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In this innovative guide, Dr. Mark Houston helps readers discover the causes of heart disease, how to prevent and treat its debilitating effects via nutrition, nutritional ...
In this innovative guide, Dr. Mark Houston helps readers discover the causes of heart disease, how to prevent and treat its debilitating effects via nutrition, nutritional supplements, exercise, weight management, and lays to rest to various myths (cholesterol is not the primary cause) based on scientific studies and medical publications.
Readers will also learn how to indentify the risk factors most likely to endager them and construct an arsenal of non-pharmacological preventitive strategies that can counteract this most deadly disease.
THIS IS A BOOK about coronary heart disease, which comes about when the arteries that carry fresh blood to the heart are blocked and the flow of fresh blood to a portion of the heart drops dramatically or ceases entirely. Depending on the extent of the blockage, the result can be anything from the chest pain of angina to a sudden and fatal heart attack. Although a number of other problems can afflict the heart, including faulty valves, coronary heart disease is what most people think about when someone says “heart disease.”
Most doctors talk about coronary heart disease prevention as if it were a matter of dodging five “bullets,” namely:
elevated cholesterol (specifically LDL “bad” cholesterol)
high blood pressure
This focus on the “Big Five” risk factors is all pervasive; you’ve probably even seen those “How Long Will You Live?” equations that supposedly calculate the power these risk factors have to induce coronary heart disease. The equations contain instructions like “Subtract 6 points if your cholesterol is over 300” and “Add 2 points if you don’t smoke.” These may be fun to play with, but they are misleading because they don’t address the real causes of heart disease.
I prefer to think of the evolution of heart disease as a trip through a giant maze. When you first enter the Heart Disease Maze, you see hundreds of little pathways that wander all over the place, leading nowhere in particular. The walls lining these pathways are low, and there’s plenty of light, so you experience no feeling of urgency or danger; instead, you feel as if you can safely wander from path to path forever. These paths represent the hundreds of biochemical and other variations in your body that are often small and, by themselves, don’t matter. But if one variation is joined by others, you may find yourself on the fast track to heart disease. Examples of these variations include your blood levels of C-reactive protein, the size and number of your LDL cholesterol particles, the type and blood level of the fat known as triglyceride, your blood level of homocysteine, the type and size of HDL “good” cholesterol, your blood level of tumor necrosis factor (a marker of inflammation), and your blood level of interleukin-6 (a protein molecule that regulates the immune system). A few variations, such as uric acid levels, are routinely measured in standard blood tests; many others can be determined through specialized blood work or other tests. These variations also include certain diseases, such as chronic obstructive pulmonary disease, and infections, such as H. pylori, that by themselves don’t lead to heart disease.
But back to the maze: If you just strolled down a few of these paths for a while, then hopped over the short walls and walked out of the Heart Disease Maze, all would be well. However, if you kept walking and followed too many paths, or followed one or more for too long, you would suddenly realize that you were moving along a different kind of path—one with higher walls, less light, and a kind of spooky feeling. You would have moved from the innocuous “Variations Pathways” to one of the considerably more dangerous “Fast Track to Heart Disease Pathways.” You wouldn’t have noticed any signs indicating you were leaving the little Variations Pathways and entering the ominous Fast Track to Heart Disease Pathways, but there you’d be.
For many people, the Fast Track Pathways of greatest concern are the following seven:
Oxidative Stress Pathway
Vascular Autoimmune Pathway
Blood Pressure Pathway
Blood Sugar Pathway
Obesity and Increased Body Fat Pathway
Once you’re on a Fast Track to Heart Disease Pathway, you’ll find yourself moving faster and faster into darker, spookier territory. You’d like to stop but don’t know how, because there are no road signs or helpful people telling you how to get off. There are some doors in the very high walls that would let you out of the maze, but they’re difficult to spot unless you know what you’re looking for. Odds are you’ll keep moving ahead until you find yourself on the very dark and frightening “Faulty Arteries Pathway,” hurtling forward into the darkness. Even then there are a few ladders propped up against the very high walls that you could use to climb out of there, but they’re very hard to spot and grab hold of. That’s why there is a very good chance you’ll continue speeding forward in the darkness until you slam headlong into the brick wall called a heart attack.
