Aromasin Study (on men)...Effects on Lipid Profile and IGF-1

[Jenetic]

I've seen a lot of questions on Aromasin lately. This study on men should clearify the issues.

Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males

Nelly Mauras, John Lima, Deval Patel, Annie Rini, Enrico di Salle, Ambrose Kwok and Barbara Lippe

Nemours Children’s Clinic and Research Programs (N.M., J.L., A.R.), Jacksonville, Florida 32207; and University of Florida Health Sciences Center (D.P.) and Amersham Pharmacia Biotech (E.d.S., A.K., B.L.), Peapack, New Jersey 07977


Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14–26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P 0.002); 50 mg, 32% (P 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 ± 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.


Abbreviations: AUC, Area under the curve; CBC, cell blood count; HDL, high density lipoprotein; LDL, low density lipoprotein; PK, pharmacokinetic.

 

[lartinos]

i love this stuff......wouldn't use anything else

 

[Guvna]

good post. k to ya.

 

[Goodfellow]

great

 

[b1ewsw32]

Great read dude!.....Check your PM's

B32

 

[bicepts101]

i know what ill be using next cycle...ldex doesnt work for me

 

[b1ewsw32]

I was just wondering? Since I know that Aromasin is a irreversible aromatase inhibitor(suicidal) and that new enzymes are formed eventually. Is it possible that with some kind of dysfunction/disposition that you could permanently supress conversion of T to E due to irreversible death of the aromatase enzymes.Similar to the need for HRT because of decreased sensitivity of the Leydig cells due to age or AAS abuse or possibly compromised piuitary or hypothalamus efficiency.
Would you have to take ERT. lol. or is the estrogen from the adrenal glands. ie. cholesterol>pregnenolone>DHEA>estrogen+testosterone be sufficient.

Jenetic,Huck,Ulter,Fonz or any member with experience or reasonable hypothesis please let me know what you think. Thanks.

B32

 

[ketogenic]

I believe its an aromatase inactavor not inhibitor. femara and arimidex are inhibitors.
keto

 

[brianzganjar]

I was just wondering? Since I know that Aromasin is a irreversible aromatase inhibitor(suicidal) and that new enzymes are formed eventually. Is it possible that with some kind of dysfunction/disposition that you could permanently supress conversion of T to E due to irreversible death of the aromatase enzymes.Similar to the need for HRT because of decreased sensitivity of the Leydig cells due to age or AAS abuse or possibly compromised piuitary or hypothalamus efficiency.
Would you have to take ERT. lol. or is the estrogen from the adrenal glands. ie. cholesterol>pregnenolone>DHEA>estrogen+testosterone be sufficient.

Jenetic,Huck,Ulter,Fonz or any member with experience or reasonable hypothesis please let me know what you think. Thanks.

B32

Aromasin binds to the aromatase protein molecule only, resulting in a distortion in its tree dimensional structure and it can no longer catalyze the conversion. It will not alter production of the enzyme. One would not ever have to go on ERT even if there were no aromatase production whatsoever. In elderly men with serum test levels <350 ng administration of arimidex increased test levels to youthful levels as you would expect but also estradiol levels remained in the normal male range despite total aromatase inactivity.


Leder BZ, Rohrer JL, Rubin SD, et al.
Effects of aromatase inhibition in elderly men with low or borderline-low serum testosterone levels.
J Clin Endocrinol Metab (United States), Mar 2004, 89(3) p1174-80

Concern over estradiol levels in genuine as you know due to the significant lipid abnormalities that occur and their subsequent acute affects on the liver which is often overly taxed to begin with.

 

[Jenetic]

Aromasin binds to the aromatase protein molecule only, resulting in a distortion in its tree dimensional structure and it can no longer catalyze the conversion. It will not alter production of the enzyme. One would not ever have to go on ERT even if there were no aromatase production whatsoever.

The first statement would make sense due to the fact that the CYP19 gene resposible for production of the P450 aromatase is unaffected, therefore it would not affect the production of the aromatase enzyme. A direct mutation of the CYP19 gene would be necessary for a loss in production to occur.

But to say that ERT would not be needed if the P450 aromatase was not in production whatsoever does not make much sense due to the fact that, in males, estrogens derive from circulating androgens. Aromatization of the C19 androgens, testosterone and androstenedione, to form estradiol and estrone, respectively, is the key step in estrogen biosynthesis, which is under the control of the aromatase enzyme.