor, myostatin levels, etc.

So even though this research was super thorough, it, like most studies, left scientists with more questions than answers.

As I read over this study for the tenth time, one thing is for sure: the athletes were right. Testosterone does increase strength, power, and muscle size without negatively affecting the kidneys, liver or, prostate � you just have to take enough of it (i.e., at least 300 mg/week). Now that Testosterone has been shown to improve muscle mass in the elderly, in normal men, and in those with wasting disorders, I wonder how long it will take for its rogue social status to disappear? Judging how the media handled the recent "anabolic steroids in baseball" scandal, we may still be a few decades away...


Tim Ziegenfuss, Ph.D., CSCS is the Chief Scientific Officer for an industry-leading, pharmaceutically-licensed nutritional supplement company. Tim is also an Adjunct Professor of Nutrition at Kent State University and has monthly columns in Physical Magazine and Muscular Development. Previously, "Dr. Z" spent five years as a college professor, teaching (Anatomy/Physiology, Sports Nutrition, Exercise Physiology) and researching sports supplements (creatine, protein, pyruvate, androstenedione, androstenediol, ma huang, ribose). You can contact Tim with questions about training, nutrition, or supplement use at: [email protected]


Reference

Bhasin, S et al. (2001). Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab 2811172-E1181.

 

[exnihilo]

The original journal article has been cited in this thread a few times already CED

 

[CEDeoudes59]

oh ...