Monosodium Glutmate: Creating Dumb, Obese, Brain Cell Fried Citizens and Children...

Monosodium Glutmate: excitotoxin; CNS toxin


This substance is used as a binder in vaccinations, but what makes it fascinating to be included in immunizations is that it's primary use in the modern world is as a flavor enhancer. There have been literally hundreds upon hundreds of scientific studies concluding that MSG is a potent excitotoxin, yet this substance continues to be used not only in vaccinations but in food and beverages we consume on the regular here in the United States. If you thought the FDA had your best interests in mind in general, read a little bit about the blatantly excitotoxic monosodium glutamate that our government is allowing to run rampant in our food supply and our vaccinations!

http://www.modern-diets-and-nutritional-diseases.com/monosodium-glutamate.html

Toxicity of Monosodium Glutamate

This series of pages is a difficult one to write. The information about free glutamic acid and other excitotoxins is very interesting, but includes a lot of scientific detail. One source is a book entitled EXCITOTOXINS The Taste that Kills by Russell L. Blaylock, M.D., a neurosurgeon. It is documented by almost 500 references in the scientific literature. He claims to have picked up on this subject from John W. Olney M.D., also a neurosurgeon, whom he quoted as follows.

"Thus, today we are witnessing an ironic situation; while knowledgeable neuroscientists are fervently attempting to develop methods for protecting CNS [brain] neurons against neurotoxic potential of endogenous (within the body) Glu [glutamate] and Asp [aspartate], other elements of society are vigorously promoting the unlimited use of exogenous (free) Glu and Asp."

In the brain the amino acid glutamate is a neurotransmitter and is present in controlled low concentrations. When found in proteins with other amino acids they are bound and not free. It has been shown that these free amino acid taste enhancers, can produce significant damage to the brain.

Dr. Blaylock’s book was copyrighted in 1997. Although the volume of research, and literature, is overwhelming to followers of this debate, there is little evidence that the industry producing these toxins is being reigned in at all. Consumers are still being taken in to the delight, I guess, of the industry and their supporters, and their profits.

Consumers may not realize that many medical researchers are strongly opposed to efforts of the excitotoxin producing industry.

Another source of information on the dangers of excitotoxins, free Glutamate, Aspartate, and others, is the supporters of www.truthinlableing.org. This website was begun by a couple, one of whom, is allergic to MSG. Their deep involvement led to the discovery of the government’s support of the excitotoxin industry. The government has seemed to work hand-in-glove with heavy handed and underhanded efforts by the excitotoxin producing industry to discredit research showing the damage free Glutamate and Aspartate, and other excitotoxins, can do to the brain. The government has also been instrumental in helping the industry hide from the public, including those who have serious reactions to excitotoxins, the presence of these substances.

http://www.cbn.com/CBNnews/107774.aspx

Headache specialist Dr. David Buchholz is certain that MSG causes migraines for literally millions of people: Buchholz said, "That's exactly right. It's an excitotoxin, and it turns on this headache mechanism and makes you hurt like heck."

An excitotoxin is any substance that overexcites cells to the point of damage -- it acts as a toxin.
And there may be more to this public poison.

MSG can directly worsen autism, attention deficit disorder, and hyperactivity.

And MSG can cause the brain to be mis-wired, especially in the womb and the first few years of life.

That damage to brain connections can mess up nearly any aspect of brain function, from the control of hormones to behavior and intelligence.

That's what happens with infant mice.

After being fed MSG, they show no signs of mental damage -- until they're older and begin to fail at complex tasks.

Bluntly put, they become stupid.

And humans are five times more sensitive to MSG than mice -- infants even more so. Blaylock believes the entire education system suffers as a result, even the ability to for students to get along with each other.

Blaylock said, "So the brain is still forming its connections, particularly the most important social part of our brain, the prefrontal cortex, continues up to age 25, 26, even 27."

http://www.holisticmed.com/msg/TheErbreportonMSGtotheWHO.pdf

A lengthy pdf file on the risks of monosodium glutamate, also addresses the issue of them in vaccinations. A worthwhile read!

http://curezone.com/foods/msg.asp

This information is found in the book by George R. Schwartz, MD a noted toxicologist, "In Bad Taste, the MSG Syndrome".

MSG has been found to be more toxic than all other food toxins, poisons and allergens.

Patients have stronger reactions to MSG than arsenic or mercury.

MSG is pervasively hidden under other names and aliases so as to go undetected.

MSG is a sodium salt of Glutamic Acid, an amino acid and is a drug.

It acts as an excitatory neurotransmitter. It basically causes the nerve cells to discharge an electrical impulse and that's the basis of its use as a flavor enhancer. Food companies learned that MSG could increase the flavor and aroma and enhance acceptability of commercial food products.

Equally important they learned that it could also suppress undesirable or "off" flavors, bitterness, and sourness and eliminated the "tinny" taste of canned foods. This is the reason food companies in general have no intention of giving up MSG as an additive in their products.USA national consumption of MSG went from roughly one million pounds in 1950 to 300 times that amount today.

http://www.jpands.org/hacienda/article27.html

Some medical journal references on the excitotoxic, brain neuron damaging effects of monosodium glutamate. This list was published in: the Medical Sentinel 1999;4(6):212-215


1. Ikonomidou C, Turski L. Glutamate in neurodegenerative disorders, in Stone TW (Ed.), Neurotransmitters and Neuromodulators: Glutamate. CRC Press, Boca Raton, 1995, pp. 253-272.

2. Whetsell WO, Shapira NA. Biology of Disease. Neuroexcitation, excitotoxicity and human neurological disease. Lab Invest 1993;68:372-387.

3. Lucas DR, Newhouse JP. The toxic effect of sodium L-glutamate on the inner layer of the retina. Arch Ophthalmol 1957;58:193-201.

4. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science 1969;165:719-721.

5. Pol ANV, Wuarin J-P, Dudek E. Glutamate, the dominate excitatory transmitter in neuroendocrine regulation. Science 1990;250:1276-1278.

6. Coyle JT, et al. Excitatory Amino Acid Neurotoxins: Selectivity, Specificity, and Mechanisms of Action. Neurosci Research Bull 1981;19(4).

7. Blackstone CD, Huganir RL. Molecular structure of Glutamate Receptor Channels, in Stone TW (Ed), CNS Neurotransmitters and neuromodulators: Glutamate. CRC Press, Boca Raton, 1995, pp. 53-67.

8. Analysis of Adverse Reactions to Monosodium Glutamate (MSG). Life Sciences Research Office, FASEB, July 1995.

9. Blaylock RL. Excitotoxins: The Taste That Kills. Health Press, Santa Fe, NM, 1997, pp. 248-254.

10. Dawson R, Simpkins JW, Wallace DR. Age and dose-dependent effects of neonatal monosodium glutamate (MSG) administration to female rats. Neurotox Teratol 1989;11:331-337.

11. Dawson R. Acute and long lasting neurochemical effects of monosodium glutamate administration to mice. Neuropharmacology 1983;22:1417-1419.

12. Olney JW. Glutamate: a neurotoxic transmitter. J Child Neurol 1989;4:218-226.

13. Choudhary P, Malik VB, et al. Studies on the effect of monosodium glutamate on hepatic microsomal lipid peroxidation, calcium, ascorbic acid and glutathione and its dependent enzymes in adult male mice. Toxicol Lett 1996;89:71-76.

14. Plaitakis A, Caroscio JT. Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann Neuro 1987;22:575-579.

15. Blaylock RL. Neurodegeneration and aging of the central nervous system: Prevention and treatment by phytochemicals and metabolic nutrients. Integrative Med 1998;1:117-133.

16. Olney JW. Excitotoxic food additives: functional teratological aspects. Prog Brain Res 1988;18:283-294.

17. Parsons RB, Waring RH, et al. In vitro effect of the cysteine metabolites homocysteic acid, homocysteine and cysteic acid upon human neuronal cell lines. Neurotoxicology 1998;19:599-603.

18. Esskes TK. Neural tube defects, vitamins and homocysteine. Eur J Pediatr 1998;157:Suppl 2:S139-S141.

19. McCaddon A, Daves G, et al. Total serum homocysteine in senile dementia of Alzheimer type. In J Geriatr Psychiatry 1998;13:235-239.

20. Banks JC, et al. Retinal pathology in Alzheimer's disease. I. Ganglion cell loss in foveal/parafoveal retina. Neurobiol Aging 1996;17:377-384.

21. Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway for neurologic disorders. New Eng J Med 1994;330:613-622.

22. Rodriguez MC, Obeso JA, Olanow CW. Subthalamic nucleus-mediated excitotoxicity in Parkinson's disease: a target for neuroprotection. Ann Neurol 1998;44:(Supp 1) S175-S188.

http://www.truthinlabeling.org/Proof_BrainLesions_CNS.html

THIS IS WHAT THE DATA SAY ABOUT MONOSODIUM GLUTAMATE TOXICITY and the CENTRAL NERVOUS SYSTEM(Compiled by Adrienne Samuels, Ph.D., May, 2009)

Excitotoxins are toxic agents capable of exciting and then poisoning cells or tissues. Two manufactured excitotoxic amino acids are presently used in quantity in processed foods. Glutamic acid (glutamate) is the most prevalent of the excitotoxic amino acids. Glutamate that has been produced through bacterial fermentation or has been freed from protein through a manufacturing process or through fermentation (MSG) will be found in ingredients including, but not limited to, hydrolyzed protein products, autolyzed yeast, calcium caseinate, sodium caseinate, textured vegetable protein, gelatin, ultra-pasteurized products, and monosodium glutamate. It is glutamate as MSG that has been administered or fed to subjects in studies where some form of glutamate produces brain lesions and/or adverse reactions. Glutamate found in intact protein has never been shown to cause brain lesions or adverse reactions.

Retinal degeneration

In 1957, Lucas and Newhouse(26) first noticed that severe retinal lesions could be produced in suckling mice (and to some extent in adult mice) by a single injection of glutamate. Studies confirming their findings using neonatal rodents (49-52) and adult rabbits(53) followed shortly, with others being reported from time to time (54-58). These studies concerned themselves not only with the confirmation of monosodium glutamate induced retinal lesions, but with the formulation and testing of hypotheses to explain the phenomenon.

In 2002, Ohguro et al.(27) found that rats fed 10 grams of sodium glutamate (97.5% sodium glutamate and 2.5% sodium ribonucleotide) added to a 100 gram daily diet for as little as 3 months had a significant increase in amount of glutamic acid in vitreous, had damage to the retina, and had deficits in retinal function.

Ohguro et al. also documented the cumulative effect of damage caused by daily ingestion of MSG.

Other reports of toxic effects of monosodium glutamate have come from studies at the University of Pecs, Hungary, where the neuroprotective effects of PACAP in the retina are being studied(28,29).

Neuronal necrosis -- which can lead to behavior disorders, learning disabilities, reproductive disorders, and obesity.

In this country, at this time, potential poisons are not administered to humans in order to determine if they are toxic or safe. Therefore, what we know about the toxic effects of MSG comes from animal studies. The first relevant studies were done between 1969 and 1980 wherein MSG was administered or fed to animals. By the early 1980s, the neurotoxicity of glutamate was accepted in animal models as glutamate was being used as an ablative and/or provocative tools(122,123), with which suspected pathophysiological abnormalities (obesity, for example) could be deliberately induced to facilitate study.

In evaluating the relevance of these studies to human ingestion of MSG in food, drugs, and dietary supplements, it is essential to understand that the glutamate given to animal subjects is invariably a manufactured product produced in food and/or chemical manufacturing plants. It is glutamate as monosodium glutamate that has been administered or fed to subjects in studies where glutamate from exogenous sources has been shown to cause brain lesions. Glutamate found in intact protein has never been shown to cause brain lesions or adverse reactions.
Lesions in the arcuate nucleus of the hypothalamus of neonatal and infant animals.

In 1957, Lucas and Newhouse(26) first noticed that severe retinal lesions could be produced in suckling mice (and to some extent in adult mice) by a single injection of monosodium glutamate. In the late 60s, Olney(59) became suspicious that obesity in mice, which was observed after neonatal mice were treated with monosodium glutamate for purposes of inducing and studying retinal pathology, might be associated with hypothalamic lesions caused by monosodium glutamate treatment; and in 1969 he first reported that monosodium glutamate treatment did indeed cause brain lesions, particularly acute neuronal necrosis in several regions of the developing brain of neonatal mice, and acute lesions in the brains of adult mice given 5 to 7 mg/g of v subcutaneously(59).

Research that followed confirmed that monosodium glutamate, which was routinely given as the sodium salt, monosodium glutamate (brand name Accent), induces hypothalamic damage when given to immature animals after either subcutaneous(60,61,62,63,64,66,67,68,69,70,71,72,73,74,75,76,77,78,81) or oral(67,73,74,76,82,83,84,85,86 doses.

Work by Lemkey-Johnston and Reynolds(86) published in 1974 included an extensive review of the data on brain lesions in mice. They confirmed the phenomenon of monosodium glutamate induced neurotoxicity; described the sequence of the lesions; and emphasized the critical aspects of species variation, developmental age, route of administration, time of examination of brain material after insult, and thoroughness of tissue sampling methods.

A review of monosodium glutamate induced neurotoxicity, published by Olney in 1976(87), mentioned species (immature mice, rats, rabbits, guinea pigs, chicks, and rhesus monkeys) demonstrating monosodium glutamate induced neurotoxicity, and efficiency of both oral and subcutaneous administration of monosodium glutamate in producing acute neuronal necrosis; discussed the nature and extent of the damage done by monosodium glutamate administration and the impact of monosodium glutamate administration to monosodium glutamate levels in both brain and blood; and discussed the similar neurotoxic effects of a variety of acidic structural analogues.

Studies of sub-human primates were thought to be particularly meaningful because monosodium glutamate toxicity found in laboratory animals might be relevant to humans. As early as 1969, Olney(61) had suggested that monosodium glutamate could be involved in the unexplained brain damage syndromes occurring in the course of human ontogenesis. Olney(61) demonstrated that the infant rhesus monkey (Macaca mulatta) is susceptible to monosodium glutamate-induced brain damage when administered a high dose (2.7g monosodium glutamate/kg of body weight) subcutaneously.

Olney et al.(74) expanded Olney's earlier work with a study of eight additional infant rhesus monkeys and, using light microscopy and the electron microscope, reconfirmed Olney's earlier findings of hypothalamic lesions, and discussed the findings of both Abraham et al.(75) and Reynolds et al.(88) who had questioned his work. Olney found his data to be entirely consistent with studies done previously by his own and other laboratories on all species of animals tested.

Neuroendocrine Disorders

Olney found not only hypothalamic lesions in 1969, but described stunted skeletal development, obesity, and female sterility, as well as a spate of observed pathological changes found in several brain regions associated with endocrine function in maturing mice which had been given monosodium glutamate as neonates(59).

Longitudinal studies in which neonatal/infant animals were given doses of monosodium glutamate and then observed over a period of time before being sacrificed for brain examination, repeatedly supported Olney's early findings of abnormal development, behavioral aberration, and neuroendocrine disorder. Animals treated with monosodium glutamate as neonates or in the first 12 days of life were shown to suffer neuroendocrine disturbances including obesity and stunting, abnormalities of the reproductive system, and underdevelopment of certain endocrine glands (59,68,70,86,88,89,90, 92,93,94,95,96,97,98,99,100,101,102,103,104,105,106) and possible learning deficits either immediately or in later life (92,95, 96,107,108,109,110,112,113).

In addition, there were reports of behavioral reactions including somnolence and seizures (114,115,116,117,119,120,121); tail automutilation (94,108); and learned taste aversion(110). Irritability to touch was interpreted as conspicuous emotional change by Nemeroff(94). Lynch(14) reported hyperglycemia along with growth suppression. He noted that hyperglycemia did not occur when subjects were given intact protein containing a large amount of glutamate.
Olney et al. (122,123,124) have written a number of review articles which summarize the data on neuroendocrine dysfunction following monosodium glutamate treatment. Nemeroff (125) has written another.

Ad libitum feeding studies

Findings of neurotoxicity and neuroendocrine dysfunction in laboratory animals raised questions about the effects that monosodium glutamate might have on humans. Since it would be unthinkable to administer doses of monosodium glutamate that might produce the same sorts of neurotoxicity and neuroendocrine dysfunction as found in laboratory animals, researchers had no alternative but to make decisions based on the best of the animal studies. "Best," in this case, would be studies that would most closely parallel the true human condition.

