BIO Mary Nash Stoddard on Twitter

PRESENTING: MARY NASH STODDARD - Co-Founder of the massive international anti-aspartame movement in the mid 1980's, following the brain tumor death of her forty two year old husband, Mike. Ms. Stoddard suffered a life threatening aspartame-related blood disorder in 1985, whereupon, The NutraSweet Co. offered her an all-expense paid vacation for two anywhere in the world, if she would agree to be tested by their doctors. She declined, with the blessing of her doctor, and the rest is history. She has conducted multi-national lecture tours and is a popular visiting professor at colleges, universities and medical schools. "Deadly Deception - Story of Aspartame" is a toxicology sourcebook, edited by Ms. Stoddard, documenting the harmful effects of the world's most toxic artificial sweetener. The companion one hour "Deadly Deception" video is further documentation - taped at a prestigious scientific conference. Stoddard's efforts, over more than two decades, led to the present rejection of the sweetener by many of the food and beverage giants of industry, as they rush to distance themselves from the liabilities associated with use of a neuro-toxic substance in their products. She has testified in court as an Expert Medical Witness and like her counterpart, Erin Brokovitch, helped with a number of lawsuits on behalf of consumers. Her powerful message has reached millions around the world through the airwaves on radio and television, in print and through popular personal appearances. Honors, Awards, Societies: • Expert Medical Witness [1992-present] * Guest Presenter Gulf War Veterans Annual Conference - [Las Vegas 1999] * Visiting Professor: U. T. Southwestern Medical School [1997] * Visiting Professor: American University School of Journalism [1999] * Visiting Professor: University of North Texas at Denton Dept. of Science [1990 and 2005] • Visiting Professor: University of Houston Bioneers Conference [2006] * Invited speaker: Hebrew Univ. Jerusalem - [1997] * Keynote speech: Mexican Government's Annual Conference on Sweeteners [1999] * Appointed Judge - State of Texas [1977-1984] * Broadcast Journalist - [1965-present] * President's Council on Food Safety - [1998-1999] * International Lecture Tours - [1996-present] * Testimony Senate Committee Hearing on Safety of Aspartame - Washington [1987] * Panelist at National News Conference Announcing Dr. John Olney's Brain Tumor/Aspartame Connection - Washington D.C. [1998] * Inducted Member Texas Radio Hall of Fame [2002-present] Representative of the Texas Rice Growers Association [Miss Rice] Board member: Irving Symphony Orchestra Board Member: Irving Community Theater Founding Board Member Radio Station KNON [public radio], Dallas Charter member City of Dallas Citizens Safety Committee Board Member Dallas Mayor’s Fee Task Force Vice President Operation Get Involved, [liaison committee of the D.P.D.] Board member Dallas Homeowners League President Save Open Space Texas Steering Committee Presidential Election Award for Public Service - Mexican Government State of Texas Board of Adjustment
Showing posts sorted by relevance for query E.COLI. Sort by date Show all posts
Showing posts sorted by relevance for query E.COLI. Sort by date Show all posts

Wednesday, August 11, 2010

Aspartame Made from E-Coli Cultures

Proof of e-coli as a culture medium for amino acids in APM:

http://www.ias.ac.in/currsci/jul10/articles20.htm

Optimization of d-hydantoinase production


d-hydantoinase was produced as an inducible enzyme in most of the microbial strains reported. Hydantoinase production in Pseudomonas species, Agrobacterium species, and Peptococcus anaerobius was observed to be induced by various substrates and substrate analogues. d-hydantoinase production was maximally induced by uracil in Pseudomonasputida19, and Agrobacterium sp.33. An unmetabolizable substrate analogue, 2,4-thiouracil, enhanced hydantoinase production up to five fold in Agrobacterium sp.41. In P. fluorescens and Bacillus stearothermophilus SD1, the enzyme was produced constitutively, and substrates or substrate analogues were unable to induce the enzyme production42,43.

Although production of hydantoinase has been reported in many organisms, only few reports about the medium optimization are available. Meat and beef extract, when used as nitrogen source, enhanced d-hydantoinase production inP. putida19, and Bacillus SD1 (ref. 43). This may be due to the high pyrimidine and purine content in these complex meat-derived nitrogen sources44. Yeast extract was used as the nitrogen source in Pseudomonas sp.42, and A. radiobacter45. Glucose or glycerol was used as a carbon source in most of the cases for the production of d-hydantoinase. In a recent study46, medium optimization studies were carried out for the production of d-hydantoinase in A. radiobacter NRRL B 1229, wherein with the use of an empirical modeling technique (response surface method) Achary et al. were able to achieve 35 U/ml of enzyme activity and 1.69 mg/ml of biomass in optimized complex medium. The optimized medium contained molasses as the carbon source, and ammonium nitrate as the nitrogen source. Mass production of d-hydantoinase from batch culture of recombinant E. coli in minimal medium with glycerol as the sole carbon source has been reported by Lee et al.47. They achieved 50 g dry cell weight per litre of broth, and an enzyme yield of 38000 U/g DCW in a 50 litre fermenter. They also reported that d-hydantoinase gene, which is expressed under its own promoter, is catabolically repressed by glucose in the recombinant strain.

