Once the battery is charged, your heart is primed to do the mechanical work of contracting and relaxing. But in order for this work to occur, your heart cells needs one more important ingredient—adenosine triphosphate, or ATP, the essential energy that fuels your body’s cells. In the analogy presented above, if your heart is a car and electrolytes power the batteries, then ATP is the gas that lets the car move forward.
And boy, is your heart a gas-guzzler! All of your body’s 100 trillion cells require ATP to function, and your cardiomyocytes are no exception. In fact, your heart muscle cells are the most voracious users of ATP—after all, it takes an enormous amount of energy to push the equivalent of 20,000 pounds of blood around your body every day! Because your heart works harder than any other organ in your body, its cells need more ATP as well. For this reason, cardiomyocytes have the body’s highest concentration of mitochondria, the cellular factories that manufacture ATP. It therefore makes sense that your heart also has the highest concentration of magnesium ions in your body. This is because magnesium is essential for the biological activation of the ATP molecule. A free magnesium ion binds to an ATP molecule, changing its shape and electrical charge and forming a new compound called Mg-ATP, from which your cells can now extract the energy they need to function. Your heart thus makes and activates the greatest supply of Mg-ATP in your body—and quickly puts it to work.
Once your cardiomyocyte has access to these Mg-ATP molecules, it is finally ready to perform the contraction that the electrical signal ordered. Fueled by Mg-ATP, the heart muscle cell contracts; as soon as it does so, its electrolytes switch back to their original positions, with calcium and sodium on the outside of the cell and potassium and magnesium on the inside. The electrical signal is thus released, passing on to the next cell; accordingly, the cardio myocyte returns to its resting state and relaxes, ready to receive the next signal. (For a more detailed explanation of the process by which the electrical signal is turned into mechanical work, see the inset on pages 80 to 81.)
CONCLUSION
Hopefully by now, you should have a clear understanding of the cardiovascular system, particularly the heart. The heart is a complex organ—it not only manages multiple circulatory functions, but also regulates this circulation through an electrical system and the secretion of its own hormones. As the hardest-working organ in your body, the heart is both a massive consumer and producer of energy, a nuclear plant that requires enormous volumes of energy in order to produce the power that keeps your body working.
As this chapter has demonstrated, minerals are integral to the two essential functions of the heart. In the form of electrolytes, they allow for the conduction of electrical impulses. And as the activator of the energy compound ATP, magnesium helps fuel muscle contractions. But what happens when your body is deprived of these important minerals? Read on! Chapter 4 will examine the consequences of magnesium loss for your heart, unveiling a new theory that raises awareness of magnesium deficiency as a potential source of cardiovascular disease.
4
The Missing Link
Magnesium Deficiency & Heart Disease
Most modern heart disease is caused
by magnesium deficiency.
—DR. MILDRED S. SEELIG
Heart disease is the single most serious health epidemic facing the United States today. It is an enormously complex problem whose causes and risk factors the medical research community is still endeavoring to understand. Despite advances in scientific understanding, medical technology, emergency response, and health education, Americans continue to suffer heart attacks and strokes in overwhelming numbers. The statistics show that the battle against heart disease is far from over—in fact, it may just be beginning.
So what causes heart disease? Why does it occur, and why is it still such a pervasive problem? What have we failed to see? Are there factors in the development of cardiovascular disease that have not previously been considered? In short—what are we missing? It is time for some new answers to this old problem.
Chapters 1 and 3 established the foundations for understanding heart disease, introducing you to the cardiovascular system and describing the most common disease conditions affecting it. This chapter delves into the causes, risk factors, and mechanisms of heart disease. First, you will learn how the medical community presently views the development of heart disease, and how it treats and controls the perceived risk factors. Then, you will be introduced to a new theory that may account for the gaps in the system, a theory that explains why people continue to die of heart attack and stroke, despite the wealth of accepted wisdom on the subjects. The starved heart theory of heart disease proposes that there is an important and overlooked factor—a missing link—that could be the root cause of all cardiovascular disease. This missing link is magnesium deficiency, and it is implicated in every stage in the development of heart disease, from beginning to end.
By showing you that magnesium deficiency is an important and underappreciated cause of cardiovascular disease, this book will empower you to make better decisions about your treatment options, putting your well-being back into your own hands. The benefits of magnesium for heart health are no secret, yet surprisingly few people are aware of this marvelous nutrient. It’s time for this to change.
THE CURRENT VIEW OF HEART DISEASE
When doctors and scientists talk about why heart disease arises, most of the time they’re discussing the development of a cardiovascular condition called atherosclerosis, in which the arteries become narrowed or hardened due to the buildup of a fatty substance called plaque. Atherosclerosis is important because it sets the stage for the development of many other serious heart conditions, including heart attack, chest pain (angina), and stroke. Find the cause of atherosclerosis, researchers reason, and you’ll find the cause of many of the most common forms of heart disease.
