Testosterone/Estradiol Ratio

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Larry B

New Member
I've been on anastrozole for 11 years. I believe since I started, science has evolved and lowering estradiol down into the 25 pg/mL range is no longer desirable as I have been told to do by my doctor all these years. Recently I've read more and more that estradiol should not be that low in men.

I always kept it low for fear of gynecomastia, fat accumulation, ED and libido but now read the opposite may be true. A few years ago I developed terrible tendinitis and now I believe it may have been associated with low estradiol. Is there a testosterone to estradiol ratio for men? Recent research has led me to believe that if one has a high testosterone level their estradiol level can and should be above the high level of normal on the Labcorp and Quest test values. Basically the higher the testosterone level the higher the estradiol level can and should be.

Does anyone know what men with naturally high levels of testosterone have for an estradiol level? I found this ratio calculator but not sure exactly what it means. My total testosterone on my last blood draw was 845 ng/dL and my estradiol was 32.2 pg/mL. It appears those are two different units of measure. Can anyone tell me based on my numbers if my ratio is in a good range? Also, what is considered a good ratio?

 
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One way to consider the ratio is as the fraction of testosterone that is converted to estradiol. Typically this ranges from around 0.3 to 0.6%. The calculation is performed by dividing estradiol in pg/mL by 10 to convert to ng/dL, and then dividing this result by total testosterone in ng/dL. It's also common to consider a T:E2 ratio, which directly divides total testosterone in ng/dL by estradiol in pg/mL. The normal range then becomes about 16-30.

There is evidence that elevated estradiol in the presence of low testosterone is harmful. However, I don't view this as a green light to sky-high estradiol when accompanied by similarly high testosterone. It's still quite possible that high absolute levels of estradiol are problematic in some ways. The obvious solution is to maintain testosterone at a level that yields normal estradiol—after all, our bodies naturally regulate testosterone mainly by the level of (free) estradiol. The exception is when aromatization is excessive, i.e. causing an E2:T ratio above a normal range and seeming to cause symptoms. Ideally the aromatization rate would be decreased naturally, such as through weight loss. But this isn't always possible.

Looking at the specific numbers you gave, estradiol is 0.38% of testosterone, and the T:E2 ratio is 26. This implies aromatization is a little below average. It would be unremarkable if it occurred naturally, but as you note, there is increasing concern about the long-term consequences of skewing the ratio via aromatase inhibition. As I said in the other thread, you have room for a significant testosterone dose reduction, so in the long run you may be able to manage estradiol appropriately without using an AI. Keep in mind that a temporary excess of aromatization is possible after non-suicidal AIs—such as anastrozole—are discontinued.
 
One way to consider the ratio is as the fraction of testosterone that is converted to estradiol. Typically this ranges from around 0.3 to 0.6%. The calculation is performed by dividing estradiol in pg/mL by 10 to convert to ng/dL, and then dividing this result by total testosterone in ng/dL. It's also common to consider a T:E2 ratio, which directly divides total testosterone in ng/dL by estradiol in pg/mL. The normal range then becomes about 16-30.

There is evidence that elevated estradiol in the presence of low testosterone is harmful. However, I don't view this as a green light to sky-high estradiol when accompanied by similarly high testosterone. It's still quite possible that high absolute levels of estradiol are problematic in some ways. The obvious solution is to maintain testosterone at a level that yields normal estradiol—after all, our bodies naturally regulate testosterone mainly by the level of (free) estradiol. The exception is when aromatization is excessive, i.e. causing an E2:T ratio above a normal range and seeming to cause symptoms. Ideally the aromatization rate would be decreased naturally, such as through weight loss. But this isn't always possible.

Looking at the specific numbers you gave, estradiol is 0.38% of testosterone, and the T:E2 ratio is 26. This implies aromatization is a little below average. It would be unremarkable if it occurred naturally, but as you note, there is increasing concern about the long-term consequences of skewing the ratio via aromatase inhibition. As I said in the other thread, you have room for a significant testosterone dose reduction, so in the long run you may be able to manage estradiol appropriately without using an AI. Keep in mind that a temporary excess of aromatization is possible after non-suicidal AIs—such as anastrozole—are discontinued.
Thank you for your reply! From your formula it sounds like I'm in range with a ratio of 26. I am going to cut back slightly on the amount of testosterone since the amount of .31 ml twice a week has given a level of 845.
 
I found this concerning Estradiol.

