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Preventing Degenerative Disease
- Heart Disease/Stroke
- Diseases of the Heart Muscle
Dr. Strands Supplement Recomendations for those with this medical issue:
I add approximately 100 mg each of grape-seed extract and CoQ10
along with some additional magnesium, about 200 to 300 mg per day. l feel it is critical for these patients to be taking a basic product that contains a mixture of vitamin E as mentioned in Table 1
.Pharmaceutical Grade Supplements
If one's homocysteine level does not drop below 7 with just the B vitamins listed in Table 1
, I will add 1-5 9 of TMG (trimethylglycine) to the patient's regimen.
Heart Disease: An Inflammatory Disease
- Dr. Ray Strand
DAILY YOU AND I HEAR REMINDERS ABOUT THE SERIOUSNESS OF America's cholesterol problem. And as I mentioned in Chapter 2, heart disease is the number-one cause of death in the United States. Like me, you probably assume what such statistics and much of the media suggest: cholesterol is the cause of heart disease.
If so, you may be as stunned as I was to learn that cholesterol is not the culprit behind heart disease; the inflammation of blood vessels is. My research revealed that more than half of heart-attack patients in the United States have normal cholesterol levels!4 And can you guess what I discovered significantly reduces, or eliminates entirely, inflammation of the blood vessels? That's right: nutritional supplements.
This finding is revolutionary to the treatment and prevention of heart attacks. Rather than concentrating only on lowering cholesterol, you need to understand the necessary steps to decreasing the cause of the inflammation in your arteries. This approach could have significant and dramatic implications in the prevention and reversal of heart disease.
Did you know that elevated cholesterol in the blood was not always considered a risk factor for coronary artery disease and stroke? When I first began practicing medicine in 1972, we considered any cholesterol level less than 320 normal. I distinctly remember telling patients who had a cholesterol level of 280 or 310 not to worry because their cholesterol levels were normal.
It really wasn't until the late seventies that we began to realize the higher the cholesterol levels, the greater the risk of developing a heart attack or stroke. This was based in large part on the Framingham studies, which followed a large population of patients who lived in Framingham, Massachusetts. Scientists noted in these studies that as the cholesterol levels increased, so did the frequency of heart attacks. Following this research, cholesterol levels greater than 200 were considered abnormal and a cholesterol level greater than 240 placed the patient at high risk of developing a heart attack.2
In the early 1980s physicians began to learn that not all cholesterol was bad. We learned that HDL (high density lipoproteins) cholesterol is actually good, and the higher our HDL cholesterol is, the better. It is the LDL (low density lipoproteins) cholesterol that is bad. LDL cholesterol accumulates along the artery walls, forming plaque and narrowing the arteries. The HDL cholesterol actually comes along and cleans up the artery.
After this discovery we started checking not only total cholesterol levels but also determining the amounts of both good and bad cholesterol present. We calculate a ratio by dividing the total cholesterol by the HDL cholesterol. The lower this ratio is, the better off the patient is when it comes to heart disease. It is now common practice to routinely check both HDL and LDL cholesterol levels. Needless to say, we are all acutely aware of the importance of cholesterol and the detrimental effects of LDL cholesterol.
What I have shared with you so far is pretty common knowledge. Are you ready for the uncommon knowledge?
The Nature of the Inflammatory Response
LDL cholesterol is really not "bad." God didn't make a mistake when He created it. Native LDL cholesterol, the kind that the body originally makes, is good. In fact it is essential for building good cell membranes, other cell parts, and many different hormones that our bodies need. We could not live without it. In fact if we don't get enough from our diet, our bodies will actually make this form of cholesterol.
Problems begin to occur only when free radicals change or oxidize native LDL cholesterol. It is this modified LDL cholesterol that is truly "bad." In a 1989 issue of the New England Journal of Medicine, Dr. Daniel Steinberg postulated that if patients had adequate antioxidants on board to quell oxidization, the LDL cholesterol would not become bad.3
In the years since Dr. Steinberg's theory was released, hundreds of studies have been conducted in an attempt to either prove or disprove his theory.
