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Recent years have shown a 600% increase in daily consumption of HFCS, often unknowingly. Of concern are not merely obesity but also the discovery of interruption of hippocampal function (memory, orientation, even behavioral regulation) and creation of neuroinflammation. HFCS-induced inflammation has also been documented throughout sensitive endothelial tissues lining the heart and blood vessels and in joints. An association with cancer has been shown as well, supporting Warburg's insistence on mitochondrial deterioration as a primary event. The staggering number of HFCS foods are dangerous not only because of their empty-calorie content (lots of calories, devoid of real food value) leading to nutritional deficiencies, and not only because they encourage increasing intake of sugary/starchy foods, but also because these very foods sponsor the development and worsening of tooth decay, obesity, cardiovascular diseases, diabetes, and the "Yeast Syndrome."
Here's a provocative observation: HFCS foods entered the food chain in about 1971, and the first book describing the Yeast Syndrome appeared in 1978, The Missing Diagnosis, by Orion Truss, MD. "Syndrome X," cardiometabolic (or just metabolic) syndrome, was first described in the 1987 Banning Lecture to the American Diabetes Association by Stanford endocrinology professor Gerald Reaven, MD. This clinical pattern clearly is the developmental step toward induced diabetes and preventable cardiovascular diseases. Key pathognomonic features of metabolic (or "insulin-resistance") syndrome are the curse of our suffering survival as we age: obesity (increasing girth, elevated body mass index), higher blood pressure, elevating blood sugar (with increasing insulin production), elevating triglycerides, and decreasing HDL cholesterol. Oh – and don't even get me started on the toxic cellular effects of "other" sweeteners such as aspartame, acesulfame potassium, sucralose, and saccharine. These were approved for limited use in foods for diabetics. Now they are widely scattered through the food chain, needlessly exposing millions to chemicals with demonstrated toxicity. (You should also be careful of Sapporo Diet Water – yes, I've seen it! – and Bernard Dehydrated Water … an empty tin!) Incidentally, the overwhelming percentage of corn, as used in production of HFCS, is a GMO – genetically modified for more robust growth. Some have declared these genetic manipulations by chemical giant Monsanto are the inevitable end of healthful foods. Gives you that warm, fuzzy feeling again, right?
GMO crops are engineered to resist herbicides, so higher concentrations can be applied to increase the commercial yield per acre. Are you ready for more and more hidden sources of glyphosate residues (broad-spectrum weed-killer Roundup) – now the world's largest-selling herbicide and another demon-invention from Monsanto? Glyphosate has been connected to, among a growing list of other health challenges, an increased rate of miscarriage, reduction in sex hormone production, and disruptions to endocrine system development. What about autoimmune inflammatory celiac enteropathy – classically described as "gluten intolerance"? Celiac patients experience a twofold increased risk for coronary artery disease, along with arrhythmias and heart failure. Glyphosate residues on grains might be the real culprit in the recent rise in apparent clinical patterns, since they create the setting for destructive inflammation throughout body tissues … in not just the intestinal linings but also mitochondria.
Recent reports suggest that glyphosate interruption of cytochrome P450 detoxification enzymes, disruption of aromatic amino acid synthesis by the gut microbiome, and impaired sulfate metabolism could amplify inflammatory pathways, resulting in many degenerative diseases … including those of the heart and blood vessels. Oddly, glyphosate "cages" (chelates?) aluminum in the gut and enhances absorption of this toxic metal. The (controversial! and challenged) speculation of glyphosate-induction of diseases has been suggested by consulting chemist Anthony Samsel and MIT computer science senior research scientist Stephanie Seneff, PhD, as the "textbook example" of "exogenous semiotic entropy": the disruption of homeostasis by environmental toxins.1 But you can rest assured: the Council on Science and Public Health of the American Medical Association has concluded that "it appears unlikely that HFCS contributes more to obesity or other conditions than sucrose." Keep in mind also that the common high-fat/high-sugar diet creates hyperinsulinemia (part of the metabolic syndrome), a key factor in promoting prostate cancer. Could enhanced inflammation (promoted by glyphosate?) along with the yeast proliferation induced by such a diet be a major feature in cancer promotion? For years, I have treated elevated prostate specific antigen (PSA) patients aggressively for the Yeast Syndrome … with uniformly encouraging results. For a provocative review of the crucial interrelationship of fungus (yeast) and cancer, consider this internet video by the television host of Know The Cause and my dear friend for over 30 years, Doug Kaufmann: http://www.knowthecause.com/index.php/cancer.
Getting on with the Drugs and Stuff
You might think that I'm spending too much time and space discussing the "food issues" – and you'd be wrong. Master teacher of the American College of Cardiology, Demetrio Sodi-Pallares, MD, practicing clinical and electro-cardiology for 60 years with impoverished Mexican citizens, has long treated dramatic degenerative heart diseases with little more than radical changes in the diet. His "nontoxic therapy" evolved from low-sodium/high-potassium diet plus infusions of "polarizing" (GIK = glucose-insulin-potassium) solutions to later include a strong electromagnetic field of 200 gauss and even later use of beta blockers, thyroglobulin, and exercise.