Recently, genes from thermophilic Bacillus sp. have been cloned by various groups43,79. A gene for nonspecific hydantoinase from B. stearothermophilus from genomic DNA which encoded a 471 amino-acid-long peptide was also cloned79. The nucleotide sequence of this gene had a homology of 91% with the sequence of d-hydantoinase from a gram-positive organism Lu1220 (ref. 80). d-hydantoinase gene from B. stearothermophilus SD1 was cloned and overexpressed inE. coli43. The cloned enzyme was expressed as 20% of the total protein in E. coli. d-hydantoinase protein sequence decoded from the gene sequence of d-hydantoinase from B. stearothermophilus SD1 showed 20–28% homology with other hydantoinases, allantoinase and dihydroorotase protein sequences. This sequence exhibited more than 89% identity with hydantoinase from other thermophiles. Among the hydantoinases from thermophiles, C-terminal regions of enzymes were completely different, implying thereby that C-terminal region plays an important role in the biochemical properties of the enzymes81. Dihydropyrimidinase gene cloned by c-DNA cloning from rat liver and human liver showed 40% similarity with the
d-hydantoinase gene sequences from various microorganisms.

43 Lee, D. C., Lee, S. G., Hong, S. P., Sung, M. H. and Kim, H. S., Ann. N. Y. Acad. Sci., 1996, 799, 401–405.

http://lib.bioinfo.pl/pmid:16466681
Metabolic engineering of the E. colil-phenylalanine pathway for the production of d-phenylglycine (d-Phg).

Ulrike Müller, Friso van Assema, Michele Gunsior, Sonja Orf, Susanne Kremer, Dick Schipper, Anja Wagemans, Craig A Townsend, Theo Sonke, Roel Bovenberg, Marcel Wubbolts
d-phenylglycine (d-Phg) is an important side chain building block for semi-synthetic penicillins and cephalosporins such as ampicillin and cephalexin. To produce d-Phg ultimately from glucose, metabolic engineering was applied. Starting from phenylpyruvate, which is the direct precursor of l-phenylalanine, an artificial d-Phg biosynthesis pathway was created. This three-step route is composed of the enzymes hydroxymandelate synthase (HmaS), hydroxymandelate oxidase (Hmo), and the stereoinverting hydroxyphenylglycine aminotransferase (HpgAT). Together they catalyse the conversion of phenylpyruvate via mandelate and phenylglyoxylate to d-Phg. The corresponding genes were obtained from Amycolatopsis orientalis, Streptomyces coelicolor, and Pseudomonas putida. Combined expression of these activities in E. coli strains optimized for the production of l-phenylalanine resulted in the first completely fermentative production of d-Phg.

courtesy: Aspartame Consumer Safety Network

Sunday, June 11, 2017

IS THERE E_COLI BACTERIA IN YOUR FAVE SWEETENER?

FECAL BACTERIA IN ASPARTAME and NEOTAME? D-Phenylalanine, 50% of Aspartame molecule, is cultured in a laboratory using Ecoli. Certain strains of the bacteria are known to cause illness, infections and even death, in some cases. Next time you hear media talk about an e.coli outbreak or epidemic somewhere, ask yourself this question: How many of the victims, (diagnosed with bacterial infections from exposure to e.coli in/on food sources), might also be reacting to their subsequent ingestion of Aspartame-sweetened products? Aspartame is routinely found in: gum; yogurt; diet beverages such as sodas, juices, sports drinks, flavored tea and waters, diet sodas, dental products, OTC medications and Rx meds for infants, children and adults. Be an alert consumer. Don't always take the most convenient or media-offered causes of an illness epidemic when you hear of one. Many illnesses and epidemics did not exist prior to the advent of Aspartame in our environment, in 1981. These include, but are not limited to: Chronic Fatigue Syndrome; Lyme disease; Alzheimers; Dementia; Obesity; Mental Illness; ADD; Autism; PTSD; Panic Anxiety Disorder; Suicidal Depressions; Bipolar; and, many forms of Cancer, which did not exist before the 1980s.
Visit ; http://www.aspartamesafety.com , marystod on Twitter; Mary_Nash_Stoddard  on Facebook for more.
-- Hon. Mary Nash Stoddard / toxicology sourcebook author Deadly Deception Story of Aspartame (Odenwald Press 1998)

https://marystod.blogspot.com/search?q=E.COLI

Friday, November 2, 2012

PREVENTION IS THE CURE - ASPARTAME OFTEN THE CAUSE


From the Townsend Letter
June 2011
Shorts
briefed by Jule Klotter

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Detecting Allergens
Doris J. Rapp, MD, has recently completed an 11-page booklet called Allergies: The Answers You Need Are Here. Rapp, one of the pioneers in identifying and treating environmental illness, is board certified in pediatrics and allergy and environmental medicine. This practical booklet explains how to recognize common and uncommon allergies and sensitivities. Most of us think that allergies manifest as itchy eyes and runny noses during pollen seasons, digestive and intestinal upsets when eating something that doesn't agree with us, or hives from a food. But allergies also cause many, many other symptoms. Young children can display hyperactivity, reluctance to keep clothes on, aversion to being touched, tics, twitches, seizures, and fatigue when exposed to allergens. Fatigue is also a symptom of allergy in older people. Other signs of allergen exposure in adults and older children include daily headaches, unexplained aggression or anxiety, sleep problems, fuzzy thinking, sudden mood changes, and sudden severe body odor (not eliminated by washing). Exposure to allergens (and toxic chemicals) can also produce a sudden difficulty with tasks that require motor coordination (writing, drawing, speaking, or walking). Most people do not realize the diverse and sometimes bizarre reactions that can arise when a sensitive person is exposed to an allergen or environmental trigger.

As Rapp explains in her new booklet, the first step in tracking down triggers is to keep a record or log of foods, other exposures, symptoms, and locations where symptoms occur. In particular, she says to be on the lookout for the following sudden changes: abnormally red earlobes or cheeks; dark eye circles; bags under the eyes; a spaced out, frightening or "demonic" look to the eyes; wiggly legs; or sudden shifts in emotions, behavior, and/or movement. In addition, blood pressure can rise and the pulse rate increase to 100 at rest.

