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Sugar toxicity: a silent epidemic: a view from the trenches of daily primary integrative medical praxis.

Sugar is the generalized name for sweet, short-chained soluble carbohydrates. Carbohydrates are composed of carbon, hydrogen, and oxygen (basically carbon + water). The term sugar refers loosely to a number of different types of carbohydrates, including monosaccharides (glucose, fructose), disaccharides (sucrose, lactose), oligosaccharides, and polysaccharides (common components of glycoproteins and glycolipids). The most biologically important and well-known monosaccharide is glucose. Glucose is the main source of energy fueling aerobic metabolism --a fundamental necessity of living mammalian cells. The most common disaccharide is sucrose (glucose + fructose) or common table sugar. Biopolymers (oligo-and polysaccharides) of sugar are common structural forms of carbohydrates in nature. Plants produce sugar and sugar biopolymers through the process of photosynthesis. These biopolymers are converted into structural polysaccharides, such as cellulose and pectin found in plant cell walls. They also may serve as a form of energy storage, such as starch or inulin. In addition, DNA and RNA are polymers of the monosaccharides deoxyribose and ribose respectively and constitute the basis of genetic blueprint and memory for almost all forms of life. The importance of sugar for life in its various functional and structural forms cannot be overstated. However, like oxygen, which is both essential for most life forms and also extremely toxic to life (physiologic function versus toxic free-radical damage), sugar also has a dark side for living tissue.

Studies in animals and humans have suggested that chronic consumption of added sugar contributes to metabolic and cardiovascular dysfunction. There is also growing evidence that added fructose is more damaging than refined glucose in terms of cardiovascular risk. Cardiac performance has been shown to be impaired by switching from a low-carbohydrate diet including fiber to a high-carbohydrate diet. Switching from saturated fatty acids to carbohydrates with high glycemic index values shows a statistically significant increase in the risk of myocardial infarction. Other studies have shown that the risk of developing coronary heart disease is decreased by adopting a diet high in polyunsaturated fatty acids and low in sugar, but a low-fat, high-carbohydrate diet showed no reduction. This suggests that consuming a diet with high glycemic load ("high glycemic" = causes a rapid rise in blood sugar) is strongly associated with the development of coronary artery disease. The consumption of added sugars has been positively associated with multiple measures known to increase cardiovascular disease risk in adolescents as well as adults. Multiple studies suggest that the impact of refined carbohydrates or high glycemic load carbohydrates is more significant than the impact of saturated fatty acids on cardiovascular disease. In addition, a connection between Alzheimer's disease and fructose has been suggested, but remains the subject of debate. Finally, the possible addictive effects of refined sugar simply adds to the scientific concern regarding the toxic effects of sugar in the development of cardiovascular disease.


One of the lesser-known structural/ functional physiologic aspects of sugar is the glycocalyx. The glycocalyx is a polysaccharide sugar polymer coating that surrounds all cell membranes. This "sugar" coating consists of several carbohydrate moieties of structural membrane glycolipids and glycoproteins which serve as a backbone for support and cell-cell communication. Pischinger's matrix theory of rapid cell to cell communication is centered on the functional aspects of the glycocalyx (Pischinger A. Matrix and Matrix Regulation Basis for a Holistic Theory in Medicine. Brussels: Haug International; 1991). This carbohydrate ("sugar") portion of plasma membranes contributes to cell-cell recognition and communication, and intracellular adhesion. The slime on the outside of a fish is a common example of a glycocalyx. It is essentially a functional "biofilm." The term glycocalyx was initially applied to the polysaccharide matrix coating epithelial cells, but its functions have been discovered to go well beyond that. The glycocalyx plays a major role in regulation of endothelial vascular tissue, including the modulation of red cell volume in capillaries. It is located on the apical surface of vascular endothelial cells which line the lumen of all blood vessels and may be up to 11 urn thick. It is present throughout a diverse range of microvascular beds (capillaries) and macrovessels (arteries and veins). The glycocalyx also consists of a wide range of enzymes (eNOS, ACE, SOD3, etc.) and proteins (growth factors, chemokines, antithrombin, etc.) that regulate and protect the endothelium. They serve to reinforce the glycocalyx barrier against vascular and other diseases. Another function of the glycocalyx within the vascular endothelium is to shield the vascular walls from direct exposure to blood flow while serving as a vascular permeability barrier. Its protective functions are universal throughout the vascular system. In microvascular tissue the glycocalyx inhibits coagulation and leukocyte adhesion. It also affects the filtration of interstitial fluid from capillaries into the interstitial space. Research has shown that the glycocalyx is composed of a negatively charged network of proteoglycans, glycoproteins, and glycolipids.

