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Anabolic Steroids

Perrin Aybara's Journey to an Elite Powerlifting Total

Perrin Aybara said:
Eman, the voice of reason, lol. I started having some trouble breathing today, but i assume it's e2 related or blood pressure from e2. I agree with you though, just gonna have to go over my inventory and see if it's feasible.
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Damn!! That's a lot of test. I know I'm glad I stocked up on test when I had the extra cash especially now that money is tight for me. I got enough for 2 years worth on 150mg week.
 
Kakarot said:
You think you might get some blood work? Just to see what that much test is actually doingo_O
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If I was a wealthier man I'd do it just out of curiosity. I'm not sure there's any value to getting them besides that. Was running two different UGLs and just switched to a third yesterday as I'm out of one of the others. What I knew was test enan I was dosing EOD and what I thought was mast prop that was actually more test enan I was dosing ED. I really wouldn't know what to expect or if it was even out of the ordinary for such a wild protocol.

I don't know though, i am really curious. I guess I'm gonna finish out the next two weeks like this. I'd say my levels would be stable by then for bloods. Actually been wondering how i should split the pins. 5cc twice a week or just keep up the ED protocol?
 
Docd187123 said:
E2 doesn't raise BP. If it is BP related which it likely is, it's bc of the gear itself. If it's only two more weeks and your breathing is back to normal I'd just keep on
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Not even indirectly? I get anxious when my e2 is high and it seems to make my BP go up and taking Adex helps. I took extra last night along with extra Lisinopril and feel much better today.

How do you think I should dose it? Keep up the high frequency? Probably doesn't matter that much at this point.
 
Marcus said:
Same thing happens with me. I always thought that high E2 can and does affect BP
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theprodgicalson said:
i think what @Docd187123 is saying is that high estrogen doesnt directly cause elevated BP. but, the side effects from high estrogen cause elevated BP

i could be wrong.







probably am lol
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Yeah, that's what I'm getting at. More of an indirect cause. I feel anxious and like I can't breathe and that in turn raises my BP. I've actually measured before and a couple hours after taking Adex and it's been lower. Could totally be in my head, but there it is.
 
Perrin Aybara said:
Yeah, that's what I'm getting at. More of an indirect cause. I feel anxious and like I can't breathe and that in turn raises my BP. I've actually measured before and a couple hours after taking Adex and it's been lower. Could totally be in my head, but there it is.
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100% with me too, exactly 2-3 hours after. Good to hear I'm not completely nuts with this. Still may be placebo I guess
 
Perrin Aybara said:
If I was a wealthier man I'd do it just out of curiosity. I'm not sure there's any value to getting them besides that. Was running two different UGLs and just switched to a third yesterday as I'm out of one of the others. What I knew was test enan I was dosing EOD and what I thought was mast prop that was actually more test enan I was dosing ED. I really wouldn't know what to expect or if it was even out of the ordinary for such a wild protocol.

I don't know though, i am really curious. I guess I'm gonna finish out the next two weeks like this. I'd say my levels would be stable by then for bloods. Actually been wondering how i should split the pins. 5cc twice a week or just keep up the ED protocol?
Click to expand...
Nah man I understand money issues:(. If it was me I'd do it just out of curiosity. If it was over 15k I'd frame it and put it on the wallo_O
 
I don't even mean indirect. I mean it's directly related to androgens and not aromatization. Here's a post from Dr. Scally:

Michael Scally MD said:
Re: A HOW TO for: SERMs, Aromatize inhibitors, Gyno and PCT *A must read








This is getting off-topic from the OP, but since E2 has been stated as causing "bloat," which is then the cause of PB [sic] problems, I will address this in a brief manner. "Newly" found elevated BP after administering AAS can be a challenge to the user as well as the caretaker.

The simple idea that this problem arises from E2 is without supportive evidence. I came to this conclusion very early in treating AAS users by the fact that no amount of E2 control managed the BP. I am sure this is the experience of many AAS users. This is further confirmed by the fact that non-aromatizable AAS can cause elevated BP. [Proviron is reported to cause an increased BP.] This observation would lead one to conclude that the AAS itself is the source of the BP problems and lowering E2 while AAS are high will have limited success.

