HORMONES AND PROSTATE CANCER: AN OVERVIEW
Doctors have long known that hormones play a major role in the life of the prostate. In 1786, an English surgeon named John Hunter became the first to demonstrate in animals that a radical operation, castration, caused the sex accessory tissues, including the prostate, to shrink.
But it wasn’t until the 1930s that anyone discovered why this happened. At the University of Chicago, a trio of investigators discovered that removing the testes shut down production of testosterone. And, when shots of testosterone were injected back into castrated animals, these tissues were restored to normal size and function. This Nobel Prize-winning research included another valuable finding—that castration also could shrink prostate cancer.
The researchers were able to achieve the same effect chemically; they found they could shut down testosterone with doses of female hormones called estrogens. Estrogens blocked a signal, transmitted in the brain by the pituitary gland, called luteinizing hormone (LH), which stimulates testosterone. The oral estrogen, called DES (diethylstilbestrol), is what’s known as a chemical castrator; it causes impotence.
Impotence is likely with almost every kind of hormone therapy; 90 percent of men on hormone therapy lose sexual drive and the ability to have an erection. In the future, however, new hormone treatments (discussed later in this chapter) may prove effective without causing impotence.
For a time, hormone therapy does control prostate cancer. But what some doctors used to believe—that prostate tumors are nourished only by hormones, that hormone starvation will stop the cancer from spreading—is, unfortunately, not the whole story. Ultimately, hormone therapy will not stop the disease’s progression.
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