At the time, a seemingly logical first step was to study the effects of monosodium glutamate on subhuman primates; and, as already noted, hypothalamic lesions had been demonstrated in monkeys as early as 1969(61). A seemingly logical second step was to study "normal" ingestion of monosodium glutamate as opposed to some kind of forced feeding. Many felt that ad libitum feeding of laboratory animals parallels the human situation more closely than either subcutaneous or gavage administration of monosodium glutamate, and that ad libitum feeding studies were, therefore, the vehicle of choice. Ad libitum feeding would give animals free access to feed or water thereby allowing the animal to self-regulate intake. Some tended to disagree, feeling that the ad libitum feeding studies were, by and large, studies that had the greatest potential for minimizing the amount of monosodium glutamate actually ingested while registering the irrelevant amount of monosodium glutamate available.

Two studies that demonstrate neurotoxic reactions after ad libitum feeding of monosodium glutamate are reported here. In a 1979 study done as part of a project designed to evaluate a developmental test battery for neurobehavioral toxicity in rats, in which rats were exposed to monosodium glutamate and other food additives mixed with ground Purina rat chow beginning five days after arrival at the laboratory(109), it was demonstrated that high doses of dietary monosodium glutamate produce behavioral variations. Monosodium glutamate was mixed with food as opposed to being administered subcutaneously or by gavage. A year later, dietary studies demonstrated that weanling mice will voluntarily ingest monosodium glutamate and that such voluntary ingestion results in readily detectable brain damage (127).

Focus on Older Animals

Most studies demonstrating retinal necrosis, brain lesions and/or neuroendocrine dysfunction, focused on neonatal or infant animals. Researchers were primarily interested in producing lesions in order to expand their knowledge of brain function; and lesions were most easily produced in the young. It was, however, also of scientific interest to understand the relationship of age of animal to type and severity of lesion or dysfunction. Thus, older animals were studied, but not to the same extent as the young.

Hypothalamic lesions have been produced in adult animals using considerably greater doses of monosodium glutamate than those required to produce lesions in younger animals. Nemeroff(125) reported that the least effective dose for a ten day old mouse, given orally, is .5g/kg of body weight, and given subcutaneously is .35g/kg of body weight. According to Olney(128) the dose required to damage the adult rodent brain is given as 1.5-2 mg/g of body weight as compared to 0.3-0.5mg/g required to damage the brain of an infant rodent. Only minimal damage is induced unless very high doses (4-8 mg/g) are used(123).

Although advances in technology have facilitated the observation of brain lesions to some extent, it is still true today, as it was in the 1960s, that simple light microscopes are adequate to identifying monosodium glutamate induced lesions if one looks in sensitive locations within 4-5 hours of monosodium glutamate administration. By 24 hours after insult, lesions will be filled in ("healed") with cells other than neurons. Thus the "hole" is filled in, but lost neurons are not replaced. The damage will have been done, but will be virtually impossible to see. Although it is now possible under optimal circumstances to count neurons in well defined areas, the arcuate nucleus of the hypothalamus is not a well defined area, and lesions in that area will defy detection after as little as 24 hours after monosodium glutamate administration. One could not, therefore, ascertain whether or not an adult animal given monosodium glutamate as an infant, had suffered a lesion in the arcuate nucleus.

Industry's response

Not all studies reported brain damage following administration or ingestion of monosodium glutamate. Adamo and Ratner(131) and Oser et al.(132) failed to reproduce findings of neurotoxicity affecting the brains of non-primates. Adamo and Ratner(131) used rats, not mice as Olney(59) had, but maintained that otherwise the experimental approach used was "very similar." Oser et al.(132) studied mice, rats, and beagles (dogs). Although their methodology varied considerably from Olney's, they concluded that they could "...offer no explanation for the fact that [their]...observations...do not confirm those of Olney...."

Arees and Mayer(64) reproduced Olney's(56,59,61) findings only in part. Their discussion focused more on the question of human consumption of monosodium glutamate as food than on reasons for differences between the various studies.

All three of these negative studies were refuted by both Olney(60,133) and Burde(73) who independently reviewed the literature and found that these early discrepancies could be attributed to: 1) failure on the part of investigators to attempt to replicate Olney's methods; and 2) use by investigators of entirely different (and inappropriate) methods of preservation and staining of brain tissue in the analysis of results.

Burde(73) speculated that the method of fixation and staining used by Adamo and Ratner(131) obscured the existence of the lesion, and noted that their dose schedule was not appropriate; that Oser et al.(132) used a minimal effective dose and did not examine the rats and mice until 24 hours after insult, even though it was known that by 24 hours after insult, in a minimal dose, such as the one used by Oser, which would produce edema, all signs of edema would have disappeared, and that necrotic cells would already have been phagocytized. Burde found the interpretation by Arees and Mayer,(64) that the lesion produced by monosodium glutamate is limited to "microglia," to be puzzling, particularly in light of the fact that most of the cells of the arcuate nucleus are known to be small neurons. Furthermore, using Olney's exact methods, Burde(73) replicated Olney's previous findings.

Olney's(60) review of the discrepancies, pointed out that the failure of Oser et al.(132) to detect brain damage in any of the three species they studied might be accounted for by their having limited the monosodium glutamate dose to a single, minimally effective dosage; failure to use a feeding tube to assure that the full dose was received by orally treated animals; failure to examine brains in appropriate post treatment intervals (which are particularly relevant in cases of minimal effective dosage); and use of relatively unrefined techniques for tissue preparation.
Olney(60) also noted that in a 1971 study done by Arees et al. (58) the authors were able to demonstrate that neuronal degeneration does occur in the infant mouse brain following subcutaneous treatment with monosodium glutamate. Thus the discrepancies noted by Arees and Mayer previously(64) became resolved.

Finally, Olney(60,133) suggested that methodological variables might well explain the failure of Adamo and Ratner(131) to demonstrate lesions in the rat.

The subject of tissue preparation has been addressed by a number of people. Takasaki(69) stated it clearly: "...changes disappeared at least 24...[hours] after injection....The results should be borne in mind when histological examination is performed on changes of the hypothalamus caused by administration with MSG. It is [especially] so in animals administered with a small dose of MSG, because necrotic neurons are few and the glial reaction that occurs secondarily is very mild in the AN [arcuate nucleus]. Without punctual preparation after administration, the effect upon the hypothalamus is apt to be overlooked in these animals"(69).

Olney(67,81,133,134) and Murakami(135) have discussed the problem in similar terms. Olney(67) has discussed such methodological problems in great detail.

In 1973, Filer and Stegink(136) published an editorial in the New England Journal of Medicine that suggested that the neurotoxic effects of monosodium glutamate and its related amino acids, aspartate and cysteine, in species other than the mouse, are debatable. In turn, Olney et al.(137) pointed out that neurotoxic effects of monosodium glutamate and its related amino acids had been well documented, and that the "null effect" reported by Filer and Stegink was a function of faulty methodology, not strain specificity--a fact which had been pointed out earlier by Burde(71,74). Olney noted that Filer and Stegink supported their argument by pointing out that no neurotoxic effects of monosodium glutamate had been reported in the guinea pig, which was, at the time, an unstudied species. Olney further reviewed the criticisms of his own research proffered by Filer and Stegink and suggested that a more careful reading of the research as presented would resolve their concerns.

There were other studies that failed to confirm toxic effects of monosodium glutamate, and there were criticisms of Olney's work. Abraham(75), mentioned earlier, found toxic effects when monosodium glutamate administration was subcutaneous, but very little when administration was oral.

Lowe(138) criticized Olney(61) for failure to provide data on plasma monosodium glutamate concentrations, and for lack of a control in his single infant monkey study. Zavon(139) criticized Olney for lack of a control animal and for lack of detail in reporting the same study. Olney(140) responded to both Lowe and Zavon with detail gathered from mouse studies and an apology that he had had only the one monkey available at the time of his study. Blood et al. (141) criticized Olney (59) for questioning the safety of monosodium glutamate after parenteral, as opposed to oral, administration; failure to clearly elucidate his methodology; and use of doses which far exceeded Blood et al.'s estimate of "...the total daily intake [of glutamate] from all reasonably possible uses... (.7 g per day) in an average adult"(141).

Olney(142), in reply to Blood et al.(141), provided the figures requested, and suggested that to truly establish the safety of monosodium glutamate if, indeed, that could be done, solid research was needed.

Two studies took exception to Olney's finding of hypothalamic lesion in sub-human primates due to loading of monosodium glutamate. Abraham et al.(75) treated four monkeys and failed to reproduce the findings of Olney and Sharpe(61). Reynolds et al.(88,144) treated 16 sub-human primates which were compared to five controls. They, too, failed to reproduce the findings of Olney and Sharpe(61), and found, instead, a "spectrum of degenerative changes" which they attributed to inadequate fixation procedures rather than to the effects of monosodium glutamate.

Olney(74) noted that elements of the research design and methodology of Abraham et al.(75) and Reynolds et al.(88,139,140) distinguished their study from his. Reynolds et al. used only a spot sampling technique when two of the rhesus infants, each treated with low oral doses of monosodium glutamate, were examined by electron microscopy, so the possible occurrence of small lesions in these brains was not actually ruled out. In addition, the method used for preparation of brains for examination by light microscopy has been found unsatisfactory for evaluating even large monosodium glutamate-induced lesions in infant rodent brains; and subsequent information provided by Reynolds indicated that some of the infants vomited an unknown portion of the administered dose.

Abraham et al.(75) supported their findings with a single light micrograph from a rhesus infant sacrificed 24 hours following oral intake of an emetic dose (4 g/kg of body weight) of monosodium glutamate, although four monkeys were studied. Moreover, little or no evidence of lesion would be expected 24 hours after monosodium glutamate insult because damaged elements are removed from the scene of an monosodium glutamate-induced lesion with such remarkable efficiency, that 24 hours after insult, without pre- and post-insult comparison, it is virtually impossible to determine if damage has been done. In general, Abraham's work appears to be vulnerable to the criticism that he maintains that he is replicating work done by Olney, but does not do so. A careful comparison of the two studies will demonstrate that age of subject, dosage administered, time between insult and examination of tissue, and methods of tissue preparation all differ. Abraham's study can also be criticized for use of methodology known to be inappropriate for identifying monosodium glutamate lesions. Finally, it was also noted by Nemeroff(125) that Abraham et al.(75) found in both control and monosodium glutamate treated monkeys a "very small proportion of necrotic or damaged neuronal cells and oligodendrocytes...in the arcuate nuclear region of the hypothalamus." One might suspect that this might happen if the placebo, as well as the test material, contained small amounts of an excitotoxin identical, or similar to, monosodium glutamate.

Also failing to reproduce neurotoxicity in primates, were studies of Abraham et al.(145), Newman et al.(146), and Stegink et al.(147). Stegink et al.(147) used the same data as Reynolds et al.(88,139,140) with two additional monkeys, and used the same methodology for tissue staining. His work, then, is subject to the same criticisms as hers. Abraham et al. stated that their present investigation was undertaken in an attempt to resolve some aspects of the controversy. However, the details of this methodology were identical to those of their earlier study(75) and are subject to the same criticisms.

Newman et al.(146) found "...no evidence in any instance of any change that could be attributed to MSG as described by Olney and Sharpe, although there were artifacts in some inadequately fixed areas as recorded by Reynolds and her co-workers." The initial study was carried out with animals of 108, 99, 60, and 3 days, with unspecified histories. Information pertaining to the animals is incomplete. Their history is uncertain. There is no information pertaining to the first 108 days of an animal's life. Quoting from the research report: "Rhesus monkeys were maintained and observed in the primate buildings of HRC, where most of them were bred." "The test solution was readily consumed voluntarily by all animals on all occasions throughout the study;" "The 3-day-old monkey had a few hypochromatic nuclei, and a minimal degree of vacuolation in the ventral hypothalamus, but these findings were not regarded as significant." "By electron microscopy, changes of the type reported by Olney and Sharpe were seen in both test and control animals, and were attributed to fixation artefact." (Emphasis added.)

In a 1976 study by Reynolds et al.(148) which produced negative results relative to abnormalities of the subinfundibular region of the monkey brain, both mice and monkeys were studied. Mice, but not monkeys, were reported to show brain lesions. The monkeys were infant macaques with age ranging between 30 minutes and 14 days. It is of interest (and concern) to note that the cross section presented in Figure 4 of "...a 7-day-old infant Macaca fascicularis monkey that ingested 4 g/kg monosodium glutamate..." appears, in every aspect, to be identical to a section of an "...infant rhesus monkey which received 4 g/kg of monosodium glutamate by stomach tube..." presented in Figure 3 of the report by Stegink et al.(147) The monosodium glutamate in Reynolds et al. study was prepared as a 20% w/v solution in water and administered as a single dose of as much as 4 g/kg monosodium glutamate.

It was reported that monkeys received various doses, but dosage by age was not given. The techniques for evaluation of mouse brains is the same used by Lemkey-Johnston and Reynolds(86) and Reynolds et al.(88) in previously reported studies. These had been found by Olney(74) to be inappropriate. No information is given about the timing involved or the techniques used for evaluation of monkey brains. Reynolds concludes, "Neither aspartame nor MSG is capable of eliciting a lesion in the neonatal monkey brain." (Emphasis added.)

In failing to replicate Olney's methods, researchers used entirely different (and inappropriate) methods of preservation and staining of brain tissue in analysis of results; limited the monosodium glutamate dose to a single, minimally effective dosage; failed to use a feeding tube to assure that the full dose was received by orally treated animals; and/or failed to examine brains in appropriate post treatment intervals (which are particularly relevant in cases of minimal effective dosage).

Delay in examination of potentially damaged tissue beyond the time that the damage could be observed was common to these studies. Delay in administering or feeding monosodium glutamate to test animals beyond the age that brain damage would most readily be inflicted, would be similarly effective.

A number of the negative studies were ab libitum studies. Ad libitum feeding gives animals free access to feed or water, allowing animals to self-regulate intake, and, therefore, would appeared to closely approximate the human condition. At the same time, the amount of monosodium glutamate actually ingested could be minimized while the amount of monosodium glutamate available (but not necessarily ingested) was reported. Olney(127) pointed out that ad libitum animal studies fall far short of approximating the human condition.

Negative results could also be assured if researchers considered the effect of monosodium glutamate on irrelevant variables, i.e., variables that had never been shown to be associated with monosodium glutamate-induced toxicity. Blood pressure and weight loss are examples. A variation used in studies of adverse reactions (as distinct from brain lesions) would be study of effects of ingestion of monosodium glutamate on plasma glutamate level. Elevated plasma glutamate has been shown to be associated with production of brain lesions, but has never been shown to be relevant to monosodium glutamate-induced adverse reactions. The logical fallacy in these studies comes when it is concluded that finding nothing while studying irrelevant variables proves that monosodium glutamate is safe.

A number of studies used non-relevant levels of otherwise relevant variables. Since females exhibit reproductive disorders and males do not, males, but not females, might be studied. Similarly, if a particular neuroendocrine change would not exhibit itself in less than 20 days following insult with monosodium glutamate, researchers would examine test animals after 15 days.

A number of studies drew conclusions not warranted by their data. Matsuzawa et al.(99) did a series of studies using both neonatal and 10 day old rats, given oral and subcutaneous doses of monosodium glutamate at a total of 4 different doses. Controls were given saline solution. The ad libitum diet was given "...for 10 days after weaning (at 20 days)." By 1979, the date of the study, it was well understood that the timing used was outside of the range of the animal's most susceptible age. Based on this methodology Matsuzawa concluded that "MSG therefore produces marked reproductive endocrine abnormalities after maturation only when injected parenterally early in postnatal life, in repeated, very large doses. The development of reproductive endocrine function is not affected by MSG unless neurological damage occurs in the hypothalamus by any route of administration." (Emphasis added.)

The identical approach was taken by Takasaki et al.(98). They report that, "Adverse effects from MSG have never been reported from dietary administration." (Emphasis added.) In this case, "never" equals four studies. They concluded that "MSG does not exert an adverse effect on somatic growth in that the hypothalamic neurons are not injured by any routes of administration, and the MSG did not induce somatic deficiency under the conditions of our experiments, which mimic the intended conditions of use of this material as a food additive."
Conclusions drawn from these studies are based on negative results. Using inferential statistics, the question raised is whether or not a difference found between two groups of subjects or two sets of measurements could have occurred by chance. If statistical analysis determines that observed differences would rarely have occurred by chance, the investigator would describe those differences as statistically significant, and would specify the probability with which differences of that magnitude would be expected to be reproduced if the experiment were replicated at another time.

