Androjel and prostate

My understanding, and I could be wrong, is that testosterone can feed the prostate cancer cells, if there are cells there to begin with but it cannot Cause prostate cancer. I hope others will answer as well although this is kind of a hot topic in the prostate cancer world!

Best of luck with the biopsy
Susan

You should probably consider stopping the T meds for 3 to 6 months and get another PSA test.

rp:

Sounds like your uro. is too quick to do a biopsy , IM(non-medical)O.

Why not go off the Androgel for a month and have your PSA re-checked ? Or stay on the Androgel and have your PSA re-checked in a month ?

Biopsies are not without risks ( infection). And CaP is very, very slow growing. You have some time to see what happens and/or get a second or third opinion - according to John Hopkins Urology.

Also, did your uro. do a "free" PSA test ?? If your free PSA is >25% , it would indicate a much lower chance of having CaP.

Again, it seems to me your uro. is acting too quickly to do a biopsy .........If he says this must be done "right now" , I would find a new uro. - FAST.

This is our experience with Androgel:  My husband was on Androgel for 2 years for low T and when his PSA went to 4.1 from 3.6 six months earlier, he was referred to a urologist.  The urologist said that taking Androgel when you have prostate cancer is like pouring gasoline on a fire.  My husband immediately went off of Androgel after that visit.  He was scheduled for a biopsy and was diagnosed with a Gleason 7 (4+3) cancer.  One of the side effects of Androgel as listed on their website and instructions states that there is an increased risk of prostate cancer.   

Peter, when there are more pies, more mice will join the party! Same with the cancer and T. Cancer begets more cancer through multiplication and little or no apoptosis.

All the T supplements warn that it may cause PSA to rise and that people who have, have had, or are at high risk to PCa should not use them. So, I wonder what the surprise is when the PSA goes up. Lesson is to read and research before you decide so that you know what to expect.

Interesting subject, I think. The "pouring gasoline on a fire" theory is certainly the conventional wisdom and it is a "safe" position for a doctor to take (his malpractice insurance company would certainly want him to follow it; it's hard to get sued for sticking to the conventional wisdom.) What'e more, most urologists have quite a bit of anecdotal clinical experience that tends to support it.

... but ...

On the other hand, when the assumption is subjected to the rigors of controlled research it proves, again and again, to be hard to find. Here are a few full-text reviews of recent research:

The benefits and risks of testosterone replacement therapy: a review

Hypogonadism in the Aging Male Diagnosis, Potential Benefits, and Risks of Testosterone Replacement Therapy

And here is a link to an interesting article by Dr. Morgantaler in Life Extension magazine:

Destroying the Myth about Testosterone Replacement and Prostate Cancer (By Abraham Morgentaler, MD) Life Extension Magazine

JNF:

I was writing this when you posted. I have read quite a bit of the research (see above). I don't think there are any urologists who prescribe T for patients with active metastatic advanced non-castrate-resistant prostate cancer.

The controversial idea is that there are two levels of T that make sense: castrate level (which halts or delays the growth of prostate cancer) and normal (which avoids the effects of hypogonadism). If you aren't going to shoot for castrate levels of T then you might as well adjust it to normal since the difference between low T and normal T, in terms of their effect on PCa, is quite small. No one denies that castrate-level T is an effective treatment when it is needed.

The reason that the T manufacturers say that men at risk for PC shouldn't use their product is not because they have done research that shows a danger, it's because it is not worth their money to do the research to try to show that it is safe and they don't want to take the liability risk.

In my metaphor the crumbs of my single pie are enough to feed all the hypothetical mice you plan to throw at me. I will merely hypothesize a bigger, crumbier pie. That's my point, actually. Once you feed the mice more crumbs don't make a difference.

Edit: Fixed the link to the Life Extension Mag article.

rp:

I was a long time user of Androgel ... and my doc wasn't watching the PSA levels (i thought she was; bad mistake). And the PCa grew to be a bit out of control ... It sounds like your PSA numbers suggest there might be something there -- i'd encourage you to make sure and catch it early. Same advice it give my brother -- if on Androgel, test PSA early and often and be prepared to stop or move to 'active surveillance' . Work with a good doctor on this stuff ... it's thin ice.

Ray

Here is an approximation of the graph that explains the "activation" theory. It tends to agree with your dad's rad onc as long as you take "some" to mean "not that much."



Activation
^........................................ . . . . .' ' ' ' ' ' ' ' '........<== 100 % Activation
|.................. . . . . . . ' ' ' ' ' '..................................<== Some protection
|...........'
|........'
|.......
|......
|....:
|...:
|..:
|.:
|..
|:
---------------------------------------------------------------------> T
Castrate..........................Low.....................'Normal'

JAVGuzzi said...
Looks like the "Activation" theory is opposed to Morgentaler's "Saturation" theory. See his article.

Actually, no. They say nearly the same thing. If you look at the activation graph and see how it flattens out as T increases that is because the androgen receptors are approaching full "activation" or are becoming "saturated". It approaches 100% activation as an asymptote.

A simplistic version of the saturation theory would have the "activation" (here the effect on the cancer cells) show a sharp linear rise and then go totally flat at the saturation point. The activation theory rounds out the elbow but still fits the saturation graph fairly well.

Peter:

Morgentaler's Saturation Theory says any level of "T" greater than a very low level should not have any effect as far as promoting additional CaP growth. It says nothing about "protection".   The theory assumes that CaP is present.  That was the point I was making by my statement.

Here's a link to his Saturation Theory:
http://www.urosource.com/fileadmin/European_Urology/european_urology/Morgentaler%20best%20art.pdf

JAVguzzi:

He repeatedly says that adding T above the "saturation" level produces "little or no effect." You and I seem to be arguing about whether that means "little effect" (my reading) or "no effect" (yours). If it is "little" then whatever little difference there is between low T and normal T would show that little effect.

Reading your statement again I wonder if you read my graph differently than I intended. I was not saying that additional T gave "protection". Instead, I was saying that having low T might offer a tiny bit of "protection" as compared to having normal T but that the difference would be tiny.

Post Edited (PeterDisAbelard) : 12/11/2012 6:57:04 PM (GMT-7)

mspt98 -

My insurance all but quit paying for Androgel.... So I asked them which one they would pay for. They said Testim. Uro said it didn't matter to him which one I took...