I know there has been lots of discussion on the subject topic. In hopes of not beating a dead horse I recall those that claimed a hydrophilic (Crestor -rosuvastatin) had no positive benefit vs a lipophillic statin such as atorvastatin. However notable studies Contradict this notion,
“Our results suggest that only atorvastatin, pravastatin and rosuvastatin were associated with improved survival in advanced PC patients receiving ADT.” urotoday.com/recent-abstrac....
Also the acclaimed prostate doc “Snuffy Myers” if I recall correctly, advocated rosuvastatin, among other statins. I’m thinking that there is more to this than “hydro” vs “ lipophillic” mechanisms and that is an over simplistic analysis. We all know cancer is very complex and based on the literature it seems the statin benefit goes beyond an explanation of hydro and lipophillic characteristics. Reason I’m bringing this up is because my pcp switched me to Crestor from atorvastatin due to very minor liver indications in my blood work. Based on the literature I see no benefit to switching in order to maximize my asssult on my mHSPCa.
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The best evidence so far is a "Mendelian randomization study" involving 655,000 people. They found that people who have a genetic mutation that simulates the HMG-CoA reductase inhibition that statins cause have exactly the same incidence of cancer (including prostate cancer) as people who have no natural HMG-CoA reductase inhibition. This means statins cannot prevent PC. Can they slow down, speed up, or have no effect on PC that is already there? There's evidence for each hypothesis, but the evidence is weak. I think that if you are taking it for cardiovascular effect anyway, it probably will do no harm and might help slightly.
Hhhmm… I'm more inclined to concur with the limitations of the study that it's authors identify, namely:
Our study has limitations. First, as mentioned, genetic variants that mimic the effect of a therapeutic agent cannot anticipate potential drug-specific adverse effects of a therapy that is not related to its mechanism of action (i.e., off-target effects). Second, genetic variants reflect the effect of lifelong exposure to a biomarker on an outcome and therefore cannot be used to estimate the expected effect of short-term pharmacologic changes in that biomarker directly.9,23,24 Third, most major adverse effects tend to be uncommon, leading to imprecise estimates of effect, particularly with genetic variants that have small effects on the exposure of interest. As a result, evaluation of the association between a genetic variant that mimics the effect of a therapeutic agent and numerous potential adverse outcomes can lead to both spurious suggestions of increased risk and false reassurances of safety owing to potential off-target effects, imprecise estimates of effect, the play of chance related to multiple testing, and difficulties in translating the observed effect of lifelong exposure into the expected effect of short-term pharmacologic changes.
Put simply, they have identified genetic variants that control/predict the short term LDL-lowering impact of statins and shown these same variants impact cardiac outcomes... and then shown that they do NOT correlate with cancer outcomes. But it feels like a bridge too far to conclude that LDL therefore has no impact on cancer outcomes, particularly in the face of population-wide studies that indicate otherwise.
Occam's razor suggests a simpler explanation may be that any cancer-related impact of LDL is not well represented by the genetic variants they have identified, and no more than that.
As I said, it does not say anything about cancer outcomes. It convincingly proves that a lifetime of statins/low LDL will not affect the incidence of prostate cancer. It proves that a lifetime of low LDL has zero impact on incidence of cancer. What it "feels like" to you is irrelevant.
"...particularly in the face of population-wide studies that indicate otherwise." You don't seem to understand the level of evidence that this rises to, which is very high. A large mendelian randomization study (MRS) like this simulates the structure of a large randomized clinical trial (which is the highest level of evidence). You can see by the enormous sample size and the genetic screening on all those people, how difficult an undertaking this was. It was a project of the UK government and several universities. It is far more reliable than any "population-wide study." We throw out all those studies when we get a MRS.
You have to let go of your confirmation bias. The simplest explanation is that those with this genetic variant, which gives them low LDL levels, has no impact on incidence of cancer.
Before launching large clinical trials to confirm the effects of statins in improving outcomes among men with prostate cancer (PC), the most appropriate target patient population and the type of statins need to be clearly identified.
