how do you reduce the bloat from anadrol??

[gorillaboy55]

i have a slight blood preasure issue in the past not bad only like 90 over 150....i have chosen to front load with an oral and this is the only one i could get my hands on. my dr. has given me a water pill. and i got the anadrol powder and am thinking of taking it at half rate or even half rate 2 day on and 2 days off.....any other suggestions....and i know why would you take an oral with a blood preasure issue........thanks for your time

 

[gorillaboy55]

just out of curiosity how did i get all this negative karma???? ive never wronged anyone on here before?

 

[KD1]

First off, if I had a BP issue I wouldent take A-Bombs. And if I did, I woudlent do 2 days on 2 days off, thats just going to fuck your HPTA and give you shit for gains.

 

[mikefear]

with something that has such a short half-life, you dont want to do 2 days on, 2 days off.. either be on it, or dont. if you want to reduce the bloat, get on a good AI.. preferably AIFM as it is one of the most powerful you can buy. you can get it frmo the banner in my signature.

it doesn't seem like you've done much research before devling into this.. it's not a joke, my man.. anabolics are serious.. prepare yourself and things will go well.. take the obstacles as they come, and you'll end up with some problems.

 

[KD1]

if you want to reduce the bloat, get on a good AI..

That may not help with Anadrol. According to Big Cat, Its not armomitization that causes the bloat, but rather the interaction of Anadrol itself with the estrogen receptor.

http://www.bodybuilding.com/fun/catanadrol.htm

 

[macrophage69alpha]

anadrol interacts with the PgR. AI's do help, by reducing PgR expression.

anadrol does not bind to the ER, though some have wrongly made that assumption based on its PgR activity.

also increasing potassium and decreasing sodium will help

 

[H_T_]

i can't handle A-bombs. i have stage II hypertension, so the outer limit BP readings are a no no......

 

[boxerjake]

Diuretics and inhibitors will help ....... oxy actually does convert but by a different mechanism .
The guys i know who still take oxy most often take it in conjunction with a diuretic of some sort .... the bloat for me is not worth it , there are better choices .

 

[macrophage69alpha]

no one has ever eludicated the "supposed" Estrogenic metabolites nor the method of reduction. Though many have made such claims. Its PgR activity has been established as well as its ability to suppress natural progesterone production

 

[Wulfgar]

Faslodex(fulvestrant) is the better estrogen antagonist during Drol admin(or any other AAS with progestin activity). The drug works by down-regulating estrogen and progesterone receptor counts. Less receptors meals less acticity

 

[macrophage69alpha]

aromatase inhibitors are just as effective, and more tolerable.
though faslodex is certainly better than nolva in this aspect as it has almost entirely antagonistic activity at the ER (hence why it down regulates the PgR).


faslodex has some other, what appear to be, not so nice activities

Mol Cancer Ther. 2006 Jun;5(6):1539-1549. Related Articles, Links


Fulvestrant (ICI 182,780) down-regulates androgen receptor expression and diminishes androgenic responses in LNCaP human prostate cancer cells.

Bhattacharyya RS, Krishnan AV, Swami S, Feldman D.

Division of Endocrinology, Department of Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Stanford University Medical Center S-025, Stanford, CA 94305-5103. [email protected].

The androgen receptor (AR) plays a key role in the development and progression of prostate cancer. Targeting the AR for down-regulation would be a useful strategy for treating prostate cancer, especially hormone-refractory or androgen-independent prostate cancer. In the present study, we showed that the antiestrogen fulvestrant [ICI 182,780 (ICI)] effectively suppressed AR expression in several human prostate cancer cells, including androgen-independent cells. In LNCaP cells, ICI (10 mumol/L) treatment decreased AR mRNA expression by 43% after 24 hours and AR protein expression by approximately 50% after 48 hours. We further examined the mechanism of AR down-regulation by ICI in LNCaP cells. ICI did not bind to the T877A-mutant AR present in the LNCaP cells nor did it promote proteasomal degradation of the AR. ICI did not affect AR mRNA or protein half-life. However, ICI decreased the activity of an AR promoter-luciferase reporter plasmid transfected into LNCaP cells, suggesting a direct repression of AR gene transcription. As a result of AR down-regulation by ICI, androgen induction of prostate-specific antigen mRNA and protein expression were substantially attenuated. Importantly, LNCaP cell proliferation was significantly inhibited by ICI treatment. Following 6 days of ICI treatment, a 70% growth inhibition was seen in androgen-stimulated LNCaP cells. These data show that the antiestrogen ICI is a potent AR down-regulator that causes significant inhibition of prostate cancer cell growth. Our study suggests that AR down-regulation by ICI would be an effective strategy for the treatment of all prostate cancer, especially AR-dependent androgen-independent prostate cancer. [Mol Cancer Ther 2006;5(6):1539-49].