In case you haven't yet grasped the significance of diet in development of disease, refer to the classical findings of Weston A. Price, DDS, research director for the American Dental Association, who documented the deleterious effects of "foods of commerce" (Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects; 1939), and those of Francis M. Pottenger Jr., MD, regarding uncooked foods (reviewed in Pottenger's Cats: A Study in Nutrition; 1995. The Price-Pottenger Nutrition Foundation offers tremendous resources at www.ppnf.org).As the science of nutritional biochemistry advanced during the mid-1900s, our understanding of health and disease dramatically expanded.
Recall that our populations were told since the 1960s to avoid salty foods, to lower the tendency to develop high blood pressure, a major risk factor for heart disease. Sure, we have made serious efforts to avoid "salting at the table." But we still eat salted peanuts, salted pretzels, salted chips, salty pickles, salty deli meats, and so on. And these salted sources don't have added iodine. Why is this an issue? Over 100 years ago, public health authorities adopted the addition of iodine to table salt, a product that virtually everyone used, in order to reduce the incidence of thyroid disease (goiter). So now we have three generations of patients who have received a steady salt intake but minimal iodine. Bingo! Broda Barnes, MD, showed some 40 years ago that low thyroid levels (associated with low iodine intake) are directly associated with a rising risk of heart attack (Hypothyroidism: The Unsuspected Illness; 1976). Denis Wilson MD, has shown that raising thyroid hormone levels (especially free-T3) and raising basal body temperatures closer to "normal" can lower heart disease risk, and blood tests are rarely reflective of adequate support levels (Evidence-Based Approach to Restoring Thyroid Health; 2014). As you might predict (note: tongue-in-cheek!), these observations continue to be challenged by the American Thyroid Association.
Magnesium holds a special place for cardiovascular diseases. Lowered intracellular levels of magnesium are difficult to detect but clearly important. When serum levels are normal, intracellular magnesium may have been scavenged to maintain that measurement. Low serum levels are, therefore, beyond critical and must be addressed, since they contribute not only to high blood pressure but also both pump (CHF, congestive heart failure) and performance (contractility and rhythm disturbances) failures, as thoroughly documented by Seelig.2 Complementing magnesium certainly are manganese, copper, and zinc – adequate levels of all are essential for the formation of SOD, superoxide dismutases, thought to be the fifth most prevalent enzyme set in the human body, since they serve critical antioxidant functions in mitochondria, intracellular cytoplasm, and in extracellular fluids. SOD enzymes outcompete the essential tissue production of superoxide, used to defend against invading bacteria, protecting body cells from internally generated oxidant injury. Back to mitochondria and that inflammation idea, right? Recently developed laboratory tests can be invaluable in helping practitioners identify patterns of nutritional deficiency that can aggravate inflammation; especially helpful are micronutrient testing to evaluate their function within leukocytes (white blood cells), urinary amino acid patterns wherein abnormalities suggest the setting for disease development or progression, and chelation challenge urinary excretion to provoke underlying essential element deficiencies, sometimes supplemented by the old standard of tissue mineral analysis by hair sampling.
Another aspect of cardiovascular disease that might relate to nutritional status and the quality of food intake involves the hypercoagulability (clotting) and rheological (flow) properties of blood. People with underlying biochemical conditions – such as diabetes, alcohol abuse, tobacco use, and even hypertension, to name a few – are more at risk for triggering abnormal clot formation. Those with "vulnerable plaque" – artery blockage that is "unstable" (inflamed and irregular in composition and shape) and more likely to have pieces "break off" and slam into tinier vessels further downstream, causing sudden vascular disasters – often suffer with a dangerous accentuation of their clotting patterns. Sometimes referred to as "sticky blood," underlying changes relate to an increased tendency to activate the clotting cascade to form a "plug" (clot or thrombus) in a blood vessel that leads to a sudden severe (even complete) interruption to flow. This ischemia pattern must be corrected as quickly as possible (infusion of a kinase "clot-buster" within 4 hours) or tissue death ensues – infarction is death of the tissue, whether heart attack, brain stroke, gangrene, retinal occlusion blindness, kidney necrosis, and so on. When a blood clot forms in deeper veins in the legs, the situation is far more ominous than painful discomfort: if dislodged, the plug can zip into the lungs, and such a pulmonary embolism can literally cause sudden death. Risks for these events are reduced by all the treatment strategies discussed along with the addition of oral "fibrinolytic" clot-buster enzymes such as nattokinase (from soy), lumbrokinase (from earthworms), or serrapeptase (from bacteria within silkworms). "Thick blood" (excessive numbers of red cells) is a different but also aggravating condition that can create similar blockage. Platelets (tiny circulating cells responsible for starting the formation of a clot) can become "irritable" when inflammatory conditions are present (including low oxygen saturations, toxic heavy metals, toxic organic chemicals, elevated blood sugars), and their undesirable activation can amplify "sticky blood" tendencies.
