Cream and prostate issues?

Mr.63

Member
I have a quick question for the cream users.

Aren't you afraid of prostate growth due to the extremely high DHT? Or even prostate cancer?

My DHT was 200 just before my evening application. So at the peak, it must be even higher.

I feel much better on the cream. In every aspect. Whereas injections, at any dose or frequency, have never worked. But with the cream, I do sometimes experience problems urinating. Which worries me as i dont want to go back on injections.
 
I have a quick question for the cream users.

Aren't you afraid of prostate growth due to the extremely high DHT? Or even prostate cancer?

My DHT was 200 just before my evening application. So at the peak, it must be even higher.

I feel much better on the cream. In every aspect. Whereas injections, at any dose or frequency, have never worked. But with the cream, I do sometimes experience problems urinating. Which worries me as i dont want to go back on injections.

Even than much more to look at when you get into serum vs tissue (local regulatory mechanisms that tightly control intracellular androgen homeostasis) and saturation point!




Key points here!

* We are reminded of Horton’s admonition some 25 years ago when he concluded that blood levels of DHT provide only a hint of tissue levels and that DHT should be regarded as a paracrine hormone formed and acting primarily within target tissues (39).


*
There is no sound current clinical evidence to indicate that elevated DHT concentrations (either short-lived peaks or sustained supraphysiological levels) are associated with risk beyond that known for androgens (most notably, T), including adverse effects on prostate.




Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels (2016)

Ronald S. Swerdloff, 1 Robert E. Dudley,2 Stephanie T. Page,3 Christina Wang,1,4 and Wael A. Salameh1


Key Conclusions and Recommendations for Future Clinical Research

Circulating levels of DHT in response to TRT do not correlate with those found in androgen-sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis. Observations from numerous clinical studies are consistent with current knowledge that androgen-sensitive tissues can self-regulate tissue DHT levels by downregulating its synthesis and upregulating metabolism during DHT excess or, conversely, upregulating synthesis and downregulating metabolism under conditions of T or DHT deprivation. We are reminded of Horton’s admonition some 25 years ago when he concluded that blood levels of DHT provide only a hint of tissue levels and that DHT should be regarded as a paracrine hormone formed and acting primarily within target tissues (39).

The modest increases observed in serum DHT and in the DHT/T ratio observed after TRT are unlikely to be a cause of clinical concern, particularly when viewed in the context of changes observed in these parameters for currently marketed T replacement products and those under development for which DHT data are available.
There is no sound current clinical evidence to indicate that elevated DHT concentrations (either short-lived peaks or sustained supraphysiological levels) are associated with risk beyond that known for androgens (most notably, T), including adverse effects on prostate.






Dihydrotestosterone Administration Does Not Increase Intraprostatic Androgen Concentrations or Alter Prostate Androgen Action in Healthy Men: A Randomized-Controlled Trial (2011)
Stephanie T. Page, Daniel W. Lin, Elahe A. Mostaghel, Brett T. Marck, Jonathan L. Wright, Jennifer Wu, John K. Amory, Peter S. Nelson, and Alvin M. Matsumoto


Conclusions

Robust supraphysiologic increases in serum DHT, associated with decreased serum T, do not significantly alter intraprostatic levels of DHT, testosterone, or prostate epithelial cell androgen–regulated gene expression in healthy men. Changes in circulating androgen concentrations are not necessarily mimicked within the prostate microenvironment, a finding with implications for understanding the impact of androgen therapies in men. (J Clin Endocrinol Metab 96: 430 – 437, 2011)




* In summary, in this study of human prostate physiology we have demonstrated that substantial increases in serum DHT concentrations mediated by high-dosage exogenous DHT, which concurrently lower serum T concentrations, do not raise intraprostatic concentrations of T, DHT, DHEA, or androstenedione in healthy men. In addition, supraphysiologic levels of serum DHT for 1 month were not associated with alterations in prostate epithelial cell proliferation or androgen-regulated gene expression. Longer-term studies that directly examine the prostate effects of androgen replacement strategies should be undertaken but, lacking those data, we should not infer that changes in serum androgen concentrations conferred by exogenous androgens are reflected within the prostate.
 

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