More than 40 years ago the concept of cholesterol’s impact upon cardiovascular disease emerged, and the misguided war on cholesterol began. (For the full story, start your research with the ‘saturated fat myth’ and ‘diet-heart myth’). Then, in the 1950’s, drug company scientists discovered the biochemical pathway to cholesterol synthesis and the now trillion-dollar statin industry began.
In the past few years the true legacy of statin drugs has emerged and it is time to acknowledge their severe over-prescription and re-evalutate their usage once and for all.
Here’s what you need to know:
- Statins are a class of drugs that lower cholesterol in the blood by reducing the production of cholesterol by the liver.
- Yes, our liver produces cholesterol, at approximately 1-2 grams per day.
- Total cholesterol is not the cause of the disease, inflammation is.
- Dietary saturated fat is not associated with an increased risk of heart disease. You can access the research here.
- Low fat diets do nothing to control your disease risk, but they will make you hungry, fat, hormonally imbalanced and inflamed.
Why does our body produce cholesterol?
Cholesterol is the major component of our cell walls, the precursor to vitamin D, vital for proper neurological functioning and importantly, the precursor to hormones including our sex hormones. Cholesterol clearly plays some pretty important roles.
When statins are administered in doses sufficient to compromise this synthesis of cholesterol, it is inevitable that nutritional uptake required for cellular function is compromised.
What are the side effects of statins?
The highest concentration (25%) of cholesterol in the body is found in the brain. When cholesterol production is blocked, the side effects can be disastrous. The potential side effects of statin usage include confusion, paranoia, disorientation, depression, memory loss and dementia.
Multiple studies have shown that statins decrease mitochondrial function (our energy powerhouses) and coenzyme Q10 (CoQ10) levels, via poisoning HMG-CoA reductase. As mitochondria are the inevitable target of statin drugs, cellular and nutritional insufficiency creates additional adverse effects, including muscular weakness, instability, fatigue and muscle aches and pains. For the sedentary person this is difficult enough, but for athletes this will impair your adaptation to and recovery from exercise.
What about my heart health/chronic disease risk?
- Cholesterol alone is not the problem. We do not need to artificially lower a vital substance that virtually every cell in your body naturally produces and requires to sustain optimal function.
- From a blood lipid panel, high total low density lipoprotein (LDL) cholesterol is not the most important factor, but rather it’s the size of the LDL particles that counts.
- High total cholesterol (TC)/high density lipoprotein (HDL) cholesterol ratio (TC/HDL-C ratio) indicates small LDL particles and correlates strongly with incidence and extent of heart disease.
- Low TC/HDL-C ratio indicates minimal small LDL particles and a reduced risk of heart disease.
- High carbohydrate diets and the presence of insulin are responsible for small LDL particles. Statin drugs do nothing to change LDL particle size, but the pharmaceutical industry would rather you didn’t know this.
- The gold standard for identifying heart disease risk is the Coronary Artery Calcium (CAC) score. This is the measurement of the calcium in the artery walls, which shows the amount of hardening or atherosclerosis that exits. Males over 45 years of age and females over 50 years should be aware of their CAC score, especially in the case of: family history of heart disease; smokers; and/or the presence of chronic diseases including diabetes and obesity.
- To first understand your inflammatory profile and therefore chronic disease risk, explore the following:
- TC:HDL: optimal <3.5, where <5.0 is good
- Triglycerides: ideal <1.0 mmol/L
- C-reactive protein (CRP): ideal <1 mg/L
- Homocysteine: ideal 7.0-7.5 umol/L
Cholesterol and statin drugs are complex topics, one that goes beyond what we believe science even understands at this point in time.
Please note: there are some cases where statins can be beneficial, but please ensure you are working with a highly skilled Cardiologist. What we do know is that there are effective strategies to assist patients who require statin therapy, including CoQ10 supplementation. This is specifically important for those people who want to participate in exercise, but are limited due to the drug side effects.
Take home messages:
- Cholesterol is important for cellular health and wellness.
- Inflammation (not high cholesterol) is the cause of disease.
- Small LDL particles correlate strongly with incidence and extent of heart disease.
- High carbohydrate diets and the presence of insulin are responsible for small LDL particles.
- Statins decrease CoQ10, an important cellular nutrient required for energy production.
- Statins have the ability to impair adaptation to exercise due to pain, fatigue, decreased improvements in performance and increased recovery time.
- In the small percentage of cases where statins are necessary, they should be co-prescribed with a high-quality coenzyme Q10 supplementation.
Image credit here.
Graveline, D, 2015. Adverse effects of statin drug: a physician patient’s perspective. Journal of American Physicians and Surgeons, 20, 1, 7-11.
Ochsner, J, 2010. Coenzyme Q10 and statin-induced mitochondrial dysfunction. The Ochsner Journal, 10, 1, 16-21.
Diechmann, D.E. et al., 2015. The interaction between statins and exercise: Mechanisms and strategies to counter the musculoskeletal side effects of this combination therapy, The Ochsner Journal, 15, 4, 429-437.
Marcoff, L. & Thompson, P. D, 2007. The role of coenzyme q10 in statin-associated myopathy: a systemic review. Journal of the American College of Cardiology, 49, 23, 2231-2237.
Siri-Tarino, P. W. et al., 2010. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Society for Nutrition, 91, 3, 535-546.