This may be an oversimplified way of looking at the development of coronary heart disease and heart attacks, but it illustrates an important point: the disease process typically starts innocently with small problems having to do with inflammation, oxidative stress, or the way the immune system functions in the arteries (vascular autoimmunity)—a few minor variations in the levels of substances that most doctors don’t measure or even connect with heart disease. I call them variations because they’re often not out-and-out problems or diseases; they’re just a bit too much or too little of a measurable substance or the presence of a certain state. But when they’re combined with others, they can become troublesome. Even then they may not hurt you, thanks to your unique biochemistry and other factors. But if you have the wrong combination of genetics and other factors, you’ll need to slam on the brakes and get off that road as soon as possible, or your journey may come to an abrupt and unfortunate end, because now you have early-stage disease of the arteries, and they’re not working the way they should.
As a hypertension and vascular specialist practicing preventive cardiology, I’ve been frustrated by the fact that most people have no idea they’re in the Heart Disease Maze until they’re already on the Faulty Arteries Pathway or have splattered into the brick wall at the end of the journey. If only they knew how easy it is to step out of the maze at the beginning of the journey or how to get off the Fast Track to Heart Disease and Faulty Arteries Pathways or, better yet, how to avoid them altogether. But they don’t know because they’re not told these things by their physicians.
That’s going to change, starting now. In this book, I’ll introduce you to hundreds of biochemical and other changes (technically called risk mediators and risk factors) that make up the Variations Pathways, as well as several of the Fast Tracks to Heart Disease—inflammation, oxidative stress, vascular autoimmune dysfunction, dyslipidemia, disturbances to blood pressure and flow, and problems with blood sugar—that arise when variations interact with one’s unique body chemistry and lifestyle. But first, let’s take a look at the terrifying Faulty Arteries Pathway (technically called endothelial dysfunction) that inevitably results from these Fast Tracks—a pathway traveled by virtually everyone who has a heart attack.
The cardiovascular system consists of a heart that pumps blood and the blood vessels that carry the blood to all parts of the body, then return it to the heart. The blood vessels that carry blood away from the heart are called arteries; those that carry it toward the heart are called veins. It’s the arteries that we’re concerned with when we speak about cardiovascular disease. Most people think of the arteries as something akin to the water pipes in a house—all they do is carry water from the street, through the house, and back out. Like water pipes, they believe, arteries are inert little tubes that have no influence on the fluid they carry or the pump that keeps that fluid moving. Nothing could be further from the truth.
Unlike the water pipes in your house, arteries are complex, multilayered, living tubes that do much more than transport fluid. The arteries and their smaller versions, the arterioles, carry freshly oxygenated blood from the heart to all parts of the body. But they also perform many tasks to ensure that the blood keeps flowing at the right speed and physical consistency, and in the correct manner. If they fail to perform correctly, the consequences can be severe.
As you can see in Figure 1, the artery is a complex structure made up of several layers of tissues, each with its own duties and characteristics.
The central part of the artery, the open area through which blood flows, is called the lumen. This is the corridor through which the blood travels, with its red blood cells, white blood cells, platelets, proteins, nutrients, oxygen, and numerous other substances.
The layer that the blood actually comes into contact with is called the intima. It’s made up of the endothelium, which serves as the smooth inner lining of the vessel, plus connective tissue. The endothelium is the tissue in which coronary heart disease originates.
Moving deeper into the arterial wall, we come to the media, a thicker layer made up of smooth muscle that contracts and relaxes at the appropriate times, which helps control the flow of blood and the pressure. The outer layer, called the adventitia, is made up of connective tissues that help the artery maintain its shape and prevent it from bulging outward.
The endothelium, the point of contact between blood and artery, is very thin—just one cell deep. It has a variety of duties, including:
acting as a barrier by allowing only specific substances to pass from the blood into the artery
fighting off disease and regulating the way the immune system behaves in the artery by producing interleukins and other substances that play important roles in the battle against bacteria and other dangers
regulating blood pressure and arterial tone by synthesizing substances such as angiotensin converting enzyme, angiotensin II, nitric oxide, and endothelin, which help regulate blood pressure
controlling inflammation and oxidative stress
maintaining homeostasis and controlling the growth of arteries by detecting and responding to changes in the oxygen content of blood, as well as other indicators of the blood’s status and composition
fine-tuning the blood and helping to keep it thin and fluid enough to flow easily through the blood vessels
controlling blood clotting
As you can see, the endothelium is much more than an inert pipe. If it is damaged, you will find yourself on the road to heart disease and may suffer from numerous other ailments as well. Even if you’re thin, a nonsmoker, and have great cholesterol levels and low blood pressure, if your endothelium is damaged, you’re in trouble.
