Why talk about the heart from a medical point of view? How boring, unless you're a doctor that is. Right?
By looking at the basic anatomy and physiology of the heart from a doctor's perspective, we gain a unique privilege. We get to evaluate that perspective. Once we understand the underlying basis of medical treatments used to correct heart problems, we can make informed decisions as to which of those treatments and medications actually make sense for us...and, more importantly, what alternatives might actually work better. So with that in mind, let's take a look at the human heart.
Your heart is located between your lungs in the middle of your chest, immediately behind and slightly to the left of your breastbone (sternum). In this location, it is protected by the breastbone in front, the spinal column in back, and the ribs on the sides. It weighs 7 to 15 ounces and is about the size of a human fist.
With each beat, the heart muscle expands and contracts, sending 2 to 3 ounces of blood on its way through the vascular system. The full circuit around the lungs and body (covering a mind boggling 50-60 thousand miles of branching blood vessels) takes only about one minute to complete when the body is at rest. In that same minute, your heart can pump some 1.3 gallons of blood to every cell in your body. Over the course of a day, we're talking about 100,000 heartbeats shuttling some 2,000 gallons of oxygen rich blood throughout your body. That works out to some 35 million beats a year and an unbelievable 2.5 - 3.5 billion beats in a lifetime. Another way of looking at it is that the heart pumps approximately 700,000 gallons a year and almost 50 million gallons in an average lifetime.
I will cover the circulatory system in detail in its own newsletter at a later date, but for now it's important to understand in our discussion of the heart that the heart actually pumps blood through two very distinct circulatory systems. They are the Systemic and the Pulmonary
The systemic system is what most people think of when they think of the circulatory system. That's the system that feeds the organs, tissues, and cells of your body. That's the system in which fresh oxygenated blood pumps out through the arteries and in which deoxygenated blood returns to the heart through the veins. The pulmonary system is actually quite different, just the opposite in fact. Deoxygenated blood is pumped out of the heart through the pulmonary arteries into the lungs, and recharged oxygenated blood returns to the heart through the veins. It is this recharged oxygenated blood that gets pumped out through the systemic circulatory system. Understanding these differences will be important later. For now, just consider the simple fact that these two separate systems must be perfectly balanced in terms of input and output. If for example, the pulmonary system is just one drop a minute behind the systemic system, in short order, the left ventricle of the heart (the chamber that pumps blood out to your body) will become under filled with blood and cease to function efficiently.
The tissue of the heart is comprised of three layers. The primary layer, the middle layer, is called the myocardium. This is the actual muscle tissue of the heart and the part of the heart that will feature most prominently when we talk later about what can go wrong with the heart. The myocardium is a thick strong muscle and comprises the bulk of the heart. It is formed of smooth involuntary muscle like your intestines and your bladder, but with a several key differences.
- It has built in rhythmicity. That is to say, unlike other muscle tissue, it is self-stimulating and doesn't require a signal from the nervous system to contract.
- The muscle tissue itself has a spiral structure that allows for the twisting action of the heart as it contracts with each beat. (We'll talk more about this later.)
The myocardium is lined on the inside (where all the blood is pumping) with a thin membrane called the endocardium. On the outside, the myocardium is enclosed by a membranous sac filled with fluid called the pericardium. The outside of the pericardium sac is pressed against the lungs and the chest wall. The inside of the sac (called the visceral pericardium) is actually attached to the heart muscle. The purpose of the sac is to hold the heart in place, protect it, and eliminate inflammation by protecting the heart from friction as it beats. If you think about it, every time the heart beats it expands and contracts rubbing and sliding against the lungs and the chest wall. It is the fluid filling the pericardial sac that allows the inner and outer parts of the sac to slide against each other with no friction thus allowing the heart to beat some 2.5 - 3.5 billion times in a lifetime without rubbing itself raw.
The heart itself is divided into four chambers: the right and left atria and the right and left ventricles. As you can see below, it is separated vertically by part of the myocardium heart muscle. Horizontally, the two halves are further divided by two valves, the mitral or bicuspid valve on the left side of the heart (right side of the illustration) and the tricuspid valve on the right.
The flow of blood through those chambers is actually quite simple.
All of the deoxygenated blood in need of "recharging" returns to the heart through the large veins called the vena cava (anterior and posterior). The two vena cavae empty into the right atrium, the first chamber in the heart. (Incidentally, one of the definitions of atrium is a forecourt of a building, which is essentially what the atria are: forecourts to the two ventricles.) From there, the blood passes through the one-way tricuspid valve into the right ventricle, which pumps it out through the pulmonary valve into the pulmonary aorta and into the lungs.
Note in the illustration above how much smaller the left ventricle is than the right and how much thicker the muscles are surrounding it (about 4 times thicker). The reason is simple. Smaller chamber and greater force of contraction means greater pressure. When you consider that the right ventricle only needs to push the blood a few inches into the lungs and back, whereas the left ventricle needs to push the blood throughout the entire body, this makes sense. In fact, the left ventricle produces about 4 times the pressure of the right ventricle. It is through this difference in pressure that the body keeps the blood supply perfectly balanced between the two chambers even though they are powering two entirely different circulatory systems.
Once oxygenated, the blood makes the short trip back through the pulmonary veins and back into the heart, entering through the left atrium. This is the pulmonary circulatory system we referred to above.
From the left atrium, the oxygenated blood passes down through the one-way mitral valve and into the left ventricle. From there, the large muscles surrounding the left ventricle squeeze the blood out through the aorta as it starts its circuit out to every single cell in the body.
In construction and function, the two valves are quite simple, but extremely important. Fundamentally they look like parachutes with tendons or cords running down into the ventricles to keep them from opening too far. (See below.) When there is no blood in the ventricle below them, there is no pressure on the valves, and they are in the open position. In the open position, blood can passively move from the atrium above down through the openings in the valve into the ventricle below. Once the ventricle fills with blood and the heart contracts creating pressure in the ventricle, that pressure pushes up on the bottom of the valve forcing it closed so the blood cannot flow back into the atrium above. At that point, the blood has only one way out of each ventricle - through the main pulmonary artery in the right ventricle and the aorta in the left ventricle. The system is brilliant, totally passive, and amazingly durable. For most people it functions flawlessly for 70-100 years, through 2.5 billion plus heartbeats.
For a great review of everything we've talked about so far, check out the medical animation from the University of Pennsylvania Health System.
Once the oxygenated blood leaves the heart and heads into the aorta, it almost immediately encounters the first two blood vessels off the aorta: the left and right coronary arteries. These are the main arteries that feed the heart muscle, the myocardium. One of the first things you'll notice in the illustration below is how much branching and redundancy there is in the arteries and veins that feed the heart.
The medical term used to describe this branching is anastomosis. You don't have to remember it. Just remember that the blood vessels of the heart have many branches that reconnect in multiple places to provide alternate pathways for the blood in case one branch is blocked. In fact, there is so much redundancy, that your heart can function with no visible symptoms with up to 70% blockage. It's almost as though nature anticipated the western fast food diet and built in a huge reserve capacity knowing how aggressively we would seek to clog the system up.
We've established the basic bio-mechanics of the heart, but there's one key question we haven't addressed yet:
Fundamentally, the contraction of the heart is an electrical phenomenon - or more precisely, a bio-electrical phenomenon based on the movement of sodium, calcium, and potassium ions across membranes. (We'll cover this in more detail in a moment.)
For now, just understand that when a muscle cell is excited, an electrical signal is produced and spreads to the rest of the muscle cell, causing an increase in the level of calcium ions inside the cell. The calcium ions bind and interact with molecules associated with the cell's contractile machinery, the end result being a mechanical contraction. To simplify this, a sodium ion starts the stimulation of the cell, a calcium ion extends that stimulation to allow the entire muscle to contract before potassium comes along and tells the muscle cell to relax for a moment and get ready for the next wave. Even though the heart is a specialized muscle, this fundamental principle still applies. (Makes you think about the importance of minerals in the diet, doesn't it?) One thing, however, that distinguishes the heart from other muscles is that the heart muscle, as we've already discussed, has built in rhythmicity. Thus, an electrical excitation that occurs in one cell easily spreads to neighboring cells.
