Forget Cholesterol - Inflammation may be bullying your heart

Alternative Medicine|January/February 2020

Forget Cholesterol - Inflammation may be bullying your heart
“Don’t worry, take a statin.” That’s the heart health advice offered by smiling faces on TV, as well as much of the medical establishment. Pharmaceutically pushing LDL cholesterol levels to near-zero is the commonly accepted cure-all for heart disease. However, nearly half of all cardiac events happen to people with low cholesterol. Maybe there is another mechanism in play— current research says there is.


Cardiovascular disease (CVD) is usually characterized by disease of the heart muscle, valvular disease, or coronary artery disease (CAD), a condition of blood vessel damage due to a combination of silent inflammation, endothelial dysfunction, and plaque buildup. As the immune system repairs damage in blood vessel walls, a silent but deadly process unfolds in time as arteries begin to calcify.

As inflammation increases, so does the likelihood that plaques in arterial walls will become unstable and rupture. When unstable plaques break open, blood clots can enter the bloodstream, become lodged in blood vessels, and block blood flow. Devastating events that stem from such a blockage include the death of heart muscle cells, stroke, or potentially dangerous arrhythmias. All of these conditions are produced by the resulting loss of oxygen to the local tissues.

Although the cholesterol theory of coronary heart disease remains controversial and poorly understood, the most recent publication in the British Medical Journal strongly negates its hypothesis. Thus, inflammation as the source of cardiovascular disease looks more promising and continues to gain momentum among progressive health care professionals.

When considering inflammation as a contributor to cardiovascular disease, evaluating for diastolic dysfunction (DD)—an early form of heart failure— as well as 5 common blood markers are helpful for assessment: fibrinogen, high-sensitivity C-reactive protein (hs-CRP), lipoprotein(a) (Lp[a]), lipoprotein-associated phospholipase A2 (LpPLA2), and myeloperoxidase (MPO). This is not a complete list of all inflammatory markers but offers a very useful set of data points.

Diastolic dysfunction is a condition that is poorly understood and currently underdiagnosed in the medical community. In comparison to diastolic heart failure, which is a clinical syndrome, DD represents frequently abnormal mechanical function without the outward signs of heart failure. For example, in early DD, the first presenting symptoms may be fatigue, a chronic cough, or exercise intolerance, yet neither imaging nor labs will suggest a diagnosis of heart failure. It is thought that DD may be caused by hypertension, narrowing of the aorta, disease of the heart muscle, aging, and CAD.

It is also suspected that defects in adenosine triphosphate (ATP) production from impaired mitochondrial function may contribute to DD. Mitochondria are mini-organs within each cell that produce the body’s most important energy molecule, ATP. The chambers of the heart require more energy to relax and fill than to contract. Because of oxidative stress and chronic inflammation, damaged mitochondria are unable to produce sufficient ATP to help the heart relax and fill with blood. All patients with heart failure have DD to some degree.

Because the requirements of muscle cells for ATP are absolute, incorporating a metabolic approach with nutritional biochemical interventions that preserve mitochondrial health and support efficient ATP production must be considered. For example, in a randomized controlled trial, 300 mg of coenzyme Q10 (CoQ10) promoted reversal of mitochondrial dysfunction in CVD patients. Such a metabolic cardiology approach does not create adverse effects and may be supportive of patients with DD.


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January/February 2020