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    http://groups.yahoo.com/group/aspartameNM/message/1302
    The Lowdown on Sweet? (Ramazzini Foundation, M Soffritti proof that
    aspartame causes cancers), Melanie Warner, The New York Times:
    Murray 2006.02.12

    http://www.nytimes.com/2006/02/12/
    business/yourmoney/12sweet.html?_r=1&oref=slogin

    Article 2 of 26 in Business

    The Lowdown on Sweet?

    By MELANIE WARNER Published: February 12, 2006

    WHEN Dr. Morando Soffritti, a cancer researcher in Bologna, Italy,
    saw the results of his team's seven-year study on aspartame,
    he knew he was about to be injected into a bitter controversy
    over this sweetener, one of the most contentiously debated substances
    ever added to foods and beverages.

    Pigi Cipelli for The New York Times
    Dr. Morando Soffritti, who led tests of aspartame on 1,900 rats,
    calls it a possible carcinogen. [ photo ]

    Pigi Cipelli for The New York Times
    A study conducted at an Italian cancer research center, above,
    has rekindled the debate on aspartame. [ photo ]

    Aspartame is sold under the brand names Nutra-Sweet and Equal
    and is found in such popular products as Diet Coke, Diet Pepsi,
    Diet Snapple and Sugar Free Kool-Aid.
    Hundreds of millions of people consume it worldwide.
    And Dr. Soffritti's study concluded that aspartame may cause
    the dreaded "c" word: cancer.

    The research found that the sweetener was associated
    with unusually high rates of lymphomas, leukemias and other cancers
    in rats that had been given doses of it starting at what would be
    equivalent to four to five 20-ounce bottles of diet soda a day
    for a 150-pound person.

    The study, which involved 1,900 laboratory rats and cost $1 million,
    was conducted at the European Ramazzini Foundation
    of Oncology and Environmental Sciences, a nonprofit organization
    that studies cancer-causing substances;
    Dr. Soffritti is its scientific director.

    The findings, first released last July, prompted a flurry of criticism
    from the Calorie Control Council, a trade group for makers
    of artificial sweeteners that has spent the last 25 years
    trying to quell fears about aspartame.

    It said Dr. Soffritti's study flew in the face of four earlier cancer
    studies that aspartame's creator, G. D. Searle & Company,
    had underwritten and used to persuade
    the Food and Drug Administration to approve it for human consumption.

    "Aspartame has been safely consumed for more than a quarter of a
    century and is one of the most thoroughly studied food additives,"
    read one news release from the council.

    At the same time, Dr. Soffritti's findings have energized a vociferous
    group of researchers, health advocates and others who say they are
    convinced that aspartame is a toxin associated with a variety of
    health troubles, including headaches, dizziness, blindness and seizures.

    DR. SOFFRITTI, who oversees 180 scientists and researchers
    in 30 countries who collaborate on toxin research,
    says that since last July, he has been contacted by some of these critics,
    including a member of Parliament in Britain and a number of
    conspiracy theorists, some of whom say they have suffered from
    "aspartame poisoning" and filled Web pages with cloak-and-dagger
    speculation about why the F.D.A. approved aspartame for sale
    a quarter-century ago.

    No regulatory agency has yet acted on Dr. Soffritti's findings,
    although Roger Williams, a member of Parliament,
    called for a ban on aspartame in Britain last December.

    Last month, the European Food Safety Authority,
    an advisory body for the European Commission,
    began to review 900 pages of data from Dr. Soffritti;
    the goal is to finish by May.
    A commission spokesman, Philip Tod, said it was too early
    to know what the next steps would be if the scientists
    reviewing the data concurred with Dr. Soffritti's findings.

    In the United States, the Food and Drug Administration
    says it has also taken note of the study, which is available online (
    http://ehp.niehs.nih.gov/docs/2005/8711/abstract.html )
    and is scheduled to be published next month in a medical journal
    financed by the National Institutes of Health.

    F.D.A. officials say that they, too, intend to conduct a thorough review.
    But both the F.D.A. and the European Commission have cautioned
    that there is no need for people to avoid aspartame.
    "We don't see any concerns at this stage," said George H. Pauli,
    associate director for science policy in the F.D.A.'s
    Office of Food Additive Safety. "We've gone through a humongous
    amount of data on aspartame over the years."

    Putting restrictions on aspartame would come at a significant cost.
    Food companies and consumers around the world bought
    about $570 million worth of it last year.
    New regulatory action on aspartame would also jeopardize
    the billions of dollars worth of products sold with it.
    Already, in the United States, many companies are opting to
    use sucralose, or Splenda, in their new low-calorie products,
    in part because it is less controversial.

    [ Dr. Soffritti's journal article on his findings is at
    nytimes.com/business ]

    Lance Collins, chief executive of Fuze Beverage in Englewood Cliffs,
    N.J., said that safety concerns about aspartame were a
    "major contributing factor" in his decision to use sucralose
    in his tea and juice drinks.

    Sucralose, however, is made by under a patent by just one company,
    Tate & Lyle of London, and is in desperately short supply.

    Dr. Soffritti, who has spent 28 years doing research on potential
    carcinogens, said he was trying to steer clear of the growing political
    maelstrom. But he added that he was concerned about the large
    numbers of people who use aspartame,
    particularly children and pregnant women.
    "If something is a carcinogen in animals," he said, "then it should not
    be added to food, especially if there are so many people
    that are going to be consuming it."

    Lyn Nabors, executive vice president of the Calorie Control Council,
    said Dr. Soffritti's study was not valid because the rats used
    in it had been allowed to live longer than the two-year standard
    established by the United States government's
    National Toxicology Program. "It's difficult to determine if the cancers
    you find are due to something else," Ms. Nabors said.
    "Just as in humans, the rat's body slows down later in life,
    and the aging process causes all kinds of things."

    But John R. Bucher, deputy director of environmental toxicology
    at the National Toxicology Program, the government's agency
    for research on toxic chemicals, called the design of the Ramazzini
    study "impressive" and "thorough," and said that he did not think
    the fact that rats were allowed to live until their natural deaths
    had skewed the results.

    Dr. Jose Russo, director of the breast cancer and environmental
    research center at the Fox Chase Cancer Center in Philadelphia,
    says that lifetime studies are "ideal" but that they are not done often,
    partly because they are more expensive than limited-time tests.
    Dr. Russo, however, criticized the Ramazzini study for not allowing
    outside pathologists to analyze all of the tissue samples where
    cancerous tumors were found. "People need to see every tumor,"
    he said.

    Dr. Bucher of the National Toxicology Program said pathologists
    at the program, with which Ramazzini collaborates, looked at 70
    tumor slides.
    But with the study producing over 9,000 tumor-containing slides,
    James Swenberg, professor of environmental science
    at the University of North Carolina at Chapel Hill,
    says that this falls short of standard practice.

    While Dr. Soffritti's methods have drawn some criticism,
    the Ramazzini cancer lab, which is financed
    by private bank foundations, governments and 17,000
    individual members, has earned considerable credibility
    since it was founded in 1971 for its pioneering research
    on chemicals.

    It was the first research body to do studies showing that
    vinyl chloride and the gasoline additive methyl tertiary-butyl ether,
    or M.T.B.E., are carcinogenic, research that eventually
    encouraged the United States to strictly regulate vinyl chloride
    and that led 21 states to ban M.T.B.E.

    Dr. Soffritti said he was inspired to look at aspartame
    because of what he calls "inadequacies" in the cancer studies done
    by Searle in the 1970's. He said that those studies did not
    involve large-enough numbers of rats and did not allow them
    to live long enough to develop cancer.

    The Ramazzini study was conducted with 1,900 rats,
    as opposed to the 280 to 688 rodents used in Searle's studies,
    and the rats lived for up to three years instead of being sacrificed
    after two, which is the human equivalent of age 53.
    "Cancer is a disease of the third part of life," Dr. Soffritti said.
    "You have 75 percent of cancer diagnoses for people
    who are 55 years old or older. So if you truncate the experiments
    at 110 weeks and the rats are supposed to survive
    until 150 to 160 weeks, it means you avoid the development
    of cancer at the time when cancer would be starting to arise."

    Others have also challenged Searle's studies.
    Documents from the F.D.A. and records from the Federal Register
    indicate that, in the years before the F.D.A. approved aspartame,
    the agency had serious concerns about the accuracy and credibility
    of Searle's aspartame studies. From 1977 to 1985 - during much
    of the approval process - Searle was headed by
    Donald H. Rumsfeld, who is now the secretary of defense;
    Searle was acquired by Monsanto in 1985.

    Monsanto later spun Searle's assets out into two companies:
    Merisant, which owns the brands Equal and Canderel, and NutraSweet,
    which is owned by J. W. Childs Equity Partners,
    an investment firm in Boston.

    A 1976 report from an F.D.A. task force, for example,
    found that Searle's studies on aspartame and several of the company's
    pharmaceutical drugs were "poorly conceived, carelessly executed, or
    inaccurately analyzed or reported." It cited what it called a lack of
    training by the scientists analyzing tissue samples, a "substantial"
    loss of information because of tissue decomposition
    and inadequate monitoring of feeding doses.

    In response to the report, the F.D.A. asked the Justice Department
    to open a grand jury investigation into whether two of Searle's
    aspartame studies had been falsified or were incomplete.

    In a 33-page letter in 1977, Richard A. Merrill, the F.D.A.'s
    chief counsel at the time, recommended to Samuel K. Skinner,
    then the United States attorney for the Northern District of Illinois,
    that a grand jury investigate the company,
    which was based in the Chicago suburb of Skokie,
    for "concealing material facts and making false statements
    in reports of animal studies conducted to establish the safety
    of the drug Aldactone and the food additive aspartame."

    A grand jury was never convened, however.
    Shortly after the letter was sent, Mr. Skinner left the
    Justice Department to join Sidley & Austin,
    a law firm that represented Searle.

    After 12 years at that firm, now Sidley, Austin, Brown & Wood,
    Mr. Skinner was appointed to be President George H. W. Bush's
    transportation secretary; later he became his chief of staff.

    In 1978, a year and half after Mr. Skinner left the United States
    attorney's office in Chicago, his deputy, William F. Conlon,
    also left to work at Sidley & Austin.

    Mr. Skinner, now a lawyer at Greenberg Traurig LLP,
    said that as soon as he began looking for a new job
    and interviewing with Sidley & Austin,
    he recused himself from the Searle investigation.
    Mr. Conlon, who is still at Sidley & Austin, did not return phone calls.

    Over the next few years, Searle's petition for aspartame approval
    led to much disagreement within the F.D.A.
    The commissioner at the time, Alexander M. Schmidt,
    convened a three-member public board of inquiry,
    which concluded that one of Searle's studies on rats showed
    an increase in brain tumors from aspartame.
    The board members - all of them scientists at universities - voted
    to withhold approval of aspartame until more studies were done.

    But yet another F.D.A. review, this one of Searle's tumor tissue
    slides - paid for by Searle and conducted by an academic group
    that is now defunct - concluded that Searle's studies had
    demonstrated that aspartame was safe.

    In 1981, a new F.D.A. commissioner, Arthur Hull Hayes,
    concurred with this assessment and granted approval to aspartame
    shortly after President Ronald Reagan appointed him to run the agency.

    And in a move that fueled the conspiracy theories,
    Mr. Hayes left the F.D.A. a little more than a year after approving
    aspartame and took a job as a consultant to Burson-Marsteller,
    which at the time was Searle's public relations agency.
    Mr. Hayes did not return calls seeking comment.