In statistical parlance, we would say that the investigator had tested the hypothesis that there would be no difference between two groups (the "null hypothesis"), and had rejected that hypothesis when he found that there was, indeed, a significant difference. The statistical model on which these statistics are based allows the investigator to conclude that it is highly likely (the probability being 95 percent or 99 percent) that differences found were not due to chance. The statistical model does not allow the investigator to conclude that there is no difference between the two groups when a statistically significant difference is not found.

The following examples illustrate the reasoning.

Example 1: Suppose it is known unequivocally from space missions that there is life on Mars, and that all Martians (group 1) have 2 heads. On Thursday an alien spacecraft lands in your back yard, and several aliens emerge (group 2). If the visiting aliens had three heads, we would know that the three-headed aliens were not from Mars, and that there must be life on other planets. (There is clearly a difference between the two groups of aliens.) However if the visiting aliens had two heads (just like the Martians), they might be from Mars, or they might come from another planet. Perhaps there are 2-headed aliens on another planet.

Example 2: Suppose that subjects are given purple dye number 12 or a placebo, and that the numbers of headaches reported by each group are the same. If reports of headache had been significantly greater in the group given purple dye, we could have concluded, with a certain amount of confidence, that purple dye caused headaches. But since reports of headaches were approximately the same for both groups, we would not know what to conclude. It might be that purple dye does not cause headaches. It might have been that subjects were eating something with purple dye in it during the studies, giving the placebo group headaches; or that purple dye only causes headaches in females and all of the subjects were males.

Drawing conclusions based on failure to find a difference (i.e., on failure to reject the null hypothesis) is grossly inappropriate(23,24,25). Given the statistical model, rigorous demonstration of the truth of the null hypothesis (that there is no difference between groups) is a logical impossibility(23).

<>In their 1979 summary of monosodium glutamate toxicity in laboratory animals, Heywood and Worden(149) cite nine chronic animal studies in which various species were given ad libitum feedings of monosodium glutamate over extended periods of time. These include studies by Ebert(150), Owen et al.(151,152), Semprini et al.(153), and Wen et al.(154). Because we have no data on chronic animal studies from persons other than those who have produced negative studise, and, therefore, have no records of positive results, we have no basis for evaluating the levels of variables used in these studies. And because they are incomplete and imprecise in detailing their methodology, it is difficult to evaluate the research, as a whole. Ebert(150,155) apparently used data from a 1953 study done at Arthur D. Little, Inc., entitled, "Report on a study of L-monosodium glutamate, DL monosodium glutamate and L glutamic acid with respect to potential carcinogenicity." His mice were clearly older than Olney's mice(87). The 1970 report of these data(150) was in the form of an abstract. The 1979 reports(155,156) were expanded abstracts done, "...to comply with the suggestion of the Select Committee on GRAS Substances during hearings on glutamates, held at Bethesda, Maryland on July 25-27, 1977"(155).

We know that these studies producing negative results and thereupon claiming to "prove" that monosodium glutamate is a safe food additive, are subject to the limitations of the statistics that they use, and that from the point of view of the statistical model, any conclusion of safety based on failure to find a difference between two groups is invalid. We also know that the procedures of Wen et al.(154) are subject to the same criticisms(60,73,133) as studies by Adamo and Ratner(131).In another 1979 summary of results of dietary administration of monosodium glutamate, Anantharaman(157) stated that studies indicated that "...dietary administration of MSG at even very high doses was not found to result in any of these symptoms [produced by other routes of administration], including the endocrine disturbances." They cited Huang(158), Wen(154), Takasaki(159), Bunyan(160), Owen(151), and Trentini(105). They also cited two year rat studies by Ebert(150) and Owen et al.(151), where no abnormalities were found in successive generations. And in their own study(157), they also produced negative results.

Studies by Owen(151), Takasaki(159), and Wen(154) have already been discussed in some detail. The additional studies mentioned here are subject to previously discussed statistical limitations.

The study reported by Anantharaman(157) must be criticized on additional grounds. Unlike most of the research reported, Anantharaman provides a great deal of detail, including detail of the exact nature of the basal diet provided. And in that basal diet we note that "yeast food" is listed as a component of the protein (page 236, Table 3). When we checked in 1990, yeast food invariably contained either protease (which creates MSG, the toxic component of monosodium glutamate, during manufacture) or L-cysteine which produces neurotoxic effects somewhat different from, but more extensive than, the effects of monosodium glutamate. We are suspicious, then, that the failure to find differences in growth of control and experimental groups may be due to the fact that both groups were receiving neurotoxic substances in their basal diet.

Using inappropriate placebo materials has been discussed by others previously. In 1981, Rippere(161) criticized the use of common food allergens as placebo materials, noting that even a minute trace of an allergen might trigger severe symptoms in a sensitized individual. In a study by Abraham et at.(145) cited earlier, it was noted that the control group exhibited some small evidence of brain damage just as the experimental group did, raising a question of what placebo materials might have been used there. In 1990, this author questioned research done by Goldschmiedt, Redfern, and Feldman(162) which used beef broth as a placebo for controls. In the United States, one cannot purchase commercially prepared beef broth that does not contain some MSG-containing ingredient (hydrolyzed protein, yeast extract, textured vegetable protein, natural flavoring, or monosodium glutamate, for example). This author questioned the possible unwitting bias in placebo material in a letter to the editor of the American Journal of Clinical Nutrition. The letter was not published and no informative reply was received. The author questioned Dr. Feldman about the contents of the placebo. He replied that he did not know the contents of the various materials used.

A 1977 study by Heywood et al.(163) which focused on neurotoxicity, came to the same conclusion as Anantharaman. Heywood et al. concluded from one study of ad libitum feeding of monosodium glutamate over a period of four days, using 20 day old mice that, "There is indeed no evidence from any dietary study yet reported that would suggest a lack of safety of MSG as a food additive." Details of the amounts of monosodium glutamate consumed are not given. In the discussion where it states that "...dose levels as high as 45.5 g [monosodium glutamate]/kg body weight were achieved...", we are not told if that is per day, per animal, or total. Nemeroff(125) noted that their study did not present representative histological micrographs for evaluation(149).

In a second 1979 report, Takasaki et al.(164) again reviewed a number of studies and this time reported that, among other things, "Weanling, pregnant, and lactating mice fed large amounts of MSG in the diet ... did not develop hypothalamic lesions." As evidence they cited studies by Semprini et al.(165), Huang et al.(158), Wen et al.(154), and Takasaki (159). In addition, they reported findings from their own research(164) which compared the effects of monosodium glutamate fed ad libitum to other routes of administration. In their report, they build from a discussion of findings of brain lesions to relationships of lesions to plasma glutamate levels, to relation of ad libitum dietary feeding to plasma monosodium glutamate levels, to histological effects of ad libitum feeding of monosodium glutamate, to the statement that "...plasma glutamate levels... remained much lower than those required to induce hypothalamic lesions." (Emphasis added.) It must be understood that it has never been determined that any particular level of plasma monosodium glutamate is required for the production of brain lesions.
Unfortunately, Takasaki(164) did not provide sufficient detail for one to evaluate the reports, and the reports, themselves, are lacking. Again, it will be observed that Wen(154) appears to have used the same techniques as Adamo and Ratner(131) and Oser(132) which Olney(60,133) and Burde(73) criticized in 1971.

A study by Iwata(108) failed to find behavioral abnormalities as a function of ingestion of monosodium glutamate. Iwata did not examine the brains histologically, yet concluded that there had to be lesion damage prior to there being behavioral effects. Iwata concluded that "...dietary administration... caused no behavioral latent effect in later life." (Emphasis added.)
Prabhu et al.(166) failed to demonstrate differences in a battery of behavioral tests and drug applications. They mentioned that the results are based on surviving mice, but fail to state the mortality rate. Lengvari(167) also reported no differences between control and experimental groups in a number of variables. One must question the meaning of their failure to find a significant difference when they report a mortality rate of 45.1% (to day 30) as opposed to a 20% mortality rate for controls.

Related, but with a slightly different focus, are a pair of studies reported by Takasaki in 1979(84) and 1980(85), in which he studied the effect on brain lesions of administering various materials simultaneously with monosodium glutamate. Takasaki reported that certain mono- and disaccharides and arginine hydrochloride, leucine and the prior injection of insulin significantly reduced the number of necrotic neurons in the arcuate nucleus of the hypothalamus.

In general, the detail provided about the study is incomplete, and the procedure is difficult to follow. It is not clear whether reduction in effect of monosodium glutamate might have been due to inclusion of additional materials, thus diluting the test material. Moreover, statistics pertaining to the values for number of necrosed neurons observed appear to be based on analysis of one representative section from each animal. And values for representative brain sections appearing in Tables 1 and 2(82) have vastly different values (195 +/- 18 and 263 +/- 15) for what would appear should be the same thing. One is compelled to question the meaning of "representative" under these circumstances.

In the research report of Heywood and Worden (149) reports of lesions (or failure to find lesions) were accompanied by discussion of plasma glutamate levels and levels of glutamate found in the brain. According to Heywood and Worden, Perez and Olney had found that "A fourfold increase in the levels of glutamate in the arcuate nucleus of the hypothalamus followed the elevation of plasma glutamate after a single subcutaneous injection of MSG. Peak plasma levels occurred after 15 min, and peak levels in the arcuate nucleus were attained after 3 hr." Heywood and Worden(149), not Perez and Olney(63), went on to conclude that "The results indicate that plasma concentrations above a certain level were necessary to induce brain lesions." (Emphasis added.)

With rare exception, the negative studies were openly sponsored by the glutamate industry.

