This is not a diet book or an attempt to push a new fad; Dare to Live is a first-of-its-kind look at atherosclerosis from the naturopathic medical standpoint. Rather than just telling us what to do, Parcell presents in language accessible to everyone the causes of the disease, the rationale behind assessing risk for it, the purpose of the various tests he recommends, and the scientific evidence behind his recommendations.
Understanding what our bodies are trying to tell us is the first big step in preventing heart disease, and the next big step-acting on our knowledge-can teach us more than we might believe possible. By pursuing natural, scientific methods, we can keep health close to our hearts and keep a major killer away from ourselves and our loved ones.
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Dare to LiveA Naturopathic Doctor's Complete Guide to the Prevention and Treatment of Coronary Artery Disease
By Stephen W. Parcell
iUniverse, Inc.Copyright © 2011 Stephen W. Parcell
All right reserved.
Chapter OneWhat Is Arterial Plaque, How Does it Form, and Why?
Atherosclerosis is a complex subject under continuous study by cardiology researchers. Why do humans get plaque? What is plaque? What is it made of? Why does plaque form in some areas and not others? The answers to these questions may surprise you. Our understanding of atherosclerosis is still evolving, and new risk factors continue to emerge. Atherosclerosis (arterial plaque) results from the process of atherogenesis, and unchecked atherogenesis often results in a heart attack. Arteriosclerosis is a similar-sounding term but refers to hardening (and loss of elasticity) of the arteries. It causes high blood pressure. In the most basic terms, plaque is the body's response to injury at the artery wall. We used to call the plaque in arteries a "callus" analogous to the thickening of the skin in response to mechanical friction and pressure.
Injury comes in two types: mechanical and chemical. Mechanical injury includes arterial stretching caused by the effects of blood pressure on the artery wall and shear stress caused by the frictional forces of passing blood cells over the inner lining of an artery over a lifetime, plus the stretching of the vessels with each pulse. Chemical injury includes factors such as oxidative stress (not enough antioxidants or too much oxidative stress), dietary deficiencies, hormone imbalances, smoking, pollution, too much (or the wrong kind of) cholesterol, immune system dysfunction, and lack of nitric oxide.
In CAD, coronary arteries (the arteries that supply the heart) can become narrow with plaque, or the plaque itself can rupture. If a clot forms in a coronary vessel, it could block blood flow and lead to a myocardial infarction, or heart attack. The most common cause of a clot in a coronary vessel is a plaque rupture. The rupture attracts platelets and other clotting factors and causes a clot to form. We call this a thrombus. When the heart muscle does not get enough blood, part of it can die. So, both heart attacks and strokes are mediated by blood clots.
Heart attacks are not always symptomatic, especially the small ones. Also some plaques may rupture but not cause an obstruction. But, if the blocked artery is not fixed, the part of the heart that it supplies can become permanently damaged. Damage to the heart muscle affects electrical patterns in the heart; these electrical abnormalities are what doctors pick up on an electrocardiogram.
Quantifying plaque is achieved through noninvasive coronary calcium scoring with electron beam tomography (EBT), carotid artery ultrasound, or 64-slice heart scanners. While an angiogram shows us if you have a blockage or narrowing of the artery, the heart scan allows us to identify plaque years before it will cause a heart attack. Plaque is the ultimate risk factor. If your calcium score or carotid artery plaque is growing, you have active disease; if it is regressing or remains the same each year, you have coronary plaque reversal or stable disease.
A stroke occurs when a blood clot forms and travels to the brain, where it lodges in an artery providing the blood supply to a particular region of the brain. The clot can occur from a ruptured plaque in the arteries that feed the brain, or it can happen spontaneously, usually because of untreated high blood pressure. The blockage causes damage to the brain because brain cells need oxygen and glucose to survive. Doctors call this an ischemic stroke. The severity and type of symptoms depend on where and how extensive the ischemia is. The more damage to the brain, the harder it is to recover. Some people do not recover; others have long-lasting speech or walking problems. Transient ischemic attacks, or TIAs, are a type of ministroke where the clot is so small that the body is able to break it up and heal the damage.