    Ms. Nabors of the Calorie Control Council said that suggestions or
    innuendoes that Searle was trying to influence government officials
    with lucrative job offers were baseless. Artificial sweeteners are
    unfairly targeted for suspicion, she said, citing the government's
    decision to ban the sweetener cyclamate in 1969 after studies
    showed that it caused cancer in animals. "Cyclamate was banned,
    saccharin was required to have a warning label for a while,
    and there's all these conspiracy theories on aspartame," she said.

    She added that there were more than 100 published scientific studies
    showing no adverse effects from aspartame, and said that in 2002,
    the European Commission reviewed many of these studies and
    reaffirmed the sweetener's safety. The bulk of the studies
    investigated neurological effects; none were animal cancer studies,
    which are lengthy and expensive.

    In any case, critics say that most of these studies were financed either
    directly or indirectly by manufacturers of aspartame, and that the results
    of aspartame studies tend to depend on who paid for them.

    In an analysis of 166 articles published in medical journals
    from 1980 to 1985, Dr. Ralph G. Walton, a professor of psychiatry
    at Northeastern Ohio Universities College of Medicine
    found that all 74 studies that were financed by the industry
    attested to sweetener's safety.

    Of the 92 independently funded articles,
    84 identified adverse health effects.
    "Whenever you have studies that were not funded by the industry,
    some sort of problem is identified," said Dr. Walton,
    adding that he has not looked at studies performed since 1985.
    "It's far too much for it to be a coincidence."

    Dr. Walton, who, like some other psychiatrists, has studied aspartame
    from a neurological perspective, said he had also seen problems from
    the sweetener firsthand. At Safe Harbor Behavioral Health,
    a mental health facility in Erie, Pa., where he is clinical director,
    Dr. Walton said he had observed that for many people with mood
    disorders, such as depression or bipolar disorder, aspartame
    exacerbates the condition. "For people with panic disorders,
    for instance, we've seen that when we eliminate aspartame,
    it's much easier to control their illness," he said.
    "The number of panic attacks goes down."

    Dr. Walton and others say that this is probably attributable to
    aspartame's phenyalanine component. (Aspartame is made up
    of two amino acids, phenyalanine and aspartic acid.)
    He said that an excess of phenyalanine could upset the body's
    balance of neurotransmitters, causing a range of neurological symptoms.

    Defenders of aspartame often point out that phenyalanine is naturally
    present in many protein-intensive foods. But Dr. William M. Pardridge,
    a professor of endocrinology at the David Geffen School of Medicine
    at the University of California, Los Angeles, says that when it comes
    from food, phenyalanine is absorbed into the brain more slowly.
    "If your blood phenyalanine level was increased five times,
    in my view there would be a safety concern," Dr. Pardridge said.
    "The question is whether aspartame use could ever increase levels
    that much, and the answer is yes. We've known that for 20 years."

    Dr. Soffritti said he had not studied the effects of phenyalanine.
    He theorized that the tumors in his study were related to the methanol,
    or wood alcohol, that is produced as the body metabolizes aspartame.

    When the body breaks down methanol, the result is formaldehyde,
    a known carcinogen. "I know that when I treat animals with methanol,
    you end up with lymphomas and leukemias," he said.

    BUT Dr. Kenneth E. McMartin, a methanol expert and professor of
    pharmacology, toxicology and neuroscience at the Louisiana State
    University Medical Center, said he believed that it was unlikely
    that someone could consume enough aspartame to let harmful levels
    of formaldehyde build up in the body.

    Dr. Soffritti said he thought that more research and open debate
    were needed on whether aspartame was a carcinogen.
    "It is very important to have scientists who are independent and
    not funded by industry looking at this," he said.

    Michael F. Jacobson, executive director of the
    Center for Science in the Public Interest, a nutrition advocacy group,
    said he did not think that Dr. Soffritti's study could be considered
    definitive, but that it should prompt an "urgent re-examination.

    "For a chemical that is used by hundreds of millions of people
    around the world, it should be absolutely safe," Mr. Jacobson said.
    "There shouldn't be a cloud of doubt."
    ************************************************** *****

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    ************************************************** *****

    http://www.splendaexposed.com/articl...a_the_art.html

    Splenda, the Artificial Sweetener, Adds a Brown Sugar Blend
    By MELANIE WARNER Published: April 4, 2005

    Splenda, the popular artificial sweetener, is going brown.

    The manufacturer of Splenda, the brand name given to the chemical
    sweetener sucralose, is releasing a version that can be used as a
    replacement for brown sugar.
    It will be called Splenda Brown Sugar Blend.

    "People can use it for baking their favorite recipe or sprinkle it on top
    of cereal the same way they would use brown sugar," said John Leahy,
    marketing director for Splenda at McNeil Nutritionals,
    the division of Johnson & Johnson that sells and markets the sweetener.

    Made from a blend of regular brown sugar and sucralose that has been
    colored brown, Splenda's brown sugar will give consumers a 50 percent
    reduction in calories because a smaller amount will be needed for baking
    and other purposes.

    For instance, if a recipe calls for one cup of brown sugar, Mr. Leahy said, only a half-cup of Splenda brown sugar will be necessary.
    Splenda brown sugar will come in one-pound and two-pound bags
    when sales start in September.

    The popularity of Splenda took its manufacturers by surprise last year.
    In November, Tate & Lyle, the British ingredients company that makes
    sucralose, told its customers that its supply of sweetener would have to
    be rationed because of high demand. McNeil markets Splenda
    in the United States under a contract with Tate & Lyle.

    Over the last year and a half, nearly every major food company has
    incorporated sucralose into one or more of its products. Both PepsiCo
    and Coca-Cola have opted to use the sweetener for new colas.
    This month, for example, Pepsi is introducing PepsiOne with Splenda
    and Coke will make a new version of Diet Coke sweetened
    with Splenda that will be in stores in several months.

    Splenda brown sugar is likely to add to the legal debate brewing over
    Splenda's marketing campaign. The Sugar Association, which represents
    the sugar industry; Merisant, the maker of the aspartame-based
    artificial sweetener NutraSweet; and a lawyer in San Diego
    have filed lawsuits against McNeil contending that Splenda's
    marketing misleads consumers.

    "The average consumer assumes that Splenda is related to sugar,"
    said Howard M. Rubinstein, the San Diego lawyer. "They're exploiting
    the fear some people have around other artificial sweeteners
    like NutraSweet and presenting this as a more natural alternative."

    Mr. Leahy said that its marketing for the new brown sugar product
    would "remain consistent with Splenda's existing brand communication."

    Neither the Sugar Association, based in Washington, nor Merisant,
    which is based in Chicago, would comment. If Splenda brown sugar
    catches on with consumers, it is likely to accelerate the decline of
    old-fashioned sugar.
    Sales of both white and brown sugar in the United States have been
    declining for years.
    Sales have dropped 10 percent since 1999, Mintel International,
    a research firm based in Chicago, has reported.
    ************************************************** *****

    February 12, 2006

    Any unsuspected source of methanol, which the body always quickly
    and largely turns into formaldehyde and then formic acid, must be
    monitored, especially for high responsibility occupations, often with
    night shifts, such as pilots and nuclear reactor operators.

    In particular, the next review gives many recent mainstream
    peer-reviewed studies that show formaldehyde,
    always inevitably derived in the body from any methanol source,
    including aspartame, causes endothelial injury,
    ie, diabetic neuropathy -- among the most serious and complex
    complications of diabetes.

    http://groups.yahoo.com/group/aspartameNM/message/1263
    many studies on endothelial injury (diabetic neuropathy) by adducts of
    formaldehyde derived from methylamine from many of the same sources
    as also supply methanol (formaldehyde), including aspartame:
    PH Yu et al: DJ Conklin et al: Murray 2005.12.04

    http://groups.yahoo.com/group/aspartameNM/message/1237
    ubiquitous potent uncontrolled co-factors in nutrition research are
    formaldehyde from wood and tobacco smoke and many sources,
    including from methanol in dark wines and liquors, in pectins
    in fruits and vegetables, and in aspartame: Murray 2006.01.13

    http://groups.yahoo.com/group/aspartameNM/message/925
    aspartame puts formaldehyde adducts into tissues, Part 1/2
    full text Trocho & Alemany 1998.06.26
    Universitat Autònoma de Barcelona : Murray 2002.12.22

    http://groups.yahoo.com/group/aspartameNM/message/1250
    aspartame causes cancer in rats at levels approved for humans,
    Morando Soffritti et al, Ramazzini Foundation, Italy &
    National Toxicology Program
    of National Institute of Environmental Health Sciences
    2005.11.17 Env. Health Pers. 35 pages: Murray

    http://groups.yahoo.com/group/aspartameNM/message/1271
    combining aspartame and quinoline yellow, or MSG and brilliant blue,
    harms nerve cells, eminent C. Vyvyan Howard et al, 2005
    education.guardian.co.uk, Felicity Lawrence: Murray 2005.12.21

    http://groups.yahoo.com/group/aspartameNM/message/1279
    all three aspartame metabolites harm human erythrocyte [red blood cell]
    membrane enzyme activity, KH Schulpis et al, two studies in 2005,
    Athens, Greece, 2005.12.14: 2004 research review, RL Blaylock:
    Murray 2006.01.14

    As a medical layman, I suggest that evidence mandates immediate
    exploration of the role of these ubiquitious, potent formaldehyde
    sources as co-factors in epidemiology, research, diagnosis,
    and treatment in a wide variety of disorders.

    Folic acid, from fruits and vegetables, plays a role by powerfully
    protecting against methanol (formaldehyde) toxicity.

    Many common drugs, such as aspirin, interfere with folic acid,
    as do some mutations in relevant enzymes.

    The majority of aspartame reactors are female.

    In mutual service, Rich Murray
    ************************************************** *****

    "Of course, everyone chooses, as a natural priority,
    to actively find, quickly share, and act upon the facts
    about healthy and safe food, drink, and environment."

    Rich Murray, MA Room For All rmforall@comcast.net
    505-501-2298 1943 Otowi Road Santa Fe, New Mexico 87505

    http://groups.yahoo.com/group/aspartameNM/messages
    group with 151 members, 1,302 posts in a public, searchable archive
    http://RMForAll.blogspot.com http://AspartameNM.blogspot.com

    Dark wines and liquors, as well as aspartame, provide
    similar levels of methanol, above 100 mg daily, for
    long-term heavy users, 2 L daily, about 6 cans.

    Methanol is inevitably largely turned into formaldehyde,
    and thence largely into formic acid.
    It is the major cause of the dreaded symptoms of "next
    morning" hangover.