REFERENCES
14. Lynch, JF Jr, Lewis LM, Adkins JS. Monosodium glutamate-induced hyperglycemia in weanling rats. Fed Proc. 1971;30(2):460Abs (Abstract #1477).
23; Ferguson GA. Statistical Analysis in Psychology and Education. New York: McGraw-Hill, 1959.
24; Weinberg GH, Schumaker JA. Statistics: An Intuitive Approach. Belmont: Wadsworth, 1962.
25; McNemar Q. Psychological Statistics. New York: Wiley, 1949.
26. Lucas DR, Newhouse JP. The toxic effect of sodium-L-glutamate on the inner layers of the retina. AMA Arch Ophthalmol. 1957;58(2):193-201.
27; Ohguro H, Katsushima H, Maruyama I, et al. A high dietary intake of sodium glutamate as flavoring (Ajinomoto) causes gross changes in retinal morphology and function. Exp Eye Res. 2002;75(3):307-15.
28; Babai N, Atlasz T, Tamas A, et al. Search for the optimal monosodium glutaamte treatement schedule to study the neuroprotective effects of PACAP in the retina. Ann N Y Acad Sci. 2006;1070(July):149-155.
29; Szabadfi K, Atlasz T, Horvath G, et al. Early postnatal enriched environment decreases retinal degeneration induced by monosodium glutamate treatment in rats. Brain Res. 2009;1259(March):107-12.
49. Potts AM, Modrell RW, Kingsbury C. Permanent fractionation of the electroretinogram by sodium glutamate. Am J Ophthalmol. 1960;50(Nov): 900-907.
50. Freedman JK, Potts AM. Repression of glutaminase I in the rat retina by administration of sodium L-glutamate. Invest Ophthalmol. 1962;1(Feb):118-121.
51. Freedman JK, Potts AM. Repression of glutaminase I in rat retina by administration of sodium L-glutamate. Invest Ophthal. 1963;2(June):252-258.
52. Potts AM. Selective action of chemical agents on individual retinal layers. In: Graymore CN, ed. Biochemistry of the retina. New York: Academic Press; 1965:155-161.
53. Hamatsu T. Experimental studies on the effect of sodium iodate and sodium L-glutamate on ERG and histological structure of retina in adult rabbits. Acta Soc Ophthalmol Jpn. 1964;68(11):1621-1636. (Abstract)
54. Hansson HA. Ultrastructure studies on long-term effects of MSG on rat retina. Virchows Arch [Zellpathol]. 1970;6(1):1-11.
55. Cohen AI. An electron microscopic study of the modification by monosodium glutamate of the retinas of normal and "rodless" mice. Am J Anat. 1967;120(2): 319-356.
56. Olney JW. Glutamate-induced retinal degeneration in neonatal mice. Electron-microscopy of the acutely evolving lesion. J Neuropathol Exp Neurol 1969;28(3):455-474.
57. Hansson HA. Scanning electron microscopic studies on the long term effects of sodium glutamate on the rat retina. Virchows Arch ABT B (Zellpathol). 1970; 4(4): 357-367.
58. Arees E, Sandrew B, Mayer J. MSG-induced optic pathway lesions in infant mice following subcutaneous injection. Fed Proc. 1971;30(2):287Abs (Abstract # 521).
59. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science. 1969;164(880):719-721.
60. Olney JW, Ho OL, Rhee V. Cytotoxic effects of acidic and sulphur containing amino acids on the infant mouse central nervous system. Exp Brain Res. 1971;14(1):61-76.
61. Olney JW, Sharpe LG. Brain lesions in an infant rhesus monkey treated with monosodium glutamate. Science. 1969;166(903):386-388.
62. Snapir N, Robinzon B, Perek M. Brain damage in the male domestic fowl treated with monosodium glutamate. Poult Sci. 1971;50(5):1511-1514.
63. Perez VJ, Olney JW. Accumulation of glutamic acid in the arcuate nucleus of the hypothalamus of the infant mouse following subcutaneous administration of monosodium glutamate. J Neurochem. 1972;19(7):1777-1782.
64. Arees EA, Mayer J. Monosodium glutamate-induced brain lesions: electron microscopic examination. Science. 1970;170(957):549-550.
66. Everly JL. Light microscopy examination of monosodium glutamate induced lesions in the brain of fetal and neonatal rats. Anat Rec. 1971;169(2):312.
67. Olney JW. Glutamate-induced neuronal necrosis in the infant mouse hypothalamus. J Neuropathol Exp Neurol. 1971;30(1):75-90.
68. Lamperti A, Blaha G. The effects of neonatally-administered monosodium glutamate on the reproductive system of adult hamsters. Biol Reprod 1976;14(3):362-369.
69. Takasaki Y. Studies on brain lesion by administration of monosodium L-glutamate to mice. I. Brain lesions in infant mice caused by administration of monosodium L-glutamate. Toxicology. 1978;9(4):293-305
70. Holzwarth-McBride MA, Hurst EM, Knigge KM. Monosodium glutamate induced lesions of the arcuate nucleus. I. Endocrine deficiency and ultrastructure of the median eminence. Anat Rec. 1976;186(2):185-196.
71. Holzwarth-McBride MA, Sladek JR, Knigge KM. Monosodium glutamate induced lesions of the arcuate nucleus. II Fluorescence histochemistry of catecholamines. Anat Rec. 1976;186(2):197-205.
72. Paull WK, Lechan R. The median eminence of mice with a MSG induced arcuate lesion. Anat Rec. 1974;180(3):436.
73. Burde RM, Schainker B, Kayes J. Acute effect of oral and subcutaneous administration of monosodium glutamate on the arcuate nucleus of the hypothalamus in mice and rats. Nature. 1971;233(5314):58-60.
74. Olney JW, Sharpe LG, Feigin RD. Glutamate-induced brain damage in infant primates. J Neuropathol Exp Neurol. 1972;31(3):464-488.
75. Abraham R, Doughtery W, Goldberg L, Coulston F. The response of the hypothalamus to high doses of monosodium glutamate in mice and monkeys: cytochemistry and ultrastructural study of lysosomal changes. Exp Mol Pathol.1971;15(1):43-60.
76. Burde RM, Schainker B, Kayes J. Monosodium glutamate: necrosis of hypothalamic neurons in infant rats and mice following either oral or subcutaneous administration. J Neuropathol Exp Neurol. 1972;31(1):181.
77. Robinzon B, Snapir N, Perek M. Age dependent sensitivity to monosodium glutamate inducing brain damage in the chicken. Poult Sci. 1974;53(4):1539-1542.
78. Tafelski TJ. Effects of monosodium glutamate on the neuroendocrine axis of the hamster. Anat Rec. 1976;184(3):543-544.
81. Olney JW, Rhee V, DeGubareff T. Neurotoxic effects of glutamate on mouse area postrema. Brain Res. 1977;120(1):151-157.
82. Olney JW, Ho OL. Brain damage in infant mice following oral intake of glutamate, aspartate or cystine. Nature. 1970;227:609-611.
83. Lemkey-Johnston N, Reynolds WA. Nature and extent of brain lesions in mice related to ingestion of monosodium glutamate: a light and electron microscope study. J Neuropath Exp Neurol. 1974;33(1):74-97.
84. Takasaki, Y. Protective effect of mono- and disaccharides on glutamate-induced brain damage in mice. Toxicol Lett. 1979;4(3): 205-210.
85. Takasaki, Y. Protective effect of arginine, leucine, and preinjection of insulin on glutamate neurotoxicity in mice. Toxicol Lett. 1980;5(1):39-44.
86. Lemkey-Johnston, N, Reynolds WA. Nature and extent of brain lesions in mice related to ingestion of monosodium glutamate: a light and electron microscope study. J Neuropath Exp Neurol. 1974;33(1):74-97.
87. Olney JW. Brain damage and oral intake of certain amino acids. In: Levi G, Battistin L, Lajtha A, eds.Transport Phenomena in the Nervous System: Physiological and Pathological Aspects. New York: Plenum Press; 1976.
88. Reynolds WA. Lemkey-Johnston N, Filer LJ Jr, Pitkin RM. Monosodium glutamate: absence of hypothalamic lesions after ingestion by newborn primates. Science. 1971;172(990):1342-1344.
89. Matsuyama S. Studies on experimental obesity in mice treated with MSG. Jap J Vet Sci. 1970;32:206.
90. Redding TW, Schally AV, Arimura A, Wakabayashi I. Effect of monosodium glutamate on some endocrine functions. Neuroendocrinology. 1971;8(3):245-255.
92. Araujo PE, Mayer J. Activity increase associated with obesity induced by monosodium glutamate in mice. Am J Physiol. 1973;225(4):764-765.
93. Nagasawa H, Yanai R, Kikuyama S. Irreversible inhibition of pituitary prolactin and growth hormone secretion and of mammary gland development in mice by monosodium glutamate administered neonatally. Acta Endocrinol. 1974;75(2):249-259.
94. Nemeroff CB, Grant LD, Bissette G, Ervin GN, Harrell LE, Prange AJ Jr. Growth, endocrinological and behavioral deficits after monosodium L-glutamate in the neonatal rat: Possible involvement of arcuate dopamine neuron damage. Psychoneuroendocrinology.1977;2(2):179-196.
95. Nemeroff CB, Konkol RJ, Bissette G, et al. Analysis of the disruption in hypothalamic-pituitary regulation in rats treated neonatally with monosodium glutamate (MSG): Evidence for the involvement of tuberoinfundibular cholinergic and dopaminergic systems in neuroendocrine regulation. Endocrinology. 1977;101(2):613-622.
96. Pizzi WJ, Barnhart JE, Fanslow DJ. Monosodium glutamate administration to the newborn reduces reproductive ability in female and male mice. Science. 1977;196(4288):452-454.
97. Tafelski TJ, Lamperti AA. The effects of a single injection of monosodium glutamate on the reproductive neuroendocrine axis of the female hamster. Biol Reprod. 1977;17(3):404-411.
98. Takasaki Y, Sekine S, Matsuzawa Y, Iwata S, Sasaoka M. Effects of parenteral and oral administration of monosodium L-glutamate (MSG) on somatic growth in rats. Toxicol Lett. 1979;4(5):327-343.
99. Matsuzawa Y, Yonetani S, Takasaki Y, Iwata S, Sekine S. Studies on reproductive endocrine function in rats treated with monosodium L-glutamate early in life. Toxicol Lett. 1979;4(5):359-371.
100. Matsuyama S, OkiY, Yokoki Y. Obesity induced by monosodium glutamate in mice. Natl Inst Anim Health Q(Tokyo). 1973;13(2):91-101.
101. Pizzi WJ, Barnhart JE. Effects of monosodium glutamate on somatic development, obesity and activity in the mouse. Pharmacol Biochem Behav. 1976;5(5):551-557.
102. Nikoletseas MM. Obesity in exercising, hypophagic rats treated with monosodium glutamate. Physiol Behav. 1977;19(6):767-773.
103. Redding TW, Schally AV. Effect of monosodium glutamate on the endocrine axis in rats. Fed Proc. 1970;29(2):378Abs (Abstract #755).
104. Holzwarth MA, Hurst EM. Manifestations of monosodium glutamate (MSG) induced lesions of the arcuate nucleus of the mouse. Anat Rec. 1974;178(2):378.
105. Trentini GP, Botticelli A, Botticelli CS. Effect of monosodium glutamate on the endocrine glands and on the reproductive function of the rat. Fertil Steril. 1974;25(6):478-483.
106. Lynch JF Jr, Lewis LM, Hove EL, Adkins JS. Effect of monosodium L-glutamate on development and reproduction in rats. Fed Proc. 1970;29(2):567 Abs (Abstract 1795).
107. Pradhan SN, Lynch JF Jr. Behavioral changes in adult rats treated with monosodium glutamate in the neonatal state. Arch Int Pharmacodyn Ther. 1972;197(2):301-304.
108. Iwata S, Ichimura M, Matsuzawa Y, Takasaki Y, Sasaoka M. Behavioral studies in rats treated with monosodium l-glutamate during the early stages of life. Toxicol Lett. 1979;4(5):345-357.
109. Vorhees CV, Butcher RE, Brunner RL, Sobotka TJ. A developmental test batter for neurobehavioral toxicity in rats: a preliminary analysis using monosodium glutamate, calcium carrageenan, and hydroxyurea. Toxicol Appl Pharm. 1979;50(2):267-282.
110. Vogel JR, Nathan BA. Learned taste aversions induced by high doses of monosodium L-glutamate. Pharmacol Biochem Behav. 1975;3(5):935-937.
112. Berry HK, Butcher RE, Elliot LA, Brunner RL. The effect of monosodium glutamate on the early biochemical and behavioral development of the rat. Devl Psychobiol. 1974;7(2):165-173.
113. Weiss LR, Reilly JF, Williams J, Krop S. Effects of prolonged monosodium glutamate and other high salt diets on arterial pressure and learning ability in rats. Toxicol Appl Pharmacol. 1971;19(2):389.
114. Bhagavan HN, Coursin DB, Stewart CN. Monosodium glutamate induces convulsive disorders in rats. Nature. 1971;232(5308):275-276.
115. Johnston GAR. Convulsions induced in 10-day-old rats by intraperitoneal injection of monosodium glutamate and related excitant amino acids. Biochem Pharmacol. 1973;22(1):137-140.
116. Mushahwar IK, Koeppe RE. The toxicity of monosodium glutamate in young rats. Biochem Biophys Acta. 1971;244(2):318-321.
117. Nemeroff CB, Crisley FD. Lack of protection by pyridoxine or hydrazine pretreatment against monosodium glutamate induced seizures. Pharmacol Biochem Behav. 1975;3(5):927-929.
119. Wiechert P, Gollinitz G. Metabolic investigations of epileptic seizures: the activity of the glutamate decarboxylase prior to and during experimentally produced convulsions. J Neurochem. 1968;15(11):1265-1270. (Abstract)
120. Wiechert P, Herbst A. Provocation of cerebral seizures by derangement of the natural balance between glutamic acid and y-aminobutyric acid. J Neurochem. 1966;13(2):59-64.
121. Wiechert P, Gollnitz G. Metabolic investigations of epileptic seizures: investigations of glutamate metabolism in regions of the dog brain in preconvulsive states. J Neurochem. 1970;17(2):137-147.
122. Olney JW, Price MT. Neuroendocrine interactions of excitatory and inhibitory amino acids. Brain Res Bull. 1980;5:Suppl 2, 361-368.
123. Olney JW, Price MT. Excitotoxic amino acids as neuroendocrine probes. In: McGeer EG, Olney JW, McGeer PL eds. Kainic Acid as a Tool in Neurobiology New York: Raven Press; 1978.
124. Olney JW. Excitotoxic amino acids: research applications and safety implications. In: Filer LJ Jr, Garattini S, Kare MR, Reynolds WA, Wurtman RJ, eds. Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press; 1979:287-319.
125. Nemeroff CB. Monosodium glutamate-induced neurotoxicity: review of the literature and call for further research. In: Miller SA, ed. Nutrition & Behavior. Philadelphia: The Franklin Institute Press; 1981.
126; Stegink LD, Reynolds WA, Filer LJ, Jr, Baker GL, Daabees TT, Pitkin RM. Comparative metabolism of glutamate in the mouse, monkey, and man. In: Filer LJ Jr, Garattini S, Kare MR, Reynolds WA, Wurtman RJ, eds. Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press; 1979:85-102.
127. Olney JW, Labruyere J, De Gubareff T. Brain damage in mice from voluntary ingestion of glutamate and aspartate. Neurobehav Toxicol. 1980;2(2 ):125-129.
128. Olney JW, Cicero TJ, Meyer ER, De Gubareff T. Acute glutamate-nduced elevations in serum testosterone and luteinizing hormone. Brain Research. 1976;112(2):420-424.
131. Adamo NJ, Ratner A. Monosodium glutamate: Lack of effects on brain and reproductive function in rats. Science. 1970;169(946):673-674.
132. Oser BL, Carson S, Vogin EE, Cox GE. Oral and subcutaneous administration of monosodium glutamate to infant rodents and dogs. Nature. 1971;229(5284):411-413.
133. Olney JW. Monosodium glutamate effects. Science. 1971;172(980):294.
134. Olney JW. Toxic effects of glutamate and related amino acids on the developing central nervous system. In: Nyhan WL. ed. Heritable Disorders of Amino Acid Metabolism New York: Wiley; 1974:501-512.
135. Murakami U, Inouye M. Brain lesions in the mouse fetus caused by maternal administration of monosodium glutamate. Congenital Anomalies. 1971;11:161,171-177.
136. Filer LJ, Stegink LD. Safety of hydrolysates in parenteral nutrition. N Engl J Med. 1973;289(8):426-427.
137. Olney JW, Ho OL, Rhee V, De Gubareff T. Neurotoxic effects of glutamate. New Engl J Med. 1973;289(25):1374-1375.
138. Lowe CU. Monosodium glutamate: specific brain lesion questioned. Science. 1970;167(920):1016.
139. Zavon MR. Monosodium glutamate: specific brain lesion questioned. Science. 1970;167(920):1017.
140. Olney JW, Sharpe LG. Monosodium glutamate: specific brain lesion questioned. Science. 1970;167(920):1017.
141. Blood FR, Oser BL, White PL. Monosodium glutamate. Science. 1969;165(897):1028-1029 .
142. Olney JW. Monosodium glutamate. Science. 1969;165(897):1028-1029.
144. Reynolds WA, Lemkey-Johnston N, Filer LJ Jr, Pitkin RM. Monosodium glutamate: absence of hypothalamic lesions after ingestion by newborn primates. Science 1971;172(990):1342-1344.
145. Abraham R, Swar J, Goldberg L, Coulston F. Electron microscopic observations of hypothalami in neonatal rhesus monkeys (Macaca mulatta) after administration of monosodium L-glutamate. Exp Mol Pathol. 1975;23(2):203-213.
146. Newman AJ, Heywood R, Palmer AK, Barry DH, Edwards FP, Worden AN. The administration of monosodium L-glutamate to neonatal and pregnant rhesus monkeys. Toxicology. 1973;1(3):197-204.
147. Stegink LD, Reynolds WA, Filer LJ Jr, Pitkin RM, Boaz DP, Brummel MC. Monosodium glutamate metabolism in the neonatal monkey. Am J Physiol. 1975;229(1):246-250.
148. Reynolds WA, Butler V, Lemkey-Johnston N. Hypothalamic morphology following ingestion of aspartame or MSG in the neonatal rodent and primate: a preliminary report. J Toxicol Environ Health. 1976;2(2):471-480.
149. Heywood R, Worden AN. Glutamate Toxicity in Laboratory Animals. In: Filer LJ Jr, Garattini S, Kare MR, Reynolds WA, Wurtman RJ, eds. Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press; 1979:203-215.
150. Ebert AG. Chronic toxicity and teratology studies of monosodium L-glutamate and related compounds. Toxicol Appl Pharmacol. 1970;17(1):274.
151. Owen G, Cherry CP, Prentice DE, Worden AN. The feeding of diets containing up to 4% monosodium glutamate to rats for 2 years. Toxicol Lett 1978;1(4):221-226.
152. Owen G, Cherry CP, Prentice DE. Worden AN. The feeding of diets containing up to 10% monosodium glutamate to Beagle dogs for 2 years. Toxicol Lett. 1978;1(4): 217-219.
153. Semprini ME, D'Amicis A, Mariani A. Effect of monosodium glutamate on fetus and newborn mouse. Nutr Metabol. 1974;16(5):276-284.
154. Wen CP, Hayes KC, Gershoff SN. Effects of dietary supplementation of monosodium glutamate on infant monkeys, weaning rats, and suckling mice. Am J Clin Nutr. 1973;26(8):803-813.
155. Ebert AG. The Dietary administration of monosodium glutamate or glutamic acid to C-57 black mice for two years. Toxicol Lett. 1979;3(2):65-70.
156. Ebert AG. The dietary administration of L-monosodium glutamate, DL-monosodium glutamate and L-glutamic acid to rats. Toxicol Lett. 1979;3(2):71-78.
157. Anantharaman K. In utero and dietary administration of monosodium L-glutamate to mice: reproductive performance and development in a multigeneration study. In: Filer LJ Jr, Garattini S, Kare MR, Reynolds WA, Wurtman RJ, eds. Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press New York: Raven; 1979:231-253.
158. Huang PC, Lee NY, Wu TJ, Yu SL, Tung TC. Effect of monosodium glutamate supplementation to low protein diets on rats. Nutr Rep Int. 1976;13(5):477-486.
159. Takasaki, Y. Studies on brain lesions after administration of monosodium L-glutamate to mice. II Absence of brain damage following administration of monosodium L-glutamate in the diet. Toxicology. 1978;9(4):307-318.
160. Bunyan J, Murrell EA, Shah PP. The induction of obesity in rodents by means of monosodium glutamate. Br J Nutr. 1976;35(1):25-29.
161. Rippere V. Placebo-controlled tests of chemical food additives: are they valid? Medical Hypotheses 1981;7(6):819-823.
162. Goldschmiedt M, Redfern JS, Feldman M. Food coloring and monosodium glutamate: effects on the cephalic phase of gastric acid secretion and gastrin release in humans. Am J Clin Nutr. 1990;51(5):794-797.
163. Heywood R, James RW, Worden AN. The ad libitum feeding of monosodium glutamate to weanling mice. Toxicol Lett. 1977;1(3):151-155.
164. Takasaki Y, Matsuzawa Y, Iwata S, O'Hara Y, Yonetani S, Ichimura M. Toxicological studies of monosodium L-glutamate in rodents: relationship between routes of administration and neurotoxicity. In: Filer LJ Jr, Garattini S, Kare MR, Reynolds WA, Wurtman RJ, eds. Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press; 1979:255-275.
165. Semprini ME, Conti L, Ciofi-Luzzatto A. Mariani A. Effect of oral administration of monosodium glutamate (MSG) on the hypothalamic arcuate region of rat and mouse: a histological assay. Biomedicine. 1974;21(10):398-403.
166. Prabhu VG, Oester YT. Neuromuscular functions of mature mice following neonatal monosodium glutamate. Arch Int Pharmacodyn. 1971;189(1): 59-71.
167. Lengvari I. Effect of perinatal monosodium glutamate treatment on endocrine functions of rats in maturity. Acta Biol Acad Sci Hung. 1977;28(1):133-141.

Formaldehyde: Carcinogen in Vaccinations

Formaldehyde: carcinogen

http://www.atsdr.cdc.gov/mhmi/mmg111.html

The Agency for Toxic Substances and Disease Registry: the CDC's own information on the substance:

Formaldehyde is synthesized by the oxidation of methanol. It is among the 25 most abundantly produced chemicals in the world and is used in the manufacture of plastics, resins, and urea-formaldehyde foam insulation. Formaldehyde or formaldehyde-containing resins are used in the manufacture of chelating agents, a wide variety of organic products, glass mirrors, explosives, artificial silk, and dyes. It has been used as a disinfectant, germicide, and in embalming fluid. In the agricultural industry, formaldehyde has been used as a fumigant, preventative for mildew in wheat and rot in oats, a germicide and fungicide for plants, an insecticide, and in the manufacture of slow-release fertilizers. Formaldehyde is found in construction materials such as plywood adhesives.

