As you can see my free e2 is very high before I am on TRT. My latest sili
Here are my blood estradiol readings
Estradiol 67 (55 - 165) 39.3 (9 - 41) Units? 96 (<160) pmol/L 77 (<160) 132 (<160) 112(<150) 112 ( <160 ) pmol/L 12.71 ( 11.0 - 43.9 ) pgml (On ATD) 92(<150) 35 (11.0 - 43.9) pg/ml 21.97 (11.0 - 43.9) pg/ml (On letrozole)
70(<160)pmol/l Latest reading done in australia on nothing. This was done a few weeks before the before TRT reading.
So it seems for me free estrogen is always way too high. Blood seems to be ok.
Latest 44(15-50)nmol/l on nothing. This has risen about 10 points over the last few years.
Could it be possible that something is binding to SHBG with greater affinity than e2? Thus displacing E2 giving me high free E2 despite in range blood e2?
The only recoveries I have had were when taking anti estrogens. They helped get my libido back but did not feel 100 percent normal.
I have found my hydroxy progesterone is 3 times the range when not on TRT. It falls down into the range when I go on TRT. Kind of indicated FSH / LH stimulation is resulting in the production of hydroxy prog.
Vincentv- why didn’t you stay on anti estrogens without using testosterone boosters. Could it be possible our testo is fine but being supressed by estrogen? The more testo we add the more it gets converted to estrogen.
Tumbleweeds is reporting some good success on just anti estrogens.
Thanks for posting labwork. TRT and steroid users report when estrogen isn’t controlled (reduced) using an AI during a cycle or TRT, oftentimes, estrogen will get too high. Symptoms of high estrogen are loss of libido, loss of erections, loss of morning/night wood, gyno etc.
The reason this happens is the body aromatasizes much of the extra testosterone into estrogen. The reason that happens is the body’s homeostatic reference point for testosterone and estrogen, is fixed. Iow, the body ‘knows’ how much testosterone and estrogen it should have floating around. As external testosterone is injected, the body says, ‘hey, we’ve got too much testosterone here! Convert most of it to estrogen’!! When that happens, estrogen goes even higher, and the body shuts down natural testosterone production via the HPTA.
That’s essentially what happened to you, in this case. TRT could work, but you’ve got to take an aromatase inhibitor with TRT, otherwise, all you’ll do is shutdown your balls and get no qualitative benefit in terms of boners, wood, libido etc.
I think part of the problem with us PFS guys; finesteride ‘reset’ the bodies homeostatic point for testosterone and estrogen. Basically, it reset our systems to create more estrogen and keep less testosterone around.
How can this happen? I don’t know. But I have anecdotal proof, using a corollary; Aromasin users note that after prolonged use of the AI, they don’t need as much anymore to keep estrogen levels reduced. What that means is their bodies essentially reset the homeostatic point for estrogen (lower) and testosterone (higher). If an anti-estrogen drug can reset estrogen levels lower for men, why can’t an anti-androgen drug reset estrogen levels higher in men (finesteride)?
hey there. Just as I mentioned; several steroid users reported Aromasin gets stronger with prolonged use (meaning, less Aromasin is required to control estrogen). This means, in some cases, after prolonged use, the body is ‘retrained’ to convert less Testosterone to estrogen, using Aromasin. That has gigantic implications.
Now, is the corollary also true? That an anti-androgen, like finesteride, can in some cases, reset estrogen higher in the body, after prolonged use?
If you wait around for randomized, double-blind, placebo controlled, peer-reviewed studies in major medical journals, you’ll have a floppy dick for a long time, friend…
Here is what’s fascinating. I have low estrogen and low testosterone , but I have all the symptoms of adrenal fatigue/estrogen dominance. If my theory is correct, which is that the progesterone receptors are wiped out, then even low levels of estrogen can make you estrogen dominant and supressed thyroid function/ testosterone. Let’s start with that premise. Legendary reported that he felt good when his estrogen was “almost undetecible” in his body. Basically almost all traces of estrogen (estradiol) out if his system. That’s incredible because it suggests a few things, one of which is even with low estrogen you can have estrogen dominance. Now think about this, regular doctor sees my blood work, low estrogen, low testo, and decides to boost my testo, well if the aromatize inhibitor or anti estrogen simply keeps my now seemingly higher estrogen at what it is or even higher, then I won’t feel any of he effects. I read an article that said even .75 to 1mg of letrozole can lower estrogen by 50 percent
Interesting. I’ll do more research on the progesterone-estrogen connection. Also read that DHT is a potent anti-estrogen…
Why would an aromatase inhibitor not suppress estrogen, while on TRT? Something I learned after reading hundreds of posts about the subject; reference ranges established by the labs aren’t the end-all, be-all to this problem. Go by how YOU FEEL. NOT by bloodwork.
