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Estrogens

Many men, for many reasons, don’t want to undergo surgical castration, so they opt for chemical castration—taking drugs that accomplish the same result without the cosmetic change.

DES, the main oral estrogen, targets a different checkpoint—the hypothalamus and pituitary connection, instead of the testicles. It works by blocking the release of LHRH, which in turn blocks the release of LH and FSH, virtually shutting down the Leydig cells, the testicles’ testosterone-making factories. So testosterone drops to the castrate range.

The effect is not as speedy as with surgical castration; it generally takes ten to fourteen days for testosterone to fall to the castrate range. And, it’s not permanent—in most cases, the testicles start making testosterone again soon after a man stops taking DES.

We talk about DES here because it’s the most widely used oral estrogen, and it’s the gold standard of estrogen therapy for prostate cancer. Other drugs, such as Premarin and ethinyl estradiol (both medications used by women during menopause) are considered as effective as DES; neither is better. Another drug, called cholotriansene (TACE), is a synthetic estrogen that lowers testosterone but doesn’t completely shut down its production; it also permits the body to make a litde bit of LH. (It has proven to be ineffective, and is no longer used in attempts to lower testosterone levels to the castrate range.) A drug called polyestradiol phosphate (Esradurin), injected once a month, may be easier to tolerate for men with gastrointestinal problems; And for men with advanced prostate cancer who haven’t responded to other estrogen drugs, diethylstilbestrol diphosphate (Stilphostrol) may bring relief of symptoms. It is administered intravenously, at 500 to 2,000 milligrams a day.

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