The Deadlifting Dog

so I am going to add 12.5. (or 25mg EOD?) ED of aromasin starting week 2 going til PCT. Is that sufficient?

Week 7Considering adding masteron enenthate, but i am not keen on the potential massive natural test suppression.

I was watdark_sideng an AAS documentary recently and the professor of endocrinology was saying the tests produce naturally between 50-75mg/ test /week. So 250mg test e is still significantly higher than natural output or what is called a physiologic dose.

You wont crash your estrogen with an even higher dose of an AI,adex or aromasin 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 Blood was withdrawn in the morning, between 0800-0900 h at the beginning of each treatment cycle and 24 h after the last dose of each treatment cycle (4 blood draws) for various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.

by the way I still think my figures are correct

I’m trying a few calculations here. Let’s say we’re going with a daily dose of 80mg. (I’m actually doing 70mg but 80 is easier for calculations). If you take 80mg once a day (every 24 hours)… then you peak at 80mg and you bottom out at 13mg. If you take 40mg twice a day (every 12 hours)… then you peak at 40mg and you bottom out at 16mg. If you take 20mg four times a day (every 6 hours)… then you peak at 20mg and you bottom out at 12.6mg. Actually I might start taking it once a day just to get that peak of 80mg. Wooohoooo!