Because the endothelium produces substances that alter the actions of the arteries and makes “executive decisions” about which substances are allowed to pass through it, the endothelium qualifies as an organ and is, in fact, the largest organ in the body. If you took it out of the arteries, flattened it, and laid it out, it would cover six and a half tennis courts!
Even though the endothelium is the “brain” of the arteries, it is not encased in a protective sheath or buried safely within the artery wall. Instead, it is in direct contact with the bacteria, hormones, and other substances in the blood that can either harm it or alter its behavior. And it is right up against the pounding of the blood that continuously rushes through the arteries, like a beach subjected to the forces of heavy waves, twenty-four hours a day. While it may not matter whether a beach is reshaped by the ceaseless action of the water, the endothelium cannot allow itself to be altered by the tremendous force of the blood flowing past. It must maintain its structural and functional integrity. Unfortunately, it can’t always do that.
When the endothelium is damaged, its ability to serve as an intelligent barrier between the blood and the arteries is compromised. We call this condition endothelial dysfunction. When this occurs, several things can happen. The wrong substances—LDL cholesterol, white blood cells called monocytes, and other immune system cells and proteins—may pass from the blood into the arterial wall. The endothelium may over-or underproduce key mediators, substances, or hormones. Its ability to keep blood viscosity at the right level may falter, possibly allowing the blood to become thick, sluggish, and more likely to clot inappropriately. And since the endothelium is responsible for releasing substances that relax the arterial muscles and help regulate blood flow, the arteries may become constricted. This can cause blood pressure to rise and, depending on where the constriction is, blood flow to the heart to decrease.
Endothelial dysfunction leads to many problems with the arteries themselves, including
thickening of the endothelium (which should only be one cell thick) and the arterial wall
increased arterial inflammation
increased oxidative stress (free radical damage)
autoimmune dysfunction of the artery (the immune system mistakenly attacks the arteries)
increased deposits of protein, fats, and inflammatory cells into the artery walls
As damage to the endothelium accumulates and intensifies, the entire artery may become stiff, blocked, or otherwise ineffectual. Unfortunately, the problems triggered by endothelial dysfunction can make the condition worse, setting in motion a vicious circle and an intensification of the disease. For example, problems with the endothelium can make it impossible for the arteries to relax at the appropriate times, elevating the blood pressure. As blood pressure rises, the extra force exerted by the blood can further damage the endothelium and increase the endothelial dysfunction—which makes blood pressure rise even higher.
There are more than four hundred biochemical and biomechanical mediators of endothelial dysfunction—that is, things that can harm the endothelium. That’s an almost infinite number of insults the endothelium and artery may suffer, but there are only a finite number of responses, or things the endothelium and artery can do to protect themselves when they’re harmed. These responses are to trigger inflammation, oxidative stress, and autoimmune dysfunction of the arteries. These are standard “weapons” the body uses when attacked, but, unfortunately, they can make the problem worse, leading to endothelial dysfunction, abnormal arterial stiffness, and a lack of compliance, or the ability of the arteries to bend and relax in response to changing conditions.
For years we believed that heart disease began with atherosclerosis (“clogged arteries”), a process initiated when excess cholesterol and fat in the bloodstream stuck to the inner lining of an artery. More and more stuck and eventually blocked the flow of blood in an artery supplying the heart, triggering a heart attack. That idea is now obsolete. Today we understand that heart disease begins with an injury to the endothelium. Think of this injury as a microscopic scratch, like a paper cut on your finger that you can’t even see. Many things may have caused the scratch, including substances in cigarette smoke, elevated levels of glucose (sugar) or homocysteine in the bloodstream, chronic infections. toxins or heavy metals, oxidized LDL cholesterol, elevated blood pressure, or sheer stress on the arterial wall.
