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SOD B Extramel Improves Physical, Mental Performance
 
AVIGNON, France—A new study confirmed the quick and lasting efficiency of Bionov’s SOD B Extramel in improving mental and physical performance. (Nutrients. 2014 July;6(6) 2348-2359. doi: 10.3390/nu6062348)
SOD B Extramel contains the high activity bioactive SuperOxide Dismutase (SOD) that fights one of the major consequences of stress and mental disorders: oxidative stress. Chronic stress,decreased cognitive performances and physical fatigue are associated with an over-production of Reactive Oxygen Species. –The results showed a significant reduction of stress and physical fatigue, as well as an improvement in cognitive performances and over all life quality. The double-blind, placebo-controlled trial was performed on 61 people. Participants reported a reduction of stress (-8.8 percent) and physical fatigue (-9.4 percent), as well as improved cognitive performances (13.9 percent) after three months of oral supplementation at 10 mg/day.—More than 450 million people worldwide have a mental disorder, according to the World Health Organization. SOD B Extramel represents another solution to the growing segment of stress and cognition. In 2008, it was awarded the European Anti-Stress Promising Ingredient of the Year Award
Recipe—THE simplest way to increase SOD is by combining Zinc ( citrate) 15mgs to copper 1mg—this would be the easiest way to increase SOD levels
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[F1]Or in todays times a polymer material as well as nanoparticle—an example would be vaccines or other methods of delivery or containment
[F2]In the case of internal exposure the same principles apply such as formulations ( TSP –Borax Peroxide- MMS-Turpentine-Vitamin C-Iodine-Herbals and Botanicals that can have an impact on the removal-exposure time –would be indicating the amount of time to utilize the components—Temperature can be utilize by either swear lodges—heat from saunas—hot tubs—baths—mechanical activity can be utilized as devices that can either send frequencies or signals or currents through the body
[F3]Which would be to our organs-tissues—skeletal structure
[F4]Why is this not alarming or surprising—do you ever get the feeling your being involved in a experiment—and you happen to be the experiment!!!
[F5]Medical uses—
Epinephrine vial 1mg (Adrenalin)
Adrenaline is used to treat a number of conditions including: cardiac arrest, anaphylaxis, and superficial bleeding.[20] It has been used historically for bronchospasm and hypoglycemia, but newer treatments for these that are selective for beta2 adrenoceptors, such as salbutamol, a synthetic epinephrine derivative, are currently preferred. Currently the maximum recommended daily dosage for patients in a dental setting requiring local anesthesia with a peripheral vasoconstrictor is 10 mg/lb of total body weight [2
[F6]One may want to maintain a study intack of tyrosine or phenyalanine to assist in the sustaining of proper adrenal function as well as B% and vitamin A
[F7]Part of the reason you cannot see them is that there size is a factor and what they are being mixed with in regard to aluminum—titanium dioxide—which actually camoflauges the particles
[F8]I find this –playing ignorant to the cause is ridiculously deceiving—almost to a level of playing innocent—when in fact they know there are self replicating and smart dust nanoparticles airborne not to mention the manufatucring processes that use the nano is leaking out of there containment
[F9]As you can see they are omitting out of the explanation aerosoling the skies with chemtrails which are nanosmart dust programmable material that self replicates and the results of this exposure can be seen on the trees and plants and insects
[F10]This is called pollen
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Show of the Month September 13 2014
Allergic reaction to antibiotic residues in foods? You may have to watch what your fruits and veggies eat
How skin falls apart- Pathology of autoimmune skin disease revealed at the nanoscale
Vibration may help heal chronic wounds
Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer’s
Copper as a Anti Viral
 
Liposome research meets nanotechnology to improve cancer treatment
 
Stealth Liposomes
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Allergic reaction to antibiotic residues in foods? You may have to watch what your fruits and veggies eat
Source-American College of Allergy, Asthma and Immunology (ACAAI)
People with food allergies always have to watch what they eat. Now, they may have to watch what their fruits and vegetables eat, as it seems it’s possible to have an allergic reaction to antibiotic residues in food.–An article published in the September issue of Annals of Allergy, Asthma and Immunology, the scientific publication of the American College of Allergy, Asthma and Immunology (ACAAI), examines the case of a 10 year-old girl who had an anaphylactic (severely allergic) reaction after eating blueberry pie. Although she had a medical history of asthma and seasonal allergies, and known anaphylaxis to penicillin and cow’s milk, she wasn’t known to be allergic to any of the ingredients in the pie.–After weeks of testing on both the young girl and a sample of the pie, the article authors decided that what had caused the reaction was a streptomycin-contaminated blueberry. Streptomycin, in addition to being a drug used to fight disease, is also used as a pesticide in fruit, to combat the growth of bacteria, fungi, and algae.–“As far as we know, this is the first report that links an allergic reaction to fruits treated with antibiotic pesticides,” said allergist Anne Des Roches, MD,FRCP, lead study author. “Certain European countries ban the use of antibiotics for growing foods, but the United States and Canada still allow them for agricultural purposes.”-[F1]The authors note that new regulations from the Food and Drug Administration may help to reduce antibiotic contaminants in food, which will help reduce antibiotic resistance and may also help reduce this type of event.–“This is a very rare allergic reaction,” said allergist James Sublett, MD, ACAAI president-elect. “Nevertheless, it’s something allergists need to be aware of and that emergency room personnel may need to know about in order to help determine where anaphylactic reactions may arise. Anyone who is at risk for a life-threatening allergic reaction should always carry epinephrine[F2]. They also need to know how to use their epinephrine [F3]in an emergency situation.”–Story Source–The above story is based on materials provided by American College of Allergy, Asthma and Immunology (ACAAI). Note: Materials may be edited for content and length
Recipe—if one has allergies sustaining a good dose of vitamin C will block or minimize the histamine release which may trigger a allergic response and sustain using nettle leaf or root as tea—utilizing as well pine bark –quercitrin and zinc ( which all would support the bronchrial area and strengthen and support the lungs as well from infection ) also things like feverfew—methionine – and Korean ginseng ( minimize use with young people since it can be overpowering) and aloe vera
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How skin falls apart- Pathology of autoimmune skin disease revealed at the nanoscale
Date:
September 10, 2014
Source:
University at Buffalo
 