The glycocalyx plays a crucial role in cardiovascular system health. Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized LDL cholesterol. In the microvessels, dysfunction of the glycocalyx leads to internal fluid imbalance and potentially edema. In arterial vascular tissue, glycocalyx disruption causes inflammation and atherothrombosis. Fluid shear stress is also a potential problem if the glycocalyx is disrupted for any reason. This type of frictional stress is caused by the movement of viscous fluid (i.e., blood) along the lumen boundary, damaging the delicate glycocalyx. Minimal ischemic damage to the glycocalyx increases capillary hematocrit. Endothelial (glycocalyx) dysfunction can be tested by a variety of methods. Of all the current tests employed in a research setting, flow mediated dilatation (postocclusive reactive hyperemia; PORH) is the most widely used noninvasive test for assessing endothelial dysfunction. This technique measures endothelial function by inducing reactive hyperemia via temporary arterial occlusion and measuring the resultant relative increase in blood vessel (capillary) diameter via ultrasound or plethysmography. A reduction of small arteriole/capillary compliance is a marker for endothelial (glycocalyx) dysfunction that is associated with both functional and structural changes in the microcirculation and is predictive of subsequent morbid events. These changes can be distinguished from large artery (macrocirculation) stiffness and obstruction by the use of pulse volume recording (PVR).


The endothelium is a thin layer of squamous endothelial cells that line the inner surface of blood and lymphatic vessels, forming an interface between circulating blood or lymph fluid in the lumen and the vessel wall. Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph fluid are known as lymphatic endothelial cells. Endothelium is mesodermal in embryonic origin. Vascular endothelial cells line the entire circulatory system, from the heart ("endocardium") to the smallest capillaries. These cells have unique functions in vascular biology. Both blood and lymphatic capillaries are composed of a single layer of cells called a monolayer. All endothelial cells are coated with glycocalyx biopolymers. Endothelial dysfunction is a hallmark for vascular disease, and is often regarded as a key early event in the development of cardiovascular disease. Impaired endothelial function has been related to hypertension and vascular thrombosis and is seen in patients with coronary artery disease, diabetes mellitus, and hypercholesterolemia. Endothelial dysfunction is a systemic pathological state of the inner lining of blood vessels and can be broadly defined as an imbalance between vasodilating and vasoconstricting forces acting on endothelial cells. Endothelial dysfunction has been shown to be of prognostic significance in independently predicting vascular events including stroke and myocardial infarction. Endothelial dysfunction can result from and contribute to several disease processes (hypertension, diabetes) and can also result from environmental factors such as smoking and exposure to air pollution. Thus, endothelial dysfunction is a major pathophysiological mechanism of vascular disease. Endothelial dysfunction is synonymous with glycocalyx dysfunction.

Macro- vs. Microcirculation

There are actually two "functionally interrelated" blood circulatory or vascular systems found in the human body: the macrocirculation and the microcirculation. The macrocirculation consists of the larger "conduit" arteries that conduct blood to the major organs. Included among these arteries are the aorta (chest and abdomen), carotid (neck), femoral (legs), coronary (heart) arteries, and others. These are the blood vessels commonly treated with surgery and angioplasty (balloon therapy/stenting). The acute treatment of these large conduit "macro" vessels is commonly the focus of cardiologists, vascular surgeons, the news media, websites, and television shows. These treatments are routinely used and "sold" by scientific (more properly called statistical) "evidenced-based" medical practitioners. These macrovessels are the arteries said to be chronically "plugged up" (arterial plaque buildup) from the common "statistical" risk factors promoted by "evidence-based" scientific medicine: cholesterol, "bad" genes, high blood pressure, smoking, and so on. Please note that no one who speaks from scientific authority has ever said that cholesterol or smoking actually "causes" plaque. No, that's not what has been said, but commonly that is what is heard. What is being "said" is these factors are statistically associated with plaque, but science still does not know what actually causes arterial plaque to form.

