Atherosclerosis and What You Can Do About It PDF Print E-mail
Post by Hollie Greenwood, MS, NC/Dr. Feder.com   
Friday, 12 March 2010 16:00

Heart Health
Atherosclerosis: What is Atherosclerosis?
by Hollie Greenwood, MS, NC via Dr.Feder.com

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).

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

Atherosclerosis: An Epidemic (Part 2)
by Hollie Greenwood, MS, NC

According to the American Heart Association, coronary artery disease alone accounts for over a half million deaths — the single leading cause of death in the United States. 70 million Americans have had one or more forms of cardiovascular disease (CVD) with nearly a million people dying from it every year (8).

It’s interesting to note that in the early 20th century, atherosclerotic-related heart diseases were relatively rare accounting for approximately only 8% of all deaths in the U.S. Myocardial infarctions (MI) were almost nonexistent in 1910 — and by 1930 caused no more than 3,000 deaths per year (9).

However, by 1950, coronary heart disease (CHD) was the leading cause of mortality and in 1960, 500,000 people died from MI related-deaths (10). What can account for such diverging statistics?

Leading cardiologists, pharmaceutical manufacturers, the American Heart Association, and the American Medical Association aren’t quite sure; yet they continue to maintain that the Lipid Hypothesis still holds relevancy. In very simplified terms, this theory states that when foods rich in saturated animal fats and dietary cholesterol are consumed, that cholesterol is then deposited in our arteries, causing plaque and contributing to a series of cardiovascular-related events that are life threatening (11).

This fifty-year-old hypothesis has continued to dominate the medical establishment’s thinking on which factors contribute to heart disease due in part to the work of the famous Framingham Heart Study of 1948 and the work of Ancel Keys, a public health scientist at the University of Minnesota. The Framingham Study looked at diet, lifestyles and environments and tried to draw correlations between high cholesterol and heart disease. Around the same time, Keys conducted his well-publicized Seven Countries Study to try and prove his hypothesis that there was indeed a relationship between dietary fat composition and serum cholesterol levels.

When one researches Keys’ findings they find serious flaws. There were twenty countries that participated in the study, yet only data from the seven countries that supported his hypothesis ever got reported (12). Even within the reported data there are in congruencies. For example, Greece (specifically the Greek island of Crete) was found to be the country with the lowest rate of heart disease. Yet, their cholesterol levels were well over 200 and they ate plentifully of goat cheese and full-fat yogurt.

In France, similar findings were found — very high cholesterol levels. Interestingly, the medical establishment has arbitrarily linked this “French Paradox” to red wine instead of the French diet, which is rich in butter and creamy sauces (13). Despite this manipulation of data, Keys’ relentless push back in the 50s for a low-fat, low-cholesterol diet became mainstream. Cardiologists at the time were hesitant to support this theory. But they eventually succumbed to the pressure — despite the fact that the “research” didn’t correlate with the anecdotal evidence seenin their practices. These published studies later became the catalyst for the American Heart Association’s first official endorsement of a low-fat diet and its ability to prevent heart disease (14).

The following is an excerpt from Good Calories, Bad Calories, by Gary Taubes. The book chronologically depicts the shift in consciousness that surrounded the historical Lipid Hypothesis debate: “From the end of World War II, when the USDA statistics became more reliable, to the late 60s (where coronary heart-disease mortality rates supposedly soared), per capitaconsumption of whole milk dropped steadily and the use of cream was cut by half. We ate dramatically less lard (13 lbs per person per year compared with 7 lbs) and less butter (8.5 lbs versus 4). Yet, we ate more margarine 4.5 lbs versus 9 lbs), vegetable shortening (9.5 lbs versus 17), and vegetable cooking oils 7 lbs versus 18). As a result, during the worst decades of the heart-disease “epidemic,” vegetable fat consumption per capita in America doubled, while the average consumption of all animal fat (including the fat in meat, eggs and dairy products) dropped from 84 lbs to 71. So the increase in total fat consumption, to which Ancel Keys and others attributed to the “epidemic” of heart disease, paralleled the increased consumption of vegetable fats, which were considered to be heart-healthy, with a decreased consumption of animal fats.” (15)

Despite many attempts, researchers in the 50s were unable to establish a correlation between patients with atherosclerosis who had significantly more cholesterol in their bloodstream to those who didn’t. Furthermore,
if the Lipid Hypothesis held true then those with the genetic disorder known as hypercholesterolemia should be getting atherosclerosis and dying of heart attacks — yet the opposite was happening (16).

The Lipid Hypothesis is still indoctrinated in mainstream cardiology circles today despite these historical findings, and as a result, cholesterol continues to be made guilty by association. Yet, as previously discussed, cholesterol accumulates at the site of a cardiovascular injury as it works to help heal damaged tissue. This takes place regardless of whether serum cholesterol levels are high or not because one of cholesterol’s primary roles is that of an antioxidant carrier, helping to reduce inflammation (17).

