T Nation

TRT Info

www.lef.org/protocols/abstracts/abstr-130.html

  1. Effects of testosterone supplementation in the aging male.

Reports an increase in PSA, a sustained increase… over a 3 month duration. There is nothing presented to determine if the PSA increase was from the increase in T or the increase in E that occurs when an AI is not used.

My last three PSA tests have been .8 now, and .8 then 1.0 6 and 12 months ago. [0.0 - 4.0 ng/ml]. Three years ago it was 0.6 and 0.5 before that. So my PSA did increase. Note that sexual activity increases PSA for a while and can affect the lab results. If you have a DRE [digital rectal exam] at the doctor’s office, and get a blood draw before you leave; PSA can increase and this makes the result of suspect diagnostic value.

Just before my TRT started 2 years ago, my PSA was 0.5 and E2=17; so we have a good baseline for me. And that type of increase is expected.

There is the decrease to PSA=0.8 after been 1.0. Part of that may be my decrease in E2 from 37 down to most recently 19.

My prostate is not a problem and my urine flow is fine, better that several years ago. The big improvement came when Arimidex as added to my TRT. Some are now seeing high levels of E as a greater threat to the prostate than T or DHT. Noting that when old men get prostate problems, their T and DHT levels are low.

When some get really high E2 levels from TRT, there is a possibility that this will be harmful to the prostate. Few doctors are aware of this connection and might laugh you out the door.

AbstractFull CitationRelated ArticlesEmail this Abstract
Desgrandchamps F, Droupy S, Irani J, Saussine C, Comenducci A
Effect of dutasteride on the symptoms of benign prostatic hyperplasia, and patient quality of life and discomfort, in clinical practice. [Journal Article]
BJU Int 2006 Jul; 98(1):83-8.

Aim: To assess the improvements in symptoms, quality of life (QoL), discomfort and satisfaction in patients with symptomatic benign prostatic hyperplasia (BPH) treated with dutasteride in clinical practice. In a prospective, multicentre open-label study, we evaluated the efficacy and safety in clinical practice of dutasteride, 0.5 mg/day for 24 weeks, in patients with symptomatic BPH. The primary endpoint was the proportion of patients achieving at least a 3-point decrease from baseline in the International Prostate Symptom Score (IPSS) after 24 weeks of treatment. The secondary endpoints included changes from baseline in measures of QoL (IPSS item 8 and BPH Impact Index score, BII), and patient discomfort and satisfaction (visual analogue scales, VAS) at 12 and 24 weeks. Of the 366 patients assessed, 72.5% achieved at least a 3-point reduction in IPSS at 24 weeks; the IPSS decreased from 15.3 at baseline to 10.2 at 12 weeks, and to 9.1 at 24 weeks.

There were significant (P < 0.001) decreases in all the individual IPSS items at 12 and 24 weeks, with more marked improvements in voiding symptoms than storage symptoms. There were also significant (P < 0.001) improvements in the BII and VAS scores for patient discomfort and satisfaction at both times. Dutasteride treatment for 24 weeks significantly improved BPH symptoms, QoL and patient discomfort and satisfaction, and was well tolerated in clinical practice.


More from this journal
BJU international. [BJU Int]

What you say makes sense…then I read this.

[quote]fedorov wrote:

What you say makes sense…then I read this.[/quote]

…but they’re treating the test subjects with Dutasteride. That’s a totally different scenario than KSman’s is it not?..hebs

[quote]hebsie wrote:
fedorov wrote:

What you say makes sense…then I read this.

…but they’re treating the test subjects with Dutasteride. That’s a totally different scenario than KSman’s is it not?..hebs
[/quote]

KSman is making the point that high levels of estradiol are the reason for BPH, if I understand him correctly, and that by keeping these levels in the low range will keep the situation under control.
The current medical establishment does not seem to agree with this.
By the way, I am taking Avodart (a androgen inhibitor) to reduce levels of DHT, which many Doctors think is the culprit.
This is the conflict, which is it?

I read into this a lot more:
www.lef.org/protocols/abstracts/abstr-130.html

There is a huge amount of research into the E-BPH connection. More than I expected.

So why the great focus on 5-alpha reductase inhibitors?

As probably all men are getting this to one degree or an other, what are the implications of dealing with the E-BPH connection. What are the implications of taking every older man an putting them on something like arimidex. Many would howl at the drug companies for trying to over medicate and make huge amounts of money. Would that be “Preventative” medicine. Would urologist fight that to protect their cash flow?

