Help me understand these 2 studies on adex vs aromasin

[Swolberham_Lincoln]

While researching clinical studies/trials in regards to estragen control I came across this study on adex and aromasin

https://www.ncbi.nlm.nih.gov/pubmed/14671195 -aromasin

This study was done on males 14-26 yrs old.
This study from my understanding says that there was not a significant difference between 25mg of 50mg of aromasin daily, in regards to estrogen control. Estrogen was decreased by 38% with 25mg/day and 32% with 50mg/day. This actually found that 25mg suppressed estrogen slightly better than 50mg! Right?
Half life is 9 hours. and after 12 hours of administration estragen was by 62% +/- 14% 12 hours after administration.

Test was raised by 60%
Lipids and igf levels were unaffected

Arimidex study https://www.ncbi.nlm.nih.gov/pubmed/10902781

This study was done on males age 15-22
This study from my understanding says that there is no significant difference between .5mg and 1mg daily. Both dosages lowered estrogen by 50%.
Testosterone increased by 58%
Igf levels decreased by 18%
There were no changes in bone density
Lipids were unaffected.

Conclusions:

So these studies lead me to believe that arimidex is better at suppressing e2 than aromasin (50%reduction for adex) (38% reduction for aromasin)

I've concluded that there is no advantage of 1mg/day over .5mg/day of adex. Same goes for 25 vs 50mg of aromasin.

Both raise testosterone by about 60%
Adex decreases igf by 18% while aromasin does not affect igf.
Blood lipids and bone composition was unaffected by either a.i.

Are my conclusions correct? Did I comprehend these studies correctly?

[numbere]

Arimidex is better for keeping e2 within range when using large amounts of exogenous test.

For normal doses of aromatizing compounds both arimidex and exemestane work sufficiently well.

You're conclusion that 0.5mg of arimidex has no advantage over 1.0mg of arimidex is incorrect.

To understand why you need to read the full study from which the abstract above was taken.

After being treated with either 0.5mg or 1.0mg of arimidex, both groups had sensitive estradiol readings of less than 3.0 pg/ml.

To put this in perspective the normal range for the tanner aged men tested is 10.0−36.0 pg/ml.

This means these males had extremely low e2.

The same procedure was followed using 3.0mg of arimidex and similar e2 levels were achieved.

Aromatase inhibition is dose dependent.

However, aromatase is less suppressed in the testis than adipose and muscle tissue.

This incomplete inhibition of aromatase is likely the cause for the low e2 results, and why the results weren't completely zero, in the above mentioned study.