  • When researchers monitored the estrogen levels of 501 men with chronic heart failure, men with estradiol (the most "potent" form of estrogen) in the normal range (between 21.80 pg/ml and 30.11 pg/ml) had the fewest deaths during a three-year period. Men with the highest levels (above 37.99) had 133 percent more deaths during the same period. However, the men with the lowest estrogen levels (below 12.90) fared the worst as they experienced 317% more deaths.

    Here's a list of the median estradiol levels by age, as established by the authors of a study that appeared in the journal Clinical Endocrinology:
    • Age 2-29: 28.0 pg/ml
    • Age 30-39: 25.7 pg/ml
    • Age 40-49: 24.7 pg/ml
    • Age 50-59: 22.1 pg/ml
    • Age 60-69: 21.5 pg/ml
    • Age 70-80: 21.9 pg/ml
    Furthermore, as you get older, SHBG levels rise and bind up more hormone, so while estrogen levels might appear "normal," your amount of "free" estrogen might be too low. Ideally, both SHBG and estrogen blood levels should fall in the mid-range of normal values so that you can get an actual snapshot of your estrogen situation.



 
One way to consider the ratio is as the fraction of testosterone that is converted to estradiol. Typically this ranges from around 0.3 to 0.6%. The calculation is performed by dividing estradiol in pg/mL by 10 to convert to ng/dL, and then dividing this result by total testosterone in ng/dL. It's also common to consider a T:E2 ratio, which directly divides total testosterone in ng/dL by estradiol in pg/mL. The normal range then becomes about 16-30.

There is evidence that elevated estradiol in the presence of low testosterone is harmful. However, I don't view this as a green light to sky-high estradiol when accompanied by similarly high testosterone. It's still quite possible that high absolute levels of estradiol are problematic in some ways. The obvious solution is to maintain testosterone at a level that yields normal estradiol—after all, our bodies naturally regulate testosterone mainly by the level of (free) estradiol. The exception is when aromatization is excessive, i.e. causing an E2:T ratio above a normal range and seeming to cause symptoms. Ideally the aromatization rate would be decreased naturally, such as through weight loss. But this isn't always possible.

Looking at the specific numbers you gave, estradiol is 0.38% of testosterone, and the T:E2 ratio is 26. This implies aromatization is a little below average. It would be unremarkable if it occurred naturally, but as you note, there is increasing concern about the long-term consequences of skewing the ratio via aromatase inhibition. As I said in the other thread, you have room for a significant testosterone dose reduction, so in the long run you may be able to manage estradiol appropriately without using an AI. Keep in mind that a temporary excess of aromatization is possible after non-suicidal AIs—such as anastrozole—are discontinued.
Do u take anything to manage E2?
 
I found this concerning Estradiol.

  • When researchers monitored the estrogen levels of 501 men with chronic heart failure, men with estradiol (the most "potent" form of estrogen) in the normal range (between 21.80 pg/ml and 30.11 pg/ml) had the fewest deaths during a three-year period. Men with the highest levels (above 37.99) had 133 percent more deaths during the same period. However, the men with the lowest estrogen levels (below 12.90) fared the worst as they experienced 317% more deaths.
    ...

A concern about the underlying study is that it used a standard immunoassay test to measure estradiol. If C-reactive protein was able to inflate the measurements then the conclusions cannot be trusted.

Do u take anything to manage E2?
Not currently, though I have experimented with anastrozole in the past. I generally lowered estradiol from 50s to 30s pg/mL. The only effect I'm pretty sure about is a reduction in the emotional responsiveness seen at higher levels of estradiol.
 
A concern about the underlying study is that it used a standard immunoassay test to measure estradiol. If C-reactive protein was able to inflate the measurements then the conclusions cannot be trusted.


Not currently, though I have experimented with anastrozole in the past. I generally lowered estradiol from 50s to 30s pg/mL. The only effect I'm pretty sure about is a reduction in the emotional responsiveness seen at higher levels of estradiol.
What dose of anastrozole did u take to get u from 50’s to 30’s?
 
Based on no medical education whatsoever - but a few years of sticking myself with needles and rubbing cream in odd places - I sometimes wonder if it might be a better approach to tune in E2 to just below top of the range (without AIs) and let TT/FT be wherever they may be based on that.

We go about it the opposite way.
 
