High Estradiol in Men: Article that Fueled Hysteria

JimBob

Active Member
Thread starter #1
I'm looking for a Life Extension article on estradiol that has been criticized as being flawed in its conclusions. A Search didn't bring it up. Any help? I want to show it to my FNP.

I'm referring to something Nelson posted here:

Role of Estradiol in Men and Its Management

"Not one study has looked at the effect of estradiol on cardiovascular, edema, erectile function, gynecomastia incidence and mood in men on TRT with TT levels above 500 ng/ml. NOT ONE. I am not saying high estradiol is not a problem. What I am saying is that men with higher TT can accommodate more estradiol than men with low TT. Using the same upper limit for both populations makes no sense at all unless proven by a study. The Life Extension article that started this craze plus our preconceived judgment of a "female" hormone has not served us well in this field."
 
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#3
Are you talking about the 3 page article? It was pretty lengthy and packed full of info. I’m pretty sure it was posted in one of the E2 threads that got out of control and then locked down.
 

JimBob

Active Member
Thread starter #5
I'm referring to something Nelson posted here:

Role of Estradiol in Men and Its Management

"Not one study has looked at the effect of estradiol on cardiovascular, edema, erectile function, gynecomastia incidence and mood in men on TRT with TT levels above 500 ng/ml. NOT ONE. I am not saying high estradiol is not a problem. What I am saying is that men with higher TT can accommodate more estradiol than men with low TT. Using the same upper limit for both populations makes no sense at all unless proven by a study. The Life Extension article that started this craze plus our preconceived judgment of a "female" hormone has not served us well in this field."
 
#8
The cliff note here is a testosterone deficiency is creating estrogen dominance in men is what is believed to increase the risk of cardiac events, not high estrogen as the sole cause of cardiac events.

Using the wrong estrogen testing in men who more than likely have inflammation
(C-reactive protein) is another area of concern as Vince Carter points out.

There are a ton of junk studies out there and must be validated before leading people and doctors down the wrong path.
 
#9
LEF can't even convince itself that it uses the wrong E testing for males
Hey @Vince Carter, can you share the specifics you are referring to? I have not delved into all the LEF info. What wrong methodology are they using and what do you consider the correct methodology?

Edit: The three I am aware of are ECLIA. LC/MS/MS and seemingy your favorite for your personal circumstances; Free estradiol

Thanks,
 
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#10
The cliff note here is a testosterone deficiency is creating estrogen dominance in men is what is believed to increase the risk of cardiac events, not high estrogen as the sole cause of cardiac events.

Using the wrong estrogen testing in men who more than likely have inflammation
(C-reactive protein) is another area of concern as Vince Carter points out.

There are a ton of junk studies out there and must be validated before leading people and doctors down the wrong path.
IMO it's really marketing to call the sensitive E2 a "male" test because that isn't really what it is.

Females who are menopausal also have low E2, and they are just as likely to have higher C-reactive protein as men. They should also get the sensitive test.

And if I have low C-reactive protein levels then either E2 test should give the same results for me. I can see where LEF is coming from, though both those for and against this seem overly dogmatic about the issue. To me it's not as big a deal as most make it.

Bottom line, it's not an important issue for me as the sensitive test can be bought for reasonable prices Vs the regular E2 test, so if Defy wants the sensitive test, it's a big shrug for me.
 
#13
This seems like splitting semantic hairs.

Is it not appropriate in general to call LC/MS/MS more appropriate for men than ECLIA ?
I think it;s more appropriate in general to call LC/MS/MS better for any individual with lower E2 and or with high c-reactive protein.

Can anyone explain why women with low E2 and higher c-reactive protein should NOT take the LC/MS/MS version of the test?

Also, doesn't it seem a pointless test in those men that contend HIGH E2 is preferable for them, meaning higher than 50, why not take the typical "women's" test? At that point of E2 level, they aren't any different (regarding E2) than women in their Follicular phase 12.5 - 166.0 or Luteal phase 43.8 - 211.0.