You can appreciate why scientists and researchers met Dr. Steinberg's new theory with such enthusiasm. After all, of the approximately 1.5 million heart attacks in the United States this year alone, almost half of these patients will be under the age of sixty-five.4 We have all known friends or loved ones who seemed to be in excellent health only to find out that they have died suddenly of a heart attack. If Steinberg's theory turned out to be true, doors would open wide to a vast array of new preventive and treatment protocols.
In 1997 researcher Dr. Marco Diaz made an impressive review of all of the studies that had appeared in mainline medical journals since Dr. Steinberg had first presented his theory. Diaz concluded that patients with the highest levels of antioxidants in their bodies indeed had the least amount of coronary artery disease.5
Animal studies done during this time also supported Dr. Steinberg's theory.6 Antioxidants and their supporting nutrients have become the new hope in the war against our number-one killer: heart disease.
LDL cholesterol isn't the only instigator behind inflammation of the blood vessels. Other main causes include something called homocysteine
and the free radicals that cigarette smoking, hypertension, fatty foods, and diabetes cause.
The inflammation that takes place in our arteries is quite similar to the inflammatory reactions found elsewhere in the body. I will attempt to explain this process in lay terms so that you will have a better understanding of what is actually taking place on a cellular level. Don't get caught up in trying to understand the minute details of this process. (This is difficult even for most physicians to understand, so don't feel bad if you are not getting all of it.) I will then explain how you can best protect yourself against this insult to your arteries-it is really quite simple.
When you look at the cross section of a typical, medium-sized artery (Figure 1) you simply need to look at the first layer of cells called the endothelium. This is the tissue-thin lining of the artery. Everything that I am going to talk about involves this thin layer of cells and the area just under the lining's surface called the sub-endothelial space (see Figure 2).
The inflammatory response is a four-step process.
Step 1: The Initial Insult to the Endothelium
The endothelium is an extremely sensitive lining that is vulnerable to even the slightest irritation. Almost all research scientists now believe that hardening of the arteries begins when oxidative stress damages or irritates this single cell layer.
Oxidized LDL cholesterol, homocysteine
, and excessive free radicals cause the oxidative stress that injures the endothelium. This occurs when native LDL cholesterol is able to pass into the area just beneath the lining of the artery (called the subendothelial space) where it becomes oxidized. This cholesterol then begins to irritate the lining of the artery
Step 2: Inflammatory Response
Our body has a defense system designed to protect this endothelium of the artery. In the event of injury, our body responds by sending in certain white cells (mainly monocytes) in an attempt to eliminate the harmful oxidized LDL cholesterol. Here the defense team of monocytes starts gobbling up the enemy in an attempt to minimize the irritation to the endothelium. If this inflammatory response is successful, the problem is over and the lining of the artery will be repaired. But this is not what usually happens.
Think of a monocyte as a white minivan. As it drives around, picking up children and letting them off in their proper places, it is limited to the number of children it can carry at any one time because it has only so many seats and seat belts. On a good day the same is true for monocytes. When we're healthy they zoom around, picking up native LDL cholesterol and dropping off other native LDL cholesterol. And just like a minivan, monocytes can carry only so many native LDL cholesterol particles at a time. This is known as a natural feedback mechanism.
When native LDL cholesterol becomes oxidized, the cholesterol particles are no longer harmless little children. Instead, they now pose a threat to the body, and the monocytes pick them up via a totally different method. Monocytes continue to gather the delinquent oxidized LDL cells, but they don't let any out. This would be like a gang of severely obese juveniles clamoring into the minivan through the rear door without its driver having any control whatsoever on the number of kids getting in. If this were to happen, the van would be immobilized and soon begin to jam up traffic.
When the monocyte encounters bad cholesterol, it is in a similar fix. Because there is no natural feedback mechanism, the monocyte gets crammed so full of oxidized I.DL cholesterol (fat) that it becomes a foam cell. This is just like what you are picturing in your mind: it is a cell that looks like a ball of fat. This foam cell then attaches itself to the lining of the artery and eventually forms the initial defect of hardening of the arteries, which is called afatty streak.
