AI & E2 rebound effect?

[BuzzSaw]

I've been hearing people mention that if you don't keep taking an AI (ie Arimidex), that you can end up with an E2 rebound, and that you end up with higher levels of E2.

Is this true? How does it work? Does it only apply to Arimidex?

Thanks.

 

[Cataceous]

It may be true with AIs that are not suicide inhibitors. These include anastrozole, but not exemestane. I think the theory is that with any AI use the body attempts some compensation by increasing aromatase production. So there is an excess of aromatase, though it is not active while tied up by the AI.

In the case of anastrozole the aromatase enzyme can be released and used when concentrations of the drug drop. So if you stop taking it then you may well be left with excess aromatase, and consequently excess estradiol, until the body adjusts and aromatase concentrations fall to normal.

With suicide inhibitors such as exemestane the aromatase enzyme is permanently deactivated. When you stop the drug aromatase must be made from scratch to replace what was lost. Although the production rate for aromatase may initially be higher than baseline, the more gradual rise may be enough to allow adaptation and no overshooting of normal levels.

 

[BuzzSaw]

Many thanks for the clear explanation!

I take it exemestane is the only suicide inhibitor AI?

 

[Systemlord]

I have experienced the E2 rebound effect, but not everyone will. I never experiencing a rebound effect with suicide inhibitors which kills aromatase, that only happens with AI's that work similar to anastrozole by blocking aromatase.

 

[Cataceous]

...
I take it exemestane is the only suicide inhibitor AI?

Yes, of the three pharmaceuticals generally used by men. Letrozole is reversible like anastrozole.

I'm not sure about natural AIs such as zinc, DHT, resveratrol, vitamin D and selenium. I'd suspect they are less likely to be suicide inhibitors, but can't say for sure without more research.

 

[JoeJ0eyJoeJoe]

I recently (4 weeks prior to labs) stopped HCG 500 IU 2x weekly, and compensated by stopping my anastrozole 0.5mg 2x weekly and increasing my 3x weekly 0.2ml TCyp injection to 0.22. (200mg/ml). (I’ve always understood the HCG generally causes E2 to rise).

Estradiol jumped to 49 (from 20) and free T jumped from 86 to 207 pg/ml (35-155pg/ml, Dialysis). Total T went from 654 to 962 ng/dL (250-1100).

I was surprised at both the E2 rise and the substantial free T rise with a moderate 10% increase in TCyp and removal of HCG. But the E2 rebound makes more sense after reading the above. Will be curious to see if either or both lowers in time.

 

[Cataceous]

I recently (4 weeks prior to labs) stopped HCG 500 IU 2x weekly, and compensated by stopping my anastrozole 0.5mg 2x weekly and increasing my 3x weekly 0.2ml TCyp injection to 0.22. (200mg/ml). (I’ve always understood the HCG generally causes E2 to rise).

Estradiol jumped to 49 (from 20) and free T jumped from 86 to 207 pg/ml (35-155pg/ml, Dialysis). Total T went from 654 to 962 ng/dL (250-1100).

I was surprised at both the E2 rise and the substantial free T rise with a moderate 10% increase in TCyp and removal of HCG. But the E2 rebound makes more sense after reading the above. Will be curious to see if either or both lowers in time.

Your results for free testosterone are peculiar, to the point that I wouldn't trust them. It's not reasonable to have it more than double with a 10% increase in dose. The somewhat disproportional increase in total testosterone could possibly be explained by an increase in SHBG stemming from higher estradiol. I'm also curious about your future measurements if you care to share them.