T Nation

HPTA and AI

Hypothetical case:

Over 50 male with total T and E levels midrange of “normal” (T slightly below midpoint, E slightly above midpoint). Moderate symptoms of low T.

As I understand it, estradiol in men is produced directly in fat but is mainly produced by the conversion of T via aromatase. If this person were to use an aromatase inhibitor, would we expect E levels to drop and the HPTA to upregulate both T and aromatase production to compensate? If the AI were continued, could we then expect a net decrease in E and a net increase in T? After all, he is now producing T naturally, so what we’re really fighting are the HPTA “setpoints” for T and E. Do you think AI alone could achieve the goal of higher T and lower E? We’re not trying to achieve supraphysiologic levels, just to get into the high normal for T and low normal for E.

[quote]happydog48 wrote:
Hypothetical case:

Over 50 male with total T and E levels midrange of “normal” (T slightly below midpoint, E slightly above midpoint). Moderate symptoms of low T.

As I understand it, estradiol in men is produced directly in fat but is mainly produced by the conversion of T via aromatase. If this person were to use an aromatase inhibitor, would we expect E levels to drop and the HPTA to upregulate both T and aromatase production to compensate? If the AI were continued, could we then expect a net decrease in E and a net increase in T? After all, he is now producing T naturally, so what we’re really fighting are the HPTA “setpoints” for T and E. Do you think AI alone could achieve the goal of higher T and lower E? We’re not trying to achieve supraphysiologic levels, just to get into the high normal for T and low normal for E.[/quote]

You have described my exact situation except my E levels are much higher. I see a new doc in 10 days and will insist on AI or find a new doc. I expect the reduction of E will raise T overall in addition to FT.

[quote]happydog48 wrote:
Hypothetical case:

Over 50 male with total T and E levels midrange of “normal” (T slightly below midpoint, E slightly above midpoint). Moderate symptoms of low T.

As I understand it, estradiol in men is produced directly in fat but is mainly produced by the conversion of T via aromatase. If this person were to use an aromatase inhibitor, would we expect E levels to drop and the HPTA to upregulate both T and aromatase production to compensate? If the AI were continued, could we then expect a net decrease in E and a net increase in T? After all, he is now producing T naturally, so what we’re really fighting are the HPTA “setpoints” for T and E. Do you think AI alone could achieve the goal of higher T and lower E? We’re not trying to achieve supraphysiologic levels, just to get into the high normal for T and low normal for E.[/quote]

Yes, that is the expected outcome. SERMs can have the same actions, the E usually goes up, but the HPTA is blinded to the E by the SERM. But the SERMs can have some other estrogenic side effects and are not a good choice for long term use. But long term use of Nolvadex has been reported on this BB to increase T as an alternative to TRT.

Some E is produced in the testes as well. You can reduce fat, but not…

[quote]happydog48 wrote:
Hypothetical case:

Over 50 male with total T and E levels midrange of “normal” (T slightly below midpoint, E slightly above midpoint). Moderate symptoms of low T.

As I understand it, estradiol in men is produced directly in fat but is mainly produced by the conversion of T via aromatase. If this person were to use an aromatase inhibitor, would we expect E levels to drop and the HPTA to upregulate both T and aromatase production to compensate? If the AI were continued, could we then expect a net decrease in E and a net increase in T? After all, he is now producing T naturally, so what we’re really fighting are the HPTA “setpoints” for T and E. Do you think AI alone could achieve the goal of higher T and lower E? We’re not trying to achieve supraphysiologic levels, just to get into the high normal for T and low normal for E.[/quote]

Its never a good idea to use an AI as a T replacement therapy. Mainly because E’s effects on the brain are still not properly understood. Endocrine disrupters will be proven unnecessary. Not only that, driving E down will only cause a minimal increase in T.

[quote]V R wrote:
happydog48 wrote:
Hypothetical case:

Over 50 male with total T and E levels midrange of “normal” (T slightly below midpoint, E slightly above midpoint). Moderate symptoms of low T.

As I understand it, estradiol in men is produced directly in fat but is mainly produced by the conversion of T via aromatase. If this person were to use an aromatase inhibitor, would we expect E levels to drop and the HPTA to upregulate both T and aromatase production to compensate? If the AI were continued, could we then expect a net decrease in E and a net increase in T? After all, he is now producing T naturally, so what we’re really fighting are the HPTA “setpoints” for T and E. Do you think AI alone could achieve the goal of higher T and lower E? We’re not trying to achieve supraphysiologic levels, just to get into the high normal for T and low normal for E.

Its never a good idea to use an AI as a T replacement therapy. Mainly because E’s effects on the brain are still not properly understood. Endocrine disrupters will be proven unnecessary. Not only that, driving E down will only cause a minimal increase in T. [/quote]

The cost benefit ratio for some guys will lower T that do not qualify for TRT might be quite good. And for some that have E levels that interfere with T docking at receptors, the results might be quite good. Certainly better than supplements that claim to do such things. The way that we see guys on TRT benefiting from AI is also encouraging.

I just discovered a link from another thread that leads to a study that answers my question with very encouraging results, indeed!

Here’s the link:

http://jcem.endojournals.org/cgi/content/full/89/3/1174

The name of the study is:

Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels

Here’s the study group and what they were given:

“We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62 to 74 yrs) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14).”

The results were nothing short of amazing:

“Mean SD bioavailable testosterone increased from 99 + or - 31 to 207 + or - 65 ng/dl in group 1 and from 115 + or - 37 to 178 + or - 55 ng/dl in group 2”

“Total testosterone levels increased from 343 + or - 61 to 572 + or - 139 ng/dl in group 1 and from 397 + or - 106 to 520 + or - 91 ng/dl in group 2”

“Serum estradiol levels decreased from 26 + or - 8 to 17 + or - 6 pg/ml in group 1 and from 27 + or - 8 to 17 + or - 5 pg/ml in group 2”

“These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range.”