Under normal circumstances, the initial electrical excitation that starts the beat of the entire heart originates in the pacemaker cells of the sinoatrial node, located on top of the right atrium. This small group of cells pretty much serves as the impulse-generating pacemaker for the heart and normally discharges about one hundred times per minute. These impulses move down through fibers in the myocardial wall and come together in the atrial ventricular node where they are slowed down before entering and stimulating the controlled contraction of the muscles surrounding the two ventricles.
A simplified picture of the electrical system of the human heart. The direction of the activation is indicated by the arrows and is:
SAN (= sinoatrial node), AM (= atrial myocardium), AVN (= atrioventricular node),
PF (= Purkinje fibers), VM (= ventricular myocardium).
As mentioned in the paragraph above, there is a moment of rest in the contraction of the muscle cells as the heart prepares for its next beat. This moment of rest is actually critical as we will discuss in the next newsletter as a spurious impulse during this rest period can cause premature contractions leading to compromised filling and poor ejection of blood from the heart. This can lead to life threatening arrhythmias that so severally compromise the heart's ability to pump that death can occur quickly.
As an interesting side note, when doctors or EMTs use a defibrillator to get a "fluttering" heart going again, the primary effect is to depolarize the heart muscle and actually stop the heart. The electric shock from the defibrillator doesn't switch the heart back on. Instead, defibrillation actually stops the heart briefly! It's this stoppage of the heart that allows the sinoatrial node to reestablish control of the heartbeat.
And that's probably a good place to stop for the moment, as we are edging into physiology. In the next issue of the newsletter, we will actually explore the physiology of the heart in some detail, specifically talking about:
- What can go wrong with it.
- What things must be handled by a medical doctor.
- The side effects associated with many medical options. (In most cases, it's not a free ride.)
- What things can be handled by diet, lifestyle, and supplement choices. (Surprisingly, much more than you might think.)
In the last newsletter, we worked through the anatomy of the heart -- primarily to lay the groundwork for this issue. By using what we learned in the last issue, we can now explore:
- Things that can go wrong with the heart.
- Medical treatments.
- Limitations that may be inherent in some of those treatments.
- What you can do to change the equation.
As you may remember, the epicardium is the lining that surrounds the heart muscle -- inside and out. On the inside, It's called the endocardium, and on the outside It's called the pericardium. Let's start our discussion of heart problems by looking at the epicardium -- not because It's the most important part of the heart, but because It's a simple place to start and lets us dip our toes into the subject before plunging into deeper waters.
Problems that can occur with the heart lining pretty much fall into two categories
- Physical damage.
- Inflammation caused by infection.
Physical damage is easy to understand, and usually easy to repair. you're driving in your car, you get into an accident. you're slammed against the steering wheel or an airbag. Your body stops suddenly but your heart, powered by inertia (an object in motion tends to stay in motion) keeps moving forward and tears the pericardium that holds it in place before bouncing back and coming to rest. This causes bleeding in the pericardial sac, which serves as the buffer between the heart and the chest wall and lungs. The extra fluid (blood) pumps into the sac under pressure which expands the sac, thereby squeezing and constricting the heart. If the pressure isn't relieved, it can build to the point where it constricts the heart so much that it prevents it from beating. Herbs and neutraceuticals are not much use here. Fortunately, medical intervention tends to be easy and effective in these situations. A catheter inserted into the sac to drain the excess blood and relieve the pressure will usually do the trick -- along with stopping the bleeding.
Inflammation (known as "itis" in medical terminology) is a little more complex. The primary cause of inflammation of the heart lining is infection, both viral and bacterial. Depending on which part of the lining is affected, it will be called pericarditis, endocarditis, or epicarditis. The inflammation can cause chest pain, difficulty pumping, or fever. These symptoms can be mild, acute, or even chronic. Standard treatment includes the use of antibiotics and antivirals. These are "usually" effective unless the underlying infection is resistant to the arsenal of drugs at your doctor's disposal, which is a growing problem. Fortunately, there are natural alternatives including garlic, olive leaf extract, oil of oregano, grapefruit seed extract, etc. that can work even in the case of drug resistant infections.
Also, as we discussed last issue, your heart valves are constructed like parachutes with tendons or cords anchoring them to the heart muscle to keep them from opening too far. Their role is to allow blood to flow down from the atria into the ventricles, and then to seal shut when the ventricles pump so that blood doesn't back up into the atria, but is instead forced out into the main pulmonary artery from the right ventricle or into the aorta from the left ventricle. Problems with the valves are easy to understand and fall generally into two categories.
- Backflow, or regurgitation, is caused by misshapen or damaged valves or ruptures to the tendons that hold the valves in place. These things cause the valves to imperfectly seal with each heartbeat, thus allowing backflow into the atria.
- Stenosis, or hardening of the valves, caused by disease or aging prevents the valves from fully opening. This limits the flow of blood into the ventricles so that they cannot fill completely in the fraction of a second the valves are open. Since the ventricle chamber is now partially empty when it pumps, it generates less pressure with each beat, which ultimately reduces the amount of blood that flows through the body.
- Either you were born with a problem. This can be genetic or it can be the result of nutritional problems in your parents' diet (either before you were conceived or while you were gestating).
- Over time, as a result of aging and poor nutrition, the valves shrink and change shape.
- Infection has caused the valves to inflame so that they no longer seal perfectly.
- Diseases such as rheumatic fever and syphilis have scarred and hardened the valves.
- Valvular tissue can be damaged in the same way as heart muscle tissue as the result of a heart attack.
- Valve tendons may rupture, which means the valve no longer stays in place when backpressure is created by the squeezing of the ventricles.
The bottom line is that the pumping process becomes less efficient, and your heart has to pump harder and faster to compensate. Treatments can range from doing nothing, to using drugs to reduce infection and inflammation, to surgically replacing the damaged valves with artificial valves.
Doing nothing you might ask? Absolutely! In most cases, that's what doctors do. Why? The heart has tremendous reserve capacity. Last issue we mentioned that you can have 70% blockage of your coronary arteries and never experience any outward symptoms. It doesn't stop there. Your heart also has a tremendous reserve pumping capacity and when called upon can increase output 5-8 times if needed. For example, in mitral valve prolapse (a condition in which the mitral valve "falls down", or prolapses too far into the left ventricle allowing for backflow into the right atrium), there are usually few symptoms or any problems. In most cases doctors will just make note of it and watch for any changes.
On the other hand, sometimes, there are symptoms. These can include:
- That old standby, chest pain.
- Fatigue and/or dizziness.
- Shortness of breath.
- Low or high blood pressure, depending on which valve is affected.
- Palpitations caused by irregular heartbeats.
- Even migraine headaches.
In those cases the valves are often replaced with mechanical valves. At one time, you could actually hear the mechanical valves make a slight clicking sound as they opened and closed 70-80 times a minute. This drove some people crazy when they tried to sleep at night. Newer models have overcome that problem and are silent.
Now you might think since problems with valves are mechanical in nature that nutrition and supplements would not play much of a role in resolving them. If so, you would be wrong. Most medical doctors are not aware of this fact, but there are numerous studies showing nutrients matter -- and supplementation can actually change the mechanical aspects of valve function. For example, it has been shown that magnesium plays a role in mitral valve prolapse.
- Therapeutic effect of a magnesium salt in patients suffering from mitral valvular prolapse and latent tetany.
- Magnesium Deficiency in the Pathogenesis of Mitral Valve Prolapse.
This is just the tip of the iceberg. In fact, nutrition and supplementation can play a primary role in maintaining optimum heart health -- and even reversing many chronic heart problems. We will talk more about this later; but for now let's explore problems that happen within the coronary arteries.
