Tag Archives: prostate cancer risk

Gentlemen, Start your Moustaches !


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Movember is both a month and a cause, the latter being one you should commit to supporting. Adam Gerone described his journey starting this remarkable movement in a TED talk that you should watch, just for it’s inspirational value if nothing else. This year, Movember has morphed ahead and is challenging all of us to not only support the research into men’s health (and especially prostate and testicular cancers), but to get off the couch and MOVE, with the tagline “30 MOVEs in 30 days“. As my faithful readers will know, exercise is an incredible way to fight both cancer and the side effects of androgen deprivation.

So here’s the deal: I think you should sign up with Movember to raise money for our cause AND you should commit to exercising more this month. If you don’t have a team to join or don’t want to grow your own moustache to remind your friends of how important our health is, you can support my scraggly moustache by clicking on THIS LINK, but in any case, enjoy this fabulous month and get off the couch! That’s it for today – I’m off to the gym.

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What is going to kill me? – the cloudy crystal ball


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With an intense focus on prostate cancer, it is easy to overlook the reality of other causes of death or disability in making decisions about therapy. An example of this issue is the proliferation of molecular tests that have been validated to separate patients with “intermediate risk”, or “low risk” into “even lower” or “even higher” risk disease categories using a number of different gene expression profiles on the tumor or biopsy material. For example, Genomic Health offers the Oncotype Dx test that provides a “Genomic Prostate Score” that gives a patient who (based on clinical criteria such as PSA and number of biopsy cores positive) falls into a low or intermediate risk category another lab value (GPS) that can potentially be useful in making a decision about treatment. GenomeDx has a test that can evaluate high risk men after prostatectomy to more accurately predict metastatic disease at 5 years. There is a very balanced article on the challenges of using these tests (which are a potential step forward to be sure) in the real world of the clinic here.

However, in all of the excitement and marketing of these and other tests, a couple of key facts are often overlooked (and may be much more important in decision making). Prostate cancer is generally a slow disease anyway. Competing mortality looms large as patients get older. And most importantly, there are validated ways to put the “whole patient” into the picture before ordering these tests, whether they be a PSA, biopsy, or molecular analysis. The Charlson comorbidity index can be extremely useful in predicting survival and is barely ever mentioned in the molecular analysis literature/reports. It is a simple yes/no answer to whether a patient has any of these 12 conditions: diabetes, bleeding gastrointestinal ulcer, chronic lung disease, congestive heart failure, stroke, myocardial infarction, angina or chest pain, cirrhosis or liver disease, arthritis, inflammatory bowel disease, hypertension, and depression. In a lovely article published last year, the use of this analysis in relationship to prostate cancer mortality gave a vivid picture of prostate cancer mortality in the larger setting of 3533 men with prostate cancer. A snapshot of their data looks like this:

Screen Shot 2014-06-19 at 9.15.54 AM

Very often, the comorbid conditions lead to death from another cause. In my opinion (and in my practice), we too often ignore our ability to quantify the risk of dying from “something else” when we focus so intensely on the PSA or other tests in counseling patients about what to do. It is also true that patient perception of test results can vary dramatically. One patient with a “GPS score” of 10 might be reassured, while another will perceive it as “not low enough” and opt for aggressive treatment rather than observation. To some extent this exposes the fallacy of “we need to separate the issue of treatment from that of diagnosis” thinking. Until the crystal ball becomes crystal clear, management of prostate cancer will remain challenging and requires the kind of wholistic thinking that is often better done by primary care physicians or public health professionals than by prostate cancer docs, or their patients.

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PCPT rides again – finasteride (proscar) to the rescue?