UB researchers have pinpointed important changes in cellular behavior that occur in Pemphigus Vulgaris, the rare, blistering skin disease —-University at Buffalo researchers and colleagues studying a rare, blistering disease have discovered new details of how autoantibodies destroy healthy cells in skin. This information provides new insights into autoimmune mechanisms in general and could help develop and screen treatments for patients suffering from all autoimmune diseases, estimated to affect 5-10 percent of the U.S. population.–The research, published in PLoS One on Sept. 8, has the potential to help clinicians identify who may be at risk for developing Pemphigus vulgaris (PV), an autoimmune skin disorder, by distinguishing pathogenic (disease-causing) autoimmune antibodies from other nonpathogenic autoimmune antibodies.–PV results in the often painful blistering of the skin and mucous membranes. Generally treated with corticosteroids and other immunosuppressive agents, the condition is life-threatening if untreated.–“Our work represents a unique intersection between the fields of biology and engineering that allowed for entirely new investigational strategies applied to the study of clinical disease,” says Animesh A. Sinha, MD, PhD, Rita M. and Ralph T. Behling Professor and chair of the Department of Dermatology in the UB School of Medicine and Biomedical Sciences and senior author on the study.-The immediate application of the research, Sinha explains, is in helping scientists pinpoint important changes in cell behavior.–“These changes could be the differentiation of stem cells or the development of metastases in cancer or, as we are studying it, the point at which a cell is going to implode because it’s under autoimmune attack,” he says.–Sinha’s research team, in collaboration with scientists at Michigan State University, describe the use of atomic force microscopy (AFM), a technique originally developed to study nonbiological materials, to look at cell junctions and how they rupture, a process called acantholysis.–“It has been very difficult to study cell junctions, which maintain the skin’s barrier function by keeping cells attached to each other,” says Sinha. “These junctions, micron-sized spots on cell membranes, are very complex molecular structures. Their small size has made them resistant to detailed investigation.”–Sinha’s interest lies in determining what destroys those junctions in Pemphigus Vulgaris.–“We haven’t understood why some antibodies generated by the condition cause blisters and why other antibodies it generates do not,” says Sinha.–By studying the connections between skin cells using AFM and other techniques that probe cells at the nanoscale, Sinha and his colleagues report that pathogenic antibodies change structural and functional properties of skin cells in distinct ways.–“Our data suggest a new model for the action of autoantibodies in which there are two steps or ‘hits’ in the development of lesions,” says Sinha. “The first hit results in the initial separation of cells but only the pathogenic antibodies drive further intracellular changes that lead to the breaking of the cell junction and blistering.”–The researchers examined the cells using AFM, which requires minimal sample preparation and provides three-dimensional images of cell surfaces.–The AFM tip acts like a little probe, explains Sinha. When tapped against a cell, it sends back information regarding the cell’s mechanical properties, such as thickness, elasticity, viscosity and electrical potential.–“We combined existing and novel nanorobotic techniques with AFM, including a kind of nanodissection, where we physically detached cells from each other at certain points so that we could test what that did to their mechanical and biological functions,” Sinha adds.–Those data were then combined with information about functional changes in cell behavior to develop a nanomechanical profile, or phenotype, for specific cellular states.–He also envisions that this kind of nanomechanical phenotyping should allow for the development of predictive models for cellular behavior for any kind of cell.–“Ultimately, in the case of autoimmunity, we should be able to use these techniques as a high-throughput assay to screen hundreds or thousands of compounds that might block the effects of autoantibodies and identify novel agents with therapeutic potential in given individuals,” says Sinha. “Such strategies aim to advance us toward a new era of personalized medicine.”–Story Source–The above story is based on materials provided by University at Buffalo. The original article was written by Ellen Goldbaum. Note: Materials may be edited for content and length.–Journal Reference-Kristina Seiffert-Sinha, Ruiguo Yang, Carmen K. Fung, King W. Lai, Kevin C. Patterson, Aimee S. Payne, Ning Xi, Animesh A. Sinha. Nanorobotic Investigation Identifies Novel Visual, Structural and Functional Correlates of Autoimmune Pathology in a Blistering Skin Disease Model. PLoS ONE, 2014; 9 (9): e106895 DOI: 10.1371/journal.pone.0106895
 
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Vibration may help heal chronic wounds
Date:
March 31, 2014
Source:
University of Illinois at Chicago
 
Eileen Weinheimer-Haus, first author, and Timothy Koh, principal investigator.
Wounds may heal more quickly if exposed to low-intensity vibration, report researchers at the University of Illinois at Chicago.–The finding, in mice, may hold promise for the 18 million Americans who have type 2 diabetes, and especially the quarter of them who will eventually suffer from foot ulcers. Their wounds tend to heal slowly and can become chronic or worsen rapidly.–Timothy Koh, UIC professor of kinesiology and nutrition in the UIC College of Applied Health Sciences, was intrigued by studies at Stony Brook University in New York that used very low-intensity signals to accelerate bone regeneration.–“This technique is already in clinical trials to see if vibration can improve bone health and prevent osteoporosis,” Koh said.–Koh and his coworkers at UIC collaborated with Stefan Judex of Stony Brook to investigate whether the same technique might improve wound healing in diabetes. The new study, using an experimental mouse model of diabetes, is published online in the journal PLOS One.–The low-amplitude vibrations are barely perceptible to touch.–“It’s more like a buzz than an earthquake,” said Eileen Weinheimer-Haus, UIC postdoctoral fellow in kinesiology and nutrition, the first author of the study.–The researchers found that wounds exposed to vibration five times a week for 30 minutes healed more quickly than wounds in mice of a control group.–Wounds exposed to vibration formed more granulation tissue, a type of tissue important early in the wound-healing process. Vibration helped tissue to form new blood vessels — a process called angiogenesis — and also led to increased expression of pro-healing growth factors and signaling molecules called chemokines, Weinheimer-Haus said.–“We know that chronic wounds in people with diabetes fail to form granulation tissue and have poor angiogenesis, and we believe these factors contribute to their wounds’ failure to heal,” said Koh. He and his colleagues want to determine whether the changes they see in cell populations and gene expression at wound sites underlie the observed improvement in healing.—“The exciting thing about this intervention is how easily it could be translated to people,” Koh said. “It’s a procedure that’s non-invasive, doesn’t require any drugs, and is already being tested in human trials to see if it’s protective of bone loss.” A clinical study, in collaboration with Dr. William Ennis, director of the Wound Healing Clinic at UIC, is planned, Koh said.–Story Source–The above story is based on materials provided by University of Illinois at Chicago. The original article was written by Jeanne Galatzer-Levy. Note: Materials may be edited for content and length.–Journal Reference-Eileen M. Weinheimer-Haus, Stefan Judex, William J. Ennis, Timothy J. Koh. Low-Intensity Vibration Improves Angiogenesis and Wound Healing in Diabetic Mice. PLoS ONE, 2014; 9 (3): e91355 DOI: 10.1371/journal.pone.0091355
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Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer’s
Date:
September 9, 2014
Source:
BMJ-British Medical Journal
 
