My LDL cholesterol has gone up considerably in the last couple years. I'm not sure if it is an inflammatory response to all the radiation, but regardless, I am thinking of adding a statin. I have read and my MO agrees there may be a mild benefit in the prostate cancer battle to adding a statin.
Does anybody know if there is a difference in that regard between the different statins? My preference would be Pravastatin. Even though it is not as strong, apparently it has fewer side effects, but I do not know if it as effective against PCa.
Interestingly, I have been primarily vegan for the last year, I am not overweight, and I exercise a lot. It was a surprise (and disappointment) that the LDL continued to increase with a "heart healthy" diet.
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jdm3
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According to these studies, hydrophobic statins (like simvastatin) may be preferable to hydrophilic statins (like pravastatin) for PC, although side effects may be higher.
Since side effects increase with dose, and the PC benefits are uncertain, I would go with the lowest dose available. Of course, if you have high LDL levels, your doctor may want you on some other dose.
There are many studies that suggest a benefit in PC and many studies that suggest no benefit. There is no proof either way. My personal opinion is that, for most men, the side effects of low dose statins are low, the possible benefits to cardiovascular health are high, and it is inexpensive. So I can't think of any good reason not to take it. The same reasoning applies to aspirin and metformin, btw.
You should discuss with your doctor. He will want to run lipid tests and a fasying blood glucose test before deciding appropriate doses. He will also monitor you as you take them.
When I asked our PCP about changing my husband's Pravastatin to Crestor(sp?) he noted the latter was harder on the liver. Anyone heard this before?
I take an acid reducer called omeprazole for GERD / reflux due to a hiatal hernia. Simvastatin was horrible -- it seemed to counteract the omeprazole completely such that I was suffering from heartburn. Atorvastatin (lipitor) worked for me so, I'll stick with it regardless of whether it is the best statin for prostate cancer or not.
I took Pravastatin for 8 years to control my mild hypercholesterolemia until I read the following article, then I immediately switched to Simvastatin. The article mentions that Pravastatin affects the immune system and has been linked to Prostate Cancer.
I was taking Simvistatin and Dr. Myers switched me to Crestor due to a lower risk of drug interactions and its effectiveness. I've been able to reduce the dose after a couple years on the Meditteranean diet he recommended and by excercising daily. He didn't want my LDL to go too low as it could impact my already impacted cognitive abilities.
During my final consult with Snuffy I complained about the cognitive SE's from Xtandi, Lupron, etc. He acknowledged that was likely the cause especially with the length of time I've been on it. He was also concerned about my LDL levels going too low since it is essential for proper brain function - my current level is 54. So he reduced my dosage of Crestor from 20mg to 5mg. That reading of 54 is after 6 months at the lower dose.
No just that T starved PCa will use LDL to make DHT so it is best to keep it low but not too low. I seem to recall he liked to keep it around 60, there's probably a video on YouTube where he discusses it. What's the deal with "small particle" LDL?
Small LDL particles are a far more destructive force than their larger counterparts. Like finely tuned weapons designed to wreak maximum damage, smaller particles more effectively penetrate the cellular barrier and enter arterial walls, contributing to atherosclerotic plaque. They also persist longer in the circulation, which allows more opportunity to cling like little magnets to tissues within the walls.
Once in the arterial wall, small LDL particles are more prone to oxidation, which stimulates the release of inflammatory and adhesive proteins. Small, dense LDL promotes endothelial dysfunction and enhanced production of pro-coagulants by endothelial cells. Small, dense LDL thus appears to be more atherogenic—that is, more likely to contribute to the build-up of plaque within arteries—than normal LDL.12,13
Small LDL can be an inherited predisposition that is activated by unhealthy lifestyles and weight gain. When the genetic factors are strong, it can occur in healthy people who are not overweight. It frequently causes heart disease and is found in more than half of all people who suffer heart attacks. Small LDL particles triple the likelihood of developing coronary plaque and suffering a heart attack.14
This one little measure also holds a world of hidden information. Not only does it indicate a higher risk for heart attack, but small LDL suggests that you are more resistant to insulin and more likely to develop metabolic syndrome, or even diabetes, if you become overweight.15 It also suggests that a very low-fat diet (deriving less than 20% of calories from fat) may paradoxically heighten your heart disease risk.16
Small LDL can augment the dangers of other cardiac risk factors, such as high total cholesterol, increased LDL particle number, or high C-reactive protein (a measure of inflammation). Researchers have noted that while elevated small LDL particle count alone can raise heart attack risk by up to 300%, heart attack risk is sixfold higher (600%) when elevated C-reactive protein is also present.17
Thank you all for the information and references. As with many of our decision points, this one is not clear cut, but it does appear that simvastatin gets the nod for possibly being mildly beneficial in the cancer battle. I will continue to research and report back if I find anything new and/or interesting. Thanks.
I take rosuvastatin (Crestor) and my chloresterol data is great. And I’m not a vegan . I’ve seen posts that say simvastatin is best for PCa but my RO (who follows Dr Myers) disagrees and no other statin has performed as well as Crestor has for me.
Been taking simvistatin for years. Has worked very well for me. I think, like PCa (and other) drugs, what works and doesn’t work for you is in part determined by your individual biology.
I asked my doctor for Simvastatin over 7 years ago, based on the PCa studies available. My LDL-C was not particularly high, but doctors seem convinced that lower is better, even though most heart attacks occur in men who do not have elevated cholesterol. So he had no problem prescribing the highest dose (40mg - the 80mg is grandfathered in the U.S., but new users can't get it.) Studies indicate the the benefit of any statin is dose-related.
"Atorvastatin, lovastatin, and simvastatin are lipophilic, whereas pravastatin, rosuvastatin, and fluvastatin are more hydrophilic." [1]
Lipophilic (hydrophobic) is best for PCa cell uptake.
Regarding LDL-C, it is the very small LDL that get cholesterol into cells, so one must be concerned if VLDL-C is high.
ADT messes with one's lipids. Difficult to prevent. Another good reason for starting a statin at the same time.
Typically, a vegan diet can improve lipids - except triglycerides.
I am planning on getting a test to differentiate the LDL to see the proportions of small to large (or short to long as some people say), but will probably start a low dose simvastatin for the PCa more than the LDL.
To you point about LDL and heart attacks, I was reading a paper that suggests in inverse correlation over age 60....
"Setting, participants and outcome measures: We sought PubMed for cohort studies, where LDL-C had been investigated as a risk factor for all-cause and/ or CV mortality in individuals ≥60 years from the general population.
Results: We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all- cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.
Conclusions: High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies."
A really good read (well-researched) on the sad history of CVD - saturated fat - cholesterol - etc, research (in America) is "The Big Fat Surprise" by Nina Teicholz.
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