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From the Townsend Letter
May 2016

Sugar Toxicity: A Silent Epidemic
A View from the Trenches of Daily Primary Integrative Medical Praxis
by David A. Edwards, MD, HMD; Jean Malik, MD, APH; Edna Espig, CNA, CHA; Renoir Morillo, BSN, CHA; Erika Bryant, EECP Tech; and Jesusa Ludahl
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There are several neurological syndromes related to microvascular disease caused by sugar toxicity Included are asymptomatic leukoaraiosis, symptomatic leukoaraiosis, stroke/lacunar infarct syndromes, cognitive decline, Alzheimer's syndrome, lateral temporal sclerosis and/or autonomic dysfunction. Leukoaraiosis in the absence of "symptoms" is generally considered to be related to aging and of no consequence, but recent science now contradicts this "accepted" thinking.85-128,162,163 The different symptomatic clinical syndromes are generally treated with "standardized" drug therapy, depending on specific clinical pattern (aspirin, antiplatelet agents, antiseizure drugs, anticoagulants, memory enhancing drugs, sedative-hypnotics, SSRI drugs, etc.). All drugs only treat symptoms and not the cause of the problem. The underlying "cause" in these clinical syndromes is microvascular disease from sugar toxicity. Symptomatic treatment may be necessary, but treating the underlying causative microvascular disease is more logical, clinically astute and critical. Biological Maillard reactions (sugar toxicity) are fundamentally progressive, degenerative, chronic inflammatory, aging/disease processes that glycate, caramelize, and chronically immune activates ("inflame") specific tissues, organs, and organ systems. The pharmacologic drugs currently used to treat symptoms of Alzheimer's disease and other labeled "idiopathic" forms of cognitive decline consist of two classes: cholinesterase inhibitors and NMDA receptor blockers. Cholinesterase inhibitors are basically insecticides.266 Their short-term effectiveness is marginal and only lasts for months on average.267-269 Side effects and cost are limiting factors for their use. Additional conventional methods that are helpful include exercise, melatonin, growth hormone, and testosterone.270-273 There is mounting evidence that low-level environmental toxic metal accumulation (aluminum, mercury, lead, cadmium, etc.) contribute to cognitive decline/memory loss. This problem can only be treated medically with the process of chelation therapy. Certain vitamins, other nutrients, and herbs have also shown effectiveness anecdotally.274-283

A common problem with understanding the academic, scientific classification of memory loss/cognitive dysfunction syndromes is language. True Alzheimer's "disease" (cognitive decline and autopsy evidence of amyloid/tau protein with neurofibrillary tangles) as originally described and defined by Alois Alzheimer always occurred, by definition, before 55 years of age. Because of this relatively young age it was also sometimes also referred to as presenile dementia or dementia praecox (psychiatric label). If the patient was 56 years old or older, the problem was called "senile" dementia or chronic organic brain syndrome. The two conditions and terms are now commonly mixed and referred to as Alzheimer's-like senile dementia (ALSD) or Alzheimer's syndrome. In addition, there are other "syndromic" variations of memory loss problems (Pick's disease, Parkinson's disease, age-related cognitive decline, Huntington's disease, and others).To add to this taxonomic confusion, microvascular ischemic cognitive dysfunction, the underlying cause of most "Alzheimer's-like senile dementia (ALSD, Alzheimer's "syndrome," leukoaraiosis, or neurological microvascular sugar toxicity) is much more common than true Alzheimer's "disease" (genetics, abnormal amyloid or tau proteins, and anatomic neurofibrillary tangles). There are many theories about how Alzheimer's disease develops.284 Alzheimer's syndrome and other forms of leukoaraiosis are caused or aggravated by microvascular sugar toxicity.79,80 The similarities and overlap between the two conditions (Alzheimer's disease vs. Alzheimer's syndrome/vascular dementia) are clinically difficult to discern.285 Despite the clinical and scientific name differences, they are all conventionally treated with the same pharmaceutical drugs (cholinesterase inhibitors and/or NMDA blockers), either on or off label.267-269