Taking benzodiazepines — widely prescribed drugs to treat anxiety and insomnia — is associated with an increased risk of developing Alzheimer’s disease, particularly for long-term users, suggests a new study.—Taking benzodiazepines — widely prescribed drugs to treat anxiety and insomnia — is associated with an increased risk of developing Alzheimer’s disease, particularly for long-term users, suggests a new study.—The researchers warn that unwarranted long-term use should be considered a public health concern. Dementia currently affects about 36 million people worldwide and this number is expected to double every 20 years, reaching 115 million by 2015. Although a increased risk of dementia has been identified in benzodiazepine users, the nature of this association, whether causal or not, remains unclear.–So a team of researchers based in France and Canada set out to investigate the relationship between the risk of Alzheimer’s disease and benzodiazepine exposure over a several years, as well as a potential dose-response relationship.–Using data from the Quebec health insurance program database (RAMQ), they tracked the development of Alzheimer’s disease in a sample of elderly residents living in Quebec, Canada who had been prescribed benzodiazepines.–Over a period of at least six years, they identified 1,796 cases of Alzheimer’s disease. They then compared each case with 7,184 healthy people matched for age, sex, and duration of follow-up.–Results show that past use of benzodiazepines for three months or more was associated with an increased risk (up to 51%) of Alzheimer’s disease. The strength of association increased with longer exposure and with use of long-acting benzodiazepines rather than short-acting ones.–Further adjustment for symptoms that might indicate the start of dementia, such as anxiety, depression or sleep disorders, did not meaningfully alter the results.–In this large case-control study, benzodiazepine use was associated with an increased risk of Alzheimer’s disease, say the authors. They emphasise that the nature of the link is still not definitive, but say the stronger association seen with long-term exposures “reinforces the suspicion of a possible direct association, even if benzodiazepine use might also be an early marker of a condition associated with an increased risk of dementia[F8].”–Benzodiazepines are “indisputably valuable tools for managing anxiety disorders and transient insomnia” they write, but warn that treatments “should be of short duration and not exceed three months.”–They conclude that their findings are of “major importance for public health, especially considering the prevalence and chronicity of benzodiazepine use in elderly populations and the high and increasing incidence of dementia in developed countries.”–In view of the evidence, they conclude that “it is now crucial to encourage physicians to carefully balance the benefits and risks when initiating or renewing a treatment with benzodiazepines and related products in elderly patients.”–In an accompanying editorial, Professor Kristine Yaffe of the University of California at San Francisco and Professor Malaz Boustani of the Indiana University Center for Aging Research, point out that in 2012 the American Geriatrics Society updated its list of inappropriate drugs for older adults to include benzodiazepines, precisely because of their unwanted cognitive side effects.–Yet almost 50% of older adults continue to use these drugs, they say. And without any formal monitoring system, the potential long term consequences on brain health are likely to be missed, adding to the growing prevalence of cognitive impairment among older people, they suggest.–Given the expanding numbers of older people likely to be treated with several drugs at a time, and/or who are at risk of Alzheimer’s disease, this gap needs to be plugged, they say.–Story Source–The above story is based on materials provided by BMJ-British Medical Journal. Note: Materials may be edited for content and length.-Journal References–S. Billioti de Gage, Y. Moride, T. Ducruet, T. Kurth, H. Verdoux, M. Tournier, A. Pariente, B. Begaud. Benzodiazepine use and risk of Alzheimer’s disease: case-control study. BMJ, 2014; 349 (sep09 2): g5205 DOI: 10.1136/bmj.g5205 -K. Yaffe, M. Boustani. Benzodiazepines and risk of Alzheimer’s disease. BMJ, 2014; 349 (sep09 6): g5312 DOI: 10.1136/bmj.g5312
 
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Copper as a Anti Viral
 
In 1964, Yamamoto and colleagues [53] reported on the inactivation of bacteriophages by copper. Jordan and Nassar [54] in 1971 showed that copper (0.2 mg/l) present as copper carbonate or colloidal copper inactivated infectious bronchitis virus. Totsuka and Ohtaki [55] in 1974 showed that the effect of copper sulfate on poliovirus RNA is proportional to its concentration, and that most amino acids except cysteine had a protective effect as did Fe2+ and Al3+. Similarly, Coleman and colleagues [56] in 1974 reported that herpes simplex virus (HSV) type I was quite sensitive to silver. Sagripanti and colleagues [57,58] found in 1992 that cupric and ferric ions were by themselves able to inactivate five enveloped or nonenveloped, single- or double-stranded DNA or RNA viruses (phi X174, T7, phi 6, Junin, and HSV). The metals were even more effective than glutaraldehyde in inactivating the viruses. The metal virucidal effect was enhanced by the addition of peroxide, particularly for Cu2+. In every case, the viruses were more resistant to iron-peroxidase than copper-peroxidase on a metal concentration basis. The inactivation of HSV by copper was enhanced by the following reducing agents at the indicated relative level: ascorbic acid >> hydrogen peroxide > cysteine. Treatment of HSVinfected cells with combinations of Cu2+ and ascorbate completely inhibited virus plaque formation to below 0.006% of the infectious virus input. The logarithm of the surviving fraction of HSV mediated by 1 mg of Cu2+ per liter and 100 mg of reducing agent per liter followed a linear relationship with reaction time. The kinetic rate constant for each reducing agent was – 0.87 min-1 (r = 0.93) for ascorbate[F9], -0.10 min-1 (r = 0.97) for hydrogen peroxide, and -0.04 min-1 (r = 0.97) for cysteine. The protective effects of metal chelators and catalase, the lack of effect of superoxide dismutase, and the partial protection conferred by free-radical scavengers suggest that the mechanism of copper-mediated HSV inactivation is similar to that reported for copper mediated DNA damage [59].Sagripanti and Lightfoote [60] reported that Human Immunodeficiency Virus Type 1 (HIV-1) was inactivated by both cupric or ferric ions when the virus was free in solution and also 3 hr after cell infection. Fifty percent inactivation of cell-free HIV-1 was achieved with Cu2+ at a concentration between 0.16 and 1.6 mM, or by 1.8 to 18 mM Fe3+. Thus, the dose to inactivate 50% of infectious HIV-1 (IC50) by Cu2+ or Fe3+ is higher than that reported for glutaraldehyde (0.1 mM), for sodium hypochlorite (1.3 mM), and for sodium hydroxide (11.5 mM). It is however significantly lower than that required for HIV-1 inactivation by ethanol (360 mM). Treatment of infected cells for 30 min at 20°C with 6 mM Cu2+ or Fe3+ completely inhibited the formation of syncytia and the synthesis of virus-specific p24 antigen in HIV-infected cells, while still preserving cell viability. We have recently reported the use of copper in free flow filters that deactivate HIV-1 and West Nile Virus. The copper filters reduced the infectious titers of both viruses by 5 to 6 log [19]. Wong et al [61] reported a 106-fold reduction in bacteriophage R17 infectivity due to RNA degradation in the presence of both ascorbate and Cu2+. A study published in 2001 reported on the inactivation of poliovirus and bacteriophage MS-2 in copper pipes containing tap water as a result of a synergistic effect between copper and free chlorine [62]. It was found that the log reduction/hour of the bacteriophage MS-2 in the presence of 400 μg/l of leached copper was 0.385, in 20 mg/l free chlorine 7.605 and with both copper and chlorine, 10.906. This suggests that an oxidizing agent such as chlorine or hydrogen peroxide is necessary to break open the virus protein coat and allow the copper to bind to and denature the nucleic acid. The International Copper Association, Ltd. investigated the effects of copper on the survival of waterborne viruses [63]. They found that poliovirus was completely inactivated by copper sulfate (20 mg/l) in the presence of hydrogen peroxide (10 μM), confirming observations of a synergistic effect of copper ions in the presence of oxidizing agents. The effect was reduced by the presence of a protective agent, L-histidine. Other proposed protective agents, disodium hydrogen orthophosphate, bovine serum albumin and catalase, were found to be relatively ineffective. Similarly, they found that copper reduced coxsackie virus types B2 & B4, echovirus 4 and simian rotavirus SA11 infectivity by over 98%. They concluded that there does not appear to be any significant difference between the capacity of copper to inhibit the different types of virus tested. The polio, coxsackie and echo viruses may be expected to behave similarly as they are have a similar size and are common members of the enterovirus group. However, the rotaviruses are considerably larger (75 nm diameter as opposed to 28 nm) and belong to the Reovirus group, a completely different family of viruses. They thus suggest that whatever mechanism is removing or inactivating the viruses, it is not dependent on subtle properties associated with the surface of the viruses. In another study, the efficacy of copper and silver ions, in combination with low levels of free chlorine, was evaluated for the disinfection of hepatitis A virus, human rotavirus, human adenovirus, and poliovirus in water [64]. There was little inactivation of Hepatitis A virus and human rotavirus under all conditions. Poliovirus showed more than a 4 log titer reduction in the presence of copper and silver combined with 0.5 mg of free chlorine per liter or in the presence of 1 mg of free chlorine per liter alone. Human adenovirus remained active longer than poliovirus with the same treatments, although it remained active significantly less than hepatitis A virus and human rotavirus. The addition of 700 μg of copper and 70 μg of silver per liter did not enhance the inactivation rates after exposure to 0.5 or 0.2 mg of free chlorine per liter, although on some occasions it produced a level of inactivation similar to that induced by a higher dose of free chlorine alone. This data indicates that copper and silver ions alone in water systems may not provide a reliable alternative to high levels of free chlorine for the disinfection of viral pathogens.
 
