MR10X

Originally Posted by Mr.BB

There are studies in which they give 1mg daily to men, im in mobile out of town, cant pull the link.
They never mention the low e2 simptoms that ramdomly appears here in forum.

My opinion, some peeps are ultrasensitive to low e2, but only a very small %%. Many times low e2 is confused with other conditions IMO

These study were done with men not taking AAS,if you use AAS then your E2 will rise even more so you will need a higher dose of AI…If your using more than 500mg of test a week you will need a higher dose of AI,below that you might not need any,only a blood test will confirm that……Doubling the dose doesn’t double the response to lowering E2,you can see in the studys that 50mg wasnt much different than 25 mg daily of Aromasin ..You can crash your E2 with letro dose for dose compared to Adex and Aromasin but its much more potent and requires a lot lower dose…I did 2.5 mg a day of letro trying to get rid of a little gyno i had for a long time and it totally killed my libido to where even cialis wouldn’t do me any good…

arimidex – Anastrozole

Type-II Aromatase Inhibitor

Arimidex binds reversibly to the aromatase enzyme through competitive inhibition. This suppresses the conversion of androgens into estrogen. Circulating plasma estrogen can be reduced by nearly 85% in women using Arimidex. A common misconception is that aromatase inhibition is similar in men and women.

However in trials when males were merQistered 1mg of Arimidex daily, circulating estrogen was only reduced by about 50%. Anastrozole is rapidly absorbed orally (time to reach maximum concentration, 1 hour) with a slow apparent clearance of 1.54 liters/h and a terminal half-life of 46.8 h.

aromasin

Study I: dose finding
Two different doses of exemestane (Aromasin, 25-mg tablets) were merQistered orally in random order for 10 d with a 14-d washout in between. Twelve subjects were divided into 2 groups (treatment sequences): group I received 25 mg in period 1 and 50 mg in period 2, and group II received 50 mg in period 1 and 25 mg in period 2. Blood was withdrawn in the morning, between 0800–0900 h at the beginning of each treatment cycle and 24 h after the last dose of each treatment cycle (4 blood draws) for various pharmacodynamic assays. These included estradiol, estrone, estrone sulfate, androstenedione, testosterone , free testosterone, dehydroepiandrosterone sulfate, cortisol, SHRonin, IGF-I, IGF-binding protein-3, and plasma lipid profiles [triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, and low density lipoprotein (LDL) cholesterol]. Safety data, including general chemistries, cell blood count (CBC), urinalysis, and liver profiles, were measured as well. All adverse events were recorded.
Study I: dose finding
Analysis of the data on hormone concentrations after the 25- and 50-mg doses showed no difference in any of the parameters measured due to an order effect; hence, the data were grouped for analysis by dose. The 25- and 50-mg doses of daily exemestane had comparable effects in suppressing circulating estrogen concentrations, with 38 ± 24% (mean ± sd; P = 0.002 vs. baseline) and 32 ± 29% (P = 0.008) decreases in estradiol concentrations, 71 ± 12% (P < 0.0001) and 74 ± 12% (P < 0.0001) decreases in estrone concentrations, and 45 ± 27% (P = 0.004) and 51 ± 20% (P = 0.02) decreases in estrone sulfate concentrations after doses of 25 and 50 mg, respectively. 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 ± 36%; P = 0.004) and 50 mg (47 ± 59%; P = 0.052) exemestane, respectively (Fig. 1 and Table 2). SHRonin concentrations were decreased by 21 ± 7% (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 SHRonin and the increase in total testosterone. No effect on circulating dehydroepiandrosterone sulfate was observed at either dose. Serum cortisol concentrations increased significantly (38 ± 39%; P = 0.008) with the 25-mg dose, but not the 50-mg dose, yet the increase was well within the normal range of cortisol concentrations. Plasma IGF-I decreased significantly (−13 ± 11%; P = 0.008) after the 25-mg dose, but not the 50-mg dose. Similarly, IGF-binding protein-3 showed a trend toward lower concentrations after the 25-mg dose (−7 ± 13%; P = 0.09), but not the 50-mg dose. There were no changes in circulating serum triglycerides, cholesterol, or LDL or HDL cholesterol concentrations with either dose of exemestane. Table 2 summarizes the results of the hormonal and lipid data.