The first blood vessels off the aorta are the two coronary arteries, which subsequently split off into numerous branches that feed the heart. Blockage of these arteries through the build up of arterial plaque is one of the most common causes of death. The net result is ischemia, which means a "reduced blood supply." As I mentioned last issue, because there is so much redundancy in the branching of the coronary arteries, you can have up to 70% blockage and yet have no obvious symptoms. At some point, though, you will have a heart attack, also known as myocardial infarction. The myocardium is the name of the heart muscle, and infarction means the "death of tissue." In other words, a heart attack is the result of loss of blood flow to the heart muscle, which causes death of heart muscle tissue. The severity of the attack is determined by:
- Which part of the muscle is damaged. (Some parts are more critical than others.)
- How extensive the damage is.
In some cases, people do indeed die from their first heart attack. In most cases, though, the attacks are progressive -- with each attack killing more and more tissue until the remaining heart muscle can no longer carry the load. Depending on the extent of the damage, standard medical treatments include:
- Drugs, such as:
- Beta-blockers to slow heart rates and decrease blood pressure -- thus lowering the heart's demand for oxygen.
- Nitroglycerin to open coronary arteries and reduce the heart's demand for oxygen.
- Calcium channel blockers to open coronary arteries to increase blood flow to the heart muscle.
- Angiotensin-converting enzyme to allow blood to flow from the heart more easily, decreasing the workload on the heart.
- Angioplasty uses a balloon inflated inside the blocked artery to press the plaque against the arterial wall, thus clearing the blockage -- at least temporarily.
- Stents are like angioplasty on steroids. Instead of just pressing the plaque against the wall of the artery, the balloon is also used to also press a wire mesh against the arterial wall to hold the artery open.
- Bypass surgery involves using a vein (usually taken from the leg) to literally create a bypass around the clogged area of the coronary artery.
- Heart transplants.
None of these options are perfect. Angioplasty and bypass surgery (even though they have been in use for years) are actually unproven (for those of you who think everything in medicine is backed by peer reviewed studies). In fact, recent studies indicate that they may actually give only slight temporary relief with no extension of life -- not to mention an increased risk of stroke. Both stents and angioplasties (and bypasses too, for that matter) quickly re-plug, a problem called restenosis, and need to be periodically redone or replaced. New forms of stents are coated with drugs to slow down restenosis but come with their own set of problems. Bypass surgery produces a dramatically increased risk of stroke, infection and profound depression. And heart transplants force you to stay on immunosuppressant drugs for the rest of your life.
Far and away the biggest problem with all of these treatments, though, is that they only treat one manifestation of the problem, not the underlying cause -- the fact that the arteries are blocking in the first place. It is here that alternative therapies excel -- both short term, and long term. For example:
- Dietary changes can have a profound impact in reversing coronary heart disease as can a number of supplements.
- Shifting the balance of Omega-6 to Omega-3 fatty acids can eliminate a major source of heart attacks.
- Hawthorne berries are tonic for the heart, working to support the relaxation and dilation of coronary arteries and increasing the flow of blood and oxygen to and from the heart. In effect, Hawthorne berries work much like prescription drugs, but without the side effects.
Another aspect of coronary heart disease is the blood clot or thrombus. (If it becomes dislodged and floats free, It's called an embolus.) In larger arteries, a clot will only impede the flow of blood. In smaller arteries, it can completely block it. Thrombi form most often in the veins of the leg, where they then float off (now called emboli) and end up lodging in and blocking the smaller arteries of the heart, lungs, and brain. There can be many triggers for the formation of clots and emboli, but one of the more interesting is deep vein thrombosis -- the formation of blood clots as the result of prolonged sitting in airplanes and cars.
Preventing blood clots reduces the risk of stroke, heart attack and pulmonary embolism. The standard treatment for those at risk of embolisms involves the use of drugs such as Heparin or warfarin (a form of rat poison), which are anticoagulants used to inhibit the formation and growth of existing blood clots.
But these drugs are dangerous and require constant watching and regulating since they can cause internal bleeding. Far safer (and better since they also dissolve arterial plaque and help promote the repair of arterial tissue) are proteolytic enzyme formulations that incorporate specialized enzymes such as nattokinase.
In the end, when you're talking about the heart, it mostly comes down to the myocardium -- the heart muscle. The danger of coronary heart disease, for example, is that it starves the myocardium of oxygen and kills it. The danger of a valve problem is that it forces the myocardium to work too hard. The danger of a bio-electrical/conductivity problem is that it throws the heart muscle out of rhythm and causes it to lose its beat, or to fibrillate. (Fibrillation occurs when a heart chamber "quivers" due to an abnormally fast rhythm and can no longer pump blood well. Fibrillation of the atrium is called atrial fibrillation; in the ventricle It's called ventricular fibrillation. Ventricular fibrillation usually leads to death.) To paraphrase the Clinton campaign in the 90's, "It's all about the myocardium."
For the most part, problems in the atria are not life threatening. Even if both atria totally lose their ability to pump or weaken and balloon out, you lose maybe 30% of your total heart function. Without pumping, gravity and suction will still bring most of the blood down into the ventricles. There are, of course, times your doctor will want to address problems, but for the most part, you can live for years with barely functioning atria.
Ah, but the ventricles are a different story. When the left ventricle goes into fibrillation, we're talking cardiac arrest. It's time to pull out the electric paddles. So what kinds of problems are we talking about?
- Myocarditis, or inflammation of the heart, is a form of cardiomyopathy (which literally translates as "heart muscle disease"). The problem here is that blood flows more slowly through an enlarged heart, which increases the likelihood of blood clots. In addition, people with cardiomyopathy are often at risk of arrhythmia and/or sudden cardiac death. When cardiomyopathy results in a significantly enlarged heart, the mitral and tricuspid valves may not be able to close properly, resulting in murmurs. There may be multiple causes of myocarditis, including viral infection. Common culprits include: influenza, herpes, Epstein-Barr, hepatitis, and salmonella.
- Ischemic cardiomyopathy is a weakness in the muscle of the heart due to inadequate oxygen delivery to the myocardium, with coronary artery disease being the most common cause. (Ischemia simply means "reduced blood flow.") Anemia, sleep apnea, and hyperthyroidism can also contribute to ischemic myocardium.
- Myocardial infarction literally means the "death of heart muscle tissue." Since heart muscle does not grow back, this has a snowball effect. If you have a heart attack that starves part of the heart muscle of oxygen so that it dies, that scar tissue does not recover. You now have a weakened heart that is more likely to suffer a subsequent attack -- leading to more heart muscle damage and increased chances for a third attack. And so on. It's not too hard to see where this leads -- to long-term loss of heart muscle activity and chronic heart failure.
- Congestive heart failure (CHF) is a condition in which your weakened heart can no longer pump out all the blood that flows into it. CHF is the most common cause of hospitalization for people over age 65. It kills more than 50,000 people a year in the US and costs the health care system more than $50 billion per year. The heart is just like other muscles. When it is weakened, it becomes enlarged and inefficient. This leads to congestion and flaccid muscle tone. In fact, it can even lead to prolapse of the heart in which the heart literally "drops" from its original position in the chest. It is not unusual to require a stethoscope placement three to five inches below the normal area when listening to a weakened heart.
Unfortunately, modern medicine comes up short when it comes to problems of the myocardium. Mostly it just deals with the aftermath.
- If the heart stops beating, use the electric paddles to get it going again
- If no paddles are near, pop a nitroglycerine tablet.
- Perform a coronary bypass to try and prevent any further damage.
- Use nitroglycerine tablets to open up the arteries in an emergency and prevent a heart attack.
When it comes to the muscle itself, nothing! But as luck would have it, here is where alternative therapies shine.
- All of the B vitamins, but especially vitamin B4 are essential for heart health.