A couple of last points on foods. Bioflavonoids (polyphenols), cell-signaling sugars, and a wide range of other goodies are essential for well-being. Colorful vegetables are the source of bioflavonoids (and other "live" factors) on the planet. These are critical in biological functions (believe it or stop reading the basic science journals!) and virtually all of them are now being also shown to have powerful antifungal (and even anticancer) activities. Other goodies include items such as intracellular glutathione (difficult to absorb unless enhanced by liposomal packaging, synthesis rate limited by scarce availability of L-cysteine, essential for antioxidant activity and detoxification), CoQ10, and (induced production of) nitric oxide. These latter two are critical for control of cardiovascular efficiency – pump and performance issues – while the last aids in dilatation (widening … or reduced constriction) of the pipes. While these and other factors are not readily "replenished" by direct supplementation, their synthesis and incorporation can be encouraged by specific nutritional support beyond merely the regular "multivitamin/-mineral formulas."
Mitochondrion Basics
Likely derived from prokaryotic ancient "bacterial" invaders into eukaryotic cells, these tiny "power plants" produce the ATP-based (adenosine triphosphate) energy used by virtually every cellular process. Cell life and division – even cell death – relate to mitochondrial status. Think of a "mito" as a "Dagwood sandwich" from the comic strip Blondie, with outer bread slices encasing a pile of layers of meats and cheeses. The "bread" in this illustration serves as a limiting outer membrane, through which sugars and fats can enter and ATP compounds can exit. The layers of meats and cheeses are equivalent to "shelves" (called cristae) inside the mito, stacked one upon another and separated by an insulating matrix. Enzymes and substrates involved oxidative phosphorylation (processing of sugars through to the end products of the electron-transport system) are aligned along these shelves in specific order, much like you would search for the volume of an encyclopedia from A to Z, not randomly. When all is working well, an innocent "sugar" molecule tumbles its way along, much like a Slinky toy trips its way down stairs, going quickly from one to the next chemical reaction, in order.
Lead and other toxic heavy metals (and even iron, in excess) disrupt the inner shelf arrangements (apparently by inflammatory changes) and diminish enzyme efficiencies, reducing the rate of energy production. Further, as the mito becomes sickened and less able to perform, it can accumulate calcium ions and swell, distorting the shelf arrangements even more. While specific studies have not been done, EDTA chelation therapy appears a likely prospect to reduce internalized calcium and to restore more normal mito shape and function. Whether lead and other toxic metals are actually removed from within the mito is unclear, but in vitro laboratory studies demonstrate increased energy production in heart muscle as a result of chelation. As an interesting side note, Denham Harman, PhD, MD, who proposed the free-radical theory of aging, was frustrated by observing no increase in lifespan of research animals with the addition of antioxidant supplementation. He concluded that such nutrients did not routinely make their way into the mitochondria, which are concurrently producing as well as being damaged by free radicals. He therefore proposed the mitochondrial theory of aging in 1972, where the health of these organelles is the primary determinant of maximum lifespan.
Before settling into the comfort of "modern diagnostics and medications," be sure that exposures in the patient's setting are well understood. Especially be wary that we have less and less understanding about more and more complexities. For example, when tetraethyllead was removed from vehicle gasoline in 1976 – a good idea to reduce environmental pollution, to lower blood pressure and heart attack risk, to minimize kidney damage, to improve brain function, and so on – the replacement mineral chosen was manganese. The health hazards associated with manganese combustion products have now been debated for decades. Might we later find that our replacement is almost as challenging to human health as the original lead that aided octane performance in the gasoline?
Another provocative speculation is that the modern practice of "polypharmacy," wherein several drugs are prescribed concurrently, might induce or amplify inflammatory processes. Medications are approved for use by the Food and Drug Administration based upon limited clinical testing, where most variables are tightly controlled. The general public, though, offers nothing but variables! The dubious interactions of multiple drugs simply haven't been studied, and their role in unwittingly aggravating disease processes – or even in inducing new ones, such as through interference with mitochondrial functions – raise disturbing questions about the bases for "modern" medical practice.
Mitochondrial dysfunctions are at the root of all degenerative disease progression. Understanding that optimal cellular and tissue function requires a robust supply of ATP energy leads to the obvious realization that all body activities are impaired whenever this vital component is limited. Any reduced antioxidant capability allows for unbridled inflammatory chemistry to wantonly damage cell structures and enzymes. Impairment of energy-dependent production of immune molecules leaves an undefended body increasingly prone to opportunistic attack by uncommon organisms, including those generally considered as nonpathogenic commensals or symbiotes on body surfaces, especially in the intestinal and respiratory tracts. Reduced digestive functions lead to a plethora of chemical and biological insults to gut tissues (and, subsequently, to fragile endothelial cells lining heart and blood vessels), not to mention amplification of nutritional deficiencies.
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