Morning testosterone spike....

hhajdo, here is the final updated and revised version after all this:


By Fonz




The Dball Main cycle ramp-off explained in detail: Article
Please try to keep this flame free. I have taken great pains to explain my(and others) reasoning in a clear and concise fashion.


The Dball Main cycle ramp-off explained in detail: Article

The original Study:

Acta Endocrinol (Copenh) 1976 Dec;83(4):856-64 Related Articles, Links


Effect of an anabolic steroid (metandienon) on plasma LH-FSH, and testosterone and on the response to intravenous administration of LRH.

Holma P, Adlercreutz H.

Plasma levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as well as the response of LH and FSH to the intravenous administration of 100 mug of luteinizing hormone releasing hormone (LRH) were measured in 16 well-trained athletes (mean age 30 years) before and after 2 months of daily oral intake of 15 mg of metandienon, and anabolic steroid (Anabolin, 17 alpha-methyl-17beta-hydroxy-1,4-androstadien-3-one, Medica, Finland). All athletes continued to train regularly, just as they had done for several years. During administration of metandienon the mean plasma testosterone level fell 69%, from 29.4 +/- 11.6 nmol/1 to 9.1 +/- 7.5 nmol/1. The mean plasma levels of LH and FSH also fell significantly (P less than 0.001 and P less than 0.01, respectively), both about 50%. Because LH and FSH levels were low after administration of the steroid the maximum stimulation values after LRH administration were also lower than pre-treatment values although the mean increments did not differ significantly before and after administration of the anabolic steroid. However, after treatment, the FSH response curve had a biphasic pattern in most subjects, with peaks at 10 to 20 and 50 to 60 min after the iv injection of LRH. Administration of LRH after the treatment period had no effect on FSH secretion in two subjects and no effect on LH secretion in one. Our results show that administration of an anabolic steroid causes a pronounced lowering of plasma levels of testosterone, LH and FSH but causes no gross alteration in the response of LH secretion to stimulation by LRH. The reason for the biphasic response pattern of FSH to LRH administration in most subjects is not known.

------------------------------------------------------------------------------------


Ok, I'm making this flame-free so that no flame fests occurr and people get the right information, not all jumbled. It has actually been improved upon somewhat with the advent of some newer compounds and with the help of AF Vets.

This a more streamlined version, that should work for almost everybody.(Even those who almost always crash):

First, it was decided that the last 4 weeks, of the 8 week ramp-off should be 5mg instead of 10mg, as your HPTA should be recovered by some degree by that time.


The 10mg time/correlation:

Now, for 10mg.

10mg ------- 5mg --------- 2.5mg --------1.25mg ---------0.625mg

Half-lives = 3.4 * 4 = 13.6hrs(to 1mg)

13.6/16.0 = 85% or 0.85(As compared to 15mg)

Test decrease + LH Decrease

Normal(15mg) = 69% 50%
10mg = 58.7% 42.5%

Thats w/o arimidex

W/ arimidex(Increases Test by an average of 58% in controlled trails, and reduces estrogen by about 90%):

10mg becomes: 58.7*(1-0.58)= 24.65% Test decrease
LH is reduction is reduced from 50% to 42.5%

(These numbers do not include the addition of Clomid and Human Chorionic Gonadotropin (HCG) )

This is 5mg time/concentration correlation:


5mg ------- 2.5mg --------1.25mg ------ 0.625mg

Half-lives = 2.4 * 4 = 9.6hrs(to 1mg)

(Compared to 10mg)

9.6/13.6 = 70.59% or 0.7059

Test decrease + LH Decrease

Normal(15mg) = 69% 50%
10mg = 58.7%(-10.3%) 42.5%(-7.5%)
5mg = 41.43%(-27.57%) 30%(-12.5%)

Thats w/o arimidex

W/ arimidex:

5mg becomes: 41.43*(1-0.58)= 17.4% Test decrease
And LH, decreases to only a 30% decrease

