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The use of statins to control dyslipidemia is now over 20 years old and supported for patients with coronary artery disease by the landmark Scandanavian Simvastatin Survival Study published in 1994. That study demonstrated a significant reduction in the rate of myocardial infarction and death among treated patients and remarkable safety. Subsequently numerous trials demonstrated their efficacy and safety in the cardiovascular arena even among patients with relatively normal lipid profiles and found a wide variety of other “off target” effects of statins which were originally designed to inhibit HMG-CoA reductase, a key enzyme in the regulation of cholesterol. For example the JUPITER trial highlighted the importance of CRP, a marker of inflammation as a possible additional mechanism of action.
Fortunately, many of the “off target effects” of the statins also have the ability to suppress cancer development, some of which may relate to the evolving understanding of insulin resistance and insulin as a growth factor for prostate cancer. Dozens of articles have been published on the efficacy of statins to reduce the incidence of a wider variety of cancers, including (but not limited to) colon, breast, esophageal, gastric, and melanoma because their use is so common in the population and both cancer and heart disease are common to the aging process. The studies are often confounded by “what else” patients might have been doing (exercise, low fat diets, taking NSAIDS, finasteride, dutasteride, etc), but in general it is likely that statin use is beneficial in prevention and perhaps in prolongation of survival among patients with prostate cancer. In one of the larger articles demonstrating this effect, Yu et. al. studied 11,772 men from the UK who were newly diagnosed with non-metastatic prostate cancer between 1998 and 2009. They published these conclusions in the Journal of Clinical Oncology last year:
“During a mean follow-up time of 4.4 years (standard deviation, 2.9 years), 3,499 deaths occurred, including 1,791 from prostate cancer. Postdiagnostic use of statins was associated with a decreased risk of prostate cancer mortality (HR, 0.76; 95% CI, 0.66 to 0.88) and all-cause mortality (HR, 0.86; 95% CI, 0.78 to 0.95). These decreased risks of prostate cancer mortality and all-cause mortality were more pronounced in patients who also used statins before diagnosis (HR, 0.55; 95% CI, 0.41 to 0.74; and HR, 0.66; 95% CI, 0.53 to 0.81, respectively), with weaker effects in patients who initiated the treatment only after diagnosis (HR, 0.82; 95% CI, 0.71 to 0.96; and HR, 0.91; 95% CI, 0.82 to 1.01, respectively).”
A very balanced editorial accompanied this publication reviewing the many similar articles and came to the cautious conclusion that “the current data may be sufficient to sway some clinical decisions toward statin use for men who are on the borderline for cardiovascular disease prevention.” I would certainly concur with this opinion, and if you have family members at risk for prostate cancer, it would seem prudent for them to have their lipid profiles tested and (given the other potential benefits and low risks for statin use) have them discuss starting statins if they have not already done so. Adding statin “therapy” after prostate cancer is diagnosed is probably of little harm, but as with metformin, much less proven as an interventional strategy.