Test results for 8mg daily blend (Enan + Prop)

I am from Germany, and the product I use is called Tostran 2%. I find it has a little less alcohol content and it also dries out in a bit more time than usual.

Proviron @ 25mg should feel like something.
Also from Germany. Have the Testogel 1.62%.
I need 37mg proviron to feel an effect.
Gonna try the gel again.
 
May I ask the reason for adding TNE? And why do you think it is better (or different) than TE/TP blend?
TNE definitely different from TP. Must faster hitting. A little goes a long way in my experience.

I tried both Suspension (water based) and TNE (oil based). @Cataceous started a thread on it here:

 
Also from Germany. Have the Testogel 1.62%.
I need 37mg proviron to feel an effect.
Gonna try the gel again.
Proviron is heavily dependent on underlying trt protocol. Since all of the androgenic effects of Proviron are mediated through liberating DHT bound to SHBG. On low dose protocols, there isnt enough DHT bound to SHBG begin with and hence non-significant androgenic boost/libido.

I have used upto 75mg a day of proviron but little to effects (positive/negative) but on a high DHT protocol (topical Test) even half a proviron tab provides god like confidence and libido.
 
.... Since all of the androgenic effects of Proviron are mediated through liberating DHT bound to SHBG. ...

In steady-state conditions Proviron should not have much influence on free DHT unless it is significantly affecting 5ar activity. But I would expect a reduction, if anything, due to possible negative feedback of higher DHT-like activity. Otherwise Proviron is just adding on to existing DHT activity. A widespread misconception is that a real or virtual (Proviron-driven) reduction in SHBG affects free hormone levels. This is not the case when a new equilibrium is established.

On the other hand, maybe you're suggesting the transient behavior is driving the subjective results. As Proviron levels rise there is some displacement of SHBG-bound DHT, temporarily increasing free levels. However, as Proviron falls free DHT decreases, even going below baseline before a return to the original equilibrium.
 
In steady-state conditions Proviron should not have much influence on free DHT unless it is significantly affecting 5ar activity. But I would expect a reduction, if anything, due to possible negative feedback of higher DHT-like activity. Otherwise Proviron is just adding on to existing DHT activity. A widespread misconception is that a real or virtual (Proviron-driven) reduction in SHBG affects free hormone levels. This is not the case when a new equilibrium is established.
Assuming high free DHT doesnt have negative feedback loop-like activity on the 5ar enzyme. Why would decreasing SHBG not result in higher free androgen levels in a steady state environment? Is it because of increased liver clearance of androgens?
 
On the other hand, maybe you're suggesting the transient behavior is driving the subjective results. As Proviron levels rise there is some displacement of SHBG-bound DHT, temporarily increasing free levels. However, as Proviron falls free DHT decreases, even going below baseline before a return to the original equilibrium.
This might be true, from my experience the positive effects of proviron seems to be transient and consistent usage always result in diminishing returns.
 
In steady-state conditions Proviron should not have much influence on free DHT unless it is significantly affecting 5ar activity. But I would expect a reduction, if anything, due to possible negative feedback of higher DHT-like activity. Otherwise Proviron is just adding on to existing DHT activity. A widespread misconception is that a real or virtual (Proviron-driven) reduction in SHBG affects free hormone levels. This is not the case when a new equilibrium is established.

On the other hand, maybe you're suggesting the transient behavior is driving the subjective results. As Proviron levels rise there is some displacement of SHBG-bound DHT, temporarily increasing free levels. However, as Proviron falls free DHT decreases, even going below baseline before a return to the original equilibrium.
We were talking about achieving a peak thus no stable proviron levels. Works like a modulator to obtain quasi circadian level variations. That's how it feels for me.
 
Assuming high free DHT doesnt have negative feedback loop-like activity on the 5ar enzyme. Why would decreasing SHBG not result in higher free androgen levels in a steady state environment? Is it because of increased liver clearance of androgens?

Here is the reasoning: At steady state DHT is being cleared at the same rate it is being produced. If we can assume that clearance is proportional to the free hormone concentration then at steady state the free levels are always driven directly and proportionately by the production rate, independent of SHBG. I am applying the same argument that I've used for testosterone, explained in detail here:
 

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TRT Hormone Predictor

Predict estradiol, DHT, and free testosterone levels based on total testosterone

⚠️ Medical Disclaimer

This tool provides predictions based on statistical models and should NOT replace professional medical advice. Always consult with your healthcare provider before making any changes to your TRT protocol.

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Understanding Your Hormones

Estradiol (E2)

A form of estrogen produced from testosterone. Important for bone health, mood, and libido. Too high can cause side effects; too low can affect well-being.

DHT

Dihydrotestosterone is a potent androgen derived from testosterone. Affects hair growth, prostate health, and masculinization effects.

Free Testosterone

The biologically active form of testosterone not bound to proteins. Directly available for cellular uptake and biological effects.

Scientific Reference

Lakshman KM, Kaplan B, Travison TG, Basaria S, Knapp PE, Singh AB, LaValley MP, Mazer NA, Bhasin S. The effects of injected testosterone dose and age on the conversion of testosterone to estradiol and dihydrotestosterone in young and older men. J Clin Endocrinol Metab. 2010 Aug;95(8):3955-64.

DOI: 10.1210/jc.2010-0102 | PMID: 20534765 | PMCID: PMC2913038

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