Diabetes: Causes, Natural Control, & the Mercury/Vaccine Factor B. Windham(Ed) 2011

 

I. Introduction

 

Diabetes (hyperglycemia) incidence is increasing drastically. For individuals born in 2000, the lifetime risk of diabetes in the U.S. is 33% and over 16 million in the U.S. currently have diabetes(502d,580,598), while over 54 million have insulin resistance or pre-diabetes(1). Childhood diabetes is increasing even more rapidly than adult diabetes(82,493,502,598,1). Over the last 20 years the percent of diabetes cases below 20 years old has increased from 2% to over 30%, and there was a 70% increase in cases under 40 years of age between 1990 and 1998(502). Studies in the U.S. and Europe have found toxic metals and vaccinations to be factors in the increased diabetes cases (502,369,35,100,490-492) along with poor dietary habits(1). A greatly increased incidence of juvenile diabetes has been correlated to specific vaccination sequences and to the number of vaccines given (11,502). Autoimmune diseases with a predominant Th1 cytokine component involvement in some cases include insulin-dependent diabetes mellitus(12). Incidence of insulin resistance which a factor in many chronic conditions has also increased significantly. Diabetes and pre-diabetes are conditions rather than diseases, and usually can be prevented or controlled – see Section V. 

There are 2 basic types of diabetes, Type I (autoimmune) diabetes and Type II (insulin resistance). In type I diabetes the body’s immune system attacks its own insulin producing tissue, the beta cells of the pancreas (580). Type II diabetes involves metabolic failure related to poor diet, obesity, environmental factors, and genetic susceptibility (1). Insulin resistance is a primary factor in type 2 diabetes and results when the body cannot properly use insulin, which is secreted by the pancreas to move glucose from the blood into the cells that need it. The pancreas then produces extra insulin in a futile effort to compensate, leading to higher insulin and glucose levels in the blood along with a deficiency of glucose in the cells that need sugar to function properly. Those with either type I or type II diabetes have been found to be more likely to have other chronic conditions including heart disease, strokes, kidney disease, Alzheimer’s, eye conditions and blindness (580,581) 

II. Causes of Diabetes and the mercury/toxic metal connection

Type 2 diabetes and pre-diabetes is an epidemic among young Americans and greatly increases the incidence of heart attack, blindness, stoke, infertility, and early death. Brain inflammation has been found to be a major factor in pre-diabetes, diabetes, and the closely related metabolic syndrome which includes diabetes or pre-diabetes, high blood pressure, and high cholesterol (598,1, 581b,etc.). Causes of oxidative stress and lipid peroxidative related brain inflammation that have been documented include vaccines, mercury, aluminum, excitotoxins such as MSG, aspartame, food additives, and overconsumption of high-fructose corn sweetener, starches, sweets, and other omega 6 oils (13,424,489,494,496,596-599,1,etc.). These cause high glutamate levels in the brain and oxidative damage –resulting in inflammation of the brain and immune system, as well as damage to brain microglia cells and the mitochondrial DNA, fatigue, high triglycerides, metabolic syndrome, etc. These have been found to be factors in most chronic neurological diseases. Inflammation induced by vaccine adjuvants like aluminum and mercury or by excitotoxins like MSG has been found to play a significant role in insulin resistance (type-2 diabetes) and in high levels of LDL cholesterol (597,598,etc.). There is also evidence that the diet drink sweetener aspartame can cause or increase the effects of diabetes and hypoglycemia (450,498). Higher levels of vit D have been found to be associated with lower levels of insulin resistance and appears to be protective(580). Theoflavins from black or green tea and curcumin have been found to be significantly effective in protection against inflammation and inflammatory conditions(580). 

Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation, and are protective against these conditions (599,43). Mercury and cadmium inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes (43,198,338,505, 597). Iron overload has also been found to be a cause of insulin resistance/type 2 diabetes(595). Mercury also has synergistic effects with other toxics such as dioxins that have been found to increase insulin resistance more than simply additive effects(505). 

 

Mercury exposure levels from vaccinations have likewise shown major increases during this period and have been found to be a major factor in the increase of other conditions like autism and ADHD(8). The most common mechanism of causality has been found to be blockage by mercury and other toxic metals of the enzymatic processes related to digestion of milk casein and wheat gluten, resulting in dumping of morphine like substances in the blood of the majority of children with these conditions(9).

 

A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to allergic/immune reactive conditions(15-23,98,4). For example mercury has been found to strongly inhibit the activity of xanthine oxidase(16) and dipeptyl peptidase (DPP IV) which are required in the digestion of the wheat protein gluten or the milk protein casein (4,15,17,19,20,24-26,98,499) - the same protein that is cluster differentiation antigen 26 (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell surface glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain. Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors(15). 

Beta-casomorphine-7 is a morphine like compound that results in neural disfunction (24,25,4), as well as being a direct histamine releaser in humans and inducing skin reactions (14,21,25c). 

A similar mechanism related to mercury and toxic metals blocking the enzymatic processes related to digestion of gluten and casein have also been shown to be a significant factor in causality of children’s type I diabetes. Early introduction of feeding cow’s milk to infants rather breastfeeding has been shown to be a significant risk factor in type I diabetes incidence (4,5). 

Most infants in recent years have been found to be exposed to high levels of mercury and toxic metals through vaccines, mother’s amalgam dental fillings, and other sources(8), with toxic metals documented to block the enzymatic processes needed to digest casein and gluten. Studies have found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein in cow’s milk(9,4,etc.).  In vitro the bioactive peptide beta-casomorphin 7 (BCM-7) is yielded by the successive gastrointestinal proteolytic digestion of bovine beta-casein variants A1 and B, but this was not seen in variant A2 (4,498). In hydrolysed milk with variant A1 of beta-casein, BCM-7 level is 4-fold higher than in A2 milk. Consumption of the beta-casein A1 variant had a strong correlation to diabetes incidence (r = +0.726). Even more pronounced was the relation between beta-casein (A1+B) consumption and diabetes (r = +0.982).(4a) These latter two cow caseins yield a bioactive peptide beta-casomorphin-7 after in vitro digestion with intestinal enzymes whereas the common A2 variant or the corresponding human or goat caseins do not. BCM-7 has also been found to be a factor in autism and schizophrenia. Mercury and toxic metals have been found to disable the enzymatic process required to digest casein(9).