Becoming aware of these changes and then continuously asking questions is the key to finding the environmental trigger: What is different? Where was I when my ability to breathe well decreased or increased? Why did this happen? What did I eat, touch or smell? Allergies: The Answers You Need Are Here offers ways to track down exposures that cause symptoms. It also explains how to identify problem foods by using a one-week multiple food allergy elimination diet. The booklet costs just $5 and is available at www.dorisrappmd.com.
Leaky Gut, Autoimmunity, and Celiac Disease 
Though it is often undetected, an estimated 1 person in 133 in North America has celiac disease (CD). This autoimmune disease is characterized by inherited hypersensitivity to gluten, a difficult-to-digest protein found in grains. Bacteria living in the gastrointestinal appear to influence genetic expression. Dr. Alessio Fasano says in an article for Scientific American, "… a person whose immune system has managed to tolerate gluten for many years might suddenly lose tolerance if the microbiome [gut flora] changes in a way that causes formerly quiet susceptibility genes to become active." Stress and other factors may also turn on the susceptibility genes.

At this time, celiac disease is the only autoimmune disease whose environmental trigger (gluten) has been identified. In people with celiac disease, gluten protein fragments (peptides) stimulate the immune system to attack the gut, producing chronic inflammation and damaging the villi. (The villi in the small intestine transport nutrients across the gut wall to the bloodstream.) Impaired nutrient absorption produces a numerous and often unrecognized effects. "By robbing the body of particular nutrients," Fasano explains, "CD can thus produce such symptoms as osteoporosis, joint pain, [anemia, neurological problems,] chronic fatigue, short stature, skin lesions, epilepsy, dementia, schizophrenia, and seizure." Diarrhea, pain, and persistent indigestion are the most recognized symptoms. Staying on a gluten-free diet is the treatment for celiac disease and lets the small intestine heal.

In addition to a heightened immune response, people with acute or active celiac disease have elevated levels of the protein zonulin. Zonulin regulates permeability, which allows fluids and the substances that they carry to move from the gut to the bloodstream and from the blood into the brain. Increased gut permeability, also called leaky gut, characterizes many autoimmune diseases including celiac disease, type 1 diabetes, multiple sclerosis, and rheumatoid arthritis. Fasano, whose team discovered zonulin, helped set up Alba Therapeutics to investigate the therapeutic possibilities of a zonulin inhibitor called Larazotide. Larazotide has decreased permeability, inflammation, and gastrointestinal symptoms in celiac patients in two placebo-controlled studies as of 2009. The US Food and Drug Administration has approved studies that explore Larazotide's use in type 1 diabetes and Crohn's disease.

Fasano A. Celiac disease insights: clues to solving autoimmunity. 
Sci Am. July 27, 2009. Available at: www.scientificamerican.com/article.cfm?id=celiac-disease-insights. Accessed March 16, 2011.
Levin EB. Researchers find increased zonulin levels among celiac disease patients [online press release]. University of Maryland Medical Center. March 21, 2008.www.umm.edu/news/releases/zonulin.htm. Accessed March 24, 2011.



Heavy Metals, Mercury Amalgams, and Autoimmunity
Heavy metals are among the environmental factors that trigger autoimmune disease in genetically susceptible people. While nickel, colloidal gold, and metals used occupationally have been linked to autoimmune disease, most research has focused on mercury, particularly mercury amalgams. Air pollution and contaminated seafood are other common sources of mercury exposure. Mercury, whose toxicity particularly affects nerves and kidneys, tends to accumulate in the body with chronic exposure. As with other autoimmune triggers (such as gluten), the severity of an individual's reaction depends on inherited sensitivity and the body's ability to deal with toxins.

Several clinical studies have linked mercury amalgam fillings to autoimmune diseases. In 1994, R. L. Siblerud and E. Kienholz compared blood tests from multiple sclerosis (MS) patients who had amalgams with texts from those who had had their amalgam fillings removed. Those with amalgam fillings had significantly lower levels of red blood cells, hemoglobin, hematocrit, thyroxine, total T-cells, and CD8+ suppressor cells. In addition, MS patients with amalgams had 33.7% more exacerbations during the previous 12 months than the group without amalgams.

Patients who show sensitivity to mercury, using MELISA lymphocyte stimulation tests, tend to improve when amalgams are removed, according to Czech research. In a 2004 study, 25 out of 35 autoimmune patients who had amalgams removed reported improved health and significantly decreased lymphocyte reactivity to inorganic mercury, silver, organic mercury, and lead with MELISA testing. Those who improved tended to show high reactivity to mercury at baseline. Amalgam removal also improved health in about 70% of patients with autoimmune thyroiditis in a 2010 Czech study. Mercury-specific lymphocyte responses in vitro and antithyroid autoantibodies normalized as well. As in the 2004 study, the patients who improved were those who initially showed lymphocyte reactivity to mercury. Apparently, individual sensitivity plays a greater role than does exposure. In a metal-sensitive person, even a small exposure causes systemic reactions. Studies that have sought to connect the number and size of amalgams to the severity of symptoms have usually found no correlation.

In addition to genetic predisposition, nutrition, stress, and pathogens can increase a person's sensitivity to environmental triggers like heavy metals. "Considering the complexity of the immune system and its interaction with the nervous and endocrine systems," Stejskal and Stejskal write, "it is obvious that a combination of mechanisms is responsible for the induction of auto-immunity."

