Research: glutamate - chronic pain FM and TMJ

Discussion in 'Fibromyalgia Main Forum' started by tansy, Sep 26, 2005.

  1. tansy

    tansy New Member

    Neural mechanisms of temporomandibular joint and masticatory muscle pain: A
    possible role for peripheral glutamate receptor mechanisms.

    Pain Res Manag. 2005 Autumn;10(3):145-52.

    Lam DK, Sessle BJ, Cairns BE, Hu JW.

    University of Toronto, Toronto, Canada.

    PMID: 16175250

    The purpose of the present review is to correlate recent knowledge of the
    role of peripheral ionotropic glutamate receptors in the temporomandibular
    joint and muscle pain from animal and human experimental pain models with
    findings in patients.

    Chronic pain is common, and many people suffer from chronic pain conditions
    involving deep craniofacial tissues such as temporomandibular disorders or

    Animal and human studies have indicated that the activation of peripheral
    ionotropic glutamate receptors in deep craniofacial tissues may contribute
    to muscle and temporomandibular joint pain and that sex differences in the
    activation of glutamate receptors may be involved in the female
    predominance in temporomandibular disorders and fibromyalgia.

    A peripheral mechanism involving autocrine and/or paracrine regulation of
    nociceptive neuronal excitability via injury or inflammation-induced
    release of glutamate into peripheral tissues that may contribute to the
    development of craniofacial pain is proposed.
    [This Message was Edited on 09/26/2005]
  2. tansy

    tansy New Member

    For many years I had a chronic head pain that only varied in it's intensity. It was after reading the research from Japan below that I started taking sublingual methyl B12, then I added in 2 antioxidants that cross the blood brain barrier.

    At first the head pain got worse and then they it went away, now it's only when I am herxing that it returns in a major way. I need to continue taking methyl B12 (1,000mcg) to keep it at bay, and take higher doses when herxing.

    Have not researched Mg's role in this, but I can understand why it may help.

    love, Tansy

    Eur J Pharmacol. 1993 Sep 7;241(1):1-6. Related Articles, Links

    Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons.

    Akaike A, Tamura Y, Sato Y, Yokota T.

    Department of Neuropharmacology, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University, Japan.

    The effects of methylcobalamin, a vitamin B12 analog, on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free medium for 1 h.

    Glutamate cytotoxicity was prevented when the cultures were maintained in methylcobalamin-containing medium. Glutamate cytotoxicity was also prevented by chronic exposure to S-adenosylmethionine, which is formed in the metabolic pathway of methylcobalamin. Chronic exposure to methylcobalamin and S-adenosylmethionine also inhibited the cytotoxicity induced by N-methyl-D-aspartate or sodium nitroprusside that releases nitric oxide.

    In cultures maintained in a standard medium, glutamate cytotoxicity was not affected by adding methylcobalamin to the glutamate-containing medium. In contrast, acute exposure to MK-801, a NMDA receptor antagonist, prevented glutamate cytotoxicity. These results indicate that chronic exposure to methylcobalamin protects cortical neurons against NMDA receptor-mediated glutamate cytotoxicity.

    PMID: 7901032 [PubMed - indexed for MEDLINE]

    And from the library here

    Methylcobalamin: A Potential Breakthrough in Neurological Disease

    Japanese scientists have identified a form of vitamin B12 that protects against neurological disease and aging by a unique mechanism that differs from current therapies.

    Some of the disorders that may be preventable or treatable with this natural vitamin therapy, called methylcobalamin, include chronic fatigue syndrome, Parkinson's disease, peripheral neuropathies, Alzheimer's disease, muscular dystrophy and neurological aging. Americans have immediate access to this unique and new form of vitamin B12, and, unlike prescription drugs, it costs very little and is free of side effects.

    vitamin B12 is a general label for a group of essential biological compounds knows as cobalamins. The cobalamins are structurally related to hemoglobin in the blood, and a deficiency of vitamin B12 can cause anemia. The primary concern of conventional doctors is to maintain adequate cobalamin status to protect against anemia.

