A must read, if you care about your health and those you love

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jumpincactus

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I see that the lounge is listed a a general purpose area to talk about things in general, so I opted to post this info here. If I am in the wrong spot let me know. I have only good intentions as I feel this information is important to each and every one of us and our children and grand-kids. Along with future generations.

The first article will get you started,

the second is a long read but it most definitely is worth looking into. It is in the form of a PDF not sure how to get it up on the board so if I fail those of you that want more info PM me and I will send you the link for the pdf file. The second source of information is a real eye opener, in my opinion a must read.

Take what you want and leave the rest. If you don't agree fine, this isn't a post for debate, just sharing of what I believe to be truthful and accurate. I hope that those of you that are on board and believe will pass this knowledge on to others. Peace

If monosodium glutamate (MSG) is as safe as its food industry proponents claim, then why do they consistently labor to hide it from us with deceptive labeling?

Monosodium glutamate is in a special class of chemicals known as excitotoxins. These chemicals cross the blood brain barrier to over stimulate the neurons of the brain. It has the effect of destroying some neurons permanently, causing a variety of mental issues, including a permanent loss of intelligence. MSG poisoning will lower a person's intelligence faster than lead exposure, in addition to causing its better known mental and physical effects. This toxin is especially dangerous when combined with magnesium deficiencies, which are common in the West. MSG and magnesium deficiency is a deadly combination that can lead to sudden heart failure, and this combination is the primary reason why so many high-school athletes in the United States have mysterious heart failures.

MSG is sprayed directly upon crops, because it is a highly effective insecticide. Nevertheless, the F.D.A. has blessed its usage inside U.S. foods for decades.

"Cardiovascular signs[of MSG consumption]include hypotension, shock, and sometimes cardiac arrhythmias, which, if untreated, may precipitate circulatory collapse."

-- Handbook of Diseases, 2003

U.S. food regulators and chemical companies are intentionally making it difficult to avoid MSG, by using other names to hide its presence in ingredients lists.

Common Names Used To Hide MSG In Ingredients Lists

  • Gelatin
  • Calcium Caseinate
  • Hydrolyzed Vegetable Protein (HVP)
  • Textured Protein
  • Monopotassium glutamate
  • Hydrolyzed Plant Protein (HPP)
  • Yeast Extract
  • Sodium Glutamate
  • Glutamate
  • Autolyzed Plant Protein
  • Yeast Food

  • Yeast
  • Nutrient
  • Glutamic Acid
  • Sodium Caseinate
  • Autolyzed Yeast
  • Vegetable Protein Extract
  • Soy Protein
  • Hydrolyzed Corn Gluten
  • Natural Flavor*
  • Artificial Flavor
  • Spice*
*Since the F.D.A. has intentionally left "natural flavor" and "spice" without meaningful definitions, U.S. companies freely use these names to hide ingredients in our foods. This lack of regulations in enforcing honest labels is by design, in order to benefit the chemical industry.

[MSG's]"commercial use is permitted only due to its marketing before the 1958 Food Additive Amendments to theFood, Drug and Cosmetic Act, which in effect grandfathered hundreds of substances which had never been tested for safety, including MSG...

"... Certain neuroscientists have, for years, warned that consumption of neurotoxic amino acids (glutamic acid, aspartic acid, and L-cysteine) place consumers at risk -- with most risk to newborns and young children whose immature blood-brain barriers leave them less well protected than more mature people. There is now additional and growing concern on the part of neuroscientists that the glutamate that we eat may cause or exacerbate neuro-degenerative diseases such as ALS, Parkinson's disease, and Alzheimers disease."

-- Mission Possible Canada

"Industry has begun to proliferate products with the words 'No MSG', 'No Added MSG', or 'No MSG Added' on product labels when the products contain hydrolyzed protein (which invariably contains MSG) -- a practice that is clearly in violation of existing FDA regulations. Hidden MSG is not limited to use in food. MSG sensitive people have reported reactions to soaps, shampoos, hair conditioners, and cosmetics that contain hidden MSG. The most obvious common hiding places are in ingredients called 'hydrolyzed protein' and 'amino acids'. Drinks, candy and chewing gum are also potential sources of hidden MSG... Binders and fillers for medications, nutrients, and supplements, both prescription and non-prescription, including internal feeding materials and some fluids administered intravenously in hospitals, may contain MSG. Reactions to MSG are dose related, i.e., some people react to even very small amounts of MSG while others usually only react to relatively more. MSG-induced reactions may occur immediately after contact or after as much as 48 hours."

-- Aspartame Poisoning Information Canada

The Documented Effects Of MSG Consumption

Epilepsy
Vision disturbances
Panic attacks
Heart attacks
Parkinson's disease
Huntington's diseaseALS (Amyotrophic Lateral Sclerosis)
Alzheimer's disease
Brain lesions
Retinal damage
Obesity
Food cravings
Depleted nutrients
Hyperinsulinemia
Stunted growth
Crosses into the fetus
Ocular (eye) destruction
Liver damage
Diabetes
Kidney damage
Vastly increased chance of ADD, ADHD,
asperger's and autism
Severe headaches
Shortness of breath
Chest pains
Asthma
Gastrointestinal disturbances
Poor memory


Swelling
Numbness of hands, feet, or jaw
Chronic bronchitis
Allergy reactions
Irregular heart beat
Unstable blood pressure
Pain in joints or bones
Abrupt mood changes
Tingling in face or chest
Pressure behind eyes
Difficulty swallowing
Anxiety attacks
Explosive rages
Balance problems
Dizziness or seizures
Mini-strokes
Fibromyalgia
Multiple sclerosis
Tenderness in localized areas,
neck, back, etc.
Chronic post nasal drip
Sleep disorders
Blurred vision
Chronic fatigue
Extreme thirst or dry mouth
Hypoglycemia
Difficulty concentrating
Slowed speech

Notice the alarming number of diseases caused by, or aggravated by MSG. It is no coincidence that these symptoms match almost exactly those of insecticide ingestion, for MSG is actually used by farmers as an insecticide.

Glutamate occurs naturally in some foods, but the naturally-occurring glutamate does not cause ill-effects. It is believed to always appear in nature with its own antidote(s), for instance, taurine. The kind of MSG added to foods is a type that the F.D.A. allows manufacturers to call a "natural flavor" even though there is nothing natural about it. What follows describes that "natural" manufacturing process.

"Today, the glutamic acid component of the food additive monosodium glutamate is generally made by bacterial or microbial fermentation wherein bacteria used are often, if not always, genetically engineered. In this method, bacteria are grown aerobically in a liquid nutrient medium. The bacteria have the ability to excrete glutamic acid they synthesize outside of their cell membrane into the liquid nutrient medium in which they are grown. The glutamic acid is then separated from the fermentation broth by filtration, concentration, acidification, and crystallization, and, through the addition of sodium, converted to its monosodium salt."

-- truthinlabeling.org

In other words, the MSG added to our foods is typically produced from the putrid fermenting wastes of genetically engineered bacteria combined with powerful chemical agents. This whole process is referred to as "natural", at least by the F.D.A.'s unique version of biological science.

We recommend reading,The Slow Poisoning Of Mankind, which was an official report submitted to the World Health Organization about MSG.

