I think i got a better feel now for internet forum protocals. I was probably hijacking someone's thread again (this time Lowvolume) :0 For some reason, i felt that i was too new to this forum to be creating threads... but I get a feeling it's better than hijacking. In any case, here's a copy and paste of a few posts from another thread.

Quote Originally Posted by Jawohl
This might be a stretch... but couldn't it be that 95% of ur guys have high Total E's precisely because they have hormonal imbalances to beginwith, therefore making them want to seek medical help such as yourself? Or were you refering to assays done on healthy males with no known endocrine issues?


After trying to look up some more info on Total Estrogens and possible suppresion to the HP, I found a few posts from a thread in a different forum that I found interesting. The poster is a practicing physician and he sounds pretty knowledgable too. Here's a copy and paste of a few posts...

Quote Originally Posted by SWALE
Here is what I have seen in my clinical practice: I lower Estradiol levels with Arimidex, to mid range. But Total Estrogens go up, sometimes to 50% over the top of their collective physiological range. Since Estradiol is going down, that means Estrone and/or Estriol is going up even more. I have not gathered enough labs to figure this out yet, but am working on it.

Analysis of the metabolic pathways would make one think this could not be true, as an AI inhibits both the conversion of Testosterone to Estradiol, AND androstenedione to Estrone. Also, the conversion of Estrone to Estradiol must be inhibited as well, because, as I have said, estradiol is going down while the rest are elevating. But obvioulsy the body is not willing to be ruled by intuitive thought from a lovely picture of the metabolic pathways.
Quote Originally Posted by SWALE
Arimidex also prevents the conversion of androstenedione to estrone.

That is what is so puzzling. Why is it, if we are inhibiting the production of estrogens, and as demonstrated by lowered Estradiol levels, Total E's can remain at 50% over the top of physiological range??.

Here's a response from a diff poster..

Quote Originally Posted by Snipe
My estrone went from 23 to 104 afer discontinuing Arimidex. (0.25mg. 3x/week)

Estradiol went from 12 to 52 but is not valid since the latter value was not obtained using the extraction method. (I will retest soon.)

My total E's went down form 180 to 100 after several weeks of I3C @400mg/day, and remained at 100 after discontinuing Arimidex.

I intend to stay off Adex, remain on I3C, and retest in about 6 weeks.

Quote Originally Posted by SWALE
Let's be careful not to hang our hats on this observation I have made about Total E's rising on Arimidex. I have seen this on a few patients, not all. It is only recently I began checking Total E's. Before, that, it was cutting edge to just order E2. In those patients with good E2 but elevated Total E, I am going to begin ordering fractionated estrogens, to explore this further.

Of note, I am seeing a trend in that these are the same guys who complain of estrogen symptoms even after adding in Arimidex (and controlling E2 to mid-range).

All I have at this time is basically a few case studies. Puzzling? Yes

A good question from another poster..

Quote Originally Posted by Maxzax
HI Swale,

With the 50% increase in Total E's how does that affect LH production?

I guess my main concern is would arimidex lowering E1 and E2, be enough to restore my HPTA and fix the symptoms?

Do high Total Estrogens mean much in terms how your patients feel?


And finally...

Quote Originally Posted by SWALE
Max--That is a good question. I do not know if there is a differential in how the different varieties of estrogen inhibit the HPTA. I would hazard a guess that when Total E's goes up, even in the presence of mid-range Estradiol, that suppression is increased as well.
I quit running follow-up LH and FSH levels, except when the patient specifically requests them. So I have no data with respect to this question.

Does anyone have any ideas or know if E1 or E3 has any role in the negative feedback loop whatsoever? I also wonder if Dr.John meant 95% of his regular patients or a seperate study group of men with no known hormonal issues/imbalances?
I, much like the poster Maxzax, am wondering if lowering Total Estrogens could possibly be enough to restart the HPTA axis in some men with idiopathic hypogonadotropic hypogonadism.