Arterial plaque occurs in localized, "specific" sites within macrovessels; but, oddly enough, the statistical risk factors, which occur throughout the entire vascular system, theoretically should affect all macroarteries in the same way. Despite this, one commonly sees plaque blocking 90% of one coronary heart artery and no evidence of any blockage in the heart artery right next to the blocked one in the same patient. Isn't just as much cholesterol passing through each artery? Why the difference in presence and/or size of plaque? No one, and certainly no one in "evidence-based" scientific medicine, knows. They simply "know" statistical risk factors that are associated (statistically) with the presence of plaque. Scientific "evidence-based" statistical treatment and/or prevention consists of advising lifestyle changes (weight reduction, exercise, stress control, etc.) or prescribing pharmaceutical drugs (statin drugs, ACE inhibitors, ARB blockers, beta blockers, aspirin, Plavix, etc.), angioplasty, or surgery. The typical advice in mild to moderate plaque buildup is to reduce or lower weight, lower cholesterol, lower blood pressure, reduce inflammation, and increase blood thinning--all strategies that have been "statistically" ("evidence-based") demonstrated to reduce the risk and severity of macrovascular disease. Interestingly, these statistically based approaches are not effective in all patients, simply a "statistically significant" number of patients. Therefore, many patients following the correct "evidence-based" scientific diet and lifestyle and using appropriate "evidence-based" medications or surgery will continue to demonstrate advancing plaque buildup over time. Advanced or high grade plaque buildup (80%-100%) is mechanically (surgery, angioplasty) repaired as if it is simply defective plumbing, but this mechanical therapy does not correct the actual cause. That's about it, "scientifically speaking," for macrocirculation treatment from a scientific, "evidence-based" perspective.

Microcirculation is turning out to be radically "different." Microcirculation is also referred to in scientific medical literature as the capillary circulation, terminal circulation, or end-circulation. These are the tiny blood vessels (capillaries and capillary networks) that actually supply oxygen and nutrients and remove carbon dioxide and other metabolic waste from the vital organs (i.e., heart, brain, kidney, liver, etc.). Incredibly, it now appears from a scientific perspective that microcirculatory disease is primarily related to the biological toxicity of sugar, not fat as in macrocirculatory theory. The "joke" of Mother Nature on modern medical science is that substances that are absolutely "essential" to life (oxygen, sugar) also turn out to be extremely toxic to life. Nature has placed a hidden "tax" on aerobic-based (oxygencarbohydrate-sugar) metabolic energy efficiency. Thus, metabolically utilizing ("burning") oxygen and sugar for efficient production of energy comes at a potentially high metabolic price: free radical toxicity and protein glycation or glucotoxicity. By way of analogy, oxygen toxicity can be thought of in simple terms as being similar to "rusting" of molecules in the tissue or organ that these molecules make up (free-radical pathology). Sugar toxicity is being discovered to act by causing "glycation," or "caramelization" of essential structural and functional proteins, including the glycocalyx or endothelium. This process can be thought of in simple terms as causing protein "wrinkling." Another simple analogy would be that of melting caramel over an apple and the caramel-sugar "coating" then hardens or stiffens, thus slowly, but progressively "caramelizing" the microcirculatory endoskeleton of the affected vital organ (i.e., heart, brain, kidney, etc.). When this process involves living tissue it occurs with subtle but devastating physiological consequences over time. The "nonenzymatic" (meaning in the absence of the enzyme insulin) attaching of a sugar to a protein is currently thought to destroy (glycate or caramelize) proteins. Protein glycation is currently generally assumed to be nonreversible. This assumption is actually no longer scientifically correct.