The Poisoning of Mankind,

John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
1
The Slow Poisoning of Mankind
A Report on the Toxic Effects of the Food Additive
Monosodium Glutamate
Presented by John Erb
of Canada
to the Joint FAO/WHO Expert Committee
On Food Additives
August 2006
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
2
Table of Contents
Explanation 3
Human Exposure 3
Orally: 3
Subcutaneously: 4
Air Transmission: 4
Biological Aspects 4
Short-term toxicity of Monosodium Glutamate 5
MSG Used to Trigger Epileptic Seizures 5
MSG Used to Trigger CNS and Brain Damage 5
MSG Used to Damage Eye Cells in Vivo and in Vitro 6
Long-term toxicity of Monosodium Glutamate 7
MSG Used to Create Obese Test Subjects 7
The Ways in Which MSG Triggers Obesity In Test Subjects: 8
MSG increases the appetite. 8
MSG increases the secretion of Insulin. 10
MSG reduces the excretion of Ketones. 11
MSG reduces the excretion of Growth Hormone (GH) during adolescence. 11
MSG Triggers Diabetes In Test Subjects: 12
MSG crosses the Placenta endangering the fetus. 13
MSG’s Ocular Toxicity: 16
MSG causes Genotoxicity: 17
Other Human MSG studies: 17
MSG connected with adult-onset olivopontocerebellar degeneration: 17
MSG connected with amyotrophic lateral sclerosis (ALS) : 18
MSG and the Alteration of the brain: a model for ADHD/Autism 18
The Erb Hypothesis: 18
Accelerated and abnormal brain growth in the Autistic: 19
Possible vaccine connection with Autism: 20
MSG proven to accelerate the growth of neurons and stimulate proliferation: 20
Conclusions 21
Appendix A List of Foods Approved for MSG Addition 22
Appendix B List of Ingredients 23
Involving MSG 23
Appendix C List of Vaccines Involving MSG 24
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
3
Explanation
The Codex Alimentarius lists Monosodium Glutamate (ref #621) as a flavor enhancer
approved with no daily limit to be added to a broad range of food categories. (17th
Report of JECFA, 1974) Monosodium Glutamate is an amino acid that affects on
almost every major system and organ in the body. Glutamate receptors trigger many
different responses and can be over stimulated to cause cell death and other systemic
problems. For thirty years, scientists and researchers have used MSG in their
experiments to purposely create obese and pre-diabetic test subjects, trigger epileptic
seizures, create ischemic strokes, and destroy cell tissues in vivo and in vitro. The
amount of studies that use MSG to cause negative effects in test subjects numbers over
one thousand, published in a variety of medical and scientific journals in over a dozen
different countries.
Monosodium Glutamate added to the diet has been shown to increase the test subjects
desire to eat more food faster and more frequently.
There is mounting evidence that not only the rise in human obesity and diabetes is
linked to the ingestion of Monosodium Glutamate, but the increase in Autism and
Attention Deficit Hyperactive Disorder as well.
In light of the overwhelming evidence showing the detrimental effects of the food
additive Monosodium Glutamate, it is requested that the Joint Food and Agriculture
Committee/World Health Organization Expert Committee on Food Additives remove
Monosodium Glutamate (and ingredients that contain MSG) from the allowable
additives list of the Codex Alimentarius, and have it banned from vaccines as well.
Human Exposure
Orally:
Monosodium Glutamate is found in unlimited amounts in a wide variety of packaged
foods. The list of foods it can be found in is listed in Appendix A. MSG is also added
in unlimited amounts in restaurant and industrial food such as hospitals, retirement
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
4
homes and cafeterias. Because food processors and manufacturers do not have to list
the amount of MSG on their packaging, we have no way of knowing what a normal
person or child would ingest in a days period. According to industry research 0.6%
MSG added to food is optimal for making people eat progressively more and faster
(Bellisle F, Monneuse MO, 1991). If this is the case, as much as .6% of a person’s
daily diet could be made up of MSG. In a daily intake of 2kgs of laced food the adult
or child would receive a 12 gram dose of Monosodium Glutamate. A 12 gram dosage
of MSG is lethal to a one kg rat. JECFA Toxicology Study, FAO Nutrition Meetings
Report Series,1974, No. 53
Subcutaneously:
Though previous JECFA reports have disallowed MSG in foods for infants or those
under one year of age, many infants and children receive doses of MSG in a variety of
vaccinations. See Appendix C.
Air Transmission:
MSG is now being sprayed on crops and can become airborne. Though the Codex
Alimentarius specifically disallows MSG’s addition to fresh fruits and vegetables
(GFSA Annex to Table 3) Auxigro, with 30% MSG content, has been approved by some
countries to be sprayed on crops of fresh fruits and vegetables. Airborne effects of
MSG sprays have not been studied by the JECFA.
Biological Aspects
Monosodium Glutamate is an amino acid readily utilized by glutamate receptors
throughout the mammalian body. These glutamate receptors are present in the central
nervous system as the major mediators of excitatory neurotransmission and
excitotoxicity. Neural injury associated with trauma, stroke, epilepsy, and many
neurodegenerative diseases such as Alzheimer’s, Huntington’s and Parkinson’s diseases
and amyotrophic lateral sclerosis may be mediated by excessive activation of the
glutamate receptors. Neurotoxicity associated with excitatory amino acids encountered
in food, such as monosodium glutamate, has also been linked to glutamate receptors.
Glutamate receptors are found in the rat and monkey heart, the conducting system,
nerve terminals and cardiac ganglia. They are also present in the kidney, liver, lung,
spleen and testis. Therefore, food safety assessment should consider these tissues as
potential target sites.
Potential target sites in peripheral tissues for excitatory neurotransmission and excitotoxicity.
Gill SS, Mueller RW, McGuire PF, Pulido OM.
Bureau of Chemical Safety, Health Protection Branch, Health Canada, Ottawa.
Toxicol Pathol. 2000 Mar-Apr;28(2):277-84
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
5
Short-term toxicity of Monosodium Glutamate
MSG Used to Trigger Epileptic Seizures
Epileptic convulsions were triggered in rats using small single doses of Monosodium
Glutamate.
“Convulsive activity in 3, 10, 60 and 180-day old Sprague-Dawley rats was studied following the
i.p. administration of 4 mg g-1 of commercial MSG. The latency period increased with the age of
the animals while the duration of the convulsive period was longer in younger animals and shorter
in 60-day old rats. Convulsions were predominantly tonic in 3 and 10-day old rats, tonic-clonic in
60-day old rats, and predominantly clonic in 180-day old animals. The severity of the convulsions
and death incidence increased progressively with age.
Monosodium-L-glutamate-induced convulsions--I. Differences in seizure
pattern and duration of effect as a function of age in rats.
Arauz-Contreras J, Feria-Velasco A.
Gen Pharmacol. 1984;15(5):391-5.
“Adult rats (60 days old) were injected intraperitoneally with 5 mg/g monosodium L-glutamate
(MSG). During the convulsive period (1 h after injection), uptake and release of
[3H]norepinephrine (3H-NE) and [14C]dopamine (14C-DA) were measured. Data suggest that
catecholaminergic neurotransmission may play an important role in the etiopathology of
convulsions in the experimental model using MSG.”
Monosodium L-glutamate-induced convulsions: changes in uptake and release of
catecholamines in cerebral cortex and caudate nucleus of adult rats.
Beas-Zarate C, Schliebs R, Morales-Villagran A, Feria-Velasco A.
Epilepsy Res. 1989 Jul-Aug;4(1):20-7.
MSG Used to Trigger CNS and Brain Damage
Single doses of MSG have been used to cause CNS and brain damage in rodents and
chicks.
“Monosodium glutamate (MSG) was used to create a lesion in the CNS of the infant rat.
Subcutaneous injections of MSG in four day old rat pups caused a high degree of cell necrosis in
the arcuate nucleus of the hypothalamus”
Reaction of the hypothalamic ventricular lining following systemic administration of MSG.
Rascher K, Mestres P.
Scan Electron Microsc. 1980;(3):457-64.
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
6
“Administration of doses of glutamate (Glu) leads to selective neurodegeneration in discrete
brain regions near circumventriclular organs of the early postnatal mouse. The arcuate nucleusmedian
eminence complex (ARC-ME) appears to be the most Glu-sensitive of these brain regions,
perhaps because of the intimate relationships between its neurons and specialized astroglial
tanycytes. A dose of 0.2 mg MSG/g BW s.c. causes clear but discrete injury to specific
subependymal neurons of undetermined phenotype near the base of the third ventricle. Slightly
higher doses of MSG evoke damage of additional neurons confined to the ventral region of the
ARC traversed by tanycytes.”
Exogenous glutamate enhances glutamate receptor subunit expression during
selective neuronal injury in the ventral arcuate nucleus of postnatal mice.
Hu L, Fernstrom JD, Goldsmith PC.
Neuroendocrinology. 1998 Aug;68(2):77-88
“Various dosages of monosodium glutamate (M.S.G.) were injected to 5 day old male chicks. Body
weights, food intake, rate of obesity, semen production, some endocrine criteria and brain
pathology were studied til 235 days post injection. All M.S.G. treated birds showed brain
