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Dr. Magryta: Cholesterol Part 3

What to do?

This section really should be called: Heart Disease – What to do?

In the past two pieces, I have put forth some hypothesis that are not in line with current American College of Cardiology guidelines and I am ok with that because this is about stimulating a conversation about disease etiology and treatment.

I am not encouraging anyone to go against their physicians’ recommendations. The choice to change your current therapeutic regimen is solely between patient and  provider. Pharmacotherapy is likely necessary for patients who are unwilling to pursue aggressive lifestyle changes, have significant genetic risk factors or have advanced coronary artery disease requiring medication therapy. However, I do encourage every person to look at the science, to be informed and then discuss with their physician the possibility of non-pharmacologic treatments where possible. The statin effect is likely related to pleotrophic effects and not solely on the cholesterol lowering effect.

Now that we have settled that cholesterol is not inherently bad unless unbalanced — and that it clearly has a beneficial role in human health — we need to understand what really causes coronary artery disease. Dr. Mark Houston has written extensively on this topic and is a specialist in non-pharmacologic management of heart disease. Since this is my stated goal throughout medicinal management, he is my go-to source for information. I prefer to go to the top of the intellectual heap for insight into disease management, and he sits atop the mountain.

Coronary artery disease is caused by endothelial dysfunction which precedes arteriosclerosis and atherosclerosis that we call a narrowed artery. This narrowed artery eventually has a plaque that ruptures, causing rapid vessel closure — a heart attack or myocardial infarction, MI for short.

Physiologically, an artery is made up of a sheet of cells that are organized in interlocking rows that form the endothelium of a long tube for blood to flow through. This is straightforward plumbing. Under normal homeostatic conditions, this tube is repaired constantly for blood to flow undisturbed forever. However, under stress from unbalanced mechanical and chemical forces, these cells will become dysfunctional (endothelial dysfunction). Mechanical stress occurs with high blood pressure. Chemical stress occurs primarily through genetic risk factors, toxin exposure and poor quality diets.

For the sake of this discussion, I am going to focus on the chemical stressors, as the mechanical stressors will be reduced by the same treatments that reduce the chemical stress.

The major causes of chemical stress on the coronary artery are: 1) unbalanced macronutrients – fats, carbohydrates and proteins, 2) unbalanced micronutrients – minerals primarily, 3) host genetics, 4) dysfunctional intestinal microbiota, 5) toxins. There are more thn 395 other causes; however, these are the big 5 that account for a large part of the disease.

Let us look primarily at Inflammation and oxidative stress as they are two of the most damaging events occurring in the heart and the rest of the body — primarily due to poor dietary choices, but also from exposure to drugs, chemicals, excessive exercise, excessive sun exposure and smoking. Oxidative stress is basically the event that occurs in the body when naturally beneficial oxygen radicals are overproduced by our cells — to clear infections.

These radicalized molecules have unpaired electrons that are in a mad search for another electron to balance their sensibilities. When free and radical, they can destroy a bacterial or viral cell wall via this unpaired electron. When we have a pathogen to kill, this is good. What is not good is when they run into our liver cell or heart cell first. This damage when it occurs to our cell wall and enzymes has a catastrophic effect, if it occurs in high frequency. This is one of the major pathways to endothelial dysfunction and ultimately heart disease.

If for example, you consume too much mercury via excessive consumption of tuna and you smoke cigarettes, you can start this cascade of reactive oxygen species that cause inflammation and cellular damage to the artery wall. Now let us say you have a genetic predisposition for small and dense lipoproteins like LDL cholesterol and have apolipoprotein E3/4 genotype while consuming a high refined carbohydrate diet, then you have the ripe condition for the small dense LDL particle to squeeze between artery wall cells and become oxidized and engulfed by an immune cell, thus begining the process of atherosclerosis.

Since prevention is about catching disease where it begins, this is a conversation that parents need to have with their children.

Next week we will discuss the process from beginning to end of a plaque formation.

Dr. M

Deep Nutrition, Catherine Shanahan, MD

Statin Article



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