Fun adventures with E2

[idmd]

Recap....

Scenario 1: Test + AI = E2 low with rock solid erections, crappy orgasms, no libido and tight nuts.

Scenario 2: Test with no AI = E2 in the 20-30 range, some libido, good but not great erections, still crappy orgasms and tight nuts

Scenario 3: Test with no AI and 250ui hCG every 3-4 days = E2 at 45, GREAT libido, GREAT orgasms, erections at 40% unless I jack it like a rabbit and nice low hanging nuts.

Seriously I've NEVER had ED issues EVER. So the trade off for me seems to be rock solid erections but sex that's just fine because my orgasm sucks and I feel 7 with tiny nuts or horny as shit with low hanging manly nuts and orgasms that almost make me pass out but I have to beat a half limp dick to do it?

Does an AI cross the blood-testicle barrier? Does it lower E2 driven by hCG?

 

[LW64]

Seriously I've NEVER had ED issues EVER.

You've also never had your E2 at 45 since you started TRT with an AI. Is that result in range, btw? (I'm betting it is.) What was your E2 before starting TRT?

Does an AI cross the blood-testicle barrier?

I dont know.

Does it lower E2 driven by hCG?

I dont know. But first you might try lowering the HCG dose to 100 IUs 2x/week or 250 IUs once a week.

 

[Michael Scally MD]

What I find interesting is you are apparently convinced this has to do with E2. I am still waiting for "A" study to show such evidence, particularly for E2 within the reference range.

 

[foreveryoung]

...

Does an AI cross the blood-testicle barrier? Does it lower E2 driven by hCG?

I've seen it theorized that letrozole might be different than arimidex in different tissues of the body, and I do notice better results from letrozole than arimidex seemingly without regard to dose response, so I am interested in some studies on this specific thing, so far we might just be guessing

I must say that letrozole does a whole lot more good for me than arimidex

 

[LW64]

What I find interesting is you are apparently convinced this has to do with E2. I am still waiting for "A" study to show such evidence, particularly for E2 within the reference range.

Based on my own experience and because he and I are both (IMO) E2 sensitive. Once I'm on IM T only (no AI) for 2 or 3 months, my E2 will drift up and over the top of the normal range and loss of morning wood and ED will kick in about a month before.

 

[biceps72]

I've seen it theorized that letrozole might be different than arimidex in different tissues of the body, and I do notice better results from letrozole than arimidex seemingly without regard to dose response, so I am interested in some studies on this specific thing, so far we might just be guessing

I must say that letrozole does a whole lot more good for me than arimidex

I guess I use letrozole?? I bought it from ADC. It definitely works and I have used the brand name armidex too; it works!!

Personally I hate using this stuff!! I use it very very sparingly. At 63 with more body fat than ever I need it because of androgel usage.

Life on TRT can be dammm complicated for us old guys who have low testosterone!!!

Not that it would matter but I wish I knew why my testosterone production crashed at 56? It definitely was not from steroid use/abuse!! I guess enviromental causes, agent orange exposure or football injury early in life (basically kicked in nuts) like a million other guys ????

 

[idmd]

What I find interesting is you are apparently convinced this has to do with E2. I am still waiting for "A" study to show such evidence, particularly for E2 within the reference range.

What I didn't say is I've been "playing" with this for the past few weeks. I've been using hCG for the past few weeks with no AI. I love the libido boost and full sensation of my testicles. I had my E2 tested and posted the result in the 40's. Last night I took 0.5mg arimidex.... today in the afternoon my erection is back at 90% and hopefully by tomorrow 100%.

While I can't be 100% sure I'm reasonably convinced E2 is the major issue here since all things being equal arimidex returns my erections back to 90%. I understand a legit published article would make this easier to swallow and my experience can't be generalized but based on my experience E2 seems to be the issue.

I believe I'm extremely sensitive to E2 and while still in the normal range I seem to have adverse side effects. While pure conjecture perhaps this is what precipitation my secondary hypogonadism in the first place - I'm extremely sensitive to E2? I may try and drive my E2 down even further just to see what the result is.....my guess is my erections will be back at 100%.

I'm assuming any AI I use is just killing the extra-gonadal E2 being aromatized in fat and that the hCG induced E2 is still being produced in my testicles.....any idea if AI's affect E2 produced by the testicles? Do they cross the testicle-blood barrier?