Additional "nonstandard" treatments for cognitive decline related to brain microvascular disease are intravenous EDTA (ethylenediaminetetraacetic acid) chelation therapy, intravenous orthomolecular therapy (glutathione/Myers cocktail), and EECP.262-266,286-292  Although considered "off-label" (i.e., not FDA approved for this clinical use), there is mounting evidence for effectiveness in reversing cognitive dysfunction.262,296-292 In addition, ongoing research has demonstrated that modifying standard EDTA chelation (a modification called metabolic or metachelation) to reverse microvascular glycation can lead to further clinical improvement in memory loss/cognitive decline.293 Capillary microvessels are essentially naked, functional endothelium without the additional connective and muscular tissue found in macrovessels. Microvascular capillary endothelial networks perfuse through all tissues and organs, providing the biophysical, biomechanical, and biochemical matrix for normal physiologic function. When capillary microvessels maximally dilate during cardiac systole ("contraction"), they are 10 microns in diameter. During cardiac relaxation (diastole), they collapse to 5 microns. A red blood cell is 8 microns in diameter. Red blood cells must pass through these pulsating capillary networks in single file. Caramelized/glycated capillaries (endothelium) and/or red blood cells (HbA1c) gradually become rigid (loss of compliance/abnormal PORH/PVR), leading to small areas of ischemia (lack of oxygen) or cellular/tissue damage (i.e., heart "infarct," brain lacunar "stroke," kidney "nephrosclerosis," muscle "trigger point," joint "degenerative arthrosis," etc.). Standard EDTA chelation therapy acts biochemically to provide therapeutic effects involving free radical toxicity (toxic metals), blood viscosity (anticoagulant), metabolism (lowers blood sugar), tissue decalcification, and other probable unspecified mechanisms. Metachelation incorporates additional intravenous nutrients, minerals and supplements to reverse protein glycation. Orthomolecular therapy acts biochemically to support cell and mitochondrial metabolism. EECP therapy works by biomechanically disrupting ("fracturing") the sugar stiffened endothelial glycocalyx via increasing diastolic blood pressure ("diastolic augmentation") and biophysically reentraining physiologic cardiac pulsation in the endothelial microvascular matrix.

In an interesting study, diabetic patients with cognitive decline due to microvascular ischemic brain atrophy treated in a clinical trial with "intensive" glucose control failed to show improved cognitive function. However, patients in the intensive treatment group had significantly greater brain volume at 40 months of treatment.294 Brain atrophy is common as we age and considered to be "normal aging" in conventional medicine, but it really is not "normal" in healthy aged.295 The cause is the gradual (years to decades) development of global microvascular ischemic atrophy of the brain. The study demonstrated that while late application of intensive sugar control for a defined period of time did not benefit functional decline, it had a positive and dramatically beneficial effect structurally.294 Function may be preserved if the process is treated much earlier. By slowing glycation, the preservation of brain volume strongly suggests improved microcirculation function (fluid balance, oxygenation, nutrients, waste removal, end circulation pulsatile waves). This strongly suggests that the earlier clinical evidence of sugar toxicity is detected, the more likely the process can be treated and potentially reversed.98,99,101-106

Autonomic dysfunction diagnosed by clinical symptoms (palpitations, anxiety, insomnia, dizziness, etc.) or testing (abnormal PORH, EAV testing, etc.) can be treated and improved or eliminated by improving the underlying metabolic syndrome and/or removing toxic minerals with chelation therapy.236-238 In addition, following homeopathic-isopathic concepts, dysautonomia is commonly associated with the homeopathic-isopathic nosodes Coxsackie-/enterovirus. Interestingly, scientific evidence has been documented that enteroviruses, such as Coxsackie and other neurotropic enteroviruses (EV 68-71), cause dysautonomic syndromes by attacking the brainstem and spinal cord.296-300 Interestingly, Coxsackievirus has also been implicated as a cause of type 1 diabetes.301 Additional therapy directed at viral issues include intravenous ozone therapy (major autohemotherapy), intravenous hydrogen peroxide therapy, ultraviolet blood irradiation (UVBI) intestinal antibiofilm therapy, and Coxsackie isopathic nosode therapy.

Free radical chemistry is both necessary for life, but also toxic to life. Sugar interactions with biological molecules are likewise essential for life (glycosylation) but also toxic to life (glycation). The important difference between the two processes is that physiologic glycosylation is regulated and controlled by enzymes while pathological glycation is not. Glycation is hazardous in its deactivation and caramelization of structural and functional proteins.302 With the clinical realization that sugar-driven microvascular disease is the fundamental pathophysiologic and pathological process underlying most chronic degenerative syndromes and diseases, sugar excess has become the main dietary element that should be identified and avoided before and after symptomatic disease appears.108-115,117-129,303 Perhaps modern society should revisit the ancient Greek Delphic oracular admonition of "Nothing in excess (Meden agan)." When one considers the extreme amounts of sucrose, glucose, and fructose now found in the American diet and the underlying pathology caused by such dietary madness, the clinical implications for treatment and, more importantly, prevention become staggering. Treatment to reverse such microvascular and protein glycotoxic pathology is time consuming, expensive and could become almost unnecessary if the process is recognized early and effective preventive measures are adopted by government, politicians, and medical science. Unfortunately, the politics, economics, and rampant scientism currently shaping scientific nutritional and medical thought seem incapable of addressing this problem. One bright glimmer on the horizon, however, is the new science of the "microbiome." This new science is beginning to relate the microbes that live in and on the human body to overall health and disease patterns, including glycotoxicity syndromes.304,305 Perhaps one day treating chronic glycotoxic degenerative diseases may be as simple as fecal transplant or providing an encapsulated freeze-dried sample of healthy fecal microorganisms from those who are to those unfortunate enough to be plagued by these chronic diseases. Until that time, however, practicing physicians will have to make do with the current state of praxis in dealing with sugar toxicity.

References (pdf)

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