11-Sterone verses Suppress-C
- 08-14-2011, 05:24 PM
- 08-14-2011, 05:35 PM
I just started Supress-C... cant give any feedback yetBy believing passionately in something that still does not exist, we create it. The nonexistent is whatever we have not sufficiently desired.
08-14-2011, 07:12 PM
Well as far as cost/gains is concerned i would say Suppress C since its a bit cheaper to run than 11oxo>>>especially be on clearnce here at Nutraplanet
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08-14-2011, 09:12 PM
08-14-2011, 11:30 PM
i know 11-sterone is hormonal, i think supress c isn't hormonal.
how different is supress c than 7-spray?
08-15-2011, 12:44 AM
08-15-2011, 12:47 AM
08-15-2011, 05:33 PM
08-15-2011, 05:35 PM
08-16-2011, 01:56 AM
08-16-2011, 01:59 PM
08-16-2011, 08:45 PM
08-16-2011, 09:16 PM
10-08-2011, 01:35 PM
10-08-2011, 01:43 PM
I ran it at 450 and honestly it was ok but next time I will run it at 900
Log of EPIC by FRL - http://anabolicminds.com/forum/supplement-reviews-logs/202576-should-epic-frl.html
10-16-2011, 08:39 AM
11-sterone is awesome .. As for your question .. Are you looking for a bridge or just a cycle ?
S.n.S team member
10-16-2011, 09:11 AM
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10-16-2011, 03:07 PM
By adding suppress-c to most of these designers you can get both anabolism and anti-catabolism simultaneously. This cortisol rebound crap that people like to think happens is moot. maybe it happens on something that directly inhibits cortisol biosynthesis or strongly inhibits 11b-hsd1, but not after a typical anabolic steroid cycle.
10-17-2011, 04:43 PM
an increase in androgens will lead to an increase in cortisol as the body is attempting to balance itself out.
another one of the reasons i say to start cortisol control when pct starts.
10-17-2011, 08:25 PM
The effects on plasma proteins of the anabolic steroids oxymetholone, methandrostenolone, stanozolol, fluoxymesterone, oxandrolone, norethandrolone, ethylestrenol, nandrolone phenpropionate and methandriol dipropionate, as well as 17α-methyltestosterone, given orally and sublingually, testosterone propionate sublingual and parenteral aqueous testosterone, were studied on both volunteers and patients. The responses of thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), cortisol-binding globulin (CBG), serum cortisol and nonprotein-bound cortisol (NPC) were studied. The 17α-alkylated anabolic steroids induced marked changes, with significant elevations of TBPA and depression of TBG; CBG was significantly increased by oxymetholone and methandrostenolone. Both the latter steroids have conjugated and unsaturated resonating systems in ring A. On the other hand, the non-17α-alkylated androgens did not produce these changes. The C-3 ketone group, absent from ethylestrenol, seemed also to be important for effects upon these plasma protein concentrations. These effects on plasma proteins are dose related and different from the ones obtained with estrogens or during an acute phase reaction. Only methandrostenolone produced a significant increment in cortisol, and none of the anabolic steroids significantly changed NPC. A negative correlation (r= −0.78; p<0.01) was found between the ability to produce nitrogen retention in man and the degree of depression of TBG serum levels, for different anabolic steroids. It is concluded that in general a 17α-alkyl group, and to a lesser degree a C-3 ketone group, are necessary for those changes in plasma proteins. Additional unsaturation in ring A (other than the α, β unsaturation) may result in changes in CBG and is consistent with the effect of estrogen on this protein.
Endocrine effects of self-administration of high doses of anabolic steroids and testosterone were investigated in five power athletes during 26 wk of training, and for the following 12-16 wk after drug withdrawal. After 26 wk of anabolic steroid and testosterone administration, serum testosterone concentrations had increased 2.3-fold. This was associated with increased concentrations of serum estradiol, which rose 7-fold to values (0.48 nmol[middle dot] l-1) typical for females. There was a major decrease in serum FSH and LH concentrations, but they returned to control levels following drug withdrawal. However, serum testosterone concentrations stayed at low levels (9 nmol[middle dot] l-1) during this follow-up period, indicating long-lasting impairment of testicular endocrine function. Serum ACTH concentrations were also decreased during steroid administration, possibly due to a corticoid-like effect of some of the anabolic steroids taken in high doses. However, no changes were seen in serum cortisol. The only consistent change in the control group was an increase in serum LH concentrations during the most intensive training, suggesting that a decreasing tendency of serum testosterone was compensated for by augmented LH secretion.
As you can see^^, it seems like if there is a uniform anti-glucocorticoid action of anabolic steroids, it is certainly not an obvious one because cortisol concentrations remain steady throughout administration according to this data, which makes me think rebound or elevations after disontinuation are not a likelihood on many of them.
Of course there could be anti-G action at the receptor level, as has been observed in oxandrolone(http://www.ncbi.nlm.nih.gov/pubmed/15219414), but not all anabolic steroids possess this unique action.
10-19-2011, 03:39 PM
10-30-2011, 10:35 PM
10-30-2011, 10:39 PM
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