While you or I would probably ignore an insignificant scratch, the body is much more thorough. It triggers the inflammation process, rushing white blood cells, platelets, and other immune cells to the injured area to patch things up. But these immune cells don’t simply slap a kind of “molecular bandage” on the scratch and leave. Instead, some of these cells bind to the site, while others burrow through the endothelium and into the artery wall. These immune system cells, along with small, dense LDL cholesterol (which becomes oxidized and modified), smooth muscle cells, inflammatory cells, cytokines, chemokines, and clotting substances combine to form a toxic brew within the inner artery wall. It’s like an improvised explosive device buried in one of the walls of your arteries.
The toxic brew is walled off from the bloodstream. But it is not harmless, for it sends out signals that increase inflammation, oxidative stress, and harmful autoimmune activity. With time, the toxic brew inside the artery wall grows larger and more dangerous and becomes covered by a fibrous cap—a sort of arterial scab. If the toxic brew is large enough, it may cause the intima to bulge inward, interfering with the flow of blood. But even if a bulge grows large enough to block 50, 60, or even 80 percent of the passageway, it may not cause a problem. Even obstructions of 98 percent may be relatively asymptomatic—unless the fibrous cap ruptures or is ripped off, which is the thing we fear the most.
If the fibrous cap comes off, the toxic brew spews into the bloodstream. The toxic brew contains certain substances that, upon contact with the blood, cause an instantaneous blood clot. So even if a coronary artery is completely clear and the blood has been flowing through it freely, that sudden release of clotting substances can trigger the formation of a clot big enough to fill the artery, stop the flow of blood, and cause an instantaneous heart attack.
There’s no doubt about it: endothelial dysfunction leads to the arterial damage that’s a key factor in heart disease, even if there is no elevated cholesterol, no signs of “hardening of the arteries,” and no evidence of high blood pressure. That’s why simply taking medicines that lower cholesterol or blood pressure, or counteract elevated blood sugar, is not the answer if your endothelium is malfunctioning.
Ron, a forty-two-year-old man, was rushed to the emergency room when he complained of chest pain. He told the doctors that he had been having “moderate” chest pain off and on for several months. Ron, who was severely overweight, also divulged that he smoked a pack of cigarettes every day and was under a lot of stress. He was given the standard tests, which revealed that he had elevated levels of total cholesterol, LDL “bad” cholesterol, blood pressure, and fasting blood sugar. However, his cardiac angiogram showed that his coronary arteries were all “wide open,” with only minimal blockages. (That’s not surprising, for toxic brews can be hidden in the arterial walls and not protrude much into the lumen.) Ron’s doctors assured him that he was fine and just needed to stop smoking, lose weight, take medicines to control his cholesterol, and otherwise keep his Big Five risk factors under control.
Ron was an excellent patient and took his medicines exactly as prescribed. He also lost 20 pounds and cut back from one pack to half a pack of cigarettes a day. At his regular check-ups, his doctor was delighted. Then, three years later, Ron had his first heart attack.
He was sent to see me, and the tests I performed showed significant damage to the endothelium—which could have been detected earlier, had someone looked. If Ron had worked to reduce the factors that contributed to his endothelial dysfunction, he probably wouldn’t have had that heart attack.
Let me be clear: I don’t mean to imply that it’s okay to have elevated cholesterol, blood pressure, or blood sugar, or to smoke or be obese. But our decades-long insistence that the Big Five are the be-all and end-all of heart disease is a tragic myth that has led millions to an early grave. Endothelial dysfunction is much more important than any of these factors.
Endothelial dysfunction can be detected easily by several tests performed in the doctor’s office. They are accurate, giving a clear indication of the risk of coronary heart disease. They are also noninvasive, relatively inexpensive, and take less than fifteen minutes to complete. They include the following tests:
Computerized Arterial Pulse Waveform Analysis (CAPWA)—This test measures the elasticity of large and small arteries (their ability to widen and narrow in reaction to the pulsing of the blood). A poor result means the arteries are stiffer than they should be, indicating early endothelial dysfunction. A CAPWA is quick and simple; small monitors attached to the body feed information to a computer over the course of ten minutes. The patient simply lies on a table during the test.
