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Ultrasensitive Estradiol results

30 picograms of estradiol per milliliter of blood is always 30 pg/ml regardless of the "normal range" the lab tags it with.
 
Dr. Crisler wrote about how standard E2 testing isn’t a good value for men and they need ultrasensitive Estradiol for testing. I’ve always just done E2 but recently did ultrasensitive to compare. My last blood work is here
http://www.professionalmuscle.com/f...cle-forum/139996-everyday-im-trt-results.html

Since then I’ve had a few more tests using the 25mg IM TRT protocol. Total and free test are around 1100-1200 and free test around 280-320. I wanted to see how low I could go with arimidex to control estrogen. At .5mg 2x per week my E2 was around 20 or so. Then I went to .25mg 3x per week and E2 was 35 range <=39 but I had ultrasensitive Estradiol done as well to compare and it was 10. Range <=29. So that surprised me. I don’t want estro that low so my last test was I switched to .125mg Adex 3x per week. It’s a bitch splitting the tabs that low but I just used a .01g scale and it would always be around .12-.15mg so a total of around only .36-.45mg/wk of total Adex. I figured this would be too low but I just got my ultrasensitive Estradiol results back and it’s 20. Same range <=29. I wouldn’t even mind being closer to 29 since my test is in the high range the ratio would be equal. I figure .10mg Adex 3x per week will be my sweet spot. I recommend anyone who gets estrogen tested to get ultrasensitive Estradiol done instead of standard E2. Much more accurate.

What brand and dose of arimidex are you using? I wonder if mine is the same where I could measure it on a scale. Mine is manufactured by Accord and they are white tablets that say AHG from Walgreens
 
What brand and dose of arimidex are you using? I wonder if mine is the same where I could measure it on a scale. Mine is manufactured by Accord and they are white tablets that say AHG from Walgreens



You could split any pill brand doesn’t matter. It’s just relying that the dose is equally dissolved throughout the whole pill. I’d say it’s prolly
More likely with pharma vs ugl presses tab but not guaranteed. But I guess either way in the long run you’ll still reach the same amount and it would be more split up than one dose.
 
What brand and dose of arimidex are you using? I wonder if mine is the same where I could measure it on a scale. Mine is manufactured by Accord and they are white tablets that say AHG from Walgreens



Same. Accord.
 
30 picograms of estradiol per milliliter of blood is always 30 pg/ml regardless of the "normal range" the lab tags it with.

30 is a good rough number. 25 is ok and so is 40 imo...but it DOES matter because if you read my post earlier, my E2 was 34.1 while my sensitive Estradiol was 19.4...so it absolutely matters which test it is. These readings were taken simultaneously/at the same draw.
 
30 is a good rough number. 25 is ok and so is 40 imo...but it DOES matter because if you read my post earlier, my E2 was 34.1 while my sensitive Estradiol was 19.4...so it absolutely matters which test it is. These readings were taken simultaneously/at the same draw.



So when getting the sensitive what would the new “good range”? Considering on regular estradiol you want to be around 25-40?
 
Sorry guys I had the numbers wrong. When using the .25adex 3x per week E2 was 22 not 35. Range <=39. Ultrasensitive was 10 range <=29. Then dropping Adex to .125mg 3x per week ultrasensitive was 20 range <=29

So from calculating it having an E2 of 22 with range <=39 means my E2 was approx 57% of max value(39x.57). When calculating ultrasensitive I was approx 35% of max value(29x.35).

So pretty significant difference about 20% difference. Although both tests measure in pg/mL

Now with Adex at .125mg 3x/wk ultrasensitive is 20 range <=29

I think this is a decent range to stay at I might drop the Adex a tad more to let’s say .10mg 3x/wk and check again in a few weeks. The goal would obviously be to not use Adex at all and if I dropped the testosterone just a little bit like maybe from 25mg ED to 20mg ED that alone may let me avoid using any anti estrogens. I found it interesting my estrogen was higher when doing every day subQ shots vs shallow IM. But then I read the following article by Dr. Crisler.

http://www.allthingsmale.com/word_docs/TRT.doc

Under the transdermal topic he states:

“Gels and creams, like all transdermal delivery systems, provide a greater boost in DHT levels, compared to injectable testosterone preparations. As DHT is responsible for all the things of manhood--literally, AllThingsMale--the transdermals are better at treating sexual dysfunction than are injectables. However, issues of hair loss (which I treat with a compounded topical DHT blocking mixture) and possible prostate morbidity (a contentiously debatable point, to be sure, but resolved in the negative to my mind) then come into play. This might be a good time to mention I vehemently oppose adding finasteride or similar medication.

