HERE IS THE FDA LIST OF 92 SYMPTOMS ON THEIR STATIONERY: www.mpwhi.com/92_aspartame_symptoms.pdf ___________________________________
Whereas, the Ramazzini Studies by the European Foundation for Oncology in Italy conducted exhaustive studies over three years with thousands of rats, and proved aspartame to be multipotential carcinogen, thus confirming the United States Food and Drug Administrations original findings; and
THIS WAS PEER REVIEWED BY 7 WORLD EXPERTS. THIS RAMAZZIN REPORT WAS ALSO POSTED ON THE WEBSITE FOR THE NATIONAL INSTITUTE OF HEALTH, A BRANCH OF THE UNITED STATES GOVERNMENT. ________________________________
Whereas, the United States Food and Drug Administration admitted that aspartame caused cancer over two decades ago when the Administrations toxicologist, Dr. Adrian Gross, told Congress at least one of Searles studies has established beyond any reasonable doubt that aspartame is capable of inducing brain tumors in experimental animals and that this predisposition of it is of extremely high significance. In view of these indications that the cancer causing potential of aspartame is a matter that had been established way beyond any reasonable doubt, one can ask: What is the reason for the apparent refusal by the FDA to invoke for this food additive the so-called Delaney amendment to the Food, Drug, and Cosmetic act? Given the cancer causing potential of aspartame, how would the FDA justify its position that it views a certain amount of aspartame as constituting an allowable daily intake or safe level of it? Is that position in effect not equivalent to setting a tolerance for this food additive and thus a violation of that law? And if the FDA itself elects to violate the law, who is left to protect the health of the public?
Congressional Record, August 1, 1985, SID835: 131: and THIS GIVES THE REFERENCE TO THE CONGRESSIONAL RECORD. ______________________________________ Whereas , aspartame is linked to sudden death, multiple sclerosis, lupus, and many neurodegenerative diseases, as cited in many medical texts, most notably: Aspartame Disease: An Ignored Epidemic, by H.J. Roberts, M.D., and Excitotoxins: The Taste That Kills, By Russell Blaylock, M.D., and
Whereas, on November 3, 1987, Dr. Louis Elsas told Congress: I am a pediatrician, a Professor of Pediatrics at Emory and have spent twenty-five years in the biomedical sciences, trying to prevent mental retardation and birth defect caused by excess phenylalanine, and therein lies my basic concern, that aspartame is in fact a well known neurotoxin and teratogen which, in some as yet undefined dose, will irreversibly in the developing child or fetal brain, produce adverse effects: and
DR. ELSAS TESTIMONY IS DISCUSSED IN THE UPI INVESTIGATION: http://www.wnho.net/upi_1987_aspartame1.htm THIS WAS IN THE NOV 3, 1987 CONGRESSIONAL RECORD, AND THE ACTUAL PAGE WILL BE FAXED. ____________________
Whereas, there are tens of thousands of case histories and anecdotal accounts from victims of aspartame poisoning who have come forward to make their case histories known; now, therefore,
WE HAVE THESE AT MISSION POSSIBLE BEING TAKEN IN THE LAST 17 YEARS, AS WELL AS THOSE THE FDA ADMITS TO, AND THEY ARE BEING COLLECTED BY MISSION POSSIBLE CHAPTERS IN 38 NATIONS. _________________
BE IT RESOLVED by the Senate of the Twenty-Fourth Legislature of the State of Hawaii, Regular Session of 2008, the House of Representatives concurring, that the Department of Health is requested to create, within their existing budget, an evidentiary repository accessible to the public for patients and physicians to submit of the next year their cases involving victims of aspartame poisoning; and
BE IT FURTHER RESOLVED that the Director of Health is requested to report to the Legislature on the status of the evidentiary repository during periodic interim meetings with the Chairs of the Hawaii State Senate Committees on Health and Human Services and Public Housing, the House of Representatives Committees on Health and Human Services and Housing, and the state Attorney General; and
In 1980, Stephen Fox founded New Millennium Fine Art, a Santa Fe gallery specializing in Native American and Landscape, and is very active in New Mexico Legislative consumer protection politics, trying above to get the FDA to rescind its approval for the neurotoxic and carcinogenic artificial sweetener, Aspartame. [http://www.prlog.org/10070694]
In a strictly legislative context, his most important writing has been for the Hawaii Senate: http://www.prlog.org/10056715-hawaii-senate
In his capacity as Contributing Editor of the Santa Fe Sun News, Fox recently interviewed Mikhail Gorbachev: http://www.prlog.org/10064349-mikhail-gorbachev
He has been adamant and resourceful about exposing the charlatans of the sometimes-organic food movement. Take the time to read this press release concerning California Attorney General Jerry Brown's suits against Whole Foods, Avalon, and others, for either knowingly or negligently adding a deadly carcinogen to their body care products and soap, as in Whole Foods 365 Label products: http://www.prlog.org/10079593
He cordially invites all Op Ed News readers to visit New Mexico in 2008!
[ See also: methanol impurity in alcohol drinks [ and aspartame ] is turned into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Rich Murray 2008.02.24 http://rmforall.blogspot.com/2008_02_01_archive.htm Sunday, February 24, 2008 http://groups.yahoo.com/group/aspartameNM/message/1524 ]
Direct and indirect cellular effects of aspartame on the brain. Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa, Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12 http://groups.yahoo.com/group/aspartameNM/message/1463
"The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders (DSM-IV-TR 2000) and also in compromised learning and emotional functioning."
Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print] Direct and indirect cellular effects of aspartame on the brain. Humphries P, Pretorius E, resia.pretorius@up.ac.za; Naude H. [1] Department of Anatomy, University of Pretoria, Pretoria, Gauteng, South Africa [2] Department of Anatomy, University of the Limpopo, South Africa.
The use of the artificial sweetener, aspartame, has long been contemplated and studied by various researchers, and people are concerned about its negative effects.
Aspartame is composed of phenylalanine (50%), aspartic acid (40%) and methanol (10%).
Phenylalanine plays an important role in neurotransmitter regulation, whereas aspartic acid is also thought to play a role as an excitatory neurotransmitter in the central nervous system.
Glutamate, asparagines and glutamine are formed from their precursor, aspartic acid.
Methanol, which forms 10% of the broken down product, is converted in the body to formate, which can either be excreted or can give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives.
Previously, it has been reported that consumption of aspartame could cause neurological and behavioural disturbances in sensitive individuals.
Headaches, insomnia and seizures are also some of the neurological effects that have been encountered, and these may be accredited to changes in regional brain concentrations of catecholamines, which include norepinephrine, epinephrine and dopamine.
The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders (DSM-IV-TR 2000) and also in compromised learning and emotional functioning.
European Journal of Clinical Nutrition advance online publication, 8 August 2007; doi:10.1038/sj.ejcn.1602866. PMID: 17684524
Received 25 October 2006; revised 26 April 2007; accepted 27 April 2007 Correspondence: Professor E Pretorius, Department of Anatomy, University of Pretoria, BMW Building, Dr Savage Street, PO Box 2034, Pretoria 0001, Gauteng, South Africa. E-mail: resia.pretorius@up.ac.za
c 2007 Nature Publishing Group, All rights reserved 0954-3007/07 $30.00 www.nature.com/ejcn
[ Figures 1-6 not included herein ]
REVIEW
Introduction
The artificial dipeptide sweetener, aspartame (APM; Laspartyl-L-phenylalanine methyl ester), is present in many products in the market, especially in unsweetened or sugar free products.
People trying to lose weight or patients with diabetes, including children, frequently use these products.
A recent observation indicated that aspartame is slowly making its way into ordinary products used every day, which do not carry any indication of being for people on diets or diabetics.
Thus, aspartame is used not only by the above mentioned group of people, but also by unsuspecting individuals.
Although there is concern and research evidence suggesting possible adverse neurological and behavioural effects due to aspartame's metabolic components (phenylalanine, aspartic acid (aspartate), diketopiperazine and methanol), which are produced during its breakdown, research suggests that aspartame is not cytotoxic.
This debate still continues 20 years after the FDA had approved the use of aspartame.
As seen later in the literature study, phenylalanine may cross the blood-brain barrier and cause severe changes in the production of very important neurotransmitters.
Methanol breaks down into formate, which in turn is very cytotoxic and can even cause blindness.
The effects of aspartame have been studied on various species, including humans, rats, mice and rabbits.
Most studies described in the literature have a macroscopic approach.
If no adverse effects are visible after a single large administered dose of aspartame, it is believed that aspartame has no effect.
Further studies are not carried out microscopically to demonstrate possible adverse effects on the cellular basis.
Thus, results obtained from different studies vary from severe adverse effects to none observed.
The aim of this study was to investigate the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders (DSM-IV-TR 2000) and also in compromised learning and emotional functioning.
Most diet beverages and food products currently in the market contain aspartame as an artificial sweetener.
However, controversy surrounds the effects of this non-nutritive artificial sweetener, as it is made up of three components that may have adverse effects on neural functioning, particularly on neurotransmitters (Figure 1), neurons and astrocytes.
In light of the possible adverse effects of aspartame, the research questions directing this study are formulated as follows: What are the direct and indirect cellular effects of aspartame on the brain? How might excessive aspartame ingestion contribute to the pathogenesis of certain mental disorders? What are the implications for early brain development, emotional status and learning following high ingestion of aspartame?
Aspartame is composed of phenylalanine (50%), aspartic acid (40%) and methanol (10%).
The first two are known as amino acid isolates.
It has been reported that consumption of aspartame could cause neurological and behavioural disturbances in sensitive individuals (Anonymous, 1984; Johns, 1986).
Headaches, insomnia and seizures are some of the neurological disturbances that have been encountered, and this may be accredited to changes in regional brain concentrations of catecholamines, which include norepinephrine, epinephrine and dopamine (Coulombe and Sharma, 1986), all important neurotransmitters regulating life-sustaining functions.
The effects of phenylalanine, aspartic acid and methanol are first reviewed, followed by a discussion of altered neurotransmitter functioning, that is dopamine, serotonin, glutamate, g-aminobutyric acid (GABA), and acetylcholine.
The discussion is concluded with implications for early brain development, emotional status and learning following high ingestion of aspartame.
Effects of phenylalanine
Phenylalanine not only plays a role in amino acid metabolism and protein structuring in all tissues, but is also a precursor for tyrosine (Hawkins et al., 1988), DOPA, dopamine, norepinephrine, epinephrine (Ganong, 1997), phenylethylamine (Young, 1988) and phenylacetate (as phenylacetate interferes with brain development and fatty acid metabolism).
Phenylalanine also plays an important role in neurotransmitter regulation (Caballero and Wurtman, 1988).
Phenylalanine can follow one of the two pathways of uptake in the body.
A part is converted into tyrosine (a nonessential amino acid) in the liver (Caballero and Wurtman, 1988) by the enzyme phenylalanine hydroxylase (Figure 2a)
The remaining portion of phenylalanine (not converted in the liver) will bind to a large neutral amino acid transporter (NAAT) to be carried over the blood-brain barrier (BBB) (Figure 2b).
A large number of compounds, including phenylalanine and tyrosine, compete with each other for a binding site on the NAAT, because it is the only manner in which they can cross the BBB.
Importantly, tyrosine cannot be synthesized in the brain and has have to enter the BBB via NAAT (Figure 2c) for production.
Memory loss is thought to be due to aspartic acid and phenylalanine being neurotoxic without the other amino acids found in protein.
These neurotoxic agents might cross the BBB and deteriorate the neurons of the brain (Mehl-Madrona, 2005).
NAAT is also a co-transporter for phenylalanine, tryptophan (an important precursor for synthesis of serotonin), methionine and the branch-chained amino acids.
All the above-mentioned amino acids (tyrosine, phenylalanine, tryptophan and methionine) compete for the NAAT transporter, so a large quantity of one amino acid in the blood stream will occupy most of this transporter.
This results in a phenylalanine overload in the surrounding areas, greatly limiting the amount of important amino acids (for example, tyrosine, tryptophan and methionine) entering the brain (Figure 2c).
If high concentration of aspartame is taken through the daily diet, 50% of it is broken down to phenylalanine.
Phenylalanine will then be either converted into tyrosine or cross the BBB as it is.
Tyrosine is converted into dihydroxyphenylalanine (DOPA) once it is in the brain, by the enzyme tyrosine hydroxylase, with the help of the co-factors oxygen, iron and tetrahydrobiopterin (THB) (Figure 2d).
Dopamine, a catecholamine, is formed from DOPA by an aromatic amino acid decarboxylase.
Tyrosine hydroxylase activity is inhibited by high concentrations of dopamine through its influence on the THB co-factor (negative feedback, Figure 2d).
This system is very necessary to prevent large amount of dopamine being produced, as dopamine is an inhibitory neurotransmitter.
However, if phenylalanine, as the main part of aspartame, competes with tyrosine for NAAT, a compromised dopamine production will result, because phenylalanine will bind more frequently and freely than tyrosine, owing to its higher concentration, and thus lead to lower concentrations of dopamine in the brain.
After administration of aspartame to humans, the increases in blood levels of both phenylalanine and tyrosine have been well documented (Fernstorm, 1988; Filer and Stegink, 1988).
Therefore, phenylalanine (formed by breakdown of aspartame) will increase in the brain owing to the ingestion of aspartame, and tyrosine will increase as a breakdown byproduct of phenylalanine in the liver (Fernstorm, 1988; Filer and Stegink, 1988).
Thus, aspartame and its components could potentially disrupt a wide range of processes in the body, including amino acid metabolism, protein structure and metabolism, nucleic acid integrity, neuronal function and endocrine balances.
Aspartame ingestion directly results in an increase in phenylalanine and tyrosine levels in the brain, which in turn leads to changes in the regional brain concentrations of catecholamines (for example, dopamine) (Fernstorm et al., 1983).
According to Mehl-Madrona (2005) aspartame changes the dopamine level in the brain, affecting people suffering from Parkinson's disease.
Bowen and Evangelista (2002) noted a substantial increase in the levels of plasma phenylalanine and aspartic acid after ingestion of aspartame.
This increased phenylalanine, thereby causing a PKU (phenylketonuria) effect.
PKU, also known as phenylpyruvic oligophrenia, is a disorder characterized by accumulation of phenylalanine and its keto derivatives in the blood, tissues and urine.
This disorder is a direct result of a hereditarydeficiency or absence of phenylalanine hydroxylase.
As described previously, this enzyme is necessary for conversion of phenylalanine into tyrosine.
The enzymes required for the reduction of circulating phenylalanine are overwhelmed, thus also interfering with other metabolic reactions that utilize these enzymes, resulting in the PKU effect.
This causes reduced dopamine and serotonin production as the enzyme actions controlling numerous types of neurotransmitters (and their precursor amino acids) are debilitated by overdoses of the competitive circulating phenylalanine isolates (and aspartic acid isolates; Bowen and Evangelista, 2002).
Serotonin, an indolamine, causes powerful smooth muscle contraction (Ganong, 1997).
Physiologically, it is also important for behaviour and control of sleep, temperature, appetite and neuroendocrine functions.
Tryptophan, independently utilized for synthesis of serotonin in the brain, is transported across the BBB via NAAT.
Therefore, if NAAT is occupied with phenylalanine, tryptophan will not be adequately carried across the BBB and serotonin production can ultimately be compromised (Figure 3).
Aspartame administered orally in mice as single doses gave contradictory results;
norepinephrine and dopamine (precursor of norepinephrine) concentrations in various brain regions increased significantly, and not as observed above.
However, mice have a different metabolism for aspartame and its breakdown products are different from those of human beings; this could be the reason for these contradictory results.
Sharma and Coulombe (1987) also analysed different regions for catecholamine (for example, dopamine) and indoleamine (for example, serotonin) neurotransmitters and their major metabolites.
Results from this study indicated that single dose exposure increased adrenergic chemicals, which were not apparent after repeated dosing with aspartame.
In contrast to the above observation, decreased serotonin and its metabolite, 5-hydroxyindoleacetate, was found in several regions (Sharma and Coulombe, 1987).
The lowered levels of serotonin might cause the following:
A compromised BBB -- due to lower levels of activity of cAMP, which plays an important role in the complexity of the tight junctions in the epithelial cells of the capillaries (Figure 3).
Lowered activity of the GABA transporters -- thus GABA is absorbed at a lower rate into the astrocytes, which results in the continuous inhibition of depolarization of the postsynaptic membrane (Figure 4).
Maher and Wurtman (1987) suggested that aspartame consumption could cause neurological or behavioural reactions in some people.
When mice were given aspartame in doses that raise plasma phenylalanine levels more than those of tyrosine (which probably occurs after any aspartame dose in humans), the frequency of seizures increased, especially following the administration of the epileptogenic drug, pentylenetetrazole
Equimolar concentrations of phenylalanine stimulate this effect and are blocked by synchronized administration of valine, which blocks phenylalanine's entry into the brain (Maher and Wurtman, 1987).
Glutamate, the most common neurotransmitter in the brain, is formed from its precursor a-ketoglutarate from the Kreb's cycle (Figure 5).
Glutamate is primarily produced in neurons as excitatory neurotransmitters, owing to an increased flow of positive ions (sodium and calcium) by opening the ion-channel after binding to appropriate receptors.
Stimulation of these receptors is terminated by a chloride-independent membrane transport system, which is used only for reabsorbing glutamate and aspartate across the presynaptic membrane.
Glutamate can also be reabsorbed into the neurons for later use.
Excess glutamate released into the synapses is converted into glutamine (non-excitotoxic molecule) by nearby astrocytes (glial cells).
Glutamine is safely transported back to neurons, for reconversion into glutamate.
Swollen astrocytes contribute to the excitotoxicity of glutamate, owing to their inability to absorb excess glutamate.
Glutamate acts on its postsynaptic N-methyl-Daspartate (NMDA) and non-NMDA receptors.
The NMDA receptor is an ion channel for calcium, sodium and potassium ions.
Glutamate and aspartate exert their action through three separate receptors, characterized by selective interaction with NMDA, quisqualate and kainate (Hidemitsu et al., 1990).
The glutamate recognition sites might directly be acted upon by aspartame in the brain synaptic membranes.
This interaction might play a vital role in mediating the potentiation of hippocampal excitability as reported by Fountain et al. (1988).
As discussed above, aspartame may act on the NMDA receptors, leading to continuous activation of these receptor sites, resulting in no binding space for glutamate.
Continuous activation might cause damage to brain neurons, as suggested by Choi and Rothman (1990).
Thus, aspartame acts as an agonist of glutamate on the NMDA receptor (Fountain et al., 1988).
GABA is also primarily produced by neurons in the citric acid cycle from succinate and is inactivated by absorption into astrocytes (Figure 5).
GABA is secondarily produced in astrocytes from glutamine.
It can be released from the astrocytes as GABA or it can be reabsorbed into the neuron as glutamine (for conversion into either glutamate or GABA).
If the neuroenergetics of the cells were compromised by the presence of aspartame, thus lowering glucose and oxidative metabolism, this important feedback system of tryptophan and tyrosine will be inhibited (Ganong, 1997).
Owing to a lowered level of oxidative metabolism and low glucose levels in the cells, pyruvate would not be converted into acetyl CoA, necessary for production of acetylcholine in synapses (Figure 6).
Thus, it could lead to a decreased stimulation of second messengers (often cyclic AMP) to indirectly open the ion channels.
Since aspartame causes neurodegeneration (destruction of neurons), the neurons in the Meynert nucleus will also be decreased.
The Meynert nucleus is the primary cholinergic input for the cerebral cortex, and loss of neurons in this nucleus has been shown in Alzheimer's patients.
Thus, aspartame might be involved in the cause/mimic of Alzheimer's disease (Ganong, 1997; Bowen and Evangelista, 2002).
Effects of aspartic acid
One of the largest studies commissioned by the aspartame manufacturers are of the opinion that: 'in most cases aspartate concentrations were not significantly affected by aspartame ingestion' (Stegink et al., 1988; Stegink et al., 1989).
If read in another way, it suggests that in some cases aspartic acid was, indeed, increased.
Aspartic acid is thought to play a role as an excitatory neurotransmitter in the central nervous system (Watkins, 1984; Stone and Burton, 1988).
Glutamate, asparagines and glutamine are formed from their precursor, aspartic acid (Stegink et al., 1989).
Aspartate is inactivated by reabsorption into the presynaptic membrane and it opens an ion channel (Olney, 1975).
Aspartate is an excitatory neurotransmitter and has an increased likelihood for depolarization of the postsynaptic membrane.
Even short-lived increases of a powerful neural stimulator are enough to induce neuroendocrine disturbances (Olney, 1975).
In addition, Mehl-Madrona (2005) observed that when the temperature of aspartame exceeds 86 degrees F, the wood alcohol in aspartame is converted into formaldehyde and then to formic acid, which in turn causes metabolic acidosis.
The methanol toxicity is thought to mimic the symptoms of multiple sclerosis.
According to them, symptoms of fibromyalgia, spasms, shooting pains, numbness in the legs, cramps, vertigo, dizziness, headaches, tinnitus, joint pain, depression, anxiety, slurred speech, blurred vision or memory loss have been attributed to aspartame.
Effects of methanol
As mentioned previously, aspartame breaks down to form phenylalanine, aspartic acid and methanol, which forms 10% of the break down product.
The methanol in the body is converted to formate, which is then excreted.
It can also give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives (Clarke, 2000
The absorption-metabolism sequence of methanol-formaldehyde-formic acid also results in synergistic damage (Bowen and Evangelista, 2002).
The accumulation of formate, rather than methanol, is itself considered to cause methanol toxicity (Stegink et al., 1989), but research has shown that formaldehyde adducts accumulate in the tissues, in both proteins and nucleic acids, after aspartame ingestion (Trocho et al., 1998).
The formed adducts of the metabolic poisons alter both mitochondrial DNA and nucleic DNA.
Methanol and formaldehyde are also known to be carcinogenic and mutagenic.
The damaged DNA could cause the cell to function inadequately or have an unbalanced homoeostasis, thus initiating disease states (Bowen and Evangelista, 2002).
In addition, it is thought that the methanol is the aspartame is converted to formaldehyde in the retina of the eye, causing blindness (Mehl-Madrona, 2005).
As seen from the above discussion, tryptophan, tyrosine and phenylalanine are precursors for the neurotransmitters serotonin, dopamine and norepinephrine.
Glutamate (glutamic acid) and aspartate (aspartic acid), as neurotransmitters, have no direct access to the brain and have to be synthesized in the neuronal cells of the brain.
Proteins rich in aspartate and glutamate have no effect on the levels of acidic amino acids in the brain.
If aspartame is ingested in large amounts, it will increase the levels of acidic amino acids in the brain (Fernstrom, 1994).
Effects of aspartame on the blood brain barrier
A compromised BBB (altered lipid-mediated transport or active carrier transport) will result in the transport of excitotoxins (aspartame) across BBB and within the cerebrospinal fluid, causing several adverse reactions to occur:
The nerves will be stimulated to fire excessively by the excitotoxins.
The offset of induced, repeated firing of the neurons mentioned above will require normal enzymes, which are negated by the phenylalanine and aspartic acid present in aspartame.
These compulsory enzyme reactions mentioned above require a normal functioning energy system.
Thus, it could be stated that the neurons become compromised from (Bowen and Evangelista, 2002):
diminishing intracellular ATP stores;
the presence of formaldehyde; intracellular calcium uptake been changed (e.g. phenylalanine binds to NMDA receptor, not glutamate, thus altering calcium channels);
cellular mitochondrial damage;
destruction of the cellular wall; and
subsequent release of free radicals.
These preceding reactions potentiate oxidative stress and neurodegeneration.
Secondary damage is caused by the toxic by-products, which in turn will increase capillary permeability, continuing to destroy the surrounding nerve and glial cells, thus further obstructing enzyme reactions and promoting DNA structural defects.
Cellular death occurs over the next 1-12 h (Bowen and Evangelista, 2002).
Excitotoxic-saturated placental blood flow, caused by maternal aspartame consumption, could lead to the damage or impairment of the development of the foetal nervous system, contributing to cerebral palsy and all-encompassing developmental disorders (Bowen and Evangelista, 2002).
Mehl-Madrona (2005) also cited findings implicating aspartame consumption at the time of conception to consequent birth defects, because the phenylalanine concentrates in the placenta, causing mental retardation.
Laboratory tests showed that animals developed brain tumours as a result of aspartame administration. It was also pointed out that phenylalanine breaks down into 1-deoxy-D-xylulose-5-phosphate (DXP), a brain tumour agent.
In keeping with these findings, neuronal (brain) damage is also produced by excitotoxins circulating in the fetal brain areas, as a result of an incompetent BBB.
This is especially true for those areas adjacent to the brain's ventricular system.
The methanol components of aspartame are thought to mimic fetal alcohol syndrome, which is a direct result of the maternal ingestion of aspartame (Bowen and Evangelista, 2002). [ See: methanol impurity in alcohol drinks [ and aspartame ] is turned into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Rich Murray 2008.02.24 http://rmforall.blogspot.com/2008_02_01_archive.htm Sunday, February 24, 2008 http://groups.yahoo.com/group/aspartameNM/message/1524 ]
The amino acids that constitute meat contain a chain of 80-300 amino acids, of which 4% are phenylalanine.
This chain also includes the amino acid valine.
Valine inhibits the transport of phenylalanine into the brain across the BBB.
In aspartame, phenylalanine makes up 50% of the molecule; thus, in a can of diet soda, which contains 200 mg aspartame, 100 mg is phenylalanine.
No valine is present in aspartame to block the entry of toxic levels of phenylalanine into the brain, thus resulting in lowered concentrations of dopamine and serotonin, owing to NAAT occupation by phenylalanine.
Thus, it can be concluded that the usage of aspartame should be carefully considered as it (and its metabolites) causes detrimental effects, ranging from alterations in concentrations of neurotransmitters to causing infertility.
Thus, human health at the macroscopic, microscopic and cellular level is at risk of being destroyed.
Comparison between human and animal reaction to aspartame
Physiologically, the animals tested for phenylalanine toxicity are approximately 60 times less sensitive than human beings.
Humans are 10 - 20 times more sensitive to methanol poisoning, both as a subchronic and chronic toxin/carcinogen.
The differences in enzyme concentrations of the species suggest that animals studied are more sensitive to the more common ethanol found in alcoholic beverages.
Test animals being used are 8 -10 times less sensitive than humans to the effects of aspartic acid and glutamates (Bowen and Evangelista, 2002).
Implications of aspartame consumption for early brain development and everyday living
Ingestion of aspartame results in a craving for carbohydrates, which will eventually result in weight gain, especially because the formaldehyde stores in the fat cells, particularly in the hips and thighs; therefore, aspartame is believed to cause problem in diabetic control. (Mehl-Madrona, 2005).
In addition, prenatal consumption of aspartame might result in mental retardation, impaired vision, birth defects and is thought to play a role in the pathogenesis of Alzheimer's disease;
furthermore, it is implicated in disruption of learning and emotional functioning due to its involvement in alteration of certain neurotransmitters.
The earlier research findings show that aspartame consumption might affect early brain development and neurotransmitter systems, which might result in specific emotional, behavioural and learning difficulties as discussed below.
[ for much more, use initial URSs..... ]
by
Rich Murray (0 articles, 0 quicklinks, 1 diaries, 13 comments)
on Thursday, April 10, 2008 at 3:40:45 PM
formaldehyde from aspartame causes contact dermatitis
formaldehyde from many sources, including aspartame, is major cause of Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging 2005 Dec.: Murray 2008.03.27
"For example, diet soda and yogurt containing aspartame (Nutrasweet), release formaldehyde in their natural biological degradation.
One of aspartame's metabolites, aspartic acid methyl ester, is converted to methanol in the body, which is oxidized to formaldehyde in all organs, including the liver and eyes. 22
Patients with a contact dermatitis to formaldehyde have been seen to improve once aspartame is avoided. 22
Notably, the case that Hill and Belsito reported had a 6-month history of eyelid dermatitis that subsided after 1 week of avoiding diet soda. 22"
"We present a case of a medical student who presented with erythematous eczematoid plaques on her trunk and legs and fine vesiculation of her scalp, 3 weeks after starting anatomy class.
Of note, she routinely washed her face and arms after leaving the anatomy lab, but remained in her scrubs for the rest of the day.
Formaldehyde and Quaternium-15 positive reactions in the same patient."
"Our patient underscores the importance of appropriate patch testing and education. Once we identified the allergy to formaldehyde and quaternium-15, we provided patient education materials regarding the common and not-so-common locations of these chemicals and cross-reactors. We also gave the patient information on avoidance and safe alternatives (see Table 5).
Fortunately, with technical advances, this student completed the anatomy section via electronic learning tools.
By avoiding formaldehyde, including anatomy lab, FRP in her shampoo and cosmetics, and aspartame in her diet, this patient dramatically improved.
As with all contact dermatitides, the mainstay of treatment for allergic contact dermatitis is avoidance."
Allergen Focus: Focus on T.R.U.E. Test Allergens #21, 13 and 18: Formaldehyde and Formaldehyde-Releasing Preservatives -- By Sharon E. Jacob, M.D., Tace Steele, B.A., [now MD] and Georgette Rodriguez, M.D., M.P.H.
Allergic Contact Dermatitis is an important disease with a high impact both in terms of patient morbidity and economics.
The contact dermatitides include irritant contact dermatitis, contact urticaria and allergic contact dermatitis.
Irritant contact dermatitis, the most common form, accounts for approximately 80% of environmental-occupational based dermatoses.
Contact urticaria (wheal and flare reaction) represents an IgE and mast cell-mediated immediate-type hypersensitivity reaction that can lead to anaphylaxis, the foremost example of this would be latex hypersensitivity. While this is beyond the scope of this section, we acknowledge this form of hypersensitivity due to the severity of the potential reactions and direct the reader to key sources. 1,2
Allergic contact dermatitis, on the other hand, is a delayed type IV hypersensitivity reaction. The primary focus of this section is to highlight the educational component of allergic contact dermatitis.
Clinical Illustration
We present a case of a medical student who presented with erythematous eczematoid plaques on her trunk and legs and fine vesiculation of her scalp, 3 weeks after starting anatomy class. Of note, she routinely washed her face and arms after leaving the anatomy lab, but remained in her scrubs for the rest of the day.
Formaldehyde and Quaternium-15 positive reactions in the same patient.
History of Formaldehyde and the Formaldehyde-Releasing Preservatives
The desire to improve one's appearance with topical applications dates back to the Egyptian Queen, Cleopatra, who was fond of using creams and make-up for skin beautification. 3
What once was fit for a queen has become a $30 billion a year cosmetic industry. 4
With the cosmetic boom came the concern of microorganisms in cosmetic creams introduced during manufacture or transferred to the product through use. 5
A variety of reports of cosmetic contamination from Klebsiella pneumoniae have been reported.
In addition, this bacterium has been linked to septicemia after contact with a contaminated hand cream dispenser. 6,7
Consequently, considerable attention has been given to topical pharmaceutical preparations with effective methods of antimicrobial preservation.
Preservatives are biocidal chemicals added to cosmetics, topical medicaments and foods to protect against spoilage, bacterial and fungal contamination, and biological degradation. 7
The ideal preservative should be stable, antimicrobial, nontoxic, non-irritating and active over a broad range of pH values.
In 1938, the FDA passed the Food, Drug and Cosmetic Act requiring the cosmetic industry to prove product safety before marketing to consumers. 8
Prior to that, products such as Lash-Lure (by the Los Angeles-based company) containing paraphenylenediamine had caused blindness, and a whitening foundation containing lead oxide had caused muscle paralysis. 9
Soon thereafter, formaldehyde preservation of cosmetics was being streamlined for its many advantages. It was cheap and effective in eliminating a wide range of microorganisms and aggressively destroying degradation enzymes, thus slowing product decomposition. Formaldehyde remains a commonly used preservative in cosmetics today with an average concentration between 0.02% and 0.3%. 10
How It Was Discovered
A formaldehyde-based white brittle material, polyformaldehyde was discovered during the incomplete combustion of carbon in 1859 by the Russian chemist, Alexander Mikhailovich Butlerov. This leader in isomer chemistry (and synthesizer of the first artificial sugar) has had a crater on the moon named after him to commemorate his work. 11,12
Ten years after the polymer discovery, the German chemist, August Wilhem von Hofman, found that by passing methanol and air over a heated platinum spiral, he could create pure formaldehyde (a technique is still used today). 13
In 1892, the year of Hofman's death, Friedrich August Kekule von Stradonitz, the scientist who introduced the concept of chemical bonds, isolated pure formaldehyde by the catalytic oxidation of methanol.
First Commercial Uses
One of the first mass commercial uses of formaldehyde was in medical embalming (a practice known to be utilized during the Civil War). 14
Interestingly, formaldehyde use evolved with medical advancement. In 1883, Robert Koch made a landmark discovery with a weighty economic impact to the food industry. He found that the bacterium, Vibrio cholerae, the cause of cholera, could be transmitted via food and water. This discovery initiated the demand for government regulation of food industry sanitation and the necessitation of antimicrobial food additives. 8
In 1900, San Franciscan Chinese immigrants suffered from an outbreak of the bubonic plague. The city board of health quarantined Chinatown and dusted the district with a mixture of lime and formaldehyde to control the spread of disease. 15
In 1912, Dr. Harvey Wiley, Head of the Department of Chemistry in Washington D.C. (Predecessor to the Food and Drug Administration), founded the "poison squad". This squadron of volunteers ate food to test the safety of added preservatives (for example, borax, benzoic acid, sulfuric acid and formaldehyde). The poison squad was so popular with the public that minstrel shows sang about it:
"Next week he'll give them mothballs, a la Newburgh or else plain; O, they may get over it, but they'll never look the same." 8
After 5 years of experiments, vomiting and stomach pain, Dr. Wiley publicly resolved that preservatives in food and medications should "only be used when absolutely necessary," despite big business fighting him "tooth and nail". 8
In the 1950s, formaldehyde again made its mark in the medical news. Jonas Salk's team created a polio vaccine. This was made possible through the use of formaldehyde to kill the poliovirus. 15
Success with Plastics
Although the medical and food industries had mixed experiences with formaldehyde, the plastics industry thrived because of it.
Prior to innovation of formaldehyde-derived plastics, the celluloid plastics had been highly flammable and not suitable for mass marketing. 16 At the turn of the century, the International Galalith Gesellschaft Hoff and Company compounded formaldehyde and fat-free milk curd to formulate a new synthetic plastic (casein-formaldehyde), which became a main constituent of buttons. 16,17
The biggest landmark in formaldehyde-based plastics came in 1910. Leo H. Baekeland condensed phenol and formaldehyde to make the first non-flammable synthetic plastic, Bakelite, which had high utility as an electronics insulator. 10,18 Bakelite sales skyrocketed, as it was marketed in toys, jewelry and cameras. The Bakelite Museum in England even boasts a Bakelite coffin! 19
Its amber color contributed to its popularity in jewelry, but limited its potential when transparency was needed. 10 During the Bakelite heyday, circa 1912, scientists, Daniel J. O'Conor and Herbert Faber, added formaldehyde to a urea polymer to develop a novel insulation substitute for mica, aka formica. 18
The 1920s and '30s, saw the explosive age of the urea formaldehyde resins whose colorless properties allowed new lines of plastic products in bright colors, i.e the trendy plastic versions of marble dishes, bandalasta. 11,21
Today, urea-formaldehyde resins and melamine-formaldehyde laminates dominate the commercial market. What began as a reach for a new plastic alternative and preservative has become a $500 billion industry, representing 5% of the United States' gross national product. 11
Formaldehyde is used to make plywood, asphalt shingles, car gears and bearings.
Specifically, p-tert-Butylphenol formaldehyde resin is used in bonded leather, construction materials and waterproof glues.
In addition, fertilizers and photographic developers are also known to contain formaldehyde. 11
A Powerful Allergen
The rates of sensitization to formaldehyde have risen to 9.2%. 22,23
Formaldehyde is second only to fragrances as the most common sources of cosmetic-associated contact dermatitis. 24
To decrease sensitization and lower the concentration of formaldehyde, the formaldehyde-releasing-preservatives (FRPs)\ are often used in place of frank formaldehyde, for example quaternium-15 (see Table 1). 7,22,25
Herbert and Rietschel explain that if the concentration of formaldehyde that is released by FRPs is below the threshold of reactivity for virtually all formaldehyde-sensitive patients (somewhere between 30 and 250 ppm), there would not be an allergy to the FRP. 25
Many cases of contact dermatitis to formaldehyde/FRPs present as eyelid dermatitis associated with the use of cosmetics (mascara, blush and foundation), shampoos, medical creams or nail hardeners, to name a few.
Other important sources of exposure include permanent press clothing, cleaning agents, baby wipes, disinfectants, paper and even cigarette smoke. 22
As is often the case in contact dermatitis, the distribution of the dermatitis can provide insight into the exposure. For example, patients sensitized to formaldehyde from adorned permanent-press clothing tend to present with a chronic dermatitis around their body folds, where the clothes rub against the skin. 22
Patients sensitized to formaldehyde in clothing textiles have been found to become secondarily sensitized to quaternium-15, presenting with a diffuse nummular dermatitis or erythroderma. 24
Systematized dermatitis is seen with both formaldehyde and the FRPs.
Inhalation (smoking) and ingestion of formaldehyde containing foods are important systemic sensitization sources (see Table 2) .27-30
For example, diet soda and yogurt containing aspartame (Nutrasweet), release formaldehyde in their natural biological degradation.
One of aspartame's metabolites, aspartic acid methyl ester, is converted to methanol in the body, which is oxidized to formaldehyde in all organs, including the liver and eyes. 22
Patients with a contact dermatitis to formaldehyde have been seen to improve once aspartame is avoided 22
Notably, the case that Hill and Belsito reported had a 6-month history of eyelid dermatitis that subsided after 1 week of avoiding diet soda. 22
Formaldehyde-Releasing Preservatives
The formaldehyde releasers are reversible polymers of formaldehyde. 31
Formaldehyde is formed in different amounts based on the pH, temperature, and amount of water. 31,32 The antibacterial effects are independent of the amount of formaldehyde released. 29
An allergic reaction can be seen specifically to the FRP, formaldehyde or both. 31
Quaternium-15, a colorless, odorless, biocidal FRP is highly water-soluble, stable, and active over a broad range of pH.
It has broad antimicrobial activity, particularly Pseudomonas aeruginosa, yeasts, and molds. 22
As the most common sensitizer among the formaldehyde-releasers, it is included on the T.R.U.E. test and has many alternative names (see Table 3). 23
Occupational sources
Occupation is one of the biggest risk factors for quaternium-15 exposure. Occupations such as hair dressing, painting, printing, textile dyeing, paper processing and working with disinfectants all have greater risks of developing allergies to quaternium-15, according to Haz-Map, an organization that evaluates occupational risks for exposures to hazardous chemicals.
Formaldehyde is both an irritant and a contact allergen.
Contact urticaria and anaphylaxis to formalin have been described in a patient after a root canal and in a hemodialysis patient, respectively (see list of systemic formaldehyde effects in Table 4). 28,33
Garment industry workers, hemodialysis nurses, embalmers, pathologists, and dermatologists are at great occupational risk for occupational-based formaldehyde allergy.
Due to the notoriety it has received as a potential carcinogen, irritant, and sensitizer, formaldehyde use in cosmetics has significantly decreased. Notably, formaldehyde is prohibited in cosmetics in Sweden and Japan. 22
Testing for Allergy to Formaldehyde and FRPs
Patch testing for formaldehyde, quaternium-15, and p-tert-Butylphenol formaldehyde resin allergy can be accomplished with the Thin-layer Rapid Use Epicutaneous (T.R.U.E.) test (sites 18, 21, and 13, respectively).
The T.R.U.E. test is the commercially available, globally used, allergen screening system.
While it is widely used, the discrepancy in allergen prevalence and uncertain relevance has led to scrutiny of its utility.
The T.R.U.E test contains 23 allergens and one negative control.
At best, the T.R.U.E test is a minimum screening tool because it tests only 23 of the more than 3,700 possible allergens that can cause allergic contact dermatitis.
Krob et al. recently demonstrated that nickel, thimerosal, cobalt, fragrance and balsam of Peru are the most prevalent allergens detected by the T.R.U.E. test, yet a significant number of relevant allergens, not present on the T.R.U.E. test, are potentially missed by this screening tool used alone. 34
Value of this Patient Case
Our patient underscores the importance of appropriate patch testing and education
Once we identified the allergy to formaldehyde and quaternium-15, we provided patient education materials regarding the common and not-so-common locations of these chemicals and cross-reactors.
We also gave the patient information on avoidance and safe alternatives (see Table 5).
Fortunately, with technical advances, this student completed the anatomy section via electronic learning tools.
By avoiding formaldehyde, including anatomy lab, FRP in her shampoo and cosmetics, and aspartame in her diet, this patient dramatically improved.
As with all contact dermatitides, the mainstay of treatment for allergic contact dermatitis is avoidance.
[ for much more, use initial URLs.... ]
by
Rich Murray (0 articles, 0 quicklinks, 1 diaries, 13 comments)
on Thursday, April 10, 2008 at 3:48:53 PM
methanol from aspartame becomes neurotoxic formic acid
methanol impurity in alcohol drinks [ and aspartame ] is turned into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Rich Murray 2008.02.24 http://rmforall.blogspot.com/2008_02_01_archive.htm Sunday, February 24, 2008 http://groups.yahoo.com/group/aspartameNM/message/1524 ____________________________________________________
[ Rich Murray comments: As a medical layman volunteer information activist for aspartame and related toxicity issues since January 1999, I note with appreciation the remarkable exponential progress on all fronts, including a rapidly emerging consensus about the primary importance of all toxicity challenges for our world.
This lengthy review features in detail two quite different, revolutionary contributions, from Canada, and England and China.
It is indicative of our times that the CL Nie et al. study, 2007 appears in a free, open access journal-- indeed, as all life and death information must.
Following rather vigorously, indeed blindly, the imperatives of single-minded, profit-driven capitalist competition -- manipulating adroitly research, education, media, citizens, governments -- many great global corporations have inevitably created results that oppose the common good. Alcohol and tobacco are well known.
Realistically, any further manipulations can only lead to inevitable and even sudden corporate meltdowns, in the context of an unfettered, cooperative, democratic global information forum, the Internet.
Now, it is as easy and cheap to compose and instantly post a 30-page review as 3 pages a decade ago -- and such reviews are archived forever in multiple collections, open via global search engines to a billion Net citizens.
Perforce, and increasingly happily, all societal entities will have to operate by high and shared voluntary universal standards for the common good. ]
Alcoholism: Clinical and Experimental Research Volume 31 Issue 12 Page 2114-2120, December 2007
Bhushan M. Kapur, b.kapur@utoronto.ca; Arthur C. Vandenbroucke, PhD, FCACB Yana Adamchik, Denis C. Lehotay, dlehotay@health.gov.sk.ca; Peter L. Carlen carlen@uhnres.utoronto.ca; (2007) Formic Acid, a Novel Metabolite of Chronic Ethanol Abuse, Causes Neurotoxicity, Which Is Prevented by Folic Acid Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120. doi:10.1111/j.1530-0277.2007.00541.x
Abstract
Background: Methanol is endogenously formed in the brain and is present as a congener in most alcoholic beverages.
Because ethanol is preferentially metabolized over methanol (MeOH) by alcohol dehydrogenase, it is not surprising that MeOH accumulates in the alcohol-abusing population.
This suggests that the alcohol-drinking population will have higher levels of MeOH's neurotoxic metabolite, formic acid (FA).
FA elimination is mediated by folic acid.
Neurotoxicity is a common result of chronic alcoholism.
This study shows for the first time that FA, found in chronic alcoholics, is neurotoxic and this toxicity can be mitigated by folic acid administration.
Objective: To determine if FA levels are higher in the alcohol-drinking population and to assess its neurotoxicity in organotypic hippocampal rat brain slice cultures.
Methods: Serum and CSF FA was measured in samples from both ethanol abusing and control patients, who presented to a hospital emergency department. [ CSF = Cerebral Spinal Fluid ]
FA's neurotoxicity and its reversibility by folic acid were assessed using organotypic rat brain hippocampal slice cultures using clinically relevant concentrations.
Results: Serum FA levels in the alcoholics (mean ± SE: 0.416 +- 0.093 mmol/l, n = 23) were significantly higher than in controls (mean ± SE: 0.154 +- 0.009 mmol/l, n = 82) (p < 0.0002).
FA was not detected in the controls' CSF (n = 20), whereas it was >0.15 mmol/l in CSF of 3 of the 4 alcoholic cases.
Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours to the rat brain slice cultures caused neuronal death as measured by propidium iodide staining.
When folic acid (1 umol/l) was added with the FA, neuronal death was prevented. [ umol = micromole ]
Conclusions: Formic acid may be a significant factor in the neurotoxicity of ethanol abuse.
This neurotoxicity can be mitigated by folic acid administration at a clinically relevant dose.
From the Department of Clinical Pathology (BMK), Sunnybrook Health Science Centre, Division of Clinical Pharmacology and Toxicology, The Hospital for Sick Children, Toronto, Ontario, Canada;
St. Michael's Hospital (ACV), Toronto, Canada;
Department of Laboratory Medicine and Pathobiology (BMK, ACV), Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada;
Departments of Medicine (Neurology) and Physiology (YA, PLC), Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada;
and University of Saskatchewan (DLC), Saskatchewan, Canada.
Received for publication May 1, 2007; accepted September 24, 2007.
Reprint requests: Dr. Bhushan M. Kapur, Department of Clinical Pathology, Sunnybrook Health Science Centre, 2075 Bayview Ave, Toronto, Ontario, M4N 3M5, Canada; Fax: 416-813-7562; E-mail: b.kapur@utoronto.ca;
Copyright 2007 by the Research Society on Alcoholism. DOI: 10.1111/j.1530-0277.2007.00541.x Alcoholism: Clinical and Experimental Research 2007 Dec. Alcohol Clin Exp Res, Vol. 31, No 12, 2007: pp 2114-2120
NEUROTOXICITY AND BRAIN damage are common concomitants findings of chronic alcoholism (Carlen and Wilkinson, 1987; Carlen et al., 1981; Harper, 2007).
The cause of ethanol-induced neurotoxicity is still unclear.
We present here a novel hypothesis for neurotoxicity: increased formic acid (FA) levels produced from methanol (MeOH), whose catabolism is blocked by ethanol.
Axelrod and Daly (1965) demonstrated the endogenous formation of MeOH from S-adenosylmethionine (SAM) in the pituitary glands of humans and various other mammalian species.
Presence of MeOH in the breath of human subjects was reported by Ericksen and Kulkarni (1963).
Most alcoholic beverages also have a small amount of MeOH as a congener (Sprung et al., 1988).
As ethanol (EtOH) has a higher affinity for alcohol dehydrogenase (ADH) than MeOH, EtOH is preferentially metabolized (Mani et al., 1970).
As a result, MeOH accumulation from endogenously produced MeOH, and/or, that consumed as part of an alcoholic beverage, has been reported in concentrations up to 2 mmol/l in heavy drinkers (Majchrowicz and Mendelson, 1971).
Toxicity resulting from MeOH consumption is extensively documented in both humans and animals and has been attributed to its metabolite, FA (Benton and Calhoun, 1952; Roe, 1946, 1955; Wood, 1912; Wood and Buller, 1904).
The rate of formate oxidation and elimination is dependent on adequate levels of hepatic folic acid, particularly hepatic tetrahydrofolate (THF) (Johlin et al., 1987; Tephly and McMartin, 1974).
Significantly higher formate levels were obtained when folate-deficient animals were exposed to MeOH as compared with folate-sufficient animals (Lee et al., 1994; McMartin et al., 1975; Noker et al., 1980).
To understand ethanol's toxicity, one must consider FA produced from MeOH, and its elimination mediated by folic acid.
We postulate that in the chronically drinking patient, we will find higher levels of FA than in the nondrinking population, and that formate is neurotoxic.
We also hypothesize that treatment with folic acid, which is a critical factor in the catabolism of FA, can prevent or diminish FA neurotoxicity.
[ for much more, use initial URLs..... ]
by
Rich Murray (0 articles, 0 quicklinks, 1 diaries, 13 comments)
on Thursday, April 10, 2008 at 3:57:19 PM
We still need help in readers contacting the Senate Office of Hawaii Senator David Ige, if you want this to advance. If he declines, at least everyone will know it was him and will wonder why.
16th Senatorial District Hawaii State Capitol, Room 215 415 South Beretania Street Honolulu, HI 96813 phone 808-586-6230; fax 808-586-6231 E-mail sendige@Capitol.hawaii.gov
Aspartame, in due course, will be one of those things like asbestos, leaded gasoline, thalidomide, Vioxx: the list is huge of products and chemicals the industries profiting off of them always saying that their products are harmless, and when the body count is too great to believe that anymore, they just take them off the market.
Accountability on this issue? Not in America, unless you sue them for damages, like the tobacco suits in the 1990's, which with aspartame would be a comparative slam dunk.
by
Stephen Fox (64 articles, 2 quicklinks, 10 diaries, 267 comments)
on Thursday, April 10, 2008 at 9:17:25 PM
4 comments
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