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Articles : Nutrition
  
Atherosclerosis: Lab Tests and Lifestyle (Part 3): Back to Articles
by Hollie Greenwood, MS, NC

Contrary to cholesterol’s negative reputation, the body cannot function without it. It’s the basic raw material for making steroid hormones (such as estrogen, progesterone, testosterone and cortisol), and bile acids needed for digestion. It makes almost all phospholipids in the brain, so is very important for brain functionality and mental acuity. Cholesterol also helps convert sunlight into vitamin D, regenerates damaged endothelial cells, is an important constituent for maintaining the integrity of cell membranes, is needed by neurotransmitters in the brain, and helps bind mercury and other heavy metals in the body (18).

It is only when cholesterol becomes oxidized that it starts to be identified by the immune system and becomes problematic.

So if dietary cholesterol and saturated fats aren’t to be blamed for atherosclerosis, what is?

Oxidative Stress

Cholesterol oxides are forms of cholesterol that have been damaged by oxidative stress (not to be confused with that of dietary cholesterol, which can be obtained by eating saturated animal fats). These forms of cholesterol cause white blood cells to proliferate within the arterial walls, which has been shown to cause atherosclerosis (19).

The more oxidative stress a person has, including inflammation, the more damage there is to cholesterol, leading to the formation of these cholesterol oxides.Smoking, high serum iron levels, chronic infection and dietary antioxidant deficiencies can all increase cholesterol oxide formation and will be discussed individually in more detail below (20). Additionally, trans-fatty acids, non-fat milk solids (used to give body and sustenance to low-fat or non-fat commercial dairy products), processed cheeses and egg substitutes (such as Egg Beaters) contain oxidized cholesterol.

Lipoprotein(a)

By in large, cholesterol is very protective to the body for reasons already described. However there is a circumstance whereby cholesterol can turn a healthy situation into an unhealthy one. This occurs when LDL cholesterol becomes chemically bound to an additional molecule of adhesive-like protein called apolipoprotein(a). In a healthy body, Lp(a) restores and repairs damaged blood
vessel walls acting as a artery patch by promoting blood clotting. But, in the presence of atherosclerosis, this molecule can become a risk factor for heart disease. When inflammation is present, the body will produce more to meet the repair demand and Lp(a) will concentrate at the site of the damage. Oxidized LDL will start depositing and circulating, thereby contributing to the buildup of plaque. Because one of Lp(a)’s functions is to clot blood, it continues to do this on top of the forming plaque, narrowing blood vessels and likely closing off an artery (21). Studies have shown there to be 10 times greater risk of heart disease with Lp(a) then with elevated LDL (22).

Hyperinsulinemia

When there is too much insulin in the body and cell membranes can no longer respond to the body’s signal that there is too much of the hormone, the result is
hyperinsulinemia. Glucose and triglycerides are no longer able to enter cells and as a result, build up in the circulation. Over time, if not corrected, the high blood ugars and insulin can cause major cardiovascular complications as arterial inflammation starts to set in. Blood becomes thicker and stickier (increasing probabilities for blood clot formations), cells become damaged by free radicals, blood vessels constrict and spasm, blood pressure increases, and C-reactive protein levels increase (23).

Homocysteine

Homocysteine is an amino acid, which if elevated can become an atherosclerotic risk factor. As already discussed, when cholesterol becomes damaged by
oxidation, plaque will be produced in the arterial wall. Homocysteine is a catalyst for this oxidation reaction to occur and coordinates the many reactions that precipitates plaque build-up such as: irritation of the endothelial lining, free-radical damage, the production of a dense form of LDL and thrombosis. With high homocysteine, the blood vessels ability to dilate becomes inhibited (24). Low levels of vitamin B6, B12 and folic acid have been known to increase homocysteine.

C-Reactive Protein

CRP is an antibody-like blood protein that can be a significant indicator of heart disease. CRP levels are known to rise when a person is experiencing any type of
infection such as the flu; but after recovery, levels usually fall back down. When there is a persistent elevation of CRP in the blood that doesn’t subside, then arterial inflammation can set in. CRP levels can rise with any of the following conditions: chronic inflammation, high blood sugar, overweight status, and antioxidant and essential fatty acid deficiency — creating pro-inflammatory substances that increase the likelihood of developing atherosclerosis (25).

