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Truth About Bad Cholesterol

From eNewsletter 12/16/2019

DID YOU KNOW that in a study from Journal of the American College of Nutrition, researchers found with better diet quality, levels of carotenes, lutein, cryptoxanthin, adiponectin (regulates glucose levels), and HDL (good) cholesterol were significantly higher, whereas levels of C-Reactive Protein (inflammation), leptin (craving hormone), total cholesterol, triglycerides, glucose, and insulin were negatively associated with diet quality.

These findings confirm the association between diet quality and nutrition-related biomarkers and support the idea that a high-quality diet positively influences pathways involved in chronic disease development across all different ethnic groups.


We are elated to announce that researchers have finally busted a myth we have been harping on for years regarding LDL, the bad cholesterol. According to a study from International Journal of Nanomedicine, a particular subclass of LDL, known subclass B, is a much better predictor of potential heart attacks than the mere presence of LDL, which is incorrect more often than not.

75 percent of patients who suffer heart attacks have cholesterol levels that don't indicate a high risk for such an event. That's because of the three subclasses that comprise LDL, only subclass B causes significant damage. Subclass B was found to be the most damaging to endothelial function and can contribute to the development of atherosclerosis. In addition to subclass B, the other two that are benign, subclass A and subclass I, should be used to diagnose atherosclerosis and the risk of heart attack.

Understanding could greatly improve the accuracy of diagnosis for the evaluation of cardiovascular disease rates, as well as severely curtail the number of prescriptions, especially statins. This is prescient given the following...

New FDA Warning for Statins

The FDA added a new statin warning: Immune-mediated necrotizing myopathy, which should be appearing on label inserts beginning of 2020. Also known as Necrotizing Autoimmune Myopathy, it causes muscle cell death (necrosis) that leads to weakness of the skeletal muscles.

Two Explanations for Why Statins Damage Muscle

Research in JACC: Basic to Translational Science made a discovery that could help prevent the most prevalent side effect of statins, muscle pain. Statins cause spontaneous and irregular leaks of calcium from storage compartments within muscle cells. Under normal conditions, coordinated releases of calcium from these stores make the muscles contract. Unregulated calcium leaks cause damage to muscle cells, potentially leading to muscle pain and weakness. In people already susceptible due to their genes or lifestyle, the leak caused by statins may overwhelm the muscle cells, giving rise to muscle pain and weakness. The researchers found that exercise can help prevent these changes.

A second discovery of why statins lead to muscle issues appeared in a recent issue of American Journal of Physiology-Cell Physiology. Who would have ever thought statins release the amino acid glutamate at much higher levels than muscle cells that are not exposed to statins?

Glutamate is a potent activator of muscle pain receptors, so of course it would trigger the sensation of muscle pain when statins enter muscle cells. The muscle then tries to increase its production of antioxidants to combat the stress. This is also why supplemental CoQ10, a protective antioxidant, is effective in mitigating statins effects. Researchers also found that administering vitamin E was successful in helping to reduce glutamate release. 

Statins for Healthy Persons

According to a study in British Medical Journal, the benefits of statins for people without heart disease is small, uncertain, and there are potential harms. What's worse, as drug companies have convinced heart organizations to continually lower cholesterol guidelines, many more healthy persons have been prescribed statins.

For example, the researchers examined the effects of guideline changes on cardiovascular disease prevention in older people in Ireland from 1987 to 2016 and found that the proportion of over 50s who would have been eligible for statins increased from 8% based on the 1987 guidelines to 61% with the 2016 guidelines.

Overall, they found no significant reductions in death from any cause, vascular deaths, and major coronary or vascular events. In fact, their analysis suggest that none of those classified as low or moderate risk in primary prevention would reach acceptable levels of risk reduction to justify taking a daily statin.


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