I see there is some confusion over TRT and prostate cancer. So, I wanted to try to help clarify.
For years it was accepted as a fact that androgens caused prostate cancer (PC), but new evidence has changed that view. Newer studies show that PC occurs in men with low T as often as those with normal T. There is also evidence showing that TRT in men with PC (that has not advanced) does NOT fuel their cancer.
Based on this and other evidence, Abraham Morgentaler, a urologist affiliated with Beth Israel Deacones, the hospital associated with Harvard Medical School, and Professor of urology at Havard Med School developed a new paradigm - the "Saturation Model of Prostate Cancer." Normal and cancerous postate cells have androgen receptors. T and DHT (mainly DHT in the prostate), bind to these AR and stimulate the prostate. However, very little of these androgens is needed to saturate the prostate' AR. Once these AR are saturated, the prostate cells are maximally stimulated. Any increase in T or DHT seems to have no further effect. This may change later if advance PC develops.
Here's the kicker. Apparently, AR saturation occurs at hypogonadal levels of T. Said another way, to have the AR less than saturated, low T is needed. In range T levels cause saturation. And saturation is saturation. Based on this theory, it shouldn't matter whether T is at the low end or high end of the range.
You may ask why PC regresses in men who have metastatic PC and have their T blocked?
Well, many PCs are androgen dependent. When T or DHT occupy these AR, they stimulate PC growth. When these cancers become advanced, or spread, blocking all androgens (androgen deprivation) causes the cancer to remit.
The saturation theory shows that PC depends on only a low amount of androgens and that above a certain point (which is likely a hypogonadal level)different levels of T do not lead to different health outcomes.
This means that a man with a slightly low T likely has the same risk of PC as a man with a normal T. This is why TRT does not increase the PC risk.
NONE of the above considers the use of suprapsiological levels of T usage.
I hope this helps.
For years it was accepted as a fact that androgens caused prostate cancer (PC), but new evidence has changed that view. Newer studies show that PC occurs in men with low T as often as those with normal T. There is also evidence showing that TRT in men with PC (that has not advanced) does NOT fuel their cancer.
Based on this and other evidence, Abraham Morgentaler, a urologist affiliated with Beth Israel Deacones, the hospital associated with Harvard Medical School, and Professor of urology at Havard Med School developed a new paradigm - the "Saturation Model of Prostate Cancer." Normal and cancerous postate cells have androgen receptors. T and DHT (mainly DHT in the prostate), bind to these AR and stimulate the prostate. However, very little of these androgens is needed to saturate the prostate' AR. Once these AR are saturated, the prostate cells are maximally stimulated. Any increase in T or DHT seems to have no further effect. This may change later if advance PC develops.
Here's the kicker. Apparently, AR saturation occurs at hypogonadal levels of T. Said another way, to have the AR less than saturated, low T is needed. In range T levels cause saturation. And saturation is saturation. Based on this theory, it shouldn't matter whether T is at the low end or high end of the range.
You may ask why PC regresses in men who have metastatic PC and have their T blocked?
Well, many PCs are androgen dependent. When T or DHT occupy these AR, they stimulate PC growth. When these cancers become advanced, or spread, blocking all androgens (androgen deprivation) causes the cancer to remit.
The saturation theory shows that PC depends on only a low amount of androgens and that above a certain point (which is likely a hypogonadal level)different levels of T do not lead to different health outcomes.
This means that a man with a slightly low T likely has the same risk of PC as a man with a normal T. This is why TRT does not increase the PC risk.
NONE of the above considers the use of suprapsiological levels of T usage.
I hope this helps.
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