 

A1 is the most frequent in Holstein-Friesian (0.310–0.660), Ayrshire (0.432–0.720) and Red (0.710) cattle(4b,498). In contrast, a high frequency of A2 is observed in Guernsey (0.880–0.970) and Jersey (0.490–0.721) cattle as well as Asian and African cattle. BCM-7 may play a role in the aetiology of many human diseases including diabetes, neurological, immune, and cardiovascular(498) . Epidemiological evidence from New Zealand claims that consumption of beta-casein A1 is associated with higher national mortality rates from ischaemic heart disease. It seems that the populations that consume milk containing high levels of beta-casein A2 have a lower incidence of cardiovascular disease and type 1 diabetes. BCM-7 has also been suggested as a possible cause of sudden infant death syndrome. In addition, neurological disorders, such as autism and schizophrenia, apprear to be associated with milk consumption and a higher level of BCM-7(4b) 

Lactose Intolerance

Lactose (milk sugar), which is a major component of milk, is a disaccharide sugar made up of the simple sugars glucose and galactose(3). Lactase is an enzyme which facilitates digestion of lactose. Over 50% of non-Caucasians are lactose intolerant, to a significant degree and about 20% of Caucasians. Infants are most lactose tolerant but lactase activity declines dramatically over time so that by adulthood to about 5 to 10 % of the level of infants. Only a relatively small percentage of people retain enough lactase activity to absorb significant amounts of lactose throughout their adult life (3). Lactose intolerance results in undigested lactose in the intestines which often causes gas, bloating, abdominal discomfort, and proliferation of bacteria in the intestines. In addition to inhibiting the enzymes such as peptidases required to digest milk casein and whey, chronic mercury exposure in animals has also been found to inhibit lactase and glucose-6-phosphatase needed to digest lactose and other polysaccharides (32). Thus chronic exposure to mercury and toxic metals also increases lactose intolerance and digestion problems of carbohydrates in general. Digestive problems have been found to commonly be improved by reducing chronic mercury and toxic metal exposures. 

Lactose intolerance can also be alleviated to some degree by supplemental enzymes, using fermented milk products such as yogurt or kefir, or using only small amounts of milk products spread throughout the day(3). 

 

Rat study findings suggest that mercury-induced changes in RT6+ T 

lymphocytes appear to be related to the development of renal autoimmune insulin-dependent diabetes mellitus disease in genetically predisposed BN rats(6). Treatment of a strain of rats that are more prone to diabetes than other strains with mercury chloride results in significantly higher incidences of autoimmunity to thyrogobulin and laminin(30). Mercury has been documented to cause autoimmune conditions like thyroiditis, MS, Lupus, eczema, etc. and people who replace amalgam fillings commonly recover or significantly improve from these conditions(369b). 

Another study found that the age or timing of vaccinations containing mercury thimerosal affects the incidence of diabetes in rats(31). Vanadium, uranium, and other toxic metals have also been found to damage pancreatic islet cells and be a factor in diabetes(490). 

Until mercury thimerosal was removed from most vaccines, vaccines were the largest source of mercury in most infants and young children(8a) and exposures far more than Government health guidelines were common. Dental amalgam has been documented to be the largest source of mercury in most who have several amalgam mercury fillings(500) with high typical exposures far more than Gov’t health guidelines. Dental amalgam has been documented to be the largest source of mercury in most mothers with several amalgam fillings and the largest prenatal mercury exposure source to the fetus, as well as significant source of mercury exposure in infants (501). 

Mercury causes release of inflammatory cytokines such as Tumor Necrosis Factor-alpha(TNFa) and Interleukin-4 which are documented to be factors in the chronic inflammatory conditions, cell death, and damage to the immune system. (47,65,101) TNFa(tumor necrosis factor-alpha) is a cytokine that controls a wide range of immune cell response in mammals, including cell death(apoptosis). Mercury has been shown to induce TNFa, deplete glutathione, and increase glutamate, dopamine, and calcium related toxicity, causing inflammatory effects and cellular apoptosis in immune cells(47). Cell signaling mechanisms like sphingolipids are part of the control mechanism for the TNFa apoptosis mechanism(101). Glutathione is an amino acid that is a normal cellular mechanism for controlling apoptosis. When glutathione is depleted, reactive oxidative species increased, and CNS and cell signaling mechanisms are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results and cellular damage. Oxidative stress including methylmercury-induced oxidative stress causes pancreatic beta-cell apoptosis (programmed cell death) and dysfunction(491,492,493,499). Thimerosal has similar toxicity to methyl mercury(8a) and dental amalgam is a significant source of methyl-mercury in those with amalgam fillings(500). 

Both immune cell type Th1 and Th2 cytokine responses are involved in autoimmunity(425c). Mercury has been found to affect both Th1 and Th2 cytokines causing an increase in inflammatory Th2 cytokines(152,181,285,404b) as well as in Th1 cytokines in some circumstances(6). In the pancreas, the cells responsible for insulin production can be damaged or destroyed by the chronic high levels of cytokines, with the potential of inducing type I or II diabetes - even in otherwise healthy individuals with no other risk factors for diabetes(502). Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam filings and normalizing of blood sugar(35,502). Mercury exposure also increases insulin resistance(505). 

Mercury exposure causes an approximately 1.8-fold increase in glucose transport. This glucose transport corresponds with an increase in GLUT 1 glucose transporters. Phosphorylation of p38 kinase increased with mercury exposure. Activation of p38 and an increase in glucose transport corresponding to an increase in GLUT 1 are indicative the induction of a stress response, which can contribute to the induction of insulin resistance in adipocytes. While the magnitude of the action of mercury is modest, its effects were sustained over many days of exposure and impacted subsequent insulin-mediated glucose transport. Pre-treatment with HgCl2 decreased insulin-mediated glucose transport 1.3-fold suggesting that exposure to mercury may contribute to pathologies associated with glucose homeostasis(10).

Studies have also found evidence of a connection between low levels of zinc and childhood-onset diabetes(72) . Zinc is an antagonist to toxic metals like cadmium and mercury, and adequate levels are required to balance the adverse effects of these toxic metals on cellular calcium and other enzymatic processes(28,74). Mercury reduces the bloods ability to transport essential nutrients such as calcium, magnesium, and zinc; and has an adverse effect on cellular levels of these essential minerals, as well as blocking the function of magnesium and zinc in cellular enzymatic functions(43,96,198,338). Part of the toxic effects of mercury, cadmium, lead, etc. are through their replacing essential minerals such as zinc at their sites in enzymes, disabling the necessary enzymatic processes. Other connections between mercury and type 1 diabetes have also been demonstrated. Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam filings and normalizing of blood sugar(35). 

  Dr. J. Bart Classen discovered it would be possible to study the effect of Hemophilus B immunization on the incidence of IDDM  using data from a large clinical trial  in Finland.  Dr. J. Bart Classen and D.C. Classen initiated and funded a collaboration with Dr. Tuomilehto in Finland. All children born in Finland between October 1st, 1985 and August 31st, 1987, approximately 116,000 were randomized to receive 4 doses of the HiB vaccine (PPR-D, Connaught) starting at 3 months of life or one dose starting at 24 months of life. Classen and Classen calculated the incidence of IDDM in both groups through age 10 and in an group which did not receive the HiB vaccine, a cohort which included all 128,500 children born in Finland in the 24 months prior to the Hemophilus vaccine study. Immediately following the completion of these two arms all children born in Finland over a two year period were randomized to receive 3 doses of the old PPR-D HiB vaccine or 3 doses of a newer HbOC HiB vaccine. The data supports  published findings that the immunization starting after 2 months of life is associated with an increased incidence of IDDM. Rises in diabetes have been seen in the UK and USA following the introduction of the hemophilus vaccine (99). Other studies have found that any vaccine that contains mercury or other substances that can induce autoimmunity can cause type I or II diabetes and that vaccinations are a common cause of autoimmunity(100). 