Based on no medical education whatsoever - but a few years of sticking myself with needles and rubbing cream in odd places - I sometimes wonder if it might be a better approach to tune in E2 to just below top of the range (without AIs) and let TT/FT be wherever they may be based on that.

We go about it the opposite way.
Roughly what number would the top of the range for E2 be?
 
... I sometimes wonder if it might be a better approach to tune in E2 to just below top of the range (without AIs) and let TT/FT be wherever they may be based on that.
...
It's a reasonable idea except for the "top of range" part. With most parameters we measure we find that bad things, such as higher mortality, are linked to higher and lower levels. Why give testosterone and estradiol a few pass? Maybe the better approach is to put estradiol in the middle of the healthy-young-man range. This could be around 30 pg/mL according to some data.
 
It's a reasonable idea except for the "top of range" part. With most parameters we measure we find that bad things, such as higher mortality, are linked to higher and lower levels. Why give testosterone and estradiol a few pass? Maybe the better approach is to put estradiol in the middle of the healthy-young-man range. This could be around 30 pg/mL according to some data.
Exactly. Everything in the human body needs to be in balance. It wouldn’t make sense if there was one or two hormones that didn’t have to abide by this

Do you personally manage ur E2 with something other than just adjusting ur dose and/ or frequency of injections? If so, what do u do to keep it in range? And do u personally have an E2 range that works for u?
 
...
Do you personally manage ur E2 with something other than just adjusting ur dose and/ or frequency of injections? If so, what do u do to keep it in range? And do u personally have an E2 range that works for u?
More recently I've been letting estradiol do what it wants in response to realistic testosterone dosing—with daily peak T at 600-800 ng/dL. My natural aromatization rate seems to be about 0.5%. This is the average I measure with only testosterone injections. When hCG is in the protocol the average E2/T jumps to 0.75%. When an AI is used with the hCG then the ratio drops back to 0.5%, though there's a large standard deviation in these latter measurements.
 
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More recently I've been letting estradiol do it wants in response to realistic testosterone dosing—with daily peak T at 600-800 ng/dL. My natural aromatization rate seems to be about 0.5%. This is the average I measure with only testosterone injections. When hCG is in the protocol the average E2/T jumps to 0.75%. When an AI is used with the hCG then the ratio drops back to 0.5%, though there's a large standard deviation in these latter measurements.

My E2 aromatization rate is low, often ~0.25%, the only time it got to 5.7% was when I took clomid.

I speculate that for those of us with a naturally low aromatization rate we tend to have more E2 receptors or are more sensitive to E2 as compensation.
 
More recently I've been letting estradiol do it wants in response to realistic testosterone dosing—with daily peak T at 600-800 ng/dL. My natural aromatization rate seems to be about 0.5%. This is the average I measure with only testosterone injections. When hCG is in the protocol the average E2/T jumps to 0.75%. When an AI is used with the hCG then the ratio drops back to 0.5%, though there's a large standard deviation in these latter measurements.
Are u currently using HCG?

What’s ur personal reasons for using HCG?

What dose of ai did u use to bring down ur E2 while on HCG?
 
Are u currently using HCG?

What’s ur personal reasons for using HCG?

What dose of ai did u use to bring down ur E2 while on HCG?
I haven't used hCG for about a year now. HCG was useful for reversing testicular atrophy, and it also helped some with libido. But for me that influence on estradiol seems to throw things out of balance, and I'm happy to be making my own LH now instead. As I mentioned previously, when I used an AI it was typically about a quarter milligram of anastrozole spread out over each week.
 
Beyond Testosterone Book by Nelson Vergel
(a) 17‐α‐estradiol (17aE2) is a relatively “non‐feminizing” estrogen which shows reduced activation of classical estrogen receptors compared with 17‐β‐estradiol (Anstead et al., 1997). Harrison et al. (2014) reported that in UM‐HET3 mice fed 4.8 mg 17aE2/kg (4.8 ppm) diet from 10 months of age, median male lifespans increased 12% (p = 0.0012, pooled across the three sites), while 17aE2 did not alter female lifespan. Strong et al. (2016) showed that using a threefold higher dose (14.4 ppm) from 10 months of age, pooled median male lifespans increased 19% (p < 0.001); the 90% lifespan increased 12%, but females still did not benefit. Thus, only males were tested in the present study. To determine whether 17aE2 treatment is effective when initiated in older mice, males were treated beginning at 16 or 20 months of age, choosing middle age, and early old age before many natural deaths.
 
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