An analogy that is frequently used in holistic circles is that cholesterol is like that of firemen at the scene of a fire — they are there to lend assistance during the accident — to help to put the fire out. They are not the cause of it.

Part 3: Lab Tests and Lifestyle

Atherosclerosis: Lab Tests and Lifestyle
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).

Atherosclerosis: Diagnosis (Part 4)
by Hollie Greenwood, MS, NC

Prevention and early diagnosis of atherosclerosis is absolutely critical. If someone has been experiencing any of the above symptomatology, or there is a known predisposition for cardiovascular disease running through family lines, it would be prudent for a person to seek medical attention early — enabling them to implement a naturally effective and safe therapy. For those needing a baseline for determining their current state of cardiovascular health then obtaining a heart panel laboratory test would be a wise choice. The Berkley Heart Panel is one such lab that offers a comprehensive cardiovascular panel, which tests for the following inflammatory markers: LDL, IIIa+b, LDL lVB, Triglycerides, Apo B, Lp(a), Homocysteine, Fibrinogen, hs-CRP, Lp-PLA2, Low HDL and HDL2b (40).

Although the VAP Lipid Profile from Atherotech, Inc. has become well-known in the medical field, it is not as comprehensive as the Berkley panel and does not test for as many markers.

The Oxidative Stress Test is another diagnostic tool that can be used. This test shows the body’s oxidative stress status, antioxidant reserves and how well the liver is detoxifying.

Other assessments used for diagnosing cardiovascular issues are:

Electron beam CAT scan: beams of electrons are used to generate x-rays of the heart. It can capture images of the heart between beats and also detect calcium deposits in the arteries.

Angiogram: considered the gold standard in evaluating heart disease. A catheter is inserted into an artery in the groin or arm and guided up to the heart. A special dye is then injected through the catheter into each of the coronary arteries providing a contrasting color that shows the severity and location of blockages via x-ray imaging.

Echocardiogram: a noninvasive ultrasound records specific geographical areas of the beating heart, revealing blood flow patterns and measuring arterial wall thickness. It also shows which valves might be too restrictive or leaky and the overall functional capacity of the heart.

EKG: Assesses the electrical activity of the heart at rest enabling one to get precise information about cardiac rhythm, heart rate, coronary blood flow and pumpaction.

Additional suggested assessments

Oddly enough, the presence of a diagonal earlobe crease is a less evasive, but more exact indicator of future myocardial infarctions than an angiogram. Because the earlobe contains numerous veins, a decrease in blood flow over a period of time is thought to result in a collapse of the vascular bed, leading to the diagonal crease (41).

Atherosclerosis: Standard Medicines: Statins (Part 5)
by Hollie Greenwood, MS, NC

Cardiovascular disease is a huge profit center for those tied to the medical field. This in and of itself is probably not significant; however, because money is what tends to influence medical treatment standards — then its impact becomes quite significant. Surprisingly, pharmaceutical drug companies seem to hold a lot of control over decisions that are made in the world of cardiovascular health. Major medical research, meetings and cardiology conferences are all funded by drug companies, and pharmaceutical advertising dollars are what pays for a majority of the professional journals. Sadly, nutritional therapies aren’t lucrative enough for hospitals, doctors, research institutions or the drug companies and therefore
are rarely recommended for treatment (42).

Some of the most common drugs that are used to treat atherosclerotic symptoms are: statins, beta blockers, ACE inhibitors, coumadin, and calcium channel blockers. A discussion of how each of these drugs behave as well as their side effects is beyond the scope of this paper; however, because there is such substantial controversy surrounding the administration of statin drugs, it will be reviewed briefly.

Statins

Approximately 15-20 million Americans currently take statin drugs for lowering cholesterol. It’s estimated that an additional 15 million will take them in the near future as doctors are now prescribing them for lowering CRP levels as well. Statin drugs are huge sellers for pharmaceutical companies, estimating $16 billion in revenue for them in 2003 alone (43).

Ironically, statins work best because they reduce inflammation, not because they influence cholesterol levels (44). Yet, it’s their cholesterol-lowering ability that is advertised the most heavily. Statins seem to reduce atherosclerotic plaque by inhibiting a variety of immune factors, while enhancing other substances (such as nitric oxide) that promote healthy dilation of arteries and inhibit abnormal platelet clotting. This classification of drugs has also been shown to increase plaque stability by increasing collagen and suppressing macrophage growth (45).

As promising as this sounds one should still proceed with caution. Inflammation is a symptom of what is going wrong in the body — by suppressing it, the root of the problem still isn’t being properly dealt with. The immune factors that statins are quenching are the very ones that are needed to maintain our body’s immune defense system.