EndoPAT—This test monitors the flow of blood, the relationship between blood flow in the arms and fingers, and the changes that occur as a blood pressure cuff on one arm is inflated and deflated. The results from the arm with the cuff are compared with those from the other arm to determine endothelial health.
Digital Thermal Monitoring (DTM)—DTM measures the ability of the arteries to widen and narrow by monitoring temperature. (Blood is warm, so changes in blood flow in the tiny blood vessels in the fingertips slightly alter the fingertip temperature, making fingertip temperature a surrogate measurement for blood flow.) A blood pressure cuff is attached to the arm, inflated to interfere with blood flow to the fingers, then deflated to allow the flow to return to normal. Changes in fingertip temperature allow the doctors to gauge endothelial health.
Carotid Artery Duplex Scan—This painless test uses ultrasound waves to generate a computerized “snapshot” of the blood flowing through the carotid arteries and identify any thickening, narrowing, or obstructions.
Ankle-Brachial Index (ABI)—This test compares blood flow in the ankle to blood flow in the brachial artery of the arm before and after exercise (walking on a treadmill for five minutes). Normally, the blood pressure at your ankle should be equal to or a little higher than the pressure in your arm, producing an ankle-brachial index or ratio of about 0.9 to 1.3. Deviations from this average suggest trouble in the arteries.
Carotid Intimal Medial Thickness (IMT)—This test uses ultrasound to measure the thickness of the intima and media of the carotid arteries, which run through the neck. As blood pressure increases and a toxic brew forms within a damaged artery, its walls become thicker. Thickening of the carotid arteries has been shown to be a strong indicator of cardiovascular disease and atherosclerosis. It also signals an increased risk of coronary heart disease, heart attack, and stroke.
Based on the results of these and perhaps other tests, your physician will be able to determine whether you are suffering from endothelial dysfunction and, if you are, to what degree. If you have signs of endothelial dysfunction, you need to take action now, because you’re on the Faulty Arteries Pathway, which can easily cause a heart attack or stroke. If you don’t show signs of endothelial dysfunction, you’re not necessarily in the clear, as you might still be on one of the Fast Track to Heart Disease Pathways. No matter what your problem, however, my Integrative Cardiovascular Disease Prevention Program has solutions. Read on to discover how to gauge the health of your heart, find out whether you’re on a Fast Track to Heart Disease or one of the earlier pathways, and what to do about it.
Genetic errors play an important role in determining whether you wind up on one of the pathways, which one you enter, and to what extent you develop faulty arteries.
Genetic errors that cause significant problems, such as the extremely high cholesterol levels known as familial hypercholesterolemia, are easy to detect. However, many of us have relatively minor genetic changes that act subtly, predisposing us to coronary heart disease that strikes only when other factors, such as poor diet or exposure to certain chemicals, come into play.
These smaller errors are slight alterations in DNA that occur when one of the four “letters” that make up the genetic alphabet—the nucleotides known as adenine (A), cytosine (C), thymine (T), and guanine (G)—is replaced by one of the other letters. For example, perhaps the sequence of nucleotides in a segment of DNA should be ACAT—but instead, the last “letter” is changed, and the segment becomes ACAG. It’s like a typo. Doctors call this a single nucleotide polymorphism (SNP).
These little “genetic typos” are common, and many are inconsequential. But suppose yours occurs within a portion of the DNA that carries instructions for the behavior of a hormone that helps regulate cholesterol. This altered hormone may not be deformed enough to trigger disease on its own, but if it is combined with other problems in the way your body handles cholesterol, it may tip the balance in favor of disease.
We know about certain genetic typos that play a role in coronary heart disease. For example, one affects the secretion of LDL and increases the risk of suffering a heart attack, while another increases the risk of coronary heart disease by interfering with one of the body’s important antioxidants, leading to increased oxidative damage.
So far, more than seven hundred SNPs related to car-diovascular health, heart disease, and hypertension have been identified. Fortunately, you can be tested for SNPs that may set you on the path toward coronary heart disease at laboratories such as Pathway Genomics, Doctor’s Data, Genova Diagnostics, and Quest Diagnostics. Remember, however, that these are genetic predispositions, not disasters written in stone. Knowing where you have weaknesses can be a blessing, as it allows you to take corrective action.
