MSG & Aspartame During Pregnancy, Potential for Causing Brain Damage at Normal Human Exposure Levels

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MSG & Aspartame During Pregnancy

Two Common Food Additives Show Potential for

Causing Brain Damage at Normal Human Exposure Levels

 

Environmental Neurotoxicology Research Project

University of South Florida, Tampa - 1997

Richard Pressinger (M.Ed.)

 

INTRODUCTION

 

There has been considerable media attention given to the harmful

health effects of MSG over the past several years. The Food and Drug

Administration (FDA) has also come out with its recent report that

MSG is " safe " for most people except for those with serious asthma

difficulties.

 

MSG is a flavor enhancer used by the food industry for several

reasons. The primary reason for its use is that it increases the

" perceived " taste of any item that contains MSG. For instance, when

Campbell's soup makes chicken soup, they found they would only have

to add only about one-half as much chicken to their product while

using MSG to achieve the same taste profile as as if they added no

MSG but added twice the amount of chicken. As you can see the

addition of MSG to consumer products increases the profit margin of

companies that use it. Unfortunately, the use of MSG is not without

consequence.

 

World production in 1976 was 262,000 metric tons per year. Studies by

Reif-Lehrer (67 in Special Article) reported that 25% of a population

sample who have been exposed to Chinese restaurant food exhibit at

least some adverse symptoms.

 

Prior to the 1970's, MSG was routinely added to baby food before the

practice was stopped following government suggestions. Commenting on

this issue, Dr. Olney, at the Department of Psychiatry, Washington

University states,

 

According to an NAS (National Academy of Science) Subcommittee, in

considering the safety of added MSG in baby foods, one must remember

that the levels added are small - not higher than 0.6 g%.... This

means that one small jar of baby food (130 g) would provide about

0.78 g of MSG or 0.13 g/kg of body weight for a human infant weighing

6 kg. Based on our finding that an oral dose of 1 g/kg in the primate

or 0.5 g/kg in the mouse is sufficient to destroy hypothalamic

neurons, this leaves a 4 to 8 fold margin of safety for a human

infant eating one jar, a 2 to 4 fold margin if two jars are eaten and

so forth. This is substantially less than the 100-fold margin

generally recommended to accommodate contingencies such as species or

individual differences in susceptibility to the mechanism of a toxic compound.

 

In support of their assumption that human infants are invulnerable to

MSG-induced brain damage, the NAS Subcommittee pointed to absence of

behavioral manifestations in human infants given intravenous

infusions of protein hydrolysates providing 0.3 g/kg/day of free

glutamic acid. Our demonstration that MSG destroys hypothalamic

neurons in monkeys as well as mice at intake doses lower than those

required to produce acute behavioral manifestations points to a

serious flaw in this line of reasoning. The subcutaneous injection of

protein hydrolysate (0.2 cc) produces, in 10 day old infant mice, a

hypothalamic lesion unaccompanied by behavior disturbances (22). "

 

There have been at least two other MSG studies using infant primates

which found no significant brain lesions after MSG exposure (Abraham

et al. (10). However, in criticism of these reports, Dr. Olney states

that because of the " remarkable efficiency " with which degenerate

elements are removed from the scene of MSG-induced lesion (minimal

lesions are cleared from mouse brain within 12 to 18 hours), it is

essential to examine the brain earlier than 24 hours (Dr. Olney's

studies examined at 3 and 5 hours). This is particularly true if, due

to vomiting, the infant retained very little MSG, and therefore,

sustained only a minimal lesion.

 

 

 

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Infant Seizures Improve After MSG Removal

 

A child experiencing " innumerable seizures " at 6 months of age showed

dramatic improvements after removal of MSG from the child's diet. The

case history, reported by Dr. L. Reif-Lehrer of Harvard Medical

School in the journal Federal Proceedings, showed the child did not

respond to dilantin treatment but had symptoms " completely alleviated

by a diet that excluded exogenously added glutamate. "

 

The child's first seizures began at 6 months of age on October 14,

1971. For the next four months the child's seizures continued even

with treatment using dilantin, mysoline and pyridoxine. At 9 months

of age the child was experiencing 100 or more seizures per day.