III. Insulin Resistance increases incidence of neurological conditions including Alzheimer’s

Higher insulin and glucose levels in the blood and deficiency of glucose in brain cells that need it has been found to lead to neurological problems such as Alzheimer’s (580,581). Diabetes also impacts memory by increasing the risk blood vessels will become obstructed, restricting blood flow to the brain.

High blood glucose levels also impact cognition through formation of sugar-related toxins called advanced glycation end products (AGEs). AGEs have been found to be a factor in aging, diabetes, and Alzheimer’s. Glycotoxins are formed when sugars interact with proteins and lipids, damaging the structure of proteins and membranes, rendering them less able to carry out their many vital processes. (581). Studies have shown that AGEs are a key factor in cross-linking of harmful beta-amyloid plaques in the brain that are implicated in Alzheimer’s. As previously documented mercury and aluminum exposure increase insulin resistance and amalgam replacement and detoxification reduce insulin resistance. Studies have also found that supplementation with chromium improves memory performance in individuals with mild memory loss, by reducing insulin resistance and increasing ability of cells to use insulin. 

IV. Effect of Persistent Organic Pollutants(POPs)

Effects of low-level exposure to some persistent organic pollutants (POPs) was surveyed in a large population (NHANES) survey(497). There was a strong dose-response relations between serum concentrations of six selected POPs and the prevalence of diabetes. Diabetes prevalence was strongly positively associated with lipid-adjusted serum concentrations of all six POPs. When the participants were classified according to the sum of category numbers of the six POPs, adjusted odds ratios were strongly significant for trend. The association was consistent in stratified analyses and stronger in younger participants, Mexican Americans, and obese individuals. Systemic detoxification has been found to be effective in reducing the levels of toxic metals and POPs and to lessen related adverse health effects. There are many alternatives for accomplishing this that have been demonstrated to have effectiveness. 

V Effective Treatment or Control of Diabetes 

Authorities referenced here suggest the following measures to prevent diabetes and insulin resistance: lower toxic exposure levels, control weight and lose weight if overweight, reduce body fat percentage where excessive, regular exercise, good diet using glycemic index or glycemic load information, take appropriate supplements in addition to a good multivitamin/multimineral supplement(see below), monitor blood glucose level . 

For those with several amalgam dental fillings and diabetes, amalgam replacement and detoxification commonly results in significant improvement (499,598,etc.). Reduced consumption of excitoxins like MSG and aspartame and of high fructose corn syrup and other omega 6 oils along with increased consumption of magnesium and omega 3 oils such as virgin olive oil and coconut oil have been found to reduce brain inflammation and improve inflammatory conditions like insulin resistance, diabetes, depression, etc. (598,599,580,etc.). Drugs such as diuretics, blood pressure medications, steroids for asthma, arthritis, or allergies, prozac, and birth control pills that can increase insulin resistance and blood sugar (1). Drugs used to treat diabetes such as Avandia and Actos have been found to cause significant increases in cardiovascular disease and heart attacks, as well as increased risk of hip fracture(581b,FDA,etc.)

Other factors that have been found to be significantly associated with cardiovascular disease and diabetes include daily consumption of soda drinks, diet drinks, fried foods, or a “Western Diet” high in fried foods, refined grains, fast foods, soda, etc. and low in fruits and vegetables (590,598,580,1). These diet patterns all have been found to be significantly associated with metabolic syndrome, a cluster of cardiovascular disease and diabetes risk factors including elevated waist circumference, high blood pressure, elevated triglycerides, low levels of high-density lipoprotein (HDL or "good") cholesterol, clogged arteries, and high fasting glucose levels. The presence of three or more of the factors increases a person's risk of developing diabetes and cardiovascular disease. Avoidance of these dietary causes of insulin resistance and metabolic syndrome along with exercise such as walking, have been found to be highly effective at preventing or controlling these conditions (1, 598 ,etc.)  Some carbohydrates elevate blood glucose almost instantly -- others much more slowly. The Glycemic Index (GI) is a measure of how quickly carbohydrates elevate glucose. A lower number indicates a slower glucose rise -- and better glucose control. Monitoring and avoiding high glycemic foods along with exercise have been found to be effective in controlling insulin resistance(1c). 

Oily fish, greens(chlorophyll) and Fenugreek are too foods that have been documented to be effective in helping to control insulin resistance(1a). Other foods supportive of controlling blood sugar include foods with high fiber content, whole grain bread, brown rice, dried beans and peas, fresh vegetables and fruit (1a). Glycemic Load (GL) takes into account not only the quality of carbohydrate but also quantity and its effects. 

Several studies have documented that lipoic acid(an antioxidant and chelator) resulted in improvement in the majority of diabetes cases it was used for, by improving glucose metabolism, increasing insulin sensitivity, and reducing nerve damage(including in diabetic neuropathy)(502e) Lipoic acid is also a mercury chelator, commonly used for that purpose. 

Several supplements have been found to be significantly effective in promoting healthy blood glucose metabolism. These include Gymnema sylvestre, bitter melon, N-acetyl-cysteine (NAC), Vitamin C and E, Goat’s Rue, Cinnamon, Quercetin, Vanadyl sulfate, Bitter melon, PolyGycopleX(PGX) (581,1). Nutrients that have been found effective at blocking AGEs include: Carnosine, Vitamin B1 and B6, NAC, Guava, chromium, Pycnogenol, B7, magnesium, and Yerbamate (581). 

Several types of organ damage can be caused by diabetes/insulin resistance. Diabetic neuropathies are one such. Supplements documented to help with such neuropathies include lipoic acid, Vit B6 and B12, Folic Acid, Fish oil, and Huckleberry leaf tea(1a). Diabetes can also be a factor in vision problems such as cataracts and diabetic retinopathy. Supplements found to help with these conditions include Taurine, bilberry, lycopene (1a). CAN-C drops (N-acytyl-Carnosine) have been found to be effective  at reducing or reversing damage cataracts or other vision problems (582). Acetyl-L carnitine(ALC) reduces effects and pain of diabetic neuropathy(581b). 

Supplements found to help with diabetic related kidney damage include Taurine, melatonin, and cranberry proanthocyanidins (1a). Supplements found to help with diabetic related cardiovascular conditions include L-Arginine, L-Carnitine, and Hawthorne which can be found in hawthorne tea or supplements (1a). 

