Use Of Statin Drugs To Lower Cholesterol

1. Diagnosed arteriosclerotic cardiovascular disease to prevent further damage or increased mortality (secondary prevention for those with established ASCVD)
2. Preventive measures for anyone with an LDL cholesterol above 190 mg/dl (primary prevention of ASCVD for those with LDL-C ≥190 mg/dL)
3. Preventive measures for anyone with diabetes and an LDL cholesterol over 70 mg/dl (primary prevention of ASCVD for individuals with diabetes mellitus and LDL-C of 70–189 mg/dL)
4. Preventive measures for anyone with increased risk of heart disease and an LDL cholesterol over 70 mg/dl (primary prevention of ASCVD for those without diabetes, with LDL 70–189 mg/dL, but with an estimated 10-year absolute risk of ≥7.5% as assessed by the pooled cohort equations)

Additionally, the 2013 guidelines also discuss other factors that might affect net risk reclassification:

1. LDL-C ≥160 mg/dL or evidence of genetic dyslipidemia (abnormal lipid/cholesterol measurements)
2. elevated lifetime risk
3. family history of premature CVD,
4. blood levels of high sensitivity C-reactive protein (CRP) ≥2.0 mg/L,
5. ankle-brachial index (used as a measure of circulation in the extremities)

However, some patients do not tolerate the statin drugs. They develop incapacitating muscle pains, brain fog and even dementia. We know that statins are HMA-CoA reductase inhibitors, and completely stop the synthesis of CoQ-10. When these statin-treated patients are taken off statin therapy, their symptoms generally improve – especially if they are given supplements to help restore the mitochondria, such as CoQ-10.

We have been taught that there is an association between cholesterol levels and coronary heart disease, morbidity (illness) and mortality. In the allopathic standard of care, the use of statin drugs for high cholesterol is almost a knee-jerk reflex. And the definition of what is a high level of cholesterol has been progressively lowered from 240 mg/dl in the late 1990s to less than 100 mg/dl in recent years.

The association between high cholesterol and mortality from coronary heart disease is not as direct or impressive as we have been taught. In a study dating from 1994, whose objective was “to determine whether elevated serum cholesterol level is associated with all-cause mortality, mortality from coronary heart disease, or hospitalization for acute myocardial infarction and unstable angina in persons older than 70 years,” the study authors concluded that their “findings do not support the hypothesis that hypercholesterolemia or low HDL-C are important risk factors for all-cause mortality, coronary heart disease mortality, or hospitalization for myocardial infarction or unstable angina in this cohort of persons older than 70 years.”

In a 2016 study which analyzed data from the Minnesota Coronary Experiment, based on lowering cholesterol levels by replacement of saturated fat with an oil rich in omega-6 linoleic acid in the intervention group, the conclusion was that “the intervention group had significant reduction in serum cholesterol compared with controls, but that “there was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts.” Progressive lowering of cholesterol levels in fact raised the probability of death by 22% for each 30 mg/dl reduction in serum cholesterol.

Why would we want to lower cholesterol levels? Simply because of the idea that high lipids are associated with cardiovascular disease? A 2004 study addressed that question. The objective of the study was “To assess the association between lipid levels and cardiovascular events in older adults.” The conclusion was “In this population-based study of older adults, most lipid measures were weakly associated with cardiovascular events. The association between low HDL-C and increased MI risk was nonetheless strong and consistent.”

Could there be another reason for people to develop coronary heart disease besides simply having high blood cholesterol levels?

There is evidence for the association of elevated homocysteine levels, elevated C-reactive protein levels and chronic inflammation with coronary artery disease. Could the explanation for coronary artery disease lie at least partly in the realm of inflammation as it relates to mortality?

A 1997 study had as its objective to examine “the relation between plasma total homocysteine levels and mortality among 587 patients with angiographically confirmed coronary artery disease.” The conclusion of the study was the finding of a “a strong, graded relation between plasma homocysteine levels and overall mortality.” Those with a homocysteine level of greater than 20 had 4.5 times increased overall mortality as compared to those with a “normal” homocysteine level.

Homocysteine is an indirect measure of the ability to produce glutathione, used by all mammalian systems for detoxification of xenobiotics and other potentially poisonous substances. Elevation of homocysteine levels is predictive of cognitive decline, as shown in a 2010 study from Holland. In this study, high homocysteine levels in combination with high CRP levels were associated with faster rates of cognitive decline. Statin drugs have a similar association with cognitive decline in some patients. Statin drugs are associated with mitochondrial dysfunction. The brain has the second highest concentration of mitochondria in the body. The heart, by the way, has the highest concentration – it has to function 24/7. The brain, at least, gets to turn off and go to sleep sometimes.

Could there be a link between mitochondrial dysfunction, cognitive dysfunction, inflammation and poor detoxification capacity? This idea does not seem outside the bounds of reasonable possibility. All the above-mentioned dysfunctions are associated with increased inflammation.

In this study dating from 2004, we read that the objective was to evaluate the “predictive value of lipid and C-reactive protein levels, as well as a possible interaction between statin therapy and CRP”. The study’s conclusions: “Lipid levels drawn at angiography were not predictive of survival in this population, but initiation of statin therapy was associated with improved survival regardless of the lipid levels. The benefit of statin therapy occurred primarily in patients with elevated CRP.”

The next question, then, is whether statins do in fact lower C-reactive protein and inflammation.

A 2001 study address that question. The objective was “to test the hypothesis that pravastatin has anti-inflammatory effects as evidenced by CRP reduction.” The conclusion was “pravastatin reduced CRP levels at both 12 and 24 weeks in a largely LDL-C-independent manner. These data provide evidence that statins may have anti-inflammatory effects in addition to lipid-lowering effects.”

Essentially the same question was studied in this 2005 study of the relationship between fibrinogen (which is elevated with inflammation) and the risk of heart disease. The objective of the study was “to assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes.” The conclusion was that “moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults.”

A similar study also in 2005 had as its objective to measure progression of atherosclerosis by coronary angiography in two groups of patients – those receiving moderate statin therapy (40 mg of pravastatin) and intensive statin therapy (80 mg of atorvastatin) for 18 months. The study’s conclusion: there was significant reduction in LDL cholesterol levels and in CRP levels in the group as a whole, not related to the intensity of statin treatment. The decrease in CRP levels was independently and significantly correlated with the rate of progression of atherosclerosis.

So clearly inflammation must play a part in the development of atherosclerotic heart disease, if all these various inflammatory markers are considered to be risk factors.

Perhaps if we can lower inflammation in the body, we can also lower the risk of heart disease, and avoid having to take a pharmaceutical drug that has some significant adverse effects (muscle aches, brain fog, heart failure…). Of course the question always arises whether the non-pharmaceutical means is both safer and as effective as the pharmaceutical route. And is the benefit of non-pharmaceutical lowering of cholesterol as great as if we simply took a pill?

This 2004 study assessed “the effects of three-month formal phase II cardiac rehabilitation and exercise training programs on high-sensitivity C-reactive protein (HSCRP) levels in patients with coronary heart disease (CHD).” The study’s conclusion: “Similar significant reductions in HSCRP occurred in the rehabilitation patients regardless of whether they received statin therapy or lost weight.”