Fibrinogen

Fibrinogen is a protein that converts to fibrin during the formation of blood clots as well as determines the stickiness of the blood’s constitution. At normal levels,
fibrinogen promotes the clotting that is necessary to stop bleeding when there has been an injury. But, when it is produced in higher quantities, it makes blood clot
faster and stimulates platelet aggregation. This creates a situation that allows atherosclerotic plaque to buildup, potentially blocking vital oxygen and nutrients
for the heart’s tissue. Smoking and insulin resistance significantly raises levels of fibrinogen (26).

Ferritin

Hemoglobin, the red blood cell pigment that carries oxygen to the cells needs iron for its production. However, if your body takes in amounts of iron that exceeds that which is needed to make hemoglobin, it can contribute to cardiovascular diseases. Too much iron can oxidize LDL cholesterol, which makes it more susceptible
to plaque formation. It also poisons the endothelial cells and promotes inflammation. Ferritin should be used as an inflammatory marker for atherosclerosis. But, its etiology should be verified as iron overload can occur from many sources: excess dietary or supplemental iron, too much vitamin C, which increases the absorption of iron, or a genetic weakness for high iron called hemochromatosis (27).

Dietary fats

The quality as well as the quantity of certain fats consumed in the diet can be a very important atherosclerotic risk factor. Surprisingly, it’s not the saturated fats that cause damage to the arterial walls, as these fats are very stable when they are heated and therefore do not oxidize easily. They also are very heart-protective in that they help protect the arteries from damage against Lp(a). Saturated fats are
also crucial to maintaining cell membrane integrity and aren’t likely to succumb to free-radical damage.

Polyunsaturated fats (such as vegetable oils) on the other hand, are quite susceptible to oxidative damage. As a result, more antioxidants are needed to counter the harmful effects that they can have on tissue damage, inflammation, and thrombosis (28).

Trans-fatty acids are by far the most damaging of the fats. Trans-fats are created during a process called hydrogenation whereby polyunsaturated vegetables oils
(usually liquid at all temperatures) are made into more solid fats by the addition of a hydrogen molecule. This has been done to give longer shelf life to packaged goods
such as cookies, crackers and other commercial snacks. However, this comes at a dangerous price to the human body, which doesn’t recognize these fats as natural
substances. This increases free-radical damage to cell membranes, causing inflammation, increased levels of Lp(a), LDL oxidation and lowered HDL (29).

Eating a diet that has the correct ratio of omega-6 to omega-3 fatty acids is also important. A normal ratio should be 4 to 1; however the American diet sees a ratio
that resembles something closer to 20 to 1, which can cause high levels of Inflammation — a precursor to atherosclerosis. When diets were high in saturated fats and lower in foods that were made with rancid oils and heavily processed, this problem was rarely seen (30).

Hypertension

When blood flows through vessels, it creates a force in the form of blood pressure that at normal levels, is asymptomatic. However when the blood pressure is consistently high it can contribute to wear and tear on the cardiovascular system, eventually damaging the arteries as a result of the extra exerted force of the heartbeat (31). Cigarette smoke, oxidized LDL, Lp(a), toxic metals, insulin resistance, and excess weight can all conspire to make hypertension worse by weakening the blood vessels, especially in the narrowed branches, accelerating the
inflammatory process (32).

Smoking

Cigarette smoking has been touted the most important risk factor for cardiovascular disease (CVD) as smokers have a 70% greater chance of dying from CVD complications than non-smokers (33). However, even passive smoke is damaging to the health of the heart. Studies have shown that environmental tobacco smoke actually has a higher concentration of certain toxic elements, making non-smokers at risk as well (34). Smoking reduces the blood’s oxygen and HDL levels, contributes to hormonal imbalances (by lowering DHEA and melatonin), elevates
blood pressure, depletes antioxidants, increases fibrinogen levels, and increases platelet aggregation (35).