- Congestive heart failure has been strongly tied to significantly low blood and tissue levels of CoQ10. Supplementation with CoQ10 can literally change the size and shape of the heart.
- Studies have shown that high concentrations of heavy metals such as mercury directly correlate to higher incidences of acute coronary events. Regular heavy metal detoxing directly reduces and eventually eliminates that risk.
- Studies have also shown a direct connection between periodontal disease and acute coronary events. Regular use of avocado soy unsaponifiables, proteolytic enzymes, immune boosters, and pathogen destroyers can reduce the risk.
- Incidentally, electric paddles are not the only thing that can get a heart muscle going again. In an emergency cayenne pepper can do the trick too. A teaspoon of cayenne pepper in a glass of warm water taken every fifteen minutes can raise the dead.
- And in the end, the heart is a muscle, and like all muscles responds to exercise. Cardiovascular exercise, particularly interval training, can improve the efficiency and strength of your heart.
The heart is an unusual organ. It has millions and millions of cells, and each cell has the potential for electrical activity. In the normal heart these electrical impulses occur in regular intervals. When something goes wrong with the heart's electrical system, the heart does not beat regularly. Unlike most organs in the body, all the cells in the heart are wired together so that if a single cell fires prematurely or late, the neighboring cells will be activated and a mistimed wave will travel over the heart. The irregular beating results in a rhythm disorder, or arrhythmia.
- Due to natural aging or disease, the SA node starts losing function and no longer produces the right number of signals at the proper rate.
- The AV node normally has one group of cells through which the electrical impulse can travel. However, due to aging or heart disease, it is possible for the AV node to develop two or more groups of conductive cells. Because of the extra conduction pathways, your heart can at times beat more quickly than normal.
- The bundle branch (see above) becomes "blocked" as a result of a heart attack which damages the inner heart muscle and nerves. This stops the signal from traveling from the AV node to the ventricles. Left to their own devices, the ventricles establish their own rhythm of about 20-40 beats per minute. This is much too slow for health and results in weakness, fainting, and shortness of breath.
- Valve stenosis (stiffness) causes increased pressure in the atria (since blood never fully clears) which causes ballooning of the walls of one or both of the atria (aka atrial dilation). Because the atrium is now bigger, it increases the distance signal has to travel. The increased distance means it takes longer for the signal to reach its final destination which throws off the pacing of the heartbeat.
Typical medical treatment involves drugs such as adenosine, calcium channel blockers (e.g., diltiazem, verapamil), short-acting beta-blockers (e.g., esmolol), and digitalis.
The other option, of course, is the pacemaker. The pacemaker uses electrodes attached to the heart that take over from the SA node to control the beating of the heart. The pacemaker is run by a small computer installed in the body. Modern pacemakers are externally programmable and allow for the selection of optimum pacing modes for individual patients. Some can even self-regulate and adapt to changing requirements such as stress or exertion. And some combine a pacemaker and defibrillator in a single device.
Drugs and pacemakers work reasonably well at keeping the heart going, but still address the problem after the fact. Keep in mind that in most cases the rhythm of the heart was lost through degradation based on nutrition or disease. Installing a pacemaker does not address that problem; it merely bypasses it. On the other hand, it is possible to reverse many of those conditions nutritionally and thus reverse many of the associated problems.
- Mineral deficiencies particularly in calcium, sodium, magnesium, potassium, and many of the trace minerals can have a profound effect on the electrical efficiency of the heart since they are responsible for running it. Supplementing with minerals and liquid trace minerals can make a profound difference.
- Supplementing with CoQ10 can significantly improve the energy level of each cell in the heart, thus improving its ability to respond to an electrical stimulus and pass the signal on to its neighbor in a timely manner.
- Shifting the balance of Omega-6 to Omega-3 fatty acids can eliminate a major source of potassium imbalance which can trigger heart attacks.
- What tests does your doctor run?
- What do they mean?
- What can you tell from them?
- What questions should you ask your doctor when viewing the results?
For now, though, It's worth reviewing a key concept:
Although many problems with the heart may seem to be biomechanical in nature and beyond the purview of nutrition and supplements, that's not necessarily true. As we've seen:
- Magnesium supplementation can change the shape and condition of heart valves.
- The B vitamins can help rebuild the heart.
- CoQ10 can reenergize every single cell in the heart and can literally remold the size and shape of the heart after the onset of congestive heart failure.
- The use of Omega-3 fatty acids can reverse damage caused by NEFAs.
- Proteolytic enzymes can provide nutritional support for your body as it works to clean out the coronary arteries and repair damage to epicardial tissue surrounding the heart.
- The use of heavy metal chelators such as cilantro and chlorellacan reduce the risk of an acute coronary event
- Regular supplementation of a tonic made with cayenne and Hawthorne berry can rebuild the strength of the heart.
- Proper dental care and the use of avocado soy unsaponifiables and proteolytic enzymes can reduce the incidence of periodontal disease, which reduces the chances of an acute coronary event.
- Regular use of immune enhancers and pathogen destroyers decreases the risk of most inflammatory heart disease and the incidence of viral and bacterial infections that can adversely affect the heart.
- And regular exercise can strengthen the heart and improve its efficiency even in your eighth and ninth decade of life.
As usual, It's not just about pharmaceutical drugs and surgical procedures. Following the principles of the Baseline of Health Program can change your heart and your prospects for long term survival.
In this issue, we're going to conclude our series by examining how your doctor unravels the secrets of your heart when you visit his/her office. My goal is not to turn you into doctors, but to take some of the mystery out of diagnosis so that you know what your doctor is looking at, listening to, and analyzing when he/she is looking at your heart -- to arm you with some basic diagnostic knowledge so you are not totally at the mercy of the medical mystique when the results of your next physical are pronounced.
Before we launch into our subject, though, we have to define two terms that will be referenced throughout: systole and diastole:
- Systole refers to the contraction of the chambers of your heart.
- Diastole refers to the relaxation of those chambers.
In fact, you can have systole and diastole in all four heart chambers, but in most cases, doctors focus on the left ventricle -- the chamber that pumps blood throughout your entire body -- when using the terms. Also, there are two kinds of systole and diastole: electrical and mechanical. Electrical systole is the electrical activity that precedes actual contraction. It's what stimulates the heart muscle of the different chambers to actually contract. The delay between electrical stimulation and actual contraction is about a tenth of a second.
The same is true of diastole, the relaxation of the heart mucles. Electrical diastole is the recovery and repolarization of the heart in preparation for the next beat. Mechanical diastole is the actual relaxation of the muscle that follows electrical diastole. This distinction becomes important when you look at your ECG.
Incidentally, the increased pressure produced in your circulatory system by the mechanical systole (contraction) of the left ventricle is referred to as systolic pressure. The reduced pressure during relaxation is called diastolic pressure. These are the two numbers your doctor gives you when reading your blood pressure (e.g., 120 over 70). We'll explore that in detail in the next series of newsletters when we explore the circulatory system.
The most basic tool your doctor has for evaluating the health of your heart is the stethoscope. It is so fundamental to medicine that it has been around in various forms for almost 200 years and is probably the most recognizable symbol of doctors in the world today. Before the stethoscope, physicians would just listen to the heart by pressing their ears against the patient's chest -- not very efficient, and often very unclean.
And what do doctors hear through a stethoscope?
Surprise! It's actually not the beating of your heart. The heartbeat itself is virtually soundless. That thumpthump your doctor listens to is the sound of blood dashing against the inner walls of the heart chambers. This is a very useful distinction. Hearing the movement of blood reveals far more than would be the case if all we heard was a mechanical contraction.
More precisely, the thumpthump of your heartbeat is the sound of the turbulence of blood against the walls of the heart and the valves during systole (contraction). In fact, thumpthump is not an entirely accurate description of the sound. As it turns out, each thump is, in reality, comprised of separate sounds in both the atria and the ventricles. But because the sound in the ventricles is so loud, it drowns out the other soundsunless there is a problem.
