This is not to say that hormone therapy does not work. It does work. It does prolong life, and it does ease many symptoms of advanced prostate cancer. The take-home message here is this: There’s no evidence that giving a man early hormone therapy, or giving more hormone therapy than is necessary, works any better than giving adequate hormone therapy if and when a patient needs it.
The other truth we have to face is that hormone therapy does not cure prostate cancer. And if a man lives long enough, this cancer will progress. Despite so many refinements in hormone therapy, the death rate for advanced prostate cancer is about the same as it has always been. And the reason these men are dying has nothing to do with the hormone-responsive cells; we can control those cells. It’s the hormone-insensitive cells we can’t seem to kill. So what we need, urgently, is a better way to target this group of cells.
But until we have such a treatment, perhaps the best strategy with hormone therapy is to find ways of lowering its costs or minimizing its side effects. Are the most expensive hormone treatments necessarily the best? Probably not. Surgical castration and one milligram a day of DES are equally effective. Even though one milligram does not lower testosterone dependably to the castrate range—as three milligrams a day does—this might not be necessary, since castration and one milligram of DES seem to be equal in terms of survival. DES is a lot cheaper than LHRH agonists, which can cost several hundred dollars a month. And DES’s biggest side effect, painful breast swelling, can be taken care of relatively cheaply with radiation treatment. However, men with a history of heart disease or thrombophlebitis should not use DES as their main form of treatment.
Another way to improve hormone therapy would be to diminish its side effects—particularly impotence. One hope in this area may be flutamide, perhaps combined with finasteride—both preserve potency in most men. The theory here is the “one-two punch.” Flutamide blocks the binding of testosterone and DHT to receptors in the prostate (the “keys-in-the-lock” idea). With help from finasteride, which decreases the amount of DHT floating around inside the prostate, only testosterone is left to bind to the receptor. Therefore, because testosterone’s link to the receptor is relatively weak, it becomes easier for flutamide to jolt testosterone out of the way—to knock the key out of the lock.
Will this work? It needs further investigation, but laboratory studies are promising. The result would be hormonal treatment that doesn’t make men impotent and doesn’t leave them feeling “unmanly,” or suffering any of the other side effects from conventional hormone therapy. This should be a major focus of research in the near future—developing effective hormone therapy with fewer side effects.
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