    Fully 11% of aspartame is methanol -- 1,120 mg aspartame
    in 2 L diet soda, almost six 12-oz cans, gives 123 mg
    methanol (wood alcohol). If 30% of the methanol is turned
    into formaldehyde, the amount of formaldehyde, 37 mg,
    is 18.5 times the USA EPA limit for daily formaldehyde in
    drinking water, 2.0 mg in 2 L average daily drinking water.

    http://groups.yahoo.com/group/aspartameNM/message/1108
    faults in 1999 July EPA 468-page formaldehyde profile:
    Elzbieta Skrzydlewska PhD, Assc. Prof., Medical U. of
    Bialystok, Poland, abstracts -- ethanol, methanol,
    formaldehyde, formic acid, acetaldehyde, lipid peroxidation,
    green tea, aging: Murray 2004.08.08 2005.07.11

    http://groups.yahoo.com/group/aspartameNM/message/835
    ATSDR: EPA limit 1 ppm formaldehyde in drinking water July
    1999: Murray 2002.05.30 rmforall

    Aspartame is made of phenylalanine (50% by weight) and
    aspartic acid (39%), both ordinary amino acids, bound
    loosely together by methanol (wood alcohol, 11%).
    The readily released methanol from aspartame is within hours
    turned by the liver into formaldehyde and then formic acid,
    both potent, cumulative toxins.
    ************************************************** *****
    Send blank post to: <br />aspartameNM-subscribe@onelist.com to join<br />free,open, list with searchable archives for toxicity issues.<br />Richard \"Rich\" T. Murray Room For All 1943 Otowi Road Santa Fe, NM 87505<br />rmforall@comcast.net 505-501-2298

  2. #2
    Join Date
    Jun 1999
    Location
    Santa Fe, NM 87505, USA
    Posts
    63

    Post

    February 12, 2006

    See also:

    http://groups.yahoo.com/group/aspartameNM/message/1271
    combining aspartame and quinoline yellow, or MSG and brilliant blue,
    harms nerve cells, eminent C. Vyvyan Howard et al, 2005
    education.guardian.co.uk, Felicity Lawrence: Murray 2005.12.21

    http://groups.yahoo.com/group/aspartameNM/message/1263
    many studies on endothelial injury (diabetic neuropathy) by adducts of
    formaldehyde derived from methylamine from many of the same sources
    as also supply methanol (formaldehyde), including aspartame:
    PH Yu et al: DJ Conklin et al: Murray 2005.12.04

    http://groups.yahoo.com/group/aspartameNM/message/1250
    aspartame causes cancer in rats at levels approved for humans,
    Morando Soffritti et al, Ramazzini Foundation, Italy &
    National Toxicology Program
    of National Institute of Environmental Health Sciences
    2005.11.17 Env. Health Pers. 35 pages: Murray

    http://groups.yahoo.com/group/aspartameNM/message/1226
    USA National Institutes of Health National Toxicology
    Program aids eminent Ramazzini Foundation, Bologna, Italy,
    in more results on cancers in rats from lifetime low levels
    of aspartame (methanol, formaldehyde), Felicity Lawrence,
    www.guardian.co.uk: Murray 2005.09.30

    http://groups.yahoo.com/group/aspartameNM/message/1186
    aspartame induces lymphomas and leukaemias in rats, full plain text,
    M Soffritti, F Belpoggi, DD Esposti, L Lambertini: Ramazzini
    Foundation study 2005.07.14: main results agree with their previous
    methanol and formaldehyde studies: Murray 2005.09.03

    http://groups.yahoo.com/group/aspartameNM/message/1189
    Michael F Jacobson of CSPI now and in 1985 re aspartame
    toxicity, letter to FDA Commissioner Lester Crawford;
    California OEHHA aspartame critique 2004.03.12; Center for
    Consumer Freedom denounces CSPI: Murray 2005.07.27

    http://groups.yahoo.com/group/aspartameNM/message/1143
    methanol (formaldehyde, formic acid) disposition: Bouchard M
    et al, full plain text, 2001: substantial sources are
    degradation of fruit pectins, liquors, aspartame, smoke:
    Murray 2005.04.02
    ************************************************** *****

    http://groups.yahoo.com/group/aspartameNM/message/1279
    all three aspartame metabolites harm human erythrocyte [red blood cell]
    membrane enzyme activity, KH Schulpis et al, two studies in 2005,
    Athens, Greece, 2005.12.14: 2004 research review, RL Blaylock:
    Murray 2006.01.14

    "High or abuse concentrations of ASP hydrolysis products significantly
    decreased the membrane enzyme activity,
    which was completely or partially prevented by L-cysteine
    or reduced GSH."

    [ Definition of Erythrocyte
    Erythrocyte:
    A cell that contains hemoglobin and can carry oxygen to the body.
    Also called a red blood cell (RBC).
    The reddish color is due to the hemoglobin.
    Erythrocytes are biconcave in shape,
    which increases the cell's surface area
    and facilitates the diffusion of oxygen and carbon dioxide.
    This shape is maintained by a cytoskeleton
    composed of several proteins.
    Erythrocytes are very flexible
    and change shape when flowing through capillaries.
    Immature erythrocytes, called reticulocytes,
    normally account for 1-2 percent of red cells in the blood. ]


    Eur J Clin Nutr. 2005 Dec 14; [Epub ahead of print]
    The effect of L-cysteine and glutathione on inhibition of
    Na(+), K(+)-ATPase activity by aspartame metabolites
    in human erythrocyte [red blood cell] membrane.
    Schulpis KH, Kleopatra H. Schulpis, MD, PhD.
    Institute of Child Health, Aghia Sophia Children's Hospital,
    GR-11527 Athens (Greece) +30 1 7708291, Fax +30 1 7700111
    inchildh@otenet.gr;
    Papassotiriou I, biochem@paidon-agiasofia.gr;
    Parthimos T,
    Tsakiris T,
    Tsakiris S. Stylianos Tsakiris. stsakir@cc.uoa.gr;
    1 Institute of Child Health, Research Center,
    'Aghia Sophia' Children's Hospital, Athens, Greece.
    ggbriass@med.uoc.gr; ersi_voskaridou@yahoo.com;
    mmoschov@med.uoa.gr; siahanidou@hotmail.com;


    Background:
    Reports have implicated Aspartame
    (N-L-a-aspartyl-L-phenylalanine methyl ester, ASP)
    in neurological problems.

    Aim:
    To evaluate Na(+), K(+)-ATPase activities in human erythrocyte
    [red blood cell] membranes
    after incubation with the ASP metabolites,
    phenylalanine (Phe),
    methanol (MeOH) and
    aspartic acid (Asp).

    Methods:
    Erythrocyte [red blood cell] membranes
    were obtained from 12 healthy individuals and
    were incubated at 37 degrees C for 1 h
    with the sum or each of the ASP metabolites separately,
    which are commonly measured in blood after ASP ingestion.

    Na(+), K(+)-ATPase and Mg(2+)-ATPase activities were measured
    spectrophotometrically.

    Results:
    Membrane Mg(2+)-ATPase activity was not altered.

    The sum of ASP metabolite concentrations corresponding
    to 34, 150 or 200 mg/kg of the sweetener ingestion
    resulted in an inhibition of the membrane
    Na(+), K(+)-ATPase by -30, -40, -48%, respectively.

    MeOH concentrations of 0.14, 0.60 or 0.80 mM
    decreased the enzyme activity by -25, -38, -43%, respectively.

    Asp concentrations of 2.80, 7.60 or 10.0 mM
    inhibited membrane Na(+), K(+)-ATPase by -26, -40, -46%,
    respectively.

    Phe concentrations of 0.14, 0.35 or 0.50 mM
    reduced the enzyme activity by -24, -44, -48%, respectively.

    Preincubation with L-cysteine or reduced glutathione (GSH)
    completely or partially restored
    the inhibited membrane Na(+), K(+)-ATPase activity
    by high or toxic ASP metabolite concentrations.

    Conclusions:
    Low concentrations of ASP metabolites had no effect
    on Na(+), K(+)-ATPase activity.

    High or abuse concentrations of ASP hydrolysis products significantly
    decreased the membrane enzyme activity,
    which was completely or partially prevented by L-cysteine
    or reduced GSH. [reduced glutathione]

    European Journal of Clinical Nutrition advance online publication,
    14 December 2005; doi:10.1038/sj.ejcn.1602355. PMID: 16391576
    ************************************************** *****

    http://groups.yahoo.com/group/aspartameNM/message/1213
    aspartame (methanol, phenylalanine, aspartic acid) effects, detailed
    expert studies in 2005 Aug and 1998 July, Tsakiris S, Schulpis KH,
    Karikas GA, Kokotos G, Reclos RJ, et al, Aghia Sophia Children's
    Hospital, Athens, Greece: Murray 2005.09.09

    Rich Murray, MA Room For All rmforall@comcast.net
    505-501-2298 1943 Otowi Road Santa Fe, New Mexico 87505
    http://groups.yahoo.com/group/aspartameNM/messages
    group with 148 members, 1,213 posts in a public, searchable archive

    [ The lowest dose level tested, 34 mg aspartame per kg body weight,
    well below the FDA daily human limit of 50 mg/kg, 16 12-oz cans,
    caused enzyme activity reduction by -33% in human red blood cell
    membranes. ]

    However, a missed opportunity in both studies is that the inevitable,
    extremely and cumulatively toxic products of methanol in the human
    body, formaldehyde and formic acid, which are responsible for the
    toxicity of methanol, were not independently tested.

    " It is concluded that low concentrations of ASP metabolites had no
    effect on the [human red blood cell] membrane enzyme activity,
    whereas high or toxic concentrations partially or remarkably decreased
    the [human red blood cell] membrane AChE activity, respectively.
    Additionally, neurological symptoms, including learning and memory
    processes, may be related to the high or toxic concentrations of the
    sweetener metabolites. " ]

    Pharmacol Res. 2005 Aug 26; [Epub ahead of print]
    The effect of aspartame metabolites on human [red blood cell]
    erythrocyte membrane acetylcholinesterase activity.
    Tsakiris S,
    Giannoulia-Karantana A,
    Simintzi I,
    Schulpis KH.
    Department of Experimental Physiology, Medical School,
    University of Athens, P.O. Box 65257, GR-154 01 Athens, Greece.

    Stylianos Tsakiris. stsakir@cc.uoa.gr;

    Giannoulia-Karantana A. First Department of Pediatrics,
    Aghia Sophia Children's Hospital, University of Athens, Greece.

    Kleopatra H. Schulpis, MD, PhD. Institute of Child Health,
    Aghia Sophia Children's Hospital, GR-11527 Athens (Greece)
    Tel. +30 1 7708291, Fax +30 1 7700111 inchildh@otenet.gr;

    Papoutsakis T. tina.papoutsakis@hua.gr;

    Papadopoulos G. Department of Biochemistry and Biotechnology,
    University of Thessaly, Ploutonos 26, 41221 Larisa, Greece
    papg@chem.auth.gr;

    Abstract:

    Studies have implicated aspartame (ASP) with neurological problems.
    The aim of this study was to evaluate acetylcholinesterase (AChE)
    activity in human erythrocyte [red blood cell] membranes
    after incubation with the sum of ASP metabolites,
    phenylalanine (Phe),
    methanol (met) and
    aspartic acid (aspt),
    or with each one separately.

    Erythrocyte [human red blood cell] membranes were obtained from
    12 healthy individuals and were incubated with ASP hydrolysis
    products for 1h at 37 degrees C.
    AChE was measured spectrophotometrically.

    Incubation of membranes with ASP metabolites corresponding
    with 34 mg/kg, 150 mg/kg or 200 mg/kg of ASP consumption
    resulted in an enzyme activity reduction by -33%, -41%, and -57%,
    respectively.

    Met concentrations 0.14 mM, 0.60 mM, and 0.80 mM decreased
    the enzyme activity by -20%, -32% or -40%, respectively.

    Aspt concentrations 2.80 mM, 7.60 mM or 10.0 mM inhibited
    membrane AChE acitivity by -20%, -35%, and -47%, respectively.

    Phe concentrations 0.14 mM, 0.35 mM or 0.50 mM reduced the
    enzyme activity by -11%, -33%, and -35%, respectively.