    The most common form of vitamin B12 is called cyanocobalamin. However, over the last ten years, a number of central and peripheral neurological diseases have been linked to a deficiency of a very specific cobalamin, the methylcobalamin form, that is required to protect against neurological diseases and aging. The liver converts a small amount of cyanocobalamin into methylcobalamin within the body, but larger amounts of methylcobalamin are necessary to correct neurological defects and protect against aging.

    Published studies show that high doses of methylcobalamin are needed to regenerate neurons as well as the myelin sheath that protects nerve axons and peripheral nerves.CFIDS and B-12In the Summer 1998 issue of Healthwatch, an important research article reported a fascinating new finding. Over 60% of CFIDS and FM patients cerebral spinal fluids contained subnormal levels of vitamin B12. On the other hand, vitamin B12 levels in the blood did not significantly deviate from normal ranges.

    According to Dr. Paul Cheney's treatment pyramid for CFIDS, vitamin B12 in its non-cyanocobalamin form (the type commercially available) is a potent detoxifier of the brain. Recent studies in Europe suggest that it needs to be given in large doses in the range of 10 - 20 mg per day, or even more. This supplementation of methylcobalamin might protect the cognitive function of patients with CFIDS by preventing the death of brain cells.

    One cause of brain cell death is glutamate toxicity. Brain cells use glutamate as a neurotransmitter, but unfortunately glutamate is a double-edged sword in that it can also kill brain cells. The release of glutamate from the synapses is a usual means by which neurons communicate with each other.

    Effective communication means controlled release of glutamate at the right time to the right cells, but when glutamate is released in excessive amounts, intercellular communication ceases. The flood of glutamate into the receiving neurons drives them into hyperactivity, and the excessive activity leads to cellular degradation.The good news is that it may now be possible to protect brain cells against glutamate toxicity by taking methylcobalamin supplementation. In a study in the European Journal of Pharmacology, it was shown that methylcobalamin protected against glutamate-, aspartate- and nitroprusside- induced neurotoxicity in rat cortical neurons.

    Researchers concluded that methylcobalamin protects against neurotoxicity by enhancing brain cell methylation. The CFIDS & Fibromyalgia Health Resource recommends methylation-enhancing therapies such as vitamin B6, vitamin B12, folic acid and trimethylglycine (TMG), taken together, to protect against heart disease, stroke and other aging-related diseases.

    The scientists who conducted the methylcobalamin studies emphasize that ongoing intake of methylcobalamin is necessary to protect against neurotoxicity. Thus for methylcobalamin to be effective in protecting against neurological disease, daily supplementation may be required.
    An appropriate dose to protect against neurological aging might be 1 to 5 mg a day taken under the tongue in lozenge form.


    A recent German study appearing in Neuropharmacology showed methylcobalamin reduced the amount of time subjects slept; sleep quality was better and subjects awoke feeling refreshed, with better alertness and concentration. Part of this effect was apparently due to melatonin suppression during the daytime because morning methylcobalamin supplementation reduces drowsiness by decreasing daytime melatonin levels.

    Multiple Sclerosis

    According to a recent study at Vanderbilt University, chlamydia pneumoniae might link multiple sclerosis (MS) to CFIDS. This makes the published effect of methylcobalamin treatment on MS of great importance to those who suffer from CFIDS.

    A study in the Journal of Internal Medicine investigated the daily administration of 60 mg of methylcobalamin to patients with chronic progressive multiple sclerosis (MS), a disease that has a poor prognosis and feature side spread demyelination in the central nervous system.Although motor disability did not improve, there were clinical improvements in visual and auditory MS related disabilities. The scientist stated that methylcobalamin might be an effective adjunct to immunosuppressive treatment for chronic, progressive MS. Those with less serious forms of MS may consider adding methylcobalamin to their daily treatment regimen.

    The effects of methylcobalamin were studied on an animal model of muscular dystrophy. This study, published in Neuroscience Letter looked at degeneration of axon motor terminals. In mice receiving methylcobalamin, nerve sprouts were more frequently observed and regeneration of motor nerve terminals occurred in sites that had been previously degenerating.