The most widely scientifically recognized clinical condition involving abnormal tissue glycation leading to clinical microcirculatory disease is diabetes. This is the biochemical, structural, and regulatory basis of the commonly encountered condition of diabetic gangrene. Once a "black toe or foot" develops in diabetes, there is no bypass vascular operation, angioplasty, or drug that will help. There is only amputation of the dead tissue and usually problems with wound healing due to the subclinical microvascular disease in the remaining "viable" tissue. Diabetes is a condition that exists in the annals of "evidence-based" scientific medicine by definition and is, "by definition," irreversible. Diabetes is defined as a blood sugar that goes "too high ..." that exceeds the statistically derived "normal" height or peak of blood sugar seen in an "average" population. The definition includes establishing the "normal" and "abnormal" blood sugar levels during fasting, after eating, or during a laboratory glucose tolerance test. This definition of diabetes focuses on how high the blood sugar goes. It turns out that glycation from glucotoxicity also occurs from glucose (sugar) being in prolonged contact with tissue. Thus, the newly described "metabolic syndrome" (also called dysmetabolic syndrome, syndrome X, or insulin resistance), which also exists by definition (and is "by definition" reversible), involves the inability of potentially toxic sugar to exit or, in more technically correct scientific terminology, be "disposed of" from the blood into the cellular metabolism as quickly as possible. Thus, diabetes, by definition, is about how high blood sugar goes and metabolic syndrome, by definition, is also about how long sugar remains in the blood (impaired glucose disposal).

The pathological effect of microcirculatory protein glycation is a stiffening of the capillaries throughout the affected organ--actually a caramelization of the microvascular skeleton within the organ involved. This process involves both abnormal biochemistry (protein glycation) and structural circulatory regulation changes (increased microvascular resistance). The gradual glycation of protein molecules ("endothelium") lining the small capillary microcirculation stiffens those microvessels so that they cannot pulsate with the heartbeat. In addition, glycation of the proteins on the red blood cell stiffens their external membranes, making it more difficult for the stiffened red cells to pass through the caramelized capillary beds one at a time. The resultant structural problem is the inability of the microcirculation to pulsate open with the kinetic (pumping) force of the heartbeat, coupled with the red blood cells' inability to bend, twist, and deform to slip through these stiffened capillaries one at a time. A capillary that is pulsed open during cardiac systole is 10 microns in diameter. During diastole, the capillary reduces to 5 microns in diameter. A red blood cell is 8 microns in diameter. Thus, the caramelized capillary cannot dilate effectively, and the older caramelized red cell has reduced flexibility. This situation results in small capillary "infarcts or strokes" in the affected microcirculatory vessel directly involving the affected organ or tissue (i.e., brain, heart, kidney, etc.).

Over time (years to decades) the collective effects of this process appears clinically. Interestingly, the clinical syndrome that appears depends on which organ(s) is (are) affected. Microcirculatory disease somewhat mimics macrocirculatory disease in that it may "skip" around, affecting different organs or areas of the body differently. Thus, if microcirculatory glycation occurs in the heart there will be a development not of a major clinical "heart attack" (myocardial infarction), but small areas of tissue damage (i.e., slight elevation of enzymes without ECG changes) or, more importantly, the gradual development of diastolic heart failure. This process does not involve the active process of the heart contracting but its inability to relax effectively (diastole) after contraction due to microvascular stiffening of capillaries within the involved heart muscle. Thus, the heart fails to fill effectively and clinical congestive heart failure (CHF; fluid backup into the lungs, legs, etc.) develops. CHF is the now the most common and least curable form or heart disease affecting the American population, with a large proportion being diastolic heart failure. Similarly, if capillary glycation involves primarily the kidney, high blood pressure will develop. Interestingly, diastolic dysfunction, diastolic heart failure, high blood pressure, and sugar toxicity ("metabolic syndrome") are now "epidemic" among Americans, old and young. If capillary glycation occurs mainly in the brain, a condition called leukoaraiosis or coalescing tiny (lacunar) strokes leading to scaring of the gray matter in the brain occurs, and memory loss/cognitive dysfunction and/or small strokes (lacunar infarcts) will develop. Leukoaraiosis is still being taught in scientific medical schools as "a result of aging" and is of "no medical consequence." This outdated thinking has been clearly and scientifically disproved. The presence of leukoaraiosis on an MRI or CT brain scan should be taken as direct clinical evidence of abnormal microvascular glycation (endothelial dysfunction). The connection between heart disease, hypertension, and Alzheimer's syndrome, suggesting a common underlying mechanism (microvascular disease), is now being formally recognized.