Some people experience cardiac chest pain without having a heart attack. This is called angina pectoris and indicates that there is compromised blood flow to the heart, causing pain but not necrosis (tissue death) to the heart muscle. If you are having chest pain, it's a good thing that you are reading this book! Put it book down right now and go see your local cardiologist. Also get an EBT heart scan and get all the blood work I discuss in the book. Cardiologists typically won't run a lot of preventively oriented blood tests. Their specialty is intervention once you have a problem.
Plaque is composed of lipids (fats and cholesterol), calcium, white blood cells, muscle cells, and connective tissue. It is metabolically active and can be hotter than surrounding tissues. White blood cells enter and modify the plaque by becoming part of its structure and by secreting enzymes that degrade the fibrous cap that covers the plaque. Plaque formation starts in early adulthood and progresses at varying rates depending on many factors. Generally, as plaque grows, more calcium accumulates within the plaque structure.
Because cholesterol is a significant component of plaque, it became a major focus of drug research—to the detriment, I believe, of investigating other promoters of atherosclerosis. Though elevated cholesterol can accelerate atherosclerosis, it is not the only cause of the problem. Some people with high cholesterol never get heart disease, and others with normal cholesterol develop extensive atherosclerosis. The reason for this is that not all cholesterol is the same, and cholesterol is not the only factor to consider.
Plaque goes through many stages. Plaque usually progresses from being soft (and vulnerable to rupture) to a harder, relatively more stable stage. Because soft plaque is more unstable than hard plaque, it is more dangerous. Mixed plaque contains soft and hard forms and is also likelier to rupture than hard plaque. Total plaque burden and rate of plaque growth also predict plaque rupture and heart attack risk regardless of plaque type (Boudi 2006).
Plaque forms and becomes stable or unstable for complex reasons. The cells found in plaque—endothelial cells, smooth muscle cells, platelets (a fragment from a cell called a megakaryocyte), and white blood cells—interact with their environment, such as during expansion and contraction of the blood vessel. The health of the blood vessel wall, the state of activation of the blood clotting mechanism, and inflammation are other interrelated processes that contribute to plaque formation.
How Plaque Forms
Exactly how and why plaque forms is still being researched. The "response-to-injury" theory is most widely accepted. The first step in this is endothelial injury. The endothelium is the skinlike inner lining of the vessel walls that is in direct contact with the blood. The endothelium for the blood is like the skin on your body. When your skin is exposed to irritants it becomes inflamed. When it is exposed to mechanical stress (golf, tennis, raking leaves, etc.) it forms a callus. Normally the endothelium has a good working defense system. When this defense system is compromised, injury to the artery wall may ensue.
Endothelial injury causes inflammation, and this attracts white blood cells, which try to fix the damage. Endothelial injury can be caused by oxidized low-density lipoprotein (LDL) cholesterol, infectious agents (viruses), toxins (heavy metals, cigarette smoke, pollution, etc.), elevated blood sugar, and metabolic by-products (Boudi 2006). This is how arterial plaque starts!
Elevated levels of LDL cholesterol are bad because they can overwhelm the endothelium's defenses like an army of cholesterol-fueled ninja warriors. If those defenses are inadequate or the LDL particles are too numerous, the LDL particle becomes oxidized and can cause a wide range of vessel wall dysfunctions that are associated with the development of atherosclerosis. We call this wall dysfunction "endothelial dysfunction," and it's like a force field breaking down and losing power.
Furthermore, oxidized LDL can activate other inflammatory processes through acting on DNA. Oxidized LDL and inflammatory molecules can stimulate the DNA of the endothelial cell to produce more toll-like receptors (TLR) (Boudi 2006). These receptors play a major role in activating the immune system by regulating the production of immune system chemicals (chemokines and cytokines), which further promote atherosclerosis. Oxidation of LDL is common in smokers and people who have low antioxidant levels. This is why the role of antioxidants in heart disease has been a subject of continued research. Too much LDL is definitely bad.
Endothelial dysfunction can impair relaxation/dilation of the artery, causing increased blood pressure and further damage to the blood vessel wall. These dysfunctions arise (at least in part) from the inability of a protective chemical called nitric oxide (NO) to do its job at maintaining a healthy vessel tone. To make matters worse, the decrease in NO is also associated with increased platelet stickiness and increased risk of clot formation, which can lead to heart attack and stroke.