There are certain instances however where statins have been shown to be useful: in those with proven coronary artery disease, prior stent implementation, bypass or angioplasty, and those having a history of previous myocardial infarctions or stroke. Statins are contraindicated for those with no history of previous cardiovascular disease, heart attacks, or for those with normal CRP levels (46). These drugs also shouldn’t be prescribed to lower cholesterol as lowered cholesterol results in lowered immunity.

The list of statin’s side effects and potential dangers is shockingly large given that it is such a popular drug prescribed by doctors. Some side effects are: muscle weakness (including the heart muscle, which increases the incidence of congestive heart failure), muscle pain, mental and cognitive decline, increased fibrinogen evels, increased risk of hemorrhagic stroke, decreased longevity, adrenal and gonad disruption, increase in immune disorders, vitamin E depletion, shortness of breath, cancer, chronic fatigue (from lack of ATP), and aggressiveness, hostility, depression, suicidal tendencies (all from the reduction in neuropeptides that control behavior and psychological tendencies) (47). Perhaps the biggest and most known side effect of statins is that they have the ability to block CoQ10 production, which is vital for proper heart functionality.

Besides drug intervention, there are other allopathic approaches that are used regularly. Surgical procedures such as coronary artery bypass surgery, angioplasty and stent implementation are conducted frequently when atherosclerotic plaque has become very mature and calcified or coronary arteries have become clogged.
Coronary artery bypass surgery is a surgical procedure where new arteries are grafted onto the heart to “bypass” clogged arteries, restoring blood flow to the heart tissue. Angioplasty on the other hand, is a medical procedure that places a balloon into a clogged artery, and inflates it to break away plaque from the artery wall, opening it to restore blood flow. After the angioplasty has widened the coronary artery, an expandable wire mesh tube (a stent) is inserted to hold the artery open (48).

According to research, these invasive cardiologic approaches aren’t necessarily the best despite the frequency in which they are used by leading cardiologists.Generally within five or six years following bypass surgery, the arteries are found to be blocked again. This is due in part because the surgery creates additional cardiovascular damage, which allows more oxidized cholesterol to be deposited (49). It has also been found that 90% of bypass procedures may be unnecessary even to begin with. The predominant factor to consider when deciding if one needs coronary artery bypass surgery isn’t the degree of blockage or the number of arteries that may be affected, but the condition of the left ventricular pump (50). This fact should be heavily considered when weighing treatment options as the complications and risks involved with cardiovascular surgeries are numerous. One study has found that 61% of patients having bypass surgery suffer from nervous system disorders (51). In addition, 2-5% of individuals who have the surgery die soon after the operation with an additional 10% having myocardial infarctions (52).

Atherosclerosis: Holistic and Nutritional Approaches (Part 6)
by Hollie Greenwood, MS, NC

Ethylenediamine Tetraacetic Acid (EDTA) Chelation Therapy is an alternative to coronary artery bypass surgery and angioplasty. It has been proven to be a much safer, effective and inexpensive option and is FDA approved. EDTA is a synthetic amino acid-like substance that when saturated into the bloodstream, has the potential to bind with minerals like calcium, iron, copper and lead, carrying them to the kidneys, where they are then properly excreted. This type of chelation therapy has been commonly used for lead poisoning, but since the 1960s has been found to be helpful for those with athersclerosis. EDTA therapy improves blood flow throughout the body as well as aids in chelating out excess iron an copper that in the presence of oxygen can stimulate free radicals — significantly impacting atherosclerosis (53). This more naturally-based therapy has also been shown to respond better to immature plaque detection than allopathic procedures.

Lifestyle and dietary support

• Eat an omnivores diet that includes saturated fat and cholesterol from high quality animal sources as this will be very heart protective.
• Eliminate all refined and processed foods whose additives, preservatives, and ingredients deplete vital nutrients and cause more oxidative stress to the body.
• Avoid all sources of hydrogenated fats, refined vegetable oils, sugar and oxidized cholesterol.
• Eat a diet that is 4 to 1 omega 6 to omega 3 to reduce inflammation and cardiovascular complications.
• Daily intake of foods should have a 5 to 1 potassium to sodium ratio. This can be achieved by eating a diet high in fruits and vegetables and low in processed or canned foods.

• Stress management is crucial to maintaining good cardiovascular health. Deep breathing exercises, yoga, meditation, prayer, massage, good time management, living in the present and practicing forgiveness are all ways to help alleviate stress.
• Weight training and cardiovascular exercise are a must for keeping the heart in shape. The heart is in fact a muscle that needs to be worked out in order to increase blood supplies and oxygen and keep it working efficiently. Physical activity also enhances mood, increases energy levels, decreases stress and improves stamina.

