I never checked DHT.
I didn’t experience hair loss not any other side effects, so I didn’t bother to test it.
Thanks for the DHT answer! I’d like to point out something:
- A lot of times when taking Aromatase Inhibitors as monotheraphy (so off cycle) users feel like being crushed in the beginning because it takes time for the body to react via the feedback loop. So the dose wasn’t necesairily too high for you, but it was too high too fast. I strongly believe you could have gone up with the dose in 2 week increments from 1/4 pill twice a week. That way you would give your body to first produce more testosterone adapting to the feedback, which means more test in the testes where neither aromatase nor suicide inhibitors have a large effect, so your E2 doesn’t crush, and this allows you to increase the dose. It is also true the other way around. If you would have just ‘rided it out’ the feeling crushed would most likely have disappeared in a week or two.
Based on your numbers though, even if your goal was to max our your free test possibilities with this for gaining an edge (using it instead of a cycle), not curing your preexisting symptoms, half a pill twice a week would probably been enough to get you to the 190ish free test numbers that seemed to be the max reachable in the studies, and you wouldn’t have needed 1/2 a pill EOD.
If you have a high response to AI’s, your E2 will be crushed and stay there. I promise. The E2 you make in the testes won’t amount to much.
Hi,
‘If you have a high response to AI’s, your E2 will be crushed and stay there. I promise.’
I absolutely agree. Also: If you weigh more, it will be harder for someone to lift you up. I promise. 
Jokes aside: Please note that in the case of an AI monotherapy we are talking about an existing OPEN FEEDBACKLOOP. Not about when you are ‘on cycle’ or ‘on trt’ when you have a suppressed/shut down natural production, and adding an AI can’t drive your free test levels up, because you are getting in a fixed exogenous amount and that’s it. With AI monotherapy what ends up as your free test is produced by your testes. When you increase the dose your own production is driven up. When you have double the amount of free test, then you’ll have double the amount of what is possible to be aromatized in the testes to estrogen. And the AI can’t inhibit that (it’s nowhere near as effective in the testes as everywhere else).
" Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens [15]."
Now that 60% stays rather intact.
Now I am not saying that:
- You absolutely can’t have low estrogen sides if your estrogen falls to 60% of it’s default value, but in MOST cases people don’t.
- There aren’t individual cases where the above 60% value turns out to be much less (let’s call the guy an overresponder).
What I am saying is:
If you look around on internet forums everyone seems to get ‘crushed’. In the studies on AI monotheraphy (either exemestane or anastrozole) nobody seems to get ‘crushed’. So when you are trying to draw conclusions from the internet dosages:
- Pay close attention if the dosages that you are looking at that seem to ‘crush’ the guys on the internet are infact a case of an intact open feedback loop (so monotheraphy, or HCG+AI, or SERM(most often clomid)+AI) not where somebody is ‘on cycle’ or ‘on trt’ dosages of aromatizable exogeneous compounds. Beacuse that would be irrelevant for this purpose.
- If you made sure the case was with an intact open feedback loop, in MY OPINION in 90% of the time users are shouting ‘I am an overresponder’ too early. If they tried to either ride it out, or taper up the dosage with a slow start instead - every two weeks (like week 1-2 1/4 pill twice a week, week 3-4 1/4 pill EOD, week 5-6 1/2 pill twice a week, week 7-8 1/2 pill EOD) till satisfaction then these 90% wouldn’t be ‘crushed’.
In the other 10% you’re absolutely right and it is the case you mentioned. I promise.
‘also after 1 month from 2nd blood test the SHBG was still low.’
That is great news. Would you be as kind and post the bloodwork for that as well (if possible)? I’d be interested in how your total T, free T, and estradiol looked after stopping the aromasin compared to the 2nd blood test.
The total estradiol production rate in the human male has been estimated to be 35-45 μg (0.130-0.165 μmol) per day, of which approximately 20% is directly produced by the testes - from your quoted study.
That leaves 80% coming from processes outside of the testes and therefore open to AI interference.
