Question on the "NEW" Hypertrophics

jminis

jminis

Well-known member
Since these new products (HH by AX and Jungle Warefare by ALRI) are supposed to increase free testosterone would these products be good to use while "on". Would this enable you to run lower dosages but still having the same amount of free test?
 
Personally I think that sounds too good to be true. Sorry I don't have anything scientific to back up my opinion with.
 
Think of it this way: just because you're shut down, do you really think the test that's already in your bloodstream just disappears? ;)
 
Then I'm gonna say using ActivaTe or anything to free bound test will indeed work.. This is why many like to use Proviron with test.. ;)
 
I would think that SHBG would bind test, regardless of whether it is exo or endo, so Activate "on" sounds logical.
 
Don't forget the possibility that these new "Hypertrophics-JW" could possibly act as a androgen agonist. Roughly meaning that your T is increased, your SHBG is decreased keeping the T levels constant, all while your AR's are hungry for something to bind to.

Sounds very interesting.
 
From what I know, SHBG definitaly binds Test on cycle as much as it does off cycle. It would be a great log if someone could get bloodwork on TestE and something that binds SHBG (like activate). :stick: :stick:
 
I don't have any blood work, but I have been taking 17-hd + methyl dien @16mg(ed)+ cissus/nettles combo for the last two weeks. I feel great and look ripped. Size is the same, I just started strength training after a longer than usual lay off. I am also using Melting point +green tea. This has a very promising start to a great cycle. I will be dropping the 17-HD for 1,4 adiol and drop the MDien for Meo-TRN. I will continue to use the nettles/Cissus combo + betositosterol through out this trip. So far, I would agree that the SHBG modifiers are a good addition to any cycle.
 
bigpetefox said:
Then I'm gonna say using ActivaTe or anything to free bound test will indeed work.. This is why many like to use Proviron with test.. ;)
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Piss poor idea to use proviron on-cycle. While it has a higher affinity towards SHBG the same holds true of the AR. Therefore while it competetively binds to SHBG it will do so to the AR as well. So you get a poor anabolic preferentially binding to the AR thus diminishing the effects of the stronger anabolic.
 
doggzj said:
From what I know, SHBG definitaly binds Test on cycle as much as it does off cycle. It would be a great log if someone could get bloodwork on TestE and something that binds SHBG (like activate). :stick: :stick:
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The affinity is the same but I'm not so sure the rate is as SHBG production is decreased with exogenous androgen usage. Therefore it is my belief that it might be wasteful to use a product that binds to or interrupts SHBG in some manner.

J Clin Endocrinol Metab. 1996 Mar;81(3):896-901. Related Articles, Links


Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. II. Pharmacokinetics and pharmacodynamics of once weekly administration of testosterone enanthate.

Anderson RA, Wu FC.

Medical Research Council Reproductive Biology Unit, Edinburgh, Scotland.

Hormonal suppression of spermatogenesis is currently being investigated as a method of reversible male contraception. However, administration of exogenous testosterone (T) induces azoospermia in only 40-70% of Caucasian men, whereas the remainder suppresses to severe oligozoospermia (< 5 x 10(5)/mL). The reason(s) for the heterogeneity in the spermatogenic response is not clear. We have prospectively investigated the possibilities that higher plasma concentrations of T and/or differences in the extent and rate of gonadotropin suppression could maintain a low level of spermatogenesis in subjects taking part in a clinical efficacy trial of hormonal male contraception. Thirty-three healthy adult men, aged 21-41 yr, were given 200 mg T enanthate (TE), im, weekly for up to 18 months. Azoospermia was achieved in 18 men (55%) after 20 weeks of treatment, at which time the remaining 15 (45%) stabilized at a mean sperm density of 2.0 +/- 0.8 (+/- SD) x 10(6)/mL. These 15 subjects remained oligozoospermic for the rest of the efficacy study. To compare the pharmacokinetics and pharmacodynamics of TE between the azoospermic and oligozoospermic responders, plasma samples were obtained immediately before and 1, 2, 4, and 7 days after the 1st and 16th TE injections. Further samples were taken after 2, 4, 8, and 12 weeks of treatment. Plasma concentrations of total, free, and non-sex hormone-binding globulin (non-SHBG)-bound T, estradiol, LH, and FSH were measured. Compared to baseline, preinjection levels of total T increased 2.5-fold, reaching a steady state around 12 weeks of treatment. Peak concentrations of total T increased by 5-fold, but free and non-SHBG-bound T levels were increased by 10-fold after 16 weeks. The plasma levels of estradiol showed similar changes as T. However, neither T (bound or free) nor estradiol was significantly different between azoospermic and oligozoospermic responders. Plasma SHBG was reduced to a similar degree in both groups of men after 16 weeks of TE treatment. Plasma concentrations of both LH and FSH decreased rapidly after the first TE injection; a significant decline in LH was detectable after 24 h. Mean levels of both gonadotropins decreased to less than 0.5 U/L by the end of 4 weeks and to below the limit of sensitivity of the assays (0.05 IU/L) by 12 weeks. There were no significant differences in plasma concentrations of LH or FSH or in the rates of suppression between azoospermic and oligozoospermic responders. We conclude that the polymorphism of spermatogenic suppression in response to exogenous T is unlikely to be due to differences in the pharmacokinetics or pharmacodynamics of TE or in the sensitivity of the hypothalamo-pituitary-testicular axis to sex steroid inhibition. Measurements of total plasma T considerably underestimate the increase in bioavailable T during the weekly TE regimen.

PMID: 8772547 [PubMed - indexed for MEDLINE]
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Another study where participants 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.

This table shows that those who received higher amounts of TE had a greater reduction in SHBG. Invalid Link Removed
 
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