Interestingly, in addition to the toxic microcirculatory effects of glucose and subsequent endothelial glycation now being described in Alzheimer's-like senile dementia, scientific evidence also shows that the accumulation of abnormal proteins ([beta]-amyloid and tau protein) in Alzheimer's disease also causes reduced microcirculation (vasoconstriction) in the brain. [beta]-amyloid protein also reduces endothelium-dependent brain vasodilation. As if to add insult to injury, any temporary lack of oxygen in the brain can also lead to increased production of [beta]-amyloid protein. Thus, it is apparent that microcirculatory compromise plays a very large role in the development of memory loss, cognitive dysfunction, and dementia syndromes, regardless of the actual "official name" of the clinical syndrome. In addition to and as further proof of this situation, the microscopic changes in brain tissue that are thought to be "specific" for Alzheimer's disease [beta]-amyloid, tau protein, neurofibrillary tangles) have also been described in patients with heart vascular disease and no evidence of dementia. The increase in body fat that is part of "metabolic syndrome" also contributes to the "bad" situation. Centralized body fat is actually a functioning endocrine organ. Body fat secretes certain pro-inflammatory cytokine hormones (tumor necrosis factor alpha and interleukin-6, etc.). Thus, increased body fat leads to increased inflammation (a statistical risk factor for macrocirculation disease). Inflammation can be measured using the blood test C-reactive protein or CRP. Thus, many previously recognized "independent risk factors" can now be connected through the understanding of the biologically toxic properties of sugar related to malfunction of cellular insulin receptors.

Insulin Resistance/Metabolic Syndrome

The underlying metabolic basis of glucotoxicity is the inability of the enzyme insulin to activate insulin receptors on cell surfaces ("membranes") that allow the sugar to move quickly from the blood into the cellular metabolism, where it can be used for energy production (and the production of free radicals!). Thus insulin acts as a "key" that must fit into an insulin receptor or "lock" and open that lock so that potentially toxic sugar can be transported ("disposed of") quickly and efficiently from the blood into the cellular metabolism. When sugar is not disposed of quickly, several "bad" things begin to happen: (1) glycated microvessels and cellular red corpuscles "stiffen" and lose their ability to pulsate with the heart; (2) the undisposed-of sugar is immediately shunted into centralized body fat production. One of the clinical markers used to define metabolic syndrome is centralized body fat (a large waistline); (3) additional pathological events related to poor glucose disposal include excess sorbitol production leading to nerve damage (diabetic neuropathy) and cataracts. The "defining components" of metabolic syndrome that have been "suggested" or adopted by various scientific groups and societies are high blood pressure, high cholesterol, high triglycerides, high fasting insulin levels, and high fasting blood sugar. Interestingly, all the different criteria put forth by various scientific medical groups (the WHO, American College of Cardiology, American Association of Clinical Endocrinology, etc.) do not include any evidence of direct tissue sugar-protein glycation as criteria for diagnosis. Usually, the presence of three or more of these statistical risk factors "qualifies" as a diagnosis of "metabolic syndrome." In reality, by the time any individual actually "qualifies" for the formal diagnosis of metabolic syndrome, they are already manifesting significant and late-stage clinical evidence of severe microvascular glycation (i.e., high blood pressure, obesity, heart disease, dementia, etc.).

The main biochemistry involved in the pathology of glucotoxicity is known as the Maillard reaction. This common chemical reaction has been known for over 100 years. The main scientific focus of this reaction usually involves food spoilage and industrial applications. Other than in diabetes mellitus ("sugar diabetes"), there was really little medical scientific interest in the Maillard reaction in medical science or practice. However, with the recent and gradually increasing scientific realization that the cholesterol ("fat" toxicity) theory of cardiovascular disease is at best incomplete, or more likely simply wrong, more scientific interest and resources have been reevaluating the pathophysiological effects of the Maillard (sugar toxicity) reaction. There is also overwhelming scientific evidence rapidly accumulating that in vivo pathological Maillard reactions accumulate both from internal dysmetabolism of sugar and ingesting advanced glycation end products (AGEs) created by excessive heating of food that are toxic in living tissue. In addition to the Maillard reaction, the Amadori rearrangement and Schiff base reactions are also part of the complex biochemistry of sugar toxicity.