Health Effects

Formaldehyde is an eye, skin, and respiratory tract irritant.

Children may be more susceptible than adults to the respiratory effects of formaldehyde.

Formaldehyde solution (formalin) causes corrosive injury to the gastrointestinal tract, especially the pharynx, epiglottis, esophagus, and stomach.

The systemic effects of formaldehyde are due primarily to its metabolic conversion to formate, and may include metabolic acidosis, circulatory shock, respiratory insufficiency, and acute renal failure.

Formaldehyde is a potent sensitizer and a probable human carcinogen.

Formaldehyde vapor produces immediate local irritation in mucous membranes, including eyes, nose, and upper respiratory tract.

Ingestion of formalin causes severe injury to the gastrointestinal tract.

The exact mechanism of action of formaldehyde toxicity is not clear, but it is known that it can interact with molecules on cell membranes and in body tissues and fluids (e.g., proteins and DNA) and disrupt cellular functions.

High concentrations cause precipitation of proteins, which results in cell death. Absorption from the respiratory tract is very rapid; absorption from the gastrointestinal tract is also rapid, but may be delayed by ingestion with food. Once absorbed, formaldehyde is metabolized to formic acid, which may cause acid-base imbalance and a number of other systemic effects.


Metabolic

Accumulation of formic acid can cause an anion-gap acid-base imbalance. If formalin is ingested, absorption of the methanol stabilizer may contribute to the imbalance and can result in an osmolal gap, as well as an anion gap.

Immunologic

In persons who have been previously sensitized, inhalation and skin contact may cause various skin disorders, asthma-like symptoms, anaphylactic reactions and, rarely, hemolysis. The immune system in children continues to develop after birth, and thus, children may be more susceptible to certain chemicals.

Gastrointestinal

Ingestion of aqueous solutions of formaldehyde can result in severe corrosive injury to the esophagus and stomach. Nausea, vomiting, diarrhea, abdominal pain, inflammation of the stomach, and ulceration and perforation of the oropharynx, epiglottis, esophagus, and stomach may occur. Both formaldehyde and the methanol stabilizer are easily absorbed and can contribute to systemic toxicity.

http://www.cancer.gov/cancertopics/factsheet/Risk/formaldehyde

Formaldehyde and cancer: current evidence and future perspectives

Can formaldehyde cause cancer?

Although the short-term health effects of formaldehyde exposure are well known, less is known about its potential long-term health effects. In 1980, laboratory studies showed that exposure to formaldehyde could cause nasal cancer in rats. This finding raised the question of whether formaldehyde exposure could also cause cancer in humans. In 1987, the U.S. Environmental Protection Agency (EPA) classified formaldehyde as a probable human carcinogen under conditions of unusually high or prolonged exposure (1). Since that time, some studies of industrial workers have suggested that formaldehyde exposure is associated with nasal sinus cancer and nasopharyngeal cancer, and possibly with leukemia. In 1995, the International Agency for Research on Cancer (IARC) concluded that formaldehyde is a probable human carcinogen. In June 2004, after evaluating all existing data, the IARC reclassified formaldehyde as a known human carcinogen (2).

Several NCI studies have found that anatomists and embalmers, people who are potentially exposed to formaldehyde in their professions, are at an increased risk of leukemia and brain cancer compared with the general population. In 2003, a number of cohort studies were completed among workers exposed to formaldehyde. One study, conducted by NCI, looked at 25,619 workers in industries with the potential for occupational formaldehyde exposure and estimated each worker’s exposure to the chemical while at work (3). The results showed an increased risk of death due to leukemia, particularly myeloid leukemia, among workers exposed to formaldehyde. This risk was associated with increasing peak and average levels of exposure, as well as with the duration of exposure, but not with cumulative exposure. Using an additional 10 years of data, a follow-up study published in 2009 continued to show a possible link between formaldehyde exposure and cancers of the hematopoietic and lymphatic systems, particularly myeloid leukemia, as was previously reported (4). As in the previous study, the risk was highest earlier in the follow-up period and declined steadily over time, such that the cumulative excess risk of myeloid leukemia was no longer statistically significant. The researchers noted that similar patterns of risks over time had been seen for other agents known to cause leukemia.
A separate study of 11,039 textile workers performed by the National Institute for Occupational Safety and Health (NIOSH) also found an association between the duration of exposure to formaldehyde and leukemia deaths (5).

Formaldehyde undergoes rapid chemical changes immediately after absorption. Therefore, some scientists think that formaldehyde is unlikely to have effects at sites other than the upper respiratory tract. However, some laboratory studies suggest that formaldehyde may affect the lymphatic and hematopoietic systems. Based on both the epidemiologic data from cohort studies and the experimental data from laboratory research, NCI investigators have concluded that exposure to formaldehyde may cause leukemia, particularly myeloid leukemia, in humans. However, inconsistent results from other studies suggest that further research is needed before definite conclusions can be drawn.

Selected References

1 U.S. Environmental Protection Agency, Office of Air and Radiation. Report to Congress on Indoor Air Quality, Volume II: Assessment and Control of Indoor Air Pollution, 1989.
2 International Agency for Research on Cancer (June 2004). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans Volume 88 (2006): Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. Retrieved May 4, 2009, from: http://monographs.iarc.fr/ENG/Monographs/vol88/index.php.
5 Pinkerton LE, Hein MJ, Stayner LT. Mortality among a cohort of garment workers exposed to formaldehyde: An update. Occupational Environmental Medicine 2004; 61:193–200.

http://monographs.iarc.fr/ENG/Monographs/vol88/mono88-6.pdf

(pgs 57-62 for cancer related charts)

http://oehha.ca.gov/air/acute_rels/pdf/50000A.pdf

Studies on formaldehyde's causation as a carcinogen:

Zhang L, Freeman LE, Formaldehyde and leukemia: Epidemiology, potential mechanisms, and implications for risk assessment.Environ Mol Mutagen. 2009 Sep 29.

Excerpt: Here, we provide a summary of the symposium at the Environmental Mutagen Society Meeting in 2008, which focused on the epidemiology of formaldehyde and leukemia, potential mechanisms, and implication for risk assessment, with emphasis on future directions in multidisciplinary formaldehyde research. Updated results of two of the three largest industrial cohort studies of formaldehyde-exposed workers have shown positive associations with leukemia, particularly myeloid leukemia, and a recent meta-analysis of studies to date supports this association. Recent mechanistic studies have shown the formation of formaldehyde-induced DNA adducts and characterized the essential DNA repair pathways that mitigate formaldehyde toxicity.

Hauptmann M, Lubin JH, Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries. J Natl Cancer Inst. 2003 Nov 5;95(21):1615-23.

Feron VJ, Til HP, Formaldehyde must be considered a multipotential experimental carcinogen.Toxicol Ind Health. 1990 Dec;6(6):637-9.

Soffritti M, Belpoggi F, Results of long-term experimental studies on the carcinogenicity of formaldehyde and acetaldehyde in rats.Ann N Y Acad Sci. 2002 Dec;982:87-105.

Soffritti M, Maltoni C, Formaldehyde: an experimental multipotential carcinogen. Toxicol Ind Health. 1989 Oct;5(5):699-730.

Excerpt: The experimental results presented in this report give scientific support to the epidemiological observation of a higher incidence of leukemias and of gastro-intestinal cancers among the people occupationally exposed.

Blackwell M, Kang H, Formaldehyde: evidence of carcinogenicity.Am Ind Hyg Assoc J. 1981 Jul;42(7):A34, A36, A38, passim.

Shaham J, Bomstein Y, DNA--protein crosslinks, a biomarker of exposure to formaldehyde--in vitro and in vivo studies. Carcinogenesis. 1996 Jan;17(1):121-5.

Excerpt: Formaldehyde (FA) is a widely produced industrial chemical. Sufficient evidence exists to consider FA as an animal carcinogen. In humans the evidence is not conclusive. DNA-protein crosslinks (DPC) may be one of the early lesions in the carcinogenesis process in cells following exposures to carcinogens... We conclude that our data indicate a possible mechanism of FA carcinogenicity in humans and that DPC can be used as a method for biological monitoring of exposure to FA.

Antibiotics in Vaccinations

A brief description of the antibiotics used in vaccinations followed by information on the harm of antibiotics to the pediatric population.

Neomycin

http://www.novaccine.com/vaccine-ingredients/results.asp?sc=15

Interferes with Vitamin B6 absorption. An error in the uptake of B6 can cause a rare form of epilepsy and mental retardation.

Streptomycin

http://www.novaccine.com/vaccine-ingredients/results.asp?sc=25

An adverse effect of this medicine is ototoxicity. It can result in permanent hearing loss.

Wikipdeia.com http://en.wikipedia.org/wiki/Streptomycin

Polymyxin B

http://www.novaccine.com/vaccine-ingredients/results.asp?sc=18

A mixture of polymyxins B1 and B2, obtained from Bacillus polymyxa strains. They are basic polypeptides of about eight amino acids and have cationic detergent action on cell membranes. Polymyxin B is used for infections with gram-negative organisms, but may be neurotoxic and nephrotoxic.

http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=602977

Chemical Descriptions:United States National Library of Medicine:

PubChemhttp://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5702105Adverse effectshttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed&term=%22Polymyxin%20B%2fadverse%20effects%22[Mesh%20Terms%3anoexp

Toxicity

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed&term=%22Polymyxin%20B%2ftoxicity%22[Mesh%20Terms%3anoexp

Poisoning

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed&term=%22Polymyxin%20B%2fpoisoning%22[Mesh%20Terms%3anoexp

Gentamicin Sulfate

http://www.novaccine.com/vaccine-ingredients/results.asp?sc=8

Gentamicin (also gentamycin) is an aminoglycoside antibiotic. Gentamicin can cause deafness or a loss of equilibrioception. Gentamicin can also be highly nephrotoxic, particularly if multiple doses accumulate over a course of treatment. – wikipedia.com

ANTIBIOTICS

http://www.hpakids.org/holistic-health/articles/58/1/Excessive-Antibiotic-Use

Unfortunately, antibiotics are excessively prescribed, especially to children. The Center for Disease Control estimates that of the 235 million doses of antibiotics given each year, between 20 and 50 percent are unnecessary. Tragically, this overuse of antibiotics can cause devastating health consequences to children.

Antibiotics Don't Discriminate

Antibiotics do not just go after the pathogenic or "bad" bacteria. They also indiscriminately destroy the beneficial bacteria necessary and vital to good health. Among the more important beneficial bacteria are lactobacillus acidophilus and bifidobacterium bifidus. They help protect the body against infection. Depleting these organisms can disrupt the balance of the body, suppress immunity, and lead to increased susceptibility to infections by fungi, bacteria, viruses and parasites. Additionally, when antibiotics are used excessively, depleting the beneficial bacteria, there may be an overgrowth of yeast in the body. A yeast infection can suppress immunity, which may lead to recurrent infections.

What's more, antibiotics adversely affect many nutrients, particularly the ones needed by the immune system to fight infection, such as vitamins A and C. One of the most common side effects of antibiotics is diarrhea. This causes a loss of nutrients, especially magnesium and zinc. Some children are on antibiotics for months or even years. Nutritional loss over such a long period of time is debilitating for the body and sets up an environment for more infections.

Serious Infectious Diseases Resistant to Antibiotics

A very frightening consequence of indiscriminate use of antibiotics is the development of antibiotic-resistant bacteria. These bacteria have "learned" to outsmart the drugs and have reproduced a generation of stronger, more resistant bugs. Consequently, there are some serious infectious diseases that are no longer responding to antibiotics. If an infection does respond, it often requires five to ten times the amount of the drug that used to be effective.

When your child is continually treated with antibiotics, the bacteria in his or her body may eventually be able to survive the drugs, making it much harder to cure an infection. In the event of a serious bacterial infection, such as meningitis, a much higher dosage of antibiotic may be required or a doctor may have to try different drugs before finding one that will work. The time this takes can potentially be a matter of life or death, since meningitis can be fatal and needs to be treated immediately. Unfortunately, with each try at a different treatment, the bacteria are given another chance to build up their resistance against even more powerful drugs.

Antibiotic resistance can affect the whole family and everyone around the child with a history of frequent antibiotic use. If the child develops resistant bacteria, he or she can pass them along to others through coughing, sneezing, and kissing.

http://www.hopkinschildrens.org/web-based-tool-streamlines-approval-reduces-excessive-antibiotic-use.aspx

Between one-third and a half of all hospital patients receive antimicrobial drugs, such as antibiotics, antifungal and antiviral medications but up to half of these prescriptions are unnecessary, researchers estimate, fuelling an already serious bacterial drug resistance problem.

To address the problem, Hopkins and other hospitals, have put more than 30 antimicrobial drugs on a "restricted" list, requiring approval by an infectious disease specialist before the pharmacy can dispense them to a patient.

(the over use of antibiotics is so serious the CDC even concedes to how dangerous it is, how it leads to more virulent organisms like MRSA, and major pro vax hospitals like Hopkins up there have restricted lists for antibiotics, yet these are never questioned as components in childhood vaccinations?)

http://www.drgreene.com/21_646.html

http://www.cpmc.org/advanced/pediatrics/patients/topics/antibiotics.html

Bacterial Resistance

When bacteria becomes resistant to an antibiotic, that antibiotic can no longer kill that type of bacteria. Excessive use of antibiotics is the number one cause of resistant strains of bacteria, and research shows that 50% of prescriptions for antibiotics are inappropriate (mainly when they are given for coughs and colds). This makes future treatment of bacterial infections more difficult. Many bacteria are now resistant to antibiotics that used to control them. When we turn to newer and more expensive antibiotics, bacteria develop resistance to them as well. In the battle between antibiotics and bacteria, the bacteria seem to be winning.


http://environment.about.com/od/healthenvironment/a/superbugs.htm

But the effectiveness of these so-called miracle drugs has waned in recent years as some of the very bacteria they are meant to control have been mutating into new forms that don’t respond to treatment. Many medical experts blame this phenomenon on both the misuse and overuse of antibiotics in recent years in both human medicine and in agriculture.

Antibiotic Resistance a Pressing Health IssueDoctors first noticed antibiotic resistance more than a decade ago when children with middle ear infections stopped responding to them. Penicillin as a treatment for strep has also become increasingly less effective. And a recently discovered strain of staph bacteria does not respond to antibiotic treatments at all, leading medical analysts to worry that certain "super bugs" could emerge that are resistant to even the most potent drugs, rendering some infections incurable. The U.S. Centers for Disease Control and Prevention (CDC) calls antibiotic resistance one of its "top concerns" and "one of the world’s most pressing health problems."

http://medind.nic.in/icb/t05/i10/icbt05i10p877.pdf

http://www.chiro.org/LINKS/ABSTRACTS/Antibiotic_Use_In_Infants_Linked_To_Asthma.shtml

Antibiotic Use In Infants Linked To Asthma

Posted on Wednesday, June 13, 2007

New research indicates that children who receive antibiotics before their first birthday are significantly more likely to develop asthma by age 7. The study, published in the June issue of CHEST ["Increased Risk of Childhood Asthma From Antibiotic Use in Early Life" ~ Chest 2007 (Jun); 131 (6): 1753–1759 ~ FULL TEXT], the peer-reviewed journal of the American College of Chest Physicians (ACCP), reports that children receiving antibiotics in the first year of life were at greater risk for developing asthma by age 7 than those not receiving antibiotics. The risk for asthma doubled in children receiving antibiotics for nonrespiratory infections, as well as in children who received multiple antibiotic courses and who did not live with a dog during the first year.

http://www.chiro.org/LINKS/FULL/Challenge_of_Antibiotic_Resistance.shtml

Really good and really long article on the problematics of antibiotic resistance as a result of over exposure.

Animal Products (Contaminants) in Vaccinations

Animal products in vaccination: Monkey kidney cells, sheep red blood cells, chick embryonic fluid, fetal bovine serum, bovine gelatin, guinea pig embryo cells= risk and history of contamination.

http://www.sailhome.org/Concerns/Vaccines.html

Calf fetus, chick embryo, chick kidney, chicken egg, cow heart, dog kidney, duck egg, guinea pig embryo, horse blood, monkey kidney, monkey lung, mouse blood, pig blood, rabbit brain, sheep blood and others. These are used in various vaccine production lines. Residues are not completely purified out of the final packaged product. Contamination can introduce new pathogens.

Studies of contamination via animal products in vaccinations:

Wessman SJ, Levings RL. Benefits and risks due to animal serum used in cell culture production, Dev Biol Stand. 1999;99:3-8.

Excerpt: Infection with bovine viral diarrhoea virus (BVDV) and other viruses is frequent in the bovine population. In utero infection leads to virus and antibody contamination of foetal and other serum used in cell culture production. The use of contaminated cells for vaccine production may result in contaminated vaccines.

Schuurman R, van Steenis B, Frequent detection of bovine polyomavirus in commercial batches of calf serum by using the polymerase chain reaction, J Gen Virol. 1991 Nov;72 ( Pt 11):2739-45.

Excerpt: The results indicate that the use of calf serum to supplement tissue culture media involves a serious risk of contaminating cell cultures with BPyV.

Johnson JA, Heneine W. Characterization of endogenous avian leukosis viruses in chicken embryonic fibroblast substrates used in production of measles and mumps vaccines. J Virol. 2001 Apr;75(8):3605-12.

Johnson ES.Poultry oncogenic retroviruses and humans. Cancer Detect Prev. 1994;18(1):9-30.Harris RJ, Dougherty RM, Contaminant viruses in two live virus vaccines produced in chick cells. J Hyg (Lond). 1966 Mar;64(1):1-7.

Contreras G, Bather R, Activation of metastatic potential in African green monkey kidney cell lines by prolonged in vitro culture. In Vitro Cell Dev Biol. 1985 Nov;21(11):649-52.

Schuurman R, van Steenis B, Bovine polyomavirus, a frequent contaminant of calf serum. Biologicals. 1991 Oct;19(4):265-70.

Wang J, Horner GW, Detection and molecular characterisation of bovine polyomavirus in bovine sera in New Zealand.N Z Vet J. 2005 Feb;53(1):26-30.

van der Noordaa J, Sol CJ, Bovine polyomavirus, a frequent contaminant of calf sera; Dev Biol Stand. 1999;99:45-7.

Monkey kidney cells and SV40 contamination in Polio vaccines:

***Polio vaccine has also been definitively linked to carcinogen SV-40. Unfortunately some bad monkey kidney cells happened to contaminate many batches of Polio vaccines (since that is one of the ingredients in the polio vaccine) and this has caused a prominant incidence of Cancer in the United States because of the nature of this contamination.

Below is documentation regarding the connection.

http://thinktwice.com/s_polio.htm

1. Monkey kidneys are used to develop polio vaccines.
2. SV-40, a cancer-causing virus, thrived in monkey kidneys.
3. Polio vaccines were contaminated.
4. Millions of people in the USA and throughout the world were infected.
5. Cancer rates have increased. SV-40 is found in brain tumors, bone cancers, lung cancers, and leukemia.

The Polio Vaccine Has Been Linked to Cancer:

Shah, K and Nathanson, N. "Human exposure to SV40." American Journal of Epidemiology, 1976; 103: 1-12.

Innis, M.D. "Oncogenesis and poliomyelitis vaccine." Nature, 1968; 219:972-73.

Soriano, F., et al. "Simian virus 40 in a human cancer." Nature, 1974; 249:421-24.

Weiss, A.F., et a;. "Simian virus 40-related antigens in three human meningiomas with defined chromosome loss." Proceedings of the National Academy of Science 1975; 72(2):609-13.

Scherneck, S., et al. "Isolation of a SV-40-like papovavirus from a human glioblastoma." International Journal of Cancer 1979; 24:523-31.

Stoian, M., et al. "Possible relation between viruses and oromaxillofacial tumors. II. Research on the presence of SV40 antigen and specific antibodies in patients with oromaxillofacial tumors." Virologie, 1987; 38:35-40.

Stoian, M., et al. "Possible relation between viruses and oromaxillofacial tumors. II. Detection of SV40 antigen and of anti-SV40 antibodies in patients with parotid gland tumors." Virologie, 1987; 38:41-46.

Bravo, M.P., et al. "Association between the occurrence of antibodies to simian vacuolating virus 40 and bladder cancer in male smokers." Neoplasma, 1988; 35:285-88.

O'Connell, K., et al. "Endothelial cells transformed by SV40 T-antigen cause Kaposi?s sarcoma-like tumors in nude mice." American Journal of Pathology, 1991; 139(4):743-49.

Weiner, L.P., et al. "Isolation of virus related to SV40 from patients with progressive multifocal leukoencephalopathy." New England Journal of Medicine, 1972; 286:385-90.

Tabuchi, K. "Screening of human brain tumors for SV-40-related T-antigen." International Journal of Cancer 1978; 21:12-17.

Meinke, W., et al. "Simian virus 40-related DNA sequences in a human brain tumor." Neurology 1979; 29:1590-94.

Krieg, P., et al. "Episomal Simian Virus 40 Genomes in Human Brain Tumors." Proceedings of the National Academy of Sciences of the USA, 1981, 78(10):6446-6450.

Krieg, P., et al. "Cloning of SV40 genomes from human brain tumors." Virology 1984; 138:336-40.

Geissler, E. "SV40 in human intracranial tumors: passenger virus or oncogenic 'hit-and-run' agent?" Z Klin Med, 1986; 41:493-95.

Geissler, E. "SV40 and Human Brain Tumors." Progress in Medical Virology, 1990; 37:211-222.

Bergsagel, D.J., et al. "DNA sequences similar to those of simian virus 40 in ependymomas and choroid plexus tumors of childhood." New England Journal of Medicine, 1992; 326:988-93.

Martini, M., et al. "Human Brain Tumors and Simian Virus 40." Journal of the National Cancer Institute, 1995, 87(17):1331.

Lednicky, JA., et al. "Natural Simian Virus 40 Strains are Present in Human Choroid Plexus and Ependymoma Tumors." Virology, 1995, 212(2):710-17.

Tognon, M., et al. "Large T Antigen Coding Sequence of Two DNA Tumor Viruses, BK and SV-40, and Nonrandom Chromosome Changes in Two Gioblastoma Cell Lines." Cancer Genetics and Cytogenics, 1996, 90(1): 17-23.

Carbone, M., et al. "SV-40 Like Sequences in Human Bone Tumors." Oncogene, 1996, 13(3):527-35.

Pass, HI,, et al. "Evidence For and Implications of SV-40 Like Sequences in Human Mesotheliomas." Important Advances in Oncology, 1996, pp. 89-108.

Rock, Andrea. "The Lethal Dangers of the Billion Dollar Vaccine Business," Money, (December 1996), p. 161. [Article]

Carlsen, William. "Rogue virus in the vaccine: Early polio vaccine harbored virus now feared to cause cancer in humans." San Francisco Chronicle (July 15, 2001), p. 7. [Article: Research by Susan Fisher, epidemiologist, Loyola University Medical Center.]

Bookchin, D. and Schumacher J. "Tainted polio vaccine still carries its threat 40 years later." The Boston Globe (January 26, 1997). [Article]

Rosa, FW., et al. "Absence of antibody response to simian virus 40 after inoculation with killed-poliovirus vaccine of mothers offspring with neurological tumors." New England Journal of Medicine, 1988; 318:1469.

Rosa, FW., et al. Response to: "Neurological tumors in offspring after inoculation of mothers with killed poliovirus vaccine." New England Journal of Medicine, 1988, 319:1226.

Martini, F., et al. "SV-40 Early Region and Large T Antigen in Human Brain Tumors, Peripheral Blood Cells, and Sperm Fluids from Healthy Individuals." Cancer Research, 1996, 56(20):4820-4825.

Aluminum: Neurotoxic Vaccine Adjuvant

Aluminum: neurotoxin

http://www.novaccine.com/vaccine-ingredients/results.asp?sc=91

Aluminum adjuvants are used in vaccine manufacturing to "stimulate" the immune system. The presence of aluminum adjuvants has been associated with injection-site reactions such as nodules, granulomas and erythema. aluminium adjuvants may lead to the syndrome macrophagic myofascitis, a histological finding where aluminium-containing macrophages infiltrate muscle tissue, and may be accompanied by a clinical syndrome of myalgia, arthralgia and fatigue. A systematic review of controlled safety studies reported that vaccines containing aluminium produce more erythema and induration than other vaccines in young children (up to 18 months of age), and greater local pain in older children (10–18 years).Animal and human studies have shown that aluminum can cause nerve cell death [1] and that vaccine aluminum adjuvants can allow aluminum to enter the brain, [2,3].

References:1. Kawahara M et al. 2001. Effects of aluminum on the neurotoxicty of primary cultured neurons and on the aggregation of betamyloid protein. Brain Res. Bull. 55, 211-217

.2. Redhead K. et al. 1992. Aluminum-adjuvanted vaccines transiently increase aluminum levels in murine brain tissue. Pharmacol. Toxico. 70, 278-280.

3. Sahin G. et al. 1994. Determination of aluminum levels in the kidney, liver and brain of mice treated with aluminum hydroxide. Biol. Trace. Elem. Res. 1194 Apr-May;41 (1-2):129-35.

http://emedicine.medscape.com/article/165315-overview

Subsequent purification processes that remove organic compounds take away many of the same compounds that bind the element in its free state, further increasing aluminum concentration.
All metals can cause disease through excess, deficiency, or imbalance.3 Malabsorption through diarrheal states can result in essential metal and trace element deficiencies. Toxic effects are dependent upon the amount of metal ingested, entry rate, tissue distribution, concentration achieved, and excretion rate. Mechanisms of toxicity include inhibition of enzyme activity and protein synthesis, alterations in nucleic acid function, and changes in cell membrane permeability.

No known physiologic need exists for aluminum; however, because of its atomic size and electric charge (0.051 nm and 3+, respectively), it is sometimes a competitive inhibitor of several essential elements of similar characteristics, such as magnesium (0.066 nm, 2+), calcium (0.099 nm, 2+), and iron (0.064 nm, 3+). At physiological pH, aluminum forms a barely soluble Al(OH) 3 that can be easily dissolved by minor changes in the acidity of the media.2

Up to this time, no biological function has been attributed to this metal, and, more importantly, aluminum accumulation in tissues and organs result in their dysfunction and toxicity.2 Aluminum is absorbed from the GI tract in the form of oral phosphate-binding agents (aluminum hydroxide), parenterally via immunizations, via dialysate on patients on dialysis or total parenteral nutrition (TPN) contamination, via the urinary mucosa through bladder irrigation, and transdermally in antiperspirants. Lactate, citrate, and ascorbate all facilitate GI absorption. If a significant load exceeds the body's excretory capacity, the excess is deposited in various tissues, including bone, brain, liver, heart, spleen, and muscle. This accumulation causes morbidity and mortality through various mechanisms.

Pathophysiology

Aluminum causes an oxidative stress within brain tissue. Since the elimination half-life of aluminum from the human brain is 7 years, this can result in cumulative damage via the element's interference with neurofilament axonal transport and neurofilament assembly. Some experts believe it plays a role in leading to the formation of Alzheimerlike neurofibrillary tangles.
Aluminum also has a direct effect on hematopoiesis. Excess aluminum has been shown to induce microcytic anemia. Daily injections of aluminum into rabbits produced severe anemia within 2-3 weeks. The findings were very similar to those found in patients suffering from lead poisoning.

Aluminum may cause anemia through decreased heme synthesis, decreased globulin synthesis, and increased hemolysis. Aluminum may also have a direct effect on iron metabolism: it influences absorption of iron via the intestine, it hinders iron's transport in the serum, and it displaces iron's binding to transferrin. Patients with anemia from aluminum toxicity often have increased reticulocyte counts, decreased mean corpuscular volume, and mean corpuscular hemoglobin.

Other organic manifestations of aluminum intoxication have been proposed, such as a slightly poorer immunologic response to infection, but the mechanism by which it exerts its effect is complex and multifactorial.

http://www.hbci.com/~wenonah/hydro/al.htm

Aluminum has been exempted from tesitng for safety by the FDA under a convoluted logic wherein it is classified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety and there are NO restrictions whatever on the amount or use of aluminum.
There are over 2000 references in the National Library of Medicine on adverse effects of alumium. The following were extracted to provide a small sample of the range of toxicity of aluminum.

Aluminum-induced anemia.
From: Am J Kidney Dis (1985 Nov) 6(5):348-52

... many questions still remain unanswered, it is clear that aluminum causes a microcytic hypoproliferative anemia and is a factor responsible for worsening anemia in patients with end-stage renal disease.

Arch Dermatol (1984 Oct) 120(10):1318-22

Three patients had subcutaneous nodules at the sites of previous injections of vaccine containing tetanus toxoid, showed aluminum crystals in the nodules from two patients. From the evidence available, we believe that these nodules are a complication of inoculations with aluminum-containing vaccines.

Persistent subcutaneous nodules in patients hyposensitized with aluminum-containing allergen extracts. Garcia-Patos V. – Pujol R.M. Arch Dermatol (1995 Dec) 131(12):1421-4

These lesions have been mainly attributed to a hypersensitivity reaction to aluminum hydroxide, which is used as an absorbing agent in many vaccines and hyposensitization preparations. Patch tests with standard antigens and aluminum compounds and histopathologic and ultrastructural studies were performed on 10 patients with persistent subcutaneous nodules on the upper part of their arms after injection of aluminum-adsorbed dust and/or pollen extracts. The nodules appeared 1 month to 6.5 years after injections.

Aspects of aluminum toxicity.
Hewitt C.D. – Savory J. – Wills M.R.
From: Clin Lab Med (1990 Jun) 10(2):403-22

Attention was first drawn to the potential role of aluminum as a toxic metal over 50 years ago, but was dismissed as a toxic agent as recently as 15 years ago. The accumulation of aluminum, in some patients with chronic renal failure, is associated with the development of toxic phenomena; dialysis encephalopathy, osteomalacic dialysis osteodystrophy, and an anemia. Aluminum accumulation also occurs in patients who are not on dialysis, predominantly infants and children with immature or impaired renal function. Aluminum has also been implicated as a toxic agent in the etiology of Alzheimer's disease, Guamiam amyotrophic lateral sclerosis, and parkinsonism-dementia.

Vaccination granulomas and aluminium allergy: course and prognostic factors.
Kaaber K. – Nielsen A.O. – Veien N.K.
From: Contact Dermatitis (1992 May) 26(5):304-6

21 children who had cutaneous granulomas following immunization with a vaccine containing aluminium hydroxide, and who had positive patch tests to aqueous aluminium chloride and/or to a Finn Chamber, were followed for 1 to 8 years. During the period of observation, the symptoms cleared in 5 children, improved in 11, and remained unchanged in 5.

Distribution of aluminum in different brain regions and body organs of rat.
Vasishta R.K. – Gill K.D.
From: Biol Trace Elem Res (1996 May) 52(2):181-92

In the present study, an attempt has been made to investigate the distribution of aluminum in different regions of brain and body organs of male albino rats, following subacute and acute aluminum exposure. Aluminum was observed to accumulate in all regions of the brain with maximum accumulation in the hippocampus. Aluminum was also seen to compartmentalize in almost all the tissues of the body to varying extents, and the highest accumulation was in the spleen.

http://www.generationrescue.org/autism/08-aluminum-toxicity.htm

Studies of aluminum-alzheimers and neurotoxicity causation

1: J Alzheimers Dis. 2006 Nov;10(2-3):179-201.Aluminum and Alzheimer's disease: a new look.Miu AC, Benga O.

2: J Alzheimers Dis. 2006 Nov;10(2-3):223-53.Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration.Yokel RA.

3: J Alzheimers Dis. 2006 Nov;10(2-3):135-44.Mechanisms of aluminum-induced neurodegeneration in animals: Implications forAlzheimer's disease.Savory J, Herman MM, Ghribi O.

4: Brain Res Rev. 2006 Aug 30;52(1):193-200. Epub 2006 Mar 10.Some aspects of astroglial functions and aluminum implications forneurodegeneration.Aremu DA, Meshitsuka S.

5: J Alzheimers Dis. 2005 Nov;8(2):171-82; discussion 209-15.Effects of aluminum on the nervous system and its possible link withneurodegenerative diseases.Kawahara M.

6: Curr Opin Pharmacol. 2005 Dec;5(6):637-40. Epub 2005 Sep 28.Aluminum: new recognition of an old problem.Klein GL.