In this instance, for you, you’ve got low estrogen. But do you have symptoms of estrogen driven too low? Ie achy, sore, clicky joints? If not, try taking your estrogen lower with an AI, and see how u feel.
The point is that being within the reference range, doesn’t mean squat. You might need below detectable estrogen to feel good, have boners, while at the same time, your joints could be fine. Very similar to Legendary, just like you said!! While I might need my estrogen around the middle of the range, to get the same effect. This is all very individual. This is why doctors are reluctant to mess with hormones; each persons optimal hormonal balance is unique only to them. Iow, everyone’s optimal hormonal balance is DIFFERENT.
The science behind that comes down to sensitivities, receptor population and cell efficiency. For you, even though your estrogen is low, maybe you’ve got a tonne of estrogen receptors on any given cell. Therefore, even though your estrogen is low, there’s so many estrogen receptors, you get triggered all the time. This is how a GP explained it to me.
Right now, I can tell I drove my estrogen too low, as my hip joints have been sore and achy the past few days. Stopped the Aromasin and waiting until boners return before dosing again etc…
It’s how the drug works. It destroys aromatase enzymes rather than simply block them like other inhibitors. Clearly prolonged usage would have an accumulative effect.
Not that I think that will help our condition mind.
I am on formestane now and on TRT. Foremestane has helped with some things. But I still have PFS without a doubt.
I will be doing another siliva test next week to see if my free estrogens have decreased.
If they have not and my free cortisol is still low I will be looking at other areas. Cortisol binding hormone is increased by estrogens. My siliva cort is always very low and blood levels are always good.
People here talk about blood estroen levels. Unfortunately this includes both free and bound estradiol. So you do not know how much is free and acting on the cells. We can not make any assumptions with PFS and assuming your free estrogens match your total estrogens is one such assumption.
I have learnt that androstane en.wikipedia.org/wiki/5%CE%B1-An … CE%B2-diol
which seems to be a 5a reduced DHEA metabolite can act as a potent estogen. If my free estrogens are reduced and I still am having problems I will be looking into this more.
I am going to try out epistane which is a hormone that is still legal, it binds to and blocks the estrogen B receptor. This way I should be able to block any estrogenic metabolites which may be causing problems.
I am also planning to try androsterone which is anabolic / androgenic hormone that does not convert into estrogen or DHT.
The results clearly indicate that androsterone (ADT, chemical structure on the left; source: HMDB: Androsterone), a potent neurosteroid, some “bros” misunderstand as a precursor or pro-hormone to testosterone and estrogen (actually it is a testosterone metabolite), has a regulative effect on sexual function in men.
The scientists measured cerebrospinal fluid (CSF) levels of several steroids and monoamine metabolites and found low androsterone levels to be the major correlate of decreased sexual desire:
The more testing we do the more we will know about this condition. Please do what you can.
I also did a test with letrozole. I took a small dose and tested my T and E within 24 hours. T went over range and E dropped to lower in the range. I did not notice much change in symptoms really.
Vincentv- interesting, if you can remember how small of a dose, and his low was the estrogen? I am starting to think if my theory is right, then estrogen needs to be almost undetectable in the body, extremely low traces
Btw- I am not necessarily thinking this is a cure because I feel only when receptors come back “online” can this condition start resolving but I do think driving estrogen to near non existent in our bodies may provide is some relief
I know girls who are on TRT and takes nothing for Estrogen and yet reap the full benefits of TRT. I have spoken hypogonadal in real life and they use only T injections and nothing. AI is invention of guys on steriods and dr.shippen etc.
How’s the Formestane? Is it trans-dermal? I’ve heard great things about TD Formestane; boners, libido, mood. Apparently, it reduces into a weak androgen responsible for pronounced mood and libido effects.
Interesting about the androsterone.
Thanks for trialing different methods. I applaud your efforts. We all need to be little guieni pigs if we’re to have hope of recovery. Let us know how it goes.