How Does Heart Disease Develop?
Over the last twenty years, the medical community has come to believe that the root cause of atherosclerosis—and thus much heart disease—is chronic inflammation. This idea was first formally introduced in the mid-1990s by then-president of the American Heart Association Valentin Fuster and further refined a decade later by Peter Libby, the director of the Donald W. Reynolds Cardiovascular Clinical Research Center at Harvard University. According to Fuster and Libby, inflammation is the mechanism that drives the development of both atherosclerotic (hard) plaque and vulnerable (soft) plaque—an unstable material that can easily rupture, producing clots that can block arteries and cause heart attack or stroke.
To understand Fuster and Libby’s theory of how heart disease works, we first need to look at the concept of inflammation. Inflammation is essentially an immune response—your body’s way of coping with an injury or threat to its well-being. There are two types of inflammation: acute and chronic. Acute (short-term) inflammation occurs in response to a bodily insult: a cut, an infection, a burn, or other physical injury. Within seconds of cutting your finger, for example, your body’s immune response kicks in, sending blood cells, proteins, and other compounds to the affected area and begin the healing process. Your finger turns red, bleeds, and swells as blood rushes to the area. Eventually, the blood clots around the cut, and the redness and swelling reduces as the healing process advances. That is your body’s immediate “acute inflammation” response at work.
Chronic (long-term) inflammation occurs when an acute inflammation response fails to heal or resolve an injury, or in response to prolonged exposure to a stressor. Sometimes chronic inflammation can even occur in the absence of any harmful or invasive agent. As your body tries to heal itself without success, the types of cells that are present at the site of the injury start to change, potentially causing extensive damage to both healthy and the already-impaired tissue. Because it often affects internal organs, chronic inflammation usually lacks the obvious symptoms that characterize acute inflammation, and can be difficult to diagnose. Its effects, however, are quite powerful: Because of
the progressive damage it inflicts on your tissues, chronic inflammation has been linked to a number of serious health conditions, including arthritis, asthma, gastrointestinal disorders, cancer, and, of course, heart disease.
According to the inflammation model of heart disease, when an artery is torn, ruptured, or otherwise damaged by infection, high blood pressure, cigarette smoke, or other offending factors, your body initiates an inflammatory response, ordering cholesterol, blood cells, clotting proteins, minerals, and other agents to the site of the damage in order to protect and heal it. These agents embed in the wall of the artery and slowly accumulate, forming a pliable substance called soft plaque, whose outer surface is covered by a fibrous cap. Unfortunately, sometimes this cap is very thin, making the plaque unstable, easily damaged, and prone to rupture. For this reason, scientists refer to this type of plaque as vulnerable plaque.
After a time, the body begins to treat this vulnerable plaque as a new invader, essentially instigating an inflammatory cascade, or an inflammatory response to the original inflammatory response. In this new inflammatory response, fresh blood cells, cholesterol, minerals, and other healing agents are sent to fight the plaque. There are two possible outcomes to this event. When attacked by these blood cells, the fibrous cap that covers vulnerable plaque can rupture, spilling the powerful coagulants found in its interior into the bloodstream, where they thicken the blood and can form large and lethal clots. Left untreated, these clots can block the arteries—a condition called thrombosis, which ultimately leads to heart attack or stroke.
Alternatively, the calcium and other minerals sent to the plaque can help stabilize it, adhering to the plaque’s sticky surface and solidifying its fibrous cap. At first glance, this inflammatory response might seem like a good thing—an attempt to protect your body against further damage—since the plaque can no longer rupture, causing thrombosis. But in fact, this outcome is still troublesome, since the plaque is now there to stay, building up in the artery walls and causing them to harden and narrow. In short, as a result of the inflammatory cascade, atherosclerosis develops—opening up new risk for a host of other cardiovascular conditions, including angina, heart attack, stroke, and more.
The discovery of vulnerable plaque has been instrumental in changing the way doctors understand heart disease. While atherosclerosis is still an important point of focus, vulnerable plaque’s capacity to rupture and cause heart attacks make it potentially more dangerous than an artery blockage, no matter how extensive.
Knowing what they know, how do doctors then decide to treat heart disease?
How is Heart Disease Treated?
Because scientific understanding of inflammation is still developing, physicians in the United States treat and prevent heart disease in part by attempting to control the risk factors that seem to contribute to its development. As you’ll recall from Chapter 1, some of the most commonly recognized risk factors for heart disease include smoking, poor diet, lack of exercise, being overweight or obese, stress, high blood pressure, diabetes, high LDL cholesterol or triglycerides, and low HDL cholesterol.
Many of these risk factors can be reduced or removed by adopting lifestyle changes—quitting smoking, eating a more wholesome diet, becoming more physically active, maintaining a proper weight, and eliminating or limiting stressors. In addition, doctors often prescribe drugs to help control these risk factors, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and beta blockers.