Aminzadeh KK, Etminan M. Dental amalgam and multiple sclerosis: a systematic review and meta-analysis [abstract]. J Public Health Dent. Winter 2007;67(1):64–66. Available at: www.ncbi.nlm.nih.gov/pubmed/17436982. Accessed March 24, 2011.
Hybenova M, Hrda P, Procházková J, Stejskal V, Sterzl I. The role of environmental factors in autoimmune thyroiditis [abstract]. Neuro Endocrinol Lett. 2010;31(3): 283–289. Available at: www.ncbi.nlm.nih.gov/pubmed/20588228. Accessed March 21, 2011.
Procházková J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. The beneficial effect of amalgam replacement on health in patients with autoimmunity [abstract]. Neuro Endocrinol Lett. June 2004; 25(3):211–218. Available at:www.ncbi.nlm.nih.gov/pubmed. Accessed March 24, 2011.
Schiraldi M, Monestier M. How can a chemical element elicit complex immunopathology? Lessons from mercury-induced autoimmunity. Trends Immunol.2009. Available at www.toxcenter.de/artikel/Quecksilber-crasht-Autoimmunitaet.pdf. Accessed March 18, 2011.
Siblerud RL, Kienholz E. Evidence that mercury from silver dental filings may be an etiological factor in multiple sclerosis [abstract]. Sci Total Environ. March 15, 1994;142(3):191–205. Available at www.ncbi.nlm.nih.gov/pubmed/8191275. Accessed April 12, 2011.
Stejskal J, Stejskal VDM. The role of metals in autoimmunity and the link to neuroendocrinology. Neuroendocrinol Lett. 1999:20;351–364. Available at: www.i-gap.info/app/dokumente/Autoimmunity%20and%20metals.pdf. Accessed March 17, 2011.
Methanol and Multiple Sclerosis
What do canned fruits and vegetables, cigarette smoke, and aspartame have in common? All are sources of methanol (wood alcohol), a known toxin that produces symptoms identical to those of multiple sclerosis (MS). In an heavily referenced 2007 article, retired food science professor Woodrow C. Monte, PhD, presents a convincing argument that links methanol consumption to the growing rate of multiple sclerosis worldwide. "The symptoms of multiple sclerosis, chronic and acute methanol poisoning, and Aspartame toxicity are in all ways identical," Monte writes. Headaches, memory loss, nervousness, depression, tingling sensations, pain in the extremities, optic neuritis, bright lights in the visual field, seizures, and inability to urinate or to keep from urinating characterize all three conditions.

French neurologist Jean-Martin Charcot presented the first documented case of multiple sclerosis during a lecture in 1868. Although the disease was rare, Monte says that incidence rose as access to canned fruits and vegetables increased. The first food cannery, devoted primarily to canning meats at first, opened in England around 1813. Gradually, the canning industry grew and began to process fruits and vegetables as well. As canned foods became more common, prices declined; and more people began using them. Monte says, "… when the fruits and vegetables and their naturally occurring pectin is placed in a sealed container (as in canning) that is then sterilized, heated or even just stored at room temperature for months, the normally unavailable, chemically bound methanol is released from the pectin. The methanol slowly builds up, trapped in the container, to hundreds of times more than when fresh. Very simply it is canned fruits and vegetables that were (before aspartame) the major source of free methanol in the human diet." Canned and bottled fruit juices and also tomatoes (fresh and canned) have high methanol levels. Fresh juice, made and consumed within minutes, has little or no free methanol. Depending upon the fruit, methanol levels in fresh juice rise within 30 minutes of storage. Tobacco leaves also have pectin-bound methanol. Fermentation of tobacco leaves, part of the manufacturing process, separates the plant's methanol from its pectin. Cigarette smoking is known to trigger MS relapses.

In addition to pectin, unprocessed fruits and vegetables have another safeguard against methanol's toxic effects: ethanol. Ethanol is a "natural outcome of digesting plant material in the gut," Monte explains. Both ethanol and methanol are broken down by alcohol dehydrogenase (ADH), an enzyme found throughout the body. ADH prefers to metabolize ethanol, which becomes acetylaldehyde and acetic acid. When ethanol isn't available or when the methanol level is 10 times greater than ethanol's, ADH turns its attention to methanol. Here is the source of methanol's toxicity. ADH breaks methanol down into formaldehyde and then into formal hydrate (formic acid). Formaldehyde causes cancer and birth defects. Formal hydrate, an extremely acidic and powerful esterifying agent, readily reacts with proteins, including the proteins in myelin, the insulation that protects nerve fibers in the central nervous system. Monte says: "… the location of ADH in our bodily tissue seems to vary with our genetic makeup. ADH might, for reasons not fully understood, be found in the liver, gut, brain, eye, skin and sinew. These hereditary differences are most likely responsible for the varied manifestations of autoimmunity. Higher enzyme representation in the brain might predispose the individual to develop MS while its presence in the skin would be required for the evolution of lupus." The chemical sweetener aspartame breaks down into two amino acids (phenylalanine and aspartic acid) and methanol (wood alcohol). Unlike plants, aspartame has neither pectin nor ethanol to mitigate the damage produced by methanol.

For decades, MS has been more prevalent in cooler latitudes. While people in tropical climates are exposed to more sunshine (and vitamin D), they also have access to an abundance of fresh fruits and vegetables and lower consumption of canned foods. The exceptions have been Australia and New Zealand, where canned foods are inexpensive and common and MS rates have been high. In contrast, Japan, which lies at a cooler latitude, has had a low incidence of MS. The Japanese tend to eat fresh produce in season rather than rely on canned foods. In recent years, both Japan and countries with warmer climates are reporting higher MS rates and increased MS relapse rates during the summer – when aspartame-containing sodas, juices, and "thirst quenchers are most frequently consumed," Monte says.