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Liposome research meets nanotechnology to improve cancer treatment
Date:
September 11, 2014
Source:
Boise State University
 
In the race to find more effective ways to treat cancer, Boise State University biophysicist Daniel Fologea is working outside the rules of general mathematics that say one plus one equals two. In his world, one plus one adds up to a whole lot more.—While radiotherapy can precisely target just the tumor site, systemic chemotherapy spreads a wide net, sending drugs speeding throughout the entire body in an attempt to kill cancer cells while also killing many healthy cells. Neither of these methods is highly effective when applied alone, therefore separated sessions of chemo and radiotherapy are required when fighting against solid tumors.–Reports have shown that ideally, both methods would be employed at the same time. But doing so produces levels of toxicity that often are deadly[F1]. To reduce the remote toxicity inherent to chemotherapy, the drugs can be administered into solid tumors by using liposomes, which are nanoscale vesicles made from fats and loaded with anti-cancer drugs. Liposomes self-accumulate within the tumor but the loaded drugs will be released very slowly from their encasing.—-A new patent awarded to Fologea, a professor in the Department of Physics, and co-researchers from the University of Arkansas in August 2014 holds promise of a way to combine the oomph of chemotherapy with the precision of radiotherapy, without harm to healthy cells.—In the new approach, said Fologea, “The liposomes are designed to release their precious cargo upon exposure to x-ray[F2]. Not only does this target where the medication goes, it also allows for a huge concentration of the drug to be released [F3]at once at the tumor site, thus increasing its efficacy. In addition, this combined modality of treatment employing concomitant radio and chemotherapy is supra-additive, which means it is several times more efficient than each therapy applied alone.”–Here’s how it works: liposomes have small scintillating[F4] nanoparticles embedded within them. When hit with the x-ray, they emit ultraviolet (UV) light. UV light triggers the release of Ca2+ entrapped into a photolabile cage inside the liposomes. The free Ca2+ activates an enzyme called phospholipase A2 that starts chewing the fats in the wall of the liposomes and triggers the fast release of the drug.–Now that they have a patent on the technique, researchers still expect several years of testing before the method is approved and available for cancer patients.–In the meantime, Fologea completed the initial phase of another method to provide similar results by using only materials previously approved by the FDA for treatment of cancer and other diseases. This approach will pave the way for earlier translational studies.
Working with Boise State biology professor Cheryl Jorcyk, he is looking for ways to put antibodies on the surface of the liposome, allowing them to recognize and attack cancer cells that are circulating in the body. A distinct approach to develop liposomes useful for treatment of diabetes is under development with Boise State biology professor Denise Wingett.—Story Source–The above story is based on materials provided by Boise State University. The original article was written by Kathleen Tuck. Note: Materials may be edited for content and length.
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Stealth Liposomes
Further advances in liposome research have been able to allow liposomes to avoid detection by the body’s immune system, specifically, the cells of reticuloendothelial system (RES). These liposomes are known as “stealth liposomes”, and are constructed with PEG[F5] (Polyethylene Glycol) [F6]studding the outside of the membrane. The PEG coating, which is inert in the body, allows for longer circulatory life for the drug delivery mechanism. However, research currently seeks to investigate at what amount of PEG coating the PEG actually hinders binding of the liposome to the delivery site. In addition to a PEG coating, most stealth liposomes also have some sort of biological species attached as a ligand to the liposome in order to enable binding via a specific expression on the targeted drug delivery site. These targeting ligands could be monoclonal antibodies (making an immunoliposome), vitamins, or specific antigens. Targeted liposomes can target nearly any cell type in the body and deliver drugs that would naturally be systemically delivered. Naturally toxic drugs can be much less toxic if delivered only to diseased tissues. Polymersomes, morphologically related to liposomes, can also be used this way.
In case of tumor development, certain anticancer drugs such as doxorubicin (Doxil) and daunorubicin are provided through liposomes. Liposomal cisplatin has received orphan drug designation for pancreatic cancer from EMEA
[F1]Cancer therapy from the medical is dangerious
[F2]This is still not a good idea anything nano never reacts the same way chemically and to addd Xray to this is again counter productive —
[F3]Anything nano would not need to be with anything high volume
[F4]scintillating :brilliantly lively, stimulating, or witty
[F5]PEG compounds themselves show some evidence of genotoxicity vi,vii and if used on broken skin can cause irritation and systemic toxicity.— Also, PEG functions as a “penetration enhancer,” increasing the permeability of the skin to allow greater absorption of the product — including harmful ingredients.
[F6]Depending on manufacturing processes, PEGs may be contaminated with measurable amounts of ethylene oxide and 1,4-dioxane. i The International Agency for Research on Cancer classifies ethylene oxide as a known human carcinogen and 1,4-dioxane as a possible human carcinogen. Ethylene oxide can also harm the nervous system ii and the California Environmental Protection Agency has classified it as a developmental toxicant based on evidence that it may interfere with human development. iii 1,4-dioxane is also persistent. In other words, it doesn’t easily degrade and can remain in the environment long after it is rinsed down the shower drain
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A liposome encapsulates a region of aqueous solution inside a hydrophobic membrane; dissolved hydrophilic solutes cannot readily pass through the lipids. Hydrophobic chemicals can be dissolved into the membrane, and in this way liposome can carry both hydrophobic molecules and hydrophilic molecules
 