As the elegant study below shows, androgens (Testosterone) do appear to be the cause. I have never argued against E2 control, but directed therapies at their cause, thus SERM for gynecomastia. In the clinical context where an AI is being used for E2 control and BP is a problem do not look at more AI to further lower E2, but treat the BP.


The researchers present new evidence on genomic and nongenomic mechanisms of testosterone action on vascular smooth muscle cells in arterial hypertension through modulating associated cellular events, thus setting the stage for further aggravation of hypertension. Using animal models of normotension and polygenic hypertension, the investigators found that, in vascular smooth muscle cells from male animals, testosterone regulates cellular processes, which mediates vascular contraction and hypertrophy, key events contributing to the increased vascular resistance in hypertension. They also observed greater production of reactive oxygen species in response to testosterone in vascular smooth muscle cells from hypertensive as compared with normotensive animals. These effects were not attributed to conversion of testosterone to 17Beta-estradiol, because the aromatase inhibitor anastrazole had no effect on reactive oxygen species formation.


Barton M, Prossnitz ER, Meyer MR. Testosterone and Secondary Hypertension: New Pieces to the Puzzle. Hypertension. Testosterone and Secondary Hypertension


Chignalia AZ, Schuldt EZ, Camargo LvL, et al. Testosterone Induces Vascular Smooth Muscle Cell Migration by NADPH Oxidase and c-Src-Dependent Pathways. Hypertension. Testosterone Induces Vascular Smooth Muscle Cell Migration by NADPH Oxidase and c-Src–Dependent Pathways

Testosterone has been implicated in vascular remodeling associated with hypertension. Molecular mechanisms underlying this are elusive, but oxidative stress may be important. We hypothesized that testosterone stimulates generation of reactive oxygen species (ROS) and migration of vascular smooth muscle cells (VSMCs), with enhanced effects in cells from spontaneously hypertensive rats (SHRs). The mechanisms (genomic and nongenomic) whereby testosterone induces ROS generation and the role of c-Src, a regulator of redox-sensitive migration, were determined.

VSMCs from male Wistar-Kyoto rats and SHRs were stimulated with testosterone (10?7 mol/L, 0–120 minutes). Testosterone increased ROS generation, assessed by dihydroethidium fluorescence and lucigenin-enhanced chemiluminescence (30 minutes [SHR] and 60 minutes [both strains]). Flutamide (androgen receptor antagonist) and actinomycin D (gene transcription inhibitor) diminished ROS production (60 minutes). Testosterone increased Nox1 and Nox4 mRNA levels and p47phox protein expression, determined by real-time PCR and immunoblotting, respectively. Flutamide, actinomycin D, and cycloheximide (protein synthesis inhibitor) diminished testosterone effects on p47phox. c-Src phosphorylation was observed at 30 minutes (SHR) and 120 minutes (Wistar-Kyoto rat). Testosterone-induced ROS generation was repressed by 3-(4-chlorophenyl) 1-(1,1-dimethylethyl)-1H-pyrazolo[3,4-day]pyrimidin-4-amine (c-Src inhibitor) in SHRs and reduced by apocynin (antioxidant/NADPH oxidase inhibitor) in both strains. Testosterone stimulated VSMCs migration, assessed by the wound healing technique, with greater effects in SHRs. Flutamide, apocynin, and 3-(4-chlorophenyl) 1-(1,1-dimethylethyl)-1H-pyrazolo[3,4-day]pyrimidin-4-amine blocked testosterone-induced VSMCs migration in both strains.

Our study demonstrates that testosterone induces VSMCs migration via NADPH oxidase–derived ROS and c-Src–dependent pathways by genomic and nongenomic mechanisms, which are differentially regulated in VSMCs from Wistar-Kyoto rats and SHRs.
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Eman said:
One of the God damn bodybuilders running around here must have sabotaged the pizza parlor, bastards.
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This made doc almost shart from laughing :(

Perrin, the deliciousness of a meat lover's pizza is inversely proportional to the amount of ch**se on it. Super duper über deliciousness = ch**se prohibition for your entire county
 
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