Manipulating Natural Test Production

[superfrk]

=/
Manipulating Natural Test Production
By Superfrk

One of the biggest problems faced in the use of anabolic and androgenic steroids are the effects it has on our natural production of testosterone. The good news is that there are ways that we can minimize these effects as well as returning natural function of the HTPA as fast as possible.

The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand how natural test production is shut down we need to understand how it is made and how it is regulated. The HTPA first receives signals from the various hormones, it then decides weather or not more sex hormones are needed, if hormone levels are high then it will decides that little or no sex hormones are needed.
The hypothalamus does not actually produce any sex hormones; instead it produces LHRH (luteinizing releasing hormone.) This is sent as a signal to the pituitary gland
The pituitary gland then uses the LHRH to decide how much LH (luteinizing hormone) it needs to make. This is then sent as a message to the testes.
Once the LH gets to the testes it then signals the testicles to produce testosterone.

Now that we know how the HTPA works, lets take a look at how we can manipulate it.
When on a heavy cycle the HTPA will slow or stop production of test. While we cannot stop the hypothalamus and the pituitary gland from shutting down we can manipulate the testes into still producing test. LH is one of the very few hormones in the body that does not have a feed back mechanism. What I mean by this is that as long as LH is present the testes will continue to produce natural test.
Armidex and HCG have been both shown to mimic LH, by using armidex and HCG through out the cycle, (.5 – 1mg of armidex ed and 500 – 700ui of HCG ed) we can maintain or increase natural levels of test, even while on a heavy cycle. This will give us better gains and also help keep the testes from a state of atrophy. This will make it easier to restart the HTPA as well as keeping the girl friend happy.
Jumpstarting the HTPA
Since HCG, does not help restart the HTPA, we will discontinue its use and replace it with clomid. Armidex and clomid work very well together at fastly restoring the HTPA, remember speed is the name of the game, the faster we can restart the HTPA the more gains we will keep. I suggest frontloading the Clomid so that we can peak concentrations as fast as possible. Use 100mg of clomid for the first week with .5 – 1mg of armidex, then drop the dose down to 50mg of clomid for the next 2 weeks, you do not need the armidex for these last 2 weeks because a little bit of estrogen is actually good for proper function of the HTPA.
This is my modern approach to the gains keeper formula; I hope you find it of
Good use in your future endeavors- Superfrk

[Stroyer]

Good post/info super !!

[mballs]

thanks for the info....

hey, do you think tribulus would be helpful in stimulating LH, thus increasing test production while on? or even while coming off? just a thought here.

[sust251]

Excellent post superfrk, you have obviously done your home work I see. A quick question for you. You mention 500-700iu of HCG ed. That dosage for the entire duration of the cycle i.e. 60-90 days? That dosage for that duration seems a little high. At that dosage I’d be growing like a weed without any gear =). The old “bibles” speculated that the prolonged use of HCG could repress the body’s own production of gonadotrophins permanently. Have you found information to dispute this? (=n)

[bigtito]

i think this mechanism or arimidex is misunderstood.

i believe that arimidex increases testosterone production by inhibiting estrogen synthesis, this then allows the GnRh to be secreted and finally Lh then test. Fsh is almost entirely regulated by estrogen



the third article states this more definitively



here is some journal articles:

Aromatization mediates testosterone's short-term feedback restraint of 24-hour endogenously driven and acute exogenous gonadotropin-releasing hormone-stimulated luteinizing hormone and follicle-stimulating hormone secretion in young men.

Schnorr JA, Bray MJ, Veldhuis JD.

Division of Endocrinology, Department of Internal Medicine, General Clinical Research Center, Center for Biomathematical Technology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.

The present clinical study examines the neuroregulatory hypothesis that feedback restraint of LH and FSH secretion by testosterone requires in vivo aromatization. To test this postulate, we prospectively and randomly assigned 47 healthy young men to 1 of 5 parallel short-term (5-day) double-blind interventions with: 1) placebo; 2) high-dose ketoconazole (KTCZ, 400 mg orally 4 times daily) to block both Leydig-cell and adrenal steroidogenesis; 3) KTCZ and transdermal testosterone delivery (7.5 mg daily); 4) KTCZ and transdermal estradiol (0.05 mg daily); or 5) KTCZ, testosterone, and the selective and potent aromatase inhibitor, anastrazole (5 mg orally twice daily). Blood was sampled every 10 min for 27 h on the last day of intervention to quantitate 24-h mean spontaneous and 3-h post-GnRH-stimulated (100 ng/kg iv bolus) LH and FSH release. KTCZ administration lowered the serum total testosterone concentration markedly from (mean +/- SEM) 423 +/- 57 ng/dL (15 +/- 2.0 nmo/L) during placebo ingestion to 58 +/- 8.6 ng/dL (2.0 +/- 0.3 nmol/L) (P < 10(-3)). Transdermal androgen addback along with KTCZ blockade increased testosterone levels to 607 +/- 57 ng/dL (21 +/- 2.0 nmol/L). KTCZ exposure alone drove a 3-fold increase in serum LH concentrations (P < 10(-3)) and a 2.5-fold rise in FSH secretion (P = 0.015), as assessed by high-specificity immunoradiometric assays. Concomitant transdermal testosterone (or estradiol) delivery repressed the elevated secretion of both LH and FSH to mid-normal baseline values. A 3-fold administration of anastrazole, KTCZ, and testosterone completely opposed exogenous testosterone's suppression of 24-h LH and FSH secretion. Anastrazole coadministration likewise abolished testosterone-dependent inhibition of 3-h GnRH-stimulated LH and FSH release. In summary, assuming the specificity of anastrazole's inhibition of aromatase activity, we conclude that circulating testosterone in healthy men curtails endogenously driven as well as exogenous GnRH-stimulated LH and FSH secretion conditional on its in vivo aromatization.