Liposomes can also be designed to deliver drugs in other ways. Liposomes that contain low (or high) pH can be constructed such that dissolved aqueous drugs will be charged in solution (i.e., the pH is outside the drug’s pI range). As the pH naturally neutralizes within the liposome (protons can pass
Recipe—take any mineral or antioxidant and fuse this is any sunflower lecithin or even fats —and when you fused them in a blender the intake of what your using will not only improve but released longer in the system
 
[F1]Cancer therapy from the medical is dangerious
[F2]This is still not a good idea anything nano never reacts the same way chemically and to addd Xray to this is again counter productive —
[F3]Anything nano would not need to be with anything high volume
[F4]scintillating :brilliantly lively, stimulating, or witty
 
 
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[F1]Why is this not alarming or surprising—do you ever get the feeling your being involved in a experiment—and you happen to be the experiment!!!
[F2]Medical uses—
Epinephrine vial 1mg (Adrenalin)
Adrenaline is used to treat a number of conditions including: cardiac arrest, anaphylaxis, and superficial bleeding.[20] It has been used historically for bronchospasm and hypoglycemia, but newer treatments for these that are selective for beta2 adrenoceptors, such as salbutamol, a synthetic epinephrine derivative, are currently preferred. Currently the maximum recommended daily dosage for patients in a dental setting requiring local anesthesia with a peripheral vasoconstrictor is 10 mg/lb of total body weight [2
[F3]One may want to maintain a study intack of tyrosine or phenyalanine to assist in the sustaining of proper adrenal function as well as B% and vitamin A
[F4]Part of the reason you cannot see them is that there size is a factor and what they are being mixed with in regard to aluminum—titanium dioxide—which actually camoflauges the particles
[F5]I find this –playing ignorant to the cause is ridiculously deceiving—almost to a level of playing innocent—when in fact they know there are self replicating and smart dust nanoparticles airborne not to mention the manufatucring processes that use the nano is leaking out of there containment
[F6]As you can see they are omitting out of the explanation aerosoling the skies with chemtrails which are nanosmart dust programmable material that self replicates and the results of this exposure can be seen on the trees and plants and insects
[F7]This is called pollen
[F8]Don’t you like the dance—they are saying a 51% increase on one hand and on the other they are saying this may be and there are strong indicators butt…and there is always a butttt
[F9]Vitamin C mix
 
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HOME
 
Show of the Month September 20 2014
Vitamin E intake Critical to being healthy—- Vitamin E
Four new quassinoids from the roots of Eurycoma longifolia Jack
Anti-tumor activity of Eurycoma longifolia root extracts against K-562 cell line
Aspartame Toxicity Information
Ultrafine Particles Cross Cellular Membranes by Nonphagocytic Mechanisms in Lungs and in Cultured Cells
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Vitamin E intake Critical to being healthy
Date:
September 15, 2014
Source:
Oregon State University
 
Sunflower seeds and oil are a particularly good dietary source of vitamin E.–Amid conflicting reports about the need for vitamin E and how much is enough, a new analysis published today suggests that adequate levels of this essential micronutrient are especially critical for the very young, the elderly, and women who are or may become pregnant.-A lifelong proper intake of vitamin E is also important, researchers said, but often complicated by the fact that this nutrient is one of the most difficult to obtain through diet alone. It has been estimated that only a tiny fraction of Americans consume enough dietary vitamin E to meet the estimated average requirement.-Meanwhile, some critics have raised unnecessary alarms about excessive vitamin E intake while in fact the diet of most people is insufficient[F1], said Maret Traber, a professor in the College of Public Health and Human Sciences at Oregon State University, principal investigator with the Linus Pauling Institute and national expert on vitamin E.-“Many people believe that vitamin E deficiency never happens,” Traber said. “That isn’t true. It happens with an alarming frequency both in the United States and around the world. But some of the results of inadequate intake are less obvious, such as its impact on things like nervous system and brain development, or general resistance to infection.”-Some of the best dietary sources of vitamin E — nuts, seeds, spinach, wheat germ and sunflower oil — don’t generally make the highlight list of an average American diet. One study found that people who are highly motivated to eat a proper diet consume almost enough vitamin E, but broader surveys show that 90 percent of men and 96 percent of women don’t consume the amount currently recommended, 15 milligrams per day for adults.–In a review of multiple studies, published in Advances in Nutrition, Traber outlined some of the recent findings about vitamin E. Among the most important are the significance of vitamin E during fetal development and in the first years of life; the correlation between adequate intake and dementia later in life; and the difficulty of evaluating vitamin E adequacy through measurement of blood levels alone.
Findings include:
Inadequate vitamin E is associated with increased infection, anemia, stunting of growth and poor outcomes during pregnancy for both the infant and mother.
Overt deficiency, especially in children, can cause neurological disorders, muscle deterioration, and even cardiomyopathy.
Studies with experimental animals indicate that vitamin E is critically important to the early development of the nervous system in embryos, in part because it protects the function of omega-3 fatty acids, especially DHA, which is important for brain health. The most sensitive organs include the head, eye and brain.
One study showed that higher vitamin E concentrations at birth were associated with improved cognitive function in two-year-old children.
Findings about diseases that are increasing in the developed world, such as non-alcoholic fatty liver disease and diabetes, suggest that obesity does not necessarily reflect adequate micronutrient intake.
Measures of circulating vitamin E levels in the blood often rise with age as lipid levels also increase, but do not prove an adequate delivery of vitamin E to tissues and organs.
Vitamin E supplements do not seem to prevent Alzheimer’s disease occurrence, but have shown benefit in slowing its progression.
A report in elderly humans showed that a lifelong dietary pattern that resulted in higher levels of vitamins B,C, D and E were associated with a larger brain size and higher cognitive function.
Vitamin E protects critical fatty acids such as DHA throughout life, and one study showed that people in the top quartile of DHA concentrations had a 47 percent reduction in the risk of developing all-cause dementia.
“It’s important all of your life, but the most compelling evidence about vitamin E is about a 1000-day window that begins at conception,” Traber said. “Vitamin E is critical to neurologic and brain development that can only happen during that period. It’s not something you can make up for later.”–Traber said she recommends a supplement for all people with at least the estimated average requirement of vitamin E, but that it’s particularly important for all children through about age two; for women who are pregnant, nursing or may become pregnant; and for the elderly.-Story Source–The above story is based on materials provided by Oregon State University. Note: Materials may be edited for content and length.—Journal Reference–Maret Traber. Vitamin E Inadequacy in Humans: Causes and Consequences. Advances in Nutrition, September 2014
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Vitamin E1
Maret G. Traber*
1. School of Biological & Population Health Sciences and the Linus Pauling Institute, Oregon State University, Corvallis, OR
Danny Manor
+ Author Affiliations
1. Departments of Nutrition and of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, OH
Vitamin E refers to the plant-derived, lipid-soluble antioxidants: tocopherols and tocotrienols. They terminate the chain reaction of lipid peroxidation. Vitamin E biological activity is different from its antioxidant activity, and there is a preference for α-tocopherol. This preference is achieved through the selective degradation and excretion of other vitamin E forms and the selective retention of α-tocopherol, mediated by the hepatic α-tocopherol transfer protein (α-TTP). Hepatic α-TTP facilitates the selective incorporation of α-tocopherol into circulating lipoproteins that distribute the vitamin to nonhepatic tissues. α-TTP is therefore considered to be the major regulator of vitamin E status in humans.
 