The risk factor that doctors most frequently focus on and treat through medication is high cholesterol. Although many new studies show that cholesterol is simply not the evil it is made out to be, large-scale research studies consistently identify cholesterol as one of the prime culprits in raising the likelihood of heart disease. As a result, doctors often try to lower cholesterol in their patients by prescribing a class of drugs called statins. Recommended by most major medical institutions, including the American Medical Association (AMA), the American Heart Association, the American College of Cardiology, and many others, statins are among the most widely prescribed medications in the United States. Statins do work—but not for everyone. Studies reliably show that statins either reduce or prevent the recurrence of coronary events (heart attacks, strokes, etc.) in patients who have already experienced one.
The problem is, statins are also overwhelmingly prescribed for patients who have high cholesterol levels but who have never experienced a cardiac event. In an important review of eleven of the largest-scale studies investigating the use of statins, with a combined data pool of over 65,000 subjects, a recent report published in the Journal of the American Medical Association found that there was no evidence that statins had any benefits for heart disease prevention in patients who had never before been diagnosed with a cardiovascular condition. While other studies have indicated limited benefits for using statins to prevent coronary events in those with no history of heart disease, much evidence suggests that if you have never had a heart attack or stroke, statins may not help you avoid them. For some, statins may even do more harm than good, as many patients suffer unpleasant side effects without definite proof of benefit.
If statins can’t prevent heart disease in people who are at risk for developing it, why prescribe them so liberally? Moreover, why do people with normal cholesterol levels sometimes die of heart attacks? Is it possible that there are risk factors for heart disease that scientists have not yet considered? Or, more significantly, is it possible that there is a potential cause of heart disease that the medical community has overlooked—one that would allow us to formulate better treatment and prevention options by remedying the problem at the source? What is the missing link that will allow us to better understand heart disease—and prevent it?
The next section will outline an important emerging model that provides us with this missing link. The starved heart model presents compelling evidence as to a potential cause of cardiovascular disease, and proposes a simple way to both treat it and prevent it from ever developing in the first place.
THE STARVED HEART MODEL
Without food, your body begins to degenerate, and you will starve to death within thirty to sixty days. Without water, the starvation process is even quicker; you die in less than a week. The principle is straightforward: When deprived of the fuel that allows it to function, your body’s vital processes begin to break down, and shortly thereafter, your body simply ceases to work, with death occurring first at the cellular level before progressing to your organ systems.
Similarly, when your heart is deprived of the energy it needs to keep blood flowing through your system, it also stops working and begins to die. Your heart needs many different ingredients to make the energy (ATP) it needs in order to function properly. If you are denied food and water, as above, you’ll lack almost all the elements needed to produce ATP. But your heart can suffer and fail even when you receive seemingly adequate nutrition. Although you might not be able to see it, your heart is still starving—not for food or water, but for the most important component of ATP: magnesium. As you’ll recall from Chapter 2, in order for ATP to be used by your body, it must first be bound to magnesium. Magnesium activates ATP, allowing it to perform all of its essential tasks.
Thus it is magnesium, or, rather, the lack of magnesium, that forms the foundation of the starved heart model. Deprived of magnesium (usually as the result of stress), your heart cannot produce enough energy; without energy, your heart, arteries, and veins quickly begin to deteriorate, leading to heart cell death. In turn, heart cell death leads to calcification, and calcification to the inflammation that Fuster and Libby observed. Moreover, research has shown that magnesium deficiency independently plays a role in many critical heart conditions, ranging from arrhythmia to heart attack. Both directly and indirectly, magnesium starvation is at the very core of heart disease.
Accordingly, by taking steps to avoid or rectify magnesium deficiency, you can help stop heart disease before it
even starts. Research shows that by maintaining optimal levels of magnesium, you can protect against heart disease, preventing or decreasing your risk of heart attacks, stroke, and high blood pressure (hypertension). Simply put, magnesium is the most essential nutrient for promoting and maintaining proper heart function.
A Closer Look at the Starved Heart Model
As this brief overview indicates, the starved heart model asserts that heart disease is the end result of a degenerative process initiated by lack of magnesium. In order to properly understand this process—and how magnesium deficiency is integral to every part of it—this section breaks down the starved heart model into simple, easy-to-understand steps. For a quick reference guide, please see the chart on page 96.
Stress
What causes magnesium deficiency in the first place? As detailed in Chapter 2, the primary source of magnesium deficiency is stress. Stress evolved as a way for primitive humans to cope with perceived threats. When confronted with an immediate danger (say, a hungry lion looking for its next meal), the bodies of your ancient ancestors released stress hormones—including epinephrine (adrenaline), cortisol, and aldosterone—that allowed them to either fight their foe or run away from it. This “fight-or-flight” response is an evolutionary gift, a survival mechanism that has historically allowed humans to thrive and avoid extinction.
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