damage in the rotundus nuclei, and in the area located dorsolaterally to the ventromedial
hypothalamic nuclei (V.M.H.). In some of the M.S.G. treated birds, additional brain regions were
damaged, i.e. V.M.H., mammillary nuclei, dorsomedial anterior nuclei, ovoid nuclei, subrotundus
nuclei, archistriatum and lateral forebrain bundles.”
The relation between monosodium glutamate inducing brain damage, and body weight,
food intake, semen production and endocrine criteria in the fowl.
Robinzon B, Snapir N, Perek M.
Poult Sci. 1975 Jan;54(1):234-41.
MSG Used to Damage Eye Cells in Vivo and in Vitro
Single doses of MSG have been used to trigger damage to various structures of the eye.
“Monosodium L-glutamate is known to cause intracellular swelling, necrosis, and
disappearance of most inner retinal neurons, with concomitant thinning of inner retinal
layers within hours after subcutaneous injection into neonatal rodents. A similar process can be
observed in adult rat retina after intravitreal glutamate injection. To better describe and compare
this process with that reported after systemic application, adult Sprague-Dawley rat eyes were
intravitreally injected with 1 mumol monosodium L-glutamate and the retinas studied by LM and
EM over a 2-month period. Results demonstrated that adult rat retina experienced severe
degenerative changes which progressed in two stages: an initial stage of massive intracellular
swelling and a second stage of necrosis and cell loss.”
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
7
Histologic changes in the inner retina of albino rats following intravitreal
injection of monosodium L-glutamate.
Sisk DR, Kuwabara T.
Graefes Arch Clin Exp Ophthalmol. 1985;223(5):250-8.
“Monosodium glutamate added to 12-day chick embryo retinas in culture causes severe
morphologic damage to the retina as judged by light microscopic examination. Damage is evident
after a few hours with concentrations as low as 0.3 mM. Glutamyltransferase induction is also
appreciably inhibited by the amino acid. General protein synthesis and RNA synthesis appear to be
less affected.”
Effects of monosodium glutamate on chick embryo retina in culture.
Reif-Lehrer L, Bergenthal J, Hanninen L.
Invest Ophthalmol. 1975 Feb;14(2):114-24.
Long-term toxicity of Monosodium Glutamate
MSG Used to Create Obese Test Subjects
In studies of new diet and diabetes drugs and treatments, a test subject must be used
that will exhibit the characteristics of obesity and hyperinsulinemea. For scientists to
create replicable results the factor that triggers obesity in the experimental test group
must be 100% replicable. For guaranteed results researchers regularly use injections of
MSG subcutaneously on test subjects on the day of birth or shortly thereafter.
“Monosodium glutamate (MSG) was administered by various methods to mice and rats of various
ages and the incidence of obesity was later measured. Newborn mice were injected subcutaneously
with 3 mg MSG/g body-weight at 1, 2, 3, 6, 7, and 8 d of age; 16% died before weaning. Of the
survivors, 90% or more became markedly obese. The proposed schedule of injections in the
newborn was almost 100% reliable in inducing a high extent of adiposity. “
The induction of obesity in rodents by means of monosodium glutamate.
Bunyan J, Murrell EA, Shah PP.
Br J Nutr. 1976 Jan;35(1):25-39.
This replicable finding has been given the names ‘monosodium glutamate obese rat’ or
‘MSG treated rat’.
Here are a few of the hundreds of studies that have used the rodent scientifically
categorized as the MSG Treated Rat, a term synonymous with obesity, lethargy and
hyperinsulinaemia:
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
8
Effect of adrenalectomy on the activity of small intestine enzymes in
monosodium glutamate obese rats.
Mozes S, Sefcikov Z, Lenhardt L, Racek L. Physiol Res. 2004;53(4):415-22.
Effect of fasting and refeeding on duodenal alkaline phosphatase activity in monosodium glutamate obese rats.
Racek L, Lenhardt L, Mozes S. Physiol Res. 2001;50(4):365-72.
Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity
in monosodium glutamate (MSG) treated-rats.
Dolnikoff M, Martin-Hidalgo A, Machado UF, Lima FB, Herrera E. Int J Obes Relat Metab Disord. 2001 Mar;25(3):426-
33
Effects of chronic administration of sibutramine on body weight, food intake and motor activity in neonatally
monosodium glutamate-treated obese female rats: relationship of antiobesity effect with monoamines.
Nakagawa T, Ukai K, Ohyama T, Gomita Y, Okamura H.
Exp Anim. 2000 Oct;49(4):239-49.
Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum
leptin and blood flow to brown adipose tissue.
Iwase M, Ichikawa K, Tashiro K, Iino K, Shinohara N, Ibayashi S, Yoshinari M, Fujishima M.
Hypertens Res. 2000 Sep;23(5):503-10.
Obesity induced by neonatal monosodium glutamate treatment in spontaneously hypertensive rats: an animal
model of multiple risk factors.
Iwase M, Yamamoto M, Iino K, Ichikawa K, Shinohara N, Yoshinari M, Fujishima M.
Hypertens Res. 1998 Mar;21(1):1-6.
The Ways in Which MSG Triggers Obesity In Test
Subjects:
MSG increases the appetite.
MSG added to food of sheep has resulted in an increase in appetite:
Sheep with oesophageal fistulas were used in sham-feeding experiments to assess how sham
intakes were affected by additions of monosodium glutamate (MSG) to the various straw diets.
MSG at 5-40 g/kg fine and coarse ground straw increased sham intakes by 146% (P = 0.04)
and 164% (P = 0.01) respectively. These findings indicated that the intakes of poor-quality
diets can be increased by improving their palatability with MSG.
Factors affecting the voluntary intake of food by sheep. The effect of monosodium glutamate on the
palatability of straw diets by sham-fed and normal animals.
Colucci PE, Grovum WL.
Br J Nutr. 1993 Jan;69(1):37-47.
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
9
MSG alters rat’s ability to regulate food intake:
Caloric regulation and the development of obesity were examined in rats which had received
parenteral injections of monosodium glutamate (MSG) as neonates. Rats were injected with
either 2 mg/g or 4 mg/g MSG on alternate days for the first 20 days of life. In adulthood, the
ability to regulate caloric intake was tested by allowing animals access to diets of varying
caloric densities. While control animals maintained relatively constant caloric intakes across
dietary conditions, MSG-treated animals demonstrated an inability to respond to caloric
challenges. Treated animals decreased caloric intake on a diluted diet and consumed
more calories than controls when presented with a calorically dense diet.”
Juvenile-onset obesity and deficits in caloric regulation in MSG-treated rats.
Kanarek RB, Meyers J, Meade RG, Mayer J.
Pharmacol Biochem Behav. 1979 May;10(5):717-21
A connection can be found in human test subjects: Two findings with MSG and
human appetite are discovered:
1.When a human subject eats a meal with MSG, they become hungry again, sooner.
2. Humans will eat more food laced with MSG than control food without it.
“Subjects consumed soup preloads of a fixed size containing different concentrations of
monosodium L-glutamate (MSG). Effects on appetite following these preloads, and when no
soup was consumed, were assessed in 3 studies.The most important finding concerning MSG
showed that motivation to eat recovered more rapidly following a lunchtime meal in which
MSG-supplemented soup was served.”
Umami and appetite: effects of monosodium glutamate on hunger and
food intake in human subjects.
Rogers PJ, Blundell JE.
Physiol Behav. 1990 Dec;48(6):801-4.
“MSG’s effects on the palatability of two experimental foods were investigated in 36 healthy
young men and women. MSG improved palatability ratings, with an optimum at 0.6%. Weekly
tests of free intake showed that subjects fed the experimental foods with 0.6% MSG added ate
progressively more and faster, indicating increasing palatability with repeated exposure. MSG
facilitated intake of some but not all target foods, and was associated with positive (increased
calcium and magnesium intake) or adverse (increased fat intake) nutritional effects. It is
concluded that MSG can act as a palatability enhancer in the context of the French diet. It can
facilitate long-term intake in both young and elderly persons but it should be utilized
cautiously so as to improve nutrition.
Monosodium glutamate as a palatability enhancer in the European diet.
Bellisle F, Monneuse MO, Chabert M, Larue-Achagiotis C, Lanteaume MT, Louis-Sylvestre J.
Physiol Behav. 1991 May;49(5):869-73.
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
10
MSG increases the secretion of Insulin.
MSG has been shown in rats to over stimulate the pancreas resulting in
hyperinsulinemia. The excess insulin in the blood increases the conversion of
glucose into adipose tissue.
“Early postnatal administration of monosodium glutamate (MSG) to rats induces obesity,
hyperinsulinemia and hyperglycemia in adulthood, thus suggesting the presence of insulin
resistance. We therefore investigated the effects of insulin on glucose transport and lipogenesis
in adipocytes as well as insulin binding to specific receptors in the liver, skeletal muscle and
fat tissues. An increase of plasma insulin was found in 3-month-old rats treated with
MSG during the postnatal period”
Late effects of postnatal administration of monosodium glutamate
on insulin action in adult rats.
Macho L, Fickova M, Jezova, Zorad S.