Chromium has been found to aid insulin transportation into cells. Cinnamon has been found to lower blood sugar levels. Lipoic acid has been found to improve glucose balance for people with type II diabetes. CoQ10 has cardiovascular benefits and prevents high blood pressure in people with blood glucose control problems. (581b)

VI. Diabetes Tests: 

Fasting Glucose Test(optimal: 76-81 mg/dL, normal: 82-85 mg/dL prediabetic: 86-125, diabetic: >126 mg/dL), Glucose test insulin level: (optimal: =< 7mcU/ml, prediabetic: 8-25 mcU/ml, diabetic: >25 mcU/ml); Fasting Glucose Tolerance Test with glucose and insulin levels: (normal: glucose < 140 mg/dL & insulin level <55 mcU/ml, prediabetic: blood glucose level of 140 to 159 mg/dL or insulin level of 56-90 mg/dl, dangerous: glucose> 160 mg/dL or insulin >90 mcU/ml); Hemoglobin A1C(HbAiC) (measures damage to blood proteins by free radicals created) (normal: 4.5-4.9%, prediabetic: 5-6.9%, Diabetic: >7%)

References:

(1) (a)The 24 Hour Pharmacist, S. Cohen, R. Ph., Rodale Press, 2008; & (b) STRIDDE, NIH, Amer. J. of Cardiology, Dec 2007; & Effect of Diet and Exercise Intervention on Blood Pressure, Insulin, Oxidative Stress, and Nitric Oxide Availability; Christian K. Roberts, PhD; Nosratola D. Vaziri, MD; R. James Barnard, PhD; Circulation. 2002;106:2530.; & Effect of a short-term diet and exercise intervention on oxidative stress, inflammation, MMP-9, and monocyte chemotactic activity in men with metabolic syndrome factors; Christian K. Roberts, Dean Won, Sandeep Pruthi, Silvia Kurtovic, Ram K. Sindhu, Nosratola D. Vaziri, and R. James Barnard; J Appl Physiol 100: 1657-1665, 2006. (high fiber, low fat diet) ; & (c ) Stuart A. Seale, MD, medical director of Lifestyle Center of America, a diabetes center in Sedona, Arizona,  The 30-Day Diabetes Miracle (Perigee). www.diabetesmiracle.org.

(3) Understanding Nutrition, 11th Edition; E. Whitney, S.R. Rolfes, Wadsworth Cengage Learning, 2008, p 110,111, etc. 

(4) Type I (insulin-dependent) diabetes mellitus and cow milk:
casein variant consumption. Diabetologia 1999 Aug;42(8):1032;
Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE; & (b) Polymorphism of bovine beta-casein and its potential effect on human health, J Appl Genet 48(3), 2007, pp. 189–198, Stanis³aw Kamiñski1, Anna Cieoeliñska1, El¿bieta Kostyra2 ; &(c)Sokolov OIuKost NV et al,
 [Regulatory peptides and psychomotor development in infants], Vestn Ross Akad Med Nauk. 2007;(3):33-9 & Influence of human B-casomorphin-7 on specific binding of 3H-spiperone to the 5-HT2-receptors of rat brain frontal cortex;  Protein Pept Lett. 2006;13(2):169-70; &(d) Dubynin VA, Malinovskaia IV, et al; Delayed effect of exorphins on learning of albino rat pups], [Article in Russian] Izv Akad Nauk Ser Biol. 2008 Jan-Feb;(1):53-60; & (e) Findings in normal rats following administration of gliadorphin-7 (GD-7), Sun Z, Cade R. Peptides. 2003 Feb;24(2):321-3

(5) Early infant feeding and risk of type 1 diabetes mellitus-a nationwide population-based case-control study in pre-school children. Diabetes Metab Res Rev. 2007 Oct 29, Rosenbauer J, Herzig P, Giani G.; & Environmental risk factors in prediction of childhood prediabetes.  Skrodenienė E, Marčiulionytė D, Padaiga Z, Jašinskienė E, Sadauskaitė-Kuehne V, Ludvigsson J. Medicina (Kaunas). 2008;44(1):56-63; & Worldwide childhood type 1 diabetes incidence--what can we learn from epidemiology?  Pediatr Diabetes. 2007 Oct;8 Suppl 6:6-14, Soltesz G, Patterson CC, Dahlquist G; EURODIAB Study Group.

(6) Reduction of the RT6.2+ subset of T lymphocytes in brown Norway rats with mercury-induced renal autoimmunity.  Cell Immunol. 1991 Jun;135(1):154-67, Kosuda LL, Wayne A, Nahounou M, Greiner DL, Bigazzi PE.

(8) The mercury/vaccine connection to recent increases in autism and ADHD. B. Windham(Ed), Annotated bibliography www.myflcv.com/kidshg.html & www.myflcv.com/tmlbn.html (over 400 peer-reviewed references) http://www.myflcv.com/autismgc.html

(9) Mercury/toxic metal/vaccine related enzymatic blockages in digestion of casein and gluten as common cause of schizophrenic behavior in autism and schizophrenia, B. Windham (Ed), 

(10) Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Barnes DM, Kircher EA. Toxicol In Vitro. 2005 Mar;19(2):207-14.
(11)
 Walter Last, The Natural Way to Heal , page 309

(12) Differential involvement of Th1 and Th2 cytokines in autoimmune diseases. Autoimmunity. 1996;24(1):25-33, Kroemer G, Hirsch F, González-García A, Martínez C.

(13)(a) S.Hussain et al, “Mercuric chloride induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain”,J Environ Sci Health B 1997 May;32(3):395 409; & P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36 ; & D.Jay, “Glutathione inhibits SOD activity of Hg”, Arch Inst cardiol Mex, 1998,68(6):457-61 &(b) S.Tan et al, “Oxidative stress induces programmed cell death in neuronal cells”, J Neurochem, 1998, 71(1):95-105; & Matsuda T, Takuma K, Lee E, et al. Apoptosis of astroglial cells [Article in Japanese] Nippon Yakurigaku Zasshi. 1998 Oct;112 Suppl 1:24P-;  & Lee YW, Ha MS, Kim YK.. Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells. Neurochem Res. 2001 Nov;26(11):1187-93. & (c)Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002 Dec 1;70(5):694-702;

(14) Kurek M, Przybilla B, Hermann K, Ring J. An opioid peptide from cows milk, beta-casomorphine-7, is a direct histamine releaser in man. Int Arch Allergy immunol 1992; 97(2): 115-20.

(15) Tejwani GA, Hanissian SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal ions and histidine. Neuropharmology 1990; 29(5): 445-52.