I’M A TRADITIONALLY trained physician who is well versed in the use of standard medicine and surgery, but I’m also very interested in integrative, functional, and metabolic medicine (previously called complementary and alternative medicine). Over the course of my career, I’ve taken what I consider to be the best of both approaches to create my eight-step Integrative Cardiovascular Disease Prevention Program. The steps are:
Get thoroughly checked by a physician who goes beyond the traditional Big Five coronary heart disease risk factors to examine the biochemical variations and disease pathways I’ll be discussing in the chapters to come.
Reduce inflammation, oxidative stress, and immune dysfunction with nutritional supplements, proper nutrition, weight loss, improvement in body composition, exercise, and medications and treat or eliminate factors that are causing or exacerbating these problems anywhere in your body. Dealing with these three problems is key, for everything else that poses a risk of coronary heart disease eventually triggers one or more of these three “late-stage” problems.
Counteract problems with cholesterol and blood fat; stabilize blood pressure and normalize blood flow through the arteries; and correct abnormalities in glucose and insulin levels with optimal nutrition, exercise, weight loss, nutritional supplements, and medications. Remember that all of these problems contribute to the inflammation, oxidative stress, and immune dysfunction that damage the endothelium and set the stage for disease and possibly disaster.
Exercise using the ABCT (Aerobics, Build, Contour, and Tone) Exercise Program, the only one that fully taps into the muscles’ ability to communicate with the rest of the body and encourage healing, slow aging of the arteries/aging in general, reduce morbidity and mortality, and promote better health.
Attend to any other diseases or states that may be contributing to inflammation, oxidation, autoimmune dysfunction, and/or endothelial damage or otherwise increasing the risk of coronary heart disease.
Make lifestyle changes to achieve ideal body weight and body composition, eliminate or reduce stress, stop smoking, sleep more, and improve your outlook on life.
Use standard medications as appropriate, and understand the importance of integrating scientifically proven medications with nutritional supplements.
Stop using all tobacco products.
My plan is the only one that takes into consideration all that we’ve learned about coronary heart disease over the past several decades, including the fact that the Big Five risk factors are not the best indicators of an impending heart attack.
The key to reducing your coronary heart disease risk is early detection, plus early and aggressive prevention and treatment of all identified risk predictors—in other words, everything that can damage the endothelium. It is never too late to begin. You can slow, stabilize, prevent, and even reverse coronary heart disease. My plan helps you do so by combining the best of standard functional and metabolic medicine.
In the next five chapters, we’ll look at the Fast Track to Heart Disease Pathways, how and why you may find yourself on one or more of them, their dangers, plus treatments and preventive strategies.
WE USED TO BELIEVE that “hardening of the arteries” (atherosclerosis) was triggered by excess cholesterol and fat in the bloodstream that somehow attached itself to the inner lining of an artery, like a barnacle sticks to the hull of a ship. More and more would attach, glomming on to what was already there, until sooner or later, one of these little “barnacle groups” would grow large enough to block the flow of blood. If the blockage happened to occur in an artery that fed the heart, the part of the heart that was no longer receiving fresh blood would die—in other words, a heart attack would strike. But that idea was rendered obsolete when numerous studies conducted during the past decade showed that the genesis of a heart attack involves a lot more than a clump of fat damming blood flow. We now know that one of the primary coronary heart disease risk factors is inflammation, and it plays an important role in promoting heart disease from the very beginning.
Inflammation is a natural response of the body designed to prevent infection and repair damage. You’re undoubtedly familiar with the outward signs of inflammation: swelling, redness, warmth, and pain. In simple terms, here’s how it works: You cut your finger, and bacteria race in through this break in the skin. Your body recognizes the bacteria as foreign invaders and undertakes to defend itself. The defense begins as the walls of nearby blood vessels “loosen up” so that plasma (the liquid part of the blood) can leak into the surrounding tissue. As the infected area floods, immune system cells in the plasma come into contact with the invading bacteria and begin to do battle. The flooding also causes swelling and creates tension in the area, triggering pain. Some red blood cells also escape from the blood vessels into the surrounding tissue, causing redness. The increased circulation of fluids promotes warmth.