(These numbers do not include the addition of Clomid or Human Chorionic Gonadotropin (HCG) )

Finalizing(W/arimidex included):


Testosterone decrease + LH Decrease

15mg == 69% 50%(Study)

10mg == 24.65% 42.5%(This for you weeks 1-4)

5mg == 17.4% 30%(This for you weeks 5-8)

(These numbers are in comparison to the 15mg dosage and do not include the addition of Clomid or Human Chorionic Gonadotropin (HCG) or other compounds which both stimulate LH, FSH and endo test)

End(Finalized Ramp-off):

(6-8 weeks) before end of Main cycle: Start 25mg Proviron

End Main Cycle.

AM Dball off-ramp: 8 weeks

#1.Start ramp-off at 10mg Dball in the AM upon
waking up.(Weeks 1-4) and 5mgs(Weeks 5-8)
#2 Make damn sure you take the 10mg dball(Weeks 1-4) at the
same damn time every day. As soon as you wake up. This
wake up time (if 8 or 9 or 10 AM) must be used for the rest of
the ramp-off(8 weeks)(Circadian Rhythm is VERY important to
the success of the ramp-off) Same with the 5mg dose(Weeks
5-8).
#3 Proviron at 25mgs/day(LH booster)(Weeks 1-8)
#4 Arimidex at 1mg ED or more.(2mg is as high as I would go).
(Also on weeks 1-8)
#5 Human Chorionic Gonadotropin (HCG) at 5000IU’s 2X/week on Weeks 5,6,7,8
(Endo Test Booster)
#6 Clomid at 300mgs Day 1, and then 100mgs/day from then on
until the end of the bridge(LH and FSH Booster)

Weeks 1-4: Are designed to reduce androgen levels(10mg Dball here) and stimulate the HPTA to start its own endo test production, and increase FSH, and LH levels.

10mg == 24.65% 42.5%(This for you weeks 1-4)

Your HPTA will be pretty much zero at the beginning off the ramp-off, and a combination of compounds that only decrease normal test levels by 24.65% and substances that increase LH and FSH and stimulate endo test(Clomid and Proviron) will let your HPTA recover by some margin.

Weeks 5-8: Are designed to reduce androgen levels even further(Only 5mg dball here), due to the fact that they are not needed because your HPTA has partially recovered in Weeks 1-4.

5mg == 17.4% 30%(This for you weeks 5-8)

With the reduction of androgens from 10mg to 5mg, you have changed the Test decrease to only 17.4% and let LH reduction only be 30%. Again, you will be on Clomid and Proviron, and these two will help you boost LH levels and increase test levels further. But now comes the interesting part. The introduction of Human Chorionic Gonadotropin (HCG). Human Chorionic Gonadotropin (HCG) is probably the best booster of endo test at your disposal for short periods of time, via the stimulation of the Leydig Cells in the testes. Human Chorionic Gonadotropin (HCG) at the specified dosage will boost endo test levels back to the normal pre-main cycle range.
(Remember that 5mg dball only causes a 17.4% decrease in Test).
Human Chorionic Gonadotropin (HCG) should help nullify that.

And after those 8 weeks of the ramp-off, you come off.
Both Test and LH levels should be within the normal range, and you will not crash or suffer muscle loss like pretty much all post-cycle recovery methods.

Special thanks goes to the guys who helped me put all this into
a clear and concise article. You know who you are.

NEW:

As an addition: Androgel might be of definate use in Weeks 5-8 as it roughly doubles Test levels, w/o any decrease in LH. Which will further boost ending ramp-off test levels. If you have the time, this preparation shows great promise for further enhancing the ramp-off.

References:

(Thanks to Mr. Nobody and got Wood)

1. Swerdloff, RS, and Wang, C., et al., Long-term pharmacokinetics of transdermal testosterone gel in hypogonadal men., J Clin Endocrinol Metab. 2000 Dec;85(12):4500-10.