    Aspt or Phe concentrations 0.82 mM or 0.07 mM, respectively,
    did not alter the membrane AChE activity.

    It is concluded that low concentrations of ASP metabolites had
    no effect on the membrane enzyme activity,
    whereas high or toxic concentrations partially or remarkably
    decreased the membrane AChE activity, respectively.
    Additionally, neurological symptoms, including learning and memory
    processes, may be related to the high or toxic concentrations of the
    sweetener metabolites. PMID: 16129618
    ************************************************** ****

    http://groups.yahoo.com/group/aspartameNM/message/1213
    aspartame (methanol, phenylalanine, aspartic acid) effects, detailed
    expert studies in 2005 Aug and 1998 July, Tsakiris S, Schulpis KH,
    Karikas GA, Kokotos G, Reclos RJ, et al, Aghia Sophia Children's
    Hospital, Athens, Greece: Murray 2005.09.09

    http://groups.yahoo.com/group/aspartameNM/message/939
    aspartame (aspartic acid, phenylalanine) binding to DNA:
    Karikas July 1998: Murray 2003.01.05 rmforall
    Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
    Measurement of molecular interaction of aspartame and
    its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
    Dept. of Chemistry, University of Athens, Greece
    http://www.chem.uoa.gr gkokotos@atlas.uoa.gr
    K.H. Schulpis inchildh@otenet.gr G.J. Reclos reklos@otenet.gr


    http://groups.yahoo.com/group/aspartameNM/message/1277
    50% UK baby food is now organic -- aspartame or MSG
    with food dyes harm nerve cells, CV Howard 3 year study
    funded by Lizzy Vann, CEO, Organix Brands,
    Children's Food Advisory Service: Murray 2006.01.13
    ************************************************** *****
    Send blank post to: <br />aspartameNM-subscribe@onelist.com to join<br />free,open, list with searchable archives for toxicity issues.<br />Richard \"Rich\" T. Murray Room For All 1943 Otowi Road Santa Fe, NM 87505<br />rmforall@comcast.net 505-501-2298

  3. #3
    Join Date
    Jun 1999
    Location
    Santa Fe, NM 87505, USA
    Posts
    63

    Post

    http://groups.yahoo.com/group/aspartameNM/message/1090
    aspartame, MSG, excitotoxins, NMDA glutamate receptors, multiple
    sclerosis: Blaylock: Martini: Murray 2004.06.09 rmforall

    Rich Murray: I have corrected typos and spelling, and added spacing
    to improve readability. I found abstracts for 7 of the 9 references, and
    added more abstracts that show a vigorous scientific advance, with
    scores of scientists and studies. These studies may well be relevant
    to very recent research that aspartame hurts memory in rats:

    http://groups.yahoo.com/group/aspartameNM/message/1088
    Murray, full plain text & critique:
    chronic aspartame in rats affects memory, brain cholinergic receptors,
    and brain chemistry, Christian B, McConnaughey M et al, 2004 May:
    2004.06.05 rmforall

    http://www.rense.com/general53/ms.htm
    The connection between MS and aspartame
    Russell L. Blaylock, M.D. Neurosurgeon 2004.06.07
    http://www.russellblaylockmd.com

    Recently, much controversy has surrounded a claim that aspartame
    may produce an MS-like syndrome.
    A current review of recent peer-reviewed scientific studies have
    disclosed a pathophysiological mechanism to explain this connection.

    As far back as 1996 it was shown that the lesions produced in the
    myelin sheath of axons in cases of multiple sclerosis were related to
    excitatory receptors on the primary cells involved, called
    oligodendroglia.
    Recent studies have now confirmed what was suspected back then.
    The loss of myelin sheath on the nerve fibers characteristic of the
    disease are due to the death of these oligodendroglial cells at the site
    of the lesions (called plaques). Further, these studies have shown
    that the death of these important cells is as a result of excessive
    exposure to excitotoxins at the site of the lesions.

    Normally, most of these excitotoxins are secreted from microglial
    immune cells in the central nervous system.
    This not only destroys these myelin-producing cells, it also breaks
    down the blood-brain barrier (BBB), allowing excitotoxins in the
    blood stream to enter the site of damage.

    Aspartame contains the excitotoxin aspartate as 40% of its
    molecular structure. Numerous studies have shown that consuming
    aspartame can significantly elevate the excitotoxin level in the blood.

    [ Rich Murray: A Searle Laboratories team in 1976 reported that
    in 4 monkeys fed aspartame, by 12 hours: "...the major fraction
    (70%) of the [aspartate] label appeared in the expired air (Fig.6)...
    Urinary and fecal 14C [ aspartate derived ] amounted to 4--6%
    of the administered [ aspartate ] label."
    This gives a total of a maximum 76% excreted aspartate
    from the aspartame, indicating that 24% of this excitotoxin
    was retained in the body.
    It is reasonable to conclude that daily use of aspartame must lead to
    substantial accumulation of this excitotoxin, aspartate, in body tissues.

    Their 1979 review said: "Aspartame... is hydrolyzed in the gut to yield
    aspartic acid, phenylalanine, and methanol....
    Aspartate may also be incorporated into body constitutents such as
    other amino acids, proteins, pyrimidines, asparagine, and
    N-acetylaspartic acid."

    J Environ Pathol Toxicol. 1979 Mar-Apr; 2(4): 979-85.
    A review of the metabolism of the aspartyl moiety of aspartame in
    experimental animals and man.
    Ranney RE, Oppermann JA.
    Department of Drug Metabolism and Radiochemistry,
    Searle Laboratories, Skokie, Illinois.

    Aspartame (3-amino-N-(alpha-carboxyphenethyl) succinamic acid,
    methyl ester; the methyl ester of aspartylphenylalanine, SC-18862)
    is hydrolyzed in the gut to yield aspartic acid, phenylalanine,
    and methanol.
    This review of the literature describes the metabolic paths
    followed by aspartate in its conversion to CO2
    or its incorporation into body constituents.
    About 70 percent of 14C from [asp-14C]-aspartame is
    converted in the monkey to 14CO2.
    Some of the aspartate is converted at the intestinal mucosal level to
    alanine by decarboxylation.
    This amino acid may be oxidized to CO2 by entering the
    tricarboxylic acid cycle via pyruvate and acetyl CoA.
    In addition, transamination of aspartate to oxaloacetate
    permits this product also to enter the tricarboxylic acid cycle.
    Aspartate may also be incorporated into body constitutents such as
    other amino acids, proteins, pyrimidines, asparagine,
    and N-acetylaspartic acid.
    It is concluded that the aspartate moiety of aspartame
    is metabolized in a manner similar to that of dietary aspartic acid.
    Publication Types: Review PMID: 376770 ]

    There is a common situation during which the excitotoxin
    exposure is even greater.
    When aspartate (as aspartame) is combined in the diet with
    monosodium glutamate (MSG) blood levels are several fold higher
    than normal.
    With the BBB damaged, as in MS, these excitotoxins can freely enter
    the site of injury, greatly magnifying the damage.
    So, we see that dietary excitotoxins, such as aspartame and MSG,
    can greatly magnify the damage produced in multiple sclerosis.
    Likewise, excitotoxins have been shown to breakdown the BBB as well.

    Of equal concern is observation that we know that about 10% of the
    population (based on autopsy studies of elderly) have MS lesions without
    ever developing the full blown disease,
    a condition called benign MS.

    A diet high in excitotoxins, such as aspartame, can convert this benign,
    subclinical condition into full-blown clinical MS.
    The amount of excitotoxins consumed in the average American diet is
    considerable, as shown by several studies.

    In addition, the toxin methanol is also in the aspartame molecule.
    Methanol is an axon poison.
    Combined toxicity of the aspartate and the methanol adds up to
    considerable brain toxicity, and can convert benign, subclinical MS
    into full-blown MS.
    Once the MS becomes full-blown, further consumption of
    excitotoxins magnifies the toxicity, increasing disability and death.

    Recent studies have also shown that even single exposures to these
    food-based excitotoxins can produce prolonged worsening of
    neurological lesions.

    In addition, it has been demonstrated that autoimmune reactions
    (as occurs with MS) greatly magnifies the toxicity of aspartate
    and glutamate (the excitotoxins).

    We also know liquid forms of excitotoxins are significantly more
    toxic because of rapid absorption and higher blood levels.

    In the face of this connection between excitotoxicity and the
    pathophysiology of MS, it would be ludicrous to allow further use
    of this excitotoxin containing sweetener.

    TREATMENT FOR MS:
    It is now known the cause for the destruction of the myelin in the
    lesions is overactivation of the microglia in the region of the myelin.
    An enzyme that converts glutamine to glutamate, called glutaminase,
    increases tremendously, thereby greatly increasing excitotoxicity.

    Mercury also activates microglia, even in subtoxic doses.

    Any dietary excitotoxin can activate the microglia, thereby greatly
    aggravating the injury.
    This includes the aspartate in aspartame.
    The methanol adds to this toxicity as well.

    Now, the secret to treatment appears to be shutting down, or at least
    calming down, the microglia.
    It has been found that the antibiotic minocycline powerfully shuts
    down the microglia.
    I tried this treatment on a friend of mine who just came down with
    fulmanant MS.
    He was confined to a wheelchair.
    I had him placed on minocycline and now, just a few weeks later,
    he is walking.

    The good news is that other things also calm the microglia --
    the most potent are: silymarin, curcumin and ibuprophen.
    Phosphatidylcholine helps re-myelinate the nerve sheaths that are
    damaged, as does B12, B6, B1, vitamin D, folate, vitamin C,
    natural vitamin E (mixed tocopherols) and L-carnitine.

    DHA plays a major role in repairing the myelin sheath.

    Vitamin D may even prevent MS, but it acts as an immune modulator,
    preventing further damage -- the dose is 2000 IU a day.

    Magnesium, as magnesium malate, is needed
    in a dose of 500 mg 2X a day.

    They must avoid all excitotoxins, even natural ones in foods --
    such as soy, red meats, nuts, mushrooms and tomatoes.

    Avoid all fluoride and especially all vaccinations, since these
    either inhibit antioxidant enzymes or trigger harmful immune reactions.


    Dr. Blaylock is a recently retired board-certified neurosurgeon
    with more than twenty six years experience. He is a recently retired
    Clinical Assistant Professor of Neurosurgery at the Medical University
    of Mississippi. Author of thirty scientific papers on various medical
    subjects, chapters in three medical textbooks and a booklet on multiple
    sclerosis, he recently completed a booklet on bioterrorism and is the
    author of "Excitotoxins: The Taste That Kills",
    "Health & Nutrition Secrets to Save Your Life", and
    "Natural Strategies for Cancer Patients".
    http://www.russellblaylockmd.com/
    He serves on the editorial staff of The Journal of American Physicians
    and Surgeons, the Journal of the American Nutraceutical Association,
    and acts as a medical advisor to the American Nutraceutical Association.
    His excellent newsletter can be gotten at
    http://www.blaylockreport.com/
    He lives in Ridgeland, Mississippi.

    References and additional abstracts:

    1. Neurobiol Dis. 1999 Dec; 6(6): 475-85.
    AMPA and kainate receptors each mediate excitotoxicity in
    oligodendroglial cultures.
    Sanchez-Gomez MV, Matute C.
    Departamento de Neurociencias, Universidad del Pais Vasco,
    Leioa, Vizcaya, 48940, Spain.
    Sanchez-Gomez MV has 11 abstracts in PubMed since 1992
    on this line of research, while Matute C has 63 abstracts since 1985.
    Carlos Matute Almau +34-946-012-865 onpmaalc@lg.ehu.es;

    Recent studies indicate that oligodendrocytes are vulnerable to
    excitotoxic insults mediated by glutamate receptors.
    The present study was carried out to characterize the type of glutamate
    receptors triggering cell death in optic nerve oligodendrocyte cultures.
    Acute activation of either AMPA or kainate receptors was toxic to
    oligodendrocytes, an effect that was prevented by CNQX.
    However, exposure to agonists of the NMDA and metabotropic
    glutamate receptors did not impair cell viability.
    Dose-response curves showed that toxicity was mediated
    by three distinct populations of receptors:
    an AMPA-type receptor and high- and low-affinity kainate-type
    receptors.
    Expression and immunocytochemical studies suggested that the
    glutamate receptor subunits give rise to the native receptors
    in each population.
    In all instances, Ca(2+) entry was a major determinant
    of glutamate receptor excitotoxicity.
    However, its influence varied for each receptor subtype.
    These results indicate that aberrantly enhanced activation of
    AMPA and/or kainate receptors may be involved
    in demyelinating diseases.
    Copyright 1999 Academic Press. PMID: 10600403

    J Neurosci. 2003 Oct 22; 23(29): 9519-28.
    Caspase-dependent and caspase-independent oligodendrocyte
    death mediated by AMPA and kainate receptors.
    Sanchez-Gomez MV, Alberdi E, Ibarretxe G, Torre I, Matute C.
    Departamento de Neurociencias, Universidad del Pais Vasco,
    E-48940 Leioa, Vizcaya, Spain.
    Department of Neurosciences, Faculty of Medicine and Dentistry,
    University of the Basque Country, Leioa, Vizcaya, Spain
    Carlos Matute Almau +34-946-012-865 onpmaalc@lg.ehu.es;

    Oligodendrocytes are vulnerable to excitotoxic signals mediated
    by AMPA receptors and by high- and low-affinity kainate receptors.
    Here we investigated the nature of the cell death triggered by activation
    of these receptors in primary cultures of oligodendrocytes
    from the rat optic nerve.
    Activation of AMPA receptors at both submaximal and maximal
    concentrations of the agonist induced massive calcium entry,
    mitochondrial depolarization, and a rise in the level of reactive oxygen
    species that correlated with a decrease in the levels of reduced
    glutathione.
    In addition, excitotoxicity initiated by submaximal, but not maximal,
    activation of AMPA receptors was prevented by caspase-3 blockade
    and by the concomitant blockade of caspases 8 and 9.
    In turn, maximal activation of high- or low-affinity kainate receptors
    induced mitochondrial events and toxicity levels similar to those observed
    with submaximal activation of AMPA receptors.
    In contrast to AMPA receptor-mediated insults, calcineurin inhibition
    or caspase-9 blockade was sufficient to prevent cell death triggered
    by both types of kainate receptors.
    Consistent with these results, prolonged glutamate receptor activation in
    freshly isolated optic nerves caused selective activation of caspase-3
    and chromatin condensation in oligodendrocytes.
    Overall, the evidence presented here indicates that oligodendrocyte
    death by excitotoxicity is mediated
    by caspase-dependent and -independent mechanisms.
    PMID: 14573531

    free full text http://www.ehu.es/ingles/paginas/prin_i.htm
    Glia. 2002 Sep; 39(3): 304-13.
    Multiple angiotensin receptor subtypes
    in normal and tumor astrocytes in vitro.
    Fogarty DJ, Sanchez-Gomez MV, Matute C.
    Department of Neurosciences, Faculty of Medicine and Dentistry,
    University of the Basque Country, Leioa, Vizcaya, Spain.
    Carlos Matute Almau +34-946-012-865 onpmaalc@lg.ehu.es;

    A role for neuropeptide receptors in glial tumorigenesis has recently
    been proposed.
    Although angiotensin receptors are known to mediate proliferative
    effects in many cell types, including brain astrocytes, the possible
    participation of these receptors in glial tumorigenesis remains unknown.
    In the present study, we have examined the expression of the molecularly
    defined angiotensin receptor subtypes AT(1a), AT(1b), and AT(2) in
    normal perinatal rat astrocytes
    and in a panel of tumor adult astrocytoma cells,
    using the reverse transcriptase-polymerase chain reaction (RT-PCR).
    Subsequently, we compared the mitogenic effect of the angiotensins
    A(1-8), A(2-8), A(3-8) and the heptapeptide "metabolite" A(1-7),
    on both normal and tumor astrocytes,
    measured in terms of the incorporation of tritiated thymidine.
    Our results indicate that AT(1a), AT(1b), and AT(2) angiotensin
    receptor mRNA is commonly expressed by many of these cells.
    Of notable exception is the astrocytoma U373 which was not found
    to express AT(1) or AT(2) mRNA.
    Chronic (24-h) incubation of cells with A(1-8) and A(1-7) lead to the
    induction of mitogenesis, even in the AT(1) and AT(2) mRNA negative
    astrocytoma cell line U373.
    Moreover, pharmacological analysis indicated that the observed
    mitogenic effects are not mediated by the AT(1) or AT(2) type
    receptors, but rather by a novel, specific A((1-7)) angiotensin
    receptor, since mitogenesis was shown
    to be partially blocked by the A(1-7) analogue D-Ala(7)A(1-7)
    and by the protease inhibitor orthophenanthroline (100 microM).
    Using Fura-2 spectrophotometry, we found that activation of this
    receptor does not alter intracellular calcium levels;
    however, preincubation with the protein kinase kinase inhibitor
    U0126 (10 microM) was found to inhibit these mitogenic effects
    partially.
    Overall, these results which demonstrate that normal and tumor
    astrocytes express a greater variety of angiotensin receptor subtypes
    than previously thought,
    support the idea that A(1-7) and its receptor signaling system may
    play an important role in shaping the astrocyte population during
    development.
    Moreover, the untimely expression of this A((1-7)) receptor
    may represent an important etiological component in the development
    of brain astrocytomas.
    Copyright 2002 Wiley-Liss, Inc. PMID: 12203396

    free full text http://www.ehu.es/ingles/paginas/prin_i.htm
    Carlos Matute, Elena Alberdi, Gaskon Ibarretxe,
    Maria Victoria Sanchz-Gomez.
    Excitotoxicity in glial cells.
    European J. Pharmacology 2002; 447: 239-246.
    Carlos Matute Almau +34-946-012-865 onpmaalc@lg.ehu.es;

    Excitotoxicity results from prolonged activation of glutamate receptors
    expressed by cells in the central nervous system (CNS).
    This cell death mechanism was first discovered in retinal ganglion cells
    and subsequently in brain neurons.
    In addition, it has been recently observed that CNS glial cells can also
    undergo excitotoxicity.
    Among them, oligodendrocytes are highly vulnerable to glutamate signals
    and alterations in glutamate homeostasis may contribute to demyelinating
    disorders.
    We review here the available information on excitotoxity in CNS glial
    cells and its putative relevance to glio-pathologies. PMID: 12151015

    Trends Neurosci. 2001 Apr; 24(4): 224-30.
    The link between excitotoxic oligodendroglial death and demyelinating
    diseases.
    Matute C, Alberdi E, Domercq M, Perez-Cerda F, Perez-Samartin A,
    Sanchez-Gomez MV.
    Departamento de Neurociencias, Universidad del Pais Vasco,
    48940 Leioa, Spain. Carlos Matute Almau +34-946-012-865
    onpmaalc@lg.ehu.es;

    Oligodendrocytes, the myelinating cells of CNS axons, are highly
    vulnerable to excitotoxic signals mediated by glutamate receptors of the
    AMPA and kainate classes.
    Receptors in these cells are commonly activated by glutamate that is
    released from axons and glial cells.
    In addition, oligodendrocytes contribute to the control of extracellular
    glutamate levels by means of their own transporters.
    However, acute and chronic alterations in glutamate homeostasis
    can result in overactivation of AMPA and kainate receptors
    and subsequent excitotoxic oligodendroglial death.
    Furthermore, demyelinating lesions caused by excitotoxins
    can be similar to those observed in multiple sclerosis.
    This, together with the effect of AMPA and kainate receptor
    antagonists in ameliorating the neurological score of animals with
    experimental autoimmune encephalomyelitis
    (an animal model of multiple sclerosis), indicates that
    oligodendrocyte excitotoxicity could be involved in the pathogenesis of
    demyelinating disorders. Publication Types: Review Review Literature
    PMID: 11250007

    Adv Exp Med Biol. 1999; 468: 97-107.
    On how altered glutamate homeostasis may contribute to demyelinating
    diseases of the CNS.
    Matute C, Domercq M, Fogarty DJ, Pascual de Zulueta M,
    Sanchez-Gomez MV.
    Departamento de Neurociencias Universidad del Pais Vasco,
    Vizcaya, Spain.
    Carlos Matute Almau +34-946-012-865 onpmaalc@lg.ehu.es;

    Glial cells communicate reciprocally with neurons in multiple ways,
    both in synaptic and non-synaptic regions of the central nervous system.
    In the latter, neuron to glial and glial to glial signals can be mediated by
    neurotransmitters.
    Here, we review the presence and some of the functional properties of
    glutamate transporters and receptors in oligodendrocytes.
    In addition, we present data illustrating that alterations in glutamate
    homeostasis can be excitotoxic to oligodendroglia and that the tissue
    lesions caused by overactivation of glutamate receptors resemble those
    observed in demyelinating diseases such as multiple sclerosis.
    Overall, this information indicates that aberrant glutamate signaling may
    contribute to the development of some white matter pathologies.
    Publication Types: Review Review, Tutorial PMID: 10635022

    2. J Neurosci Res. 1996 Nov 15; 46(4): 427-37.
    Pathophysiology of oligodendroglial excitotoxicity.
    Yoshioka A, Bacskai BJ, Pleasure DE.
    Division of Neurology, Children's Hospital of Philadelphia, PA 19104, USA.
    DAVID E PLEASURE pleasure@email.chop.edu; 215-590-2090

    Oligodendrocyte-like cells (OLD) derived from the rat oligodendroglial
    precursor line, CG-4, express Ca(2+)-permeable
    non-methyl-D-aspartate glutamate receptor channels (GluR).
    Exposure to kainate, an L-glutamate analogue,
    markedly elevates OLC Ca2+ influx and cytosolic [Ca2+],
    and results in damage to
    both OLC plasma membrane and OLC nuclear DNA.
    Two observations indicate that kainate-induced OLC internucleosomal
    DNA nicking is not simply a delayed consequence of cell necrosis:
    1) there is no temporal lag between onset of plasma membrane injury and
    of DNA nicking; and
    2) aurintricarboxylic acid, an endonuclease inhibitor, blocks
    kainate-induced damage to the plasma membrane.
    N-acetyl-L-cysteine also inhibits OLC kainate injury, suggesting that
    reactive oxygen species participate in OLC excitotoxicity.
    Kainate-induced OLC Ca2+ influx and excitotoxicity are blocked by
    alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA),
    indicating that these kainate effects are mediated by AMPA-GluR.
    AMPA and L-glutamate
    fail to elicit OLC damage unless cyclothiazide,
    an AMPA-GluR desensitization blocker, is present.
    OLC express both the "flip" and "flop" forms of GluR2,
    GluR3, and GluR4 mRNAs, but neither flip nor flop GluR1 mRNA.
    These data, together with the restriction of the desensitization-blocking
    activity of cyclothiazide to GluR containing flip-encoded GluR subunits,
    and the sharply diminished Ca2+ permeability of GluR
    ontaining edited GluR2,
    suggest OLC excitotoxicity is mediated by AMPA-GluR
    that contain flip GluR3 and/or flip GluR4 protein subunits,
    but neither flip nor flop GluR2 protein subunits.
    Rapid desensitization of these GluR is likely to be important in protecting
    cells of the oligodendroglial lineage from excitotoxicity. PMID: 8950702