For example, if there's stenosis (hardening) of the mitral valve, part of the heartbeat is slowed down because it takes longer for the stiff valve to close so that the multiple sounds start to separate. Instead of the normal thumpthump, you hear something that sounds more like thumppa pa. On the other hand, if you have an incomplete closer of a valve, as in aortic regurgitation, you lose the clean thump and get sort of a chortling "woosh" sound as in whoosh...thump. (If you're interested, here's a link to more heart sounds.)
Invariably, then, listening to your heart through a stethoscope is one of the fundamental parts of any checkup. It provides the first clues as to the health of your heart.
Note: for those of you interested in coaching your doctor through anything they may have forgotten in medical school, here's a more detailed tutorial.
When most people think of heart tests, they think of the ECG. ECG stands for electrocardiogram. It's also called an EKG, from the German elektrokardiogram. Although it may look like an ECG is recording heartbeats, It's not. In fact, it records the electrical activity (the electrical triggers, if you will) that presage the actual heartbeat. The mechanical beats follow the electrical triggers by about a tenth of a second -- unless, of course, there's a problem. Or to state it in "medicalese," electrical systole and diastole precede mechanical systole and diastole (contraction and relaxation) of the heart by about a tenth of a second.
The ECG is an important tool for your doctor, but is hardly complete and comes with several limitations.
- It's a static test, which means it doesn't necessarily identify problems that appear only when the patient's heart is under stress. An example would be a patient complaining of intermittent chest pain. This might actually be an indicator of a severe underlying problem, and yet a standard ECG could easily read as perfectly normal.
- ECG readings indicate only general problems. In most cases, abnormalities in the reading are non-specific as to cause, and in fact, many times, may mean nothing at all.
- Bottom line:
- A normal ECG reading doesn't necessarily mean that there is no problem.
- An abnormal reading doesn't necessarily mean that there is.
- It's merely a piece of the puzzle that can help point the doctor in a direction.
That said, an ECG provides four primary pieces of information for your doctor.
- First, an ECG can show how fast your heart is beating -- or more accurately, how fast the electrical activity is moving through your heart. By measuring the intervals between beats, your doctor can determine if the electrical signal is moving through your heart too slow or too fast.
- It also shows the strength and timing of the beat. By measuring the amount of electrical activity passing through your heart muscle, your doctor can get an indication as to which parts of your heart are too large or are overworked or if It's not pumping forcefully enough.
- It can provide evidence of damage to various parts of the heart muscle caused by:
- Previous heart attacks.
- Congenital heart abnormalities.
- Diseases such as thyroid problems, rheumatic fever, diabetes, and high blood pressure.
- Inflammation to either the heart muscle or its lining (inside and out).
- Very low or very high levels of electrolytes including calcium, magnesium, and potassium.
- And it can indicate problems with impaired blood flow in the coronary arteries supplying oxygen to your heart muscle.
Your doctor performs an ECG by hooking you up to a series of electrodes scattered over your chest, arms, and legs. (Accurate placement is important.) Each electrode reads the same signal, but because of its unique vantage point, provides a different view of that signal. Think of it like watching a speeding train from the front coming at you, from behind racing away, and from the side whizzing by. It's the same train, at the same point in time, but each vantage point provides very different information about the train.
Here's a snippet of an EKG showing several electrodes tracking a heart. Notice how the electrodes start providing noticeably different information concerning the same beat about 2/3 of the way through.
All well and good you might say, but what does it mean? How do I read it? Does it mean I'm healthy or unhealthy? Can I run a marathon, or do I need bypass surgery? All good questions.
In order to understand better what your doctor sees when he looks at an ECG printout, let's focus on a single beat from a single electrode.
Alright, I agree. that's certainly pretty meaningless at first glance. However, with a little decoding, it starts to make much more sense. In fact, the heartbeat as represented in an ECG breaks down into four primary pieces: the PR interval, the Q wave, the QRS complex, and the T wave. Let's explore them for a bit. (Refer back to the graphic as needed.)
- The PR interval on the left side of the graph shows the electrical impulse for the contraction of the atria, immediately followed by its depolarization (or clearing of the electrical charge to that part of the heart muscle) so it can relax and gear up for the next contraction. As mentioned earlier, the actual contraction of the muscle follows the signal by about 1/10 of a second -- in this case during the PR segment. (See graphic.)
- The Q wave (labeled Q above) is the initial downward (negative) deflection related to the initial phase of depolarization of the ventricular heart muscle. Again, depolarization is preparation for receiving an electrical stimulus.
- The QRS complex in the center of the graphic shows the electrical stimulation of the ventricles, immediately followed by their depolarization. Not surprisingly (considering how much more powerful ventricular contraction is), the amplitude of the electrical signal for the ventricles is much larger than that of the atria.
- The T wave on the right side shows the repolarization of the ventricles in preparation
for the next beat. Note: The ST segment represents the period from the end of ventricular depolarization
to the beginning of ventricular repolarization. In English, the T wave represents the recovery period of the
ventricle in preparation for the next beat.
- Now, if you've really been paying attention, you might be asking yourself an obvious question, "Where's the corresponding T wave for the atria following their PR interval. don't the atria have to repolarize just like the ventricles?" And the answer is, "Yes, they do." Good call there! The problem is that the repolarization of the atria happens during the QRS complex, and because the ventricular signal is so much stronger than the atrial signal, you can't see the atrial repolarization -- kind of like a flashlight turned on during the midday sun. Give yourself a pat on the back for catching its existence though.
- And lastly, we have the QT interval. The QT interval is not a separate section, but is a combination of the QRS complex and its following T wave. It represents the time between the start of ventricular depolarization and the end of ventricular repolarization. It is useful as a measure of the duration of repolarization.
So what's your doctor looking for when she examines your ECG? To put it simply, she's looking for normal intervals and normal amplitudes in all key segments of the wave. For example:
- The PR interval is indicative of the movement of the cardiac impulse from the atria to the ventricles via the atrioventricular node (see The Anatomy of the Heart), which is normally between 0.12 - 0.20 sec (3 - 5 small boxes wide). If the PR interval is greater than 0.20 sec, that's an indicator that an AV block is present (see Heart Problems).
- The QT interval will vary depending on the heart rate, age, and gender of the patient. It increases with bradycardia (slow heartbeat) and decreases with tachycardia (rapid heartbeat). Men have shorter QT intervals (0.39 sec) than women (0.41 sec). The QT interval is also influenced by the electrolyte balance, drugs, and ischemia. Your doctor will be looking for any interval outside the norm.
- A QRS interval of 0.04 to 0.10 seconds -- no larger than half a large box -- and of normal amplitude.
- Differences in the sizes of the Q waves read from different electrodes at the same point in time are indicative of previous heart attacks -- the differences are usually caused by areas of dead muscle tissue. A trained cardiologist can accurately pinpoint the area of damage according to which leads are producing which signals.
- Inverted T waves may indicate ischemia, or low blood flow to the heart.
- Deviations in the ST segment can show ischemia and infarction (i.e., lack of blood flow to the heart muscle and dead muscle tissue). In general, a depression in the ST segment indicates ischemia while an elevation indicates infarction.
If you got lost in the last few bullet points, don't worry about it. The important point is to understand the "kinds" of anomalies your doctor is looking for -- not necessarily to identify them yourself. However, for those of you interested in keeping up with your doctor, here's a more detailed tutorial.
And for those of you who just want to walk away with something to hold onto, you can use your ECG to easily calculate your heart rate by counting the number of large squares between R waves (the high point in each beat).