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Deficiencies:
Vitamin E deficiency occurs in humans as a result of genetic abnormalities in α-TTP or in lipoprotein synthesis or occurs secondary to fat malabsorption. Genetic defects in α-TTP are associated with a characteristic syndrome, ataxia with vitamin E deficiency (AVED). More than 20 mutations in α-TTP have been identified in human AVED patients.
Diet recommendations:
The vitamin E dietary reference intake (DRI) for adult men and women (and individuals 14–18 y) was set in 2000 at a daily estimated average requirement (EAR) of 12 mg α-tocopherol and an recommended daily allowance (RDA) of 15 mg.[F2] There are no increases for pregnancy, but for lactation the RDA is 19 mg/d. The adequate intake (AI) for infants (0–6 mo) was estimated to be 4 mg and for 7 through 12 mo to be 5 mg. The RDA for children 1 to 3 y is 6 mg; for those 4–8 y, it is 7 mg and 11 mg for those 9 to 13 y. –Plant-synthesized α-tocopherol is RRR-α-tocopherol; chiral carbons are in the R-conformation at positions 2, 4′, and 8′. Chemical synthesis results in an equal mixture of 8 different stereoisomers (RRR, RSR, RRS, RSS, SRR, SSR, SRS, SSS) that is called all-rac-α-tocopherol. The 2 position of α-tocopherol, the junction of the ring and tail, is critical for in vivo α-tocopherol vitamin activity. Only 2R forms meet human requirements.
Food sources:
Major dietary vitamin E sources, as commonly eaten portions [USDA National Nutrient Database for Standard Reference, Release 24 (January 2012; http://www.nal.usda.gov/fnic/foodcomp/search/)] are fortified ready-to-eat cereals; nuts, especially almonds; seeds, such as sunflower seeds; greens, such as spinach; and vegetable oils, especially sunflower and safflower.
Clinical uses:
Humans with defects in the TTPA gene (encoding α-TTP) have extraordinarily low (1/100 of normal) plasma vitamin E concentrations, but if they are given vitamin E supplements, plasma concentrations normalize within hours; if supplementation is halted, plasma vitamin E concentrations decrease within days to deficient levels. A daily α-tocopherol dose (800–1200 IU) is usually sufficient to prevent further deterioration of neurologic function, and in some cases, improvements have been noted. Postmortem analysis of a brain from a vitamin E–supplemented AVED patient demonstrated vitamin E accumulation and prevention of Purkinje cell loss. -Vitamin E deficiency due to impaired lipoprotein synthesis or fat malabsorption syndromes (e.g., abetalipoprotenemia, cystic fibrosis, short bowl disorder, choleastasis, and inherited defects in bile acid synthesis) is also treated with daily vitamin E supplements (100 mg/kg body weight). –The benefit of vitamin E supplements in individuals who are not vitamin E deficient is controversial. In the elderly, impaired immune function was improved with vitamin E supplementation. Patients with macular degeneration benefited from a supplement cocktail that included vitamin E. Vitamin E supplements have decreased heart attack risk in those with the haptoglobin 2–2 genotype, which results in a dysfunctional protein and causes increased oxidation by free heme. A follow-up study of the Alpha-Tocopherol Beta-Carotene Cancer Prevention trial showed that men at baseline who consumed 12 mg α-tocopherol daily (equivalent to the vitamin E EAR) had considerably lower risk of total and cause-specific mortality 13 y later.
Toxicity:
The upper limit of tolerable intakes (UL) is 1000 mg/day, equivalent to 1100 iu synthetic or 1500 iu natural vitamin E. The UL was based on the adverse effect of an increased bleeding tendency observed in rat studies. This tendency to bleed was found to have beneficial effects in preventing venous thrombosis in a trial of vitamin E supplements in women. –Subsequent to the publication of the DRI, there have been several meta-analyses evaluating the outcomes of human vitamin E supplementation trials. Thus far, there have been no uniform mechanisms identified for the claim in meta-analyses of increased mortality associated with vitamin E supplements.
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Recent research
Vitamin E in the central nervous system:
Vitamin E deficiency manifests primarily as cerebellar ataxia in humans, underscoring the unique sensitivity of the central nervous system to oxidative stress. Interestingly, α-TTP is expressed in the cerebellum. α-Tocopherol supplementation in α-TTP knockout mice normalizes its status in all tissues except the brain. Thus, a unique relationship exists between localized vitamin E levels, expression of α-TTP, oxidative stress, and optimal cerebellar function. The detailed description of this relationship and the molecular mechanisms that underlie it are critical research questions.
Homeostasis:
An important fundamental question in vitamin E biology is “are there compensatory mechanisms in response to oxidative stress to increase α-tocopherol concentrations or distribution?.” Provocatively, brain α-TTP expression levels respond to oxidative stress, [F3]but liver α-TTP does not.
Fertility:
Vitamin E was discovered as an essential dietary factor for reproductive health in female rodents. Surprisingly, very little is known regarding human vitamin E status and reproductive health. In mice, α-tocopherol sufficiency is essential for placentation. α-TTP is expressed in the uterine wall of pregnant female mice and in the human placenta. Research in this field is of great importance because 96% of U.S. women do not meet vitamin E EAR.
Interactions with other nutrients:
The untoward effects of vitamin E supplements on blood clotting may result from vitamin E and K interactions because these supplements increase undercarboxylation of prothrombin, suggesting lower vitamin K activity. More than 90% of dietary, plant-derived vitamin K is phylloquinone (vitamin K1) with a 20-carbon phytyl side chain that is identical to that of tocopherol. Phylloquinone is converted to menadione and then to MK-4 (extrahepatic tissue vitamin K). Based on their similar structures, vitamins E and K likely share the same pathways for metabolism and excretion. Possible mechanisms for the vitamin E and K interaction have been proposed, but none have been proven.
The interactions of vitamins E and C are likely dependent on their roles as antioxidants; vitamin C can regenerate tocopherol from the tocopheroxyl radical. When α-tocopherol kinetics were evaluated in cigarette smokers, smokers had higher F2-isoprostane concentrations and faster plasma α-tocopherol disappearance rates than nonsmokers. When smokers received vitamin C supplementation (500 mg twice daily) for 2 weeks, α-tocopherol disappearance rates were normalized. Thus, in smokers with greater oxidative stress, additional vitamin C is needed to restore the α-tocopheroxyl radical to its reduced form. Importantly, vitamin C supplementation did not change F2-isoprostane concentrations, showing that α-tocopherol does not prevent radical formation or the initial oxidation of fatty acids, but halts the chain reaction of lipid peroxidation.
