In the full text of their original paper, Gat and his colleagues describe how, in a very high proportion of men diagnosed with prostate cancer, testosterone may reach the prostate directly from the testes as a consequence of an age-associated malfunction of the testicular and the prostatic venous drainage systems, allowing testosterone to bypass the normal systemic circulation and massively over-stimulate the androgen receptors in the prostate. They go on to describe two different procedures (using either microsurgery or an invasive radiological procedure) that can be used to stop these high levels of testosterone from reaching the prostate, and the effects of one of these techniques in a small set of patients.
The actual paper describes two experiments. In the first experiment, Gat et al. examined 72 randomly selected patients with localized prostate cancer for varicocele — an abnormal enlargement of one or both of the internal spermatic veins in the scrotum that drain the testes. They showed that all 72 patients had malfunctioning one-way valves of the internal spermatic veins (bilateral varicocele). They postulate that this type of malfunction of these valves could have led to massive overstimulation of the prostate by testosterone.
In their second experiment, Gat et al. describe the use of “percutaneous selective sclerotherapy” to seal off the flow of high levels of testosterone from the testes to the prostate that had resulted from this malfunction of the internal spermatic veins. This procedure was carried out on 6 patients, all of whom had Gleason 3 + 3 = 6 disease and were being managed on an active surveillance protocol. The results of this second experiment were as follows:
Before the procedure, the patients’ average prostate volume was 65.3 ml (range 41.7–114 ml), and their average PSA level was 8.89 ng/ml (range 3.69–14.5 ng/ml).
At 6 months after the procedure
The patients’ average prostate volume had decreased to 36 ml (range 26.2–71.4 ml), and their average PSA level had decreased to 5.95 ng/ml (range 2.24–9.5 ng/ml).
In 5/6 patients (83.3 percent) there were no prostate cancer cells observed on post-treatment follow-up biopsies.
In 1/6 patients (16.7 percent) the post-treatment follow-up biopsy showed persistence of localized prostate cancer.
Why are we re-commenting on this paper? Two reasons. (1) Because the first time we wrote about it, there was surprisingly deathly silence, but yesterday a respected regional support group leader, who had not seen our original report, brought this paper to our attention again. (2) Because this may prove to be the most important paper on prostate cancer published in 2009 — which would make it a good gift to pass out on Christmas Day!
The hypothesis proposed by Gat and his colleagues may seem completely “off the wall” to many. However, The “New” Prostate Cancer InfoLink thinks that their hypothesis makes some sound physiological sense — and their hypothesis appears to receive confirmation from their initial experiments. We believe that someone at a major prostate cancer center (in the US or elsewhere) needs to repeat these experiments in an attempt to confirm or disprove the findings published by Gat and his colleagues. This group of investigators won’t have their careers shattered if their hypothesis is shown to be unsound. However, if they are correct in their hypothesis, then we need to know this soon!
Radically new theories that propose ”off the wall” causes for common disorders take time to filter their way into the medical mainstream — even when those theories are right and are supported by relatively compelling data. One of the best, and relatively recent, examples of this was Marshall and Warren’s “outrageous” suggestion (in 1982) that most gastric ulcers might be caused by a very common bacterium found in the gastrointestinal tract of half the people on the planet. In took Marshall and his colleagues the best part of 10-15 years to convince the medical establishment that this was, in fact, true. In the end, however, Marshall and Warren were awarded a Nobel Prize for this work in 2005. Even if Dr. Gat and his colleagues are correct in their hypothesis, it may take a similar effort over a similar time period to convince people that the cause for most prostate cancers is physiological in nature. But if they are, another Nobel Prize may well be in order.