It was my understanding that Femara reduces the body's production of estrogen. It is an aromatase inhibitor which lowers estrogen levels. Is this not true? For those who have used Femara, isn't it true that your E2 level can't be matched with your follicle growth?

And for those who have used Clomid, doesn't your E2 level go up, but the the receptors in the uterus and pituitary and/or hypothalamus just don't register the estrogen?

Someone posted on another board a quote from Sher's website which says Clomid is an anti-estrogen and Femara is not. I thought it was the opposite. I know Clomid blocks estrogen receptors, but it doesn't reduce actual estrogen production, does it?

Can anyone provide any feedback on this, particularly if you've had b/w done while on both or either? Or do you just have any input?

Thanks.

Clomid binds to estrogen receptors and blocks estrogen from attaching.

That explains the difference between the two. I know that my lining was thin on Clomid but thick on Femara. I think it is because Femara clears quickly and your lining has time to build before you O. I don't usually have b/w done, so not much help with that. http://www.infertilityspecialist.com/letrozole.html

xoxo, Tracy

So, you were just monitored with u/s while on Femara? It was my understanding that the estrogen would not match follicle size, but the follicles grow despite not producing estrogen. But what I don't understand is how the lining in the uterus can build up with reduced estrogen. Is it that the estrogen is just lower per follicle, but maybe with 2 or more follicles, there is still enough estrogen to "plump up" the uterus?

I do think there is a problem with the use of the terminology "anti-estrogenic". I think the docs are using it for both "anti-estrogenic to receptors" and "anti-estrogenic in terms of production of estrogen". So, that makes it confusing.

The only cycle I had b/w was my IVF and I did Femara + Stims. My E2 was low for the 5 eggs I got. I want to say it was around 400? Although only 3 of the 5 were mature and only 2 fertilized....so I always rationalized it was on par with the two that became embies. I think you are right that the estrogen is obviously in there building the lining......maybe looking for research on it and Tamoxifen for breast cancer treatment would give us more details. For that treatment....you don't want the body responding to estrogen because if the cancer has estrogen positive receptors it will grow. Hmm.....

xoxo, Tracy

PS: Just found this brief article that gave me a bit more insight. http://breast-cancer.emedtv.com/femara/femara-uses-p2.html

That is helpful to see that your E2 level was low for the number of follicles, but still high enough to build a lining. I'm still fascinated about how the follicles can grow, but not produce as much estrogen as they normally would. Did you by any chance have your LH tested during that cycle while you were taking the Femara? I know many docs don't do that, but I was curious if the Femara had any impact on LH. Supposedly Clomid does, but yet I've seen a lot of women being monitored who do not have an increase in LH while on it. The limited times I took Clomid, I did not see an increase in LH, but I had been on lupron prior to the Clomid and that residual effect may have played a part. But still, there are others without the lupron who didn't get a rise in LH while on Clomid. Anyway, I'm just curious how Femara affects LH levels, too.

Thanks so much for the input.

I did clomid and femara a few years back. Femara kept my E2 really, really low (my E2 was only in the 100's even though I had 7 mature follicles). Clomid kept the E2 high, but of course with my thin lining, clomid is really not an option for me. I didn't get a thick lining on femara either but that is just because I have thin lining.

That is so helpful to see how low your E2 was despite the mature follicles. Like I said to Tracy, it fascinates me how the follicles grow and don't produce estrogen. It makes sense that if your E2 is around 200 or more, you typically could have enough E2 to thicken the lining. Did you by any chance get your LH tested while you were on Femara? Like I mentioned to Tracy, I'm really curious how Femara affects the LH, too.

Thanks so much for the input.

Dr. Licciardi from NYU explains the diff btwn Clomid vs. Femara mechanisms of action in a series of blog posts at [email protected]

I've read through his posts and will look at them again. Now, I'm pretty confident that I understand the basics of Femara and Clomid. I will admit I still am perplexed how follicles will grow without having the normal estrogen levels. It just shows that the standard medical text explanations aren't as accurate as some think they are. I remember a doc who was TTC on another board years ago telling that the E2 level of a follicle reached 200 for 48 hours and that is what triggered an LH surge. Well, I had personal experiences (b/w and u/s) that proved that medical text explanation wrong! I know there were other factors involved in triggered an LH surge since I could surge with lower levels for shorter periods of time. And I'd seen other women whose experiences disproved that theory, too.