"Viewing methanol toxicity as the ethnologic cause of MS seems to answer all of the nagging questions and unexplained anomalies that have stalled the cure for this increasingly persistent disease," Monte states. What if methanol triggers multiple sclerosis just as gluten triggers celiac disease?

Hou C-Y, Lin Y-S, Wang YT, Jiang C-M, Wu M-C. Effect of storage conditions on methanol content of fruit and vegetable juices [abstract] J Food Composit Anal. August 2008;21(5):410–415. Available at: www.sciencedirect.com. Accessed March 27, 2011.
Monte WC. A Deadly Experiment. Fitness Life. December 2007;34:38–42. Available at: http://thetruthaboutstuff.com/review2.html. Accessed March 19, 2011.
Monte WC. Methanol: Where is it found? How can it be avoided? [online article]. TheTruthAboutStuff.com.http://thetruthaboutstuff.com/published/Monte%20Diet.pdf. Accessed March 19, 2011.
Monte WC. Aspartame: methanol and the public health. J Appl Nutr. 1984;36(1). .
Managing Autoimmune Disease
Conventional medicine tends to view autoimmune illness as the result of an overstimulated immune system that attacks organs and tissues as if they were foreign invaders. "Immune suppression, the mainstream medical treatment of choice for auto-immune disorders, completely overlooks the upstream cause, toxic overload, and the downstream detoxification deficiency that leads to the immune system's confusion in distinguishing self from invader," write Jodi Friedlander, MS, and Ed Bauman, MEd, PhD. Autoimmune diseases such as rheumatoid arthritis, type 1 diabetes, systemic lupus erythematosis (SLE), Addison's disease, and Crohn's disease affect 5% to 8% of the US population. It is the third most prevalent type of illness after heart disease and cancer. According to the molecular mimicry hypothesis, amino acid sequencing (peptides) in pathogens and some body tissues are similar enough so that lymphocytes (particularly Th-1 cells from the thymus) attack invader and self. Normally, the body has regulating mechanisms that keep Th-1 and Th-2, which produce an allergic response, in balance. In autoimmune diseases, Th-1 dominates. Th-1 cells emit cytokines that produce inflammation.

While molecular mimicry appears to have a role in disease progression, it does not explain why the immune response becomes so imbalanced in the first place. Genetic variations that affect detoxification processes, sensitivity to specific antigens (e.g., the protein gluten), and/or immune reactivity make some people more prone to autoimmune diseases than others. As with many other diseases, genetics alone does not determine the presence and/or severity of autoimmune disease.

Friedlander and Bauman state that when a body becomes overwhelmed and is unable to eliminate foreign molecules (antigens), the antigens "can form complexes with antibodies and becomes part of our joints, nerves, and endocrine tissue." Agricultural and household chemicals, heavy metals, petrochemicals, prescription drugs, organic solvents, and silica have triggered autoimmune disease in genetically susceptible people. Stress is another trigger. "High levels of [the stress hormone] cortisol suppress the immune system," Friedlander and Bauman explain, "by reducing the amount of secretory IgA, the main mucosal antibody responsible for eliminating pathogens from the intestinal tract and in other mucus membranes [e.g., lungs]." With prolonged stress, the adrenals eventually produce less cortisol. Without cortisol to keep IgA in check, IgA reactions will produce inflammation in the GI lining and the lungs. Over time, inflammation will damage the mucosa, producing leaky gut syndrome. This increased permeability allows more foreign antigens into the bloodstream, perpetuating the inflammation response. Increased gut permeability is a common factor in autoimmunity. Bacterial imbalance in the GI tract can also promote inflammation that contributes to autoimmune disease, according to research by Tlaskalová-Hogenová et al. (
Immunology Letters. May 15, 2004;93[2–3]:97–108).

A multifaceted treatment approach that addresses the many contributors to autoimmune disease is more likely to reduce damage and symptoms than a conventional drug approach. Friedlander and Bauman offer supportive dietary and supplement suggestions in their article "Self Destructive Tendencies: Natural Strategies for Managing Autoimmunity." Avoiding refined carbohydrates and sugar (especially fructose and high-fructose corn syrup) is perhaps one of the best dietary measures a person can take to stem the inflammatory-autoimmunity cycle. Processed, sugary foods disturb gut bacteria balance and contribute to inflammation. Friedlander and Bauman suggest numerous supplements, herbs, and foods that have anti-inflammatory effects, including olive oil (extra virgin), sesame oil, green tea (epigallocatechin gallate), and spices and herbs (ginger, turmeric/curcumin, rosemary, oregano). Short fasts using fresh vegetable and fruit juices, vegetable broths, and herbal teas also calm inflammation. People with an autoimmune diagnosis should be supervised by a knowledgeable practitioner during fasting.

Friedlander J, Bauman E. Self destructive tendencies: natural strategies for managing autoimmunity. Bauman College. 2008. Available at:www.nanp.org/downloads/NANP_Newsletters/BCArticle.Autoimmunity.pdf. Accessed March 27, 2011.



Gastrointestinal Microbes and Rheumatoid Arthritis
What effect do toxic bacteria in the gastrointestinal tract have on autoimmune disease? Laboratory rodent studies indicate that GI bacteria and their toxins (e.g., gram-negative bacteria cell wall components) contribute to the development of autoimmune diseases. Absorption of these toxins from the GI tract stimulates inflammatory and immune responses. J. Vaahtovuo et al.reported significant difference in the GI bacterial makeup in people with early rheumatoid arthritis (RA) compared with controls in their 2008 study (J Rheumatol 2008;35:1500–1505). Is it possible to relieve the symptoms of rheumatoid arthritis by reducing toxic bacteria in the GI tract?