 

[Dr JIM]

Yea on spot DOC, Dadgum it seems I've been looking for years to locate ANY credible study whereupon a "low E-2" is even remotely associated with erectile dysfunction PROVIDING TT parameters are WNL, and that's no BS (bull-shit)

However the predominant acceptance of lowering E-2 "to much" causes ED is BS (bro-science) and IS NOT based on the literature.

(Considering the duration and commitment of those scientists evaluating "all cause" ED yet NADA has surfaced after more than FIFTY years of research is telling, IMO)

I have seen two articles which seemed to imply AI's themselves MAY have a REMOTE association (DOC posted one of those articles a while back) but nothing even suggestive hypoestrogenemia is an etiologic basis for the development of SD.

It is known that lowered E-2 has an adverse effect on lipids and musculoskeletal metabolism, but nothing more has been proven in MALES.

So what good is E-2 for mates?

Well not much since it decreases GnRH and LH secretion from the HTPA, suppresses testicular steroidal genesis and MAY compete with TT at androgen receptor sites. (E-2 has been shown to "bind" the AR yet the EFFECT of said attachment is essentially unknown)

Nonetheless to prevent complications from excessively depressed E-2,
I strongly suggest an E-2 maintenance level above 20 pg/ml and preferably closer to 40 pg/ml.

Finally since the lipid and
M-S metabolic complications require considerable time to develop MOST folks will not develop these adverse effects regardless of cycle content IF the duration is limited to no more than EIGHT-TWELVE WEEKS.

Dr Scally, what's your range preference or is the best value "that which is asymptomatic", IYO?

 

[idmd]

Yea on spot DOC, Dadgum it seems I've been looking for years to locate ANY credible study whereupon a "low E-2" is even remotely associated with erectile dysfunction PROVIDING TT parameters are WNL, and that's no BS (bull-shit)

However the predominant acceptance of lowering E-2 "to much" causes ED is BS (bro-science) and IS NOT based on the literature.

(Considering the duration and commitment of those scientists evaluating "all cause" ED yet NADA has surfaced after more than FIFTY years of research is telling, IMO)

I have seen two articles which seemed to imply AI's themselves MAY have a REMOTE association (DOC posted one of those articles a while back) but nothing even suggestive hypoestrogenemia is an etiologic basis for the development of SD.

It is known that lowered E-2 has an adverse effect on lipids and musculoskeletal metabolism, but nothing more has been proven in MALES.

So what good is E-2 for mates?

Well not much since it decreases GnRH and LH secretion from the HTPA, suppresses testicular steroidal genesis and MAY compete with TT at androgen receptor sites. (E-2 has been shown to "bind" the AR yet the EFFECT of said attachment is essentially unknown)

Nonetheless to prevent complications from excessively depressed E-2,
I strongly suggest an E-2 maintenance level above 20 pg/ml and preferably closer to 40 pg/ml.

Finally since the lipid and
M-S metabolic complications require considerable time to develop MOST folks will not develop these adverse effects regardless of cycle content IF the duration is limited to no more than EIGHT-TWELVE WEEKS.

Dr Scally, what's your range preference or is the best value "that which is asymptomatic", IYO?

But my experience is NOT that low E2 causes SD....quite the opposite in fact...undetectable to an E2 of 10-15 results in EXCELLENT erectile function (clubbing baby seal boners) but low libido and high normal E2 results in ED but excellent libido.

All things being equal I prefer the low E2 good boners but low libido since I can make the decision to have sex and as long as my boner cooperates I'm GTG.

FWIW....like I said decent research would make this easier to swallow but hypogonadism itself is the red headed step child of medicine and so just because no one has taken the time to give a shit about the role of E2 in male sexual function doesn't mean it doesn't have an effect.

There's a difference between something that has been exhaustively studied and "bro-science" that says something else vs something that has not been studied and the only data available is anecdotal "bro-science".

 

[LW64]

But my experience is NOT that low E2 causes SD....quite the opposite in fact...

Right. The problem here is increased E2 and it doesn't even have to be above the lab range to cause problems. [I think you will find - anecdotally, of course - that the common thread here among men who have this issue is low SHBG.]

If the issue for you is E2 induced reduction in erectile strength, then why do you prefer an AI to injecting more frequently? Or, just popping a PDE5-I instead?

How long does the 0.5 mg arimidex do its job before you have to take another?

 

[Dr JIM]

Well after 50 years of investigating all cause ED if E-2 was problematic and or causative rest assured SOME LINK would have been discovered by now.

I mean come on now idster it's not like E-2 was some recently detected hormone!

