My bad. Free t does not produce but a small % of the benefit, estrogen and dht produce majority. im going to find the papers or documentation and speak to my doctor on this.
I totally misunderstood my doc.
Yes i misunderstood my doc. Apologies.
Lets put it this way. The majority of the benefits we seek when doing trt are realized via dht and estrogen. Fitness and etc comes at the bottom of the list for men on TRT.
Ill dig through the details of what free t does and post that info when i speak to my doc again.
I am not even trying to discuss anything with you. I saw Yeti respond to you and you totally disregarded him in everything he spoke about, yet he is an expert in the field, and you arent even closely qualified.
TRT Expert with hundreds of clients and years of experience with Dr. Rouzier as his mentor, versus you who has zero real world experience or education on the subject.
Who are you to refute these two?
I literally repeat what they say with a goal of helping other men, and i make mistakes at times, but im not sitting around acting like im a genius who knows more than an expert.
On the other handā¦ YOU DO.
Sad reality you live in.
I am not saying the benefits from DHT donāt exist in adult men, I just havenāt seen much evidence of them existing in a way that is exclusive to DHT (meaning T or another androgen can have the same benefits). No doubt it is important in development.
It seems after development DHT can be replaced by several different androgens without much impact to the guy on those androgens in many cases. Some even do well on Nandralone only therapy. They basically get E and an androgen from it (but have very low DHT values).
What exactly have I refuted?
Iāve stated what has worked for me and stated Iām not suggesting other people need to do what is working for me.
Your posts all imply an A.I. means very low or zero e2. For me a small amount means mid range e2. Iām not treating numbers- but with those numbers Iām at a place that works well for me.
You and others before you (Iām still not convinced you arenāt Dannyās second troll account), basically say that no one needs an a.i.
Iām living proof this one size fits all ideology isnāt the case.
Again- I repeat, Iām not suggesting everyone should go out and add an a.i. into their protocol.
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Ok but thats just going out of the norms of what your body already produces, lacking in production and were trying to replace. I was trying to explain simple that we are benefiting form trt due to e/dht.
Heres a link to a couple of great literature discussing E, DHT and their benefits. Androgen Physiology, Pharmacology, Use and Misuse.pdf - Google Drive
You can find where DHT is discussed in both of these by using CTRL + F and typing out DHT or its full name.
They also discuss oral agents as you mentioned and the differences of how they function in the body. very interesting stuff.
This is something that will fill your brain with a deeper understanding if you wish.
I was going to share with the forums the details of these, but i truly feel its a waste of time because nobody goes with facts today, they just go with a self realized truth and nothing applies to āmeā.
Here you go and let me know if you find anythign interesting. We can chat about that. For example this is a very interesting take from one of the articles.
"The role of aromatization in androgen action was originally identified by the 1970s in the brain (222) whereby local expression of the aromatase enzyme within brain regions leads to local production of estradiol to mediate testosterone effects selectively in that region via ER and not AR mechanisms.
Subsequently, the importance of aromatization to androgen action on bone was identified through investigations of inactivating mutations in ERĪ± in men (223) and mice (150, 224).
The role of aromatization in the estrogen-mediated effects of testosterone action is clearly shown by studies of Finkelstein et al who use the paradigm of complete suppression of endogenous testosterone production by administration of a depot GnRH analog with a range of doses of add-back testosterone without and with an aromatase inhibitor (anastrozole), the latter to investigate the effects of selective estrogen deficiency (225).
These studies showed that aromatization was important in mediating testosterone effects in reducing fat mass and sexual function but not on muscle mass or strength.
However,in another study using a different design, a high dosage of the non-aromatizable androgen dihydrotestosterone (vs. placebo) to induce selective complete estrogen deficiency in healthy men, demonstrated complete preservation of sexual function (161). Testosterone effects on bone involve dual mediation via indirect mechanisms, via aromatization to estradiol and ER-mediated effects, as well as via direct AR-mediated effects (226).