One major problem faced by clinicians interested in prevention of and early intervention in the manifestations of abnormal tissue glycation is that there is no single test in "evidenced-based" medicine that can "diagnose" metabolic syndrome. Abnormal glycation diseases can be diagnosed using several clinical and laboratory findings, but not by a single laboratory test. A simple blood test called the hemoglobin Ale or glycohemoglobin (HbA1c) test easily and cheaply provides critical clinical information about the ongoing degree of glycation in the body due to inadequate glucose disposal from blood. The "trick" in using this scientific (evidence-based) test as a "new and emerging risk factor for clinical vascular disease" (as it is now being discovered and described in scientific medical journals) is to understand that the laboratory statistical "norms" are not related to individual optimal values. A value for HbA1c above 4.6 should be considered "abnormal" (meaning evidence of accelerated cellular membrane glycation). In most commercial laboratories, diabetes is said to be present, by definition, if the value is 6.4 or higher. This is why most diabetics demonstrate severe vascular disease before scientific medicine diagnoses it. Membrane receptor resistance to the hormone Insulin is not acknowledged until late in the process (advanced tissue glycation) or a "high" HbAlc. Objectively testing using PORH for disturbed microcirculatory function and/or pulse volume recordings (PVR; microvascular disease of the vasa vasorum in macrovessels) can also demonstrate the effects of abnormal vascular glycation (loss of microvascular compliance).

As an aside regarding laboratory measurement of insulin or any other "hormone level," the clinical reality is that no hormone actually works in the blood (or urine, or saliva); hormones do their metabolic work by activating a hormone receptor (i.e., the "key in lock" analogy) located on a specific cell or nuclear membrane. The hormone receptor is usually located on the cell membrane (i.e., insulin receptor) or the nuclear membrane (i.e., thyroid receptor). Thus, in many individual ("not statistical") cases the "blood level" (and urine or saliva, for that matter) of a given hormone (i.e., thyroid, insulin, vitamin D, etc.) may be "statistically" normal or even "optimal" and yet the clinical symptoms of the particular hormone "deficiency" may clearly be present. This is a very common clinical phenomenon seen with insulin resistance syndrome. Blood simply acts as a transport medium to get the hormone from where it was made to where it will have its metabolic effect. As stated earlier, the insulin receptor is located on the cell membrane--and some cells have many more insulin receptors than others. This is the functional basis of IPT (insulin potentiation therapy) cancer chemotherapy: to use insulin to activate the insulin receptors on cancer cells. Cancer cells revert to a more primitive cellular metabolism referred to as anaerobic ("without oxygen") glycolysis (fermentation). Thus, cancer cells have significantly more insulin receptors on their cell surface than noncancer cells. Giving insulin to cause a drop in blood sugar, and at the low point of the blood sugar very small (15% to 20% of standard, recommended) doses of chemotherapy drugs to allow the cancer cell to preferentially take in the drugs as they are in their insulin activated sugar "feeding frenzy," creates a physiologic "Trojan horse" approach that significantly minimizes side effects and yet maximizes therapeutic benefit of chemotherapy to actually target the problem cancer cells, thus sparing drug toxicity to normal cells and tissue. The clinical results in cancer can be quite amazing when appropriately employing IPT.

Returning to the discussion of microvascular glycation related stiffening or lack of pulsatile ability of vascular tissue, pulsation of the microcirculation turns out to be critical for all major organ health. This is the simple reason that scientific medicine has not yet developed an effective implantable artificial heart. Pulsatile flow is something that is required in normal physiology. Any experimental animal that is put on a heart bypass pump that uses nonpulsatile or laminar flow dies within days of progressive, multiple organ (kidney, heart, brain) failure due to progressive microvascular dysfunction--called scientifically increased peripheral vascular resistance. Our best technological engineers can make pumps smaller than a dime that can operate in climates as alien as the Martian surface, but they have not yet mastered the essential, life-sustaining properties of biologically imperative pulsatile flow. The main physiologic cause of pathological microvascular stiffness is glucotoxicity. Clinical counterparts of this "laboratory" phenomenon of increased organ microcirculatory stiffness are commonly encountered, but just as commonly, the causal underlying mechanism (microvascular stiffening due to glycocalyx/endothelial caramelization) is usually not clinically recognized and thus crude, noncurative symptomatic drug or surgical therapy follows. One commonly missed clinical example of this phenomenon may be heart and peripheral arterial vascular stunning and hibernation. Integrative medicine employing chelation therapy has demonstrated clinical effectiveness in reversing stunning and hibernation, in both entire organs (heart microcirculation) and extremities (leg macrocirculation/vasa vasorum). The actual cause of the phenomenon of stunning and hibernation is "unknown" in evidence-based medicine, but glucotoxicity of the microcirculation in the corresponding capillary bed of the heart muscle or the vasa vasorum (or microcirculation) of the macrovessel arterial wall may be involved.

