Longterm use of FEMARA (LETROZOLE)

very interesting JGUNS but just a remark, all these studies are about boys not adult men. The age could be an important factor too, just a supposition ...

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In the testosterone-plus-placebo-treated group, the high-density lipoprotein cholesterol concentration did not change

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Am I missing something or did you? In the PLACEBO group HDL did not change...

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but in the testosterone-plus-letrozole-treated group the concentration decreased.

In the letro group the HDL concentration DECREASED...

Knowing the basics of how an aromatase inhibitor works would lead me to the conclusion that the greater the suppression of estrogen via the aromatase enzyme the greater Testosterone levels will be. I've quoted the difference below (adex in the first block and letro in the second). There is a significant difference in the suppression of estrogen between the two drugs. Therefore, it would be jumping the gun to conclude that because adex may have no impact on lipid profiles that all aromatase inhibitors have no effect on lipid profiles. There are many studies that show estrogen playing an important role in the way our profiles read...I believe it would be premature to dismiss this.

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Testosterone increased 117% in the Rx group (from 304 +/- 31 to 626 +/- 64 ng/dl)

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Originally posted by JGUNS but during the letro zole treatment, the increase was more than fivefold higher than in the group treated with testosterone alone.[/B]

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The first study said that lipids did not change in Anastrozole groups and no testosterone was administered.

The second study says that estradiol levels did not change in the testosterone treated boys AFTER they began treatment with letrozole. So, estrogen did not rise but did not lower with letrozole and testosterone.

The third study, yes, shows that HDL lowered, but LDL, the truly bad cholesterol remain unchanged.

So, with all of these studies posted up on PM women, who have small amounts of estrogen in their systems, I would think that studies done on boys, some receieving exogenous testosterone, would be a little closer to the mark. The point is, you can't look at these studies with 98% suppression and then think that it in any way relates to you. In the first group, I believe it was closer to 60% suppression WITHOUT any extra testosterone, whereas with letrozole when testosterone was added, E2 levels remained unchanged.

So, what is generally accepted to be the length of time it is ok to be on letrozole?

The reason I ask is, I have been on a test/EQ/tren cycle for 16 weeks, only the last 11 have I used letrozole. Before that, i was usunf formestane from 1fast100 at a dosage of 400mg per day. With the formestane, I had a lot of water and did not fell like it was working. I was all the way up to 308lbs!

I switched to letrozole and went low carb, and in 5 (count 'em 5) days lost 18 lbs. of water! I honestly felt so much better the next frickin morning after the first dose! I peed like a mofo. lol...

My cycle ended a few weeks ago, and I did my usual PCT, which is 5000IU's of HCG every 5-6 days 3x, and 100mg clomid ED for the first week then 50mg ed for the next two weeks. All the while taking letrozole ED.

I wanted to continue the letro while I am on my low carb diet to keep the stubborn estrogen out of the fat cells, which letro is best at. I figured this would keep my test levels higher, estrogen lower, thereby aiding in fat loss.

I don't want to continue the letro if it is going to screw up my heart over the longterm.

So, should i only take it during a test cycle and for the three weeks afterwards? Kepp in mind i have been doing 16 week cycles.

Thanks for all the feedback so far, it is appreciated.

Posted by: JGUNS

The first study said that lipids did not change in anastrozole groups and no testosterone was administered.

The second study says that estradiol levels did not change in the testosterone treated boys AFTER they began treatment with letrozole. So, estrogen did not rise but did not lower with letrozole and testosterone.

The third study, yes, shows that HDL lowered, but LDL, the truly bad cholesterol remain unchanged.

So, with all of these studies posted up on PM women, who have small amounts of estrogen in their systems, I would think that studies done on boys, some receieving exogenous testosterone, would be a little closer to the mark. The point is, you can't look at these studies with 98% suppression and then think that it in any way relates to you. In the first group, I believe it was closer to 60% suppression WITHOUT any extra testosterone, whereas with letrozole when testosterone was added, E2 levels remained unchanged.

After looking at the info again, maybe it would be more accurate to say that suppressing estrogen while the body is experiencing supraphysiological levels of androgens is dangerous to your lipid profile?

Posted by: ready2explode

After looking at the info again, maybe it would be more accurate to say that suppressing estrogen while the body is experiencing supraphysiological levels of androgens is dangerous to your lipid profile?

You mean "ISN'T experiencing supraphysiological amounts of test "correct?

The studies that show little if any change in plasma lipid profiles with aromatase inhibition may be very deceptive. There is an emerging view that the local aromatization of T to E2 within the coronary vessel walls is what is cardioprotective, not circulating E2.

Note that in the 2nd study below the testes intact/anastrazole administered mice had no significant difference in plasma lipids as compared to controls, but had accelerated plaque development.

This goes to my point that circulating lipids are not a reliable maker of plaque development when using aromatase inhibitors.

Posted by: Nandi

The studies that show little if any change in plasma lipid profiles with aromatase inhibition may be very deceptive. There is an emerging view that the local aromatization of T to E2 within the coronary vessel walls is what is cardioprotective, not circulating E2.

Note that in the 2nd study below the testes intact/anastrazole administered mice had no significant difference in plasma lipids as compared to controls, but had accelerated plaque development.

This goes to my point that circulating lipids are not a reliable maker of plaque development when using aromatase inhibitors.

So what do you recommend while on cycle with high estrogenic side effectsi?

Also, would you recommend taking an AI even if high E symptons dont arise (high BP, gyno, etc), as a precautionary (health) measure? Or would it be more *healthy* to leave it off?

also, how would you add nolva in there, if at all?

thanks, governor

My response was to the original post where the question was raised about any possible health risks with staying on an AI for months, or even permanently. I would say yes, definitely, there are risks.

For the typical several week cycle, if you are worried about gyno or estrogen related water retention contributing to high blood pressure, then it's doubtful AI would pose any serious health risks.

So, Nandi, in your opinion, would 16 week cycles be too much?

TTT I was looking for these studies posted by Nandi.