(16) Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. J Inorg Biochem 1996; 62(4): 271-9; &Lead and mercury mutagenesis: Role of H2O2, superoxide dismutase, and xanthine oxidase,  Maria E. Ariza, Gautam N. Bijur, Marshall V. Williams, Environ. Mol. Mutagen. 31:352-361, 1998; & Naidu BV, Fraga C, Salzman AL, Szabó C, Verrier ED, Mulligan MS. 2003. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant 22:784-93; &

Liaudet L, Szabó G, Szabó C. 2003. Oxidative stress and regional ischemia-reperfusion injury: the peroxynitrite – PARP connection. Coronary Artery Dis. 14:115-122; & Naidu BV, Fraga C, Salzman AL, Szabó C, Verrier ED, Mulligan MS. 2003. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant. 22: 784-93; & Virág L, Szabó E, Gergely P, Szabó C. 2003. Peroxynitrite- induced cytotoxicity: mechanisms and opportunities for intervention. Toxicology Letters 140:113-124;& Xanthine oxidase and neutrophil infiltration in intestinal ischemia. Grisham MB, Hernandez LA, Granger DN.  Am J Physiol. 1986 Oct;251(4 Pt 1):G567-74 

(17) Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating agents: Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol 1978; 20(6): 729-35; & W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro effect of mercury on enzyme activities”, Environ Res, 1992, 57(1):96-106; & Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT; Gastrointestinal abnormalities in children with autistic disorder. J Pediatr 1999, 135:559-63.

(18) Mc Fadden SA, Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways. Toxicology, 1996, 111(1-3):43-65; &  Markovich et al, "Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat 1", Toxicol Appl Pharmacol, 1999,154(2):181 7; & Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide bonds. J Biol Chem 1991; 266(19): 12695-702; & T.L. Perry et al, “Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985, 18(4):482-489; &  Ceaurriz et al, Role of gamma  glutamyltraspeptidase(GGC) and extracellular glutathione in disposition of inorganic mercury",J Appl Toxicol,1994, 14(3): 201 

(19) Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996;10(6):435-40; & Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993 Jul;44(1):13-8; & Puschel G, Mentlein R, Heymann E, 'Isolation and characterization of dipeptidyl peptidase IV from human placenta', Eur J Biochem 1982 Aug;126(2):359-65; & Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta 1978; 82(1-2): 185-92; & Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174,etc., www.autismndi.com/

(20) Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998; 8(5): 278-84. 

(21) Crinnion WJ. Environmental toxins and their common health effects. Altern Med Rev 2000, 5(1):52-63.

(24) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999.  ;& Autism and Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000. http://www.feingold.org/Research/cade.html & http://www.paleodiet.com/autism/ ; & "Beta-casomorphin induces Fos-like immunoreactivity in discrete brain regions relevant to schizophrenia and autism" Autism March 1999 vol 3(1) 67-83; Sun, ZJ, Cade JR, et al ;http://aut.sagepub.com/cgi/reprint/3/1/67 &  A Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in Rats, J.R. Cade, Z. Sun , Univ of Florida, USA , Autism, Vol. 3, No. 1, 85-95 (1999) DOI: 10.1177/1362361399003001007 © 1999 The National Autistic Society, SAGE Publications http://aut.sagepub.com/cgi/content/abstract/3/1/85 ; & Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone, Leboyer M, et al., Encephale 1993 Mar-Apr;19(2):95-102; & Food allergy and infantile autism. Lucarelli S, et al., Panminerva Med 1995 Sep;37(3):137-41; http://www.feingold.org/Research/autism.html ; & Peptides from Casomorphin & Gliadorphin, The Great Plains Laboratory, www.greatplainslaboratory.com/russian/glutencasein.html ; & Why Use the Gluten-Free and Casein-Free Diet in Autism and What the Results have Shown so Far, Peptides and Autism, Karl Reichelt, MD, PhD1 and A. M. Knivsberg PhD, Fall Defeat Autism Now!TM 2003 Conference *** Portland, Oregon *** October 3-5, 2003, http://www.autism.com/treatable/diet_reichelt.htm

(25) Reichelt KL. Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen 1994, 114(12):1432-4; & Reichelt KL et al, Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv 

Biochem Psychopharmocol 1981; 28: 627-43; Lucarelli S, Cardi E, et al, Food allergy and infantile autism. Panminerva Med 1995; 37(3):137-41; & Shel L, Autistic disorder and the endogenous opioid system. Med Hypotheses 1997, 48(5): 413-4; & 

(26) Huebner FR, Lieberman KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides 1984; 5(6):1139-47; & Wheat gluten as a pathogenic factor in schizophrenia. Singh MM, Kay SR, Science 1976 Jan 30;191(4225):401-2; & Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates.  Huebner FR,Lieberman KW, Rubino RP, Wall JS.  Peptides. 1984 Nov-Dec;5(6):1139-47; & Naloxone antagonises effect of alpha-gliadin on leucocyte migration in patients with coeliac disease. Horváth K, Gráf L, Walcz E, Bodánszky H, Schuler D. Lancet. 1985 Jul 27;2(8448):184-5

(28) Stewart-Pinkham, S M. The effect of ambient cadmium air pollution on the hair mineral content of children. The Science of the Total Environment 1989; 78: 289-96. 

(30) Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes-prone (DP) BB rats. Kosuda LL, Greiner DL, Bigazzi PE.Autoimmunity. 1997;26(3):173-87; & Chronic effects of methylmercury in rats. II. Pathological aspects.Eto K, Yasutake A, Miyamoto K, Tokunaga H, Otsuka Y.Tohoku J Exp Med. 1997 Jul;182(3):197-205

(31) Classen, JB, MD, "The Timing of Immunization Affects The Development of Diabetes in Rodents", Autoimmunity, 1996, 24:137-145.

(32) Changes in the activities of some digestive enzymes , exposed chronically to mercuric 

chloride; Sastry KV, Gupta PK. J Environ Sci Health B. 1980;15(1):109-19

(35) (a)Huggins HA, Levy,TEUniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc; & (b) Hal Huggins,Its All in Your Head, 1997; & (c) Huggins, HA,  Solving the MS Mystery: Help, hope and recovery, 2002; &(d) Toxic Elements Research Foundation, Colorado Springs Colorado, “Survery of 1320 patients being treated for heavy metal toxicity”, 2001. 800-331-2303; (e)Center for Progressive Medicine, 1999, 

autoimmune conditions (arthritis, diabetes, Lupus, Parkinson’s, Alzheimer’s, Leukemia, etc. )  www.myflcv.com/hgremove.html

(43) Knapp LT; Klann E. Superoxide induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem 2000 May 22; & Effect of zinc pretreatment on mercuric chloride-induced lipid peroxidation in the rat kidney. Toxicol Appl Pharmacol. 1984 May;73(3):395-401, Fukino H, Hirai M, Hsueh YM, Yamane Y.

(47) (a)Noda M, Wataha JC, Lockwood PE, Volkmann KR, Kaga M, Sano H. Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes Dent Mater. 2003;19(2):101-5; &(b) Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: differential modulation of NF- kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002 Aug;7(1):67-74; & (c) Dastych J, Metcalfe DD et al, Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999, 103(6):1108-14; & Hide I. [Mechanism of production and release of tumor necrosis factor implicated in inflammatory diseases] Nippon Yakurigaku Zasshi. 2003 Mar;121(3):163-73; & (e)Chen L, Nordlind K, Liden S, Sticherling M., Increased expression of keratinocyte interleukin-8 in human contact eczematous reactions to heavy metals. APMIS. 1996 Jul-Aug;104(7-8):509-14. 

