ofonorow wrote:At a high level, the statin is artificially lowering an important substance in your blood stream, i.e., treating a symptom. A substance, cholesterol, that is not only required for good health, but may also be elevated because of dental or other toxicity. So artificially lowering your body's own natural defense mechanism seems to be tempting fate.
Thanks to Pauling/Rath we know that ordinary cholesterol doesn't generally adhere to arterial walls like Lp(a) will, and really poses little threat (and a lot of theoretical benefit as described in Dr. Levy's STOP AMERICA'S #1 KILLER - livonbooks.com). A high Lp(a) number, with small molecular weights, would be a sign of significant CVD risk. (Larger Lp(a) molecules are not as atherogenic.)
LDL
does adhere to arterial walls - one way through which this occurs is through binding to proteoglycans in the extracellular matrix of the arterial wall.
In the case of LDL, there are several lines of evidence that indicate that lowering LDL through statins has a benefit and that LDL has a causal role.
There is no evidence that heart risk increases with the number of dental amalgams - in fact, a Swedish study found that there was an
inverse association between heart risk and the number of dental amalgams, but this association disappeared once they controlled for factors like socioeconomic status.
Apparently, taking CoQ10 can mitigate many of the risks (e.g. the stories of vegetarian women who were put on statins for "prevention" and lost major internal organs. If a cell doesn't have CoQ10 it dies. A meat diet provides at least 5 to 10 mg of CoQ10.) And the destruction of muscle fiber, explains why many statin users experience muscle pain, and lets not forget the threat of heart failure seems to be connected to CoQ10 depletion.
The effect statins have on lowering CoQ10 was recognized almost immediately, because the CoQ10 researchers were from Merck. (Remember the Merck patent to add CoQ10 to HMG-COA reductase inhibitors). What else may these foreign agents to the body interfere with? The drug companies have been reduced to saying that statins are necessary because of other effects, such as reducing inflammation. However, vitamin C is an excellent way to reduce inflammation, and Thomas Levy introduces a theory in his book is that inflammation is the way we have evolved to "move" ascorbate to the site of injury, as white blood cells are the first to saturate with vitamin C.
CoQ10 supplementation might be a good idea, but primarily based on the precautionary principle. The evidence for its benefits in reducing side effects of statins is still inconclusive.
As we have discussed previously, because of the magic 95% confidence interval, 1 in 20 studies might produce an erroneous results.
A meta-analysis would take this into account - even if one in 20 studies is based on a chance finding, the results of the other 19 would by and large correct this. Recent meta-analyses of statins for both primary and secondary prevention have been positive.
In any case, this assumes that all the primary endpoint results have a p-value of 0.05, when in fact the statistical signficance is even higher for many trials (e.g. for JUPITER it was <0.01, IIRC)
In my humble opinion, this is why Pfizer has run more than 400 studies on Lipitor. The odds are that something like 20 studies would erroneously produce a positive result. (Unfortunately, I don't believe they really even have a single one
)
I don't think Pfizer has run 400 studies on Lipitor - many of them were probably run by universities, government agencies, etc. A search for "atorvastatin" on clinicaltrials.gov yields 376 results. A search for "atorvastatin" with Pfizer as a sponsor yields
87 results. If you look through the results, you'll see that there are studies for a wide variety of indications and in different subpopulations.
At best, statins might not harm you, but there is surprisingly little evidence given all the studies that they will help you in any way. At worst, these drugs will make matters much worse.
Your "at best" scenario is inaccurate, given that the evidence clearly shows that statins do provide a benefit in reducing heart attacks and strokes, and also reducing all-cause mortality. The magnitude of the benefit, however, varies depending on whether it is used as primary prevention (as I assume in Scott's case) or secondary prevention. The benefits are more pronounced in the latter case, since the absolute risk of cardiovascular death is much higher to begin with for these patients.
They are not a magic bullet - successful prevention strategies will address a variety of risk factors and make use of lifestyle interventions as well as pharmacological agents (including supplements) where appropriate. Scott can choose to address other risk factors like his hypertension, high CRP, etc through other interventions, but LDL still poses an independent risk. No one can predict the future, but there are ways to estimate what someone's risk of having a heart attack and stroke in the next 10 years is based on evidence from large cohort studies like Framingham. We also know from a
recent meta-analysis that the relative risk reduction in major coronary events is roughly 30%, and the relative risk reduction in deaths is roughly 12%, over a mean follow-up period of 4 years. So if you have a 3% chance of having a heart attack in the next five years, you reduce your absolute risk by about 1%. For some, a 1 in 100 chance of avoiding a heart attack over a five-year period is not worth it - for others, it may be.