Role of Blood Viscosity (Do You Have Summer or Winter Oil in Your Engine?)
Evidence suggests that increased blood viscosity is an independent risk factor for atherosclerotic heart disease and its complications (Becker 1993). Blood behaves more like a solid at low speeds but behaves more like a liquid at fast speeds. Blood behaves much like ketchup coming out of a bottle. Once you get it moving, it really moves fast. When the heart is resting between beats it becomes more viscous (thick or solid), and then when the heart pumps blood through the body it becomes less viscous. Another analogy is the viscosity of summer- versus winter-grade oil. Summer-grade oil is made to be more viscous because heat makes the oil thinner. Winter-grade oil is less viscous because oil becomes thicker in cold temperatures. You want the right grade of blood—not too thick or thin. To find out if you have thick blood, get a blood viscosity test.
Atherosclerosis does not develop in random locations. This is because of differences in the turbulence of blood flow and blood viscosity. The frictional forces of blood create something called "shear stress." Shear stress refers to the arterial damage caused by thick blood or very turbulent blood flow (Becker 1993). I believe, as do some of my colleagues, these factors cause the initial damage that leads to endothelial dysfunction and atherosclerosis. Atherosclerotic plaque characteristically occurs in regions of turbulence, such as branching and curvature, and where blood undergoes sudden changes in velocity or direction of flow. Shear stress and turbulence may promote plaque formation, especially at sites within the coronary arteries, the major branches of the thoracic and abdominal aorta, the large vessels of the lower extremities, and the carotid arteries (Boudi 2006).
Why do we not get plaque in our veins? We do not see plaque in our veins because the pressure and frictional forces are much lower there. Cardiac surgeons use veins to bypass arterial arteries filled with plaque because the veins are usually in good shape. Frictional forces become very important in people with a condition called "polycythemia." Polycythemia simply means "too many red blood cells." We measure this in different ways. One common way is a test that looks at packed red blood cell volume called hematocrit. The virtual forces of blood increase considerably after hematocrit reaches forty-seven with levels over fifty being of particular concern. Too many red blood cells can also raise your blood pressure.
The more viscous your blood is, the more frictional and mechanical damage you will get. Hematocrit is the percentage of red blood cells in a given volume of blood. The more red cells you have, the higher your hematocrit will be. If you are an athlete and your hematocrit is above 50 percent, donate to your blood bank to get it down to no higher than 50 percent in order to decrease stress on the arterial wall. If you're not an athlete, consider lowering your hematocrit to at least forty-seven to decrease stress on the arterial wall. If your hematocrit is over fifty and you are not an athlete, consider getting a test for sleep apnea.
Overly viscous blood is an underappreciated risk factor.
Key Points and Action Steps Regarding Blood Viscosity
Keep hematocrit below fifty; optimal is forty-seven or below.
The easiest way to maintain lower blood viscosity is to donate blood, stay hydrated, and take nattokinase, lumbrokinase, bromelain, and fish oil.
Statin drugs also lower blood viscosity through numerous mechanisms (yes, really!)
Exercise lowers blood viscosity.
Understanding the Three Main Stages of Plaque Growth
Stage One: The earliest sign of atherosclerosis is a fatty streak in the aorta and coronary arteries. It usually happens by age twenty. Autopsies on young soldiers killed in the Korean War revealed that eighteen-year-old men already had plaque in their arteries. The fatty streak results from accumulation of cholesterol inside the vessel wall.
In stage one, white blood cells enter the vessel wall and act as scavengers, ingesting cholesterol, becoming bloated with small lipid particles, and becoming what we call "foam cells." Foam cell formation is a key part of early atherosclerosis. These bloated cholesterol-filled white blood cells then release chemicals and growth factors that cause further injury (Boudi 2006).
Stage Two: The plaque grows and becomes more fibrous, resulting from progressive cholesterol deposits and the proliferation of smooth muscle cells into the plaque. Platelets, white blood cells, and dysfunctional endothelial cells also produce chemicals that promote inflammation and lead to a vicious cycle of dysfunction and plaque growth. A deficiency of nitric oxide further aggravates this stage of plaque growth (Boudi 2006).