For further information
Food and Nutrition Board, and Institute of Medicine. Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington, DC: National Academy Press; 2000.
Institute of Medicine. Dietary reference intakes: the essential guide to nutrient requirements. Washington, DC: National Academy Press; 2006.
Manor D, Morley S. The alpha-tocopherol transfer protein. Vitam Horm. 2007;76:45–65.
Traber MG, Atkinson J. Vitamin E, antioxidant and nothing more. Free Radic Biol Med. 2007;43:4–15.
Traber MG, Stevens JF. Beneficial effects from a mechanistic perspective. Free Radic Biol Med. 2011;51:1000–13.
Traber MG. Vitamin E. In: Erdman J, Macdonald I, Zeisel S, editors. Present knowledge in nutrition. 9th ed. Washington, DC: ILSI Press.
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Four new quassinoids from the roots of Eurycoma longifolia Jack.
Fitoterapia. 2014 Jan;92:105-10
Authors: Meng D, Li X, Han L, Zhang L, An W, Li X
Abstract
Seven compounds were isolated from the roots of Eurycoma longifolia, and characterized by comprehensive analysis of 1D and 2D NMR experiments along with single crystal X-ray diffraction. Among them, four new quassinoids were identified and three of them were diastereomers[F4] for each other. Compounds 1-7 were evaluated for cytotoxicities against HT-29, MCF-7, LOVO, BGC-823, MGC-803, HepG2, HeLa, and A549 cancer cell lines. Compounds 2 and 5 exhibited the lowest IC50 values [F5]of 24.9 μM, 11.8 μM, and 44.1 μM, 14.1 μM towards MCF-7, MGC-803 cancer cell lines, respectively, while compound 6 exhibited moderate cytotoxicity towards all the selected cancer cell lines.–PMID: 24513570 [PubMed – indexed for MEDLINE]
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Anti-tumor activity of Eurycoma longifolia root extracts against K-562 cell line: in vitro and in vivo study.
PLoS One. 2014;9(1):e83818
Authors: Al-Salahi OS, Ji D, Majid AM, Kit-Lam C, Abdullah WZ, Zaki A, Jamal Din SK, Yusoff NM, Majid AS
Eurycoma longifolia Jack has been widely used in traditional medicine for its antimalarial, aphrodisiac, anti-diabetic, antimicrobial and anti-pyretic activities. Its anticancer activity has also been recently reported on different solid tumors, however no anti-leukemic activity of this plant has been reported. Thus the present study assesses the in vitro and in vivo anti-proliferative and apoptotic potentials of E. longifolia on K-562 leukemic cell line. The K-562 cells (purchased from ATCC) were isolated from patients with chronic myelocytic leukemia (CML) were treated with the various fractions (TAF273, F3 and F4) of E. longifolia root methanolic extract at various concentrations and time intervals and the anti-proliferative activity assessed by MTS assay. Flow cytometry was used to assess the apoptosis and cell cycle arrest. Nude mice injected subcutaneously with 10(7) K-562 cells were used to study the anti-leukemic activity of TAF273 in vivo. TAF273, F3 and F4 showed various degrees of growth inhibition with IC50 [F6]values of 19, 55 and 62 µg/ml, respectively. TAF273 induced apoptosis in a dose and time dependent manner. TAF273 arrested cell cycle at G1 and S phases. Intraperitoneal administration of TAF273 (50 mg/kg) resulted in a significant growth inhibition of subcutaneous tumor in TAF273-treated mice compared with the control mice (P = 0.024). TAF273 shows potent anti-proliferative activity in vitro and in vivo models of CML and therefore, justifies further efforts to define more clearly the potential benefits of using TAF273 as a novel therapeutic strategy for CML management.–PMID: 24409284 [PubMed – indexed for MEDLINE]
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Aspartame Toxicity Information
12 East Side Dr., Suite 2-18
Concord, NH 03301
603-225-2110
Date: January 12, 2002
Please find below Evidence File #4: Reported Aspartame Toxicity Effects
Reported Aspartame Toxicity Effects
———————————–
Q. What are the reported reactions to aspartame ingestion?
How often are such effects seen?
Answer
——
==> What are the reported reactions to aspartame ingestion?
We will limit our discussion in this FAQ to reported toxicity
reactions to aspartame ingestion. Controlled studies showing
problems with aspartame ingestion will be discussed in another
FAQ. Toxicity reactions to aspartame can be divided into three
types:
1. Acute toxicity reactions occuring within 48 hours of ingestion of
an aspartame-containing product.
2. Chronic toxicity effects occuring anywhere from several days of
use to appearing a number of years (i.e., 1-20+ years) after the
beginning of aspartame use.
3. Potential toxicity effects that would be nearly impossible for
the user to recognize the link to aspartame.
In an epidemiological survey which appeared in the Journal of
Applied Nutrition (Roberts 1988), 551 persons who have
reported toxicity effects from aspartame ingestion were
surveyed. The adverse effects found cover a subset of reported
acute and chronic toxicity effects from aspartame.
What follows is a listing of the adverse health effects
which were found.
——————-
# of
people (%)
Eye
– Decreased vision and/or other eye problems 140 (25%)
(blurring, “bright flashes,” tunnel vision)
– Pain (or or both eyes) 51 (9%)
– Decreased tears, trouble with contact lens, 46 (8%)
or both
– Blindness (one or both eyes) 14 (3%)
Ear
– Tinnitus (“ringing,” “buzzing”) 73 (13%)
– Severe intolerance for noise 47 (9%)
– Marked impairment of hearing 25 (5%)
Neurologic
– Headaches 249 (45%)
– Dizziness, unsteadiness, or both 217 (39%)
– Confusion, memory loss, or both 157 (29%)
– Severe drowsiness and sleepiness 93 (17%)
– Paresthesias (“pins and needles,” “tingling”) 82 (15%)
or numbness of the limbs
– Convulsions (grand mal epileptic attacks) 80 (15%)
– Petit mal attacks and “absences” 18 (3%)
– Severe slurring of speech 64 (12%)
– Severe tremors 51 (9%)
– Severe “hyperactivity” and “restless legs” 43 (8%)
– Atypical facial pain 38 (7%)
Psychologic-Psychiatric
– Severe depression 139 (25%)
– “Extreme irritability” 125 (23%)
– “Severe anixiety attacks” 105 (19%)
– “Marked personality changes” 88 (16%)
– Recent “severe insomnia” 76 (14%)
– “Severe aggravation of phobias” 41 (7%)
Chest
– Palpitations, tachycardia (rapid heart action), 88 (16%)
of both
– “Shortness of breath” 54 (10%)
– Atypical chest pain 44 (8%)
– Recent hypertension (high blood pressure) 34 (6%)
Gastrointestinal
– Nausea 79 (14%)
– Diarrhea 70 (13%)
Associated gross blood in the stools (12)
– Abdominal pain 70 (13%)
– Pain on swallowing 28 (5%)
Skin and Allergies
– Severe itching without a rash 44 (8%)
– Severe lip and mouth reactions 29 (5%)
– Urticaria (hives) 25 (5%)