Kou Katayama and Japanese colleagues recently performed a small study to investigate this question. Their 2011 study involved 20 people with RA who either did not respond or were unable to take conventional medicines used to control the illness. (Eighteen completed the study). Another 18 background-matched RA patients acted as controls. Recognizing that antibiotics would contribute to further imbalance between pathogenic and nonpathogenic GI bacteria, the researchers decided to test the effect of a proprietary whey protein product containing natural milk antibodies called Bonyuno Chikara (Asama Chemicals Inc.). This whey protein concentrate contains immunoglobulins that function as antibodies against "at least 33 strains of pathogenic bacteria," according to laboratory tests. Tests with elderly volunteers indicate that the product reduces pathogenic bacteria like E. coli and Clostridium perfringens in feces and increases Lactobacilli.

Eight of the 18 receiving the whey product for three months experienced relief from GI problems and statistically significant reduction in RA symptoms. Two showed some improvement, and the remaining 8 did not respond. C-reactive protein levels and the erythrocyte sedimentation rate significantly decreased in those who responded and remained low one month after they stopped taking the product. Symptoms did eventually return, but those who had initially responded to the product improved again when it was reintroduced. When trying to determine why some patients responded and others did not, the researchers found that responders had higher serum anti-type II collagen antibody levels and higher serum IgG and IgA anti-lipopolysaccharides (from E. coli) antibody levels than the nonresponders. They suggest that these higher levels may indicate greater intestinal permeability. The researchers also found genetic differences between the two groups.

Katayama K, Matsuno T, Waritani T, Terato K, Shionoya H. Supplemental treatment of rheumatoid arthritis with natural milk antibodies against enteromicrobes and their toxins: results of an open-labeled pilot study. Nutr J. 2011:10(2). Available at: www.nutritionj.com/content/10/1/2. Accessed March 24, 2011.
Petroleum Chemicals, Mercury, and SLE
Systemic lupus erythematosis (SLE, or lupus), like other autoimmune illnesses, occurs when genetically susceptible people are exposed to environmental toxins that disrupt the immune system. In the case of lupus, antibodies react with cell nuclear material, producing inflammation and damage in organs and joints. Lacking a definitive laboratory test, doctors rely on patient symptoms to diagnose lupus. The presence of 4 or more of the "11 criteria of lupus" indicates the disease, according to the American College of Rheumatology. (See www.rheumatology.org.) People living near industrial pollution or contamination sites have a higher incidence of lupus and other autoimmune diseases, but researchers are just beginning to track down specific contaminants that trigger or worsen these illnesses.

Pristane, a component of crude oil, and mercury, which is released during oil drilling, have each caused SLE-like symptoms and autoimmunity in laboratory mice. Mercury is known to disrupt immune function in both animals and humans. While case reports and epidemiological studies indicate that mercury can trigger SLE, the evidence linking oil components to autoimmune disease is more limited. A 2007 study, initiated at residents' request, found an unusually high incidence of SLE in a six-square-block area in Hobbs, New Mexico. From 1927 until the late 1960s, the neighborhood had been the site of an active oil field. Some homes had been built over an oil field waste pit. Ninety adults who had lived in the neighborhood for at least two years enrolled in the study. The California research team used 129 volunteers from a similar Southwestern town without a history of chemical exposure as a control. Researchers collected indoor and outdoor dust samples and air samples from some exposed homes and controls. They looked for the oil components pristane and phytane in the dust samples and measured mercury (which is more volatile) in the air. Blood and urine samples were also taken from some volunteers in each group.

"We found higher levels of air mercury and house dust pristine/phytane in the affected neighborhood compared to other areas of Hobbs and the control town," James Dahlgren and colleagues write. In addition, 5 of 20 volunteers living in the exposed area and 1 of 25 controls had detectable pristane, phytane, and/or pristanic acid in their blood. All 6 had a diagnosis of lupus or symptoms associated with immune dysfunction. In addition, lymphocyte population in all exposed volunteer blood samples was abnormal, with significantly lower natural killer cells and significantly higher B-lymphocytes compared with controls. The incidence of lupus was extremely high in the exposed neighborhood: 13 cases out of an estimated 1490 inhabitants, which translates to 872/100,000. Medical literature indicates that SLE incidence "varies from 14.6 to 50.8 cases/100,000." Volunteers living in the oil-exposed area were also 10 times more likely to have rheumatic disease. In addition to other signs of immune dysfunction (e.g., mouth sores, numbness, rash), exposed volunteers were more likely to report cardiovascular, respiratory, and/or gastrointestinal problems. This study is reportedly the first one to link crude oil components to autoimmune disease.

Will oil components be linked to an increase in autoimmune disease among clean-up workers of the 2010 Deepwater Horizon oil spill? On February 28, 2011, the National Institute of Environmental Health Sciences announced a 10-year study involving oil spill clean-up workers. The NIH scientists hope to recruit 55,000 of the estimated 100,000 workers. The study is open to people aged at least 21 who did oil spill cleanup work for at least one day or who completed oil spill worker training. Only eight oil spills have been investigated for health effects on clean-up crews, and even fewer for long-term effects. This NIH study may help clarify the relationship between petroleum and autoimmune disease, particularly SLE.

Dahlgren J, Takhar M, Anderson-Mahoney P, Kotlerman J, Tarr J, Warshaw R. Cluster of systemic lupus erythematosus (SLE) associated with an oil field waste site: a cross sectional study. Environ Health. 2007;6(15). Available at:www.ehjournal.net/content/6/1/8. Accessed March 21, 2011.
National Institute of Environmental Health Sciences. NIH launches largest oil spill health study [press release]. February 28, 2011. Available at:www.niehs.nih.gov/news/releases/2011/gulfstudyfinal. Accessed March 24, 2011.