Another clinical "symptom pattern" manifestation of insulin resistance is polycystic ovary syndrome (PCOS). The currently accepted treatment for PCOS is either using synthetic hormone birth control pharmaceuticals (BCP) or the off-label use of the antidiabetic drug metformin. Interestingly, birth control helps PCOS symptomatically, although it is known to cause weight gain, high blood sugar, and, more importantly, increase vascular resistance. It appears that while improving the clinical picture, BCPs seem to be making the manifestations of endothelial dysfunction worse. The clinical and laboratory effects of metformin in PCOS were found to be clinically superior to BCPs. It is also possible that other chronic degenerative diseases may be related to underlying microvascular pathology. For example, osteoarthritis, which is really osteoarthrosis, since no true inflammation ("-itis") is involved, may be related to reduced microcirculation to the associated joint and cartilage tissue. This could explain why the simple clinical methods of heat, massage, and/or injecting ozone (prolozone therapy) into the affected joint and/or periarticular tissue results in reduction and elimination of pain by increasing microcirculation. Chronic unexplained pelvic pain in both sexes may be related to regional microvascular disease. Localized "trigger points" in muscles may also be due to localized microcirculatory disturbance. Much like the phenomenon of localized compromise of microcirculation in the brain (dementia), heart (diastolic heart failure), or kidney (hypertension) leads to different clinical patterns resulting from the same underlying pathology, perhaps other degenerative conditions will be found to be related to reduced microcirculation to an affected organ or anatomic/physiologic area.

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No part of this material may be reproduced or transmitted in any form or by any means electronic or mechanical, including photocopying, recording or by information storage and retrieval system, without the written permission from the International BioMedical Research Institute. Support for the preparation of this manuscript was provided by the International BioMedical Research Institute, a 50(c)(3) tax-exempt educational and research organization.

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Due to space limitations we are not able to print the full text and references of "Sugar Toxicity" A Silent Epidemic." Please look on our website,, under the contents for the May 2016 issue for the hyperlink to the unabridged article.

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

David A. Edwards, MD, HMD, is the medical director of Bio Health Center, an outpatient homeopathic integrative medical facility providing quality of health care dedicated to keeping pace with changing times. Dr. Edwards has nearly 35 years of experience with homeopathic integrative medicine. Dr. Edwards completed his ozone, bioresonance, homotoxicology, and electroacupuncture certification in Germany.

Jean Malik, AHP, MBBS, is an advanced homeopathic practitioner and Bio Health Center's specialist for women's health issues and NAET allergy therapy. Jean was born and grew up in Karachi, Pakistan, where she attended and graduated from St. Lawrence High School and St. Joseph's College, both located in Karachi. Jean graduated from medical school with an MBBS degree (the British equivalent of US Medical Doctor or MD) and completed postgraduate training in obstetrics, gynecology, and internal medicine. After completing postgraduate medical training, Jean served as a medical officer in internal medicine and ob-gyn at Punjab Medical Centre and Kamal Medical Centre in Pakistan for several years before coming to the United States. Jean is a graduate of the British Institute of Homeopathy (D.I. Horn. Degree) and a certified NAET practitioner.

Edna Espig, CAN, HA, is a certified nursing assistant (CNA), certified homeopathic assistant (CHA), and Bio Health Center's executive director. Edna graduated from Paso Robles Christian School and Cuesta College in San Luis Obisbo.

Renoir Morillo, BSN, is a certified homeopathic assistant (CHA) and Bio Health Center's chelation and intravenous (IV) technician. Ren attended San Francisco State University and she received her bachelor's degree in the science of nursing (BSN) from Quezon City Medical Center, Quezon City, Philippines.

Suzie Ludahl is a front office receptionist and back office assistant. Suzie moved to Reno in 1983. Suzi completed postgraduate education Truckee Meadows Community College in prenursing.

Erika Bryant is Biohealth Center's EECPO technician.
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Author:Edwards, David A.; Malik, Jean; Espig, Edna; Morillo, Renoir; Bryant, Erika; Ludahl, Jesusa
Publication:Townsend Letter
Date:May 1, 2016
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