Nutrient and herbal support

• Niacin reduces the progression of atherosclerosis and events associated with coronary heart disease (54). Inositol hexaniacinate (a safer, more tolerated form of niacin) is an alternative to statins. It lowers Lp(a) LDL cholesterol, triglycerides, CRP, and fibrinogen levels. For best results, it should be administered at night, as most cholesterol synthesis occurs at that time. 500 mg dosage at night, increase to 1500 mg after two weeks. After one month if the 1500 mg dosage does not lower
inflammatory markers, then increase to 3000 mg (55).
• Magnesium is 20x more concentrated in the heart muscle than in the bloodstream. It’s also a natural channel blocker, is excellent for plaque stabilization, improves metabolic efficiency of the heart muscle cells and helps diabetics by maintaining balanced insulin levels. 400-800 mg regardless of food intake is recommended (56).
• Cod liver oil should be taken for its high omega 3 fatty acids content. It’s also known to combat inflammation, improve endothelial function, thin the blood, decrease Lp(a), triglycerides and blood pressure, prevent plaque rupture, and has anti-coagulation properties. Dose is 1-2 teaspoons daily (57).
• Policosanol is very beneficial in helping against atherosclerotic symptoms. It prevents against excessive platelet aggregation and LDL oxidation. Recommended
dosage is 10-20 mg daily (58).

• Garlic 4000 mcg daily has functionality similar to statins, so is therefore a good natural alternative. It also inhibits platelet aggregation, breaks down fibrinogen,
helps lower hypertension and supports immunity.
• L-Arginine is an amino acid precursor to nitric oxide. When the body is deficient in nitric oxide blood vessels constrict and lose their flexibility, causing inflammation and plaque buildup. Less nitric oxide is produced in the body with age. 2-9
g daily in divided doses is recommended (59).
• L-carnitine is an amino acid that works with C0-Q10 to help fatty acids get into the mitochondria where they can be burned for fuel. This helps improve heart
functionality by decreasing triglycerides and elevated cholesterol levels. Dosage should be 2-4 g in divided doses (60).
• Vitamin C decreases incidence of cardiovascular events and related deaths by 40-60% by hindering the progression of atherosclerosis. It also: reverses endothelial dysfunction, neutralizes Lp(a), improves recovery after bypass surgery, supports detoxification, enhances immunity, neutralizes free radicals and
inhibits platelet aggregation (61). A preventative dosage is 500-1000 mg daily with a therapeutic dose at 2-6 g in divided doses. (Note that buffered C with bioflavonoids will increase the absorption of vitamin C.)
• Since homocysteine problems stem from deficiencies of B6, folic acid, and B12, it would be prudent to supplement with these B vitamins to reduce homocysteine levels. Dosages should be 50-100 mg B6, 400-800 mcg folic acid and up to 1000 mcg B12.
• Coenzyme Q10 is an essential nutrient that helps with all forms of heart disease. It’s a fat-soluable vitamin, so is best absorbed in a liquid or gel cap form. CoQ10 is a potent antioxidant and is essential for cellular and energy production. Studies have shown that supplementation of CoQ10 before bypass surgery makes for a faster recovery and less post-operative complications. Depending on he issue, CoQ10 dosages vary: preventative dose 60120 mg daily; therapeutic dose 180-360 mg daily (for angina, arrhythmia, hypertension, insulin resistance, diabetes, those taking statins, or that have gum disease); 300-400 mg daily for congestive heart failure (62).
• D-ribose helps restore depleted energy pools in the mitochondria as a result of metabolic stress such as blood and/or oxygen deprivation. When oxygen or blood flow deficits are chronic (as happens with heart disease), tissues can’t keep up with their demand for D-ribose. This is the only nutrient that can replenish diminished ATP energy stores and missing a dosage can negatively impact cellular energy by causing muscle weakness and fatigue. Dosage of 5 g for cardiovascular prevention or for athletes doing strenuous activity; 10-15 g for those with any form of heart disease; 15-30 g for those with advanced heart failure, fibromyalgia or neuromuscular disease (63).

Risk assessment checklist:

• HDL cholesterol lower than 35mg/dl
(men; 40 mg/dl (women)
• Triglyceride higher than 150 ml/dl
• Triglyceride/HDL ratio higher than 4 to 1
• Homocysteine higher than 10 umol/L
• Lp(a) higher than 30 mg/dl
• CRP (C-Reative Protein) higher than 1.5 mg/L
• Fibrinogen higher than 350 mg/dl
• Resting blood pressure above 140/90
• EBT (scan for calcified plaque) score above 200
• Fasting blood sugar more than 100 mg/dl
• Hemoglobin A1C more than 6% of total HGB

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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