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From Free Radicals to Periodontal Disease –
As we continue our deep dive into inflammation you will learn some surprising facts that may contribute to your aches and pains. Fortunately, there are many things you can do to reduce inflammation but that all begins with education.
In this session we will answer questions such as:
Free radicals are highly reactive, imbalanced molecules that steal electrons from cells to neutralize their charge. Free radicals interfere with enzymatic reactions and cause significant metabolic stress, damaging cells and DNA. Simply eating, drinking, and breathing will generate free radicals as byproducts of energy (ATP) production, and alcohol, drugs, poor diets, and radiation, among other causes, accelerate the production of free radicals in the body. Their danger is that they fan the fires of inflammation and attack cell membranes, ultimately disrupting cellular communication. When free-radical damage disturbs the integrity of your cell membranes, they leak, and excessive waste builds up inside the cells.
One of the primary ways we can protect ourselves from free-radical damage is to take oral antioxidants. Because cell membranes are composed mostly of fat, fat-soluble antioxidants, such as alpha-lipoic acid, coenzyme Q10, and vitamin E, can best penetrate into the cell. Antioxidants slow the aging process by promoting cellular repair, inhibiting inflammation, and preventing production of the inflammatory substances that accelerate aging.
Cardiologists frequently cite the process of lipid peroxidation as a focal point for the origin of atherosclerosis (hardening of the arteries). Many antioxidants, particularly coenzyme Q10 and quercetin (found in onions), actively block the oxidation of LDL that contributes to silent inflammation.
Although oxidized LDL cholesterol creates plaque that helps set the stage for atherosclerosis, there are other causes of cardiovascular disease. Controversial nanobacteria are increasingly considered an important explanation for this disease.
Nanobacteria, formally known as Nanobacterium sanguineum, are so minute that they eluded researchers for decades. They’re one-one thousandth the size of normal bacteria, and until recently, nobody believed that anything so small could even be alive. It turns out, however, that nanobacteria are not only very vital and thriving, but they may be causing damage to our health in more ways than we can imagine.
One of our missions has been to explain how and why heart disease occurs in people who don’t exhibit the traditional risk factors. If we can identify the cause, then we can help prevent thousands of unexplained deaths each year. There have been numerous hypotheses, but so many never pan out. Take Chlamydia pneumoniae, the pathogen that causes acute respiratory disease, for example. In news reports from just a few years ago, authorities proclaimed that infection with this bacterium probably accounted for much of the unexplained plaque in people. They hoped that doctors could treat the C. pneumoniae and thereby eradicate the plaque. Well, further research uncovered that C. pneumoniae was only found in a small percentage of all plaque and was certainly not pervasive enough to be a major cause for it.
An Apt Analogy
To help illuminate what the discovery of nanobacteria could ultimately mean for our health, let’s take a look at H. pylori and ulcers. It was only after years of having patients undergo gastric surgery that doctors learned that the real culprit in many ulcers was a bacterium known as Helicobacter pylori. Surgeons were putting their patients with ulcers through major surgery, cutting their vagus nerve (the extensive cranial nerve that extends to the abdomen) and revamping part of their small intestine when, in most cases, the only treatment needed was antibiotics.
In the same way, in another alarmingly common procedure, cardiac surgeons have been cutting and pasting blood vessels to bypass plaque-filled arteries. We may learn, instead, that a course of the right antibiotic is all that’s needed for severely calcified arteries.
Scientists from the Hungarian Academy of Sciences have reported finding nanobacteria in more than 60 percent of carotid-artery-clogging plaques studied. The Hungarians also validated previous research reports of how truly minuscule these bacteria are, and how easily they can enter the body via blood exchange and blood products. Their protective calcified apatite coat makes nanobacteria highly resistant to heat, radiation, and all antibiotics except tetracycline. Nanobacteria have been implicated in nephrolithiasis, polycystic kidney disease, and renal stone formation.
More research will determine whether nanobacteria are the real culprits behind coronary arteriosclerosis. For now it is prudent to keep in mind that microbes could play a substantial factor in causing the silent inflammation that can culminate in cardiovascular disease. We’ll now discuss some of the research that looks at other viruses and spirochetes as potential causes of inflammation, as well as the relationship between periodontal disease and the heart.