7: Toxicol Ind Health. 2002 Aug;18(7):309-20.Aluminum as a toxicant.Becaria A, Campbell A, Bondy SC.

8: Immunol Allergy Clin North Am. 2003 Nov;23(4):699-712.Aluminum inclusion macrophagic myofasciitis: a recently identified condition.Gherardi RK, Authier FJ.

The authors conclude that the persistence of aluminum hydroxide at the site ofintramuscular injection is a novel finding which has an exact significance thatremains to be established fully. It seems mandatory to evaluate possiblelong-term adverse effects induced by this compound, because this issue has notbeen addressed (in the past, aluminum hydroxide was believed to be clearedquickly from the body). If safety concerns about the long-term effects ofaluminum hydroxide are confirmed, novel and alternative vaccine adjuvants torescue vaccine-based strategies should be proposed.

9: Brain Res Bull. 2003 Nov 15;62(1):15-28.The role of metals in neurodegenerative processes: aluminum, manganese, and zinc.Zatta P, Lucchini R, van Rensburg SJ, Taylor A.

Aluminum has long been known as a neurotoxic agent. It is an etiopathogenic factor in diseases related to long-term dialysis treatment, and it has been controversially invoked as anaggravating factor or cofactor in Alzheimer's disease as well as in other neurodegenerative diseases.

10: Nutr Rev. 2003 Sep;61(9):306-10. Parenteral nutrition-associated cholestasis in neonates: the role of aluminum.Arnold CJ, Miller GG, Zello GA.

Aluminum loading in animals and humans causes hepaticaccumulation and damage. The degree of aluminum contamination of PN solutions hasdecreased over time, but contamination still significantly exceeds levels thatare safe for human neonates.

14: J Neurosci Res. 2001 Dec 1;66(5):1009-18.Aluminum, NO, and nerve growth factor neurotoxicity in cholinergic neurons. Szutowicz A.

15: Ann N Y Acad Sci. 1997 Oct 15;825:152-66.
Toxin-induced blood vessel inclusions caused by the chronic administration ofaluminum and sodium fluoride and their implications for dementia.
Isaacson RL, Varner JA, Jensen KF.

17: J Toxicol Environ Health. 1996 Aug 30;48(6):649-65.Systemic aluminum toxicity: effects on bone, hematopoietic tissue, and kidney.Jeffery EH, Abreo K, Burgess E, Cannata J, Greger JL.

18: J Toxicol Environ Health. 1996 Aug 30;48(6):585-97.What we know and what we need to know about developmental aluminum toxicity.Golub MS, Domingo JL.

19: J Toxicol Environ Health. 1996 Aug 30;48(6):569-84.Aluminum toxicokinetics.Exley C, Burgess E, Day JP, Jeffery EH, Melethil S, Yokel RA

http://www.whale.to/a/alum.html

Interesting info on how much aluminum is contained in vaccinations:

At the National Autism Association conference in Atlanta, Georgia November 8-11, 2007, Dr. David Ayoub gave a rousing presentation on the link between the accumulation of aluminum in the body and the development of autism spectrum disorders. He provided stunning documentation from diagnostic tests done on autistic children showing very high aluminum levels along with known symptoms of aluminum poisoning. He also brought up the Alzheimers/aluminum connection.

When going through Dr. Ayoub's PowerPoint presentation online, I decided to check out just how much aluminum was in such common products as antacids. I found that Maalox® extra strength contains 306 mg. of aluminum hydroxide for each dose and Mylanta®contains 500 mg. for each dose.

But the amount of aluminum being injected into infants as recommended by the Advisory Committee on Immunization Practices is a jaw dropper.

The average birth weight for a baby is 7.4 lbs. (3.4 kg.) They receive soon after birth a hepatitis B vaccine that, if it happens to be Recombivax Hepatitis B from Merck, contains 500 mcg. of aluminum or 147 mcg. of aluminum per kg. of body weight. If the Energix vaccine from GlaxoSmithKline is administered, the pediatric dose is 250 mcg. of aluminum as aluminum hydroxide totaling 73.5 mcg. of aluminum per kg. of body weight.

The amount of time for these doses of aluminum to be eliminated by an infant’s immature kidneys is unknown, as is the time it takes for aluminum to transfer from muscular tissue to the bloodstream and, ultimately, into the brain. Meanwhile, the infant is continually dosed with aluminum through infant formula, and even in breastmilk but to a lesser degree.

The average baby visiting their pediatrician for the two-month, well-baby checkup weighs 9.25 lbs. (4.2 kg.) and could receive as much as 1475 mcg. of injected aluminum within 30 min. or 351 mcg. of aluminum per kg. of body weight. The breakdown of vaccines the pediatrician is supposed to administer follows: Hep B (250 to 500 mcg Al); Rotateq® (oral); DTaP (Infanrix® - 625 mcg Al and DAPTACEL® - 330 mcg Al); PCV - pneumococcal vaccine with 8 antigens (125 mcg. Al); Hib – haemophilus influenza type b (225 mcg. Al) and; IPV – inactivated polio vaccine.

Then, at four and six months of age, the bolus doses of aluminum continue to be injected.
What are the risks of this accumulating aluminum considering the constant exposure in utero, while feeding, breathing the air outside, and through baby products such as baby powder? Maybe you will want to minimize the number of injections your baby will receive by giving Pediarix®, a five in one shot. Think again. This shot contains as much as 850 mcg. of aluminum. What is most shocking is the fact that an infant’s body systems are all so immature and dependent on his mother’s "raw, enzyme-rich" milk (and love) for proper development. How can such a developing human withstand this toxic assault?

In the meantime, the CDC, EPA and FDA continue to deny the toxic nature of aluminum in our environment and medications.

Allergens in vaccinations

Egg (via chick embryonic fluid), Gelatin, Soy, Yeast and Antibiotics= Allergens in Vaccinations... note that antibiotics may also serve as allergens with a risk of anaphylaxis but this is addressed in the antibiotics page.

http://www.wellness.com/reference/allergies/vaccine-allergy/symptoms-and-causes

Patients may develop an allergic reaction to a vaccine if the immune system overreacts to substances contained in the vaccine. Most allergic reactions occur when the vaccine contains antibiotics, egg proteins, gelatin, or mercury.

Typically, an allergic response is not triggered the first time the body encounters the allergen (substance that causes an allergic reaction). In fact, some people can be exposed to the allergen several times before an allergy develops. It is only after one or more episodes of exposure to an allergen that the immune system becomes sensitized. During this process, the body's white blood cells develop immunoglobulin E (IgE) antibodies to the allergens. Once sensitized, the antibodies quickly detect and bind to the allergens in the body.

After binding to allergens, antibodies trigger other immune cells to release chemicals (such as histamine) that cause allergic symptoms, such as runny nose, watery eyes, and sneezing, as well as anaphylaxis. Anaphylaxis is a severe allergic reaction that affects many parts of the body. Symptoms vary from mild to severe and may include breathing difficulties, shock, and loss of consciousness. Anaphylaxis is a potentially fatal reaction that requires immediate treatment.

SYMPTOMS

Anaphylaxis (anaphylactic shock): Anaphylaxis is a systemic allergic reaction, which means that many parts of the body are affected. Symptoms of anaphylaxis can vary from mild to severe and may include low blood pressure, breathing difficulties, chest pain, hives, and loss of consciousness. The time lapse between contact with the allergen and anaphylactic symptoms varies among individuals. Symptoms may appear immediately or may be delayed from 30 minutes to one hour after exposure. Symptoms may also disappear and then recur hours later. Once symptoms arise, they progress quickly. Anyone with symptoms of anaphylaxis should seek immediate treatment.

Angioedema: Some hypersensitive patients may experience angioedema in response to a vaccine. Angioedema refers to the swelling that occurs in the tissue just below the skin. Angioedema is similar to hives, except it occurs deeper in the skin. The swellings, known as welts, usually appear around the eyes and mouth. They may also be present on the hands, feet, and throat.

Asthma: Asthma symptoms, including coughing, wheezing, shortness of breath, or difficulty breathing, may be triggered by vaccine allergies, especially in infants and young children.

Hives: Some patients may develop hives. Hives are red, itchy swollen welts on the skin that may appear suddenly and disappear quickly. They often develop in clusters, with new clusters appearing as other areas clear up.

http://www.vran.org/vaccines/anaphylaxis/vaccine-ana.htm

Allergy 1978 Jun:33(3):155-9 Aluminum phosphate but not calcium phosphate stimulates the specific IgE response in guinea pigs to tetanus toxoid. It is hypothesized that the regular application of aluminum compound-containing vaccines on the entire population could be one of the factors leading to the observed increase of allergic diseases. PMID 707792

Pediatric Allergy Immunol 1994 May;5(2):118-23 Immunoglobulin E and G responses to pertussis toxin after booster immunization in relation to atopy, local reactions and aluminum content of the vaccines. The role of aluminum for IgG and IgE responses to pertussis toxin (PT), as well as for side effects, was investigated in 49 children with known atopy status………………the addition of aluminum to the pertussis vaccine was, thus, associated with a stronger IgG antibody response, but tended also to induce a stronger IgE antibody response. The correlation between total IgE and PT-IgE, which was most prominent in children with atopy, indicates that the role of immunization for the development of allergy merits further studies. PMID 808719

http://lrsitbrd.nic.in/IJTB/Year%201990/October%201990/october%201990%20D.pdf

A PILOT STUDY TO ASSESS POST VACCINATION ALLERGY INDUCED
AFTER BCG VACCINATION IN INFANTS VACCINATED BY AUXILIARY
NURSE-MIDWIVES IN AJMER (RAJASTHAN)

Yet, the observed mean size of post-vaccination allergy in both the groups was below 6 mm i.e. much lower than what could be expected. Since the maximum extent of post-vaccination allergy occurs three to four months following vaccination, the possible waning of allergy, if any, that could have occurred in the two to three months that elapsed after the target timing could not have been so profound.

http://www.chiroweb.com/mpacms/dc/article.php?id=31598

Do DTP and Tetanus Vaccinations Cause Asthma?
New Study Shows Vaccinated Children Twice as Likely to Get Asthma and Other Allergy-Related Symptoms
By Michael Devitt

A new study in the Journal of Manipulative and Physiological Therapeutics1 supports the findings of three previous studies that children who receive diphteria-tetanus-pertussis (DTP) or tetanus vaccines are more likely to have a “history of asthma” or other “allergy-related respiratory symptoms.” The study reviewed data from the Third National Health and Nutrition Examination Survey, which was conducted by the National Center for Health Statistics from 1988 to 1994.

http://www.vaccination.inoz.com/asthma3.html

Michel Odent found the frequency of asthma in a group of fully vaccinated children to be 11%, while a 1997 NZ study(21) found 23%. Both found the frequency in the unvaccinated children to be only 0 1%. Several studies have found the rate higher after vaccines that use aluminum hydroxide as adjuvants in the postnatal period.(22)

Significantly, there was a decrease in deaths from asthma in the U.S. for some years until the DPT vaccine was mandated in the U.S. for school entry, in 1978. Since then, deaths from asthma(23) and other immune disorders have been rising (as has also the reported incidence of whooping cough itself!).

20 JAMA 1994;272 (8): pgs 592-3, and Lancet 1994:344:140.

21 Epidemiology 1997 Nov 8:6 678-80

22 J Allergy Clin Immunol 1999;104:1128-30. Dec 1999; 104 Number 6

23 CDC MMWR reports (See Appendix B in Submission article on this web site)

http://www.vaccinetruth.org/peanut_oil.htm

Reported pertussis infection and risk of atopy in 8- to 12-yr-old vaccinated and nonvaccinated children.

1. Original Article
Pediatric Allergy & Immunology. 19(1):46-52, February 2008.

Bernsen, Roos M. D. 1, 2; Nagelkerke, Nico J. D. 2; Thijs, Carel 3; van der Wouden, Johannes C. 1

Abstract:

Pertussis infection has been suspected to be a potential causal factor in the development of atopic disease because of the effect of pertussis immunization on specific IgE antibodies. Although several studies found a positive association between pertussis infection and atopic disorders, this relationship has not yet been studied in a population stratified by vaccination status. To assess the association between pertussis infection and atopic disorders in pertussis-unvaccinated children and in pertussis-vaccinated children. Using data from a previously conducted study on the relationship between the diphtheria-tetanus-pertussis-(inactivated) poliomyelitis vaccination in the first year of life and atopic disorders, the study population of 1872 8-12 yr old was divided into children pertussis-unvaccinated and children pertussis-vaccinated in the first year of life. Within each group, the association between pertussis infection and atopic disorders (both as reported by the parents) was assessed. In the unvaccinated group, there were no significant associations between pertussis infection and atopic disorders. In the vaccinated group, all associations between pertussis infection and atopic disorders were positive, the associations with asthma [odds ratio (OR) = 2.24, 95% confidence interval (CI95%): 1.36-3.70], hay fever (OR = 2.35, CI95%: 1.46-3.77) and food allergy (OR = 2.68, CI95%: 1.48-4.85) being significant. There was a positive association between pertussis infection and atopic disorders in the pertussis vaccinated group only.


http://www.mja.com.au/public/issues/184_04_200206/eld10500_fm.html

eMJA The Medical Journal of Australia

Pediatrics 1988 Jun (81) Supplement – Report on the Task Force on Pertussis and Pertussis Immunization – extract states, For more than 25 years, it has been known that pertussis vaccine is a reliable adjuvant for the production of experimental allergic encephalitis.

Bull Eur Physiopathol Respir 1987;23 Suppl 10:111s-113s

A model for experimental asthma: provocation in guinea-pigs immunized with Bordetella pertussis states, “ Guinea-pigs were sensitized with killed Bordetella pertussis………the presence of the immediate type of immune response was verified by passive cutaneous anaphylaxis……B. pertussis not only alters adrenergic function but provocation in B. pertussis-sensitized guinea-pigs seems to be a good model for bronchial asthma. PMID 2889487

Pediatr Res 1987 Sep;22(3):262-7

Murine responses to immunization with pertussis toxin and bovine serum albumin: I. Mortality observed after bovine albumin challenge is due to an anaphylactic reaction……….the results of our experiments have established that the disease induced by coimmunizing mice with Ptx and BSA is due to an immediate type hypersensitivity…………PMID 3309858


Infect Immun 1987 Apr.;55(4):1004-8

Anaphylaxis or so-called encephalopathy in mice sensitized to an antigen with the aid of pertussigen (pertussis toxin), states, Sensitization of mice with 1mg of bovine serum albumin (BSA) or chicken egg albumin (EA) ………….induced a high degree of anaphylactic sensitivity when the mice were challenged i.v. with 1 mg of antigen 14 days later. PMID 3557617

JAMA 1994 Aug 24-31;272(8):592-3

Pertussis vaccination and asthma: is there a link?

A study of 450 children, 11% of the children who had received the pertussis vaccination suffered from asthma, as compared with only 2% of the children who had not been vaccinated. [This does not tell you if the "unvaccinated children" had no vaccinations or just other vaccainations...- bfg] PMID 8057511

Allergy 1983 May;38(4):261-71

The non-specific enhancement of allergy. III. Precipitation of bronchial anaphylactic reactivity in primed rats by injection of alum or B. pertussis vaccine: relation of response capacity to IgE and IgG2a antibody levels. …..These results show that injection of alum or B. pertussis vaccine without antigen can precipitate/enhance anaphylactic response capacity and production of specific and non-specific IgE and IgG2a. PMID 6307077

Allergy 1980 Jan;35(1):65-71

Antigen-induced bronchial anaphylaxis in actively sensitized guinea pigs. Pattern of response in relation to immunization regimen….guinea-pigs sensitized with small amounts of antigen together with alum produced IgE and IgG1 antibodies. PMID 7369497

Allergy 1978 Jun:33(3):155-9

Aluminum phosphate but not calcium phosphate stimulates the specific IgE response in guinea pigs to tetanus toxoid. It is hypothesized that the regular application of aluminum compound-containing vaccines on the entire population could be one of the factors leading to the observed increase of allergic diseases. PMID 707792

Pediatr Allergy Immunol 1994 May;5(2):118-23

Immunoglobulin E and G responses to pertussis toxin after booster immunization in relation to atopy, local reactions and aluminum content of the vaccines. The role of aluminium for IgG and IgE responses to pertussis toxin (PT), as well as for side effects, was investigated in 49 children with known atopy status…the addition of aluminum to the pertussis vaccine was, thus, associated with a stronger IgG antibody response, but tended also to induce a stronger IgE antibody response. The correlation between total IgE and PT-IgE, which was most prominent in children with atopy, indicates that the role of immunization for the development of allergy merits further studies. PMID 8087191

Adv Drug Deliv Rev 1998 Jul 6;32(3):155-172

Entitled Aluminum compounds as vaccine adjuvants stated, “Limitations of aluminum adjuvants include local reactions, augmentation of IgE antibody responses, ineffectiveness for some antigens and inability to augment cell-mediated immune responses, especially cytotoxic T-Cell responses. PMID 10837642

Annals of Asthma, Allergy and Immunology, Vol. 85, Number 1, July 2000 article T-cell subsets (Th1 versus Th2) includes Figure 7 on page 15 – “Factors responsible for the imbalance of the Th1/Th2 responses which is partly responsible for the increased prevalence of allergy in Western countries. Risk for atopy – Th2, increased exposure to some allergens and Th2-biasing vaccines (alum as adjuvant).”