    Regenerating Nerves

    Few substances have been shown to regenerate nerves in humans with peripheral neuropathies. However, a study in the Journal of Neurological Science postulated that methylcobalamin could increase protein synthesis and help regenerate nerves. The scientists showed that very high doses of methylcobalamin produce nerve regeneration in laboratory rats.

    The scientists stated that ultra-high doses of methylcobalamin might be of clinical use for patients with peripheral neuropathies. The human equivalent dose the scientists used is about 40 mg of sublingually administered methylcobalamin on a daily basis.

    Those suffering from peripheral neuropathies often take alpha lipoic acid. Based on our new understanding of peripheral neuropathy, it may be prudent that anyone using alpha lipoic acid also take at least 5 mg a day of sublingually administered methylcobalamin to ensure that alpha lipoic acid will be bioavailable to the peripheral nerves.

    Cancer/Immune Function

    A study in the journal Oncology examined the effects of methylcobalamin on several different kinds of tumors in mice. The administration of methylcobalamin for seven days suppressed liver, lung and ascites tumor growth. Mice receiving methylcobalamin survived longer than control mice did. In mice irradiated before tumor cell inoculation, methylcobalamin did not improve survival.

    The effects of methylcobalamin on human immune function was investigated in the Journal of Clinical Immunology. The study showed that methylcobalamin demonstrated remarkable T cell-enhancing effects when the T cells were exposed to certain antigens.The scientists also showed that methylcobalamin improved the activity of T helper cells. The scientists concluded that methylcobalamin could modulate lymphocyte function by augmenting regulatory T cell activities.

    Americans need to know about this important natural therapy that could extend the healthy human life span. A search of the scientific literature reveals 334 published studies on methylcobalamin. However, it would not be an exaggeration to say that virtually no doctors know of it or are recommending it.

    Methylcobalamin should be considered for the treatment of any neurological disease. For example, based on its unique mechanisms of action, methylcobalamin could be effective in slowing the progression of "untreatable" diseases such as ALS (Lou Gerhig's disease).

    Since methylcobalamin is not a drug, there is little economic incentive to conduct expensive clinical studies on it, so it may be a long time before we know just how effective this unique form of vitamin B12 is in slowing the progression of common diseases like Parkinson's disease.The sublingual intake of methylcobalamin is an affordable and effective natural therapy, and has proven even safe when given in large doses.

    (euro-journ-pharm; 1993 Sep.7;7;241 (1):1-6) (Experientia; 1992 Aug;48[8]:716-720)(Neuropharmacology; 1996;15[5]:456-464)(journ-int-med; 1994 Feb. 33(2):82-86)(Neuroscience Letter; 1994 Mar 28; 170[1] 195-197)(journ-neuro-sci 1994 Apr. 122[2]:140-143)(journ-inherited-meta-dis 1993;16[4]:762-770) (Oncology; 1987;44[3]:169-173)(journ-clin-immuno 1982 Apr 2;[2]:101-109)[This Message was Edited on 09/26/2005]
  3. Jen102

    Jen102 New Member

    I have questions about the connections. my tmj and craniofacial pain (and other CFS and FMS symptoms) have been helped by high dosages of glutathione. I wonder how all these things fit together!!!! I understand that glutathione is a tripeptide composed of the amino acid precursors glutamate, cysteine, and glycine--glutamate being discussed in the article posted. I also have read Martin Pall's theories which seem similar to those noted in the japanese research. I wish the researchers would hurry up and get these things figured out. there are just too many ways these theories fit together, and yet no one has an answer yet. any thoughts? a few people who might have knowledge and opinions are unfortunately no longer on the board. jen
  4. davebhoy

    davebhoy New Member

    but does msg have anything to do with this? since i have had m.e. i have been incredibly intolerant of msg. if there is even a tiny amount in something i eat, a residue on a pan, i get a really bad headache. if i get a full dosage it kills me.

    i have always suffered from migraines until i got them under control by eliminating foods. that was until i got a cracker last week, i think because of decorating a room at home.
  5. tansy

    tansy New Member


    It's not a stupid question at all. The controversy over msg and apartame has been going on for years, the article I have posted includes information that is 10 years old and yet the risks are still being ignored.