So, while most guys reporting an issue are using exogynous test, and therefore not producing E2 in the testes (unless they are using HCG), you still are getting a small amount of your overall E2 from that direct production. Guys on HCG also report E2 issues on AI’s. AI therapy has some success stories, but overall I would prefer a SERM for this if I was going that route. And personal experience tells me that at 200mg/week (TRT dose) my E2 is 8 on a non-sensitive assay using only 1/4 arimidex twice a week. 20% wouldn’t be enough to fix that.
I’d have to ask the subjects about that. Studies go by numbers, and generally define E2 as fine if it’s above 5. I do not feel any differently at a low number than a high number, or anything in between, except that I get pulls and strains easily with low E2.
Yes I did quote the wrong sentence and went with that number. The previous sentence said the 20% directly from the testes. My bad!
Although from the 25 and 50mg/day dose finding study:
‘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’
Also when testing a single dose of 25mg exemestane in the same study:
‘Maximal suppression of estradiol (62 ± 14%) was observed 12 h after a single 25-mg dose of exemestane. Estradiol remained suppressed by 58 ± 21% at 24 h and returned to baseline 3–6 d after treatment (Fig. 3)’
It is essentially the same idea as using a SERM. Fake out your body so that it thinks you need more test to make more E2, so it cranks up the LH. If you just have a feedback loop issue, it kick starts it. If that’s not the problem, if you have a separate issue (like CYP mutation) then it’s going to end up back where you were. If I’m going to need a medication for the rest of my life, I’ll take test over any AI or SERM.
My problem with SEMRS is from the clomid/nolva/torem trio all of them have cataracts as a side effect. I really don’t like that.
The only SERM I know of that doesn’t have the eye sideffects is raloxifene. Which is much weaker in boosting LH than the above three. Athough it could be used in combination with Aromasin as a ‘good estrogen’ at a 60mg dose.
What would also worth a try on an AI base test boositng experiment is 10mg/day of boron. It is proven to increase E2 by slowing it’s catabolism, the end result was a 42% increase caused by this effect and by decreasing SHBG by 28%. The net effect would be different with an AI base, because we don’t know how much it could decrease SHBG, as aromasin does it as well. But decresing SHBG drives up free test, which drives up the amount that can be aromatized in the testes, so would worth a try.
I could see it affecting aroma outside of the testes, but the SHBG is produced by the liver and is going to bind T that makes it out into the bloodstream. I don’t see how it could impact testicular aroma much.
The +42% effect in the study adds up by two routes, 28% SHBG decrease and estrogen catabolism decrese. The effect of the first is unsure when combined with aromasin the effect of the second is what can be counted on:
‘As already mentioned, serum concentrations of both 25(OH)D3 and 17β-estradiol increase when boron is supplemented. Because this effect is seen in postmenopausal women receiving hormone replacement therapy, a reduction in E2 catabolism, rather than increased E2 synthesis, is responsible. Each of the major routes of E2 catabolism involve hydroxylations (ie, the introduction of a vicinal hydroxyl group at the 2, 4, or 16 position of 17β-estradiol), which is already hydroxylated at the 3 and 17 positions. This addition indicates that boron is a potent inhibitor for microsomal enzymes that catalyze the insertion of hydroxyl groups vicinal to existing hydroxyl groups in steroids.’
‘personal experience tells me that at 200mg/week (TRT dose) my E2 is 8 on a non-sensitive assay’
This made me remember my greatest problem regarding this. I don’t seem to find estradiol sensitive LC/MS test here in Europe. Does anyone know of a lab that does it? I understand a non-sesnsitive 8 could be 5 or 35 in reality (on a sensitive test). So one might as well watch the HDL instead to see if E2 is oversuppressed…
This would be the first study I have found on men that uses a lower dose than 1 pill /day of AI. Group 2 uses 1 pill twice a week:
https://academic.oup.com/jcem/article/89/3/1174/2844209
There was only one subject in group 1 (1pill/day) who had a <10 estradiol result (it was 9).
In the previously linked study freeT boost was twofold in the case of the 1mg/day group1 compared to the 1mg twice weekly group 2. This suggests the effect is maxed out at 4mg/week dose.
This study further proves this:
In this case 1mg/day and 0.5mg/day resulted in the same effect. 0.5mg/day is 3.5mg/week.
This translates to ONE tablet EOD being the max dosage off cycle.
This is very close to the one tablet M/W/F which is the standard dose for hypogonadal men in various endocrinology practices.