The fatty streak is an inflammatory lesion. It is the initial step in this process called atherosclerosis. If the process would simply stop here, the body would at least have a chance to clear this defect. But this is not the case. As in any war, this process has some collateral damage. In other words the thin, vulnerable layer of cells lining our arteries is damaged even more by the very process that is supposed to heal it. This actually creates more inflammation, which attracts more monocytes and in turn changes native LDL cholesterol to oxidized LDL. This leads to a chronic inflammatory response in the area around the lining of our arteries.
Step 3. Chronic Inflammatory Response
Chronic inflammation is the underlying cause of heart attacks, strokes, peripheral vascular disease, and aneurysms. These are altogether classified as cardiovascular disease (diseases that involve the arteries of our body). When inflammation of the arteries persists, the simple fatty streak I described begins to change. Not only does the inflammation attract more white cells (primarily monocytes), the monocytes then stuff themselves with more oxidized LDL cholesterol. This leads to a much thicker plaque, and the process of hardening of the arteries is now well under way.
This chronic inflammation also causes the muscle layer of the artery to thicken by a process called proliferation, the building up of more and thicker muscle cells. As a result, the artery begins to narrow. See Figure 3.
This entire process is a vicious cycle. Not only is there a buildup of plaque, but there is also a thickening of the artery. Normally, the layer of endothelium functions well by releasing an important product called nitrous oxide. During an inflammatory response, however, the appropriate release of nitrous oxide is blocked from the endothelium, causing the endothelium to function poorly. This in turn causes platelets to adhere to the plaque and the artery around the plaque to go into spasm.
Step 4: Plaque Rupture
The final event in about 50 percent of heart attacks is the rupture of one of these plaques and the clot that forms around a ruptured plaque. A situation such as this causes acute and abrupt total closure of this artery, which blocks the blood flow to that part of the heart. Potentially dangerous plaques are often small and may not even cause significant narrowing of the artery-making a diagnosis of heart disease difficult prior to the rupture of a plaque. (You can see now why this disease is so silent and unsuspected until the plaque ruptures and actually blocks the artery.) Oxidative stress may also cause the break down of these plaques, which eventually leads to their rupture.
Arteries can keep narrowing to the point that they become occluded (shut off). Have you ever had a friend or family member who had dye injected into his arteries to find out whether he had severe narrowing of one or all of his coronary arteries? These patients have usually had symptoms of chest pain or what doctors call unstable angina. In situations like these doctors either open vessels via angioplasty (ballooning of the artery) or bypass these blockages with surgery.
If you were to spend a day following a cardiologist or cardiovascular surgeon around the hospital, you would soon realize he has to spend the major ity of his time putting out fires.' He typically treats patients who are at the end of the inflammatory process, with his entire focus on attempting heroically to save a life. Not much time is left to teach patients about the lifestyle changes necessary to slow down or even hopefully reverse this devastating disease and prevent the need for his services in the future.
True Prevention: What the Research Says
The good news is that antioxidants and their supporting nutrients can eliminate or at least significantly reduce all of the causes of inflammation in the arteries. Hundreds of clinical studies looking at heart disease report a significant health benefit with the use of nutritional supplements. Let s now look at each individual nutrient and see what its particular role is in slowing down or preventing this inflammatory reaction.
Vitamin E is the most important antioxidant when it comes to hindering the process of hardening of the arteries. The main reason vitamin E provides such a powerful defense is the fact that it is fat-soluble, making it the most potent antioxidant within the cell wall. Vitamin E actually incorporates itself within the LDL cholesterol. The higher the vitamin E levels within the cell membrane of the native LDL cholesterol, the more resistant the LDL cholesterol is to becoming modified or oxidized. Wherever the native LDL cholesterol goes, the vitamin E travels right along with it.
It is important to understand that, as I mentioned earlier, LDL cholesterol does not become oxidized within the artery itself but only when it travels through the thin lining and into the subendothelial space. Researchers now believe that the high antioxidant content of the plasma or blood does not allow for this change to occur in the artery In the subendothelial space the surrounding cells offer significantly less antioxidant protection. If the vitamin E content of the native LDL cholesterol is high, it is protected from becoming oxidized even if it passes into the subendothelial space.