- 1 square = 300 bpm
- 2 squares = 150 bpm
- 3 squares = 100 bpm
- 4 squares = 75 bpm
- 5 squares = 60 bpm
- 6 squares = 50 bpm
The easiest way to do this is find an R wave that coincides with the beginning of a large box and then simply count over to the next R wave. In our ECG snippet (two graphics above), we can find such a point in the middle of the graph. A quick count to the right shows 5 large boxes, or approximately 60 beats per minute. Is that cool or what? You can now read a good chunk of an ECG -- and without going to medical school.
Listening to your heart and monitoring its electrical activity, may not be enough. Your doctor may also want to see the heart, and there are several ways to do that.
The most basic heart picture is the chest X-ray. Skilled doctors can actually interpret a great deal from an X-ray, but that's also the problem with the technology -- it requires a great deal of interpretation. That means its accuracy, at times, can be less than desirable.
You can think of the arteriogram (AKA angiogram, angiograph, etc.) as an X-ray on steroids. It's a procedure that uses a special dye (contrast material) and X-rays to see how blood flows through your heart.
An area of your body, usually the arm or groin, is cleaned and numbed with a local anesthetic. An IV (intravenous) line is inserted into the area. A thin hollow tube called a catheter is placed through the IV and carefully moved up into one of the heart's arteries. (X-ray images help the doctor see where the catheter should be placed.)
Once the catheter is in place, the dye (contrast material) is injected into the IV. X-ray images are taken to see how the dye moves through the artery. The dye helps highlight any blockages (dark areas) in blood flow.
Here's a short instructional film on how the procedure works.
Sometimes heart problems do not show up during normal activity; they only manifest under stress (i.e., an increased load on the heart). In those cases, an arteriogram won't reveal the problem. The thallium stress test, then, is used by your doctor to determine whether exercise causes a decreased blood flow to the heart muscle. This test incorporates elements from the ECG, the angiogram, and an MRI. An IV is inserted into your hand and ECG wires are hooked up to your chest. You then walk on a treadmill until you experience symptoms such as chest pain or shortness of breath, or until you are too tired to continue walking. During the whole procedure, your blood pressure and ECG are monitored continuously. Approximately one minute before you stop walking on the treadmill, the thallium is injected. Thallium is an isotope which is "taken up" by the heart and the coronary arteries. (It flows more easily through non-diseased arteries.) You then lie down on a table, and a scanner takes a picture of your heart. Areas where blood can't flow easily under stress appear dark. (See below, lower left corner.)
The thallium stress test certainly provides more information than a simple ECG. Unfortunately, stress tests do not detect atheromata present throughout the heart or other body arteries, nor do they reveal the vulnerable plaques, which are typically flat against the walls of the arteries and which are the cause of most heart attacks.
An echocardiogram uses high frequency ultrasound waves to produce a moving image of your heart. Such an image can help your doctor assess:
- The size of your heart -- both the thickness of the heart muscle and the size of the pumping chambers.
- How well your heart is pumping blood.
- Any valve problems: An echocardiogram can easily detect valve leaks and incomplete closure.
- Blood clots or tumors inside the chambers of the heart.
- Any holes in the walls of the heart.
It's the same technology used to look at babies in the womb.
The big new gun in heart diagnostics is the moving MRI. Recent advances in the technology now allow for full motion images of the heart that can be done quickly enough to even accommodate emergency room patients. This tool is proving to be one of the most accurate heart assessment tools yet.
Sometimes technology really does work.
In today#x27;#s newsletter, we're going to talk about the vascular system, your arteries and veins. Unlike our discussion of the heart, which required a great deal of anatomy, our discussion of anatomy today will be much simpler. As I've stated previously, my goal in this series is not to make you doctors, but to help you understand enough about your body's systems and how they work so that you can communicate with your doctor and actively participate in your treatment. If you have high blood pressure, blood clots, or atherosclerosis, It's imperative that you fully understand how that happened, the physiological consequences of any medical treatments, and any viable alternatives that might be available to you.
that's what we will cover today.
As we discussed previously, you have several distinct circulatory systems.
- The pulmonary system that carries deoxygenated blood away from the heart to the lungs, and then returns the refreshed oxygenated blood back to the heart.
- The systemic system that carries the oxygenated blood away from the heart out to every single cell in your body, and then returns the spent deoxygenated blood back to the heart so that it can be sent out through the pulmonary system.
- There is actually a third system, the portal system, which loops within certain organs or areas of the body that we will discuss in future newsletters.
The important thing to understand about these circulatory systems is that they are "closed looped." Unless there is injury, no blood leaves them. As you will see, even the nourishment that every single cell in your body receives from your blood happens without that blood ever leaving the closed system. This becomes key when we talk about blood pressure.
The circulatory systems are comprised of:
All told, these four components make up some 50,000 miles of passageways in the body. Let's take a look at them in more detail.
Arteries, arterioles, and capillaries make up the arterial system. Arteries and arterioles have only one function, to move blood throughout the body. that's all they do. They are channels, tubes, pipes if you will. As long as they are unclogged, flexible, and undamaged, they do their job. The primary difference between arteries and arterioles is one of size. Arterioles are just the smallest arteries you can see with the naked eye. Again, arteries and arterioles have only one function, to move blood. They do not feed any cells of the body, not even their own. that's actually a fun little bit of trivia. The arteries of your body are not fed by the blood that flows through them. They require their own network of blood vessels called the vasa vasorum (literally, vessels of a vessel) that feed them -- from the outside!
As I mentioned, I'm not going to get into naming all of the arteries in the body; but for the most part, arteries take their names from either the organs they supply (e.g.., the hepatic artery, which feeds the liver) or the areas through which they travel (e.g., the subclavian artery, which travels under the clavical, AKA, the collar bone).
Capillaries are quite different in function. They are not designed to shuttle blood. In fact, blood hardly flows through them at all as they are so small they allow only one blood cell at a time to pass through. Instead, the capillaries are the end point of the arterial system. It is in the capillaries that food and oxygen are exchanged with every cell in your body (except your cornea and the lens of your eye). Amazingly, of the 50,000 miles of circulation in the body, capillaries comprise over 49,000 miles.
Unlike the arteries, capillaries are invisible to the naked eye. They are smaller than a human hair and microscopic. And it is because they are so small and their walls are so thin, that capillaries serve as the exchange system for food and oxygen in the body. Keep in mind that every single cell in the body (except the cornea and lens) is near a capillary. That means that as blood passes through the ultra thin capillaries, it is easy for oxygen and tiny sugar and protein molecules (the end products of digestion) to "exchange" through the walls of the vessel and feed every single cell in the body.
Capillaries also serve as the connecting point between the arterial system and venous system that returns deoxygenated blood to the heart. The same exchange system that works to feed the cells of the body works in reverse. Cells pass their waste such as carbon dioxide back through the walls of the capillaries, where the blood cells recently relieved of their oxygen payload, can now pick up the CO2 waste from the cell and carry it back to the lungs for exchange with fresh oxygen.
Surprisingly, there's more "space" inside the tiny capillaries than can be filled by your entire blood supply. If all your capillaries were "open" simultaneously, your blood pressure would drop precipitously, and you would die. What happens, though, is that your body intelligently shunts blood into different capillaries as needed. When functioning properly, this is a pressure regulating mechanism. The body can open more capillaries to lower pressure, and close off sections if needed to raise pressure.
Note: Our bodies retain the ability to sprout new capillaries throughout our entire lives.
The venous system returns deoxygenated blood to the heart, and for the most part, it pretty much parallels the arterial system in all aspects, just in reverse. Whereas the arteries start out large (the aorta) and end small (the capillaries), the venous system starts small (the capillaries) and ends large (the vena cava). Veins tend to run right next to their corresponding arteries, and in fact have similar names. The subclavian vein, for example, runs in tandem with the subclavian artery under your collar bone. The primary exception is the vena cava, which is the aorta's counterpart.
In this section, we start learning how problems occur. For it is their different construction (dictated by their different functions) that defines the nature of the things that can go wrong such as hardening of the arteries, high blood pressure, and blood clots.