Physiol Res. 2000;49 Suppl 1:S79-85.
Even just adding MSG to the mouth of a rat can trigger an increase in insulin
release:
“When the oral cavity was infused by MSG solution, a transient increase in blood insulin
level was recognized at 3 min after this oral stimulation. These observations support the
conclusion that taste stimulation of MSG induces cephalic-phase insulin secretion.”
Cephalic-phase insulin release induced by taste stimulus of
monosodium glutamate (umami taste).
Niijima A, Togiyama T, Adachi A.
Physiol Behav. 1990 Dec;48(6):905-8.
A connection can be found in human test subjects:
“To further study glutamate metabolism, we administered 150 mg/kg body wt of monosodium
glutamate (MSG) and placebo to seven male subjects who then either rested or exercised.
MSG administration resulted in elevated insulin levels.”
Glutamate ingestion and its effects at rest and during exercise in humans.
Mourtzakis M, Graham TE.
J Appl Physiol. 2002 Oct;93(4):1251-9.
“Monosodium (L)-glutamate (10 g) was given orally in a double-blind placebo-controlled
cross-over study to 18 healthy volunteers, aged 19-28 years, with an oral (75 g) glucose load.
CONCLUSIONS: Oral (L)-glutamate enhances glucose-induced insulin secretion in
healthy volunteers in a concentration-dependent manner.”
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
11
Effects of oral monosodium (L)-glutamate on insulin secretion and
glucose tolerance in healthy volunteers.
Chevassus H, Renard E, Bertrand G, Mourand I, Puech R,Molinier N,
Bockaert J, Petit P, Bringer J.
Br J Clin Pharmacol. 2002 Jun;53(6):641-3.
MSG reduces the excretion of Ketones.
MSG has been shown in rats to reduce Ketone secretion, resulting in an obese rat
with a propensity for creating adipose tissue(fat):
“MSG-treated rats showed shorter naso-anal and tail length, and a more marked intraperitoneal
fat deposition than control rats. Plasma levels of total ketone bodies were decreased in the
MSG-treated rats as compared to control rats.”
Decreased ketonaemia in the monosodium glutamate-induced obese rats.
Nakai T, Tamai T, Takai H, Hayashi S, Fujiwara R, Miyabo S.
Life Sci. 1986 Jun 2;38(22):2009-13.
A connection can be found in human test subjects:
“Production and use of ketone bodies are lower in obese women than in lean controls.”
Ketone body metabolism in lean and obese women.
Vice E, Privette JD, Hickner RC, Barakat HA.
Metabolism. 2005 Nov;54(11):1542-5.
MSG reduces the excretion of Growth Hormone (GH) during
adolescence.
MSG has been shown in rats to reduce Growth Hormone secretion, resulting in an
obese rat with stunted stature:
Rats were treated with monosodium glutamate (MSG), 4 mg/g on alternate days for the first 10
days of life, to induce lesions of the arcuate nucleus and destroy the majority of growth
hormone-releasing hormone (GHRH) neurones.
Depletion of hypothalamic growth hormone-releasing hormone by neonatal monosodium glutamate
treatment reveals an inhibitory effect of betamethasone on growth hormone secretion in adult rats.
Corder R, Saudan P, Mazlan M, McLean C, Gaillard RC.
Neuroendocrinology. 1990 Jan;51(1):85-92.
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
12
A connection can be found in human test subjects:
In obese individuals, …….GH secretion is impaired without an organic pituitary disease
and the severity of the secretory defect is proportional to the degree of obesity.
Growth hormone status in morbidly obese subjects and correlation with body composition.
Savastano S, Di Somma C, Belfiore A, Guida B, Orio F Jr, Rota F,
Savanelli MC, Cascella T, Mentone A, Angrisani L, Lombardi G, Colao A.
J Endocrinol Invest. 2006 Jun;29(6):536-43.
A recent study compared data from both humans and rats fed MSG prenatally
through the mother‘s diet, and made the following recommendation:
“Oral administration of MSG to pregnant rats affects birth weight of the offspring, and
reduces GH serum levels are lowered in animals that received MSG during prenatal life via
maternal feeding…..The flavouring agent MSG--at concentrations that only slightly surpass
those found in everyday human food, exhibits significant potential for damaging the
hypothalamic regulation of appetite, and thereby determines the propensity of world-wide
obesity. We suggest to reconsider the recommended daily allowances of amino acids and
nutritional protein, and to abstain from the popular protein-rich diets, and particularly
from adding the flavouring agents MSG.”
Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite.
Hermanussen M, Garcia AP, Sunder M, Voigt M, Salazar V, Tresguerres JA.
Eur J Clin Nutr. 2006 Jan;60(1):25-31.
MSG Triggers Diabetes In Test Subjects:
The food additive Monosodium Glutamate is used to purposely create Diabetic rodents:
“The number of diabetic patients is increasing every year, and new model animals are required to
study the diverse aspects of this disease. An experimental obese animal model has reportedly been
obtained by injecting monosodium glutamate (MSG) to a mouse. We found that ICR-MSG mice on
which the same method was used developed glycosuria. Both female and male mice were observed
to be obese but had no polyphagia, and were glycosuric by 29 weeks of age, with males having an
especially high rate of incidence (70.0%). Their blood concentrations of glucose, insulin, total
cholesterol, and triglycerides were higher than in the control mice at 29 weeks. These high
concentrations appeared in younger males more often than in females, and were severe in adult
males. Also, the mice at 54 weeks of age showed obvious obesity and increased concentrations of
glucose, insulin, and total cholesterol in the blood. The pathological study of ICR-MSG female and
male mice at 29 weeks of age showed hypertrophy of the pancreatic islet. This was also observed
in most of these mice at 54 weeks. It was recognized as a continuation of the condition of diabetes
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
13
mellitus. From the above results, these mice are considered to be useful as new experimental
model animals developing a high rate of obese type 2 (non-insulin dependent) diabetes
mellitus without polyphagia.”
Type 2 diabetes mellitus in obese mouse model induced by monosodium glutamate.
Nagata M, Suzuki W, Iizuka S, Tabuchi M, Maruyama H, Takeda SAburada M, Miyamoto K.
Exp Anim. 2006 Apr;55(2):109-15.
“Administration of monosodium glutamate (MSG) to KK mice during the neonatal period
resulted in a syndrome of obesity, stunting and hypogonadism. In some animals the genetic
predisposition to diabetes was unmasked with the development of marked hyperglycaemia and or
hyperinsulinaemia. Food intake was not increased compared to controls. The elevated plasma
glucose and insulin in fed MSG treated mice fell rapidly with food deprivation. Glucose disposal
was comparable in MSG treated and control mice after IP glucose, but after oral glucose MSG
treated mice showed impaired glucose tolerance. Insulin secretion was defective in MSG treated
mice.”
Effects of monosodium glutamate administration in the neonatal period
on the diabetic syndrome in KK mice.
Cameron DP, Poon TK, Smith GC.
Diabetologia. 1976 Dec;12(6):621-6.
Not all rodent species become obese with MSG ingestion, some just get Diabetes:
Neuronal necrosis in the arcuate and ventromedial hypothalamus regions is easily induced in 1-
day-old Chinese hamsters by the administration of monosodium glutamate (MSG). New-born
Chinese hamsters injected with MSG showed no sign of obesity, even when grown up, but
apparently developed a diabetic syndrome.
Diabetic syndrome in the Chinese hamster induced with monosodium glutamate.
Komeda K, Yokote M, Oki Y.
Experientia. 1980 Feb 15;36(2):232-4.
MSG crosses the Placenta endangering the fetus.
MSG has been shown to cross the placental barrier in rats, and new studies suggest that
in cases where human mothers who suffer from intrauterine infection are at risk to
Glutamate causing excitotoxic perinatal brain injury to the fetus:
“Monosodium-L-glutamate given subcutaneously to pregnant rats caused acute necrosis of the
acetylcholinesterase-positive neurons in the area postrema. The same effect has been observed in
the area postrema of fetal rats. The process of neuronal cell death and the elimination of debris by
microglia cells proved to be similar in pregnant animals and in their fetuses. However, embryonal
neurons were more sensitive to glutamate as judged by the rapidity of the process and the doseJohn
Erb Report on Monosodium Glutamate Presented to the WHO August 2006
14
response relationship. These observations raise the possibility of transplacental poisoning in
human fetuses after the consumption of glutamate-rich food by the mother.”
Neurotoxicity of monosodium-L-glutamate in pregnant and fetal rats.
Toth L, Karcsu S, Feledi J, Kreutzberg GW.
Acta Neuropathol (Berl). 1987;75(1):16-22.
“Monosodium glutamate (MSG) was shown to penetrate placental barrier and distribute
almost evenly among embryonic tissues using 3H-Glu as a tracer. When a lower (1.0 mg/g) and a
higher (2.5 mg/g) doses of MSG were alternatively injected to Kunming maternal mice in every
other days from mating to deliveries, obvious injury occurred in the ability of memory retention
and Y-maze discrimination learning of adult filial mice pregnantly treated with higher doses (2.5
mg/g) of MSG. Meanwhile, the neuronal damages were observed in not only arcuate nucleus but
also ventromedial nucleus of hypothalamus. Characteristic cytopathological changes induced by