To end the debate on this topic, transdermal T gels/creams are more likely to elevate estrogen than injections, as long as the shots are properly administered once per week. That is because aromatase lives in the skin, along with higher concentrations of 5-AR, which converts T to E. Even so, the benefits of TD TRT outweigh the weekly convenience of shots.”

So this leads me to believe that perhaps subQ increases estrogen more than shallow IM.

P.S. during this entire testing protocol I have also implemented 200mg/day DIM and 500mg/day calcium D-glucarate.


The latter portion of your post is interesting to me. There have been many people who have brought up SubQ injections resulting in lower estradiol levels. I believe I even read a study on it.

However I have experimented with both SubQ and higher frequency injections and neither seemed to decrease my estradiol. In fact, I had marginally higher estradiol levels with the SubQ injections. Which as you said makes sense due to higher aromatase in the skin/fat, but this goes against what many people seem to claim.

Would be interested if anyone else has experience with this through tests of their own.
 
Regarding the sensitive vs. ultrasensitive issue, I'm surprised Dr. McClain's script has been for "Estradiol, Sensitive" with CPT code 82670 as he says in his video you need the ultrasensitive.

Here is the link from Quest: **broken link removed**

"Note: For any patients for whom low estradiol levels are anticipated (e.g. males, pre-pubertal children and hypogonadal/post-menopausal females), the Quest Diagnostics Estradiol, Ultrasensitive, LC/MS/MS assay is recommended (test code 30289)."

And it seems from the OPs bloodwork that means it could be incorrectly low or high.

The tech at Quest I go to has consistently messed up my blood work and it looks like half of my tests have been ultrasensitive and the other half have been regular estradiol lol. I've had "Estradiol, Ultrasensitive" scores of 7, 13, and 23 all while on 80mg TRT and 1mg Adex per week.
 
Update:

Dropped cyp from 25mg IM ED to 20mg
Dropped Adex completely

Total test:
696 Range 250-1100

Free test:
157 Range 35-155

Ultrasensitive Estradiol

42 range <20mg




Previous results on 25mg Cyp IM ED with .125mg Adex 3x/wk

Total test:
1203. Range 250-1100

Free test:
331. Range 35-155

Ultrasensitive Estradiol
20 range <29

I will be going back to my original 25 mg protocol as it yielded far better results.

When you say the results were much better, do you mean blood work results or how you looked and performed in the gym?


I would guess the AI is suppressing E2 enough to cause some natty test production and that is why you are getting a much higher level on just 5mg more.

I would imagine it has much more to do with less artificial testosterone being converted to estradiol than it is due to natural production, which is presumably nil on 140-175mg test per week.
 
When you say the results were much better, do you mean blood work results or how you looked and performed in the gym?




I would imagine it has much more to do with less artificial testosterone being converted to estradiol than it is due to natural production, which is presumably nil on 140-175mg test per week.

Only a tinny percentage of total testosterone is converted to E2 or DHT, neither is the main path of metabolism for most of the hormone.

Natty production can be significant if GNRH and LH production are stimulated by the lack of estradiol.
 
Only a tinny percentage of total testosterone is converted to E2 or DHT, neither is the main path of metabolism for most of the hormone.

Natty production can be significant if GNRH and LH production are stimulated by the lack of estradiol.

On 80mg TRT my total test is around 600 and E2 is 40-45. On 1mg arimidex with that 80mg TRT my total test goes up to 800-900 and my E2 gets down to around 15-20 (not that low).

