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Ergopharm 6-OXO

pa1ad said:
It is my opinion that aromatase inhbitors (arimidex, 6-oxo) are much better for bodybuilders then estrogen receptor antagonists like clomid and tamoxifen. Both can raise testosterone levels but these ERT's have estrogenic activity in the liver which promotes undesirable effects like lowering of IGF-1 and raising of SHBG.

Okay....let's get back on topic

pa1ad-
I am a big fan of 1-AD. Had great luck with this past summer and hope to run an improved cycle this winter.

I ordered some 6-OXO and have decided to use that as my postcyle recovery supp. I was planning on using 300mg ED for 20 days. Does this sound like an appropriate dose? I was planning on running 1-AD @ 300-400mg for 6wks. This was a good dose for me last year. I was planning on adding some 4-AD (about 500mg ED) as well. I got good results.

Recently I read some studies that indicated aromatase inhibitors may actually lower IGF-1 levels (anastrozole-didn't see data on letrozole). As well I saw a study reporting that aromatase inhibitors (anastrozole) caused a rapid increase in atherosclerotic lesions in rat coronary arteries! Eeek!

Testosterone inhibits early atherogenesis by conversion to estradiol: Critical role of aromatase

Obviously you didn't do major clinical studies on 6-OXO, but would it have a similar side effect? Any thoughts on if the lesions would be specific to the pharmaceutical AIs or rats? 6-OXO is a suicide inhibitor so it works in a slightly different manner, correct? Besides causing aromatase to suicide does 6-OXO have any other hormonal effects like helping LH levels return to normal?

thanks,
FHG
 
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fhg43 said:


Okay....let's get back on topic

pa1ad-
I am a big fan of 1-AD. Had great luck with this past summer and hope to run an improved cycle this winter.

I ordered some 6-OXO and have decided to use that as my postcyle recovery supp. I was planning on using 300mg ED for 20 days. Does this sound like an appropriate dose? I was planning on running 1-AD @ 300-400mg for 6wks. This was a good dose for me last year. I was planning on adding some 4-AD (about 500mg ED) as well. I got good results.

Recently I read some studies that indicated aromatase inhibitors may actually lower IGF-1 levels (anastrozole-didn't see data on letrozole). As well I saw a study reporting that aromatase inhibitors (anastrozole) caused a rapid increase in atherosclerotic lesions in rat coronary arteries! Eeek!

Testosterone inhibits early atherogenesis by conversion to estradiol: Critical role of aromatase

Obviously you didn't do major clinical studies on 6-OXO, but would it have a similar side effect? Any thoughts on if the lesions would be specific to the pharmaceutical AIs or rats? 6-OXO is a suicide inhibitor so it works in a slightly different manner, correct? Besides causing aromatase to suicide does 6-OXO have any other hormonal effects like helping LH levels return to normal?

thanks,
FHG


Your 6-OXO protocol sounds fine. And yes, 6-OXO should have the ability to raise LH as it lowers estrogen.

The other questions, as you might expect, are ones I cannot answer.
 
pa1ad said:
Your 6-OXO protocol sounds fine. And yes, 6-OXO should have the ability to raise LH as it lowers estrogen.

Good-thanks for the reassurance.

The other questions, as you might expect, are ones I cannot answer.

I guess I'll take that. What did you think of the study?

thanks,
FHG
 
fhg43 said:


I guess I'll take that. What did you think of the study?

thanks,
FHG


Since its just one study and its done in rats I am not falling off my chair in fear. However, this study does give incentive to limit aromatase inhibitor usage to only those periods when it is urgently needed - i.e. post cycle
 
Let's assume that estrogen (and/or its metabolites) are anti-atherosclerotic in nature, as the above study and other studies strongly suggest.

Now let's say that a person does a cycle of non-aromatizable androgen (1-Test or 1-AD, for instance), which lowers estrogen by inhibition of the HPTA. Then, at the end of the cycle, that person takes an anti-estrogen compound for a couple of weeks with the hope of inducing faster recovery of the HPTA, before again starting on a new cycle of non-aromatizable androgen.

Isn't this kind of cycle going to cause chronically lowered estrogen levels (both on- and off-cycle)? If so, it sounds like it may be a perfect recipe for accelerated heart disease.
 
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davin8r said:
Let's assume that estrogen (and/or its metabolites) are anti-atherosclerotic in nature, as the above study and other studies strongly suggest.

Now let's say that a person does a cycle of non-aromatizable androgen (1-Test or 1-AD, for instance), which lowers estrogen by inhibition of the HPTA. Then, at the end of the cycle, that person takes an anti-estrogen compound for a couple of weeks with the hope of inducing faster recovery of the HPTA, before again starting on a new cycle of non-aromatizable androgen.

Isn't this kind of cycle going to cause chronically lowered estrogen levels (both on- and off-cycle)? If so, it sounds like it may be a perfect recipe for accelerated heart disease.

I don't think that you run into problems using non aromatizing androgens. I think you run into problems using the aromatase inhibitors post cycle-basically you are taking your lowered E levels and knocking them down more. Conversely, through negative feedback our body is increasing production of aromatase so as soon as you stop the anti-Es your body has a signifcant amount of aromatase ready to go.

I don't think this type of ycle will chronically lower E levels. Your body will return to normal. However repeated use of anabolic agents will probably screw up your bodies natural ability to regulate hormones. And chronic use of anti-Es could have a negative effect on E levels (ie working to chronically reduce E levels or causing them to be unnaturally high). Basically plan out smart cycles and don't cycle too much.

FHG

So IMO you want to taper anti-Es and use them in conjunction with other items (clomid and trib maybe) to speed recovery.
 
davin8r said:
Let's assume that estrogen (and/or its metabolites) are anti-atherosclerotic in nature, as the above study and other studies strongly suggest.

Now let's say that a person does a cycle of non-aromatizable androgen (1-Test or 1-AD, for instance), which lowers estrogen by inhibition of the HPTA. Then, at the end of the cycle, that person takes an anti-estrogen compound for a couple of weeks with the hope of inducing faster recovery of the HPTA, before again starting on a new cycle of non-aromatizable androgen.

Isn't this kind of cycle going to cause chronically lowered estrogen levels (both on- and off-cycle)? If so, it sounds like it may be a perfect recipe for accelerated heart disease.

I think the research in this area is still in its infancy so no one can really answer this
 
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