MSG showed swollen cytoplasm, dark pyknotic nuclei and loss of neurons.These experimental
findings indicated that MSG performed its transplacental neurotoxicity in a dose-dependent
manner. The excessive activation of Glu receptors and the overloading of intracellular Ca2+
induced by MSG ultimately leading to neuronal death may result in the reduction of the
capability of learning and memory in adult filial mice pregnantly treated with MSG.”
Transplacental neurotoxic effects of monosodium glutamate on structures
and functions of specific brain areas of filial mice
Gao J, Wu J, Zhao XN, Zhang WN, Zhang YY, Zhang ZX.
Sheng Li Xue Bao. 1994 Feb;46(1):44-51.
“Administering GLU to newborn rodents completely destructs arcuate nucleus neurons, and results
in permanently elevated plasma leptin levels that fail to adequately counter-regulate food intake.
Chronic fetal exposure to elevated levels of GLU may be caused by chronic maternal over-nutrition
or by reduced umbilical plasma flow. We strongly suggest abandoning the flavoring agent
monosodium glutamate and reconsidering the recommended daily allowances of protein and
amino acids during pregnancy.”
Does the thrifty phenotype result from chronic glutamate intoxication? A hypothesis.
Hermanussen M, Tresguerres JA.
J Perinat Med. 2003;31(6):489-95
Oral administration of MSG in the pregnant mother’s diet has been shown to
accumulate at twice the maternal level in the brains of fetal mice:
“Monosodium glutamate (MSG) was shown to penetrate placental barrier and to distribute to
embryonic tissues using [3H]glutamic acid ([3H]Glu) as a tracer. However, the distribution is not
even; the uptake of MSG in the fetal brain was twice as great as that in the maternal brain in
Kunming mice. Other maternal mice were given per os MSG (2.5 mg/g or 4.0 mg/g body weight)
at 17-21 days of pregnancy, and their offspring behaviors studied. The results showed that maternal
oral administration of MSG at a late stage of pregnancy decreased the threshold of convulsion in
the litters at 10 days of age. Y-maze discrimination learning was significantly impaired in the
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
15
60-day-old filial mice.”
Effects of maternal oral administration of monosodium glutamate at a
late stage of pregnancy on developing mouse fetal brain.
Yu T, Zhao Y, Shi W, Ma R, Yu L.
Brain Res. 1997 Feb 7;747(2):195-206.
In human fetal development, Glutamate is a major contributor to growth of the CNS
and brain:
“Glutamate receptors have multiple roles in the central nervous system. Recent evidence suggests
that the iontropic glutamate receptors are critical during brain development, particularly for
corticogenesis, neuronal migration, and synaptogenesis. In this study, we examined subunit mRNA
expression and binding sites of the NMDA, AMPA, and kainate receptors from gestational weeks
8-20 in human fetal brain. Expression of glutamate receptors was high during several periods in
these brains. These results demonstrate that glutamate receptors are expressed early in human
brain development.”
Ontogeny of ionotropic glutamate receptor expression in human fetal brain.
Ritter LM, Unis AS, Meador-Woodruff JH.
Brain Res Dev Brain Res. 2001 Apr 30;127(2):123-33.
Human fetal development has been shown to be jeopardized by high amounts of
Glutamate:
“Children undergoing perinatal brain injury often suffer from the dramatic consequences of this
misfortune for the rest of their lives. Despite the severe clinical and socio-economic significance,
no effective clinical strategies have yet been developed to counteract this condition. This review
describes the pathophysiological mechanisms that are implicated in perinatal brain injury. These
include the acute breakdown of neuronal membrane potential followed by the release of
excitatory amino acids such as glutamate and aspartate. Glutamate binds to postsynaptically
located glutamate receptors that regulate calcium channels. The resulting calcium influx activates
proteases, lipases and endonucleases which in turn destroy the cellular skeleton. Clinical studies
have shown that intrauterine infection increases the risk of periventricular white matter damage
especially in the immature fetus. This damage may be mediated by cardiovascular effects of
endotoxins.”
Perinatal brain damage--from pathophysiology to prevention.
Jensen A, Garnier Y, Middelanis J, Berger R.
Eur J Obstet Gynecol Reprod Biol.2003 Sep 22;110 Suppl 1:S70-9.
“We found evidence that the thrifty phenotype may be the consequence of fetal
hyperglutamatemia. Maternal glutamate (GLU) reaches the fetal circulation, as part of the maternofetal
glutamine-glutamate exchange. Glutamine is absorbed from the maternal circulation, and
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
16
deaminated for nitrogen utilization, resulting in a fetal production of GLU. GLU is extracted as it
returns to the placenta. When the umbilical plasma flow is low, GLU may be trapped in the
fetal circulation, and reaches neurotoxic levels.”
Does the thrifty phenotype result from chronic glutamate intoxication? A hypothesis.
Hermanussen M, Tresguerres JA.
J Perinat Med. 2003;31(6):489-95.
MSG’s Ocular Toxicity:
MSG given both subcutaneously and orally in diet causes long term destruction of
various ocular structures:
“In rodents, daily injection of neurotoxic monosodium L-glutamate (MSG) during the
postnatal period induces retinal lesions, optic nerve degeneration with an alteration of visual
pathway and an absence of the b-wave in the electroretinogram. Animals received daily doses of
glutamate during the first ten days after birth according to two protocols. The two treatments
similarly destroyed 56% of the overall population of the ganglion cell layer: 30% of displaced
amacrine and 89% of ganglion cells.”
Neurotoxic effects of neonatal injections of monosodium L-glutamate (L-MSG) on the retinal ganglion cell layer of
the golden hamster: anatomical and functional
consequences on the circadian system.
Chambille I, Serviere J.
J Comp Neurol. 1993 Dec 1;338(1):67-82.
“Changes in the transparency and size of lenses in rats were investigated following administration
of monosodium-L-glutamate (MSG), MSG (5 mg/g b.w.) was injected subcutaneously on the 9th
and 10th days after birth.. The incidence of cataract increased with age, reaching more than 75% at
4 months of age. Morgagni's globules were histologically detected in the opacity of the posterior
lens cortex. Degenerative changes of the lens epithelium were observed in the mature cataract. The
size and weight of the lens were smaller than those of controls. These findings indicate that
administration of MSG could be an etiologic factor in cataract formation in the developing
rat.”
Morphological studies on cataract and small lens formation in
neonatal rats treated with monosodium-L-glutamate
Kawamura M, Azuma N, Kohsaka S.
Nippon Ganka Gakkai Zasshi. 1989 May;93(5):562-8.
“The purpose of this study was to investigate the effects of glutamate accumulation in vitreous on
retinal structure and function, due to a diet high in sodium glutamate. Three different diet groups
were created, consisting of rats fed on a regular diet (diet A), a moderate excess of sodium
glutamate diet (diet B) and a large excess of sodium glutamate diet (diet C). After 1, 3 and 6
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
17
months of the administration of these diets, amino acids concentrations in vitreous were analyzed.
Significant accumulation of glutamate in vitreous was observed in rats following addition of
sodium glutamate to the diet as compared to levels with a regular diet. In the retinal morphology,
thickness of retinal neuronal layers was remarkably thinner in rats fed on sodium glutamate diets
than in those on a regular diet. Functionally, ERG responses were reduced in rats fed on a sodium
glutamate diets as compared with those on a regular diet. The present study suggests that a diet
with excess sodium glutamate over a period of several years may increase glutamate
concentrations in vitreous and may cause retinal cell destruction.”
A high dietary intake of sodium glutamate as flavoring (ajinomoto) causes
gross changes in retinal morphology and function.
Ohguro H, Katsushima H, Maruyama I, Maeda T, Yanagihashi S, Metoki T, Nakazawa M.
Exp Eye Res. 2002 Sep;75(3):307-15.
MSG causes Genotoxicity:
MSG has been shown to be Genotoxic to a variety of organs and tissues in the
mammalian body:
Monosodium glutamate (MSG) continues to function as a flavor enhancer in West African
and Asian diets. The present study examines the modulatory effects of dietary antioxidant vitamin
C (VIT C), vitamin E (VIT E) and quercetin on MSG-induced oxidative damage in the liver,
kidney and brain of rats. In addition, the effect of these antioxidants on the possible genotoxicity
of MSG was investigated in a rat bone marrow micronuclei model. MSG administered
intraperitoneally at a dose of 4 mg/g body wt markedly increase malondialdehyde (MDA)
formation in the liver, the kidney and brain of rats. The antioxidants tested protected against MSGinduced
liver toxicity significantly. VIT E failed to protect against MSG-induced genotoxicity. The
results indicate that dietary antioxidants have protective potential against oxidative stress
induced by MSG and, in addition, suggest that active oxygen species may play an important
role in its genotoxicity.
Monosodium glutamate-induced oxidative damage and genotoxicity
in the rat: modulatory role of vitamin C, vitamin E and quercetin.
Farombi EO, Onyema OO.
Hum Exp Toxicol. 2006 May;25(5):251-9.
Other Human MSG studies:
MSG connected with adult-onset olivopontocerebellar degeneration:
In patients with recessive, adult-onset olivopontocerebellar degeneration associated with a partial
deficiency of glutamate dehydrogenase, the concentration of glutamate in plasma was significantly
higher than that in controls. Plasma alpha-ketoglutarate was significantly lower. Oral
administration of monosodium glutamate resulted in excessive accumulation of this amino acid in
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
18
plasma and lack of increase in the ratio of plasma lactate to pyruvate in the glutamate
dehydrogenase-deficient patients. Decreased glutamate catabolism may result in an excess of
glutamate in the nervous system and cause neuronal degeneration.
Abnormal glutamate metabolism in an adult-onset degenerative neurological disorder.
Plaitakis A, Berl S, Yahr MD.
Science. 1982 Apr 9;216(4542):193-6.
MSG connected with amyotrophic lateral sclerosis (ALS) :
Glutamate levels were determined in the fasting plasma of 22 patients with early-stage primary
amyotrophic lateral sclerosis (ALS) and compared to those of healthy and diseased controls. There
was a significant increase (by approximately 100%, p less than 0.0005) in the plasma glutamate of the
ALS patients as compared with the controls. Oral glutamate loading (60 mg of monosodium glutamate
per kilogram of body weight, taken orally after overnight fasting) resulted in significantly greater
elevations in the plasma glutamate and aspartate levels in the ALS patients than in the controls.
Glutamate, a potentially neuroexcitotoxic compound, is thought to be the transmitter of the
corticospinal tracts and certain spinal cord interneurons. A systemic defect in the metabolism of this
amino acid may underlie primary ALS.
Abnormal glutamate metabolism in amyotrophic lateral sclerosis.
Plaitakis A, Caroscio JT.
Ann Neurol. 1987 Nov;22(5):575-9.
MSG and the Alteration of the brain: a model for
ADHD/Autism
The Erb Hypothesis:
Attention Deficit Disorder, Attention Deficit Hyper Active Disorder, Asperger’s
Syndrome and Autism are linked. They strike the same percentage of males vs females
and have similar characteristic traits. The Erb hypothesis published in 2003 states that
Monsodium Glutamate as a food and vaccine additive triggers unchecked brain cell
growth. This results in an overgrowth of certain areas of the brain rendering them
damaged or destroyed, while accelerating the development of other areas (hence
Savants). The genetics and level of MSG exposure determines what level a child will
be: ADD, ADHD, Asperger’s or Autism.
Autism (or autistic like behaviors) was only known in a handful cases world wide in
1940. ADHD and Autism did not even exist as a diagnosis. In 1950 MSG was
introduced to the food supply and the growth of these syndromes has matched the
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
19
increase in MSG intake in the western diet. As of 2006 there is reported to be one in
every hundred children now being born with Autism in the United States.
One of the main characteristics of Autism is a heavier brain. The theory of Mercury
causing Autism does not explain the brain overgrowth. Mercury does not enhance cell
tissue growth.
In the first 8 weeks of fetal growth the placental barrier is not yet fully formed. This
period is when the brain stem, brain, and eyes begin to form.
12 grams a day of MSG in a mother’s blood stream could have an enormous affect on
the fetal development. Even after the placental barrier has been formed there is not a
single human study to show that MSG does not easily transport into the fetus.
Children not born with these ADHD and Autism may have them triggered when an
MSG bearing vaccine is injected subcutaneously into them during their formative years.
Accelerated and abnormal brain growth in the Autistic:
Autism most commonly appears by 2 to 3 years of life, at which time the brain is already
abnormally large. This raises the possibility that brain overgrowth begins much earlier, perhaps
before the first clinically noticeable behavioral symptoms. OBJECTIVES: To determine whether
pathological brain overgrowth precedes the first clinical signs of autism spectrum disorder (ASD)
and whether the rate of overgrowth during the first year is related to neuroanatomical and clinical
outcome in early childhood. Within the ASD group, every child with autistic disorder had a greater
increase in HC between birth and 6 to 14 months (mean [SD], 2.19 [0.98]) than infants with
pervasive developmental disorder-not otherwise specified (0.58 [0.35]). Only 6% of the individual
healthy infants in the longitudinal data showed accelerated HC growth trajectories (>2.0 SDs) from
birth to 6 to 14 months; 59% of infants with autistic disorder showed these accelerated growth
trajectories. CONCLUSIONS: The clinical onset of autism appears to be preceded by 2 phases
of brain growth abnormality: a reduced head size at birth and a sudden and excessive
increase in head size between 1 to 2 months and 6 to 14 months. Abnormally accelerated rate
of growth may serve as an early warning signal of risk for autism.
Evidence of brain overgrowth in the first year of life in autism.
Courchesne E, Carper R, Akshoomoff N.
JAMA. 2003 Jul 16;290(3):393-4.
To establish whether high-functioning children with autism spectrum disorder (ASD) have
enlarged brains in later childhood, and if so, whether this enlargement is confined to the gray
and/or to the white matter and whether it is global or more prominent in specific brain regions.
RESULTS: Patients showed a significant increase of 6% in intracranium, total brain, cerebral gray
matter, cerebellum, and of more than 40% in lateral and third ventricles compared to controls. The
cortical gray-matter volume was evenly affected in all lobes. After correction for brain volume,
ventricular volumes remained significantly larger in patients. CONCLUSIONS: High-functioning
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
20
children with ASD showed a global increase in gray-matter, but not white-matter and cerebellar
volume, proportional to the increase in brain volume, and a disproportional increase in ventricular
volumes, still present after correction for brain volume.
Increased gray-matter volume in medication-naive high-functioning children with autism spectrum disorder.
Palmen SJ, Hulshoff Pol HE, Kemner C, Schnack HG, Durston S, Lahuis BE, Kahn RS, Van Engeland H.
Psychol Med. 2005 Apr;35(4):561-70.
Possible vaccine connection with Autism:
Virus-induced autoimmunity may play a causal role in autism. To examine the etiologic link of
viruses in this brain disorder, we conducted a serologic study of measles virus, mumps virus, and
rubella virus. Viral antibodies were measured by enzyme-linked immunosorbent assay in the serum
of autistic children, normal children, and siblings of autistic children. The level of measles
antibody, but not mumps or rubella antibodies, was significantly higher in autistic children as
compared with normal children (P = 0.003) or siblings of autistic children (P <or= 0.0001).
Furthermore, immunoblotting of measles vaccine virus revealed that the antibody was directed
against a protein of approximately 74 kd molecular weight. The antibody to this antigen was found
in 83% of autistic children but not in normal children or siblings of autistic children. Thus autistic
children have a hyperimmune response to measles virus, which in the absence of a wild type
of measles infection might be a sign of an abnormal immune reaction to the vaccine strain or
virus reactivation.
Elevated levels of measles antibodies in children with autism.
Singh VK, Jensen RL.
Pediatr Neurol. 2003 Apr;28(4):292-4
MSG proven to accelerate the growth of neurons and stimulate
proliferation:
“It has been widely accepted that neurogenesis continues throughout life. Neural stem cells can be
found in the ventricular zone of the embryonic and in restricted regions of the adult central nervous
system, including subventricular and subgranular zones of the hippocampal dentate gyrus. The
network of signaling mechanisms determining whether neural stem cells remain in a proliferative
state or differentiate is only partly discovered. Recent advances indicate that glutamate (Glu),
the predominant excitatory neurotransmitter in mature neurons, can influence immature
neural cell proliferation and differentiation, as well., Glu can influence proliferation and
neuronal commitment as well, and acts as a positive regulator of neurogenesis. Brain injuries like
ischemia, epilepsy or stress lead to severe neuronal death and additionally, influence neurogenesis,
as well. Glu homeostasis is altered under these pathological circumstances, implying that
therapeutic treatments mediating Glu signaling might be useful to increase neuronal replacement
after cell loss in the brain.”
Glutamate as a modulator of embryonic and adult neurogenesis.
Schlett K.
Curr Top Med Chem. 2006;6(10):949-60.
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
21
Conclusions
There are few chemicals that we as a people are exposed to that have as many far
reaching physiological affects on living beings as Monosodium Glutamate does. MSG
directly causes obesity, diabetes, triggers epilepsy, destroys eye tissues, is genotoxic in
many organs and is the probable cause of ADHD and Autism. Considering that MSG’s
only reported role in food is that of ‘flavour enhancer’ is that use worth the risk of the
myriad of physical ailments associated with it? Does the public really want to be
tricked into eating more food and faster by a food additive?
MSG is entering our bodies in record amounts with absolutely no limits. The studies
outlined in this report often use a smaller proportional dosage than the average child
may ingest daily.
A handful of studies prompted an immediate task force on Acrylamide. This report
contains dozens of published studies showing proven damage to the mammalian body
across a plethora of physiological systems.
Consider the children of the world who eat MSG in their school cafeterias, hospitals,
restaurants and homes. They deserve foods free of added MSG, a substance so toxic
that scientists use it purposely to trigger diabetes, obesity and epileptic convulsions.
Consider the swift deletion of MSG from the GFSA list of the Codex Alimentarius.
Perhaps we will see a reduction in obesity, diabetes, ADHD and Autism once the excess
Glutamate threat to our health has been removed.
We can stop the slow poisoning of mankind.
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
22
Appendix A List of Foods Approved for MSG Addition
01.1.2 Dairy-based drinks, flavoured and/or fermented (e.g., chocolate milk, cocoa, eggnog,
drinking yoghurt, whey-based drinks) 01.3 Condensed milk and analogues (plain) 01.4.3 Clotted
cream (plain) 01.4.4 Cream analogues 01.5 Milk powder and cream powder and powder
analogues (plain) 01.6 Cheese and analogues 01.7 Dairy-based desserts (e.g., pudding, fruit or
flavoured yoghurt) 01.8 Whey and whey products, excluding whey cheeses 02.2.1.2 Margarine
and similar products 02.2.1.3 Blends of butter and margarine 02.2.2 Emulsions containing less
than 80% fat 02.3 Fat emulsions maily of type oil-in-water, including mixed and/or flavoured
products based on fat emulsions 02.4 Fat-based desserts excluding dairy-based dessert products of
food category 01.7 03.0 Edible ices, including sherbet and sorbet 04.1.2 Processed fruit
04.2.2.2 Dried vegetables (including mushrooms and fungi, roots and tubers, pulses and legumes,
and aloe vera), seaweeds, and nuts and seeds 04.2.2.3 Vegetables (including mushrooms and fungi,
roots and tubers, pulses and legumes, and aloe vera) and seaweeds in vinegar, oil, brine, or soy sauce
04.2.2.4 Canned or bottled (pasteurized) or retort pouch vegetables (including mushrooms and
fungi, roots and tubers, pulses and legumes, and aloe vera), and seaweeds 04.2.2.5 Vegetable
(including mushrooms and fungi, roots and tubers, pulses and legumes, and aloe vera), seaweed, and
nut and seed purees and spreads (e.g., peanut butter) 04.2.2.6 Vegetable (including mushrooms and
fungi, roots and tubers, pulses and legumes, and aloe vera), seaweed, and nut and seed pulps and
preparations (e.g., vegetable desserts and sauces, candied vegetables) other than food category
04.2.2.5 04.2.2.8 Cooked or fried vegetables (including mushrooms and fungi, roots and tubers,
pulses and legumes, and aloe vera), and seaweeds 05.0 Confectionery 06.3 Breakfast cereals,
including rolled oats 06.4.3 Pre-cooked pastas and noodles and like products 06.5 Cereal and
starch based desserts (e.g., rice pudding, tapioca pudding) 06.6 Batters (e.g., for breading or batters
for fish or poultry) 06.7 Pre-cooked or processed rice products, including rice cakes (Oriental type
only) 06.8 Soybean products (excluding soybean products of food category 12.9 and fermented
soybean products of food category 12.10) 07.0 Bakery wares 08.2 Processed meat, poultry, and
game products in whole pieces or cuts 08.3 Processed comminuted meat, poultry, and game
products 08.4 Edible casings (e.g., sausage casings) 09.3 Semi-preserved fish and fish products,
including mollusks, crustaceans, and echinoderms 09.4 Fully preserved, including canned or
fermented fish and fish products, including mollusks, crustaceans, and echinoderms 10.2.3 Dried
and/or heat coagulated egg products 10.3 Preserved eggs, including alkaline, salted, and canned
eggs 10.4 Egg-based desserts (e.g., custard) 11.6 Table-top sweeteners, including those
containing high-intensity sweeteners 12.2.2 Seasonings and condiments 12.3 Vinegars 12.4
Mustards 12.5 Soups and broths 12.6 Sauces and like products 12.7 Salads (e.g., macaroni
salad, potato salad) and sandwich spreads excluding cocoa- and nut-based spreads of food categories
04.2.2.5 and 05.1.3 12.8 Yeast and like products 12.9 Protein products 12.10 Fermented
soybean products 13.3 Dietetic foods intended for special medical purposes (excluding products of
food category 13.1) 13.4 Dietetic formulae for slimming purposes and weight reduction 13.5
Dietetic foods (e.g., supplementary foods for dietary use) excluding products of food categories 13.1 -
13.4 and 13.6 13.6 Food supplements 14.1.1.2 Table waters and soda waters 14.1.4 Waterbased
flavoured drinks, including "sport," "energy," or "electrolyte" drinks and particulated drinks
14.2.1 Beer and malt beverages 14.2.2 Cider and perry 14.2.4 Wines (other than grape)
14.2.5 Mead 14.2.6 Distilled spirituous beverages containing more than 15% alcohol 14.2.7
Aromatized alcoholic beverages (e.g., beer, wine and spirituous cooler-type beverages, low alcoholic
refreshers) 15.0 Ready-to-eat savouries 16.0 Composite foods - foods that could not be placed in
categories 01 - 15
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
23
Appendix B List of Ingredients
Involving MSG
These contain Monosodium Glutamate
Glutamate Glutamic acid Gelatin
Monosodium glutamate Calcium caseinate Textured protein
Monopotassium
glutamate
Sodium caseinate Yeast nutrient
Yeast extract Yeast food Autolyzed yeast
Hydrolyzed protein
(any protein that is
hydrolyzed)
Hydrolyzed corn gluten Natrium glutamate
(natrium is Latin/German
for sodium)
These OFTEN contain MSG or create MSG during processing
Carrageenan Maltodextrin Malt extract
Natural pork flavoring Citric acid Malt flavoring
Bouillon and Broth Natural chicken
flavoring
Soy protein isolate
Natural beef flavoring Ultra-pasteurized Soy sauce
Stock Barley malt Soy sauce extract
Whey protein
concentrate
Pectin Soy protein
Whey protein Protease Soy protein concentrate
Whey protein isolate Protease enzymes Anything protein fortified
Flavors(s) & Flavoring(s) Anything enzyme
modified
Anything fermented
Natural flavor(s)
& flavoring(s)
Enzymes anything Seasonings
(the word "seasonings")
In ADDITION...
The new practice is to label hydrolyzed proteins as pea protein, whey protein, corn protein, etc.
If a pea, for example, were whole, it would be identified as a pea. Calling an ingredient pea
protein indicates that the pea has been hydrolyzed, at least in part, and that processed free
glutamic acid (MSG) is present. Relatively new to the list are wheat protein and soy protein.
List from www.truthinlabeling.org
John Erb Report on Monosodium Glutamate Presented to the WHO August 2006
24
Appendix C List of Vaccines Involving MSG
Note: Gelatin and ingredients that use the word Hydrolyzed contain Glutamate.
MMR - Measles-Mumps-Rubella Merck & Co., Inc. 800.672.6372
measles, mumps, rubella live virus, neomycin sorbitol, hydrolyzed gelatin, chick embryonic fluid, and
human diploid cells from aborted fetal tissue
M-R-Vax - Measles-Rubella Merck & Co., Inc. 800.672.6372
measles, rubella live virus neomycin sorbitol hydrolyzed gelatin, chick embryonic fluid, and human
diploid cells from aborted fetal tissue
Attenuvax - Measles Merck & Co., Inc. 800-672-6372
measles live virus neomycin sorbitol hydrolyzed gelatin, chick embryo
Biavax - Rubella Merck & Co., Inc. 800-672-6372
rubella live virus neomycin sorbitol hydrolyzed gelatin, human diploid cells from aborted fetal tissue
JE-VAX - Japanese Ancephalitis Aventis Pasteur USA 800.VACCINE
Nakayama-NIH strain of Japanese encephalitis virus, inactivated formaldehyde, polysorbate 80
(Tween-80), and thimerosal mouse serum proteins, and gelatin
Prevnar Pneumococcal - 7-Valent Conjugate Vaccine Wyeth Lederle 800.934.5556
saccharides from capsular Streptococcus pneumoniae antigens (7 serotypes) individually conjugated
to diphtheria CRM 197 protein aluminum phosphate, ammonium sulfate, soy protein, yeast
RabAvert - Rabies Chiron Behring GmbH & Company 510.655.8729
fixed-virus strain, Flury LEP neomycin, chlortetracycline, and amphotericin B, potassium glutamate,
and sucrose human albumin, bovine gelatin and serum "from source countries known to be free of
bovine spongioform encephalopathy," and chicken protein
RotaShield - Oral Tetravalent Rotavirus (recalled) Wyeth-Ayerst 800.934.5556
1 rhesus monkey rotavirus, 3 rhesus-human reassortant live viruses neomycin sulfate, amphotericin B
potassium monophosphate, potassium diphosphate, sucrose, and monosodium glutamate (MSG)
rhesus monkey fetal diploid cells, and bovine fetal serum smallpox (not licensed due to expiration)
TheraCys BCG (intravesicle -not licensed in US for tuberculosis) Aventis Pasteur USA
800.VACCINE
live attenuated strain of Mycobacterium bovis monosodium glutamate (MSG), and polysorbate 80
(Tween-80)
Varivax - Chickenpox Merck & Co., Inc. 800.672.6372
varicella live virus neomycin phosphate, sucrose, and monosodium glutamate (MSG) processed
gelatin, fetal bovine serum, guinea pig embryo cells, albumin from human blood, and human diploid
cells from aborted fetal tissue
YF-VAX - Yellow Fever Aventis Pasteur USA 800.VACCINE
* 17D strain of yellow fever virus sorbitol chick embryo, and gelatin
 
