first cycle..

[crs288]

i was thinking some form of test with maybe winstrol or eq. low dosages of each around 250-275mg/week. start pct 2 weeks after last injection using nolvadex/vitamins/etc.. my question is, i already have my bad days where my face breaks out but here lately its been clear and clearing up well and i want a test that has the is least prone to breakouts (which isnt going to happen)... i know of several different forms of test, test e, test cyp, sust, and so on but what all are the big differences? first cycle btw..
stats are 6'1'' 205lbs
maybe 16% bf..
biceps: 15''
chest: 42"
neck: 16"
forearm: 13"
thanks in advance guys..

[kfrost06]

well this is a debatable subject but there is some evidence that shows the shorter ester testosterones like test prop have a lower conversion to estrogen. The estrogen is what will give you the acne. However if you take winstol which is a DHT and acts like an AI that too will inhibit the conversion of the test to estrogen. Also taking proviron will inhibit estrogen and at the same time increas the effectiveness of your test by binding up the SHBG.

GL

[Big]

How old are you?

[Njord]

well this is a debatable subject but there is some evidence that shows the shorter ester testosterones like test prop have a lower conversion to estrogen. The estrogen is what will give you the acne. However if you take winstol which is a DHT and acts like an AI that too will inhibit the conversion of the test to estrogen. Also taking proviron will inhibit estrogen and at the same time increas the effectiveness of your test by binding up the SHBG.

GL

Where have you heard this? The closest I found was in AR's book where he states "Winstrol has been speculated to have anti-progestenic properties". I would not count on winstrol to help with estrogen control during cycle personnally.

The key in my opinion to control sides is to keep blood plasma levels as stable as possible. This means ed injections for prop and phenyl prop (including sustanon) and 2x week for Enth and Cyp.

You can also keep estrogen related sides down by controlling your estrogen with a SERM or AI while on cycle. I have never used them while on, so can't really help you there.

[crs288]

im 20 years old... i dont want to overkill the first time, i had read that some people respond well to low doses so why build tolerance off the start thats why i said 250mg/week but im open to more suggestions..if i took clomid or nolva during cycle would that help with the estrogen or is there another route?... thanks guys!

[borntobeblue]

too young dood

[kfrost06]

Originally Posted by kfrost06
well this is a debatable subject but there is some evidence that shows the shorter ester testosterones like test prop have a lower conversion to estrogen. The estrogen is what will give you the acne. However if you take winstol which is a DHT and acts like an AI that too will inhibit the conversion of the test to estrogen. Also taking proviron will inhibit estrogen and at the same time increas the effectiveness of your test by binding up the SHBG.

GL

Where have you heard this? The closest I found was in AR's book where he states "Winstrol has been speculated to have anti-progestenic properties". I would not count on winstrol to help with estrogen control during cycle personnally.

The key in my opinion to control sides is to keep blood plasma levels as stable as possible. This means ed injections for prop and phenyl prop (including sustanon) and 2x week for Enth and Cyp.

You can also keep estrogen related sides down by controlling your estrogen with a SERM or AI while on cycle. I have never used them while on, so can't really help you there.

Well, I didn't hear it, I read it. Here's one of countless studies...

http://cancerres.aacrjournals.org/cg...ment/3378s.pdf

Comparative Studies of Aromatase Inhibitors in Cultured Human Breast
Cancer Cells1

The presence of aromatase activity, estrogen receptors, and
estrogenic responsiveness in MCF-7 human breast cancer
cells has allowed this cell line to be used as a unique in vitro
system for investigating the biological activities of potentially
therapeutic aromatase inhibitors. We now report the results of
studies which have examined the cytotoxicity, antiaromatase,
and intrinsic estrogenic activities of aminoglutethimide, 1,2-
dehydrotestolactone (testolactone), dihydrotestosterone, 4-hydroxy-
4-androstene-3,17-dione, and 10-propargylestr-4-ene-
3,17-dione within MCF-7 monolayer cultures. Cell viability was
determined by trypan blue exclusion, and aromatase activity
was assessed by quantifying the amounts of [3H]estradiol
formed from [3H]testosterone. Estrogenic activity was assessed
by examining the ability of each inhibitor to increase cytoplasmic
progesterone receptor and deplete cytoplasmic estrogen
receptor concentrations in these cells during a 5-day incuba
tion period. Cytoplasmic progesterone and estrogen receptors
were measured by the single-saturating-dose technique using
[17a-metfjy/-3H]-17a,21 -dimethyl-19-norpregna-4,9-diene-
3,20-dione and [3H]estradiol as the labeled ligands for each
assay, respectively. The results showed that all of these com
pounds were noncytotoxic aromatase inhibitors in MCF-7 cells
but that these agents demonstrated marked differences in
inhibitory potency (10-propargylestr-4-ene-3,17-dione > 4-hydroxy-
4-androstene-3,17-dione :»dihydrotestosterone » tes
tolactone = aminoglutethimide). The incubation of cells with 4-
hydroxy-4-androstene-3,17-dione resulted in cytoplasmic pro
gesterone and estrogen receptor responses that were similar
in magnitude to those observed in other cultures incubated
with equimolar concentrations of estradici. None of the other
four agents demonstrated estrogenic activity in this system.
However, we have previously observed that dihydrotestoster
one has substantial antiestrogenic action in this system. Taken
together, these results indicate that some aromatase inhibitors
may influence the hormonal regulation of human breast cancer
cells by more than one mechanism.


DHTs, e.g. winstrol, proviron, masteron all act as AIs furthermore you don't control your estrogen pruduction with a SERM, it is used to compete with your estrogen not inhibit it's production.