All the while, the immune system cells fight with and destroy the bacteria, engaging the invaders in hand-to-hand combat, shooting out chemicals designed to destroy the enemy, literally engulfing and devouring them, and otherwise doing what it takes to protect the body. Sooner or later the battle is won, the excess fluid is reabsorbed, the immune system cells are recalled, the battlefield debris is cleared away, the pain recedes, and the body returns to normal. Mission accomplished!
This kind of inflammation is short term, beneficial, and absolutely necessary. Without it, we could not survive. But inflammation becomes a problem if it is chronic, lasting long after the initial danger has been dealt with—or perhaps arising for no reason at all. Then it serves no useful function and is very destructive to the body. With chronic inflammation, the body keeps sending out immune system soldiers after the battle has been won—or even when there has been no invasion or obvious damage. The system gets stuck in “fight mode,” and the chemicals continually released by immune system cells to defend the body wind up damaging or killing the body’s own cells. Thus, instead of protecting the body, the inflammatory process starts to destroy it. Chronic inflammation is believed to be the root of most degenerative diseases, including arthritis, diabetes, cancer, and heart disease.
As you recall from the discussion in chapter one, heart disease begins with a little “scratch” to the endothelium. The body repairs the injury, but during the repair process, immune system cells, oxidized LDL cholesterol, and other cells and particles can slip through the endothelium and into the artery wall, setting the stage for endothelial dysfunction and coronary heart disease.
Inflammation can start this terrible progression by causing or contributing to the initial scratch. And once the toxic brew has begun to bubble within the arterial wall, inflammation can stir the pot by serving as a beacon, drawing additional immune system cells, oxidized LDL cells, and more to the site. From start to finish, the creation and rupture of the toxic brew plaque are driven by inflammation. Among other things, inflammation:
draws immune system cells to the injured site, where they can slip through the endothelium and into the artery wall
alters the activity of the endothelium so that it attracts substances that contribute to the buildup of plaque
loosens the junctions between endothelial cells, making the migration of foreign substances into the artery wall easier
transforms helpful immune system cells called macrophages into harmful foam cells
attracts immune system cells called T cells that, upon arrival, release substances that keep the inflammatory process going
Through these actions, the toxic brew itself becomes a source of chronic inflammation, fueling its own growth. Don’t worry about the details; the key point to remember is that inflammation is present at the beginning, middle, and end of the coronary heart disease process. It is so potentially harmful that I would go so far as to say that inappropriate inflammation is much more dangerous to the artery linings than is an extra 10, 20, or even 50 cholesterol points over the ideal.
It’s easy to recognize the signs of short-term inflammation: the site of the injury becomes reddened and warm, it swells, and it becomes painful. But chronic inflammation within the cardiovascular system is hidden inside the body; you can’t see any overt signs of it. How do you know if it exists?
Your doctor can track inflammation and its fluctuations by measuring the levels of certain substances that rise as inflammation increases and fall as it fades away. One of the most prominent indicators of inflammation is high-sensitivity C-reactive protein (HS-CRP). This is the most predictive of all inflammation indicators, and of all the inflammatory risk factors and mediators, HS-CRP is backed by the best scientific research. It should be part of every blood exam done for patients. Levels over 2.0 mg/L are cause for concern.
Many things can increase levels of HS-CRP, which is a protein produced by the liver from substances such as interleukin-6 (IL-6), interleukin-1B, and tumor necrosis factor alpha (TNF-alpha). These and other inflammatory markers and substances from all over the body travel to the liver, where they are processed into HS-CRP.
Any infection will trigger an increase in HS-CRP, including periodontal disease, H. pylori infection, a sore throat, streptococcal infection, pneumonia, colitis, and sinusitis. Any acute injury that damages tissue will also trigger inflammation and increase HS-CRP. If there’s no obvious reason for a rising HS-CRP—such as a sore throat or an injury—the increase is probably due to inflammation within the arterial system. Although HS-CRP is not itself an infection, it acts in many ways to promote inflammation as well as the oxidative stress and autoimmune dysfunction that harm the endothelium.
HS-CRP is thus both a risk factor and a risk mediator for coronary heart disease. In other words, it predicts an increased risk for heart disease, but it also causes continued damage to the arteries as long as it is elevated. For these reasons, HS-CRP should be checked at regular intervals, which can be done with a simple blood test. And if it is elevated, no matter what the reason, it is very important to reduce it to normal levels as rapidly as possible to avoid damage to the arteries.
