08-21-2005, 01:18 PM #1
Rodge...synergystics between GH/l3 IGF-1/AAS
From what I'm collecting, it seems that l3 IGF-1 and AAS is going to give you the most results right away. Considering you're injecting l3 IGF-1 without waiting for the liver to produce natural IGF-1 via 2-3 months of GH therapy.
Why would using HGH, l3 IGF-1 & AAS be more beneficial? Is this because naturally occuring IGF-1 from the liver due to GH thereapy does not suffer receptor downgrade like l3? So you jump start with l3 IGF-1 to get immediate effects for the first 4 weeks then continue with AAS and GH until the 2nd or 3rd month when the liver starts producing higher amounts of IGF-1?
Wouldn't cycling l3 IGF-1 for 4 weeks on with AAS for 12 weeks then IGF-1 PCT be a good idea? The repeat that again 2-3 months later?
Last edited by Seattle Junk; 08-21-2005 at 01:20 PM.
08-21-2005, 06:59 PM #2
08-21-2005, 08:51 PM #3
The people I know that have used those 3 together, are older or have the cash to try it. I have low HGH/IGF-1 levels so I've used that combo, but the only way I'll use HGH again is if I only have to pay a co-pay, I won't buy it again
08-22-2005, 12:27 AM #4
as johnyb said hgh is most usefull in people who are older or got low igf levels.but since lr3 is gonna supress endo gh production and hgh has got other benefits then the conversion of igf-1,it makes sence to shoot a replacement dose with it.don't get me wrong igf cycled for 4 weeks on with the same time off gives some nice results and the igf is what gives you most results.i like to see the hgh with more like we add the t3 with a gh cycle,as an replacement dose.aas is beneficial cause you won't see much from hyperplasia without hypertrophy.
08-22-2005, 01:16 AM #5Originally Posted by JohnnyB
08-22-2005, 01:20 AM #6Originally Posted by rodge nl.
08-22-2005, 03:49 AM #7Associate Member
Originally Posted by Seattle Junk
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08-22-2005, 09:48 AM #8
never heard or read that either.
08-22-2005, 12:33 PM #9Originally Posted by Seattle Junk
08-22-2005, 12:37 PM #10Originally Posted by Seattle Junk
08-22-2005, 01:36 PM #11Originally Posted by JohnnyB
08-23-2005, 03:40 AM #12supersteve GuestOriginally Posted by JohnnyB
Actually, there has been a very recent study done in humans (albeit older) which suggests this to be the case.
Testosterone blunts feedback inhibition of growth hormone secretion by experimentally elevated insulin -like growth factor-I concentrations.
Veldhuis JD, Anderson SM, Iranmanesh A, Bowers CY.
Endocrine Research Unit, Mayo School of Graduate Medical Education, General Clinical Research Center, 200 First Street Southwest, Mayo Clinic, Rochester, Minnesota 55905, USA. firstname.lastname@example.org
The present study tests the hypothesis that a high dose of testosterone (Te) drives GH and IGF-I production, in part, by blunting autonegative feedback by the end-product peptide. To this end, we infused saline or recombinant human IGF-I (10 microg/kg.h iv for 6 h) in seven healthy men ages 51-72 yr after administration of placebo (Pl) and Te in randomized order. GH release was quantitated fasting before and after injection of GHRH (1 microg/kg). Statistical analyses disclosed that Te vs. Pl: 1) increased the mean concentration of GH from 0.15 +/- 0.045 to 0.48 +/- 0.11 microg/liter (P = 0.007) and IGF-I from 108 +/- 5.0 to 124 +/- 4.1 (P = 0.047) without altering GHRH-induced GH release; 2) elevated the GH nadir from 0.13 +/- 0.03 to 0.23 +/- 0.06 microg/liter (P < 0.05) in the control session and from 0.06 +/- 0.02 to 0.14 +/- 0.04 microg/liter (P = 0.038) during IGF-I infusion; 3) augmented GHRH-stimulated GH release from 3.0 +/- 0.56 (Pl) to 3.7 +/- 0.52 microg/liter (Te) (P < 0.05) during IGF-I infusion; and 4) did not influence estimated IGF-I kinetics. In summary, supplementation of a high dose of Te in middle-aged and older men attenuates IGF-I feedback-dependent inhibition of nadir and peak GH secretion. Both effects of Te differ from those reported recently for estradiol in postmenopausal women. Accordingly, we postulate that Te and estrogen modulate IGF-I negative feedback differentially.
08-25-2005, 03:21 AM #13Associate Member
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That does say it blocks the negative feedback, but it's not clear that it was the testosterone itself or it could've been the aromitization of testosterone to estrogen. I think aromitization has a role to play here...
Check this study steve:
Estrogen and testosterone, but not a nonaromatizable androgen, direct network integration of the hypothalamo-somatotrope (growth hormone )-insulin -like growth factor I axis in the human: evidence from pubertal pathophysiology and sex-steroid hormone replacement.
Veldhuis JD, Metzger DL, Martha PM Jr, Mauras N, Kerrigan JR, Keenan B, Rogol AD, Pincus SM.
Division of Endocrinology, National Science Foundation Center for Biological Timing, University of Virginia Health Sciences Center, Charlottesville 22908, USA. JDV@Virginia.Edu
Activation of the gonadotropic and somatotropic axes in puberty is marked by striking amplification of pulsatile neurohormone secretion. In addition, each axis, as a whole, constitutes a regulated network whose feedback relationships are likely to manifest important changes at the time of puberty. Here, we use the regularity statistic, approximate entropy (ApEn), to assess feedback activity within the somatotropic (hypothalamo-pituitary/GH-insulin-like growth factor I) axis indirectly. To this end, we studied pubertal boys and prepubertal girls or boys with sex-steroid hormone deficiency treated short-term with estrogen, testosterone, or a nonaromatizable androgen in a total of 3 paradigms. First, our cross-sectional analysis of 53 boys at various stages of puberty or young adulthood revealed that mean ApEn, taken as a measure of feedback complexity, of 24-h serum GH concentration profiles is maximal in pre- and mid-late puberty, followed by a significant decline in postpubertal adolescence and young adulthood (P = 0.0008 by ANOVA). This indicates that marked disorderliness of the GH release process occurs in mid-late puberty at or near the time of peak growth velocity, with a return to maximal orderliness thereafter at reproductive maturity. Second, oral administration of ethinyl estradiol for 5 weeks to 7 prepubertal girls with Turner's syndrome also augmented ApEn significantly (P = 0.018), thus showing that estrogen per se can induce greater irregularity of GH secretion. Third, in 5 boys with constitutionally delayed puberty, im testosterone administration also significantly increased ApEn of 24-h GH time series (P = 0.0045). In counterpoint, 5 alpha-dihydrotestosterone, a nonaromatizable androgen, failed to produce a significant ApEn increase (P > 0.43). We conclude from these three distinct experimental contexts that aromatization of testosterone to estrogen in boys, or estrogen itself in girls, is likely the proximate sex-steroid stimulus amplifying secretory activity of the GH axis in puberty. In addition, based on inferences derived from mathematical models that mechanistically link increased disorderliness (higher ApEn) to network changes, we suggest that sex-steroid hormones in normal puberty modulate feedback within, and hence network function of, the hypothalamo-pituitary/GH-insulin-like growth factor I axis.
So, does that mean no aromotose inhibitors while on cycle? Maybe...
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