So you think that extra 33-50% testosterone is coming from natural production?
 
On 80mg TRT my total test is around 600 and E2 is 40-45. On 1mg arimidex with that 80mg TRT my total test goes up to 800-900 and my E2 gets down to around 15-20 (not that low).

So you think that extra 33-50% testosterone is coming from natural production?

Yep, estradiol negative feedback at the hypothalamus releasing GNRH.

And it stimulates LH not FSH because pulsatile GNRH releases FSH and steady GNRH releases LH.

I'm sure some of the extra testosterone is coming from a lack of aromatization, but think about, the units are the same, E2 from 40 to 20 is only going to "use up" 20pg/ml of testosterone. Conversions rates are in the 1-3% on E2 and DHT from what I remember. The liver just fucks most of that shit up with cyto 450 :D er, I mean metabolizes most testosterone directly.
 
Last edited:
Yep, estradiol negative feedback at the hypothalamus releasing GNRH.

And it stimulates LH not FSH because pulsatile GNRH releases FSH and steady GNRH releases LH.

I'm sure some of the extra testosterone is coming from a lack of aromatization, but think about, the units are the same, E2 from 40 to 20 is only going to "use up" 20pg/ml of testosterone. Conversions rates are in the 1-3% on E2 and DHT from what I remember. The liver just fucks most of that shit up with cyto 450 :D er, I mean metabolizes most testosterone directly.

That's an interesting idea, but what level of estradiol is considered "low" to the point that the body will produce GNRH? Any time I've tested FSH and LH they've been close to zero. It's been years since I bothered testing them but whenever I did they were nonexistent while on cycle. My current levels of 13-20 don't seem like they would be that low. Is it based on an absolute level or relative to testosterone? I've not heard of significant natural production while using TRT before except perhaps with HCG.
 
That's an interesting idea, but what level of estradiol is considered "low" to the point that the body will produce GNRH? Any time I've tested FSH and LH they've been close to zero. It's been years since I bothered testing them but whenever I did they were nonexistent while on cycle. My current levels of 13-20 don't seem like they would be that low. Is it based on an absolute level or relative to testosterone? I've not heard of significant natural production while using TRT before except perhaps with HCG.

Nolvadex will block E2 and increase GNRH production also. Estradiol is the feedback mechanism for GNRH in the HPGA, so whatever is "low" to your HPGA will stimulate production.

Very high testosterone levels will prevent natty production even if you block E2 due to a second feedback mechanism involving testosterone directly.
 
Nolvadex will block E2 and increase GNRH production also. Estradiol is the feedback mechanism for GNRH in the HPGA, so whatever is "low" to your HPGA will stimulate production.

Very high testosterone levels will prevent natty production even if you block E2 due to a second feedback mechanism involving testosterone directly.

While I agree that overall low hormone levels will stimulate production from the HPGA I was under the impression that if some of the hormones are still high this will negate proper production

For example, one of the issues that can occur when someone comes off exogenous hormones is that their test crashes but they still have relatively high estrogen. Even though the testosterone may be very low, the high estrogen prevents proper production. Therefore, an AI is recommended so that estrogen will also be suppressed and proper natural production can occur.

That is what I have seen theorized at least. I have not gone through the process myself.

From what you're saying it sounds like there could be quite a balancing act between what is just high enough to still allow natural production under certain circumstances vs what is too high of a given hormone to allow any natural production.
 
While I agree that overall low hormone levels will stimulate production from the HPGA I was under the impression that if some of the hormones are still high this will negate proper production

For example, one of the issues that can occur when someone comes off exogenous hormones is that their test crashes but they still have relatively high estrogen. Even though the testosterone may be very low, the high estrogen prevents proper production. Therefore, an AI is recommended so that estrogen will also be suppressed and proper natural production can occur.

That is what I have seen theorized at least. I have not gone through the process myself.

From what you're saying it sounds like there could be quite a balancing act between what is just high enough to still allow natural production under certain circumstances vs what is too high of a given hormone to allow any natural production.

Estradiol, not testosterone, feeds back the hypothalamus and regulates GNRH production.
 

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