Saturday, July 2, 2016

ASPARTAME / NEOTAME/ AMINOSWEET/ CANDEREL, etc. FACT SHEET for Public Distribution


Aspartame Consumer Safety Network Fact Sheet

 80% of all consumer complaints to the FDA are aspartame related
[5 deaths registered prior to 1987]

THE BITTER TRUTH ABOUT ASPARTAME AND NEOTAME
"Aspartame/Neotame - the most dangerous substances in our food supply today." -  Mary Nash Stoddard
 [Founder ACSN & Pilot Hotline since 1987-present]

Illegal Actions Gained FDA Approval:

 FDA approved the new genetically engineered molecule in 1974, following a spate of criminal acts committed by G.D. Searle pharmaceutical employees and contractors. That approval was rescinded before aspartame got to market, because it was revealed a component of aspartame [diketopiperazine] caused brain tumors. Tests were "falsified."  Second approval occurred in 1981 under President Reagan's new FDA Director, Dr. Arthur H. Hayes. In 1983, Hayes' office approved the new molecule for aqueous solution [soft drinks, etc.] and three months later, Dr. Hayes left government, went to work for the NutraSweet public relations firm, Burson Marsteller for $1,000 a day. Hayes continued to craftily dodged all media requests for interviews on the topic. Hayes lost his battle with Leukemia (oft-reported to be Aspartame related blood cancer,) in 2010. His daughter, also a staunch supporter of Aspartame in Europe, died the same year of another Aspartame-related Cancer of the Pancreas. Many government officials connected with these sweeteners have defected - going to work for the industry whose products they were entrusted to approve or reject.

In the laboratory, aspartame produced:

o Brain Tumors
 o Breast Tumors
 o Uterine Tumors
 o Pancreatic Tumors
 o Seizures
 o Deaths

 These went unreported, as did the deaths and seizures of other animals in the original tests. Tumors were removed then animals put back in test as tumor free, animals who died were brought back to life on paper when results officially submitted by G.D. Searle pharmaceutical to FDA.

Aspartame changes DNA:
In tests, the third generation of pups born to animals fed aspartic acid [component of aspartame]  were born:
 1) Morbidly obese and
 2) Sexually Dysfunctional
 Components of aspartame and its breakdown products can adversely affect the brains and central nervous systems of children and adults who consume it.

"When you harm the brain, you harm the very expression of one's self." - Peter Breggin, M.D. [Psychiatrist - Bethesda, MD]

Reported psychological symptoms:

 o Suicidal Depressions
 o Panic Attacks and Anxiety [PAD] - Manias
 o Sleep Disorders
 o Severe Mood Disorders [rages, mood swings]
 o Brain Chemical Imbalance
 o Brain Wave Malfunctions [shows up in EEGs]
 o Personality Disorders
 o Hallucinations
 o Aberrant Behaviors

Medicine In Our Food?
 Aspartame Components & Breakdown Products:

Phenylalanine 50% - Lowers the seizure threshold. Causes mental retardation in some. Blocks production of serotonin [key neurotransmitter which controls: Moods / Sleep Patterns / Satiety ] Cultured in e-coli bacteria in the lab.
  
Aspartic Acid 40% - Caused lesions or holes in the brains of lab animals. Neuroexcitatory [excites brain cells to death] amino acid. Causes motor-neuronal disorders in studies.

Methanol 10% - Also known as "methyl alcohol", "moonshine", "Sterno." Damages the liver and eye. Two teaspoons can be lethal to humans. [Not processed the same in humans and animals, so lab tests do not show full impact of toxicity] Breaks down into formaldehyde [embalming fluid] and formic acid [venom in insect stings] at temperatures exceeding 86 degrees Fahrenheit. [Body temperature is 98.6 F] Implicated in birth defects and fetal alcohol syndrome in newborn infants. As a constituent of other foods in nature, it is found in combination with ethyl alcohol, which counteracts or neutralizes the toxic affects of methanol as it is metabolized by the body. There is no ethyl alcohol in aspartame, therefore methanol in aspartame is in "free form" and is immediately absorbed into the bloodstream. For every molecule of aspartame, there is a molecule of methanol released. Classic signs of methanol poisoning include: lethargy, confusion, leg cramps, back pain, severe headache, abdominal pain, slurred speech, fainting, visual loss/blindness, labored breathing.

Diketopiperazine [DKP] - Caused brain tumors in laboratory tests. Thirteen out of 320 lab animals developed brain tumors in testing. Aspartame breakdown products cross the blood brain barrier to damage the brain.

 Aspartame is known to exacerbate or trigger onset of the following medical conditions:

 o Epilepsy
 o Parkinson's
 o Alzheimer's
 o Multiple Sclerosis
 o Chronic Fatigue Syn.
 o Lymphoma
 o Fibromyalgia / Eosinophilia Myalgia
 o Mental Retardation / Birth Defects
 o Diabetes / Hypoglycemia
 o Graves Disease
 o Heart Disease
 o Lung Disease
 o Liver Disease
 o Kidney Disease
 o  Brain Tumors [astrocytoma/glioblastoma]
 o Pancreatic Disease
 o Kidney / Adrenal Disease
 o Arthritis
 o Blindness
 o Tinnitus
 o PMS
 o Carpal Tunnel
 o Lyme Disease
 o Muniere's Disease
 o Other: Rare / Hard to diagnose disorders

 [Aspartame has been called a "systemic" toxin - which means it may virtually adversely affect the function of every organ of the body. The effects are "cumulative" and do not show up in short term testing.]