Sometimes, the underlying cause of the elevation is a disease that can be identified and treated. For example, a 2010 study published in the journal Angiology reported that otherwise healthy adults with chronic periodontal disease had significantly higher levels of HS-CRP and interleukin-6 compared with a control group that did not have the disease. But when the periodontal disease was treated, the levels of these inflammation markers fell significantly. I’ve seen elevated HS-CRP in patients with a variety of diseases, including a middle-aged man suffering from severe osteoarthritis and obesity whose HS-CRP dropped from 8 to 1 mg/L when both were treated and a young woman whose HS-CRP fell from an alarming 22 to a very safe level of 2 mg/L when her chronic bronchitis was eliminated by antibiotics. In another patient with H. pylori infection, which was causing his stomach ulcers, HS-CRP dropped from 6 to 1.5 mg/L with antibiotic treatment.
In a great many cases, however, the HS-CRP elevation is due to long-term lifestyle and dietary factors. This may sound like bad news, but it’s actually good, for it means you can start making helpful changes today—and the diet and exercise regimen I discuss later will help you do so.
I urge you to have your HS-CRP checked as soon as possible to see if you are harboring inflammation that may be damaging your arteries. Your physician may want to order other tests to search for inflammation or to provide more information about the inflammation. These include tests for serum amyloid A, which is secreted in the body during the acute phase of inflammation; IL-6, which is a small molecule that promotes the immune response; TNF-alpha, which plays a role in the acute stage of the inflammatory process and the production of HS-CRP; neopterin, a substance produced by macrophages that both shows inflammation is present and may increase atherosclerosis; and uric acid, high levels of which induce arterial inflammation. Having elevated levels of any one of these or other inflammation markers is like walking on those little Variations Pathways in the Heart Disease Maze.
In addition, get yourself checked for chronic periodontal infection and other “quiet” infections that may have been festering in your body for some time, as well as for increased levels of heavy metals such as mercury, lead, arsenic, cadmium, and iron in your bloodstream and body tissues. These substances increase inflammation (and oxidative stress), damaging the arteries and leading to coronary heart disease.
The inflammation indicators I just mentioned can all be measured and quantified, but there are some others that can’t. These are items or situations that are likely to contribute to inflammation, but we can’t say that X amount of one of these leads to a 3-percent increase in inflammation or anything similar. However, we can say with certainty that the risk of inflammation rises with any of the following conditions:
increased intake of refined carbohydrates, including sugars and sweets
increased intake of trans-fatty acids and saturated fats
lack of sleep
lack of exercise
Excerpted from What Your Doctor May Not Tell You about Heart Disease by Houston, Mark Copyright © 2012 by Houston, Mark. Excerpted by permission.
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Chapter 1 The Real Reason People Have Heart Attacks 9
Chapter 2 The Integrative Cardiovascular Disease Prevention Program 26
Chapter 3 Inflammation: A Fast Track to Heart Disease 29
Chapter 4 Quenching Oxidation, a Disaster in the Making 42
Chapter 5 Fixing Cholesterol: Beyond the Numbers 62
Chapter 6 Maintaining Proper Blood Flow Through the Arteries 78
Chapter 7 Preventing Blood Sugar and Insulin from Harming the Heart 92
Chapter 8 A Potpourri of Other Risk Factors 104
Chapter 9 Eating for Optimal Heart Health 116
Chapter 10 ABCT Exercise: The Theory 139
Chapter 11 ABCT Exercise: The Practice 148
Chapter 12 New Understandings, New Possibilities 187
Appendix I Key Cardiovascular Risk Factors 195
Appendix II Homocysteine and Its Effects on Nitric Oxide and LDL Cholesterol 197
Appendix III Quenching Inflammation and Controlling High-Sensitivity C-Reactive Protein 202
Appendix IV Reducing Oxidative Stress 218
Appendix V Antioxidant and Anti-inflammatory Supplements and Other Approaches 227
Appendix VI Expanded Supplement Regimens for Specific Problems Related to CAD 253
Appendix VII Assessing Functional Heart Age 260
About the Author 303
Posted March 13, 2013