(65) Badou A et al, “HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels”J Biol Chem. 1997 Dec 19;272(51):32411-8, & D.B.Veprintsev, 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha lactalbumin”.Biochem Mol Biol Int 1996 ;39(6): 1255 65;& A. Szucs et al, Cell Mol Neurobiol, 1997,17(3): 273-8; & D.Busselberg, 1995, “Calcium channels as target sites of heavy metals”,Toxicol Lett, Dec;82 83:255 61; Rajanna B et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203.

(72) Haglund B, Ryckenberg K, Selinus O, Dahlquist G. Evidence of a relationship between childhood-onset diabtes and low groundwater concentration of zinc. Diabetes Care 1996; 19(8): 873-5; & Harris Coulter, Childhood Vaccinations and Juvenile Onset (Type 1) Diabetes, Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 16, 1997,  www.909shot.com/hcdiabetes.htm

(74) Smith JB; Dwyer SD; Smith L. Cadmium evokes inositol polyphosphate formation and calcium mobilization. 

Evidence for a cell surface receptor that cadmium stimulates and zinc antagonizes. J Biol Chem 1989 May 5;264(13):7115 8.

(96) Goyer RA, National Institute of Environmental Health Sciences. Toxic and essential metal interactions. Annu 

Rev Nutr 1997; 17:37-50; & Nutrition and metal toxicity. Am J Clin Nutr 1995; 61(Suppl 3): 646S-650S; & Goyer RA et al, Environmental Risk Factors for Osteoporosis, Envir Health Perspectives, 1994, 102(4): 390-394; ; & Lindh U, Carlmark B, Gronquist SO, Lindvall A. Metal exposure from amalgam alters the distribution of trace elements in blood cells and plasma. Clin Chem Lab Med 2001 Feb;39(2):134 142.

(98) Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism. Vojdani A, Pangborn JB, et al, Int J Immunopathol Pharmacol. 2003 Sep-Dec;16(3):189-99.

(99) Dr. J. Bart Classen, Hemophilus Vaccine Study in Finland Proves a Causal Relationship Between Vaccines and Diabetes, Autoimmunity 35:247-253,2002,  http://www.vaccines.net/hemophil.htm &  (b) Dr. J. Bart Classen, Hemophilus Meningitis Vaccine Proven to Cause Diabetes in Clinical Trial of Over 100,000 Children, Autoimmunity, Vol 39, July 2004; &  © Congressional Testimony by Dr. J. Bart Classen regarding the link between vaccines and diabetes in the military.      http://www.whale.to/vaccines/classen3.html & Classen JB.   The diabetes epidemic and the hepatitis B vaccines. N Z Med J. 1996 Sep 27;109(1030):366.

(100) Childhood Vaccinations and Juvenile-Onset (Type-1) Diabetes by Harris Coulter, Ph.D. President, Center for Empirical Medicine Testimony before the Congress of the United States, House of Representatives,  http://www.whale.to/v/coulter.html

(101)(a) Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998 Aug 7;273(32):20354-62; & Pahan K, Raymond JR, Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide synthase in lipopolysaccharide- or cytokine-stimulated C6 glial cells. J. Biol. Chem. 274: 7528-7536, 1999; & Xu J, Yeh CH, et al, Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death. J Biol Chem. 1998 Jun 26;273(26):16521-6; & Dbaibo GS, El-Assaad W, et al, Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001 Aug 10;503(1):7-12; & Liu B, Hannun YA.et al, Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death.J Biol Chem. 1998 May 1;273(18):11313-20; 

(113) Discovery of aquaporins: a breakthrough in research on renal water transport.  Pediatr Nephrol. 1995 , Apr; 9(2):228-34; van Lieburg AF, Knoers NV, Deen PM; &(b) Importance of the mercury-sensitive cysteine on function and routing of AQP1 and AQP2 in oocytes. Am J Physiol. 1997 Sep;273(3 Pt 2):F451-6, Mulders SM, Rijss JP, Hartog A, Bindels RJ, van Os CH, Deen PM.

(152) Langworth et al, “Effects of low exposure to inorganic mercury on the human immune system”, Scand J Work Environ Health, 19(6): 405-413.1993; & Walum E et al, Use of primary cultures to sutdy astrocytic regulatory functions. Clin Exp Pharmoacol Physiol 1995, 22:284-7; &  J Biol Chem 2000 Dec 8;275(49):38620-5; & Kerkhoff H, Troost D, Louwerse ES. Infammatory cells in the peripheral nervous system in motro neuron disease. Acta Neuropathol 1993; 85:560-5; & Appel Sh, Smith RG. Autoimmunity as an etiological factor in amyotrophic lateral sclerosis. Adv Neurol 1995; 68:47-57.

(181) P.W. Mathieson, “Mercury: god of TH2 cells”,1995, Clinical Exp Immunol.,102(2):229-30; & (b) Heo Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine production in vitro and in vivo. Toxicol Appl Pharmacol, 196; 138:149-57; & (c) Murdoch RD, Pepys J; Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol 1986 80: 405-11;& (d) Parronchi P, Brugnolo F, Sampognaro S, Maggi E. Genetic and Environmental Factors Contributing to the Onset of Allergic Disorders. Int Arch Allergy Immunol 2000 Jan;121(1):2-9.

(198) Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in isolated eel hepatocytes. Aquat Toxicol. 2003 Jan 10;62(1):55-65, Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A. & Fluctuation of trace elements during methylmercury toxication and chelation therapy. Hum Exp Toxicol. 1994 Dec;13(12):815-23, Bapu C, Purohit RC, Sood PP; & E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957,p853

(285) R.C.Perlingeiro et al, “Polymorphonuclear phagentosis in workers exposed to mercury vapor”, Int J Immounopharmacology”, 16(12):1011-7,1994; & Hum Exp Toxicol 1995, 14(3):281-6; & M.L. Queiroz et al, Pharmacol Toxicol, 1994, 74(2):72-5; & (b) J.W.Albers et al, “Neurological abnormalities associated with remote occupational elemental mercury exposure”,Ann Neurol 1988, 24(5):651-9 ; & © L.Soleo et al, “Effects of low exposure to inorganic mercury on psychological performance”, Br J Ind Med, 1990, 47(2):105-9; & (d)P.J.Smith et al, “Effect of exposure to elemental mercury on short term memory”, Br J Ind Med 1983, 40(4):413-9.; & (e)M.S.Hua et al, “Chronic elemental mercury intoxication”, Brain Inj, 1996, 10(5):377-84; & (f) Gunther W, et al, Repeated neurobehavioral investigations in workers ..., Neurotoxicology 1996; 17(3-4):605-14; & (g) Levine SP; Cavender GD; Langolf GD; Albers JW. Elemental mercury exposure: peripheral neurotoxicity. Br J Ind Med 1982 May;39(2):136 9.