    This article mentions the role of magnesium.


    The amino acids that are converted to glutathione require other factors including potassium, magnesium, and energy. No wonder glutamate can be a problem for many with these DDs.

    love, Tansy

    From the health4you website.


    Russell L. Blaylock, MD, has written Excitoxins: The Taste that Kills,1 in which he explains that certain amino acids when overly abundant in the brain can cause neurons to die. Many biochemicals can act as neurotransmitters in the brain—some excite our neurons; others calm them. In particular, glutamate, aspartate, and cysteine are three amino acids that excite our neurons and can be called "excitotoxins." They are now added in large amounts to our food supply.
    "Today MSG is added to most soups, chips, fast foods, frozen foods, ready-made dinners, and canned goods. And it has been heaven sent for the diet food industry, since so many of the low-fat foods are practically tasteless"

    Glutamate, as monosodium glutamate (MSG) is added to many foods. It excites our taste buds and can make bland food taste wonderful. It is contained in the sea vegetable, kombu, which has been used as a flavor enhancer "for thousands of years in Japan." In 1908 a Japanese scientist discovered that glutamate is the active chemical in kombu.

    By 1933 their annual consumption of monosodium glutamate was over ten million pounds. Japanese cooks had found that MSG made even the most bland recipes "taste scrumptious." In the Second World War it was used in the rations for the Japanese soldiers. "Unlike American rations, theirs tasted delicious." Soon the American food industry was following the lead of the Japanese and using MSG. "The use has doubled every decade since the late 40's.

    Today MSG is added to most soups, chips, fast foods, frozen foods, ready-made dinners, and canned goods. And it has been heaven sent for the diet food industry, since so many of the low-fat foods are practically tasteless. . . . Often MSG and related toxins are added to foods in disguised forms. For example, among the food manufacturers favorite disguises are 'hydrolyzed vegetable protein,' 'vegetable protein,' 'natural flavorings,' and 'spices.' Each of these may contain from 12 per cent to 40 per cent MSG."
    ". . . it [is] ironic that the pharmaceutical industry is investing vast resources in the development of glutamate receptor blockers . . . while at the same time, the food industry, with the blessing of the FDA continues to add great quantities of glutamate to the food supply."

    The human brain has two excellent natural methods of control:
    (1) balance the chemicals within and
    (2) selectively screen the chemicals allowed inside.

    Glutamate is an amino acid that is used extensively in our brains. Why would it be toxic? Unfortunately, sometimes these two natural control methods break down.

    Energy, Magnesium, and Antioxidants

    First, in the brain the correct balance is maintained by excellent processes for reducing excess glutamate (or glutamic acid) at the special glutamate receptors in many neurons. Some processes involve storing the extra glutamate in nearby glia cells.

    Activating the appropriate enzymes for this process requires a great deal of energy, which, if unavailable, will result in the continual exposure of the neurons to the excitatory glutamate, injuring them and finally, if the energy deficit persists, the neurons will die.

    Other protective processes involve sufficient magnesium to block the uptake of glutamate by the neurons and also sufficient antioxidants, such as glutathione and vitamins C and E, to dispose of the free radicals generated within the neurons by the excitotoxins such as glutamate, aspartate, and cysteine.

    The powerful antioxidant glutathione consists of two of these excitotoxins, cysteine and glutamic acid, plus glycine. However, glutathione can only be formed from these amino acids when magnesium, potassium, and sufficient energy are all present.

    In regard to the blood-brain barrier, in Alzheimer's disease the vessels have the appearance of "Swiss cheese."
    When free radicals are not quenched they can stimulate the release of more excitotoxins from storage. "This produces a vicious cycle whereby excitotoxins stimulate free radical formation and the free radicals in turn stimulate further excitotoxin accumulation." We need to be careful to have sufficient antioxidants and magnesium in our diet!

    Blood-Brain Barrier

    The second major way in which the neurons are usually protected involves the circulatory system in the brain, which has blood vessel walls that allow certain chemicals to enter the brain while excluding others—the so-called blood-brain barrier. "There is a tight junction between the cells. . . that line the capillary walls. Blood vessels in other parts of the body have relatively large spaces between the cells that allow the passage of even large molecules." Fortunately, antioxidants such as vitamins C and E can pass through the blood-brain barrier. Dr. Blaylock points out that this barrier is not well developed in the very young and it may even be still developing in the adolescent.

    "Some parts of the brain never develop a barrier system at all, for example, the hypothalamus," which is vitally involved in endocrine function. Not only have many experiments shown that excitotoxins (such as MSG) in the diet cause major endocrine problems but also an experiment giving MSG to pregnant mice has shown similar injuries in the offspring, confirming that glutamate passes across the barrier of the placenta and enters the fetal bloodstream.

    Consistently, the animals exposed to MSG were found to be short, grossly obese, and had difficulty with sexual reproduction. One can only wonder if the large number of people having difficulty with obesity in the United States is related to early exposure to food additive excitotoxins since this obesity is one of the most consistent features of the syndrome [MSG exposure].

    One characteristic of the obesity induced by excitotoxins is that is doesn't appear to depend on food intake. This could explain why some people cannot diet away their obesity. It is ironic that so many people drink soft drinks sweetened with NutraSweet® when aspartate [in it] can produce the exact same lesions as glutamate, resulting in gross obesity The actual extent of MSG induced obesity in the human population is unknown. . . . [However], humans develop higher levels of blood glutamate following ingestion of MSG than any other species of animal known.

    Pregnant mothers are seldom warned about dangers to the fetus from excitotoxins. Due to the pioneering work of John Olney, MD, pure MSG has been removed from baby food. However, the food manufacturers continue to add an "even more dangerous product, hydrolyzed vetable protein, which contains three known excitotoxins and has added MSG."

    "One can only wonder if the large number of people having difficulty with obesity in the United States is related to early exposure to food additive excitotoxins . . ."

    In regard to the intact blood-brain barrier, there are many conditions during which it "can be temporarily broken down, such as with heat stroke, brain trauma, encephalitis, strokes, hypertension, and even severe hypoglycemia." Also, in the aged the blood-brain barrier has often deteriorated.

    For example, small strokes that we may not even be aware of can leave "a point of seepage for glutamate and other excitotoxins to by-pass the blood-brain barrier. In this way normally excluded excitotoxins from food can endanger the brain." The excitotoxins glutamate and aspartate are relatively small and can pass through an injured barrier when larger molecules are still excluded.

    Neurodegenerative Diseases

    Dr. Blaylock explains in detail and with excellent illustrations exactly which areas of the brain are involved in the neurodegenerative diseases: amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease), Parkinson's, and Alzheimer's. All three diseases can develop gradually. "The symptoms of Parkinson's disease do not manifest themselves until over 80 to 90 per cent of the neurons in the involved nuclei (called the substantia nigra) have died. The neurons didn't all suddenly die at the same time, rather they slowly and silently deteriorated over many years. The same is true of Alzheimer's disease. This is why prevention is so important."

    At times, all three diseases, ALS, Parkinson's, and Alzheimer's, have developed one after the other in the same patients. For example, in Guam following World War II the natives developed exceedingly high levels of ALS and some of them later developed Parkinson's and Alzheimer's. The cause was in their diet of flour made from the seed of the false sago palm (cycad), which has poisonous constituents. They had eaten this flour for centuries but only after "soaking the sliced seeds in water for several hours. This was repeated several times, each time using fresh water. After the last soaking, a chicken was fed some of the wash water. If it lived, the seed was deemed safe to eat." However, because of famine during the war, cycad flour became a much larger part of their diet. Also, fresh water was scarce so the precautionary measures were often abandoned or at least abbreviated. Adding to the problem, the famine could result in the natives having chronically low blood sugar.

    As explained above, low energy levels can block the detoxification of neurotoxins. Thus the people would be more vulnerable to the devastating neurodegenerative diseases.

    Pregnant mothers are seldom warned about dangers to the fetus from excitotoxins.