Poor cardiovascular metabolic processes

One new theory that has been circulating among medical circles is the idea of metabolic cardiology. No longer is treating heart disease exclusively about the supply of and demand for oxygenated blood that determines the health of one’s heart — but rather the supply and demand of cellular energy. According to this theory, what’s most important is the production of adenosine triphosphate
(ATP) and whether or not the body has enough of this fuel to power the mitochondria in the body’s cells, most notably the heart cells. As the heart becomes vulnerable to toxins, arterial inflammation and plaque build-up, ATP can help restore the cellular energy in those with a wide range of cardiovascular conditions by defending heart cells from damage (36).

Additional Causes of Atherosclerosis

Peridontal bacteria and nanobacteria, toxic metals, emotional stress (type A personality), excessive weight, physical inactivity and genetics are all considered to be additional risk factors for atherosclerosis. symptomatology Cardiac symptoms for men and women can be quite different. For men, their symptoms might be: midchest pressure, shortness of breath, dull pain between their shoulder blades, achiness in the jaw, pain in the left arm or elbow, and/or profuse sweating. For women typical symptoms might be: acute breathlessness, sudden and profound fatigue, dull, aching chest discomfort, jaw or neck pain, pain in the left arm or elbow, abdominal discomfort, nausea, vomiting, dizziness or blackouts (37). Fever, heartburn, cold sweats, coughing, diagonal ear crease, edema, hair loss on the legs, lack of balance and wobbly gait, depression, memory problems, muscle cramps or spasms, numbness or tingling in the extremities, and tinnitus are also additional symptoms that can be experienced by either of the two genders (38).

What is interesting to note is that arteries can be 8090% blocked by atherosclerotic plaque before a person may even notice any symptoms, which is why myocardial
infarctions can be known as the “silent killer.” Any one of the cardiovascular diseases could be progressing for many years before any symptoms may appear. Furthermore, atherosclerosis has been found to begin quite early in life, a fact that not many realize. Research has indicated that during the Korean and Vietnam Wars, autopsies of healthy young men that died in combat showed evidence
of cardiovascular disease (39).

Read more: Part 4  Diagnosis

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

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2. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 23.
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44. Berman, Layna and Jeffrey Fawcett. “Statin Drug Side Effects.” Your Own Health and Fitness. Podcast. April 11,
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45. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 79.

46. Ibid. 80.
47. Berman, Layna and Jeffrey Fawcett. “Statin Drug Side Effects.” Your Own Health and Fitness. Podcast. April 11,
2006.
48. Bartholomy, Paula. Lecture notes from MSHN 213. Hawthorn University. 2006.
49. Ibid.
50. Winslow CM, Kosecoff JB, Chassin M, et al. The appropriateness of performing coronary artery
bypass surgery. JAMA 1988; 260: 505-509.
51. Shaw PJ, Bates D, Cartlidge NE, et al. Neurological complications of coronary artery bypass graft surgery. Six
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angine pectoris. Lancet 1982; 2:1173-1180.
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St. Louis, Missouri: Churchill Livingston Elsevier. 2006. 1478.
54. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 122.
55. Murray, Michael, T and Joseph E. Pizzorno Jr. Textbook of Natural Medicine. 3rd Ed. Vol. 2.
St. Louis, Missouri: Churchill Livingston Elsevier. 2006. 1511.
56. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 101.
57. Ibid. 99.
58. Murray, Michael, T and Joseph E. Pizzorno Jr. Textbook of Natural Medicine. 3rd Ed. Vol. 2.
St. Louis, Missouri: Churchill Livingston Elsevier. 2006. 1512.
59. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 109.
60. Bartholomy, Paula. Lecture notes from MSHN 213. Hawthorn University. 2006.
61. Sinatra, Stephen T., M.D. Reverse Heart Disease Now. Hoboken, NJ: John Wiley & Sons, Inc. 2007. 116.
62. Ibid. 150.
63. Ibid. 161.

 

 


 
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