Atherosclerosis is a biological process rather than a disease, which influences the pathology of many different cardiovascular ailments. Directly related to diet and lifestyle, atherosclerosis affects the body’s arterial blood vessels as a result of plaque buildup from chronic inflammation. Myocardial infarctions or strokes can
result as the plaque hardens and vessels become more narrow, causing blockages of an artery or plaque that ruptures to form a clot (1).
In order to understand the cascade of events that occurs with the atherosclerotic process, we first need to look at the structure of an artery. Blood vessels have three major layers with the innermost layer the intima, known as the endothelium, being of most importance. This internal lining of the artery has a layer of endothelial cells that are ined by molecules called glycosaminoglycans (GAGs). GAGs protect the endothelium from damage (as in platelet aggregation) as well as help promote repair. Endothelial health is critical to cardiovascular health. According to well-known cardiologist Dr. Stephen Sinatra, if a person has 40-50% narrowing of the
arteries and impaired endothelial function, they are at far greater risk of having an adverse cardiovascular event then if they had 80% narrowing of the arteries and their endothelial functionality was normal.
In a healthy situation the endothelium produces chemical substances that allow the blood vessels to expand and relax in a normal manner. But being that the lining is extremely delicate and sensitive to injuries, it has the potential to be damaged by a variety of insults, weakening the GAG layer that protects the endothelial cells (2).
Some of those insults can be, but are not limited to: cigarette smoke, toxic chemicals, heavy metals, free radicals, bad dietary fats, elevated insulin, bacteria, high blood pressure and excessive stress. Any of these elements singly, or in combination, can start an inflammatory process eventually leading to the
formation of plaque. This development can occur over the course of many years (sometimes going undetected for decades) or can be quite sudden (3).
Once the endothelial cells have been significantly damaged, the injury site can lead to a deadly chain of events. The breakdown of the endothelium causes an increase in vascular permeability and plasma molecules such as low density lipoproteins (LDL), cholesterol, and Lipoprotein(a) (Lp(a)) to start accumulating and attaching themselves to the GAGs. These components are mobilized by the liver to repair any damage to the arterial walls, but when LDL binds to the injury site it begins tobreak down or oxidize. Cholesterol too starts oxidizing. This oxidation releases free radicals and alerts the immune system to send out macrophages to isolate the
oxidized molecules. But the macrophages, whose role it is to scavenge the blood and ingest foreign invaders, have their own oxidizing agents which adds more oxidation to the mix. The macrophages become so swollen by engulfing the oxidized cholesterol that they become foam cells and lose their scavenging abilities.
Foam cells can become very unstable, to the point of bursting. When this happens they spill out their oxidized cellular debris along with fiber-like proteins — leaving fatty streaks on the lining of the artery. Eventually, a kind of scar tissue, called a fibrous cap (made from a combination of oxidized lipoproteins and cholesterol, fibrous protein, cellular debris, collagen and GAGs) appears on the surface of the artery, covering the endothelium and causing plaque to form. Over time, the plaque continues to grow until it eventually blocks an entire artery or ruptures to form a clot (4).
The latter scenario of unstable plaque formation poses the most dangerous threat. The fibrous cap can start to erode, spilling destructive and inflammatory substances
into the bloodstream. As the cap starts to leak, clotting factors such as fibrinogen work to help reseal the injury. But the cap will usually continue to degrade until it
suddenly ruptures. A thrombus (blood clot) will form almost immediately either obstructing the vessel on the spot, or traveling elsewhere, clogging a smaller vessel.
Inflammation is what causes the oxidized plaque to rupture and this rupture is what can account for the deaths relating to myocardial infarctions, arrhythmias or strokes (6).
Arteriosclerosis is defined as atherosclerosis in its latest stages when the fatty inflamed deposits lining the arterial wall have become very calcified and the arteries have become brittle. The wall becomes abnormally thick and hard, making it difficult for blood to pass through (7).
Read Part 2 :An Epidemic
Hollie Greenwood is a certified nutrition consultant, certified personal chef and owner of Real Cooking — a sustainably-operated business based with offices in Santa Monica, California and Missoula, Montana. Hollie became interested in how and why food influences health at a young age. With this passion, she created a business to help individuals and families with the tools needed to transition from eating processed foods to whole foods. Created in 2004, Real Cooking has always been a unique business, in that it offers holistic nutritional consulting, personal chef services, kitchen clean-outs, guided grocery shopping and farmer’s market tours, cooking instruction and custom meal plans all under one roof.
Hollie obtained a Master’s of Science degree in Holistic Nutrition with high honors from Hawthorn University and her personal chef certification from the Culinary Classroom in Los Angeles, CA. She is currently a member of the National Association of Nutrition Professionals, the Community Food and Agriculture Coalition, the Sustainable Business Council, the Montana Organic Association and is co-chapter leader for the Weston A. Price Foundation in Missoula, MT. www.realcooking.net
1. Murray, Michael, T and Joseph E. Pizzorno Jr. Textbook of Natural Medicine. 3rd Ed. Vol. 2.
St. Louis, Missouri: Churchill Livingston Elsevier. 2006. 1501.
2. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 23.
3. Bartholomy, Paula. Lecture notes from MSHN 213. Hawthorn University. 2006.
4. Murray, Michael ND. Total Body Tune-Up. New York, New York: Bantum Books. 2000.
5. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 28.
6. Ibid. 29.
7. Bartholomy, Paula. Lecture notes from MSHN 213. Hawthorn University. 2006.
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