New member
Was reading through this thread, and have on others

From the study at the end talking abuot effectiveness of various doses would it be safe to assume that we can get by with very low daily doses. Like as low as .5mg ed, etc? What is the lowest soemone on here has gone, and how did you rate the effectivness? Also what type and amoutn of Anabolic Androgenic Steroids (AAS) were you taking?

The Terminator

New member
Pretty much everything I have seen would indicate that you could get by with smaller doses. However they come in 2.5 mg. tabs only, and if you have ever seen them you know there is no way in hell you can break them into 5 pieces...I am lucky to split them in half with a pill cutter...

The Terminator

New member
Darko said:
One can also get the liquid, this would allow for much better variation in dose.

That would realistically be the only way you could try and use .5 mg/day. I would be curious to see how well estrogen related sides are controlled with that low of a dosage...maybe I should try it next time (next month)...too bad I already have a bunch of femara tabs sitting around. :rolleyes:


New member
Thanks warimte...I saw your post about this, what is even more amazing is that you waited until the sides came, I am very impressed with this product, compared to the doses I will be running I should be able to get away with even less than you. Maybe as low as 0.625mg eod

I also wonder if the lower dose would lessen the apparent rebound that one gets from fermera as well.


New member
What does concern m about this drug is the impact on cholesterol, thats why I was commenting about garlic on another thread.


New member
I plan on doing the same with my next stack.
Trying to see gains without going overboard with alot of anti-e's.

Wartime100 said:
I ran 1.25 mg eod with 1200mg of test and 50mg of dbol and it took away all my bloat.


Community Veteran
Compared to anastrozole, the dose - response of letrozole is quite different.
Anastrozole studies performed on men indicate that there is very little difference in E suppression in the dose range of 0.5 to 10 mg ED - estradiol is usually suppressed by 50 - 60 % .

Letrozole can suppress estradiol levels by 30% after a single dose of 0.02 mg:

J Clin Endocrinol Metab 1993 Aug;77(2):319-23 Related Articles, Links

Comment in:
J Clin Endocrinol Metab. 1993 Aug;77(2):316-8.

Open dose-finding study of a new potent and selective nonsteroidal aromatase inhibitor, CGS 20 267, in healthy male subjects.

Trunet PF, Mueller P, Bhatnagar AS, Dickes I, Monnet G, White G.

Research and Development Department, CIBA-GEIGY Limited, Basel, Switzerland.

The aim of this open, dose-finding study was to evaluate the effects of single dose CGS 20 267, a new oral nonsteroidal aromatase inhibitor, on the inhibition of estrogen production and also on the production of adrenal and testicular steroids in healthy male subjects. Nine dose levels ranging from 0.02-30 mg and placebo were tested, each dose being given to 3 subjects only. A total of 18 subjects were included; 12 of them received 2 single administration, the remaining 6 were exposed only once to one of the 2 highest dose levels. A reduction in serum estrogen levels when compared to baseline was already observed after 2 h, reaching maximum suppression between 10 and 48 h after administration. After 24 h, a suppression of estrone levels by 60-85% from baseline was achieved with all tested doses. A reduction in estradiol levels by about 30% from baseline was observed at the lowest dose (0.02 mg). This reduction was further enhanced dose dependently to a maximum of about 90% from baseline at 24 h after administration of the highest dose (30 mg). With the higher doses (10 and 30 mg), estrogen suppression was maintained up to 3 days. A dose-dependent increase of testosterone, LH, and FSH was observed and was most pronounced in the 10- and 30-mg dose groups, which can be considered as a consequence of the long-lasting aromatase inhibition achieved with these high doses. No effect on serum cortisol and aldosterone levels was observed up to the highest dose. No clinically relevant changes were observed in blood chemistry and hematology tests. The systemic and subjective tolerability of CGS 20 267 was good at all doses. This study has shown that CGS 20 267 is a well tolerated, potent, selective, and long-acting inhibitor of the aromatase enzyme after single administration.


The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 7 2370-2377
Estrogen Suppression in Males: Metabolic Effects1
Nelly Mauras, Kimberly O. O’Brien, Karen Oerter Klein and Valerie Hayes

...We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 ± 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies.....

...Subsequently, eight males (aged 15–22 yr; four adults and four late pubertal) had isotopic infusions of [13C]leucine and 42Ca/44Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations.....

...Three subjects also received 3 mg Arimidex in an identical paradigm, yet there was a similar percent decline in E2 concentrations and a reciprocal increase in testosterone concentrations as with the 0.5- and 1-mg doses.....


1: J Clin Endocrinol Metab 2001 Jun;86(6):2869-74

The effect of aromatase inhibition on sex steroids, gonadotropins, and markers of bone turnover in older men.

Taxel P, Kennedy DG, Fall PM, Willard AK, Clive JM, Raisz LG.

Division of Endocrinology and Metabolism, Center on Aging, University of Connecticut Health Center, Farmington, Connecticut 06030-1317, USA. taxel@nso.uchc.edu

....Fifteen eugonadal men over 65 yr were treated for 9 weeks with 2.0 mg/day of anastrozole, an aromatase inhibitor. After 9 weeks of treatment, there were significant decreases in estradiol, estrone, and sex hormone-binding globulin levels by 29%, 73%, and 16%, respectively, and total testosterone increased significantly by 56%. Despite the limited decrease of estrogen and the increase in testosterone....

J Clin Endocrinol Metab 2000 Sep;85(9):3027-35 Related Articles, Links

Comment in:
J Clin Endocrinol Metab. 2000 Sep;85(9):3024-6.

Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback.

Hayes FJ, Seminara SB, Decruz S, Boepple PA, Crowley WF Jr.

Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA. hayes.frances@mgh.harvard.edu

The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 microg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 +/- 10 to 52 +/-2 pmol/L, P < 0.005) and IHH men (118 +/- 23 to 60 +/- 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 +/- 6% in NL vs. 56 +/- 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 +/- 9 vs. 58 +/- 6% for LH, P = 0.07; and 85 +/- 6 vs. 41 +/- 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 +/- 0.9 to 14.0 +/- 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 +/- 0.7 to 8.4 +/- 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 +/- 2.4 vs. 70 +/- 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH.