Sweet Poison – Part 2

Aspartame is the technical name for the brand names NutraSweet, Equal, Spoonful, and Equal-Measure. It was discovered by accident in 1965 when James Schlatter, a chemist of G.D. Searle Company, was testing an anti-ulcer drug.

Aspartame was approved for dry goods in 1981 and for carbonated beverages in 1983. It was originally approved for dry goods on July 26, 1974, but objections filed by neuroscience researcher Dr John W. Olney and Consumer attorney James Turner in August 1974 as well as investigations of G.D. Searle’s research practices caused the U.S. Food and Drug Administration (FDA) to put approval of aspartame on hold (December 5, 1974). In 1985, Monsanto purchased G.D. Searle and made Searle Pharmaceuticals and The NutraSweet Company separate subsidiaries.

Aspartame accounts for over 75 percent of the adverse reactions to food additives reported to the FDA. Many of these reactions are very serious including seizures and death.(1) A few of the 90 different documented symptoms listed in the report as being caused by aspartame include: Headaches/migraines, dizziness, seizures, nausea, numbness, muscle spasms, weight gain, rashes, depression, fatigue, irritability, tachycardia, insomnia, vision problems, hearing loss, heart palpitations, breathing difficulties, anxiety attacks, slurred speech, loss of taste, tinnitus, vertigo, memory loss, and joint pain.

According to researchers and physicians studying the adverse effects of aspartame, the following chronic illnesses can be triggered or worsened by ingesting of aspartame:(2) Brain tumors, multiple sclerosis, epilepsy, chronic fatigue syndrome, parkinson’s disease, alzheimer’s, mental retardation, lymphoma, birth defects, fibromyalgia, and diabetes.

Aspartame is made up of three chemicals: aspartic acid, phenylalanine, and methanol. The book “Prescription for Nutritional Healing,” by James and Phyllis Balch, lists aspartame under the category of “chemical poison.” As you shall see, that is exactly what it is.

What Is Aspartame Made Of?

Aspartic Acid (40 percent of aspartame)

Dr. Russell L. Blaylock, a professor of neurosurgery at the Medical University of Mississippi, recently published a book thoroughly detailing the damage that is caused by the ingestion of excessive aspartic acid from aspartame. Blaylock makes use of almost 500 scientific references to show how excess free excitatory amino acids such as aspartic acid and glutamic acid (about 99 percent of monosodium glutamate (MSG) is glutamic acid) in our food supply are causing serious chronic neurological disorders and a myriad of other acute symptoms.(3)

How Aspartate (and Glutamate) Cause Damage

Aspartate and glutamate act as neurotransmitters in the brain by facilitating the transmission of information from neuron to neuron. Too much aspartate or glutamate in the brain kills certain neurons by allowing the influx of too much calcium into the cells. This influx triggers excessive amounts of free radicals, which kill the cells. The neural cell damage that can be caused by excessive aspartate and glutamate is why they are referred to as “excitotoxins.” They “excite” or stimulate the neural cells to death.

Aspartic acid is an amino acid. Taken in its free form (unbound to proteins) it significantly raises the blood plasma level of aspartate and glutamate. The excess aspartate and glutamate in the blood plasma shortly after ingesting aspartame or products with free glutamic acid (glutamate precursor) leads to a high level of those neurotransmitters in certain areas of the brain.

The blood brain barrier (BBB), which normally protects the brain from excess glutamate and aspartate as well as toxins, 1) is not fully developed during childhood, 2) does not fully protect all areas of the brain, 3) is damaged by numerous chronic and acute conditions, and 4) allows seepage of excess glutamate and aspartate into the brain even when intact.

The excess glutamate and aspartate slowly begin to destroy neurons. The large majority (75 percent or more) of neural cells in a particular area of the brain are killed before any clinical symptoms of a chronic illness are noticed. A few of the many chronic illnesses that have been shown to be contributed to by long-term exposure to excitatory amino acid damage include:

* Multiple sclerosis (MS)
* Memory loss
* Hormonal problems
* Hearing loss
* Epilepsy
* Alzheimer’s disease
* Parkinson’s disease
* Hypoglycemia
* Dementia
* Brain lesions
* Neuroendocrine disorders

The risk to infants, children, pregnant women, the elderly and persons with certain chronic health problems from excitotoxins are great. Even the Federation of American Societies for Experimental Biology (FASEB), which usually understates problems and mimics the FDA party-line, recently stated in a review that:

“It is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants, and children. The existence of evidence of potential endocrine responses, i.e., elevated cortisol and prolactin, and differential responses between males and females, would also suggest a neuroendocrine link and that supplemental L-glutamic acid should be avoided by women of childbearing age and individuals with affective disorders.”(4)

Aspartic acid from aspartame has the same deleterious effects on the body as glutamic acid.

The exact mechanism of acute reactions to excess free glutamate and aspartate is currently being debated. As reported to the FDA, those reactions include:(5)

* Headaches/migraines
* Nausea
* Abdominal pains
* Fatigue (blocks sufficient glucose entry into brain)
* Sleep problems
* Vision problems
* Anxiety attacks
* Depression
* Asthma/chest tightness.

One common complaint of persons suffering from the effect of aspartame is memory loss. Ironically, in 1987, G.D. Searle, the manufacturer of aspartame, undertook a search for a drug to combat memory loss caused by excitatory amino acid damage. Blaylock is one of many scientists and physicians who are concerned about excitatory amino acid damage caused by ingestion of aspartame and MSG.

A few of the many experts who have spoken out against the damage being caused by aspartate and glutamate include Adrienne Samuels, Ph.D., an experimental psychologist specializing in research design. Another is Olney, a professor in the department of psychiatry, School of Medicine, Washington University, a neuroscientist and researcher, and one of the world’s foremost authorities on excitotoxins. (He informed Searle in 1971 that aspartic acid caused holes in the brains of mice.)

Phenylalanine (50 percent of aspartame)

Phenylalanine is an amino acid normally found in the brain. Persons with the genetic disorder phenylketonuria (PKU) cannot metabolize phenylalanine. This leads to dangerously high levels of phenylalanine in the brain (sometimes lethal). It has been shown that ingesting aspartame, especially along with carbohydrates, can lead to excess levels of phenylalanine in the brain even in persons who do not have PKU.

This is not just a theory, as many people who have eaten large amounts of aspartame over a long period of time and do not have PKU have been shown to have excessive levels of phenylalanine in the blood. Excessive levels of phenylalanine in the brain can cause the levels of seratonin in the brain to decrease, leading to emotional disorders such as depression. It was shown in human testing that phenylalanine levels of the blood were increased significantly in human subjects who chronically used aspartame.(6)

Even a single use of aspartame raised the blood phenylalanine levels. In his testimony before the U.S. Congress, Dr. Louis J. Elsas showed that high blood phenylalanine can be concentrated in parts of the brain and is especially dangerous for infants and fetuses. He also showed that phenylalanine is metabolised much more effeciently by rodents than by humans.(7)

One account of a case of extremely high phenylalanine levels caused by aspartame was recently published the “Wednesday Journal” in an article titled “An Aspartame Nightmare.” John Cook began drinking six to eight diet drinks every day. His symptoms started out as memory loss and frequent headaches. He began to crave more aspartame-sweetened drinks. His condition deteriorated so much that he experienced wide mood swings and violent rages. Even though he did not suffer from PKU, a blood test revealed a phenylalanine level of 80 mg/dl. He also showed abnormal brain function and brain damage. After he kicked his aspartame habit, his symptoms improved dramatically.(8)

As Blaylock points out in his book, early studies measuring phenylalanine buildup in the brain were flawed. Investigators who measured specific brain regions and not the average throughout the brain notice significant rises in phenylalanine levels. Specifically the hypothalamus, medulla oblongata, and corpus striatum areas of the brain had the largest increases in phenylalanine. Blaylock goes on to point out that excessive buildup of phenylalanine in the brain can cause schizophrenia or make one more susceptible to seizures.

Therefore, long-term, excessive use of aspartame may provid a boost to sales of seratonin reuptake inhibitors such as Prozac and drugs to control schizophrenia and seizures.

Methanol (aka wood alcohol/poison) (10 percent of aspartame)

Methanol/wood alcohol is a deadly poison. Some people may remember methanol as the poison that has caused some “skid row” alcoholics to end up blind or dead. Methanol is gradually released in the small intestine when the methyl group of aspartame encounter the enzyme chymotrypsin.

The absorption of methanol into the body is sped up considerably when free methanol is ingested. Free methanol is created from aspartame when it is heated to above 86 Fahrenheit (30 Centigrade). This would occur when aspartame-containing product is improperly stored or when it is heated (e.g., as part of a “food” product such as Jello).

Methanol breaks down into formic acid and formaldehyde in the body. Formaldehyde is a deadly neurotoxin. An EPA assessment of methanol states that methanol “is considered a cumulative poison due to the low rate of excretion once it is absorbed. In the body, methanol is oxidized to formaldehyde and formic acid; both of these metabolites are toxic.” They recommend a limit of consumption of 7.8 mg/day. A one-liter (approx. 1 quart) aspartame-sweetened beverage contains about 56 mg of methanol. Heavy users of aspartame-containing products consume as much as 250 mg of methanol daily or 32 times the EPA limit.(9)

Symptoms from methanol poisoning include headaches, ear buzzing, dizziness, nausea, gastrointestinal disturbances, weakness, vertigo, chills, memory lapses, numbness and shooting pains in the extremities, behavioral disturbances, and neuritis. The most well known problems from methanol poisoning are vision problems including misty vision, progressive contraction of visual fields, blurring of vision, obscuration of vision, retinal damage, and blindness. Formaldehyde is a known carcinogen, causes retinal damage, interferes with DNA replication and causes birth defects.(10)

Due to the lack of a couple of key enzymes, humans are many times more sensitive to the toxic effects of methanol than animals. Therefore, tests of aspartame or methanol on animals do not accurately reflect the danger for humans. As pointed out by Dr. Woodrow C. Monte, director of the food science and nutrition laboratory at Arizona State University, “There are no human or mammalian studies to evaluate the possible mutagenic, teratogenic or carcinogenic effects of chronic administration of methyl alcohol.”(11)

He was so concerned about the unresolved safety issues that he filed suit with the FDA requesting a hearing to address these issues. He asked the FDA to “slow down on this soft drink issue long enough to answer some of the important questions. It’s not fair that you are leaving the full burden of proof on the few of us who are concerned and have such limited resources. You must remember that you are the American public’s last defense. Once you allow usage (of aspartame) there is literally nothing I or my colleagues can do to reverse the course. Aspartame will then join saccharin, the sulfiting agents, and God knows how many other questionable compounds enjoined to insult the human constitution with governmental approval.”(10) Shortly thereafter, the Commissioner of the FDA, Arthur Hull Hayes, Jr., approved the use of aspartame in carbonated beverages, he then left for a position with G.D. Searle’s public relations firm.(11)

It has been pointed out that some fruit juices and alcoholic beverages contain small amounts of methanol. It is important to remember, however, that methanol never appears alone. In every case, ethanol is present, usually in much higher amounts. Ethanol is an antidote for methanol toxicity in humans.(9) The troops of Desert Storm were “treated” to large amounts of aspartame-sweetened beverages, which had been heated to over 86 degrees F in the Saudi Arabian sun. Many of them returned home with numerous disorders similar to what has been seen in persons who have been chemically poisoned by formaldehyde. The free methanol in the beverages may have been a contributing factor in these illnesses. Other breakdown products of aspartame such as DKP (discussed below) may also have been a factor.

In a 1993 act that can only be described as “unconscionable,” the FDA approved aspartame as an ingredient in numerous food items that would always be heated to above 86 degree F (30 degree C).

Diketopiperazine (DKP)

DKP is a byproduct of aspartame metabolism. DKP has been implicated in the occurrence of brain tumors. Olney noticed that DKP, when nitrosated in the gut, produced a compound that was similar to N-nitrosourea, a powerful brain tumor causing chemical. Some authors have said that DKP is produced after aspartame ingestion. I am not sure if that is correct. It is definitely true that DKP is formed in liquid aspartame-containing products during prolonged storage.

G.D. Searle conducted animal experiments on the safety of DKP. The FDA found numerous experimental errors occurred, including “clerical errors, mixed-up animals, animals not getting drugs they were supposed to get, pathological specimens lost because of improper handling,” and many other errors.(12) These sloppy laboratory procedures may explain why both the test and control animals had sixteen times more brain tumors than would be expected in experiments of this length.

In an ironic twist, shortly after these experimental errors were discovered, the FDA used guidelines recommended by G.D. Searle to develop the industry-wide FDA standards for good laboratory practices.(11)

DKP has also been implicated as a cause of uterine polyps and changes in blood cholesterol by FDA Toxicologist Dr. Jacqueline Verrett in her testimony before the U.S. Senate.(13)

Bottom line, aspartame is a highly acidic sweet poison that will make you sick, tired and fat.

2 thoughts on “Sweet Poison – Part 2”

  1. ALS, amyotrophic lateral sclerosis, 1156 deaths in a million person study 1982-2004, correlates with years of formaldehyde exposure [ aspartame diet soda sold after fall 1983 ], MG Weisskopf et al, Harvard SPH 2008.04.16: Rich Murray 2008.09.20http://rmforall.blogspot.com/2008_09_01_archive.htmSaturday, September 20, 2008http://groups.yahoo.com/group/aspartameNM/message/1558http://www.hsph.harvard.edu/faculty/marc-weisskopf/index.htmlMarc G. WeisskopfMark and Catherine Winkler Assistant Professor of Environmental and Occupational EpidemiologyDepartment of Environmental HealthDepartment of Epidemiology401 Park Dr., Rm 3-104Landmark Center, PO Box 15697Boston, Massachusetts 02215617.384.8872 mweissko@hsph.harvard.eduEducationScB, Neuroscience, Brown University, 1989PhD, Neuroscience, University of California, San Francisco, 1994ScD, Epidemiology, Harvard School of Public Health, 2006http://www.hsph.harvard.edu/faculty/marc-weisskopf/files/AAN_ALS_chem_press_release.pdfEMBARGOED FOR RELEASE UNTIL 2:00 P.M. CT/3:00 P.M. ET, WEDNESDAY, APRIL 16, 2008Media Contacts:Angela Babb, (651) 695-2789, ababb@aan.comRachel Seroka, (651) 695-2738, rseroka@aan.comAAN Press Room 179B (April 12–18): (312) 791-7053http://www.youtube.com/watch?v=h3ISwNRe4Xk&feature=related4:15 minute video by John Gever, Medscape Todayhttp://www.4woman.gov/News/English/614428.htmhttp://www.healthfinder.gov/news/newsstory.asp?docid=614428http://www.medicinenet.com/script/main/art.asp?articlekey=88726“…there are only about 5,500 new cases in the United States each year.”Formaldehyde Linked to Lou Gehrig's DiseaseBy Randy DotingaHealthDay ReporterWEDNESDAY, April 16, 2008 (HealthDay News) — New preliminary research suggests that exposure to the chemical formaldehyde, present in a variety of workplaces, could greatly increase a person's chances of developing Lou Gehrig's disease.The findings aren't definitive, and only a few thousand Americans are diagnosed with the condition — also known as amyotrophic lateral sclerosis (ALS) — each year.Still, the study results deserve attention, especially since formaldehyde hasn't been considered an ALS risk factor before, said study author Marc Weisskopf, an assistant professor of epidemiology and environmental health at Harvard School of Public Health. “It's a result that we view as very intriguing and worthy of follow-up.”The findings were scheduled to be released Wednesday at the American Academy of Neurology annual meeting, in Chicago.ALS progressively causes damage to the nerve cells in the brain and spinal cord. Patients lose the ability to control their muscles, and they typically become paralyzed. There's no cure for ALS, and treatments have limited value.Weisskopf and his colleagues examined statistics from an American Cancer Society study of more than 1 million people who were followed for 15 years.The researchers first examined the participants' responses in 1982 to questions about exposure to 12 different chemicals, including formaldehyde. Then they followed up between 1989 and 2004 to see what happened to those people.The researchers found that 617 men and 539 women died of ALS during the study period. Only those who reported exposure to formaldehyde had a higher risk — 34 percent higher — of developing ALS.Formaldehyde is used in the manufacture of a variety of products, including particle board, clothing, glues, cosmetics and shampoo. People who work in medical facilities and mortuaries may also encounter it on the job.The pungent chemical has already been linked to higher rates of lung cancer and leukemia. It was not declared a probable human carcinogen at high exposure levels by the Environmental Protection Agency until 1987.Those who reported more than 10 years of exposure to formaldehyde were almost four times more likely to develop ALS.According to Weisskopf, the study design didn't allow him to estimate how many extra people may develop ALS because they are exposed to formaldehyde. However, he said there are only about 5,500 new cases in the United States each year.Researchers have considered pesticides to be a possible cause of ALS, but formaldehyde hasn't been raised as a villain before, Weisskopf said. It's not clear how it might be linked to development of the disease, but Weisskopf said it could set off brain damage by increasing the “stress” caused by oxygen.It's possible that other factors besides formaldehyde may be causing ALS in the study participants. Indeed, Weisskopf said the findings don't confirm a cause-and-effect relationship: “That's very hard to do. But it does provide an avenue to get more insight into the disease process, and it may give us insight that's helpful in determining other avenues to take.”Dr. Catherine Lomen-Hoerth, director of the ALS Center at the University of California, San Francisco, said it's too early for anyone to worry too much about the findings.The research “means studies can be done in ALS rats or mice to see if formaldehyde worsens the disease process,” she said, but, “I don't think we understand environmental factors very well, and in what way they affect disease processes.”“If we knew more about what causes ALS, we might know more about how formaldehydes and other chemicals might [play a role],” she added.SOURCES: Marc Weisskopf, Ph.D., assistant professor, epidemiology and environmental health, Harvard School of Public Health, Boston; Catherine Lomen-Hoerth, M.D., Ph.D., director, ALS Center, University of California, San Francisco; April 16, 2008, presentation, American Academy of Neurology annual meeting, ChicagoCopyright © 2008 ScoutNews, LLC. All rights reserved.“Regular formaldehyde exposure increased ALS risk by 34%.In addition, the longer the self-reported exposure to formaldehyde, the higher the risk for ALS.Thus, compared with those reporting no exposure, the adjusted relative risk for ALS was1.5 in individuals who reported less than four years of exposure,2.1 in those with four to 10 years of exposure, and4.1 in those with more than 10 years of exposure.Overall, 2.6% of participants reported that they had been exposed to formaldehyde.”“Nearly 25% of beauticians reported that they were exposed to formaldehyde.Pharmacists, morticians, radio/lab technicians, dentists, firemen, photographers, printers, doctors, and nurses also reported high rates of formaldehyde exposure.Individuals in these high-exposure jobs had a 28% greater risk for ALS.”“There are several possible mechanisms for formaldehyde neurotoxicity, said Dr. Weisskopf.These include hyperexcitability of dorsal horn neurons,reduced excitability of the isolated phrenic nerve,prefrontal cortex/hippocampal neurotoxicity,a decrease in superoxide dismutase activity,an increase in malondialdehyde,and toxic tau protein misfolding.”“…other factors that might contribute to ALS were controlled for, including sex, smoking status, military service, level of education, alcohol intake, occupation, vitamin E supplement use, and exposure to other chemicals.”http://www.neurologyreviews.com/08june/FormaldehydeALS.htmlNeurology Reviews.ComVol. 16, No. 6 June 2008Formaldehyde Exposure May Pose Risk for Amyotrophic Lateral SclerosisCHICAGO — Preliminary results suggest that exposure to the chemical formaldehyde may increase the risk for amyotrophic lateral sclerosis (ALS), according to a report at the 60th Annual Meeting of the American Academy of Neurology. Researchers found that people with more than 10 years of exposure to formaldehyde had a 4.1 times increased risk for ALS, compared with those who had no exposure.“While pesticides have been thought to contribute to the development of ALS, this is the first time that formaldehyde has been identified as a potential risk factor,” commented Marc Weisskopf, PhD, Assistant Professor of Environmental and Occupational Epidemiology at Harvard School of Public Health in Boston.Formaldehyde is used in particleboard and other wood products, permanent press fabrics, glues, photography chemicals, and other household products, such as cosmetics and shampoo. It is also used as a tissue preservative in medical laboratories and mortuaries and as an industrial disinfectant. About 20 years ago, the US Environmental Protection Agency designated high levels of formaldehyde as a probable carcinogen.EXPOSURE TO CHEMICALS AND RISK FOR ALSPrior research has suggested that environmental toxins, including pesticides, may be associated with ALS. This notion has been backed by case-control and genetic studies implicating genes involved in pesticide detoxification, said Dr. Weisskopf. However, the findings have been contradictory, and there have been no large prospective studies to support this hypothesis.In the present investigation, Dr. Weisskopf’s group prospectively examined the relationship between regular exposure to 12 types of chemicals and ALS in 987,229 individuals who participated in the American Cancer Society-sponsored Cancer Prevention Study II. Participants were asked about their exposure to chemicals, including formaldehyde, in 1982, and they were then followed for approximately 15 years. The researchers also analyzed exposure to asbestos, acids/solvents, coal or stone dust, coal tar pitch/asphalt, diesel engine exhaust, dyes, gasoline exhaust, pesticides/herbicides, textile fibers/dust, wood dust, and x-ray/radioactive material.Overall, 617 men and 539 women died from ALS during the follow-up period.Regular formaldehyde exposure increased ALS risk by 34%.In addition, the longer the self-reported exposure to formaldehyde, the higher the risk for ALS.Thus, compared with those reporting no exposure, the adjusted relative risk for ALS was1.5 in individuals who reported less than four years of exposure,2.1 in those with four to 10 years of exposure, and4.1 in those with more than 10 years of exposure.Overall, 2.6% of participants reported that they had been exposed to formaldehyde.By contrast, there was limited evidence for an association between ALS and pesticides/herbicides.The study also found that an increased risk for ALS was seen with certain jobs.Nearly 25% of beauticians reported that they were exposed to formaldehyde.Pharmacists, morticians, radio/lab technicians, dentists, firemen, photographers, printers, doctors, and nurses also reported high rates of formaldehyde exposure. Individuals in these high-exposure jobs had a 28% greater risk for ALS.There are several possible mechanisms for formaldehyde neurotoxicity, said Dr. Weisskopf.These include hyperexcitability of dorsal horn neurons,reduced excitability of the isolated phrenic nerve,prefrontal cortex/hippocampal neurotoxicity,a decrease in superoxide dismutase activity,an increase in malondialdehyde,and toxic tau protein misfoldingA CAUSAL RELATIONSHIP FOR ALS AND FORMALDEHYDE?Dr. Weisskopf noted that the longitudinal design of the study minimizes the possibility that the results are due to bias. Additional strengths of the study include its large size and uniform case ascertainment, as well as the fact that other factors that might contribute to ALS were controlled for, including sex, smoking status, military service, level of education, alcohol intake, occupation, vitamin E supplement use, and exposure to other chemicals.Possible limitations of the study include small numbers in some exposure categories, as well as self-assessment of exposure. In addition, only mortality data were used to identify ALS cases. Dr. Weisskopf noted, however, that because death certificates have been reported to accurately identify 70% to 80% of ALS-related deaths, they might be a reasonable surrogate for ALS incidence, due to the short survival time associated with the disease.Dr. Weisskopf emphasized that the findings are preliminary and do not establish a causal relationship between formaldehyde and ALS. “At the moment, it is premature to make broad public health recommendations, and corroboration of the data is needed,” he concluded.NR — Jill SteinSuggested ReadingMorahan JM, Pamphlett R. Amyotrophic lateral sclerosis and exposure to environmental toxins: an Australian case-control study. Neuroepidemiology. 2006;27(3):130-135.Morahan JM, Yu B, Trent RJ, Pamphlett R. A gene-environment study of the paraoxonase 1 gene and pesticides in amyotrophic lateral sclerosis. Neurotoxicology. 2007;28(3):532-540.Neuroepidemiology. 2006; 27(3): 130-5. Epub 2006 Aug 1.Amyotrophic lateral sclerosis and exposure to environmental toxins: an Australian case-control study.Morahan JM, Pamphlett R.Department of Pathology, University of Sydney, Sydney, Australia.It has been suggested that environmental toxins could be risk factors for sporadic amyotrophic lateral sclerosis (SALS).We therefore analysed epidemiological data on 179 SALS cases and 179 age-, ethnicity- and sex-matched controls in Australia using self-reporting questionnaires. SALS was associated with solvent/chemical exposure (OR = 1.92, 95% CI: 1.26-2.93),overall herbicide/pesticide exposure (OR = 1.57, 95% CI: 1.03-2.41) andindustrial herbicide/pesticide exposure (OR = 5.58, 95% CI: 2.07-15.06).Exposure to herbicides/pesticides showed a dose-response effect.All positive findings were more statistically significant in males.These findings support those from northern hemisphere studies, indicating that environmental toxins can be risk factors for SALS.Copyright (c) 2006 S. Karger AG, Basel. PMID: 16946624http://www.usyd.edu.au/research/opportunities/supervisors/128Dr Morahan, Juliaposition: Postdoctoral Research Fellowdepartment: Discipline of Pathology, School of Medical Sciencesphone: +61 2 9036 7233 fax: +61 2 9351 3429email: morahanj@med.usyd.edu.aulocation: Level 5, Room 502aaddress: D06 – BlackburnThe University of SydneyNSW 2006 AustraliaAssociate Professor Pamphlett, Rogerposition: Associate Professordepartment: Discipline of Pathology, School of Medical Sciencesphone: +61 2 9351 3318 fax: +61 2 9351 3429email: rogerp@med.usyd.edu.aulocation: Room 502Aaddress: D06 – BlackburnThe University of SydneyNSW 2006 AustraliaAbout Associate Professor Roger PamphlettTo find a genetic cause for motor neuron disease that will enable gene therapy to halt this devastating condition.Roger Pamphlett is a neurologist and neuropathologist who works with a team of molecular geneticists in trying to find a genetic cause for motor neuron disease.Prof Pamphlett’s research in the pathogenesis of ALS started by examining the role of environmental agents. He published 20 papers on the relationship between heavy metals and ALS, using both human tissue and animal models. This body of work showed that heavy metals enter motor neurons selectively, but that the metals by themselves are unlikely to cause ALS. This raised the possibility that genetic susceptibility to these environmental toxins may underlie ALS.To look for genetic susceptibilities to ALS he has set up the Australian MND DNA Bank. He travels to all Australian mainland states collecting blood samples from people with ALS as well as controls. This Bank, supported by an NHMRC Enabling Grant, now contains over 1,400 DNA samples. Participants fill in detailed questionnaires to allow gene-environment studies to be undertaken. Using DNA from this Bank it has been shown that polymorphisms in the poliovirus receptor are more common in some forms of MND, and a variety of other genes that protect against toxins and viruses are under investigation.Prof Pamphlett is now interested in novel genetic mechanisms that could underlie sporadic ALS, such as mutations that affect CNS cells predominantly (somatic mutations). To examine these possibilities he recruits ALS patients in NSW to donate their brains and spinal cords after they die to a Tissue Bank, and collaborates with other Banks in Australia and the UK to obtain further tissue samples.Epidemiology. 2008 Mar; 19(2): 324-37.Diet and amyotrophic lateral sclerosis.Morozova N,Weisskopf MG,McCullough ML,Munger KL,Calle EE,Thun MJ,Ascherio A.Natalia Morozova; Marc G. Weisskopf; Marjorie L. McCullough; Kassandra L. Munger; Eugenia E. Calle; Michael J. Thun; Alberto AscherioDepartments of *Nutrition, Harvard School of Public Health, Boston, MA 02215, USA. nmorozov@hsph.harvard.edu;mweissko@hsph.harvard.edu; marji.mccullough@cancer.org; hpklg@channing.harvard.edu; aascheri@hsph.harvard.edu; kgorham@hsph.harvard.edu; mthun@cancer.org; jcalle@cancer.org; ethacker@post.harvard.edu;BACKGROUND:Several dietary factors have been associated with risk of amyotrophic lateral sclerosis (ALS) in case-control studies, but no prospective studies have investigated diet and ALS.METHODS:We prospectively assessed the association of selected foods and beverages with ALS mortality among participants of the Cancer Prevention Study II, a cohort of over 1 million men and women enrolled in 1982.Habitual diet was assessed with a 44-item food frequency questionnaire.Participant follow-up was conducted from 1989 through 2002 for ALS mortality.RESULTS:During the follow-up period, 862 cohort participants died of ALS.The strongest finding was an inverse association between chicken consumption and risk of ALS (P for trend = 0.0006).We also observed an increased risk of ALS among study participants with a high consumption of brown rice/whole wheat/barley (P for trend = 0.006)and decaffeinated coffee (P for trend = 0.01),and a decreased risk of ALS for high consumption of tea (P for trend = 0.02)and French fries (P for trend = 0.02);however, none of these latter associations remained significant after adjusting for multiple comparisons.CONCLUSIONS:Overall, these results do not provide convincing evidence that the investigated food items are related to ALS mortality.The association observed between chicken consumption and ALS mortality should be assessed in other studies.PMID: 18300717tobacco, alcohol drinks, and aspartame all expose people to methanol, formaldehyde, and formic acid: Rich Murray 2008.09.20formaldehyde, aspartame, and migraines, the first case series, Sharon EJacob-Soo, Sarah A Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray2008.07.18http://rmforall.blogspot.com/2008_07_01_archive.htmFriday, July 18, 2008http://groups.yahoo.com/group/aspartameNM/message/1553___________________________________________________Dermatitis. 2008 May-Jun; 19(3): E10-1.Formaldehyde, aspartame, and migraines: a possible connection.Jacob SE, Stechschulte S.Department of Dermatology and Cutaneous Surgery, University of Miami,Miami, FL, USA.Aspartame is a widely used artificial sweetener that has been linkedto pediatric and adolescent migraines.Upon ingestion, aspartame is broken, converted, and oxidized intoformaldehyde in various tissues.We present the first case series of aspartame-associated migrainesrelated to clinically relevant positive reactions to formaldehyde onpatch testing. PMID: 18627677formaldehyde from many sources, including aspartame, is major cause ofAllergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin andAging 2005 Dec.: Murray 2008.03.27http://rmforall.blogspot.com/2008_03_01_archive.htmThursday, March 27, 2008http://groups.yahoo.com/group/aspartameNM/message/1533“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, isconverted to methanol in the body, which is oxidized to formaldehydein all organs, including the liver and eyes. 22Patients with a contact dermatitis to formaldehyde have been seen toimprove once aspartame is avoided. 22Notably, the case that Hill and Belsito reported had a 6-month historyof eyelid dermatitis that subsided after 1 week of avoiding diet soda.22″Avoiding formaldehyde allergic reactions in children, aspartame,vitamins, shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob,MD, Tace Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contactdermatitis, AM Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27http://rmforall.blogspot.com/2008_03_01_archive.htmThursday, March 27, 2008http://groups.yahoo.com/group/aspartameNM/message/1532Sharon E. Jacob, MD, Assistant Professor of Medicine (Dermatology)University of California, San Diego 200 W. Arbor Drive #8420, SanDiego, CA 92103-8420Tel: 858-552-8585 ×3504 Fax: 305-675-8317 sjacob@contactderm.net;Dermatitis. 2008 Jan-Feb;19(1):9-15.Systemic contact dermatitis.Jacob SE, Zapolanski T. tamar.zapolanski@gmail.com;Department of Dermatology and Cutaneous Surgery, University of Miami,Miami, FL, USA.Systemic exposure to allergens resulting in a cutaneous eruption isknown as systemic contact dermatitis (SCD).Once sensitization occurs, varying exposures to antigens via multipleroutes (including transepidermal routes, intravenous or intramuscularroutes, inhalation, and ingestion) can result in systemic flare.This article highlights the different categories of commoncontactants, metals, medications, and plants, exposure to which leadsto SCD.A comprehensive approach that takes into account all possible routesof exposure is essential in diagnosing SCD and in helping patientssuccessfully avoid their allergens. PMID: 18346390“We present a case of a medical student who presented witherythematous eczematoid plaques on her trunk and legs and finevesiculation of her scalp, 3 weeks after starting anatomy class.Of note, she routinely washed her face and arms after leaving theanatomy lab, but remained in her scrubs for the rest of the day.Formaldehyde and Quaternium-15 positive reactions in the same patient.[ photo ]”“Our patient underscores the importance of appropriate patch testingand education.Once we identified the allergy to formaldehyde and quaternium-15, weprovided 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 safealternatives (see Table 5).Fortunately, with technical advances, this student completed theanatomy section via electronic learning tools.By avoiding formaldehyde, including anatomy lab, FRP in her shampooand cosmetics, and aspartame in her diet, this patient dramaticallyimproved.As with all contact dermatitides, the mainstay of treatment forallergic contact dermatitis is avoidance.”http://www.skinandaging.com/article/5158 Skin & Aging JournalISSN: 1096-0120 – Volume 13 – Issue 12_2005 –December 2005 – Pages: 22 – 27Allergen 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 GeorgetteRodriguez, M.D., M.P.H.http://www.eczemacenter.org/eczema_center/meetfacultystaff.htm[ photo ]The Eczema CenterRady Children's Hospital of San Diego8010 Frost Street, Suite 602, San Diego, CA 92123or call… (858) 966-6774Sharon E. Jacob , MDDr. Sharon E. Jacob is Assistant Clinical Professor of Pediatrics andMedicine (Dermatology) at the University of California, School ofMedicine and Rady Children's Hospital.She earned her medical degree from the Temple University, andcompleted dermatology training at the University of Miami and advancedcontact dermatitis training at New York University (NYU).She has been board certified in dermatology.Dr. Jacob's clinical interests include atopic and contact dermatitisand education.She is considered a national expert on chemical sensitivities in theskin and has published more than 45 journal articles, book chaptersand abstracts on this topic.In 2005, Dr Jacob was the first to present contact dermatitis data onU.S. pediatric patients to the American Contact Dermatitis Society(ACDS).She has received an excellence in teaching award from the Universityof Miami Dermatology and the Clinical Research Award from the ACDS.She is an active reviewer for the following medical publicationsincluding Journal of the American Academy of Dermatology, PediatricDermatology, Dermatitis, and the Archives of Dermatology.Dr. Jacob also serves on the medical board of the Inflammatory SkinDisease Institute and the Skin and Aging Journal.Dr. Jacob enjoys taking care of children and their families and is anadvocate for children's dermatologic health.http://www.eczemacenter.org/eczema_center/index.htmAtopic dermatitis (AD) — better known as eczema — is the most commonchronic skin disorder seen in infants and children.In fact, the prevalence of this condition has risen dramaticallyduring the last three decades.Currently, 15% to 20% of children in the United States are expected toexperience this condition sometime during their lifetime, compared to7% around 1960.The negative impact of eczema is profound and insidious.It affects both the patient who suffers from it and that patient'sfamily members, and it does so on two important levels — physical andemotional.Physical:Inflamed, itchy rashes can involve any and all of the skin surfacesand are frequently complicated by skin breakdown and bacterial, viral,and fungal infections.It is linked to the development of life-long allergic conditions,including asthma, food allergies, and rhinitis.Any level of AD is extremely uncomfortable and, at times, painful.Individuals with moderate to severe disease report that eczema hugelydisturbs their sleep and impacts performance of daily activities,including adverse effects on school, sports activities, work, and peerrelationships.In studies, individuals with eczema reported more negative impact onquality of life than those with insulin-dependent diabetes!Emotional:Patients and their families experience considerable emotionaldistress, anxiety, and embarrassment because of people's response tothis illness.In fact, the emotional scarring on both patient and family members mayoutlast eczema's physical effects.Parents especially suffer because it is difficult for childrenexperiencing this condition to understand that their parents cannotmake the torment go away.The stress of caring for these children is even greater than parentscaring for a child with insulin-dependent diabetes.Patients experience considerable discrimination and social isolationbecause of this illness.People often stare, shiver with disgust or step back in fear fromthose who have this condition.The end result for patients: A life-time of struggle with their senseof worth and self esteem.http://aad2008.omnibooksonline.com/data/papers/CRS-113-F.pdf lecturewith photos___________________________________________________similar levels of daily formaldehyde and formic acid, causes of birthdefects, come from cigarettes, aspartame, and dark wines and liquors— folic acid protects most people: Rich Murray 2008.07.15http://rmforall.blogspot.com/2008_07_01_archive.htmTuesday, July 15, 2008http://groups.yahoo.com/group/aspartameNM/message/1552http://www.divine.ca/en/health-and-wellness/articles/c_16_i_3295/5-reasons-to-quit-smoking-1.html“A smoker who goes through one pack a day will smoke 7,300 cigarettesa year, inhaling the equivalent of nearly 1 gram of formaldehyde(yikes!).”That's about 2.5 mg daily formaldehyde intake for 20 cigarettes, overthe 2 mg USA FDA alarm level for formaldehyde in average 2 litersdaily drinking water, while a single 12 oz can of diet soda alsoresults in about 2 mg formaldehyde toxic products in the body,including formic acid, a notorious cause of birth defects.Dark wines and liquors usually supply even more methanol, which thebody always turns into formaldehyde and formic acid — the major causeof “morning after” hangovers.High levels of folic acid, a safe, affordable vitamin in fruits andvegetables, largely prevents formaldehyde and formic acid toxicity inmost people.It is certain that high levels of aspartame use, above 2 liters dailyfor months and years, must lead to chronic formaldehyde-formic acidtoxicity.Fully 11 % of aspartame is methanol — 1,120 mg aspartame in 2 litersdiet soda, almost six 12-oz cans, gives 123 mg methanol (woodalcohol). The methanol is immediately released into the body afterdrinking .Within hours, the liver turns much of the methanol into formaldehyde,and then much of that into formic acid, both of which in time arepartially eliminated as carbon dioxide and water.However, about 30 % of the methanol remains in the body as cumulativedurable toxic metabolites of formaldehyde and formic acid — 37 mgdaily, a gram every month, accumulating in and affecting every tissue.If only 10 % of the methanol is retained daily as formaldehyde, thatwould give 12 mg daily formaldehyde accumulation — about 60 timesmore than the 0.2 mg from 10 % retention of the 2 mg EPA daily limitfor formaldehyde in drinking water.Bear in mind that the EPA limit for formaldehyde in drinking water is1 ppm, or 2 mg daily for a typical daily consumption of 2 liters ofwater.formaldehyde and formic acid in FEMA trailers and other sources(aspartame, dark wines and liquors, tobacco smoke): Murray 2008.01.30http://rmforall.blogspot.com/2008_01_01_archive.htmWednesday, January 30, 2008http://groups.yahoo.com/group/aspartameNM/message/1508The FEMA trailers give about the same amount of formaldehyde andformic acid daily as from a quart of dark wine or liquor, or twoquarts (6 12-oz cans) of aspartame diet soda, from their over 1 tenthgram methanol impurity (one part in 10,000), which the body quicklymakes into formaldehyde and then formic acid — enough to be the majorcause of “morning after” alcohol hangovers.Methanol and formaldehyde and formic acid also result from many fruitsand vegetables, tobacco and wood smoke, heater and vehicle exhaust,household chemicals and cleaners, cosmetics, and new cars, drapes,carpets, furniture, particleboard, mobile homes, buildings, leather…so all these sources add up and interact with many other toxicchemicals.two aspartame toxicity research studies by Resia Pretorius,U. Pretoria, South Africa, debate with JD Fernstrom:Murray 2008.04.04http://rmforall.blogspot.com/2008_04_01_archive.htmFriday, April 4, 2008http://groups.yahoo.com/group/aspartameNM/message/1536methanol impurity in alcohol drinks [ and aspartame ] is turned intoneurotoxic formic acid, prevented by folic acid, re Fetal AlcoholSyndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin ExpRes 2007 Dec. plain text: detailed biochemistry, CL Nie et al.2007.07.18: Murray 2008.02.24http://rmforall.blogspot.com/2008_02_01_archive.htmSunday, February 24, 2008http://groups.yahoo.com/group/aspartameNM/message/1524opportunities re BA Magnuson, GA Burdock et al., Aspartame SafetyEvaluation 2007 Sept., Critical Reviews in Toxicology:Rich Murray 2008.07.11http://rmforall.blogspot.com/2008_07_01_archive.htmFriday, July 11, 2008http://groups.yahoo.com/group/aspartameNM/message/1550___________________________________________________“Of course, everyone chooses, as a natural priority, to enjoy peace,joy, and love by helping to find, quickly share, and positively actupon evidence about healthy and safe food, drink, and environment.”Rich Murray, MA Room For All rmforall@comcast.net505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505http://RMForAll.blogspot.com new primary archivehttp://groups.yahoo.com/group/aspartameNM/messagesgroup with 135 members, 1,564 posts in a public archivehttp://groups.yahoo.com/group/aspartame/messagesgroup with 1,137 members, 22,958 posts in a public archive___________________________________________________


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