I’ve been reading that when used for HRT/TRT, the Aromatase Inhibitor (AI) Anastrozole is commonly dosed at .25 - .50 mg. EOD (every other day).
Yet, a study in the The Journal of Clinical Endocrinology & Metabolism titled “Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels” used 1 mg. Anastrozole DAILY in 12 men (ages 62 - 74 years old) for 12 weeks with spectacular results.
Very impressive considering they weren’t on any steroids at all.
Here’s their conclusion:
“These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined.”
“Thus, anastrozole administration may be a novel means of normalizing testosterone levels in elderly men.”
Did you catch that: “Youthful normal range.” Wow!
I’m trying to reconcile why HRT/TRT merits low dose AI in the presence of high testosterone levels while “old guys” (to quote Will Smith in Men in Black) get great results on high dose AI in the presence of low testosterone.
Google “arimidex monotherapy” , “aromasin monotherapy”’ etc. The aromatase metabolism has a feedback mechanism so E2 inhibition is self-limiting when HPTA and testes are reasonably functional and there is no exogenous T to deal with.
Thank you very much, torrential! I can see how the body would operate like that. Before I posted my question, I did some research on using an AI only and though I can’t find my notes, it seemed that a lot of folks thought it was either worthless or potentially somewhat harmful. (Kind of along the lines of HCG-only and SERM-only.)
I haven’t had time (yet) to Google your suggestions but from what you’ve said and what the study proves, it seems that an AI-only approach might be a good stepping stone into the world of TRT (i.e., try Anastrozole for a few weeks to see how I feel and get follow-up testing).
I just got my blood test results back and Serum Testosterone (which is all I could get right now) is 414 (I’m 57, 6’11", 134 lbs., and training hard – I used to train competitive amateur bodybuilders back in the early '80s). If Anastrozole alone doesn’t improve quality of life and raise my numbers significantly higher, then I’d consider opting for a cycle of Cyp.
From your point of view, does this sound like a reasonable approach? Thanks again, torrential!
P.S. Just for clarification. Last spring, I finally eradicated a massive intestinal overgrowth of Candida which lasted 12 long years and caused me to be semi-bedridden. Right before Candidiasis struck, I had weighed 173 lbs. (I lost 55 lbs. in the ordeal). That’s why I presently only weigh 134 lbs. But now I’m on the rebound, training hard, training intelligently, and eating large.
That paper is a research piece intended to see what the effects are on the HPTA. You need to not be reading dosing recommendations into what you read; especially references to LD50.
In young men [in the study], the high LH increase and high intratesticular testosterone levels [ITT] that can be 80-100 times higher than serum levels, leads to levels of T–>E2 in the testes that raises serum E2 levels. AI cannot reduce E2 in serum, only reduce T–>E2 in peripheral tissues. A competitive drug like anastrozole is totally ineffective inside the testes where it is outnumbered by 100:1
I make that last point, because with TRT guys, the LH response is weak if hCG is use, otherwise zero and there is less ITT and not so much T–>E2 inside the testes. 1mg per day will crash E2 for almost all TRT cases and make one feel very unwell.
Note that the effect of low E2 from anastrozole is self limiting [in the study], ITT–>E2 cannot be prevented provides negative feedback.
1mg/day is used to take E2 to very low levels in women. For males, we need a dose that modulates E2, not killing E2.
Very few understand the above distinctions. I have never see this proposed by anyone else. We know about the LH receptor overload T–>E2 problem thanks to examples from bro science and doctors who are similarity intelligent. From that it follows to not stack hCG and a SERM[–>LH] as hCG+LH is an overload as bad as too much of either one. Note that in a TRT context, or gear use, one can use a SERM+AI, as a SERM does not lower E2 and actually increases E2 via LH–>ITT–>E2.
So the paradox of the study with 1mg/day leading to E2=17 and smaller doses in the TRT population taking E2 way lower is now understood. There are two sub cases, T+hCG where there is a degree of ITT–>E2 and T without hCG where ITT is same as serum levels. We do have a few hCG hyper-responders who have a lot of trouble with hCG–>ITT–>E2 and they need to take a much smaller dose. That seems to be quite rare, we have seen 1 or 2 cases here.