*This* I can relate to.

FYI, my Steve's only SE to Casodex was it kept him awake.  And I think
he could "feel" it in his body.  Like a formless edginess.  Haven't
heard of that from others.  But it seemed to go away.  The insomnia.
And the vague disquiet.   Of course he only was on the Casodex by
itself for a week, then came Prednisone-that was ucky.  One of the
biggest reliefs of no chemo was no prednisone.  Just the phrase 'side
effects' has my brain going in a wild scramble of all the one's we've
had, all the ones that we haven't but could, wondering what is from
what and when it will end and why even go there.  I'm sorry you're
looking at *another* treatment already again.    laurel

Actually, we can, in the sense that as long as we don't wait too long,
we can bail and end any carnage that occurred.

I.P.

I know I've left some people speechless before but....
Bev

Laurel,

The article doesn't talk about Proscar (which is 5 mg/day of F) or
Avodart, but just about F (but presumably enough F to block DHT
formation, which would make it the equivalent of Proscar or Avodart).
The important thing to remember is that they used one point of T (they
should have done a dose-response curve), so it is unknown how much
better higher levels of T might be.  All we know for sure is that F with
no T resulted in average tumor size that was ~80% compared to continual
ADT, whereas F + T resulted in average tumor size that was ~20% compared
to continual ADT.

I'm not an M.D., but based on my model, I would predict that higher
levels of T and/or adding a drug that blocks iAR, but not mAR, such as
flutamide should result in even better results.

There is an excellent reason not to do Proscar while doing RT.
According to my model, Proscar should increase bcl-2, and it is a known
fact that PCa cells with higher levels of bcl-2 are more resistant to RT.

I agree with ADT3, but only for intermittent use(the 13 months advocated
by Dr. Leibowitz seems quite reasonable.  After that, I would recommend
very high T, plus Proscar (or Avodart), plus flutamide (or Casodex if it
is shown to block iAR but not mAR as flutamide has been proven to do),
plus enough Arimidex to keep E2 at low normal levels (using ER-alpha
blockers would be far superior, but none are yet FDA approved).  From my
point of view, why would anyone want to go on continual ADT (with all of
its horrible side effects), when intermittent ADT followed by T + F
(with all of its health benefits) has been shown to be ~5 times more
effective?

My own point of view is that intermittent ADT followed by T + F should
be most effective the earliest it is used.  I.e., the ideal time to use
it is initially, in place of any surgery or radiation.  Less ideal is to
use it following radiation or surgery, although even in those cases, the
sooner it is used the better.  Waiting only increases the probability of
 fatal mutations that won't respond to any systemic treatment.
Ideally, one would shoot for a lifetime maintenance of high
physiological levels of T and low physiological levels of DHT and E2.
In order to drop the PSA, it might be necessary to go with T + F +
flutamide to totally block iAR and minimize DHT.  However, I believe
that some DHT is necessary for long term health.  More research is
needed to determine if any adverse health  consequences result with
higher than physiological levels of T when DHT and E2 are kept low.

Ed Friedman

Heck, I'd be willing to pay the whole bill myself!  (Just kidding - I'm
happily hetero and non-transvestite.)