Immunology Today, March 1998, Volume 19, p. 113-116 states, “Modern vaccinations, fear of germs and obsession with hygiene are depriving the immune system of information input upon which it is dependent. This fails to maintain the correct cytokine balance and fine-tune T-cell regulation, and may lead to increased incidences of allergies and autoimmune diseases.”

From the journal Allergy 1999, 54, 398-399

Multiple Vaccination effects on atopy, “An increase in the incidence of childhood atopic diseases may be expected as a result of concurrent vaccination strategies that induce a Th2-biased immune response. What should be discussed is whether the prize of a reduction of common infectious diseases through a policy of mass vaccination from birth is worth the price of a higher prevalence of atopy.”

Journal of Manipulative and Physiological Therapeutics, Feb. 2000; 23(2):81-90

Effects of diphtheria-tetanus-pertussis or tetanus vaccination on allergies and allergy-related respiratory symptoms among children and adolescents in the United States, “The odds of having a history of asthma was twice as great among vaccinated subjects than among unvaccinated subjects. The odds of having any allergy-related respiratory symptom in the past 12 months was 63% greater among vaccinated subjects than unvaccinated subjects.” PMID 10714532

Thorax 1998 Nov;53(11):927-32

Early childhood infection and atopic disorder, stated “Interpretation of the prediction of atopic disorders by immunisation with wholecell pertussis vaccine and treatment with oral antibiotics needs to be very cautious because of the possibilities of confounding effects and reverse causation. However, plausible immune mechanisms are identifiable for the promotion of atopic disorders by both factors and further investigation of these association is warranted.” PMID 10193389

Epidemiology 1997 Nov;8(6):678-80

Is infant immunization a risk factor for childhood asthma or allergy? This study followed 1,265 children born in 1977. The 23 children who received no DPT and polio immunizations had no recorded asthma episodes or consultations for asthma or other allergic illness before age 10 years; in the immunized children, 23.1% had asthma episodes, 22.5% asthma consultations, and 30% consultations for other allergic illness. Similar differences were observed at ages 5 and 16 years. PMID 9345669


Arerugi 2000 Jul;49(7):585-92

The Effect of DPT and BCG vaccinations on atopic disorders findings include, “From these results we conclude that DPT vaccination has some effect in the promotion of atopic disorders……. PMID 10944825

CAN VACCINES CAUSE FOOD ALLERGIES?

JAMA 2001 Apr 4;285(13):1746-8

Detection of peanut allergens in breast milk of lactating women states, “Most individuals who react to peanuts do so on their first known exposure”……………..and concluded “Peanut protein is secreted into breast milk of lactating women following maternal dietary ingestion. Exposure to peanut protein during breastfeeding is a route of occult exposure that may result in sensitization of at-risk infants.” PMID 11277829

Women have been ingesting peanut protein while breastfeeding for decades. What has changed in the last 15 years to cause infants to develop life-threatening allergies to this legume? One change has been the vaccination schedule.

The Int Arch Allergy Immunol 1999 Jul; 119(3):205-11

Pertussis adjuvant prolongs intestinal hypersensitivity concludes: Our findings indicate nanogram quantities of PT (pertussis toxin), when administered with a food protein, result in long-term senitization to the antigen, and altered intestinal neuroimmune function. These data suggest that exposure to bacterial pathogens may prolong the normally transient immune responsiveness to inert food antigens. PMID 10436392

Does this study explain why babies and toddlers react on their first exposure to the peanuts or other antigens? The babies may have been sensitized by the vaccines to the proteins through breast milk or formula ingested at the time of vaccination. This would also explain why children are anaphylactic to a variety of proteins, such as different tree nuts, peanuts, egg, legumes, milk, seeds, etc., depending on what proteins the mother ate at the time of vaccination.

IS THE INTRODUCTION OF THE HIB VACCINE CONNECTED TO THE INCREASE IN FOOD ANAPHYLAXIS IN CHILDREN?

Rates of anaphylaxis have increased dramatically since the introduction of the Hib vaccine.

Clin Exp Pharmacol Physiol 1979 Mar-Apr;6(2):139-49

Comparison of vaccination of mice and rats with Haemophilus influenzae and Bordetella pertussis as models of atopy, states “The Haemophilus influenzae vaccinated experimental animal provides a model that is possibly more related to human atopy than the Bordetella pertussis vaccinated animal.” PMID 311260

Ann Allergy 1979 Jan;42(1):36-40

States “To determine whether Haemophilus influenzae could be a factor in human atopy its effects were studied on the (para-)Sympathic Cyclic nucleotide-histamine axis in rats. Haemophilus influenzae vaccination induced changes in the cholinergic system compatible with higher cyclic GMP levels and enhanced histamine release. The authors suggest an involvement of the cholinergic system in Haemophilus influenzae vaccination effects. PMID 216288

Agents Actions 1984 Oct;15(3-4):211-5 entitled Bronchial hyperreactivity to histamine induced by Haemophilus influenzae vaccination states “……This suggests a hyperreactivity of the parasympathethic, cholinergic pathways as a result of H.influenzae vaccination.” PMID 6335351


Eur J. Pharmacol 1980 Apr 4;62(4):261-8 entitled The effects of Haemophilus influenzae vaccination on anaphylactic mediator release and isoprenaline-induced inhibition of mediator release states “These results indicate an increased sensitivity to antigenic challenge and suggest that the functioning of beta-adrenoceptors was decreased as a result of H. Influenzae vaccination.” PMID 6154589

DOES THE PERTUSSIS VACCINE CAUSE ASTHMA, ALLERGIES AND ANAPHYLAXIS?


Pediatrics 1988 Jun (81) Supplement – Report on the Task Force on Pertussis and Pertussis Immunization – extract states, For more than 25 years, it has been known that pertussis vaccine is a reliable adjuvant for the production of experimental allergic encephalitis.4

Pediatr Res 1987 Sep;22(3):262-7

Murine responses to immunization with pertussis toxin and bovine serum albumin: I. Mortality observed after bovine albumin challenge is due to an anaphylactic reaction……….the results of our experiments have established that the disease induced by coimmunizing mice with Ptx and BSA is due to an immediate type hypersensitivity…………PMID 3309858

Infect Immun 1987 Apr.;55(4):1004-8

Anaphylaxis or so-called encephalopathy in mice sensitized to an antigen with the aid of pertussigen (pertussis toxin), states, Sensitization of mice with 1mg of bovine serum albumin (BSA) or chicken egg albumin (EA) ………….induced a high degree of anaphylactic sensitivity when the mice were challenged i.v. with 1 mg of antigen 14 days later. PMID 3557617

ARE MULTIPLE VACCINES CAUSING OUR IMMUNE SYSTEMS TO FAIL?

Immunology Today, March 1998, Volume 19, p. 113-116 states, “Modern vaccinations, fear of germs and obsession with hygiene are depriving the immune system of information input upon which it is dependent. This fails to maintain the correct cytokine balance and fine-tune T-cell regulation, and may lead to increased incidences of allergies and autoimmune diseases.”

From the journal Allergy 1999, 54, 398-399

Multiple Vaccination effects on atopy, “An increase in the incidence of childhood atopic diseases may be expected as a result of concurrent vaccination strategies that induce a Th2-biased immune response. What should be discussed is whether the prize of a reduction of common infectious diseases through a policy of mass vaccination from birth is worth the price of a higher prevalence of atopy.”

Journal of Manipulative and Physiological Therapeutics, Feb. 2000; 23(2):81-90

Effects of diphtheria-tetanus-pertussis or tetanus vaccination on allergies and allergy-related respiratory symptoms among children and adolescents in the United States, “The odds of having a history of asthma was twice as great among vaccinated subjects than among unvaccinated subjects. The odds of having any allergy-related respiratory symptom in the past 12 months was 63% greater among vaccinated subjects than unvaccinated subjects.” PMID 10714532

Thorax 1998 Nov;53(11):927-32

Early childhood infection and atopic disorder, stated “Interpretation of the prediction of atopic disorders by immunisation with wholecell pertussis vaccine and treatment with oral antibiotics needs to be very cautious because of the possibilities of confounding effects and reverse causation. However, plausible immune mechanisms are identifiable for the promotion of atopic disorders by both factors and further investigation of these association is warranted.” PMID 10193389

Epidemiology 1997 Nov;8(6):678-80

Is infant immunization a risk factor for childhood asthma or allergy? This study followed 1,265 children born in 1977. The 23 children who received no DPT and polio immunizations had no recorded asthma episodes or consultations for asthma or other allergic illness before age 10 years; in the immunized children, 23.1% had asthma episodes, 22.5% asthma consultations, and 30% consultations for other allergic illness. Similar differences were observed at ages 5 and 16 years. PMID 9345669

Arerugi 2000 Jul;49(7):585-92

The Effect of DPT and BCG vaccinations on atopic disorders findings include, “From these results we conclude that DPT vaccination has some effect in the promotion of atopic disorders……. PMID 10944825

http://drgreene.mediwire.com/main/Default.aspx?P=Content&ArticleID=111728

Of the 1.9 billion doses of vaccines administered in the United States between 1991 and 2001, only 2,281 cases of allergic reactions were reported.1

(which means there were really 20,000 - 200,000 because doctors only report 1-10% of all adverse reactions to VAERS as admitted by the CDC and FDA)

Local allergic reaction to a vaccine may consist of a wheal and flare or localized urticaria at the injection site. Systemic allergic reactions may be classified as non-life-threatening or life-threatening. Non-life-threatening systemic reactions such as generalized urticaria may follow DTaP, DT, and dT administration. Transient petechiae or urticaria following DPT vaccination usually occurs within minutes and may be caused by preformed circulating antibodies to diphtheria and tetanus. Transient generalized urticaria following a vaccine is not a contraindication to further vaccination.7

An Arthus reaction is a severe local reaction with warmth, erythema, edema, petechiae, or ulceration usually occurring two to eight hours after vaccination. This reaction occurs secondary to the presence of a high level of preformed antibody in a previously vaccinated patient, and most commonly follows diphtheria and tetanus toxoid injection. For this reason, these booster vaccines should not be given more often than every 10 years,8 although, in cases of tetanus exposure, a booster injection for tetanus may be given if more than five years have passed since the last dose.

Anaphylactic reactions are life-threatening systemic allergic reactions that may manifest as hypotension, bronchospasm, generalized urticaria, angioedema, and laryngeal edema. An estimated two cases of anaphylaxis occur for every 100,000 DPT injections administered; the rate of anaphylaxis after DTaP vaccination is unknown. Anaphylaxis to hepatitis B vaccine has been estimated to occur in one of every 600,000 recipients, most of whom are adults.4 Eleven reports of anaphylaxis secondary to MMR vaccination (after 70 million MMR doses administered) have been received by VAERS.9 The frequency of anaphylaxis to tetanus toxoid is 1.6 for every million doses given.10 For all vaccines, a true anaphylactic reaction is an absolute contraindication to further immunization with that vaccine.

It is important to differentiate other, more common, nonallergic clinical syndromes from anaphylactic vaccine reactions. Vasovagal reactions with pallor, bradycardia, weakness, dizziness, and brief syncope may occur five to 15 minutes after vaccination. These reactions occur more often in adolescents and adults than in children. Over 2,000 reports of vaccine-associated syncope were received by VAERS from 1990–2001.3 A hypotonic–hyporesponsive episode (HHE) is a shock-like syndrome, occurring 10 to 48 hours after vaccination, marked by sudden loss of muscle tone, pallor, fever, and unresponsiveness. HHE has been described following whole cell pertussis vaccine and is considered a relative contraindication (the physician should weigh the benefit against the risk in determining whether to administer the vaccine) to pertussis revaccination.9

Allergic reactions to pneumococcal, Hib, hepatitis B, hepatitis A, and poliovirus vaccines occur very rarely. Allergic reactions to any vaccine may occur secondary to the vaccine antigen itself or to other vaccine components. IgE antibodies to tetanus or diphtheria toxoids have been detected in the sera of patients experiencing generalized urticaria or anaphylaxis to vaccines containing these toxoids.11

Because the live attenuated viruses used in MMR vaccine are grown in cultured chick embryo fibroblasts, minute amounts of the egg protein ovalbumin (<1 nanogram) are contained in the final vaccine preparation. Before 1997, the American Academy of Pediatrics (AAP) recommended that patients with a history of egg anaphylaxis undergo skin testing with the MMR vaccine.12 Positive skin tests would necessitate vaccine desensitization via a graded dose protocol. These recommendations were revised in 1997 after numerous reports of safe administration of MMR vaccine to children allergic to eggs.13–17 Skin testing is no longer required for egg-allergic individuals.

Instead, MMR may be routinely administered to egg-allergic children with the precaution that vaccine recipients be observed for 90 minutes post-vaccination in a facility equipped to treat vaccine anaphylaxis.18 Allergic reactions to MMR vaccine have occurred in children who are not allergic to eggs and may also be caused by sensitivity to neomycin or gelatin, both of which are contained in the vaccine. Khakoo has suggested that children with egg allergy and asthma may be at increased risk of adverse MMR reactions.19

The influenza virus vaccine contains greater amounts of ovalbumin than does the MMR vaccine, because the virus utilized in the vaccine is derived from the allantoic fluids of infected chick embryos. Generally, influenza virus vaccine is contraindicated in any child with a history of egg anaphylaxis. A recent study, however, included a protocol for relatively safe administration of influenza virus vaccine to egg-allergic individuals.20

Egg protein is also contained within the monovalent measles, monovalent mumps, yellow fever, and rabies vaccines, but not within monovalent rubella vaccine.
Stabilizers are added to vaccines to stabilize the vaccine antigen. Porcine gelatin is the stabilizer contained within MMR and its component vaccines and in varicella, viral influenza, yellow fever, Japanese encephalitis, and DTaP vaccines (Table 4).

Patients reporting clinical gelatin allergy have usually reacted to the bovine gelatin contained in foods. These patients may be at risk of allergic reactions following administration of gelatin-containing vaccines.24 It is possible that many reactions previously attributed to egg allergy in MMR recipients were due to gelatin allergy. IgE antibodies to gelatin were detected in 93% of patients reporting anaphylaxis to the monovalent measles, mumps, and rubella vaccines in Japan.25

Adjuvants are generally utilized in vaccines that contain killed microbes or toxoids. The aluminum-adsorbed vaccines DTaP, DT, Td, hepatitis A, and hepatitis B are adjuvant-containing vaccines. Administration of such vaccines may cause subcutaneous nodules that persist for weeks or months.4 Pain and tenderness at the injection site have also been attributed to aluminum contained in various vaccine preparations.

Current hepatitis B vaccines are prepared from yeast cultures. Yeast hypersensitivity is an absolute contraindication for hepatitis B vaccine administration.26

Allergy to chicken, duck, or feathers is not a contraindication to any routine pediatric vaccine.

The potential reactivity of latex-sensitive individuals to the latex contained in the rubber stoppers of vaccine vials is a concern. However, most vaccine vials contain synthetic rubber rather than the natural rubber latex associated with clinical reactivity.

Avoiding allergic reactions: Pre-vaccination screening

All patients should be screened before vaccine administration for any possible contraindications to vaccination (see the Key Points box). In addition to obtaining a detailed patient history for any food allergies (egg or gelatin) or drug allergies (such as to neomycin, polymyxin B, streptomycin), it is important to screen all vaccine recipients for a history of vaccine reactions. Revaccination is contraindicated in any patient reporting prior anaphylaxis to a vaccine or vaccine component.