Aspartame and the Media:
 1990, The Guardian [London newspaper] was sued for publishing headline story - "NutraSweet Faked Tests to Get Sweetener Approved." Later settled out of court. NutraSweet sent intimidating press releases to all U.S. media warning  they were suing.

 Documented instances are on record where the manufacturers of aspartame, threatened  to sue and/or withdraw advertising dollars, from media. Health care professionals, scientists and medical schools have been "bribed" or intimidated into silence.

Aspartame  and Flying Safety:
Many military, general aviation and commercial airline pilots have lost medical certification to fly based on seizures which occurred while they were ingesting aspartame. Grand mal seizures have been reported in flight in the cockpits of commercial airliners. A pilots' hotline in Dallas,TX was established by ACSN, in 1988 for the anonymous reporting of adverse reactions and safety-of-flight incidents. USAF Flying Safety magazine published warnings re: aspartame use by pilots. Pilot's publications around the globe have warned  readers. The FAA will not send out an official memo - because the FDA refuses to recall aspartame as a safety hazard to consumers. Is aspartame the unacknowledged "terrorist" in every cockpit on every flight?

Legal:

 ACSN co-founders Turner & Stoddard have both qualified in court as medical Expert Witnesses. Many consumer lawsuits have been dropped or settled out of court since the mid-eighties. The Washington D.C. Supreme Court refused to hear a case brought against the FDA by James Turner, Esq. Aspartame is illegal because it violated The Delaney Clause, which states no substance can be approved that is shown to cause cancer.

 In 1995, a stealth law crept across the land, which made it illegal to say anything disparaging about a perishable food product  -example: yogurt sweetened with aspartame. Oprah was later sued under this law. [Agricultural Defamation Act]

 In 1985, G.D. Searle and NutraSweet Co. became wholly-owned subsidiaries of Monsanto Chemical in St. Louis. Controversial Supreme Court Judge, Clarence Thomas is a former Monsanto attorney.

 Monsanto sold their sweetener divisions to current owner, the J.W. Childs Partnership.

 1998, Monsanto applied for FDA approval for a monster molecule, "based on the aspartame formula" with one addition: 3-dimethylbutyl [listed on EPA's most hazardous chemical list]. Thus, Neotame becomes 13,000 times sweeter than sugar.

 July 5, 2002 - Neotame, Monsanto's super bio-manipulated molecule [newest fake sweetener] was approved by FDA over formally  registered objections of the Aspartame Consumer Safety Network and others. Long term effects on humans are unknown.

 Aspartame is  in over-the-counter drugs like: Tums, Pepsid AC, Metamucil, Alka Seltzer Plus, tooth whiteners, breath mints/strips and more.


Diabetes and Aspartame / Neotame:

 Diabetics are most insidiously harmed , because they are told aspartame is their "life line" to good health, when, in fact, just the opposite is true. Remember, aspartame caused pancreatic tumors in the lab. A diabetic may see the real life effects of aspartame on blood sugar by performing this simple test with a finger-stick test kit:

 o Confirm blood sugar levels to be well within normal limits. If they are, then continue. Drink 2-3 cans [or the bottled equivalent]  of Diet Soda containing aspartame, without stopping. Then, begin to retest for blood sugar level readings approximately one hour later. In this way, the adverse effects on blood sugar levels may be proven. This test is NOT recommended for anyone except individuals who already drink more than 2 diet drinks per day.

 The American Diabetic Association and The American Dietetic Association [Registered Dietitians] have been "bought out" by the sweetener manufacturers. [ACSN has proof!]

Parents the FDA does not protect
 your children.
Greed and avarice have made government officials, industry and mainstream science, turn a deaf ear to the truth. Children are at least 4 times more susceptible to aspartame toxicity because of the developing central nervous system. Read labels. If it says:"phenylalanine" don't buy it. Insist your child's pediatric medical records contain this warning - "Never prescribe any medications containing phenylalanine [always present in aspartame and neotame]." Aspartame is a multi-billion dollar a year industry in more than 7,000 food products, chewing gums, children's antibiotics and meds, children's vitamins and pain medications for kids. In the lab, aspartame caused tragic birth defects.

Action Agenda:

 o Copy and distribute this Fact Sheet to everyone.
 o Post this brochure on the Internet.
 o Tell everyone about this problem.
 o  Ask the next 5 people you see using aspartame if they have had any of the symptoms.
 o Get off the substance for a period of 4-6 weeks to see your physical and mental condition improve.
 o If you have sought medical treatment for any of these symptoms and you are/were an aspartame user - have your doctor enter into your official medical record that you believe aspartame may have caused some or all of your symptoms and that you are ceasing use of the sweetener and want to be "monitored" by your health care team as you get better. Very important.
 o Join over 10,000 concerned consumer members of Aspartame Consumer Safety Network worldwide who are fighting this battle to educate the consuming public about artificial sweeteners that masquerade as "natural."
 o  Take all aspartame products back to the store and exchange them for healthy "real" food. This sends a message back to the manufacturer that we will no longer tolerate neurotoxins in our foods and children's items. Register a powerful complaint where it counts.
 o  Write letters to the FDA and food manufacturers who use aspartame. Copy the editor of your local newspaper, stating your displeasure about the conspiracy of silence and illicit cover up of the facts by government and industry.
  The tobacco industry got away with it far too long. Let us learn a lesson from that and vow not to repeat mistakes that let them get away with it.  The "real villains" in today's society are those who poison our food supply and that of our children - for profit.
 ____________________________________
 Published by:
Aspartame Consumer Safety Network
Mary Nash Stoddard, Founder and President
Mary Nash Stoddard