In 1982, Willy Burgdorfer discovered the cause of Lyme disease when he isolated spirochetes of the genus Borrelia from the mid-gut of ixodes ticks. Some researchers believe that as many as 60 million people in the United States are infected with Borrelia, but that Lyme disease occurs in them only when their immune systems become overloaded. Dr. Simpson estimates that at least 30 percent of his patients with Lyme disease are also mercury toxic, and he believes that this mercury toxicity severely compromises their immune systems and leaves them vulnerable to the Borrelia spirochetes.
Lyme disease has been reported in forty-seven states and on four continents, and ticks are not the only sources. Blood transfusions, fleas, mosquitoes, sexual intercourse, and unpasteurized cow’s and goat’s milk have also transmitted the disease. People with Lyme disease are often simultaneously infected with other viruses and bacteria.
The spirochetes responsible for Lyme disease do best in an anaerobic (low oxygen) environment and cannot tolerate large quantities of oxygen. They can change their shape and chemical structure, and are more evolved than bacteria in many ways. Furthermore, these spirochetes can turn off several surface proteins, which have the effect of keeping the immune system from being able to detect them. This stealth-type camouflage of theirs prevents antibodies from attaching to them, and prevents the enzymes in the blood from finding and destroying them. In this way, the spirochete can penetrate any tissue in our bodies, including our blood vessels, brain, heart, and mouth.
Many researchers now believe that coronary artery disease (CAD) is largely an inflammatory process characterized by decades of cyclic irritation, injury, healing, and reinjury to the inside of blood vessels.
Organisms like cytomegalovirus (CMV) and other viruses have been implicated in contributing to inflammation and the subsequent elevation of C-reactive protein (CRP). This elevated CRP can lead to a fivefold increase in risk for heart disease. Dr. Hannah Valentine, a cardiologist at Stanford University Medical Center, found that people with CMV who were given heart transplants developed atherosclerosis, as did rats under identical circumstances. However, if the rats were given an antiviral drug to kill CMV, they did not develop atherosclerosis.
Iron is required for the growth and reproduction of many infectious viral organisms. Research has shown that the tendency of menstruating women to have lower iron levels than men may be the reason for their longer average life span. Since natural substances like lactoferrin, malic acid, and pectin can safely chelate iron out of the system, we recommend nutraceuticals containing these components as part of your longevity program.
There is a significant relationship between periodontal (gum) disease and chronic inflammation. Multiple microbes, including bacteria, spirochetes, and viruses, can grow in and around the teeth and periodontal sections of the mouth and cause a decline in the immune system, making the area susceptible to chronic low-grade inflammation and subsequent increases in CRP levels. In one study of fifty people referred for angiography and assessed for periodontal disease, there was a significant relationship between the extent of coronary atherosclerosis and periodontal disease.
Cardiologists are especially aware of the link between gum disease, halitosis, oral hygiene, missing teeth, and a strong probability of subsequent cardiovascular disease. Practicing good oral hygiene and taking antioxidants, such as coenzyme Q10, essential fatty acids, and magnesium, can help support gum health, thereby reducing chronic inflammation.
Toxic Blood Syndrome
Toxic blood syndrome is blood that has been compromised by heavy metals, infections, and other toxins. Ninety-five percent of chronically sick people have excess blood coagulation, which hampers blood flow, and many of these have toxic blood syndrome, characterized by such markers for inflammation as elevated levels of C-reactive protein, ferritin, fibrinogen, homocysteine, Lp(a), and oxidized LDL. (Inflammation is now considered the primary culprit responsible for vascular disease.)
In a study, elevated levels of C-reactive protein (CRP) were the most significant of twelve predictors of future cardiac events in 28,263 healthy postmenopausal women, and was the strongest risk factor associated with an acute coronary event, such as plaque rupture or myocardial infarction. In acute myocardial infarctions, those with higher C-reactive protein levels have a higher death rate than those with lower CRP levels.
A higher level of homocysteine is not only a risk factor for cardiovascular disease, it has also been implicated in Alzheimer’s disease, cancer, low birth weight, neural tube defects, and osteoporosis. Homocysteine is directly toxic to blood vessels in the brain and heart. Elevated levels wreak oxidative stress, cause DNA damage to the nerves, endothelial dysfunction, and even a weakening of the mitochondrial membrane.