– Other eruptions 48 (9%)
– Aggravation of respiratory allergies 10 (2%)
Endocrine and Metabolic
– Problems with diabetes: loss of control; 60 (11%)
precipitation of clinical diabetes;
aggravation or simulation of diabetic
complications
– Menstrual changes 45 (6%)
Severe reduction or cessation of periods (22)
– Paradoxic weight gain 34 (5%)
– Marked weight loss 26 (6%)
– Marked thinning or loss of the hair 32 (6%)
– Aggravated hypoglycemia (low blood sugar 25 (5%)
attacks)
Other
– Frequency of voiding (day and night), burning 69 (13%)
on urination (dysuria), or both
– Excessive thirst 65 (12%)
– Severe joint pains 58 (11%)
– “Bloat” 57 (10%)
– Fluid retention and leg swelling 20 (4%)
– Increased susceptibility to infection 7 (1%)
——————-
There are other clinical reports in the scientific literature of
aspartame-caused toxicity reactions including Blumenthal (1997),
Drake (1986), Johns (1986), Lipton (1989), McCauliffe (1991),
Novick (1985), Watts (1991), Walton (1986, 1988), and Wurtman
(1985).
Many pilots appear to be particularly susceptible to the effects of
aspartame ingestion. They have reported numerous serious toxicity
effects including grand mal seizures in the cockpit (Stoddard 1995).
Nearly 1,000 cases of pilot reactions have been reported to the
Aspartame Consumer Safety Network Pilot Hotline (Stoddard 1995).
This susceptibility may be related to ingesting methanol at altitude
as suggested in a letter from Dr. Phil Moskal, Professor of
Microbiology, Biochemistry, and Pathology, Chairman of the Department
of Pathology, Director of Public Health Laboratories (Moskal 1990),
or it may simply be that some pilots tend to ingest large quantities
of aspartame during a flight. Whatever the case, numerous warnings
about aspartame dangers have appeared in piloting journals including
The Aviation Consumer (1988), Aviation Medical Bulliten (1988),
Pacific Flyer (1988), CAA General Aviation (1989), Aviation Safety
Digest (1989), General Aviation News (1989), Plane & Pilot (1990),
Canadian General Aviation News (1990), National Business Aircraft
Association Digest (NBAA Digest 1993), International Council of
Air Shows (ICAS 1995), and the Pacific Flyer (1995). Both the U.S.
Air Force’s magazine “Flying Safety” and the U.S. Navy’s magazine,
“Navy Physiology” published articles warning about the many dangers
of aspartame including the cumlative deliterious effects of methanol
and the greater likelihood of birth defects. The articles note that
the ingestion of aspartame may make pilots more susceptible to
seizures and vertigo (US Air Force 1992).
Countless other toxicity effects have been reported to the FDA (DHHS
1995), other independent organizations (Mission Possible 1996,
Stoddard 1995), and independent scientists (e.g., 80 cases of
seizures were reported to Dr. Richard Wurtman, Food (1986)).
Samples of some aspartame toxicity reactions reported on the
Internet can be found on the Aspartame (NutraSweet) Toxicity Info
Center web page:
http://www.tiac.net/users/mgold/aspartame/
Frequently, aspartame toxicity is misdiagnosed as a specific disease.
This has yet to be reported in the scientific literature, yet it has
been reported countless times to independent organizations and
scientists (Mission Possible 1994, Stoddard 1995). In other cases,
it has been reported that chronic aspartame ingestion has triggered
or worsened certain chronic illnesses. Nearly 100% of the time, the
patient and physician assume that these worsening conditions are
simply a normal progression of the illness. Sometimes that may be
the case, but many times it is chronic aspartame poisoning.
According to researchers and physicians studying the adverse
effects of aspartame, the following list contains a selection
of chronic illnesses which may be caused or worsened by the chronic,
long-term ingestion of aspartame. (Mission Possible 1994, Stoddard
1995)*:
Brain tumors Multiple sclerosis
Epilepsy Chronic faigue syndrome
Parkinson’s Disease Alzheimer’s
Mental retardation Lymphoma
Birth defects Fibromyalgia
Diabetes Arthritis (including Rheumatoid)
Chemical Sensitivities Attention Deficit Disorder
*Note: In some cases such as MS, the severe symptoms mimic the illness or exacerbate the
illness, but do not cause the disease.
Also, please note that this is an incomplete list. Clearly,
ingestion of a very slow poison (as discussed in other FAQs) is not
beneficial to anyone who has a chronic illness.
Finally, potential toxicity effects from aspartame including brain
cancer (as seen in pre-approval research) and effects on fetal brain
and nervous system development will be discussed in other FAQs.
==> How often are such effects seen?
Until recently approximately 90% of aspartame sales were in the
United States (Monsanto 1994). Other countries are now being inundated
with aspartame, but it will be some time until they begin to feel the
full effects of aspartame toxicity on the general population. Since the
U.S. has some history of significant use, we will limit the discussion
to the frequency of effects in the U.S.
There have been well over 7,000 aspartame toxicity reactions officially received by the U.S.
Food and Drug Administration between 1982 (after aspartame was first approved) until 1995
(DHHS 1993, DHHS 1995). From this figure, we can estimate the number of actual toxicity
reactions observed.
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References Cited
Aviation Consumer 1988. “SafeGuard,” June 15, 1988.
Aviation Medical Bulletin 1988. “Pilots and Aspartame,”
October 1988.
Aviation Safety Digest 1989. “Aspartame — not for the
dieting pilot?” Aviation Safety Digest, ASD 142, Spring
1989 (Australia – 062/5841111).
Blumenthal, H.J., D.A. Vance, 1997, “Chewing Gum Headaches,”
Headache, Volume 37, Number 10, pages 665-666.
Butchko, Harriett H., Frank N. Kotsonis 1994. “Postmarketing
Surveillance in the Food Industry: The Aspartame Case
Study,” in Nutritional Toxicology, edited by Frank N.
Kotsonis, Maureen Macky and Jerry Hjelle, Raven Press,
Ltd., New York, c1994.
CAA General Aviation (1989). Safety Information Leaflet,
April 1989, Great Britain.
Canadian General Aviation News 1990. “Fit to fly” Canadian
General Aviation News, March 1990, page 28.
DHHS 1993. “Adverse Reactions Associated With Aspartame
Consumption,” Department of Health & Human Services
Memorandum, April 1, 1993, Reprinted in preface of
“Bittersweet Aspartame: A Diet Delusion” by Barbara
Alexander Mullarkey, NutriVoice, P.O. Box 946, Oak
Park, Illinois 60303, (708) 848-0116.
DHHS 1995. Department of Health and Human Services. “Report
on All Adverse Reactions in the Adverse Reaction
Monitoring System.” (April 20, 1995).
Drake, M.E., 1986. “Panic Attacks and Excessive Aspartame Ingestion”
(Letter), Lancet, September 13, 1986, page 631.
Food 1986. Food Chemical News, July 28, 1986, page 44.

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