Remember, the monocyte white cells pick up and drop off native LDL cholesterol so buildup doesn't occur. Keeping the native LDL cholesterol from being modified would prevent the entire inflammation process from the start.
Recent studies show us that vitamin C is the best antioxidant within the plasma or fluid of the blood primarily because it is water-soluble. Vitamin C supplementation has been shown to preserve and protect the function of the endothelium.7 Remember, endothelial dysfunction is at the core of this inflammatory process. Since maintaining the integrity of this thin lining of the artery is of utmost concern, numerous studies have appeared involving supplemental vitamin C to either prevent or decrease cardiovascular disease.8
Vitamin C has also been proven effective in protecting the LDL cholesterol from becoming oxidized within both the plasma and the subendothelial space.4 Yet another benefit of vitamin C is that it has the ability to regenerate vitamin E and intracellular glutathione so they can be used again and again.
Glutathione is the most potent intracellular antioxidant and is present within every cell. Patients with known coronary artery disease have lower levels of glutathione within their cells than people whose arteries are healthy. Glutathione is a key antioxidant because it is contained in all the cells that surround the subendothelial space. When you take the nutrients needed for the cell to make more glutathione (selenium, vitamin B2, niacin, and N-acetyl-L-cysteine), you are improving the body's overall antioxidant defense system.
Thousands of bioflavanoids exist within our fruits and vegetables. Here is a rule of thumb: the more varied the color of your fruits and vegetables, the greater variety of bioflavanoids you will get. These extremely potent antioxidants also have some anti-allergen and anti-inflammatory properties. Red wine and grape juice have a product called polyphenols, for example, which have been shown to decrease the formation of oxidized LDL cholesterol. They also help protect the integrity of the endothelium.
Grape-seed extract is believed to be the best bioflavanoid antioxidant in helping prevent chronic inflammatory disease."
Nutritional Medicine: True Prevention
Research scientists are discovering that the root cause of heart disease is inflammation resulting from oxidative stress. Now clinicians (practicing physicians like me) need to take this information and make it practical and useful for you, the patient. But both physicians and researchers have a tendency to treat basic nutrients as drugs; that is, they test the body's response to just one nutrient at a time so they'll learn its exact potential.
For example, they will conduct a study with vitamin E, then a respective study will look at vitamin C, and then a separate study will examine the effects of beta-carotene. Occasionally a clinical trial does not show any significant health benefit and physicians and researchers hesitate in recommending that particular nutrient. This is what creates the controversy you see in the media and in the medical literature. Physicians want to know beyond any shadow of doubt that a particular nutrient will help before they will go on record to recommend any form of nutritional supplementation. But they are missing the all-important synergistic effects of nutritional medicine.
This refers to the ways antioxidants work together. To halt oxidative stress, the body needs enough antioxidants to handle all the free radicals, and the antioxidants need all of the supporting nutrients to do their job well. These ingredients work in synergy as they accomplish the ultimate goal of defeating oxidative stress.
I suggest that my patients provide all of the nutrients to the cell and tissues at optimal levels. I want to stop this inflammatory process from even getting started. Therefore, I recommend that they have the highest levels of vitamin E possible within the LDL cholesterol itself in order to protect it from becoming oxidized.
I have found my patients need to have optimal levels of vitamin C to protect the integrity of the endothelium, decrease the oxidation of the LDL cholesterol, and regenerate the vitamin E and glutathione. Beta-carotene, along with all the different types of carotene, is also necessary to help prevent or slow down this process.
I want to build up the glutathione levels within the cell by giving the body its precursors-selenium, vitamin B2, N-acetyl-L-cysteine, and niacin. In the next chapter, you will also learn the importance of folic acid and vitamins B6 and B12 in reducing the risk of cardiovascular disease.
Again, all of these nutrients work together either to eliminate or to decrease the inflammation in the arteries. The synergistic effect of supplementing all of these nutrients together is the key. That is why cellular nutrition is so critical to our health.
"What Your Doctor Doesn't Know About Nutritional Medicine May Be Killing You."
Dr. Ray Strand http://www.raystrand.com/bookstore.asp