    Natives of Guam who immigrated to the United States and were no longer exposed to any of the cycad flour still developed the neurodegenerative diseases years later at ten to fifteen times the American rate. Since these diseases develop very slowly, Dr. Blaylock speculates that the people from Guam were exposed here to the less potent neurotoxins glutamate (from MSG) and aspartate (from NutraSweet®), which finally resulted in sufficient additional neurons dying so that they developed the neurodegenerative diseases that had devastated the natives of Guam at even higher rates.

    Another potent toxin related to certain opiates and to certain herbicides can cause immediate Parkinson's disease.

    Often, injury to the brain can occur at a distance from the original impingement. For example, the cortex of the brain is far from the nigrostriatal neurons. However, quoting Blaylock:

    Glutamate, amphetamines, and other excitotoxins may produce Parkinsonism by overexciting the cortical glutamate cells that connect to the nigrostriatal neurons lying deep in the brain. It is sort of like lightning hitting the power line outside your house and burning up all of the appliances connected to that line. The power line represents the cortical glutamate neurons and the appliances the nigrostriatal system.

    Dr. Blaylock is concerned about many situations that can result in low blood sugar with the consequent reduced brain energy level and ability to detoxify excitotoxins. People who are trying to lose weight are likely to be cutting down on calories and at same time consuming excitotoxins in NutraSweet® and in the MSG-containing diet foods. Exercise can also "produce rather profound states of hypoglycemia. . . especially in the untrained."

    Dr. Blaylock is concerned about many situations that can result in low blood sugar with the consequent reduced brain energy level and ability to detoxify excitotoxins. People who are trying to lose weight are likely to be cutting down on calories and at same time consuming excitotoxins in NutraSweet® and in the MSG-containing diet foods.

    If one suffers heat exhaustion, the elevated body core temperature can rise sufficiently to cause (at least based on experimental studies) a temporary breakdown of the blood-brain barrier, which can result in leakage of glutamate and aspartate into the brain itself. Also, such physical stress can cause a prolonged fall in the blood glucose and hence in brain glucose, which results in greater vulnerability of the brain to excitotoxins both occurring naturally within the brain and those supplied by the diet. In addition, during extreme exercise a tremendous number of free radicals are formed within the tissues as a result of increased metabolism. This too will add to the damage.

    Dr. Blaylock cites research indicating that Alzheimer's patients may suffer from reactive hypoglycemia. One study "seemed to suggest that diabetes and Alzheimer's disease never coexist in the same patient."

    Free Radicals and Calcium

    "The final common effect of exposure to large doses of excitotoxic amino acids [is] the release of free radicals within the neurons triggered by the influx of calcium." First, the excitatory amino acids cause the influx of calcium, ordinarily controlled by the "calcium pump," which requires much energy in order to work, as does also the pump that can take care of excess excitotoxins. Therefore, when we overwhelm the protective mechanisms with excitotoxins, too much calcium enters the neuron through special channels in the cell membrane. Then an enzyme "breaks down some of the fatty acids that make up the cell membrane." One of these is arachidonic acid, a long-chain omega-6 fatty acid, essential within the membranes but when released, it is the dangerous precursor of free radicals and an inflammatory prostaglandin. Interestingly, elderly rheumatoid arthritic patients who take anti-inflammatory medications appear to have "the lowest incidence of Alzheimer's disease."

    "Magnesium helps keep the calcium channel closed so as to protect the cells. . . . Recent nutritional studies have shown up to seventy-five per cent of adults in the United States have a significant magnesium deficiency. . . . In fact, dietary studies and metabolic balance studies indicate that the amount of magnesium in the American diet has been declining during most of this century."

    "Magnesium helps keep the calcium channel closed so as to protect the cells. . . . Recent nutritional studies have shown up to seventy-five per cent of adults in the United States have a significant magnesium deficiency"

    In regard to the blood-brain barrier, in Alzheimer's disease the vessels have the appearance of "Swiss cheese. . . . Another problem seen in children is exposure to excess lead from the environment, such as old lead paint. We know that lead exposure can easily disrupt the blood-brain barrier. In fact, it is a method commonly used in laboratory experiments."