The intend of agel in the recovery program is for libido purposes, and may delay overall recovery a bit. However, its not just about fast recovery but achieving homeostasis in a managable manner, without slipping into depression and muscle loss while you wait for endo test to come back. The same goes for morning dbol.
As everyone knows already, only time will recover you completely.

from Gotwood:

testo gel lowered LH but not too much

Got Wood? note : these men ranged from 22-65. Testo enanthate (inj) lowered LH too much - to subnormal values. Testo gel lowered LH to normal, but not beyond to a subnormal range. This is evidence that the testo gel may not lower the LH too much, thereby inhibiting recovery. however again these are hypogonadal men.
============================
J Clin Endocrinol Metab 1999 Oct;84(10):3469-78

Pharmacokinetics, efficacy, and safety of a permeation-enhanced testosterone transdermal system in comparison with bi-weekly injections of testosterone enanthate for the treatment of hypogonadal men.

Dobs AS, Meikle AW, Arver S, Sanders SW, Caramelli KE, Mazer NA.

Johns Hopkins Medical Center, Baltimore, Maryland 21287, USA. adobs@jhu.edu

The pharmacokinetics, efficacy, and safety of the Androderm testosterone (T) transdermal system (TTD) and intramuscular T enanthate injections (i.m.) for the treatment of male hypogonadism were compared in a 24-week multicenter, randomized, parallel-group study. Sixty-six adult hypogonadal men (22-65 years of age) were withdrawn from prior i.m. treatment for 4-6 weeks and then randomly assigned to treatment with TTD (two 2.5-mg systems applied nightly) or i.m. (200 mg injected every 2 weeks); there were 33 patients per group. Twenty-six patients in the TTD group and 32 in the i.m. group completed the study. TTD treatment produced circadian variations in the levels of total T, bioavailable T, dihydrotestosterone, and estradiol within the normal physiological ranges. i.m. treatment produced supraphysiological levels of T, bioavailable T, and estradiol (but not dihydrotestosterone) for several days after each injection. Mean morning sex hormone levels were within the normal range in greater proportions of TTD patients (range, 77-100%) than i.m. patients (range, 19-84%). Both treatments normalized LH levels in approximately 50% of patients with primary hypogonadism; however, LH levels were suppressed to the subnormal range in 31% of i.m. patients vs. 0% of TTD patients. Both treatments maintained sexual function (assessed by questionnaire and Rigiscan) and mood (Beck Depression Inventory) at the prior treatment levels. Prostate-specific antigen levels, prostate volumes, and lipid and serum chemistry parameters were comparable in both treatment groups. Transient skin irritation from the patches was reported by 60% of the TTD patients, but caused only three patients (9%) to discontinue treatment. i.m. treatment produced local reactions in 33% of patients and was associated with significantly more abnormal hematocrit elevations (43.8% of patients) compared with TTD treatment (15.4% of patients). Gynecomastia resolved more frequently during TTD treatment (4 of 10 patients) than with i.m. treatment (1 of 9 patients). Although both treatments seem to be efficacious for replacing T in hypogonadal men, the more physiological sex hormone levels and profiles associated with TTD may offer possible advantages over i.m. in minimizing excessive stimulation of erythropoiesis, preventing/ameliorating gynecomastia, and not over-suppressing gonadotropins.

Hope some of you guys like it. If you guys want to try it be my guest. If you disagree w/ the article then simply don't try it. Pretty simple really.

Fonz
 
Billy...they finally answered your 3 questions:

1) The amount of e2 from a low dose such as 10mg Dbol
2) The amount present in ~20hrs
3) The amount of e2 necessary to cause SIGNIFICANT supression

--------------------------------------------------------------------------------
Originally posted by Juice Authority
There is now the evidence to support his claim along with numbers of people who have actually done it. Many people are still waiting for the answer to these three questions that disprove this theory:

1) The amount of e2 from a low dose such as 10mg Dbol
--------------------------------------------------------------------------------



Well had said so, if you want to talk shop I'm here for you.

