If you use TRT ( or more ) and you are always fretting about the risk of Prostate Cancer

Its past due that we stop spreading the Bro Myths about Testosterone and Prostate Cancer

No Elevated Testosterone is not the cause of Prostate Cancer

 

Yes The Human Prostate is exquisitely sensitive to Androgens

Clinical data indicate the saturation point for serum T is approximately 250 ng/dL

What this means is after you reach 250ng/dl.. the addition of ” more Androgens” has little to no cumulative effect on the Human Prostate..
 
” It is important for younger readers to understand that, prior to introduction of the Saturation Model, the universally held belief was the “Androgen Hypothesis”, which held that higher androgen concentrations caused proportionally greater growth of prostate tissue, and that higher serum T meant greater PCa risk and aggressiveness.
 

The saturation model provided a radically different view, one that resolved an awkward paradox in which androgen deprivation clearly lowered prostate-specific antigen (PSA), yet raising T in hormonally intact men had little effect on PSA or prostate size. In one swoop, the Saturation Model assembled a messy assortment of clinical observations and experimental results into a coherent picture. Simply, the Saturation Model holds that prostate tissue is exquisitely sensitive to changes in serum androgens at low concentrations, and little to no sensitivity once a saturation point is reached.

 
Clinical data indicate the saturation point for serum T is approximately 250 ng/dL 
 
What this means is after you reach 250ng/dl.. the addition of ” more Androgens” has little to no cumulative effect on the Human Prostate..
 
The mechanisms underlying the Saturation Model include the following observations:
 
a) T or its derivative, 5α-dihydrotestosterone (5α-DHT), mediate prostatic cellular function by binding to the androgen receptors (AR).
 
b) There is a finite number of AR binding sites per cell,
 

and

c) once AR sites are fully occupied with T or 5α-DHT, a saturation state is achieved, beyond which increasing circulating T or 5α-DHT cannot elicit additional biological activity via this mechanism

 
[2]. Other mechanisms are possible, yet this relationship of androgens with AR is adequate to explain observed phenomena over a wide range of experimental data.
 
More than a decade since its publication, the Saturation Model has turned out to be a robust description of the relationship between androgens and the prostate, and we are unaware of any compelling evidence to the contrary.
 

At this point we conclude that the Saturation Model should no longer be considered a hypothesis, but rather an accurate framework describing the relationship of androgens and the prostate.

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This might be of further interest to you

https://victorblackmasterclass.com/baldness-benign-prostate-hyperplasia-prostate-cancer-and-androgen-levels/

Victor Black