GDF-15, vitamin D, and risk for prostate cancer

A new study by Lambert et al. in the journal Prostate proposes that some forms of chronic prostatic inflammation, driven by low levels of a molecule known as growth differentiation factor-15 (GDF-15), may lead to prostate cancer development. Why? Because GDF-15 is normally highly expressed in the prostate and low levels of GDF-15 can lead to chronic prostatic inflammation and tumorigenesis.

In an associated post on the blog site of the University of Colorado Cancer Center, the authors also explain that the gene for GDF-15 is known to be upregulated by vitamin D, and that this gene is “notably absent” in samples of human prostate cancer driven by inflammation. Thus, if men have low levels of vitamin D, they may be at high risk for prostatic inflammation, which may drive certain subtypes of prostate cancer. (Not all prostate cancers are necessarily caused by inflammation, but some certainly are.)

It would be premature to conclude, on the basis of this one study, that the majority of prostate cancers are being caused by low levels of vitamin D and an associated risk for chronic prostatic inflammation. However, Lambert and his colleagues have developed an interesting hypothesis that does lead to ideas about new ways to prevent development of at least some types of prostate cancer. This is just an hypothesis at the present time, but we look forward to seeing whether the hypothesis can be validated.

6 Responses

  1. Ah, but, there are already many studies out that connect low (as in very low) levels of D3 and a rise in occurrence of all cancers, generally.

    As such, it’s perfectly logical to assume the same re prostate cancer. So many cells in our bodies have D3 receptors. (D3 is not actually a vitamin, it’s a hormone created by our bodies when they get sufficient sunlight).

    Further, since blacks have a higher incidence of prostate cancer, it might be further connected/correlated to their difficulty in getting enough D3 from sunlight.

    FWIW, it’s almost impossible to get enough D3 from diet. That’s why D3 supplements are so important to health and an anti-cancer regimen.

    Further, there are studies that show less PCa from traditionally warmer climes, and the opposite, that more cases of PCa come from the less sunlit places. I believe also, PCa patients from those warmer climates have greater survival rates even after PCa is found and treated.

    Very interesting indeed!! :-)

  2. Walt:

    If you read the two links in the commentary above with care, Lambert et al. do not limit the potential applicability of their findings to prostate cancer … but it was in studying prostate cancer that they made the connection.

  3. There is also a strong correlation between low levels of D3 and dementia in the elderly. Last year my family doctor started testing all of his over-50 patients for vitamin D (which is mildly controversial, because it is a fairly expensive test compared to the rest of the normal blood workup). Mine was slightly low, and he advised taking a supplement, which I have been doing. In December I’ll get my annual physical, and am curious to see if the supplement has actually raised my blood level of vitamin D.

  4. Doug,

    Just an FYI, liquid D3 has been shown to have a 30% better absorption in many people. Some of us don’t absorb the powder (in some of the pills) very well.

    Also, if you can, try to take it with a meal that has some fat in it, as D3 is fat soluble. I get my liquid D3 from a source on Amazon (not sure if I can post the link here).

  5. Very interesting, and something I have been wondering about for nearly 3 years. I was treated for high-risk prostate cancer, partly by using adjuvant ADT with Zoladex for a bit more than 3 years. Two years into that treatment-part I spoke with an oncologist in another country, i.e. not in Sweden. He told me I was getting world-class treatment (true) but asked if I had gotten a bone mineral density test. I did not know what that was, as I had never gotten one. It’s for osteoporosis, which ADT often induces between 6 months and 1 year. To be brief, no patient on ADT had been warned about this for some time, at the rapidly deteriorating Uppsala Academic Hospital. Had I known at the start, I could have taken extra vitamin D + calcium tablets then, to mitigate the standard deviations from baseline that define “confirmed osteoporosis.” I did not take this sitting down, met resistance from the very people who were doing a fine job with the cancer, got the test, learned that I have osteoporosis, and began taking D and calcium. It’s been stable for 2 years. After about five errors I discharged myself from that unit three weeks ago. Other doctors elsewhere are doing the blood work. Reading this heightens my feeling that I did the right things, especially because my rather strong insistence changed the policy at that place. Soon, all men slated for ADT of at least 6 months will get the test for osteoporosis immediately (for a baseline) and then periodically. I think every 2 years. Fine for others, but that division has seen the back of me.

  6. I should add one thing. Thanks to me, all men slated for ADT, I think for at least 6 months, who have certain risk factors, e.g., smoking, now receive the bone mineral density test. I argued that all such men in my condition should get it. I think my reasoning is interesting. As soon as one starts on ADT, one acquires a new risk factor: the increased probability of getting osteoporosis from that course of ADT. Since this is known by one’s doctors, the benefit of a test for all such men follows by standard Bayesian reasoning. If this doctor succeeds, then all men in my condition will get the test. I know this person and am almost certain that this will happen soon. Take this as a qualification of my text.

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