chickenman

chickenman

Premium Member
Supporter
Lots of reading there, plain and simple avoid, we have for years
 
2hotmomma88

2hotmomma88

Ok my ADD would not allow me to read the second part... damn MSG's but seriously between msg and fluoride in the water some of us are screwed! :banghead: :hungover: :clown: :wacky: :watching: :wideyed:
 
seaslug

seaslug

TLDR;
"If monosodium glutamate (MSG) is as safe as its food industry proponents claim, then why do they consistently labor to hide it from us with deceptive labeling?"

Marketing. The Japanese don't have a problem with it, I've read.
 
dabs4life

dabs4life

duuno much but too much sugar along with all the chemicals sets ppl up for life. i try to eat it raw or throw it in a skillet with garlic and real stuff. that and water. real food and water is a hell of a diet.

my brother swole the fuck up one time with a crazy rash and puss and stuff along with being really sick. they blamed that on maybe being related to msg or they didnt know.

my mother drank diet coke for ever and had seizures that i think are related to the absurd amount of diet coke aspertame she consumed at the time.

use vinegar and h202 to clean germs or bleach if needed no triolscan

use dr bronners soaps to bathe in and shave. i fuckin like the blue pepermint kind. shaves better than shave gel. dip a qtip in the soap to lube the razor head in between goes.
instead of crazy overprices soaps abd stuff that have stuff not needed. plus no chemicals.

ive also used dr bronners to brush my teeth. 50/50 mix of kosher salt baking soda and a small drop on top of the mixture with a small bit of water to make it wet.

use a dab of cologne instead of spraying a fuckin can. loads of chemicals everywhere that do damage. ive been on the same ck pocket bottle for almost two years.
 
urban1026835

urban1026835

jesus, I think anyone that can read through all that is already on the same page you are.
 
jumpincactus

jumpincactus

Premium Member
Supporter
jesus, I think anyone that can read through all that is already on the same page you are.
Ya farmers I get it. I lost attention span after the 1st article. I just felt it was my duty somehow to throw it out there just in case someone may be helped.

The damnest part of the whole thing is it all seems to be like a web. All of the parts are connected. On 1 side we have the food and big agra making billions and then the medical industry makes bank cleaning the mess up. Some kind of system going on. This kind of crap really trips me out. Really hard for me at times not to become jaded and stay positive. Like my buddy Dabll Do says aint nothing going on in my life today that a Dab wont fix.....LOL

Thanks for popping in boys and girls. Much love from the desert.
 
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