    J Biol Chem. 1997 Jan 3; 272(1): 647-56.
    N-methyl-D-aspartate receptors expressed in a nonneuronal cell line
    mediate subunit-specific increases in free intracellular calcium.
    Grant ER, Bacskai BJ, Pleasure DE, Pritchett DB, Gallagher MJ,
    Kendrick SJ, Kricka LJ, Lynch DR.
    for free full text http://www.jbc.org/cgi/content/full/272/1/647
    Elfrida R. Grant , Brian J. Bacskai §, David E. Pleasure §¶, Dolan B.
    Pritchett ¶, Michael J. Gallagher , Shelley J. Kendrick , Larry J. Kricka
    and David R. Lynch §¶** 73 references

    From the Departments of Pharmacology, § Neurology, ¶ Pediatrics,
    Pathology and Laboratory Medicine, University of Pennsylvania School
    of Medicine, Children's Seashore House,
    Philadelphia, Pennsylvania 19104
    DAVID E PLEASURE pleasure@email.chop.edu 215-590-2090

    N-methyl-D-aspartate (NMDA) receptors can mediate cell death
    in neurons and in non-neuronal cells that express recombinant NMDA
    receptors.
    In neurons, increases in intracellular calcium correlate with NMDA
    receptor-mediated death, supporting a key role for loss of cellular
    calcium homeostasis in excitotoxic cell death.
    In the present study, free intracellular calcium concentrations were
    examined in response to activation of recombinant NMDA receptors
    expressed in human embryonic kidney 293 cells.
    Intracellular calcium was measured in transfected cell populations by
    cotransfection with the calcium-sensitive, bioluminescent protein aequorin
    and by single cell imaging with the fluorescent calcium indicator fluo-3.
    Agonist application to NR1/2A or NR1/2B-transfected cells elicited
    robust rises in intracellular calcium.
    NR1/2A responses were inhibited by the noncompetitive antagonists
    MK-801 and dextromethorphan and were dependent on extracellular
    calcium but not on intracellular calcium stores.
    In contrast, no detectable intracellular calcium responses were observed
    in NR1/2C-transfected cells.
    These findings indicate that NMDA receptors in the absence of other
    neuron-specific factors can mediate increases in intracellular calcium with
    subunit specificity and extracellular calcium dependence.
    PMID: 8995308

    http://jpet.aspetjournals.org/cgi/co...full/300/3/717 free full text
    Pharmacology and Experimental Therapeutics.
    March 2002; 300 (3): 717-723.
    Excitotoxicity: Perspectives Based on N-Methyl-D-Aspartate
    Receptor Subtypes
    David R. Lynch and Rodney P. Guttmann
    Departments of Neurology (D.R.L.), Pediatrics (D.R.L.),
    and Pharmacology (R.P.G.), University of Pennsylvania and
    The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
    lynch@pharm.med.upenn.edu; 215-590-2242
    rodneyg@email.uky.edu; (859) 257-1412 x275

    Since excitotoxicity has been implicated in a variety of neuropathological
    conditions, understanding the pathways involved in this type of cell death
    is of critical importance to the future clinical treatment of many diseases.
    The N-methyl-D-aspartate (NMDA) receptor has become a primary
    focus of excitotoxic research because early studies demonstrated that
    antagonism of this receptor subtype was neuroprotective.
    However, initial pharmacological agents were not clinically useful due to
    the adverse effects of complete NMDA receptor blockade.
    Understanding the biochemical properties of the multitude of NMDA
    receptor subtypes offers the possibility of developing more effective and
    clinically useful drugs. With the discovery of the basis of heterogeneity
    of NMDA receptors through molecular biological approaches,
    many new potential therapeutic targets have been uncovered,
    and several model systems have been developed for the study of
    NMDA receptor-mediated cell death.
    This review discusses these models and the current understanding
    of the relationship between NMDA receptor subtypes and excitotoxicity.

    3. Mol Cell Biochem. 2003 Jan; 243(1-2): 139-45.
    Prolonged glutamate excitotoxicity: effects on mitochondrial antioxidants
    and antioxidant enzymes. [ strong toxicity of MSG in rat brains ]
    Singh P, Mann KA, Mangat HK, Kaur G.
    Neurochemistry and Neuroendocrinology Laboratory, Department of
    Biotechnology, Guru Nanak Dev University, Amritsar, India.

    Glutamate, a major excitatory amino acid neurotransmitter is also an
    endogenous excitotoxin.
    The present study examined the prolonged and delayed effects of
    glutamate excitotoxicity on mitochondrial lipid peroxidation and
    antioxidant parameters in different brain regions, namely,
    cerebral hemisphere, cerebellum, brain stem and diencephalon.
    Wistar rats (male) were exposed to monosodium glutamate (MSG)
    (4 mg x g body wt(-1), i.p.) for 6 consecutive days and sacrificed
    on 30th and 45th day after last MSG dose.
    MSG treatment markedly decreased the mitochondrial manganese
    superoxide-dismutase (Mn-SOD), catalase
    and reduced glutathione (GSH) content,
    and increased the lipid peroxidation (LPx), uric acid and
    glutathione peroxidase (GPx) activity.
    These results indicate that oxidative stress produced by glutamate in
    vulnerable brain regions may persist for longer periods and mitochondrial
    function impairment is an important mechanism of excitatory amino acid
    mediated neurotoxicity in chronic neurodegeneration. PMID: 12619899

    4. Neurobiol Dis. 2003 Dec; 14(3): 336-48.
    AMPA receptors are the major mediators of excitotoxic death in mature
    oligodendrocytes.
    Leuchtmann EA, Ratner AE, Vijitruth R, Qu Y, McDonald JW.
    Center for the Study of Nervous System Injury, Washington University
    School of Medicine, Box 8518, St. Louis, MO 63108, USA.
    John Wood McDonald JMcDonald@WUSTL.EDU;
    +1 314 454-7825 fax: +1 314 454-5300

    Myelination of axons is important for central nervous system function,
    but oligodendrocytes, which constitute CNS myelin, are vulnerable
    to excitotoxic injury and death.
    Although mature oligodendrocytes express functional
    alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA)
    and kainate-type glutamate receptors, the relative roles of these
    subtypes in excitotoxicity are not well understood.
    Using recently developed selective antagonists for subtypes of
    ionotropic non-NMDA receptors, we addressed this issue.
    By examining the pharmacological, biochemical, and morphologic
    features of kainite-induced excitotoxic death, we also determined
    whether it occurs by apoptosis, necrosis, or both.
    We conclude that when mature oligodendrocytes die after exposure
    to kainate:
    (1) AMPA receptors are the most important mediators,
    (2) kainate receptors play a smaller role, and
    (3) death occurs predominantly by necrosis, not apoptosis.
    PMID: 14678751

    5. Annals of Neurology. 2003 May; 53 5); 588 - 595.
    Interleukin-1 promotes oligodendrocyte death through glutamate
    excitotoxicity.
    Jennifer L. Takahashi, MD 1, Fabrizio Giuliani, MD 1,
    Christopher Power, MD 1, Yoshinori Imai, MD 2,
    V. Wee Yong, PhD 1 3 *
    1 Department of Clinical Neurosciences, University of Calgary,
    Calgary, Alberta, Canada
    2 National Institute of Neuroscience, Kodaira, Tokyo, Japan
    3 Department of Oncology, University of Calgary, Calgary,
    Alberta, Canada email: V. Wee Yong vyong@ucalgary.ca;
    *Correspondence to V. Wee Yong, Neuroscience Research Group,
    University of Calgary, 3330 Hospital Drive,
    Calgary, Alberta T2N 4N1, Canada
    Funded by: Multiple Sclerosis Society of Canada
    Canadian Institutes of Health Research; Grant Number: MT H246

    Glutamate excitotoxicity is implicated in the progressive loss of
    oligodendrocytes in multiple sclerosis, but how glutamate metabolism
    is dysregulated in the disease remains unclear.
    Because there is microglia activation in all stages of multiple sclerosis,
    we determined whether a microglia product, interleukin-1,
    could provide the mechanism for glutamate excitotoxicity.
    We found that whereas interleukin-1 did not kill oligodendrocytes
    in pure culture, it produced apoptosis of oligodendrocytes in coculture
    with astrocytes and microglia.
    This requirement for a mixed glia environment suggests that interleukin-1
    impairs the well-described glutamate-buffering capacity of astrocytes.
    In support, antagonists at AMPA/kainate glutamate receptors,
    NBQX and CNQX,
    blocked the interleukin-1 toxicity to oligodendrocytes.
    Another microglia/macrophage cytokine, tumor necrosis factor-,
    also evoked apoptosis of oligodendrocytes in a mixed glia environment
    in an NBQX-blockable manner.
    These results provide a mechanistic link between the persistent and
    insidious microglia activation that is evident in all stages of multiple
    sclerosis, with the recent appreciation that glutamate excitotoxicity leads
    to the destruction of oligodendrocytes in the disease.

    6. Neurology. 2003 Oct 28; 61(8): 1113-20.
    Glutamate uptake by oligodendrocytes: Implications for excitotoxicity in
    multiple sclerosis.
    Pitt DF, Nagelmeier IE, Wilson HC, Raine CS. dfpitt@yahoo.com;
    Department of Neurology, Albert Einstein College of Medicine,
    Bronx, NY, USA. Cedric S. Raine jni@aecom.yu.edu;

    BACKGROUND:
    Excitotoxic damage is a common pathologic event in a number of
    neurologic diseases occurring after accumulation of excess extracellular
    glutamate in the CNS and subsequent overstimulation
    of glutamate receptors.
    In gray matter, astrocytes take up synaptically released glutamate
    and are thus key cells in maintaining glutamate homeostasis.
    In white matter, oligodendrocytes have been shown to express
    glutamate transporters, but their role in extracellular glutamate
    removal is unclear.
    OBJECTIVE:
    To investigate whether cultured human fetal oligodendrocytes
    functionally express the main glutamate transporters
    EAAT-1 and EAAT-2.
    METHODS:
    Cultures of fetal human oligodendrocytes were examined by
    immunocytochemistry and [3H]glutamate uptake, and the findings were
    correlated with glutamate transporter expression in normal and multiple
    sclerosis (MS) CNS tissue.
    RESULTS:
    Both EAAT-1 and EAAT-2 were expressed
    by human oligodendrocytes in vitro.
    Incubation of oligodendrocytes with the proinflammatory cytokine
    tumor necrosis factor-alpha (TNFalpha) reduced EAAT-1 expression
    and inhibited glutamate uptake by &gt;75%.
    Furthermore, in normal human white matter, oligodendrocytes
    were found to be the predominant cells to express
    EAAT-1 and EAAT-2, both at the mRNA and at the protein level.
    A small number of astrocytes in white matter expressed these receptors,
    more so EAAT-1 than EAAT-2.
    In MS white matter, oligodendrocytes lost expression of
    EAAT-1 and EAAT-2 receptors in the lesion vicinity.
    CONCLUSIONS:
    Oligodendrocytes appear to be predominant cells for glutamate
    clearance in human white matter.
    Glutamate receptor expression and glutamate removal were defective
    in MS white matter, possibly mediated by TNFalpha, changes that
    might underlie high extracellular glutamate and an increased risk for
    glutamate excitotoxicity. PMID: 1458167