Clearly, anastrozole alone is a viable alternative to TRT for men who do not have access to conventional TRT therapy. I would have thought that 1mg/day was an excessive dosage, but this study would seem to indicate that it is not. I wouldn’t start that high, but it certainly gives me a new picture of the landscape, so to speak.

Thanks to mikandrea for the original link!

[quote]happydog48 wrote:
Clearly, anastrozole alone is a viable alternative to TRT for men who do not have access to conventional TRT therapy. I would have thought that 1mg/day was an excessive dosage, but this study would seem to indicate that it is not. I wouldn’t start that high, but it certainly gives me a new picture of the landscape, so to speak.

[/quote]

Very interesting post - thanks.

BTW - what dosage will you start with?

Arimidex/anastrozole is self limiting in effect. The results of the 1mg/day and 2mg/day were basically the same. I would expect that dosing smaller than 1mg/day would also be effective. Given the costs, that should be pursued.

[quote]KSman wrote:
Arimidex/anastrozole is self limiting in effect. The results of the 1mg/day and 2mg/day were basically the same. I would expect that dosing smaller than 1mg/day would also be effective. Given the costs, that should be pursued.[/quote]

Anastrozole comes in a liquid - correct? If so, is 1 ml equal to 1 mg in the research article?

Also, should you cycle it or not. If so, what are the recommended cycles? Thanks.

Apparently the well known expert Dr. Crisler doesn’t think much of AI alone as a TRT strategy:

"I occasionally hear of physicians trying to use a SERM (Selective Estrogen Receptor Modulator) such as Clomid or Nolvadex, or even an Aromatase Inhibitor (AI), such as Arimidex, as sole “TRT”.

All have been shown to elevate LH, and therefore Total Testosterone levels. However, patients report no long-term subjective benefits from these strategies, and the studies thus far reported no long-term changes in lean body mass, fatigue levels, libido, etc. An added risk of using an AI is of driving estrogen levels too low, with deleterious consequences for the lipid profile, calcium deposition, libido, etc."

[quote]KSman wrote:
Arimidex/anastrozole is self limiting in effect. The results of the 1mg/day and 2mg/day were basically the same. I would expect that dosing smaller than 1mg/day would also be effective. Given the costs, that should be pursued.[/quote]

If you look at the ratio of T to E between the 2 protocols they are not so similar. 1mg/day gives much better increase in ratio than 1mg 2xweek.

[quote]MichaelOH wrote:
KSman wrote:
Arimidex/anastrozole is self limiting in effect. The results of the 1mg/day and 2mg/day were basically the same. I would expect that dosing smaller than 1mg/day would also be effective. Given the costs, that should be pursued.

If you look at the ratio of T to E between the 2 protocols they are not so similar. 1mg/day gives much better increase in ratio than 1mg 2xweek.

[/quote]

Note that both groups 1&2 ended up with a final E level of 17. That is consistent with the diminishing non-linear dose-response for this drug. And that is good as it seems to do the right thing without any extreme effort of BW and adjustment.

Basically, if you take too much, the only harm is likely to be only the wasted cost. This is in contrast with letro that can really knock E levels down low enough to cause problems with libido and cholesterol. The other side of that coin is that taking 1/2 of a given dose will typicaly not make E bounce 1/2 back to where is was before.

I believe he is right as well. Getting E in check is only part of the problem. More often than not, its simply an issue of the testicals not producing enough T.

Yes, T receptors can be junked up with E, but if your only producing a small amount of T anyways, reducing E will help but needs to be in conjuction with added T.

[quote]happydog48 wrote:
Apparently the well known expert Dr. Crisler doesn’t think much of AI alone as a TRT strategy:

"I occasionally hear of physicians trying to use a SERM (Selective Estrogen Receptor Modulator) such as Clomid or Nolvadex, or even an Aromatase Inhibitor (AI), such as Arimidex, as sole “TRT”.

All have been shown to elevate LH, and therefore Total Testosterone levels. However, patients report no long-term subjective benefits from these strategies, and the studies thus far reported no long-term changes in lean body mass, fatigue levels, libido, etc. An added risk of using an AI is of driving estrogen levels too low, with deleterious consequences for the lipid profile, calcium deposition, libido, etc."

http://www.mesomorphosis.com/articles/crisler/testosterone-replacement-therapy.htm[/quote]

[quote]KSman wrote:
MichaelOH wrote:
KSman wrote:
Arimidex/anastrozole is self limiting in effect. The results of the 1mg/day and 2mg/day were basically the same. I would expect that dosing smaller than 1mg/day would also be effective. Given the costs, that should be pursued.

If you look at the ratio of T to E between the 2 protocols they are not so similar. 1mg/day gives much better increase in ratio than 1mg 2xweek.

Note that both groups 1&2 ended up with a final E level of 17. That is consistent with the diminishing non-linear dose-response for this drug. And that is good as it seems to do the right thing without any extreme effort of BW and adjustment.

Basically, if you take too much, the only harm is likely to be only the wasted cost. This is in contrast with letro that can really knock E levels down low enough to cause problems with libido and cholesterol. The other side of that coin is that taking 1/2 of a given dose will typicaly not make E bounce 1/2 back to where is was before.
[/quote]
E levels were the same but T increase was significantly better for the 1 mg/day group. Therefore T/E ratio rather higher.