Arterial walls are composed of elastic tissue and smooth muscle. It is their elastic nature and the presence of substantial muscle tissue that allows them to expand and contract as the heart beats. This allows them to even out the increase in pressure caused by each beat. This is one of the primary reasons why hardening of the arteries (atherosclerosis) increases blood pressure. If you pump more fluid through the same sized tube, pressure must increase. On the other hand, if the tube is flexible and can widen, the increase is less. (We will talk more about this later.)
Veins are thinner walled than arteries and have less elastic tissue, and much, much less smooth muscle tissue. Instead, veins make use of valves and the muscle contraction of your body's major skeletal muscles to squeeze blood along. This is the reason you're asked to get up and walk around on a long plane flight, to prevent blood from pooling in your legs. As a side note, the lack of muscle in the walls of veins makes them more susceptible to bleeding when injured since there's no muscle to clamp down.
There is not much mystery as to what the problem is, the build up of arterial plaque on the walls of the arteries and arterioles. There is, however, a great deal of mystery as to what causes it.
The basic problem is that arterial plaque (a combination of protein, calcium and cholesterol) starts building up on the walls of the arteries. This causes the arteries to both harden and narrow. So far so good! But what causes that buildup?
The primary theory lays the blame on cholesterol & that as cholesterol levels climb in the blood, this causes plaque to form on the walls of the arteries. But this theory begins to collapse under even the most elementary scrutiny. As I mentioned in my newsletter, the Cholesterol Myth, one of my favorite questions to ask doctors is, "If cholesterol is the main culprit in heart disease, why don't veins ever get narrowed and blocked?" And if you wanted to, you could throw capillaries into the equation too. Capillaries do not evidence the build up of arterial plaque. (They do, however, clog with amyloid plaque in the brain. But that's a different problem that we'll cover in a later newsletter.)
Think about this for a moment. If you have cholesterol circulating equally through the entire circulatory system, but it only causes plaque to build up in the arteries and arterioles, not the capillaries or veins, then how can cholesterol be the primary cause of the problem? If cholesterol caused plaque to form, wouldn't it form everywhere? Since it only forms in the arteries, doesn't the problem have to be something unique to those arteries?
A more sophisticated version of the theory says that the build up of plaque is triggered by damage to the arterial wall and the endothelial lining. The lining consists of a thin layer of endothelial cells that performs two critical functions:
- It protects the "innards" of the artery from toxic substances in the blood.
- It helps regulate the expansion and contraction of the arteries by releasing a bio-chemical (cyclic GMP) into the cells of the smooth muscle in the arterial wall that change the tone or firmness of the artery.
In an attempt to repair damage to the endothelium, your body will "patch" the damage with plaque. This produces one of two conditions or two sides of the same coin really.
Damage to the endothelial lining is #x22;managed#x22; by the smooth muscle cells surrounding the lining. Smooth muscle cells respond to endothelial injury by rapidly multiplying and producing a fibrin/calcium/cholesterol patch. These patches, called plaques occur just inside the lining and thicken the artery's inner wall. Over time, given multiple injuries, the wall of the artery begins to harden and become dysfunctional, no longer expanding and contracting to regulate blood pressure and steadily narrowing the passageway through which blood flows.
Another way of describing this process is that your body creates plaque to #x22;paste over#x22; any damaged areas, like a scab over a cut. Over time, given repeated injury, these plaques intrude more and more on the inner passage of the artery steadily compromising the ability of the artery to expand and contract and for blood to flow freely.
The damage to the arterial wall also triggers an immune response with white blood cells flooding the area. This leads to a chronic inflammatory response in the blood vessel. Continued inflammation causes even more damage, which accelerates the process.
All of this, of course, brings up the $64,000 question: "Since the entire theory hinges on damage to the endothelial lining, what actually causes the damage to the lining, and why doesn't it happen to the lining of the veins?"
Once again, oxidized fats and LDL cholesterol are named as the key culprits. Other suspected culprits include:
- Free radicals.
- High blood pressure (yes, high blood pressure begets more high blood pressure)
- High homocysteine levels.
- High C-Reactive Protein levels.
- Low levels of vitamin C (similar to scurvy).
- Low levels of nitric oxide.
- Heavy metals.
But once again, the question arises: "Are not all of these things present in the capillaries and veins too?#x22; The answer, of course, is yes they are. Which means there's still a missing piece in the equation. The answer, according to the pH theory, lies not in what flows through the arteries and veins (which is identical), but in their construction (which is different). The key difference between arteries and veins is in the amount of muscle tissue surrounding the endothelial lining. In arteries and arterioles, the smooth muscle is extensive. In veins, it is minimal. And in capillaries, it is totally absent. Why does this matter?
It matters because when muscle tissue is used it produces lactic acid. If your body is healthy (in an alkaline state) and has ready access to an abundant source of oxygen rich blood, that lactic acid can clear quickly. But for those people who eat a high acid forming diet and are in an acidic state, the lactic acid cannot clear quickly. (Remember, blood vessels do not have direct access to the oxygen in the blood that flows through them. They are dependent on the vasa vasorum.) It is the lactic acid that provides the final trigger that causes damage to occur in arterial linings, but not so in veins. It is the presence of accumulated lactic acid in the smooth muscles surrounding arteries that ultimately causes plaques to form.
But even beyond lactic acid, there's another area where muscle tissue matters: nitric oxide. The contraction of the muscles in the arterial walls is regulated by a signaling molecule that we referred to earlier called cyclic guanosine monophosphate (cyclic GMP) in the muscle cells. Cyclic GMP causes the arterial muscle to relax, in preparation for its next contraction. Cyclic GMP is triggered by nitric oxide, which is produced in the endothelial lining. The ability of the lining to manufacture enough nitric oxide to maintain artery dilation is one of its most crucial functions. As damage continues to build in the lining, it blocks nitric oxide-induced dilation, thus stiffening the arteries.
If the arterial blockages happen in your coronary arteries, the result, as we've discussed previously, is coronary heart disease and a heart attack. If it happens in the carotid arteries leading to the brain, it can cause a stroke.
In most cases, however, the damage happens systemically, throughout your arterial system, and the result is high blood pressure. As a quick review, blood pressure is a measurement of the two pressures in your circulatory system as your heart beats. The increased pressure produced in your circulatory system by the contraction of the left ventricle is referred to as systolic pressure. The reduced pressure during relaxation is called diastolic pressure. These are the two numbers your doctor gives you when reading your blood pressure (e.g., 120 over 70). Both low and high blood pressure are dangerous, but low blood pressure is usually easier to manage. High blood pressure, on the other hand, tends to be more intractable and harder to manage, and therefore more dangerous.
Your body has many mechanisms for controlling blood pressure.
- It can change the amount of blood the heart pumps.
- It can change the diameter of arteries, and the volume of blood in the bloodstream.
- To increase blood pressure, it can pump more blood by pumping more forcefully or more rapidly.
- It can also increase pressure by narrowing arteries (particularly the arterioles), forcing the blood from each heartbeat through a narrower space than normal.
- It can seal off capillaries forcing the blood into a smaller space, thereby increasing pressure.
- The body can add fluid to the bloodstream (regulated by the kidneys) to increase blood volume and thus increase blood pressure.
- And it can remove fluid from the blood (also regulated by the kidneys), thereby decreasing pressure.
All of these things happen automatically, regulated by a healthy body, without your even thinking about it. In addition, blood-pressure measurements can vary throughout the day, affected by everything from:
- And the time of day.
- Blood pressure changes that occur naturally during the day are the result of the body's internal (circadian) rhythms. In most people, blood pressure rises rapidly in the early morning hours, in anticipation of rising and beginning the day. This is not the result of the physical act of rising but is a preset system that automatically increases a person's blood pressure at that time. Likewise, pressure normally starts dropping early in the evening in anticipation of going to sleep.