    7. Neuroscience. 2004; 123(2): 441-9.
    Excitotoxic insults to the optic nerve alter visual evoked potentials.
    Soto A, Perez-Samartin AL, Etxebarria E, Matute C.
    Departamento de Neurociencias, Universidad del Pais Vasco,
    E-48940 Leioa, Vizcaya, Spain.
    Carlos Matute Almau +34-946-012-865 onpmaalc@lg.ehu.es;

    Excitotoxic oligodendroglial death is one of the mechanisms which
    has been proposed to underlie demyelinating diseases of the CNS.
    We describe here functional consequences of excitotoxic lesions to the
    rabbit optic nerve by studying the visual evoked potentials (VEPs)
    measured in the visual cortex.
    Nerves were slowly infused with the excitotoxin kainate a
    subcutaneously implanted osmotic pump which delivered the
    toxin through a cannula onto the optic nerve.
    Records of VEPs were obtained before pump implantation and at
    1, 3 and 7 days post-implantation, and weekly evaluated thereafter
    for up to 4 months.
    We observed that the VEPs generated by light stimuli progressively
    changed in both amplitude and profile after the lesion as well as in
    comparison to those generated in control animals infused with vehicle.
    Histological examination of the damage caused by the excitotoxic insult
    showed that large areas of the optic nerve were demyelinated and their
    axons distorted.
    These observations were confirmed and extended by
    immunohistochemical analyses using markers to neurofilaments,
    myelin basic protein and the oligodendrocyte marker APC.
    The results of the present paper indicate that the consequences of
    excitotoxicity in the optic nerve share functional and morphological
    alterations which are found in demyelinating disorders.
    In addition, this experimental paradigm may be useful to evaluate the
    functional recovery of demyelinated optic nerves following various
    repair strategies. PMID: 14698751

    http://www.ehu.es/ingles/paginas/prin_i.htm
    Neurobiol Dis. 2002 Mar;9(2):234-43.
    Ca(2+) influx through AMPA or kainate receptors alone is sufficient to
    initiate excitotoxicity in cultured oligodendrocytes.
    Alberdi E, Sanchez-Gomez MV, Marino A, Matute C.
    Departamento de Neurociencias, Universidad del Pais Vasco,
    Leioa, Vizcaya, Spain.

    8. Blaylock RL.
    Interactions of cytokines, excitotoxins and reactive nitrogen and oxygen
    species in autism spectrum disorders.
    Journal of American Nutraceutical Association 6: 21-35, 2003.
    [ Not in PubMed ]

    9. Blaylock RL.
    Chronic microglial activation and excitotoxicity secondary to excessive
    immune stimulation: possible factors in Gulf War Syndrome and autism.
    Journal American Physicians and Surgeons, Summer, 2004.
    [ Not in PubMed ]
    ************************************************** *****

    http://groups.yahoo.com/group/aspartameNM/message/97
    Lancet website aspartame letter 1999.07.29:
    Excitotoxins 1999 Part 1/3 Blaylock: Murray 2000.01.14 rmforall
    The Medical Sentinel Journal 1999 Fall; (95 references)
    http://www.dorway.com/blayenn.html

    Russell L. Blaylock, MD 601-982-1175 Madison, Mississippi
    "Excitotoxins: The Taste that Kills", 1977, 298 p., 493 references.
    "Health and Nutrition Secrets that can save your life", 2002, 459 p.,
    558 + 30 references, $ 30 http://www.russellblaylockmd.com/

    http://www.truthinlabeling.org/ Truth in Labeling Campaign [MSG]
    Adrienne Samuels, PhD The toxicity/safety of processed
    free glutamic acid (MSG): a study in suppression of information.
    Accountability in Research 1999; 6: 259-310. 52-page review
    P.O. Box 2532 Darien, Illinois 60561
    858-481-9333 adandjack@aol.com
    ************************************************** *****
    Send blank post to: <br />aspartameNM-subscribe@onelist.com to join<br />free,open, list with searchable archives for toxicity issues.<br />Richard \"Rich\" T. Murray Room For All 1943 Otowi Road Santa Fe, NM 87505<br />rmforall@comcast.net 505-501-2298

  4. #4
    Join Date
    Jun 1999
    Location
    Santa Fe, NM 87505, USA
    Posts
    63

    Post

    February 12, 2006

    Any unsuspected source of methanol, which the body always quickly
    and largely turns into formaldehyde and then formic acid, must be
    monitored, especially for high responsibility occupations, often with
    night shifts, such as pilots and nuclear reactor operators.

    In particular, the next review gives many recent mainstream
    peer-reviewed studies that show formaldehyde,
    always inevitably derived in the body from any methanol source,
    including aspartame, causes endothelial injury,
    ie, diabetic neuropathy -- among the most serious and complex
    complications of diabetes.

    http://groups.yahoo.com/group/aspartameNM/message/1263
    many studies on endothelial injury (diabetic neuropathy) by adducts of
    formaldehyde derived from methylamine from many of the same sources
    as also supply methanol (formaldehyde), including aspartame:
    PH Yu et al: DJ Conklin et al: Murray 2005.12.04

    http://groups.yahoo.com/group/aspartameNM/message/1237
    ubiquitous potent uncontrolled co-factors in nutrition research are
    formaldehyde from wood and tobacco smoke and many sources,
    including from methanol in dark wines and liquors, in pectins
    in fruits and vegetables, and in aspartame: Murray 2006.01.13

    http://groups.yahoo.com/group/aspartameNM/message/925
    aspartame puts formaldehyde adducts into tissues, Part 1/2
    full text Trocho & Alemany 1998.06.26
    Universitat Autònoma de Barcelona : Murray 2002.12.22

    http://groups.yahoo.com/group/aspartameNM/message/1250
    aspartame causes cancer in rats at levels approved for humans,
    Morando Soffritti et al, Ramazzini Foundation, Italy &
    National Toxicology Program
    of National Institute of Environmental Health Sciences
    2005.11.17 Env. Health Pers. 35 pages: Murray

    http://groups.yahoo.com/group/aspartameNM/message/1271
    combining aspartame and quinoline yellow, or MSG and brilliant blue,
    harms nerve cells, eminent C. Vyvyan Howard et al, 2005
    education.guardian.co.uk, Felicity Lawrence: Murray 2005.12.21

    http://groups.yahoo.com/group/aspartameNM/message/1274
    harm to fetus from formaldehyde from methanol from aspartame,
    Woodrow C. Monte: Murray 2006.01.02

    http://groups.yahoo.com/group/aspartameNM/message/1279
    all three aspartame metabolites harm human erythrocyte [red blood cell]
    membrane enzyme activity, KH Schulpis et al, two studies in 2005,
    Athens, Greece, 2005.12.14: 2004 research review, RL Blaylock:
    Murray 2006.01.14

    As a medical layman, I suggest that evidence mandates immediate
    exploration of the role of these ubiquitious, potent formaldehyde
    sources as co-factors in epidemiology, research, diagnosis,
    and treatment in a wide variety of disorders.

    Folic acid, from fruits and vegetables, plays a role by powerfully
    protecting against methanol (formaldehyde) toxicity.

    Many common drugs, such as aspirin, interfere with folic acid,
    as do some mutations in relevant enzymes.

    The majority of aspartame reactors are female.

    In mutual service, Rich Murray
    ************************************************** *****

    "Of course, everyone chooses, as a natural priority,
    to actively find, quickly share, and act upon the facts
    about healthy and safe food, drink, and environment."

    Rich Murray, MA Room For All rmforall@comcast.net
    505-501-2298 1943 Otowi Road Santa Fe, New Mexico 87505

    http://groups.yahoo.com/group/aspartameNM/messages
    group with 151 members, 1,302 posts in a public, searchable archive
    http://RoomForAll.blogspot.com http://AspartameNM.blogspot.com

    Dark wines and liquors, as well as aspartame, provide
    similar levels of methanol, above 100 mg daily, for
    long-term heavy users, 2 L daily, about 6 cans.

    Methanol is inevitably largely turned into formaldehyde,
    and thence largely into formic acid.
    It is the major cause of the dreaded symptoms of "next
    morning" hangover.

    Fully 11% of aspartame is methanol -- 1,120 mg aspartame
    in 2 L diet soda, almost six 12-oz cans, gives 123 mg
    methanol (wood alcohol). If 30% of the methanol is turned
    into formaldehyde, the amount of formaldehyde, 37 mg,
    is 18.5 times the USA EPA limit for daily formaldehyde in
    drinking water, 2.0 mg in 2 L average daily drinking water.

    http://groups.yahoo.com/group/aspartameNM/message/1108
    faults in 1999 July EPA 468-page formaldehyde profile:
    Elzbieta Skrzydlewska PhD, Assc. Prof., Medical U. of
    Bialystok, Poland, abstracts -- ethanol, methanol,
    formaldehyde, formic acid, acetaldehyde, lipid peroxidation,
    green tea, aging: Murray 2004.08.08 2005.07.11

    http://groups.yahoo.com/group/aspartameNM/message/835
    ATSDR: EPA limit 1 ppm formaldehyde in drinking water July
    1999: Murray 2002.05.30 rmforall

    Aspartame is made of phenylalanine (50% by weight) and
    aspartic acid (39%), both ordinary amino acids, bound
    loosely together by methanol (wood alcohol, 11%).
    The readily released methanol from aspartame is within hours
    turned by the liver into formaldehyde and then formic acid,
    both potent, cumulative toxins.

    http://groups.yahoo.com/group/aspartameNM/message/1141
    Nurses Health Study can quickly reveal the extent of aspartame
    (methanol, formaldehyde, formic acid) toxicity: Murray 2004.11.21
    [ Any scientist can get access to this data for free by submitting a proper
    research proposal.
    No one has admitted mining the extensive data on diet soda use
    and many symptoms for decades for about 100,000 nurses. ]

    http://groups.yahoo.com/group/aspartameNM/message/1213
    aspartame (methanol, phenylalanine, aspartic acid) effects, detailed
    expert studies in 2005 Aug and 1998 July, Tsakiris S, Schulpis KH,
    Karikas GA, Kokotos G, Reclos RJ, et al,
    Aghia Sophia Children's Hospital, Athens, Greece: Murray 2005.09.09

    http://groups.yahoo.com/group/aspartameNM/message/939
    aspartame (aspartic acid, phenylalanine) binding to DNA:
    Karikas July 1998: Murray 2003.01.05 rmforall
    Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
    Measurement of molecular interaction of aspartame and
    its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
    Dept. of Chemistry, University of Athens, Greece
    http://www.chem.uoa.gr gkokotos@atlas.uoa.gr
    K.H. Schulpis inchildh@otenet.gr G.J. Reclos reklos@otenet.gr

    http://groups.yahoo.com/group/aspartameNM/message/1088
    Murray, full plain text & critique: chronic aspartame in rats affects
    memory, brain cholinergic receptors, and brain chemistry, Christian B,
    McConnaughey M et al, 2004 May: 2004.06.05

    http://groups.yahoo.com/group/aspartameNM/message/1067
    eyelid contact dermatitis by formaldehyde from aspartame,
    AM Hill & DV Belsito, Nov 2003: Murray 2004.03.30

