Mr. Walkaway's finding again gives us incentive to update our knowledge base and not feel our initial indoctrinating is all encompassing. I didn't just read an hour for nothing so I'll post some of what I found:
...study which showed an increase in the absorption of exemestane of 40% when taken with fats.
...it takes time for the body to produce new aromatase- so its effective time is much longer than the half life indicates.
...it seems to be forgiving in the area of eliminating all estrogen - even at 50mg/day with no exogenous test - the e levels were low but still in reference range. (we need some estrogen)
...no changes in circulating serum triglycerides, cholesterol, or LDL or HDL cholesterol concentrations with either a 25mg or 50mg daily dose of exemestane.
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 Blood was withdrawn before and 24 h after the last dose of each treatment period.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.
... also BIG difference between aromasin / exemestane and arimidex / anastrozol:
There was an increase in circulating testosterone concentrations after both 25 mg (60 + 58%; P = 0.001) and 50 mg (56 48%; P = 0.003) exemestane. Androstenedione concentrations were increased as well after 25 mg (32 Ã?Â± 36%; P = 0.004) and 50 mg (47 59%; P = 0.052) exemestane, respectively (Fig. 1Go and Table 2Go).
SHBG concentrations were decreased by 217% (P = 0.0003) and 19 39% (P = 0.18) at 25 and 50 mg exemestane, respectively.
Free testosterone concentrations were increased by 117 74% (P = 0.0001) and 154 95% (P < 0.0001) at both doses, due to the decrease in SHBG and the increase in total testosterone.