Today’s NEJM has a great article written by our colleagues who headed this study designed to ask whether taking finasteride could reduce the incidence/death rate of prostate cancer. This is the same group that reported on fish oil being a risk as I have previously discussed. The main finding of the PCPT trial was that taking finasteride (Proscar™) could reduce the rate of prostate cancer, BUT that there were more high grade cancers in the group taking the drug compared to placebo. As a result of this finding (which has been the subject of extensive discussion and speculation…for example one analysis suggests that this is an artifact of making high grade cancers easier to find because the prostate volume shrinks by about 1/3 in men on finasteride), the FDA issued a warning against taking finasteride or dutasteride. In the article released today, the investigators reported on the long term outcome of the study. As usual, the results are creating much discussion, and differing points of view. Overall there was NO DIFFERENCE in the death rate among men taking finasteride vs. placebo. 78% of men in each group survived 15 years. Moreover, there was no difference in the death rate among men who did develop cancer regardless of whether they were on finasteride or placebo. The investigators suggest this means it is reasonable to take finasteride to reduce the incidence of men who must deal with a diagnosis. Of course another approach (favored by the U.S. Preventive Services Task Force) is not to screen at all (remember all the patients in the trial were being screened by psa testing). Based on these considerations, I think it would be reasonable to recommend finasteride as a preventative in men who have a positive family history. Purists would point out that this has not been tested and would require a prospective trial before making such a recommendation. Where is Diogenes when we need him???

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Something fishy with fish oil?


Several patients have commented/questioned recent news blurbs about fish oil causing prostate cancer. The article from which news sources developed  alarming headlines comes from the SELECT trial investigators. In that trial, 35,000 men over age 50-55, with PSA <4.0, and normal DRE were randomized to receive vitamin E, Selenium, both, or placebo. The results, in spite of earlier evidence for protection, did not find any protective value in the supplements.

That fact in itself should be a cautionary note in considering what supplements do and don’t do. I, myself, took selenium for a number of years based on what I thought was pretty good evidence that it might prevent prostate cancer. In the study I was relying on, patients with a history of skin cancer took selenium to see if they could prevent further skin cancers from developing. A secondary endpoint in the trial was the evaluation of other cancers, and sure enough, there was “statistically significant” less prostate cancer in men who took selenium compared to placebo. That gave rise to the proper, prospective SELECT trial which was negative. However in the article, a secondary endpoint, the rate of prostate cancer as related to long chain omega 3 fatty acid levels in serum, was evaluated. The conclusion was as follows:

“This study confirms previous reports of increased prostate cancer risk among men with high blood concentrations of LCω-3PUFA.”

Now we have the fish oil story. How can you evaluate trials like this that hit the news all the time? First, you might ask yourself how many patients were in the trial. For example, I blogged about Pomi-T earlier this summer. You can look at that blog and find that it was a very small study AND that there might have been a commercial bent to it’s analysis and presentation. I hope my blog was sufficiently cautionary – although I have suggested a few patients might try it if they want, after reading the blog. The SELECT trial passes muster with a large number of patients.

Second, it can be worthwhile to look at other articles on the same subject. My favorite way to do this is via Google Scholar. Open Google and look at “other” in the pulldown menu and you will find it – you can bookmark that or go there via this link and save the bookmark. Enter “fish oil prostate cancer” and you will find a large number of previous trials to go through. Add the word “meta” and you can find some additional articles, like this one. The conclusion seems at odds with the fish oil hype of the media last month:

“Our analyses provide no strong evidence of a protective association of fish consumption with prostate cancer incidence but showed a significant 63% reduction in prostate cancer–specific mortality.”

So my bottom line is that if you simply read the headlines, you are often misled. The real story seems more complex. I continue to recommend reducing fat intake in patients who have metastatic prostate cancer and are watching their psa. I have previously blogged on this topic here. And as for the fish oil story, maybe it could help your heart, (see this reference for the controversies there…obtained by entering “fish oil cardiac meta” at Google Scholar – then restricting to articles since 2012) but I’d say the jury is still out as regards prostate cancer. And whatever YOU decide, be aware of the media’s tendency to hype the latest finding and tell a simplified story.

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