Discussions of AI's including progesterone suppression

Jameson653

New member
I was curious what you guys thought about the different use of AIs depending on what compounds you are running. My doctor gave me a script for aromasin 25mg a day and until I started my tren ace, the 12.5mg a day was enough. I started another thread were I talked about how i started nolva and letro when i started getting puffy nips and it has helped immensely. My question after doing some research is y'alls opinion on the actual estrogen suppression of the 3 main AIs and whether letro is the only one which lowers progesterone, (even if it actually does...) I will try to post some links to get this started but any veterans advice would be appreciated.

Estrogen suppression from aromasin in males is 38%-62% at dose of 25mg ED
Estrogen suppression from arimidex in males is 30-50% at a dose of 1mg ED
Estrogen suppression from letrozole in males is 35-58% at a dose of 2.5mg ED


Also a lot of websites throw around the fact that letro lowers progesterone by 38% but I have no idea what study they are referencing and whether that is male or female...
 
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Where are you getting your information? The reason I ask is I have seen this recommendation of 1mg of Adex ED, Letro at 2.5mg etc. and even have seen some guys planning on running these doses. This is utterly rediculous, unless of course you have breast cancer and are trying to keep your E2 below 5.
 
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AI's typically reduce E2 about 50% in natty males. A bit less if they are young.

I have used AI's at the doses listed on and off for years. Never got my E2 under 5 though.
 
heavyiron thats basically what that study revealed but it was only 14 males. I AM convinced that AIs behave differently in men and women and I AM convinced SERMS behave differently in different parts of the body and whether the cells are cancerous or not. I do my best to diffuse through all the anecdotal bs but its hard. I personally am going to be continuing my letro dose thought the rest of the time I am on tren because of the people who say it reduces progesterone. that is also why i am running low dose Winstrol (winny) even though an study saying it prevents progesterone related side effects is controversial at best. I would love to have evidence of aromasin reducing progesterone but no such luck so far. At least thanks to good advice on this site I am not afraid to run nolva with my tren cause now that I know I can run it without getting puffy nips I will NEVER run a cycle without tren again!!! my back squat jumped 50 pounds in 5 days, its crazy!!!
 
Letrozole inhibits the aromatase enzyme. I've never heard of it lowering progesterone. Where did you hear this?
 
@clamp I haven't read a study, but a lot of websites throw around the "it lowers it by 37%" quote a lot! you can google letro lowers progesterone and read some stuff. i figured I have a shitload of aroma and a shit load of letro, its not gonna hurt me to switch AIs and if it helps then great, if not then atleast I know I am still covered with estrogen reduction.
 
I wouldn't believe it unless it's backed with some evidence. Too much bro science gets spread around on these boards.
 
ok Clamp then I will go back on my aroma, it doesn't kill my libido AS badly and plus it doesn't get its effectiveness reduced like letro does because I am not discontinuing the nolva. Thanks
 
Letro is fine to use as an Aromatase inhibitor (AI), just don't expect it to lower progesterone. It is hard to find the sweet spot dosage for letro because it is so potent, but once you find it you'll be golden. Letro is way cheaper than any other Aromatase inhibitor (AI) so by no means am I telling you to use aromasin instead of letro.
 
The reason your libido is dead is because you have crashed your E2.

I sand behind my previous statments. If you guys are running Adex at 1mg Ed and Letro at 2.5mg Ed you are fucking crazy. Those are literally doses for cancer patients. Your joints are going to get dry, then your going to have a hard time cumming, followed by mr softy and ending in no sex drive.

Good luck


ok Clamp then I will go back on my aroma, it doesn't kill my libido AS badly and plus it doesn't get its effectiveness reduced like letro does because I am not discontinuing the nolva. Thanks
 
Start off letro at .1 mgs eod and work your way up till you find the sweet spot. The libido loss is simply because you're using too much letrozole and your estrogen is too low.
 
SEVERLY dropping progesterone levels shouldn't be your priority. Progesterone does not CAUSE gyno but it can be a factor. Usually when progesterone is linked to gyno its bc of estrogen dominance meaning the ratio of estrogen:progesterone has increased to the point of causing gyno. And I have yet to see any proof besides unsubstantiated claims as to AI's reducing progesterone.
 
The reason your libido is dead is because you have crashed your E2.

I sand behind my previous statments. If you guys are running Adex at 1mg Ed and Letro at 2.5mg Ed you are fucking crazy. Those are literally doses for cancer patients. Your joints are going to get dry, then your going to have a hard time cumming, followed by mr softy and ending in no sex drive.

Good luck
I have run script Adex at 1mg daily for months on end with zero issues. No libido drop and no "dry" joints. I have done the same with 2.5mg Letro daily and again with 50mg Aromasin daily.

There are several studies in men without cancer using these doses brother. I'll dig them up and post them.
 
Copy and paste away. I'm still calling bullshit on 2.5mg Letro Ed....fuck it, I'm also calling bullshit on 1mg Ed of Adex. 2.5mg of Letro is the "gyno reversal" strategy dose. This stratigy is know to crash E2 resulting in the side effect of loss of sex dive.
 
I agree with prisonsex on the letro part. I ran letro at .25mg eod on test (500 pw) and dbol (30 ed) and even THAT was too much for me. Granted I am one of those lucky few who rarely need an ai.
 
Copy and paste away. I'm still calling bullshit on 2.5mg Letro Ed....fuck it, I'm also calling bullshit on 1mg Ed of Adex. 2.5mg of Letro is the "gyno reversal" strategy dose. This stratigy is know to crash E2 resulting in the side effect of loss of sex dive.