I contend the reason no association has been made between ED and E-2 (providing normalized Testosterone testing parameters exist) is because it simply doesn't exist, and fifty years of direct and indirect research is more than adequate IMO.

 

[idmd]

While not the best study ever 3 mins on Pubmed does show the concept isn't crazy.....

The relationships between sex hormones and sexual function in middle-aged and older European men.

AuthorsO'Connor DB, et al.
J Clin Endocrinol Metab. 2011 Oct;96(10):E1577-87. doi: 10.1210/jc.2010-2216. Epub 2011 Aug 17.

Abstract
CONTEXT: Limited data are available exploring the associations between sex hormones, multiple domains of sexual functioning, and sexual function-related distress in nonpatient samples in Europe.

OBJECTIVES: The aim of the study was to investigate the relationships between serum testosterone (T), estradiol (E2), and dihydrotestosterone (DHT) and sexual function in a multicenter population-based study of aging in men.

DESIGN: Using stratified random sampling, 2838 men aged 40-79 yr completed the European Male Ageing Study-Sexual Function Questionnaire and provided a blood sample for hormone measurements. T, E2, and DHT were measured using gas chromatography-mass spectrometry.

SETTING: We conducted a community-based population survey in eight European centers.

MAIN OUTCOME MEASURES: Self-reported sexual function (overall sexual function, sexual function-related distress, erectile dysfunction, masturbation) was measured.

RESULTS: Total and free T, but not E2 or DHT, was associated with overall sexual function in middle-aged and older men. E2 was the only hormone associated with sexual function-related distress such that higher levels were related to greater distress. Free T levels were associated with masturbation frequency and erectile dysfunction in the fully adjusted models, such that higher T was associated with less dysfunction and greater frequency. Moreover, there was a T threshold for the relationship between total T, sexual function, and erectile dysfunction. At T concentrations of 8 nmol/liter or less, T was associated with worse sexual functioning, whereas at T levels over 8 nmol/liter, the relationship came to a plateau.

CONCLUSIONS: These findings suggest that different hormonal mechanisms may regulate sexual functioning (T) vs. the psychological aspects (E2) of male sexual behavior. Moreover, there was a T threshold for overall sexual function such that at levels greater than 8 nmol/liter the relationship between T and sexual function did not become stronger.

 

[Michael Scally MD]

While not the best study ever 3 mins on Pubmed does show the concept isn't crazy.....

The relationships between sex hormones and sexual function in middle-aged and older European men.

AuthorsO'Connor DB, et al.
J Clin Endocrinol Metab. 2011 Oct;96(10):E1577-87. doi: 10.1210/jc.2010-2216. Epub 2011 Aug 17.

Abstract
CONTEXT: Limited data are available exploring the associations between sex hormones, multiple domains of sexual functioning, and sexual function-related distress in nonpatient samples in Europe.

OBJECTIVES: The aim of the study was to investigate the relationships between serum testosterone (T), estradiol (E2), and dihydrotestosterone (DHT) and sexual function in a multicenter population-based study of aging in men.

DESIGN: Using stratified random sampling, 2838 men aged 40-79 yr completed the European Male Ageing Study-Sexual Function Questionnaire and provided a blood sample for hormone measurements. T, E2, and DHT were measured using gas chromatography-mass spectrometry.

SETTING: We conducted a community-based population survey in eight European centers.

MAIN OUTCOME MEASURES: Self-reported sexual function (overall sexual function, sexual function-related distress, erectile dysfunction, masturbation) was measured.

RESULTS: Total and free T, but not E2 or DHT, was associated with overall sexual function in middle-aged and older men. E2 was the only hormone associated with sexual function-related distress such that higher levels were related to greater distress. Free T levels were associated with masturbation frequency and erectile dysfunction in the fully adjusted models, such that higher T was associated with less dysfunction and greater frequency. Moreover, there was a T threshold for the relationship between total T, sexual function, and erectile dysfunction. At T concentrations of 8 nmol/liter or less, T was associated with worse sexual functioning, whereas at T levels over 8 nmol/liter, the relationship came to a plateau.

CONCLUSIONS: These findings suggest that different hormonal mechanisms may regulate sexual functioning (T) vs. the psychological aspects (E2) of male sexual behavior. Moreover, there was a T threshold for overall sexual function such that at levels greater than 8 nmol/liter the relationship between T and sexual function did not become stronger.

And. how does this support your use?

 

[idmd]

They then go on to say, "E2 was the only hormone associated with sexual function-related distress such that higher levels were related to greater distress."

Did letting my E2 creep up cause frank and total ED? No, but my function is much better when E2 is lower. I've got decent serial labs showing rising E2 paralleling decreased erectile function. Too much of a coincidence that popping an AI relieves these symptoms.

 

[idmd]

If you thought the last article was shitty look out....

Testosterone:estradiol ratio changes associated with long-term tadalafil administration: a pilot study.

AuthorsGreco EA, et al. Show all Journal
J Sex Med. 2006 Jul;3(4):716-22.

Affiliation
Internal Medicine, Department of Medical Pathophysiology, University of Roma La Sapienza, Rome, Italy.

Abstract
INTRODUCTION: It has been reported that lack of sexual activity due to erectile dysfunction (ED) may be associated with testosterone (T) decline.

AIM: To investigate whether the known changes in sex hormones associated with resumption of sexual activity are sustained in the long term.

MAIN OUTCOME MEASURES: Primary endpoints were variations from baseline of steroid hormones: total T, free T (f T), and estradiol (E). Secondary endpoints were variations of erectile function domain scores at International Index of Erectile Function-5 (IIEF-5).

METHODS: In an open-label fashion, 20 patients (mean age 54.8 +/- 8.4 years) received tadalafil 10-20 mg on demand for 12 months. Exclusion criteria were those reported for phosphodiesterase inhibitors, including hypogonadism and hyperprolactinemia.

RESULTS: Tadalafil assumption was safe and well tolerated (overall adverse effects in 15% of patients) and none discontinued medication. A significant decrease in E levels occurred at the end of the study (from 19.9 +/- 9.6 to 16.6 +/- 8.1 ng/dL, P = 0.042 vs. baseline), with parallel increase in the T:E ratio (26.3 +/- 15.3 to 32.6 +/- 17.7, P = 0.05), whereas no changes in T and f T serum levels were observed, respectively (411.4 +/- 131.4 to 434.2 +/- 177.1 ng/dL and 47.7 +/- 15.3 to 49.9 +/- 19.1 pmol/L, not significant). Interestingly, nonparametric subgroup analysis for related samples revealed that E decrease was detectable only in lean (N = 14) but not in obese (N = 6, body mass index > 27.5 kg/m2) subjects (17.8 +/- 10.1 vs. 13.5 +/- 6.8, P < 0.05). A net increase in IIEF-5 scores was observed at the endpoint (13.7 +/- 5.9 vs. 25.7 +/- 2.9, P < 0.0001).

CONCLUSIONS: Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil might have a role in the regulation of erectile function.

 

[Michael Scally MD]

They then go on to say, "E2 was the only hormone associated with sexual function-related distress such that higher levels were related to greater distress."

Did letting my E2 creep up cause frank and total ED? No, but my function is much better when E2 is lower. I've got decent serial labs showing rising E2 paralleling decreased erectile function. Too much of a coincidence that popping an AI relieves these symptoms.

Not sexual function!

You have finally taken the bait! Post hoc ergo propter hoc [ame=http://en.wikipedia.org/wiki/Post_hoc_ergo_propter_hoc]Post hoc ergo propter hoc - Wikipedia, the free encyclopedia[/ame]

It is of no use debating since your evidence trumps all other. Welcome to bro lore. LOL

Oh, we will forget all of the contrary published evidence.

 

[idmd]

You have finally taken the bait! Post hoc ergo propter hoc Post hoc ergo propter hoc - Wikipedia, the free encyclopedia

Look I'm not trying to "win" an argument here....simply sharing one person's completely anecdotal experience which I think can not and should not be generalized. My purpose is simply to stimulate conversation and debate.

You tell me I'm just crazy....perhaps. While I believe in evidence-based medicine there are still gaps in our knowledge and from what I can tell the role of E2 in male sexual function/dysfunction is not well characterized.

 

[idmd]

Please define sexual-function related distress for me because to be honest I'm having sexual-function related distress

 

[idmd]

It is of no use debating since your evidence trumps all other. Welcome to bro lore. LOL

Oh, we will forget all of the contrary published evidence.

Not fair DOC....just reporting my experience and stimulating discussion. What I'm really looking for is the evidence either way. As best I can tell there isn't a wealth of evidence supporting the role of normal/high-normal E2 and SD but I also haven't seen conclusive evidence it has no effect.

Hint DOC....this isn't me taking a stand on this topic...I'm in no position to do so - it's me asking for help/more information.

 

[dogheat]

Men who function better on low e2 usually have low shbg.