(303) Heavy Metals and Chronic Diseases , Dr. Dietrich Klinghardt, M.D., PhD, http://www.klinghardtacademy.com/Neural-Therapy/

 (338) (a)W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta”, Environ Res, 1992, 57(1):96-106;& “In vitro exposure to mercury and cadmium alters term human placental membrane fluidity”, Pharmacol, 1992, 116(1): 17-23; & (b)J.Urbach et al, Dept. of Obstetrics & Gynecology, Rambam Medical Center, Haifa, Israel, “Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption”, Reprod Toxicol, 1992,6(1):69-75;& © Karp W, Gale TF et al, Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters” Environmental Research, 36:351-358; & W.B. Karp et al, “Correlation of human placental enzymatic activity with trace metal concentration in placenta”, Environ Res. 13:470- 477,1977; & (d) Boot JH. Effects of SH blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct 1995 Jun;20(3):233 8;

 

(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and 

autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; & (b) Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuro Endocrinol Lett. 2004 Jun;25(3):211-8. . http://www.nel.edu/pdf_/25_3/NEL250304A07_Prochazkova_.pdf

(404) Romani L, Immunity to Candida Albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol 1999, 2(4):363-7; 

(424) Munch G; Gerlach M; Sian J; Wong A; Riederer P. Advanced glycation end products in neurodegeneration: more than early markers of oxidative stress? Ann Neurol 1998 Sep;44(3 Suppl 1):S85 8. 

(425) (c) Hu H; Moller G; Abedi Valugerdi M. Mechanism of mercury induced autoimmunity: both T helper 1  and T helper 2 type responses are involved. Immunology 1999 Mar;96(3):348 57;

(450) H.J. Roberts, M.D.,F.A.C.P., F.C.C.P. Adverse health effects from THE USE OF PRODUCTS CONTAINING ASPARTAME (NUTRASWEET) BY PERSONS WITH DIABETES AND HYPOGLYCEMIA. 

Aspartame & Diabetes references  https://articles.mercola.com/sites/articles/archive/2012/08/09/artificial-sweeteners-worse-than-sugar.aspx; &

https://usrtk.org/sweeteners/aspartame_health_risks/

 

(485) Hulda Clark, The Cure for all Diseases, 2000, (amalgam replacement, dental revision, detoxification, and treatment for parasites) https://alternativa-za-vas.com/support-files/cure_for_all_diseases.pdf

(489) Estevez AG,Beckman JS et al, Induction of nitric oxide dependent apoptosis in motor neurons by zinc deficient superoxide dismustase. Science 1999 Dec 24;286(5449): 2498 500;

(490) Metals, toxicity and oxidative stress., Valko M, Morris H, Cronin MT.  Curr Med Chem. 2005;12(10):1161-208 & & Free radicals and antioxidants in normal physiological functions and human disease.  Int J Biochem Cell Biol. 2007;39(1):44-84. Epub 2006 Aug 4,  Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J. 

(491) American Chemical Society, Chemical Research in Toxicology. Aug. 21, 2006 & Mercury Compound Found In Fish Damages Pancreatic Cells. ScienceDaily (Sep. 29, 2006), &  Shing-Hwa Liu et al, New Scientist, 30 September 2006 , Diabetes spotlight falls onto fish

(492) Diabetes and Mercury Poisoning, International Medical Veritas Association
October, 2006   
http://www.imva.info/med_dia_mercury_poisoning.shtml ; & DNA and Mitochondrial Time Bombs: Uranium, Mercury and Diabetes Nourished Magazine Mark Sircus

(493) Kajimoto, Y., and Kaneto, H. (2004) Role of oxidative stress in pancreatic beta-cell dysfunction. Ann. N. Y. Acad. Sci. 1011, 168-176.

(494) (a)Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res 2000 Feb;32(2):115-24(PMID: 10653482; & (b)Li Y, Liu L, Barger SW, Mrak RE, Griffin WS. Vitamin E suppression of microglial activation is neuroprotective. J Neurosci Res 2001 Oct 15;66(2):163-70.

(496) Doble A. The role of excitotoxicity in neurodegenerative disease: implications for therapy. Pharmacol Ther 1999 Mar;81(3):163 221;

(497) A Strong Dose-Response Relation Between Serum Concentrations of Persistent Organic Pollutants and Diabetes: Results from the National Health and Examination Survey 1999–2002,  D Lee, B Baker, D Jacobs et al, Diabetes Care, July 2006 vol. 29 no. 7 1638-1644 (& ADA)

(498) Devil in the Milk Illness, Health, and the Politics of A1 and A2 Milk , Keith Woodford & Thomas Cowan, MD, Chelsea Green Publishing, 2009 www.westonaprice.org/Devil-in-the-Milk-by-Keith-Woodford.html & http://articles.mercola.com/sites/articles/archive/2010/04/27/does-drinking-milk-cause-upperrespiratory-congestion.aspx

(499) Review: health effects caused by mercury exposure, www.myflcv.com/amalg6.html (over 3000 peer-reviewed medical studies cited including recoveries after amalgam replacement and detoxification) 

& Results of replacement of dental amalgam fillings, www.myflcv.com/hgrecovp.html & www.myflcv.com/hgremove.html

(500) Dental amalgam is the largest source of mercury in people with several amalgam fillings and a significant source of methyl-mercury, Review article, www.myflcv.com/damspr1.html

(501) Exposure levels and effects of prenatal and neonatal mercury exposures to infants, Review, B.Windham(Ed), over 150 peer-reviewed studies, www.flcv.com/fetaln.html

(502) (a)Dr. Gerald Bernstein, Beth Israel Medical Center, NY, past Pres., Amer. Diabetes Association; & . U.S. Centers for Disease Control, 2001, www.mercola.com/2000/sept/17/diabetes_epidemic.htm; 

& Anthony Iacopino.Conference Paper,American Academy of Periodontology(AAP)at 

the US National Institutes of Health in Bethesda, Maryland, April, 2001; & (b) Diabetes: A Silent Epidemic, Newsweek, Sep 4, 2000Harris Coulter, Childhood Vaccinations and Juvenile Onset (Type 1) Diabetes, Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 16, 1997, ; & (c) Dr. Bart Classen, Vaccines are the largest cause of insulin-dependent diabetes in young children, paper given at American College for Advancement in Medicine., Nashville, Tenn., May 14, 2001; &  Classen B. ,Autoimmunity August 2002 Vol. 35 (4), pp. 247-253 & Swedish researchers, Ann. N.Y. Acad Sci. 958: 293-296, 2002, &

  1. Narayan KMV, Boyle JP,Lifetime risk for diabetes mellitus in the U.S. JAMA, 2003, 290(14):1884-90; & (e) W. Block, Lipoic Acid Helps Fight Diabetes, Life Enhancement, Dec 2003; www.life-enhancement.org http://www.vaccination.org.uk

(505) Simultaneous exposure of non-diabetics to high levels of dioxins and mercury increases their risk of insulin resistance. Chang JWChen HLSu HJLiao PCGuo HRLee CC. J Hazard Mater. 2011 Jan 30;185(2-3):749-55. 