Also, it seems little complicated by the reports there is more erroneous variation in LC/MS/MS than in ECLIA testing.

But all I am saying, I see both sides have some justification for their position.
 

JimBob

Active Member
Thread starter #15
@JimBob

The argument is made here. Watch this and you will understand the criticism of e2 studies in men.

Thanks, but that is not what I'm looking for. By the way, I've already listened to the whole video months ago.

Last time, I'm looking for the particular LE article referred to by Nelson.
 

Nelson Vergel

Founder, ExcelMale.com
#16
This is the study mentioned in the LEF article that fed the hysteria that was already in bodybuilding forums:

STUDY LOOKING AT EFFECT OF ESTRADIOL ON MORTALITY IN MEN:

Weakness of this study: Men who were older, sicker and with average T of 325 ng/dL. Can these results be extrapolated for men with higher T who are younger and healthier? I doubt it. Unless we follow T/E2 ratios, we can't conclude much from these data.

This study found that estradiol levels of < 21.80 pg/ml and > 30.11 pg/ml resulted in greater mortality in men.


Abstract

CONTEXT:

Androgen deficiency is common in men with chronic heart failure (HF) and is associated with increased morbidity and mortality. Estrogens are formed by the aromatization of androgens; therefore, abnormal estrogen metabolism would be anticipated in HF.


OBJECTIVE:

To examine the relationship between serum concentration of estradiol and mortality in men with chronic HF and reduced left ventricular ejection fraction (LVEF).


DESIGN, SETTING, AND PARTICIPANTS:

A prospective observational study at 2 tertiary cardiology centers (Wroclaw and Zabrze, Poland) of 501 men (mean [SD] age, 58 [12] years) with chronic HF, LVEF of 28% (SD, 8%), and New York Heart Association [NYHA] classes 1, 2, 3, and 4 of 52, 231, 181, and 37, respectively, who were recruited between January 1, 2002, and May 31, 2006. The cohort was divided into quintiles of serum estradiol

quintile 1, < 12.90 pg/mL;
quintile 2, 12.90-21.79 pg/mL;
quintile 3, 21.80-30.11 pg/mL;
quintile 4, 30.12-37.39 pg/mL;
and quintile 5, > or = 37.40 pg/mL.

Quintile 3 was considered prospectively as the reference group.


MAIN OUTCOME MEASURES:

Serum concentrations of estradiol and androgens (total testosterone and dehydroepiandrosterone sulfate [DHEA-S]) were measured using immunoassays.


RESULTS:

Among 501 men with chronic HF, 171 deaths (34%) occurred during the 3-year follow-up. Compared with quintile 3, men in the lowest and highest estradiol quintiles had increased mortality (adjusted hazard ratio [HR], 4.17; 95% confidence interval [CI], 2.33-7.45 and HR, 2.33; 95% CI, 1.30-4.18; respectively; P < .001). These 2 quintiles had different clinical characteristics (quintile 1: increased serum total testosterone, decreased serum DHEA-S, advanced NYHA class, impaired renal function, and decreased total fat tissue mass; and quintile 5: increased serum bilirubin and liver enzymes, and decreased serum sodium; all P < .05 vs quintile 3). For increasing estradiol quintiles, 3-year survival rates adjusted for clinical variables and androgens were 44.6% (95% CI, 24.4%-63.0%), 65.8% (95% CI, 47.3%-79.2%), 82.4% (95% CI, 69.4%-90.2%), 79.0% (95% CI, 65.5%-87.6%), and 63.6% (95% CI, 46.6%-76.5%); respectively (P < .001).

Reference:

Circulating estradiol and mortality in men with systolic chronic heart failure.
JAMA 2009 May 13;301(18):1892-901.

Estradiol and Mortality in Men with Heart Disease.jpg
 
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