    Avoiding Excitotoxins

    In summary, Dr. Blaylock recommends first and foremost that we avoid the dietary excitotoxins so prevalent in prepared foods—the MSG and the aspartame ("NutraSweet®"). He also mentions that the excitotoxin "cysteine can easily penetrate the intact blood-brain barrier and that hydrolyzed vegetable protein contains cysteine. . . . [It is] also being added to some bread dough." We need to concentrate on whole, unprocessed food. Dr. Blaylock gives us:

    a partial list of the most common names for disguised MSG. Remember also that the powerful excitotoxins, aspartate [in NutraSweet®] and L-cysteine, are frequently added to foods and according to FDA rules require no labeling at all.

    Additives that always contain MSG:

    Monosodium Glutamate
    Hydrolyzed Vegetable Protein
    Hydrolyzed Protein
    Hydrolyzed Plant Protein
    Plant Protein Extract
    Sodium Caseinate
    Calcium Caseinate
    Yeast Extract
    Textured Protein
    Autolyzed Yeast
    Hydrolyzed Oat Flour
    Additives that frequently contain MSG:

    Malt extract
    Malt Flavoring
    Bouillon Broth
    Stock Flavoring
    Natural Flavoring
    Natural Beef or Chicken Flavoring
    Seasoning Spices
    Additives that may contain MSG and/or other excitotoxins:

    Carrageeenan Enzymes (Protease enzymes from various sources can release excitotoxin amino acids from food proteins.)
    Soy Protein Concentrate
    Soy Protein Isolate Whey
    Protein Concentrate.
    In her review of Dr. Blaylock's book NOHA Honorary Member Beatrice Trum Hunter concludes:

    Excitotoxins is a valuable contribution to the understanding of the brain and the need to protect it from assaults that result in various health problems and diseases. It is a book that should be read by all health professionals. The work is understandable for concerned laypersons, too. The extensive reference list will serve as a useful tool for those who are laboring to have toxic substances officially banned, not to be permitted as intentional food additives. As noted by Richard C. Henneberry, PhD, "I consider it ironic that the pharmaceutical industry is investing vast resources in the development of glutamate receptor blockers to protect [the central nervous system] neurons against glutamate neurotoxicity in common neurological disorders, while at the same time, the food industry, with the blessing of the FDA [Food and Drug Administration], continues to add great quantities of glutamate to the food supply."2

    1Health Press, P.O. Box 1388, Santa Fe, NM 87504, 1994; 264 pages, hard back, $27.00.
    2Hunter, Beatrice Trum, "The Neurotoxicity of Food Additives," Townsend Letter for Doctors, August/September 1994, p. 954.


    NOHA Board Member Adrienne Samuels, PhD, has carefully studied the research on "glutamic acid (found in all hydrolyzed protein products), aspartic acid (found in aspartame), and L-cysteine (currently used as a dough conditioner and proposed for use as a color preservative for fresh fruit). . . .

    There are . . . double-blind studies suggesting that these amino acids are safe. A review of studies relevant to the safety and toxicity of glutamic acid, however, suggest that many of them are flawed."1 For example, "in the case of MSG toxicology studies, the placebo used to test the excitotoxin glutamate is NutraSweet®, which contains the excitotoxin aspartate.

    It has been clearly shown in a multitude of studies that aspartate produces the identical destructive reactions on the nervous system as MSG. It would seem obvious even to the layman that you would not use a control substance to compare to a known toxin if the control contained the same class of chemical toxin. But that is exactly what is being done."2

    1Samuels, Adrienne, "Excitatory Amino Acids in Neurologic Disorders," The New England Journal of Medicine, 331(4): 274-5, July 28, 1994.
    2Blaylock, Russel L., Excitoxins: The Taste that Kills, Health Press, P.O. Box 1388, Santa Fe, NM 87504, 1994, p. 200.

    Article from NOHA NEWS, Vol. XX, No. 1, Winter 1995, pages 1-4.
    [This Message was Edited on 09/26/2005]
  6. Jen102

    Jen102 New Member

    i will try to digest this tomorrow when my brain is working a bit better--get those synapses snapping. jen

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