(580) Life Extension Foundation, Life Extension, Jan 2009; & LEF (MDs), Disease Prevention and Treatment, Expanded 4th Edition, 2003. 

(581) Brain Health and Blood Sugar, Vitamin Research News, Vol 23, No. 1, Jan 2009, p1-5; & (b)  Bad Drugs, Good Alternatives, 2010, M Stengler et al, Bottom Line Publishing. 

(582) Efficacy of N-acetylcarnosine in the treatment of cataracts, Drugs R&D, 2002: 3(2): 87-103 &  Lipid peroxidation as a possible cause of human cataracts. N-acetylcarnosine as a potent ophthalmic drug for the treatment of human cataracts. Lecture by Mark Babizhayev Ph.D., at the 3rd Monte Carlo Anti-Aging Conference; &  N-acetylcarnosine, a natural histidine-containing dipeptide, as a potent ophthalmic drug in treatment of human cataracts. Peptides, Vol. 22 (6) (2001) pp. 979-994 &  Imidazole containing peptidomimetic NACA as a potent drug for the medicinal treatment of age-related cataract in humans. Journal of Anti-Aging Medicine, Vol. 3 No. 1 43- 62, 2000. &  The Natural Histidine-Containing Dipeptide N-alpha-acetylcarnosine as an antioxidant for ophthalmic Use. Biochemistry, Volume 65 (2000) number 5 &  N-alpha-acetylcarnosine is a prodrug of L-carnosine in ophthalmic application as antioxidant. Clin Chim Acta. 1996 Oct. 15; 254(1):1-21. &  Lipid peroxidation as a possible cause of cataract. Mech. Ageing Dev., 1988 July, 44(1): pp69-89. 

(590) Dietary Intake and the Development of the Metabolic Syndrome. The Atherosclerosis Risk in Communities Study , Pamela L. Lutsey MPH, Lyn M. Steffen PhD, MPH, RD*, and June Stevens PhD, MS, RD , Circulation, Jan 2008 (Journal of the American Heart Association) 

(595Insulin resistance-associated hepatic iron overload. Gastroenterology. 1999 Nov;117(5):1155-63, Mendler MH, Turlin B, Moirand R, et al. 

(596) Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc. 2008 Mar;83(3):333-42, Dandona P; & Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007;49(1):48-63, Vasdev S, Gill V, Singal P.

(597) Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol In Vitro. 2005 Mar;19(2):207-14.  Barnes DM, Kircher EA; & Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003 Oct;75(2):368-77. Epub 2003 Jul 25, Barnes DM, Hanlon PR, Kircher EA; & (b) Heavy metal-induced inhibition of active transport in the rat small intestine in vitro. Interaction with other ions. Comp Biochem Physiol C. 1986;84(2):363-8, Iturri SJ, Peña A; & Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980 May 8;598(1):100-14, Klip A, Grinstein S, Biber J, Semenza G.

(598) Overcoming Depression, Dr. Russell Blaylock, MD, The Blaylock Wellness Report, Vol 5, No. 3, March 2008, & Food Additives, What you eat can kill you, Vol 4, No. 10, Oct 2007, http://www.blaylockreport.com/

(599) High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. 2006 Dec;19(4):237-43. Rayssiguier Y, Gueux E, et al; & (b) Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006 Nov;84(5):1062-9 Bo S, Durazzo M, Pagano G. et al; & (c) Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome. Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):471-6. Guerrero-Romero F, Rodríguez-Morán

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        Dr. J. Bart Classen discovered it would be possible to study the effect of Hemophilus B immunization on the incidence of IDDM  using data from a large clinical trial  in Finland.  Dr. J. Bart Classen and D.C. Classen initiated and funded a collaboration with Dr. Tuomilehto in Finland. All children born in Finland between October 1st, 1985 and August 31st, 1987, approximately 116,000 were randomized to receive 4 doses of the HiB vaccine (PPR-D, Connaught) starting at 3 months of life or one dose starting at 24 months of life. Classen and Classen calculated the incidence of IDDM in both groups through age 10 and in an group which did not receive the HiB vaccine, a cohort which included all 128,500 children born in Finland in the 24 months prior to the Hemophilus vaccine study. Immediately following the completion of these two arms all children born in Finland over a two year period were randomized to receive 3 doses of the old PPR-D HiB vaccine or 3 doses of a newer HbOC HiB vaccine. The data supports  published findings that the immunization starting after 2 months of life is associated with an increased incidence of IDDM. Rises in diabetes have been seen in the UK and USA following the introduction of the hemophilus vaccine (see HIB)

Dr. J. Bart Classen, Hemophilus Vaccine Study in Finland Proves a Causal Relationship Between Vaccines and Diabetes, Autoimmunity 35:247-253,2002, http://www.vaccines.net/hemophil.htm

 

Congressional Testimony by Dr. J. Bart Classen regarding the link between vaccines and diabetes in the military.      http://www.whale.to/vaccines/classen3.html

 

 

 

 

Dr. J. Bart Classen, Hemophilus Meningitis Vaccine Proven to Cause Diabetes in Clinical Trial of Over 100,000 Children, Autoimmunity, Vol 39, July 2004

 

The study followed over 100,000 children which had been randomized in a large
clinical trial to receive 1 or 4 doses of the hemophilus vaccine and over
100,000 unvaccinated children.  After 7 years the group receiving 4 doses of
the vaccine had a statistically significant 26% elevated rate of diabetes, or
an extra 54 cases/100,000 children, compared to children who did not receive
the vaccine.  By contrast immunization against hemophilus is expected to
prevent only 7 deaths and 7 to 26 cases of permanent disability per 100,000
children immunized.  The study showed that almost all of the extra cases of
diabetes caused by the vaccine occurred between 3-4 years after vaccination. 
Furthermore the paper provides new data proving the vaccine causes diabetes in
mice and reviews data from 3 smaller human studies, which all had similar
results to the current study, but were too small to reach statistical
significance.

"Our results conclusively prove there is a causal relationship between
immunization schedules and diabetes.  We believe immunization schedules can be
made safer," stated Dr. Bart Classen.

 

Classen JB.   The diabetes epidemic and the hepatitis B vaccines. N Z Med J. 1996 Sep 27;109(1030):366.

 

Classen, JB, MD, "The Timing of Immunization Affects The Development of Diabetes in Rodents", Autoimmunity, 1996, 24:137-145.

 

Classen, J.B. Congressional Testimony on the connection between vaccines and diabetes, http://www.whale.to/v/classen.html