In male mice, aromatization of testosterone must occur locally within bone as circulating estradiol levels are too low to activate ERs ; however, the role of local vs circulating estradiol effects on male bone remain to be clarified. A much wider role of estrogen action in male health is now identified (227). In that light the off-label use of aromatase inhibitors carries the risk of adverse effects on brain (manifest as sexual dysfunction), fat, and bone.
and this
The amplification pathway converts ~4% of circulating testosterone to the more potent, pure androgen, DHT (50, 52). DHT has higher binding affinity to (121) and 3-10 time greater molar potency in transactivation (122-124) of the androgen receptor relative to testosterone.
Testosterone is converted to the most potent natural androgen DHT by the 5Ī±-reductase enzyme that originates from two distinct genes (I and II) (125). Type 1 5Ī±-reductase is expressed in the liver, kidney, skin, and brain, whereas type 2 5Ī±-reductase is characteristically expressed strongly in the prostate but also at lower levels in the skin (hair follicles) and liver (125).
They seem to love their anecdote and personal experience, but hate it and write off anyone elseās personal experience that goes the other way. You feel how you feel what does he want you to refute lol.
They seem to conflate lower dose, thus lowering E2, versus using an AI with a higher dose and making it a topic of crashing E2 vs not.
āE2 is no the devil, we needā, no one is even arguing that and yet they just keep coming back with the same stuff over and over.
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Good read so far, I did see one point that brought up a question: in measuring daily release of TT, they came up with 3-10mg of testosterone (quite the range), but also inter-conversion rates of 4% to DHT and .2% to e2. Would you consider anything above (or below) those rates to be ab-normal or possibly unhealthy? Would the āe2 is healthyā argument extend beyond .2% conversion from TT?
Thats a great question. Just like SHBG, it varies between person to person. But they can only produce so much of each. It cannot create infinite amounts.
My doctor gave me this and i am going to paste it here. Leads into your comment above.
The aromatase enzyme and the five alpha reductase enzyme have saturation points just like all enzymes. Itās call Michaelis Menten kinetics. You can look that up.
So once the enzymes are fully saturated with testosterone they cannot produce any more estradiol or DHT.
You can raise Testosterone into the tens of thousands but you cannot raise DHT or estradiol past a certain point. Testosterone will keep increasing but DHT and estradiol will reach a plateau.
Iāve seen some research that seems to point towards E2 and DHT being logarithmic.
Obviously, DHT and E2 canāt be negative (so the positive portion). The data didnāt have TT (the x-axis) going out forever though. I do think it had data up to like 5,000 ng/dL though. That data showed that it still was increasing (but in a logarithmic fashion). Raising like that is kinda like being saturated though (as it is much less than linear which many people assume).
@tareload, do you happen to have those charts?
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Rectangular hyperbola.
More background on the MM kinetics math: https://febs.onlinelibrary.wiley.com/doi/full/10.1111/febs.16124
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I have seen this and posted the graph, Iāll see if I can find it again. Only related to e2, I think, but that saturation happened when TT was around 3000ng/dL. I think in the realm of TRT we wouldnāt see any AE or 5AR saturation.
Edit: I see others have posted about it too. Iāll still see if I can find it
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There are graphs in the study tareload posted above.
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The graphs do beg the question of āwhere are Tareloadās 95% confidence level graphs for DHT and E2 vs dose at?ā.
FWIW, I actually snipped out those graphs and printed them. Seems like useful info to have. Just drawing on them a bit from TT to DHT and E2 make a lot of sense. My DHT numbers on cruise with no 5 AR inhibitor, and on blast with Finasteride line up well (assuming Finasteride blocks roughly 65-70%) of DHT.
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Yah you would need a huge amount ā¦ interesting. I bet thatās hell of a rideā¦
Very doable but even the TT dose response chart was probably over the top for most. Nelso Vergel has a calculator (empirical) based on the data above for E2.