Listen to the claims of doctors and Big Pharma and the only concern you should have with taking statin drugs to reduce cholesterol values is muscle damage, i.e., rhabdomyolysis due to muscle breakdown, a complication that affects less than one percent of people taking these drugs. Combine this with the wildly overinflated claims of benefits—36-55% reduction in cardiovascular events, when the real value is closer to 1%—and it seems like statins are all win-win with little downside.
But this is simply not true. There are real and substantial problems with this class of drugs. Among them:
- Muscle aches and weakness-–While outright muscle damage is uncommon, non-damaging muscle aches and weakness are exceptionally common. Having prescribed statins to thousands of people in my early years of cardiology practice, muscle aches/weakness were the rule, not the exception. It caused complaints like “I’m having trouble getting in and out of my car,” or “I feel like I aged 20 years since I started taking the drug,” or “I’m tired all the time now.” The higher the dose and the longer you take the drug, the more likely such effects become. Somebody without such complaints was, in my experience, uncommon.
- Increased insulin resistance—While it is widely accepted that insulin resistance caused by statin drugs increases likelihood of type 2 diabetes by 30-50%, the other consequences of insulin resistance are overlooked. Insulin resistance is the process underlying so many other health conditions such as fatty liver, cancer, and cognitive impairment/Alzheimer’s dementia—type 2 diabetes is only the tip of the iceberg.
- Dysbiosis—We now know that taking a statin drug disrupts the composition of bowel flora such that the microbiome of someone on a statin drug looks like that of an obese diabetic, even if the person is slender and non-diabetic. The shift in bacterial species results in dramatic reduction in intestinal butyrate that nourishes and heals the intestinal lining, as well as eradication of blood levels of butyrate that would ordinarily moderate blood sugar and other metabolic benefits. Statins also increase the levels of intestinal secondary bile acids that are believed to increase potential for colon cancer.
- Spontaneous tendon rupture—This association was first suggested by hundreds of case reports of individuals experiencing painful spontaneous tendon ruptures, a phenomenon not tracked in multiple statin clinical trials.
If you are interested in reducing or eliminating risk for coronary disease without statin drugs, why not:
- Eliminate wheat/grains and sugars that provoke formation of small LDL particles—i.e., the REAL cause of coronary atherosclerosis?
- Eliminate wheat/grains and sugars that fuel liver de novo lipogenesis that creates VLDL particles that cause heart disease and trigger formation of small LDL particles?
- Eliminate wheat/grain and sugars that reduce glycation of LDL particles (small LDL particles are exceptionally glycation-prone)?
- Eliminate wheat/grains and sugars that provoke insulin resistance?
- Correct common nutrient deficiencies that add to insulin resistance, such as vitamin D, magnesium, and omega-3 fatty acids?
- Correct dysbiosis/SIBO that reduces endotoxemia that drives inflammation?
I propose that taking advantage of all the above is substantially superior to taking a statin and suffering the metabolic downturns they provoke. If you were following various markers, such as NMR lipoproteins, triglycerides, HbA1c, fasting glucose, fasting insulin, C-reactive protein, AST, ALT, you would see that the results you obtain with this list are dramatically superior to the values obtained with a statin drug.