Everyone gets a degree of coronary hard disease [CHD]. They convinced everyone that they need low cholestol or they will die. The medical establishment and many?most doctors would have every person on a statin drug if they could. [But the generics are spoiling the [profit] motive.]

Are statins “Preventative” medicine?

I do not know what to make of things like this. I have a full expectation that profit drives the solutions.

Drug companies are making money on 5-alpha reductase inhibitors. Perhaps that therapy is needed at times. Maybe if E was controlled before BHP started, 5-alpha reductase inhibitors would not be needed. For serious BPH cases, perhaps less 5-alpha reductase inhibitor could be used in a more effective synergistic combination.

Perhaps some here can eval a combo and see if that has value for them.

It seems one could convincingly argue that TRT that drives up E2 is doing harm. One could then argue that E2 monitoring and control is needed to not do harm. [Others would say that TRT is harmful and should not be done.] Maybe someone on t-alone TRT could get into a serious prostate problem, and sue a doctor or clinic for the the damage of TRT without monitoring and controlling E2. That seems to be the only certainty; people pay attention and change when there are law suits. There certainly is a huge amount of research that lawyers could use to argue the case.

AbstractFull CitationRelated ArticlesEmail this Abstract
Suzuki K, Ito K, Ichinose Y, Kurokawa K, Suzuki T, Imai K, Yamanaka H, Honma S
Endocrine environment of benign prostatic hyperplasia: prostate size and volume are correlated with serum estrogen concentration. [Journal Article]
Scand J Urol Nephrol 1995 Mar; 29(1):65-8.

Estrogen plays an important role in the development of benign prostatic hyperplasia (BPH), as has been shown in both experimental and clinical studies. T determine the endocrine environment of BPH, serum total testosterone (Total-T), free testosterone (Free-T), and estradiol (E2) conceptions were measured, and the relationship between these levels and prostate size and volume was analyzed. Blood samples were collected from subjects who attended the mass screening for prostate disease performed by our institute. No significant correlations were found between Total-T levels, Free-T levels, and prostate size, as determined by digital rectal examination. However, E2 levels and the ratios for E2 levels and the ratios for E2/Total-T and E2/Free-T were significantly correlated with prostate size. To confirm these relationships, prostate volume was calculated from transrectal ultrasonographic images. E2 levels and these two ratios were, indeed, highly correlated with prostate volume. These results suggest that an estrogen-dominant environment plays an important role in the development of BPH.

[quote]fedorov wrote:

AbstractFull CitationRelated ArticlesEmail this Abstract
Suzuki K, Ito K, Ichinose Y, Kurokawa K, Suzuki T, Imai K, Yamanaka H, Honma S
Endocrine environment of benign prostatic hyperplasia: prostate size and volume are correlated with serum estrogen concentration. [Journal Article]
Scand J Urol Nephrol 1995 Mar; 29(1):65-8.

Estrogen plays an important role in the development of benign prostatic hyperplasia (BPH), as has been shown in both experimental and clinical studies. T determine the endocrine environment of BPH, serum total testosterone (Total-T), free testosterone (Free-T), and estradiol (E2) conceptions were measured, and the relationship between these levels and prostate size and volume was analyzed. Blood samples were collected from subjects who attended the mass screening for prostate disease performed by our institute. No significant correlations were found between Total-T levels, Free-T levels, and prostate size, as determined by digital rectal examination. However, E2 levels and the ratios for E2 levels and the ratios for E2/Total-T and E2/Free-T were significantly correlated with prostate size. To confirm these relationships, prostate volume was calculated from transrectal ultrasonographic images. E2 levels and these two ratios were, indeed, highly correlated with prostate volume. These results suggest that an estrogen-dominant environment plays an important role in the development of BPH.

[/quote]

Those are very definitive statements. DHT levels will correlate with TT and FT. So one can say that BPH does not correlate to DHT levels. But; I wish that this had been stated explicitly. This abstract does nothing to disarm the mindset that DHT causes BPH.

The sex organs need DHT during development and for maintenance. It is reasonable that killing DHT levels will turn off the prostate to some extent, reducing its size, and metabolism. But this may be treating the symptom and ignoring the root cause. E is dangerous and with low T, unopposed E is worse. In that list of abstracts I also saw some studies showing that AIs did not shrink the prostate. I can’t recall the duration of that evaluation.

Related:
http://www.andrologyjournal.org/cgi/reprint/21/2/258.pdf

KSman, thanks for your input, I always appreciate it.
For me personally, this is more than just an intellectual discussion. I’m practically obsessing about the havoc I may be causing to my hormonal balance.
I will be seeing a new Doc soon, and I will get his take on these issues.