Jim’s Prostate Cancer 101

These brief statements about Prostate Cancer (PCa) statements are necessarily incomplete. But I think they will be helpful for PCa patients.

Is it true that traditional PCa operations have not been shown to improve life expectancy?

Why does the American Academy of Family Physicians advise member doctors to not even run patients’ PSA tests unless they commit to serve as PCa patients treatment gatekeepers so they can safeguard patients against unwarranted treatments that prostate specialists commonly use? 

Many doctors say many men with PCa may need to do little or nothing. PCa patients do not have to have surgery or radiation on their prostates.

Do PCa patients demanding to get their cancer out understand they can focally destroy/ablate PCa tumors while sparing other prostate tissue, a partial prostate removal? This is somewhat like what women who have lumpectomies instead of mastectomies do to keep most breast tissue. 

Focal treatment options include HIFU (high intensity focused ultrasound) or MRI guided laser.

It seems to me that PCa can be managed with drugs, allowing PCa patients to avoid or, if management didn’t work or they change their minds, later radiate or remove their prostates. 

Some leading doctors use finasteride and dutasteride, among other drugs for other purposes, to reduce testosterone conversion into dihydrotestosterone (DHT) and estradiol, a couple of postulated PCa promoters. Tracking PSA’s rate of change, or doubling time, may be the best way to use PSAs. Sequential testing is needed. Continually rising PSAs warrant PCa management action.

A stable PSA indicates any PCa is not growing, negating the need for treatment and perhaps limiting action to watchful waiting.

Notwithstanding a Nobel Prize assertion to the contrary, research indicates testosterone does not cause PCa and may actually help control it if drugs preventing its breakdown into other hormones are taken.

It is possible to know if PCa has spread outside the prostate by using C-11 acetate, choline, or other isotope scans. These isotopes light up fatty acids which cluster around any fatty acid producing PCa tissue which has spread beyond the prostate. If PCa has spread beyond the prostate, PCa patients are not usually Focal PCa treatment candidates.

MRI guiding of biopsies can improve biopsy efficacy, offering better information than non-MRI guided biopsies.

Although testosterone may help patients control PCa, careful blood monitoring is needed because testosterone can cause red blood cell density changes and life-threatening risks.

Studies have shown that PCa patients given testosterone replacement therapy (TRT) after surgery or radiation were 50 percent less likely to have a PCa recurrence. One study has shown that men in their forties who had below normal testosterone readings and use TRT are two-thirds less likely to contract PCa as such men who do not use TRT.

Any man with any prostate tissue will have positive PSA readings.

It is my experience that medical community tribal practices may prevent doctors from referring patients to outside doctors who might do a better job or have better technology.

Abstract: Recent experiments have shown that estradiol is the primary cause of prostate cancer. Since estradiol in men is produced by the action of aromatase on testosterone, testosterone is only the secondary cause of prostate cancer. In normal prostate epithelial cells estradiol causes mitosis, whereas testosterone prevents mitosis.

Estradiol is mutagenic through the formation of depurinating estrogen–DNA adducts 4-OHE1(E2)-1-N3Ade and 4-OHE1(E2)-1-N7Gua. For decades, doctors have been taught that testosterone is the primary cause of prostate cancer. This misunderstanding has not only been believed by the medical profession, but by the general public as well.

As a result of this, too few researchers are exploring the therapeutic uses of testosterone in treating prostate cancer, funding requests are being denied due to the ignorance of funding reviewers, and volunteers for being treated with testosterone are hard to find.

The solution to all of these problems is to educate the medical profession and the general public about the true relationship between testosterone, estradiol, and prostate cancer.

Below is the conclusion paragraph of the 7/19/12 New England Journal off Medicine epidemiology prostate cancer article. Its conclusion is consistent with a 1995 Swedish study. Neither supports the efficacy of localized Prostate Cancer prostatectomy treatments. To our knowledge there has not been any evidence brachytherapy has better mortality results than radical prostatectomy.

In conclusion, our study showed that, as compared with observation, radical prostatectomy did not significantly reduce all-cause or prostate-cancer mortality through at least 12 years among men with clinically localized prostate cancer that had been diagnosed in the era of PSA testing.

Absolute differences in mortality between the study groups were less than 3 percentage points. Subgroup analyses suggested that surgery might reduce mortality among men with higher PSA values and possibly among men with higher-risk tumors, but not among men with PSA levels of 10 ng per milliliter or less or among men with low-risk tumors.