    Thrasher (2001): "The major difference is that the Japanese
    demonstrated the incorporation of FA and its metabolites into the
    placenta and fetus.
    The quantity of radioactivity remaining in maternal and fetal tissues
    at 48 hours was 26.9% of the administered dose." [ Ref. 14-16 ]

    Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
    Embryo toxicity and teratogenicity of formaldehyde. [100 references]
    Thrasher JD, Kilburn KH. toxicology@drthrasher.org
    Sam-1 Trust, Alto, New Mexico, USA.
    http://www.drthrasher.org/formaldehy..._toxicity.html full text

    http://groups.yahoo.com/group/aspartameNM/message/1052
    DMDC: Dimethyl dicarbonate 200mg/L in drinks adds
    methanol 98 mg/L [ becomes formaldehyde in body ]: EU Scientific
    Committee on Foods 2001.07.12: Murray 2004.01.22

    http://groups.yahoo.com/group/aspartameNM/message/1131
    genotoxicity of aspartame in human lymphocytes 2004.07.29
    full plain text, Rencuzogullari E et al, Cukurova University,
    Adana, Turkey 2004 Aug: Murray 2004.11.06

    http://groups.yahoo.com/group/aspartameNM/message/1237
    ubiquitous potent uncontrolled co-factors in nutrition research are
    formaldehyde from wood and tobacco smoke and many sources,
    including from methanol in dark wines and liquors, in pectins
    in fruits and vegetables, and in aspartame: Murray 2006.01.13

    http://groups.yahoo.com/group/aspartameNM/message/1264
    fructose in rats increases uric acid, obesity, insulin resistance,
    endothelial damage -- RJ Johnson et al, U. Florida: Murray 2005.12.07
    ************************************************** *****
    Send blank post to: <br />aspartameNM-subscribe@onelist.com to join<br />free,open, list with searchable archives for toxicity issues.<br />Richard \"Rich\" T. Murray Room For All 1943 Otowi Road Santa Fe, NM 87505<br />rmforall@comcast.net 505-501-2298

  5. #5
    Join Date
    Jun 1999
    Location
    Santa Fe, NM 87505, USA
    Posts
    63

    Post

    http://groups.yahoo.com/group/aspartameNM/message/1106
    hangover research relevant to toxicity of 11% methanol in
    aspartame (formaldehyde, formic acid): Calder I (full text):
    Jones AW: Murray 2004.08.05 2005.09.28

    Since no adaquate data has ever been published on the exact
    disposition of toxic metabolites in specific tissues in
    humans of the 11% methanol component of aspartame, the many
    studies on morning-after hangover from the methanol impurity
    in alcohol drinks are the main available resource to date.

    Jones AW (1987) found next-morning hangover from red wine
    with 100 to 150 mg methanol (9.5% w/v ethanol, 100 mg/L
    methanol, 0.01%, one part in ten thousand).

    http://groups.yahoo.com/group/aspartameNM/message/1182
    Joining together: short review: research on aspartame
    methanol, formaldehyde, formic acid) toxicity: Murray
    2005.07.08 rmforall

    http://groups.yahoo.com/group/aspartameNM/message/1071
    research on aspartame (methanol, formaldehyde, formic acid)
    toxicity: Murray2004.04.29 rmforall

    http://groups.yahoo.com/group/aspartameNM/message/1250
    aspartame causes cancer in rats at levels approved for humans,
    Morando Soffritti et al, Ramazzini Foundation, Italy &
    National Toxicology Program
    of National Institute of Environmental Health Sciences
    2005.11.17 Env. Health Pers. 35 pages: Murray

    http://groups.yahoo.com/group/aspartameNM/message/1226
    USA National Institutes of Health National Toxicology
    Program aids eminent Ramazzini Foundation, Bologna, Italy,
    in more results on cancers in rats from lifetime low levels
    of aspartame (methanol, formaldehyde), Felicity Lawrence,
    www.guardian.co.uk: Murray 2005.09.30

    http://groups.yahoo.com/group/aspartameNM/message/1186
    aspartame induces lymphomas and leukaemias in rats, full plain text,
    M Soffritti, F Belpoggi, DD Esposti, L Lambertini: Ramazzini
    Foundation study 2005.07.14: main results agree with their previous
    methanol and formaldehyde studies: Murray 2005.09.03

    http://groups.yahoo.com/group/aspartameNM/message/1189
    Michael F Jacobson of CSPI now and in 1985 re aspartame
    toxicity, letter to FDA Commissioner Lester Crawford;
    California OEHHA aspartame critique 2004.03.12; Center for
    Consumer Freedom denounces CSPI: Murray 2005.07.27

    http://groups.yahoo.com/group/aspartameNM/message/1143
    methanol (formaldehyde, formic acid) disposition: Bouchard M
    et al, full plain text, 2001: substantial sources are
    degradation of fruit pectins, liquors, aspartame, smoke:
    Murray 2005.04.02
    ************************************************** *****

    http://groups.yahoo.com/group/aspartameNM/message/1070
    critique of aspartame review, French Food Safety Agency AFSSA
    2002.05.07 (18 pages, in English), Martin Hirsch:
    Murray 2004.04.13

    http://groups.yahoo.com/group/aspartameNM/message/957
    safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF,
    EU Scientific Committee on Food, a whitewash; Murray 2003.01.12

    http://groups.yahoo.com/group/aspartameNM/message/1045
    http://www.holisticmed.com/aspartame...2-response.htm
    Mark Gold exhaustively critiques European Commission Scientific
    Committee on Food re aspartame ( 2002.12.04 ): 59 pages, 230 references

    http://www.HolisticMed.com/aspartame mgold@holisticmed.com
    Aspartame Toxicity Information Center Mark D. Gold
    12 East Side Drive #2-18 Concord, NH 03301 603-225-2100
    http://www.holisticmed.com/aspartame.../methanol.html
    "Scientific Abuse in Aspartame Research"

    Gold points out that industry methanol assays were too insensitive to
    properly measure blood methanol levels.

    http://www.eatright.org/
    J Am Diet Assoc. 2004 Feb; 104(2): 255-75.
    Position of the American Dietetic Association: use of nutritive and
    nonnutritive sweeteners. American Dietetic Association.

    http://groups.yahoo.com/group/aspartameNM/message/1068
    critique of aspartame review by American Dietetic Association
    Feb 2004, Valerie B. Duffy & Madeleine J. Sigman-Grant:
    Murray 2004.05.14

    "Survey of aspartame studies: correlation of outcome and funding
    sources," 1998, unpublished: http://www.dorway.com/peerrev.html
    Walton found 166 separate published studies in the peer reviewed
    medical literature, which had relevance for questions of human safety.
    The 74 studies funded by industry all (100%) attested to aspartame's
    safety, whereas of the 92 non-industry funded studies, 84 (91%)
    identified a problem. Six of the seven non-industry funded studies
    that were favorable to aspartame safety were from the FDA, which
    has a public record that shows a strong pro-industry bias.
    Ralph G. Walton, MD, Prof. of Clinical Psychology, Northeastern Ohio
    Universities, College of Medicine, Dept. of Psychiatry, Youngstown,
    OH 44501, Chairman, The Center for Behavioral Medicine,
    Northside Medical Center, 500 Gypsy Lane, P.O. Box 240
    Youngstown, OH 44501 330-740-3621 rwalton193@aol.com
    http://www.neoucom.edu/DEPTS/Psychiatry/walton.htm

    http://groups.yahoo.com/group/aspartameNM/message/857
    www.dorway.com: original documents and long reviews of flaws in
    aspartame toxicity research: Murray 2002.07.31

    http://groups.yahoo.com/group/aspartameNM/message/858
    Samuels: Strong: Roberts: Gold: flaws in double-blind studies re
    aspartame and MSG toxicity: Murray 2002.08.01

    http://www.truthinlabeling.org/ Truth in Labeling Campaign [MSG]
    Adrienne Samuels, PhD The toxicity/safety of processed
    free glutamic acid (MSG): a study in suppression of information.
    Accountability in Research 1999; 6: 259-310. 52-page review
    P.O. Box 2532 Darien, Illinois 60561
    858-481-9333 adandjack@aol.com

    http://www.dorway.com/upipart1.txt
    http://groups.yahoo.com/group/aspartameNM/message/262
    aspartame expose 96K Oct 1987 Part 1/3:
    Gregory Gordon, UPI reporter: Murray 2000.07.10

    http://www.dorway.com/enclosur.html
    http://groups.yahoo.com/group/aspartameNM/message/53
    aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06

    http://groups.yahoo.com/group/aspartameNM/message/928
    revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23

    http://groups.yahoo.com/group/aspartameNM/message/927
    Donald Rumsfeld, 1977 head of Searle Corp., got aspartame FDA
    approval: Turner: Murray 2002.12.23 rmforall
    ************************************************** *****

    http://groups.yahoo.com/group/aspartameNM/message/1280
    Aspartame: Bill would ban food containing sweetener [in New Mexico]:
    Diana Heil, The New Mexican: Murray 2006.01.14

    http://groups.yahoo.com/group/aspartameNM/message/1276
    NM EIB votes 7-0 to delay 5-day aspartame hearing until Jan 2007,
    Diana Heil, The New Mexican: comment by Stephen Fox:
    Murray 2006.01.04

    http://groups.yahoo.com/group/aspartameNM/message/1273
    citizens against aspartame (methanol, formaldehyde), made by
    Ajinomoto, at Jan 3 hearing of NM EIB in Santa Fe: Lehrman:
    Murray 2006.01.01

    http://groups.yahoo.com/group/aspartameNM/message/1272
    New Mexico Gov. Bill Richardson endorses Nutrition Council,
    mercury ban, aspartame hearings: Lehrman, Fox, Stoller:
    Murray 2005.12.27

    http://groups.yahoo.com/group/aspartameNM/message/1248
    Aspartame and Thimerosal getting banned in New Mexico
    by the Pharmacy Board? with notes by Rich Murray: 2005.11.15

    http://groups.yahoo.com/group/aspartameNM/message/1247
    Aspartame quagmire quickly deepens, methanol (formaldehyde, formic
    acid) toxicity facts spreading at the grassroots level,
    3 items in The New Mexican,
    and long article in Vanity Fair by Rich Cohen: Murray 2005.11.15

    http://groups.yahoo.com/group/aspartameNM/message/1245
    Fox, Stoller, Murray to give Citizen's Petition
    to ban aspartame (methanol, formaldehyde) and mercury
    in children's medicines and vitamins: New Mexico Board of Pharmacy,
    2:45-3:45 pm Monday Nov. 14, Albuquerque: Murray 2005.11.13

    http://groups.yahoo.com/group/aspartameNM/message/1228
    NM EIB votes 4-2 for 5-day aspartame toxicity hearing July,
    2006, requesting a Hearing Officer and a medical expert from
    Environmental Dept. and legal advice from NM Attorney
    General: Murray 2005.10.04
    ************************************************** *****
    Send blank post to: <br />aspartameNM-subscribe@onelist.com to join<br />free,open, list with searchable archives for toxicity issues.<br />Richard \"Rich\" T. Murray Room For All 1943 Otowi Road Santa Fe, NM 87505<br />rmforall@comcast.net 505-501-2298

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