All of these things mentioned so far, have nothing to do with clinical hypertension unless they result in secondary damage such as can be caused by smoking and alcohol or sustained stress. Clinical hypertension is a chronic and dangerous condition caused by:
- Constricted arteries.
- Hardened arteries.
- Malfunctioning kidneys (which we'll talk about in a subsequent newsletter).
If left untreated, chronic hypertension can cause:
- Damage to the heart muscle because of the extra load it puts on the heart.
- Kidney damage, which leads to more hypertension, which leads to more kidney damage, etc.
And ultimately, it kills you.
As we've already discussed, veins do not have a substantial amount of muscle tissue to contract and squeeze blood along. That means that without physical activity to cause the skeletal muscles to squeeze the veins:
- Blood has a tendency to pool and stop flowing in veins, particularly in the legs where gravity works against you.
- Blood that isn't flowing tends to clot.
- Clots tend to propagate more clotting around the original clot.
- Cumulatively, this can form very large clots.
Large clots that stay in place and block the flow of blood cause phlebitis.
If the clot breaks free and starts traveling through the circulatory system, It's called a thrombus. At whatever point it lodges in a blood vessel and blocks it, It's called an embolism. If you think back to our discussion of the venous system, you'll remember that veins get steadily bigger as blood moves back to the heart. That means that clots that break free in the legs are unlikely to be stopped anywhere on their way back to the heart. The first place they are likely to lodge is when the right ventricle of the heart pumps them out into the pulmonary circulatory system on the way to the lungs. If the clot is fairly small, it will lodge in the lung itself and block the flow of blood to a section of the lung, killing it. This is called a pulmonary embolism. Larger clots can actually lodge in the pulmonary artery feeding an entire lungkilling the lung just like that. Or the clot can lodge at the juncture where the pulmonary artery divides between the two lungs, which will kill both lungs simultaneouslyin an instant.
DVT, or deep vein thrombosis, is the term now commonly associated with clots that form as the result of prolonged sitting on an airplane. They tend to break free the next time you start moving again with any vigor. This can be several days or weeks after the plane flight itself, which means many people never connect the two events.
There is one other notable place that clots tend to form. As a result of low blood flow or damaged valves, clots can form in the left atrium of the heart. If the clot forms there, It's already past the pulmonary circulatory system so it can't affect the lungs. Unfortunately, the next stop for the clot is out into the systemic circulatory system, where it has a good chance of being pushed up into the brain causing a stroke.
Medical treatments for vascular problems never address the actual causes, but seek instead to force test results back into line. What is your doctor likely to offer?
Modern medicine really only has two approaches.
- Surgically repair the damaged area (bypasses and angioplasties).
- Use drugs to improve the flow of blood through the damaged area and minimize the production of cholesterol, which serves as one of the triggers.
Neither of these approaches, of course, actually deals with the real problem.
When it comes to high blood pressure, doctors rely almost exclusively on pharmaceutical drugs. The four major classes of drugs are:
- Diuretics, which reduce pressure by making you pee out water from your body. Reduce the volume of fluid in your blood, and you reduce the pressure. Unfortunately, side effects can include dizziness, weakness, an increased risk of strokes, and impotence. (Not to worry, there are medications to alleviate the side effects.)
- Calcium Channel Blockers, which work to relax and widen the arteries and thus reducing blood pressure. Then again, a major side effect of channel blockers is a 60% increased risk of heart attack.
- Beta Blockers, which work by weakening the heart so it won't pump as strongly, thereby reducing blood pressure. One of the major problems with beta blockers, though, is the increased risk of congestive heart failure.
- ACE Inhibitors (the new drugs of choice), which like the calcium channel blockers, also work to relax and widen the arteries. Unfortunately, ACE inhibitors can produce severe allergic reactions, can be deadly to fetuses and children who are breastfeeding, and can cause severe kidney damage.
Again, none of these drugs deals with the actual cause of the high blood pressure. They are merely an attempt to force test numbers into line and prevent people from immediately dying.
If doctors are worried about clots (such as after bypass surgery), they put patients on blood thinners. The standard is Coumadin (warfarin). Aside from the usual jokes that Coumadin is essentially rat poison (which it is), it has serious side effects. It can cause severe internal bleeding that can be life-threatening and even cause death. You can always tell a person on warfarin by the extensive bruising all over their body since even the slightest bump or touch is enough to cause internal bleeding. It's a bit like using dynamite to open a locked door. It can do the job, but you need to be oh so careful or you'll blow up the building at the same time. There are better choices.
Note: Some people might think aspirin is a good alternative. It's not. While aspirin may be beneficial at keeping blood flowing through arteries, studies indicate it has no effect on preventing clots from forming in veins.
As it turns out, for most major heart problems, you have a world of alternatives that iscertainly safer and often far more effective than their medical counterparts.
- Studies have shown that dietary changes alone can unplug arteries.
- Proteolytic enzymes, particularly formulas that contain either nattokinase or lumbrokinase, can break down the proteins that hold plaque together stuck to arterial walls, effectively dissolving it.
- Proteolytic enzymes can also help dissolve scarring of the endothelial lining.
- And proteolytic formulas that contain seaprose-s, serrapeptase, and/or endonase can help reduce arterial inflammation that both constricts arteries in real time and contributes to future long term damage.
- Sufficient Omega-3 fatty acids in the diet also help reduce arterial inflammation and dramatically reduce the circulating levels of damaging NEFAs.
- Antioxidants such as SOD, pomegranate, grape seed extract (AKA OPCs), and pycnogenol help heal the endothelial lining, thereby preventing future plaque and helping to heal current plaque.
- Methylating supplements such as B6, folic acid, B12, TMG, and SAMe help reduce homocysteine levels, thereby reducing damage to the endothelial lining.
- L-arginine and noni extract assist the smooth muscle in arterial walls in obtaining sufficient nitric oxide to function properly.
- Regular heavy metal detoxing can reduce a major cause of irritation to the endothelial lining and a primary instigator of plaque formation.
- And raising body pH through proper diet and the use of supplements such as coral calcium reduces lactic acid levels in the arterial smooth muscle, thereby minimizing damage to arterial linings.
As you can see, there is a world of choices you can make that can dramatically change your vascular outcomes. Virtually all of them are covered if you're following the Baseline of Health Program.
Pretty much everything you do to reduce clogging of the arteries will, by definition, help to reduce blood pressure. In addition, though, you can also consider:
- Lose weight. Simple laws of physics apply here. As we've already discussed, your blood vessels have to service every single cell in your body. The more body mass you have, the more pressure you need to force blood through the system. Lose weight; less pressure required.
- If you smoke, stop. Smoking constricts blood vessels and raises pressure.
- If you're stressed, try meditation or biofeedback. As part of your body's "flight and fight" mechanisms, stress increases heart rate and blood pressure to help respond to the short term stress of an attack from a saber toothed tiger. Twenty-four/seven stress was not designed into the system. Prolonged stress definitely impacts blood pressure levels. Even if you have clogged arteries, reducing stress levels can still help drop your blood pressure levels significantly.
- Herbs such as passionflower, apocynum venetum, hawthorne, and stevia (yes stevia) have all been shown in clinical studies to help lower blood pressure.
Proteolytic enzymes, particularly formulas that contain either nattokinase or lumbrokinase are just as effective at preventing clots, with wide ranging dosage tolerances. In other words, good proteolytic formulas work with minimal chance of side effects. In fact, a good systemic proteolytic enzyme formula that also contains enzymes such as endonase, seaprose-s, or serrapeptase can have multiple beneficial effects for the circulatory system in addition to reducing clotting. Such formulas can play a major role in reducing inflammation and scarring in the cardiovascular system and enhance cardio perfomance in athletes.
When it comes to most forms of heart disease associated with the arteries and veins, you have a world of alternatives, certainly safer and often far more effective than their medical counterparts. It's also worth noting again that if you are following the Baseline of Health Program, then you're already doing most of them.