Publication Types:
· Clinical trial
· Randomized controlled trial

PMID: 11397860 [PubMed - indexed for MEDLINE]



Estrogen suppression in males: metabolic effects.

Mauras N, O'Brien KO, Klein KO, Hayes V.

Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. nmauras@nemours.org

We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.

Publication Types:
· Clinical trial

PMID: 10902781 [PubMed - indexed for MEDLINE]


this article really states the point

Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback.

Hayes FJ, Seminara SB, Decruz S, Boepple PA, Crowley WF Jr.

Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA. hayes.frances@mgh.harvard.edu

The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 microg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 +/- 10 to 52 +/-2 pmol/L, P < 0.005) and IHH men (118 +/- 23 to 60 +/- 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 +/- 6% in NL vs. 56 +/- 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 +/- 9 vs. 58 +/- 6% for LH, P = 0.07; and 85 +/- 6 vs. 41 +/- 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 +/- 0.9 to 14.0 +/- 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 +/- 0.7 to 8.4 +/- 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 +/- 2.4 vs. 70 +/- 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH.

Publication Types:
· Clinical trial

[superfrk]

Either way you look at it when armidex is used, FH levels incress, lowering of estrogen does play a role, but in the end you still have what I stated and that is if you use armidex and hcg together you produce more natural test, methods and substances used in these studies all differ so of coarse different theorys will be made but, when all is said a done the results are the same-Superfrk

[bigtito]

lets not contribute to disinformation.

the regulation of testosterone production is bi-nomial

there are two regulatory factors..

estrogen and testosterone..

estrogen is actually more suppressive to the HPTA than testosterone.

Arimidex stops conversion to E thus enabling the HPTA to remain uninhibited however the regulation does kick in at a higher level due to the amount of T present.

Arimidex does not mimic LH.

interestingly enough some aromitization is desired!!! why?

becuase IGF-1 is dramitically more active when combined with E..

so 100% aromatization blockade may not be what we want. we just want estrogenic symptoms blocked and not all estrogen

also estrogen is a powerful modulator of the immune system

[superfrk]

At the doses I sugest you will not block all estrogen, I did not say the HTPA will not shut down parts of it will, My article is talking about bypassing it and consentrates on keeping the testes working, As long as the testes are not shut down, you have the potintal to produce natural test, hcg and armidex will produce natural test, That article is talking about the piuitary gland which will shut down, I agree with that, But the testes will produce test as long as LH, is present period. here is some more research on armidex for ya to look over:


Study Shows That Arimidex Boosts Testosterone

Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V nmauras@nemours.org.

We have shown that testosterone (T) deficiency per se is associated with
marked catabolic effects on protein, calcium metabolism, and body
composition in men independent of changes in GH or insulin-like growth
factor I production. It is not clear,,however, whether estrogens have a
major role in whole body anabolism in males. We investigated the metabolic
effects of selective estrogen suppression in the male using a potent
aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of
12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at
baseline and after 10 days of oral Arimidex given as two different doses
(either 0.5 or 1 mg) in random order with a 14-day washout in between. A
sensitive estradiol (E2) assay showed an approximately 50% decrease in E2
concentrations with either of the two doses; hence, a 1-mg dose was selected
for other studies. Subsequently, eight males (aged 15-22 yr; four adults and
four late pubertal) had isotopic infusions of [(13)C]leucine and
(42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry,
isokinetic dynamometry, and growth factors measurements performed
before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T
withdrawal, there were no significant changes in body composition (body mass
index, fat mass, and fat-free mass) after estrogen suppression or in rates
of protein synthesis or degradation; carbohydrate, lipid, or protein
oxidation; muscle strength; calcium kinetics; or bone growth factors
concentrations. However, E2 concentrations decreased 48% (P = 0.006), with
no significant change in mean and peak GH concentrations, but with an 18%
decrease in plasma insulin-like growth factor I concentrations. There was a
58% increase in serum Testosterone (P = 0.0001), sex hormone-binding globulin did not
change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum
bone markers, osteocalcin and bone alkaline phosphatase concentrations, and
rates of bone calcium deposition and resorption did not change. In
conclusion, these data suggest that in the male 1) estrogens do not
contribute significantly to the changes in body composition and protein
synthesis observed with changing androgen levels; 2) estrogen is a main
regulator of the gonadal-pituitary feedback for the gonadotropin axis; and
3) this level of aromatase inhibition does not negatively impact either
kinetically measured rates of bone calcium turnover or indirect markers of
bone calcium turnover, at least in the short term. Further studies will
provide valuable information on whether timed aromatase inhibition can be
useful in increasing the height potential of pubertal boys with profound
growth retardation without the confounding negative effects of gonadal
androgen suppression.

[Rock_Man]

This is a very informative thread. It is good to see an intellectual approach at disputes amungst each other and not have it get out of hand and into a flaming thrashing match!

I do have do say that I tend to agree with superfrk. With that being said, I read somewhere that taking armidex and hcg may hinder gains slightly, but with your info provided, I don't see why that would be now.

All in all. Great info in this thread....

Bump!

[mulestick]

"pubertal boys"..fancy...you college boys sho is smart writin dem dissirtations an all. now,in 100 words or less, do you know how to keep balls big and titties little???

[sperminater]

i read that arimedex reduce's igf-1, 18%. this is why peaple make less gain's with arimedex. maybe femara is different. it doe's not reduce igf-1.
i read that hcg increase's estrogen as well as testosterone.
i read that hcg merely delay's the inevetable.