Compared to other steroids we can safely deduce that dbol is 60-70% estrogen mediated. The amount of estrogen isn't that much, the type of estrogen is. 17-alpha-methyl estradiol has been identified as one of the most potent forms of estrogen known today.


quote:
--------------------------------------------------------------------------------
2) The amount present in ~20hrs
--------------------------------------------------------------------------------



This was actually proven at the thread at gearedup's board, when we demonstrated that this estrogen has a half-life of 2 days.


quote:
--------------------------------------------------------------------------------
3) The amount of e2 necessary to cause SIGNIFICANT supression
--------------------------------------------------------------------------------



Well if 2.5 mg of Anavar can be supressive, as a fairly weak androgen, then a potent estrogen at a similar dose given to a person with already supressed levels is surely not going to be conducive of the fastest recovery. And with that I rest my case.


__________________
Good things come to those who weight.

H.H. HAS RETURNED. We don't die, we just go to hell to regroup.

Vigor Mortis ! Even in death we remain strong ...

For those who did not know yet, next to Philiep van Nuffel's victory in June's European championships in Napoli, another client of mine, Estelle Moreau took the world championship fitness title in the medium height class in Tenerife last fall.

I am currently incommunicado due to extreme work pressure. My apologies to all those who have tried to contact me in the past 3 weeks.
 
Not really. "Not much" isnt exactly what I was looking for. Number 2 is based on number 1. And an Anavar comparison still with no quantification isnt really either.

Oh well...
 
Juice Authority said:
Billy...they finally answered your 3 questions:

1) The amount of e2 from a low dose such as 10mg Dbol
2) The amount present in ~20hrs
3) The amount of e2 necessary to cause SIGNIFICANT supression



__________________
Good things come to those who weight.

H.H. HAS RETURNED. We don't die, we just go to hell to regroup.

Vigor Mortis ! Even in death we remain strong ...

For those who did not know yet, next to Philiep van Nuffel's victory in June's European championships in Napoli, another client of mine, Estelle Moreau took the world championship fitness title in the medium height class in Tenerife last fall.

I am currently incommunicado due to extreme work pressure. My apologies to all those who have tried to contact me in the past 3 weeks.

J/W...Why do you have Big Cat's signature? LOL
 
Billy_Bathgate said:
hhajdo, here is the final updated and revised version after all this:

Thanks for keeping me updated...

Looks like it's pretty much the same post + androgel part.

"Testo gel lowered LH to normal, but not beyond to a subnormal range. This is evidence that the testo gel may not lower the LH too much, thereby inhibiting recovery."



Actually, that's not the evidence that androgel may not lower the LH too much....

I don't think he read the whole study.

The men whose LH was "normalized" by the androgel treatment were diagnosed with primary (hypergonadotropic) hypogonadism - their LH was slightly above normal range before the study....

It actually dropped from 14.6 ± 12.1 to 5.6 ± 5.1 IU/L...

http://jcem.endojournals.org/cgi/content/full/84/10/3469
 
It would be interesting to see what's the half life of dbol metabolites which are responsible for its anabolic effect.


Farmakol Toksikol 1987 Sep-Oct;50(5):48-51 Related Articles, Links


[Dynamic distribution of methandrostenolone in the body of white rats]

[Article in Russian]

Krylov IuF, Krynetskii EIu, Prokhorov BS, Sapozhnikova GA, Smirnov PA.

Dynamics of distribution of anabolic steroidal hormone methandrostenolone and routes of its elimination from the organism of Wistar rats were studied by using methods of radioisotopes and high-performance liquid chromatography. Methandrostenolone metabolites were shown to be excreted mainly in the urine. Methandrostenolone metabolism is a complicated process in the course of which redistribution of metabolites among various organs occurs. The anabolic effect of methandrostenolone is supposed to be due to the formation of its metabolites
 
So would I, Ive never found a thing about them or anything about specific e2 suppresion numbers either...least not in my school library or medline.
 
Back
Top