Stage Three: Smooth muscle cells deposit connective tissue that forms a fibrous cap, which covers the lipid core. The lipid core is made up of foam cells (a lipid-filled type of white blood cell), cholesterol, and various cellular debris. Growth of this fibrous covering progressively narrows the artery, leading to decreased blood flow and less oxygen delivery to the heart muscle.
Paradoxically, some arteries enlarge in response to plaque formation, and narrowing of the artery may only occur once the plaque occupies greater than 40 percent of the inner layer of the artery wall (Boudi 2006).
This enlargement is called the Glagov remodeling phenomenon, and understanding it is important (Glagov et al. 1987; Korshunov and Berk 2004). In this phenomenon the artery adapts to plaque formation by enlargement, resulting in a long phase of atherosclerosis without narrowing of the artery, without a blood flow limitation, and without symptoms. See the illustration below to understand it better.
This phenomenon helps explain why patients can pass treadmill tests only to have a heart attack weeks later, and why patients can have no symptoms of chest pain but still be at high risk of a heart attack. Simply put, the artery is not narrowed, and there is no blood flow limitation. This is the reason that plaque imaging using coronary calcium scoring and/or CMIT to determine risk is so critical and that a treadmill test can give false assurances.
More Detail on Plaque Progression
For those who would like more detail on the stages of plaque growth, please refer to Figures 1-2 below. The Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association (Stary et al. 1995), has classified six types. (The term "lesion," a general medical term, is used in this case to describe atherosclerotic plaque.) Type IV lesions are most prone to rupturing because of their thin fibrous cap. Types V and VI have the most calcium and fibrous tissue, and the lipid core may be replaced with fibrous tissue and calcium. In an adult, all six types of lesions may exist at once, and there is no easy way to determine what kind you might have, though we can make some assumptions based on test results.
The kind of plaque that shows up on a CT heart scan is calcified plaque. The calcium in the plaque is what the heart scan sees. The heart scan is really a fancy kind of X-ray, and X-rays see calcium (think of bones). Calcification is the result of long-term inflammatory processes in the body and can occur in tendons, muscles, or any soft tissue or organ. Calcified plaque in arteries contributes to their hardening or stiffening. Calcification is an age-related process, so a limited amount is common. Researchers are still studying why it occurs at all. Interestingly, some people who would appear to be high risk have no calcified plaque in their coronary arteries. When I see this coupled with other risk factors, I become concerned that the patient may have soft uncalcified plaque. I recommend a carotid intima-media thickness (CIMT) test in these cases to determine if soft plaque is indeed beginning to form.
Excerpted from Dare to Live by Stephen W. Parcell Copyright © 2011 by Stephen W. Parcell. Excerpted by permission of iUniverse, Inc.. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Table of Contents
Chapter 1 What is Arterial Plaque, How Does It Form, and Why?....................1
Chapter 2 Understanding Your Risk for Heart Attack (and the Concept of Risk Factors)....................14
Chapter 3 Exercise and Why It's Important....................51
Chapter 4 Understanding Cholesterol, Lipoproteins, and the Role of Statins....................65
Chapter 5 Hormones....................86
Chapter 6 Endothelial Dysfunction: Where Cardiovascular Disease Starts....................103
Chapter 7 High Blood Pressure (Hypertension) as a Risk Factor....................112
Chapter 8 The Role of Air Pollution in Heart Disease....................118
Chapter 9 Depression, Stress, and Anxiety....................120
Chapter 10 Medical Conditions that Increase Cardiovascular Risk....................126
Chapter 11 Dietary Prevention of Heart Attack and Stroke....................141
Chapter 12 Heart Attack Prevention Diet....................152
Chapter 13 Nutritional Supplements....................170
Chapter 14 Alternative and/or Controversial Treatments for Atherosclerosis....................204
Appendix 1 Lists of Tests....................215
Appendix 2 Summary of Trials/Studies/Reviews Proving that Lowering LDL with Statins Prevents Cardiovascular Events or Reverses Plaque....................218
Appendix 3 Summary of Supplements....................223
Appendix 4 Risk Tables....................225
Appendix 5 Resources for Readers....................229