Patients and methods
A retrospective cohort study was conducted using the Taiwan Cancer Registry of 2008–2014. This study included 5749 men with locally advanced and metastatic PC who received only androgen deprivation therapy (ADT) in the first year after their cancer diagnosis. Statin users were defined as anyone who was prescribed statins for >28 days. An inverse probability of treatment-weighted Cox model was used to estimate the effects of statin use on all-cause mortality and PC-specific mortality (PCSM) while treating the statin status as a time-dependent variable.
Results
Overall, 2259 patients died, and 1495 of them died of PC during a median follow-up of 3.6 years from 1 year after their diagnosis. Statin use was associated with significant reductions in all-cause mortality (hazard ratio [HR] = 0.78, 95% confidence interval [CI]: 0.70–0.86) and PCSM (HR = 0.76, 95% CI: 0.68–0.86) for metastatic disease and all-cause mortality (HR = 0.66, 95% CI: 0.54–0.81) for locally advanced disease. Patients who received atorvastatin, pravastatin, rosuvastatin or pitavastatin showed a stronger reduction in mortality than those who received other statins. Benefits of statins were consistently observed in men who received post-diagnostic statins, even in those with high comorbidities or an old age.
Conclusions
Our results suggest that only atorvastatin, pravastatin and rosuvastatin were associated with improved survival in advanced PC patients receiving ADT.
Dr. Myers has often been cited as preferring Rosuvastatin [Crestor].
Anyone who has sat through his vlog posts will know that he was always very concerned about losing patients to heart disease. At one point, he said that he prescribed statins to patients who could not control their cholesterol levels. So, although his patients did have PCa, he did not use statins to treat PCa itself.
(Some time before retirement, he came to the conclusion that Metformin was a useful anti-PCa drug. He did not restrict Metformin to diabetics or men with high fasting glucose. He had not however come to a similar conclusion regarding statins. In fact, he preferred that men lower cholesterol through lifestyle changes.)
Statins. Lipophilic versus hydrophilic.
I use Simvastatin for PCa. I have no other reason to use a statin. My decision was made over 10 years ago. There might now be a better option, so I'm not pushing Simvastatin, which is a relatively lipophilic statin.
When choosing a statin for PCa, there are two things to consider:
i) The effect on circulating cholesterol (i.e. liver production) - particularly LDL-C & VLDL-C, and how this might affect availability to PCa cells. All of the statins in use presumably do the job fairly well. In 2013, Rosuvastatin was #4 in sales. I can't say how much this was due to efficacy, marketing, (or Dr. Myers.)
Note that "Pravastatin and rosuvastatin show greater hepatoselectivity than lipophilic agents, as well as a reduced potential for uptake by peripheral cells." [1]
"Lipophilic statins cross the blood-brain barrier more readily, which may lead to central nervous system complaints such as insomnia, although this is rare." [2]
ii) The ability of the statin to get into PCa cells and prevent the manufacture of cholesterol. I believe that this requires a lipophilic statin for uptake. A member has stated that a researcher he communicated with doubted that this occurred in practice. Until we have good evidence that cells cannot be prevented from making cholesterol, I will continue to use a lipophilic statin.
Statins & Inflammation.
It has been suggested that the benefits of statins depend more on their anti-inflammatorty properties than their effects on cholesterol. In any case, the anti-inflammatory effect mightwell reduce the aggressiveness of PCa.
Statin Users.
At this point, the majority of male users are not taking it for PCa. The majority of users with PCa are not even taking it for PCa. We have little information as to the lipid profiles of users with PCa versus non-users with PCa. If PCa survival is better at lower cholesterol levels, I don't believe that statin studies have demonstrated that.
We should not make the mistake of assuming that statin users & non-users are similar populations. (On the other hand, in the U.S., pharma-promotion has been such that statin use has become the norm for men above a certain age.)
(With PCa studies of Metformin users, I have often wondered how a non-diabetic (myself) could use that information. Similarly, how does the experience of a man who is the typical statin user, predict what my experience will be?)
Statin Dosage.
Typically, we would expect a statin dose to be tied in some way to a desired cholesterol level. However, some PCa studies indicate that the dose itself, rather than the target cholesterol, is related to the benefit.
RE dosage: I am currently taking 10mg Crestor per day, which keeps my cholesterol where my cardiologist wants it. I'm due to see him in a couple of weeks and thought I'd explore with him the idea of increasing my dose, for PCa reasons. But to what? He will have no idea, I expect.
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