High levels of homocysteine have been shown to double the incidence of Alzheimer’s disease. In one study of 1,092 people who were initially dementiafree, over an eight-year follow-up, 111 developed dementia and 83 developed full-blown Alzheimer’s disease. Those with high homocysteine levels had double the Alzheimer’s risk of those with lower homocysteine levels, and as the homocysteine levels went up, so did the risk levels.
One of the most important factors in lowering homocysteine is the use of the B vitamins, including B6, B12, betaine hydrochloride (trimethylglycine), calcium folinate, folic acid, and pyridoxal phosphate. Beets, broccoli, garlic, and SAMe are also effective in reversing toxic homocysteine back into harmless methionine. A large percentage of people, however, particularly those of European and French Canadian decent, cannot adequately metabolize synthetic folic acid. For these people, homocysteine levels will persist despite the use of B vitamin components.
What are acceptable levels of homocysteine? A homocysteine level less than 7 is ideal. Levels over 10 are unacceptable, especially in those with presenile dementia or arteriosclerotic cardiovascular disease. And high homocysteine levels are especially treacherous in the company of elevated lipoprotein(a) (Lp[a]) because together they can induce clots. On an anecdotal note, Dr. Sinatra has seen elevated homocysteine in the company of high Lp(a) in many of his patients who have heart disease, and he treats it aggressively in them, as well as in those at risk for developing it.
Lipoprotein(a) is a cholesterol particle that is highly inflammatory and thrombotic. In a ten-year follow-up of myocardial infarctions in 5,200 participants, those with the highest Lp(a) levels had a 70 percent increase in myocardial infarctions. For the cardiologist, Lp(a) is a difficult risk factor to neutralize because the statin drugs are known to increase Lp(a), so it is important for physicians to track Lp(a) levels whenever they are treating high cholesterol with any statin drugs.
We have found that the toxic effects of Lp(a) can often be neutralized by using targeted nutraceuticals. The liver-supporting nutrients are especially helpful, along with coenzyme Q10, Policosanol, and the omega-3 essential fatty acids, such as fish oils, in combination with niacin.
High fibrinogen is a phenomenon increasingly observed in postmenopausal women and smokers, and levels greater than 360 milligrams have been associated with coronary calcification. This coagulation protein has been successfully neutralized with bromelain, fish oils, garlic, and natural Cox-2 inhibitors, such as ginger and green teas, as well as enzymes (to be discussed later in this chapter).
Serum ferritin (high levels of stored iron) is also associated with increased risk for myocardial infarctions. The high levels of iron that can oxidize LDL cholesterol may reflect iron overload or hereditary high iron levels. If you have this condition, it is important to cut iron consumption to a minimum and use high-dose vitamin C with caution, as megadoses greater than 500 milligrams daily may lead you to absorb too much iron from your diet.
Toxic Blood and Plaque
In summary, it’s important to assess all these toxic-blood components, particularly when treating an individual with a family history of early-onset, or what we call premature, cardiovascular disease. We know that homocysteine and Lp(a) can be genetic, and in assessing arteriosclerosis we need to go beyond cholesterol and triglyceride monitoring and look at these toxic blood components that are becoming increasingly implicated in the formation of plaque.
Younger plaque is soft and covered by a thinner fibrous cap, loaded with cholesterol. It is quite volatile and often goes unnoticed on angiograms. To some extent, many of us have atherosclerosis—the real question is, “Do you have an unstable plaque?” Inside these young fatty plaques, macrophages (the scavenger white blood cells of the immune system) can become engorged and incompetent to do the job they are designed to do. Instead, they evolve into angry foam cells, releasing proinflammatory toxic substances that may result in further instability to the plaque.
It used to be thought that cholesterol was the major marker for atherosclerosis. This is no longer the case. Proinflammatory messengers, referred to as cytokines and leukotrienes, are now recognized as behind-the-scene culprits. When inflammation is present, specific cytokine messengers are put into service to instruct the liver to increase intermediary inflammatory substances, such as CRP, that are released into the blood and serve as indicators of underlying chronic inflammation. By interrupting and arresting, we can help to prevent atherosclerosis, hypertension, heart disease, stroke, and even sudden death. Let us look at what we can do to lower inflammatory mediators and minimize silent inflammation in the body.
In our next article we will continue to discuss a variety of causes behind inflammation and help you build a clearer understanding of what you can do about it. Learn how AlphaFlex can help you feel better.