Why do men get prostate cancer?

The answer to this question, some 70 to 80 years after we started to see if we could answer it, is still: “We haven’t got a clue.” But every so often people come up with a new or a revised hypothesis, and it can take years to work out whether each specific hypothesis is viable.

So the latest hypothesis is laid out in a new paper by Costello and Franklin that was just published in Oncology Reviews. For those who are interested, the entire text is freely accessible on line.

The authors lay out a detailed argument as to why — in their opinions — the development and evolution of clinically significant prostate cancer is potentially dependent on

  • The accumulation of high levels of zinc for secretion into prostatic fluid
  • The consequent production of high levels of zinc citrate
  • Down-regulation of the production of zinc citrate (necessary to prevent the cytotoxic impact of high zinc levels in malignant cells)
  • The roles of testosterone and prolactin in influencing these effects

Those who are interested in understanding the details behind this hypothesis are politely referred to the original article, which includes a description of what the authors refer to as their concept of “the ongogenic development of prostate malignancy.”

Despite his arguably “antique” degree in biochemistry, your sitemaster is not able to be able to provide any definitive insight into the potential accuracy of the authors’ hypothesis. (Strictly, to be an antique, something must be at least 100 years of age; your sitemaster’s biochemistry degree will actually be 50 years of age in June 2019, so there is a little literary license being taken here. As far as your sitemaster is aware, there were no undergraduate degrees in biochemistry available in 1918 or earlier and so no one really has — or has ever had — an antique degree in biochemistry.)

Does the hypothesis sound feasible? Yes, it does. Does the hypothesis have an inherent logic? Again, yes it does.

But actually proving that this is the process that stimulates the growth of tumors inside and later outside the prostate is going to require some very sophisticated research over time.

Editorial note: We thank one of our regular readers for bringing this hypothesis to our attention.

4 Responses

  1. Thank you, as always, for your insights. I assume that it is much, much too early to make any assumption about dietary, medicinal, or activity changes based solely on this article and it’s hypothesis?

  2. Dear SteveMc:

    Yes. I think so. After all, it’s only an hypothesis at present.

  3. Thank you!

  4. Sitemaster,

    Dr. Costello (a dentist?) had a subsequent abstract published in 2019 in which she claims she cured an advanced prostate cancer patient by prescribing cabergoline, which reduced the patient’s prolactin level from 11.3 to 1.3 micrograms/ml, and “therefore” reduced the CTC count from 5.4 to zero.

    One would think that if there were something to this hypothesis (which is also mentioned in Dr. Strom’s book, Prostate Cancer: Essentials for Survival (2013), there would be some serious investigation of cabergoline’s effectiveness in relation to suppressing prolactin and CTCs in advanced prostate cancer. I am very wary of a “one patient” success story as a basis to believe a such fantastic claim, and this abstract, in my mind, only serves to discredit the author.

    Best regards,


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