J Clin Endocrinol Metab. 2005 Oct;90(10):5717-22. Epub 2005 Jul 26.

Comparative assessment in young and elderly men of the gonadotropin response to aromatase inhibition.

T'Sjoen GG, Giagulli VA, Delva H, Crabbe P, De Bacquer D, Kaufman JM.
Department of Endocrinology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. guy.tsjoen@ugent.be

Abstract

CONTEXT: Aging in men is associated with a decline in serum testosterone (T) levels.
OBJECTIVE: Our objective was to assess whether decreased T in aging might result from increased estradiol (E2) negative feedback on gonadotropin secretion.
DESIGN AND SETTING: We conducted a comparative intervention study (2004) in the Outpatient Endocrinology Clinic, Ghent University Hospital.
PARTICIPANTS: Participants included healthy young and elderly men (n = 10 vs. 10).
INTERVENTIONS: We used placebo and letrozole (2.5 mg/d) for 28 d, separated by 2 wk washout.
MAIN OUTCOME MEASURES: We assessed changes in serum levels of free E2, LH, and FSH, free T, SHBG, and gonadotropins response to an i.v. 2.5-microg GnRH bolus.
RESULTS: As assessed after 28 d of treatment, letrozole lowered E2 by 46% in the young men (P = 0.002) and 62% in the elderly men (P < 0.001). In both age groups, letrozole, but not placebo, significantly increased LH levels (339 and 323% in the young and the elderly, respectively) and T (146 and 99%, respectively) (P value of young vs. elderly was not significant). Under letrozole, peak LH response to GnRH was 152 and 52% increase from baseline in young and older men, respectively (P = 0.01).
CONCLUSIONS: Aromatase inhibition markedly increased basal LH and T levels and the LH response to GnRH in both young and elderly men. The observation of similar to greater LH responses in the young compared with the elderly does not support the hypothesis that increased restraining of LH secretion by endogenous estrogens is instrumental in age-related decline of Leydig cell function.

PMID: 16046582 [PubMed - indexed for MEDLINE]

Comparative assessment in young and ... [J Clin Endocrinol Metab. 2005] - PubMed - NCBI
 
J Clin Endocrinol Metab. 2005 Oct;90(10):5717-22. Epub 2005 Jul 26.

Comparative assessment in young and elderly men of the gonadotropin response to aromatase inhibition.

T'Sjoen GG, Giagulli VA, Delva H, Crabbe P, De Bacquer D, Kaufman JM.
Department of Endocrinology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. guy.tsjoen@ugent.be

Abstract

CONTEXT: Aging in men is associated with a decline in serum testosterone (T) levels.
OBJECTIVE: Our objective was to assess whether decreased T in aging might result from increased estradiol (E2) negative feedback on gonadotropin secretion.
DESIGN AND SETTING: We conducted a comparative intervention study (2004) in the Outpatient Endocrinology Clinic, Ghent University Hospital.
PARTICIPANTS: Participants included healthy young and elderly men (n = 10 vs. 10).
INTERVENTIONS: We used placebo and letrozole (2.5 mg/d) for 28 d, separated by 2 wk washout.
MAIN OUTCOME MEASURES: We assessed changes in serum levels of free E2, LH, and FSH, free T, SHBG, and gonadotropins response to an i.v. 2.5-microg GnRH bolus.
RESULTS: As assessed after 28 d of treatment, letrozole lowered E2 by 46% in the young men (P = 0.002) and 62% in the elderly men (P < 0.001). In both age groups, letrozole, but not placebo, significantly increased LH levels (339 and 323% in the young and the elderly, respectively) and T (146 and 99%, respectively) (P value of young vs. elderly was not significant). Under letrozole, peak LH response to GnRH was 152 and 52% increase from baseline in young and older men, respectively (P = 0.01).
CONCLUSIONS: Aromatase inhibition markedly increased basal LH and T levels and the LH response to GnRH in both young and elderly men. The observation of similar to greater LH responses in the young compared with the elderly does not support the hypothesis that increased restraining of LH secretion by endogenous estrogens is instrumental in age-related decline of Leydig cell function.

PMID: 16046582 [PubMed - indexed for MEDLINE]

Comparative assessment in young and ... [J Clin Endocrinol Metab. 2005] - PubMed - NCBI

Holy shit that's a lot of letro, even for a short amount of time. Perhaps there is a point of diminishing returns rather than a direct relationship between dosage and estrogen levels. If I took that much letro I'd feel like death.

Regardless I'm sticking with my original advice. Find your personal sweet spot by starting at a low dose and slowly increasing it till you find the desired dosage.
 
The full study stated that the drug was well tolerated.

Its different for different folks for sure but I have used AI's for years and much of what you read on the boards is parroted info. I also absolutely love Aromasin at high doses. Its an Aromatase inhibitor (AI) that really agrees with me.
 
I agree with you on that parroted info part. People don't want to take the time to understand how our bodies function so they just repeat what everybody else says and pretend they are smart. As for your aromasin part, I've never used it so I can't compare. Still, if it is on par with 2.5 mgs of letro that seems a little overkill. That is based on my own personal experience as well, although once again I don't have to deal with estrogenic sides like most people do.
 
These two studies were summarized and showed Arimidex decreased Estradiol by about 50% while raising Testosterone by about 58% in males.


Estrogen suppression in males: metabolic effects.

Mauras N, O'Brien KO, Klein KO, Hayes V.
Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. nmauras@nemours.org


Comment in:
J Clin Endocrinol Metab. 2001 Apr;86(4):1836-8.

We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. 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 [(13)C]leucine and (42)Ca/(44)Ca, 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. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.

PMID: 10902781 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/10902781
 
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