 

The following medical bibliography lists chronologically the events

observed from removal of MSG from the child's diet:

 

February 15, 1972

 

 

 

Physicians removed all MSG containing foods from the child's diet

 

February 20, 1972

 

(Age 10.5 mo.)

 

No seizures for past 3 days, first free period since onset.

Reduction of anticonvulsants begun

 

March 20, 1972

 

(Age 11.5 mo.)

 

Off all anticonvulsants.

No seizures.

 

May 10, 1972

 

(Age 13 mo.)

 

Attacks 2-3 hr after surreptitious ingestion of pizza

( " Snitched " from the refrigerator with the help of an older brother).

 

August, 1972

 

(Age 17 mo.)

 

Several attacks after ingestion of family hog, locally prepared

sausage later found to contain MSG.

 

February, 1973

 

(Age 2.0 years)

 

No attacks for 7 months.

 

August, 1973

 

(Age 2.5 years)

 

Deliberate trial of a spaghetti dinner with

commercially prepared sauce containing MSG.

Seizures within 3 hours, the first one in 1 year.

 

February, 1974

 

(Age 3.0 years)

 

Diet-watch continues.

No attacks since spaghetti trial in August 1973.

 

The child's physician, Dr. M. G. Stemmermann, M.D., noted there were

still no attacks as of September, 1975, except after annual test

trials with an " MSG meal. " Commenting on this case, Dr. Reif-Lehrer states,

 

" The case of the child with shudders (seizures), as well as some of

the symptoms reported in a questionnaire study in our laboratory

indicates a very wide spectrum of sensitivity toward MSG and suggests

that perhaps some individuals should avoid exogenously added MSG. In

some individuals, glutamate (or some other chemical that results from

glutamate ingestion) may be getting through the blood-brain barrier,

or, e.g., to certain areas of the hypothalamus, and may result in

undesirable effects..... One wonders, particularly in countries where

the per capita consumption of MSG is high, if there is any

possibility that any subtle nervous disorders or unexplained retinal

pathology could be due to cumulative effects of MSG in individuals

with pre-existing abnormalities that may make them more susceptible. "

 

Dr. Liane Reif-Lehrer,

Department of Ophthalmology, Harvard Medical School; Department of

Connective Tissue Research, Boston Biomedical Research Institute

Federation Proceedings 1(11);2205-2212 (1976)

 

 

 

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Brain Damage in Primates Evident 5 Hours After MSG Ingestion

Brain lesions were found in 6 rhesus infant monkeys exposed to

varying levels of a single MSG dose. Researchers at the Departments

of Psychiatry and Pediatrics at the Washington University School of

Medicine conducted the study with rhesus monkeys because of

hypotheses from other researchers stating that susceptibility to MSG

induced brain damage may be limited to sub-primates (mice, rats, rabbits, etc.)

 

A subcommittee of nutritional experts appointed by the Food

Protection Committee of the National Academy of Sciences (NAS)

declared MSG to be a safe food additive requiring no regulation. The

nutritional experts did admit susceptibility of infant rodents to

brain damage from orally administered MSG at even the low doses of 1

gram per kilogram body weight (g/kg) but reasoned that the primate

infant was most likely not at risk to MSG brain damage because it had

a more mature central nervous system and more highly developed blood

brain barrier at birth.

 

However, this theory did not hold true when tested by Dr. John Olney

and colleagues at the Department of Psychiatry and Pediatrics at

Washington University School of Medicine. Here, the researchers

exposed 6 infant rhesus monkeys to a single MSG dose ranging from 1

to 4 g/kg and were compared to 3 control monkeys exposed in the same

manner to sodium salt (table salt). The researchers found that all

MSG exposed monkeys developed damage to the brain area known as the

infundibular region of the hypothalamus (this corresponds to the

arcuate nucleus hypothalamus area in mice).

 

Results of their study were as follows:

* Infant monkey A was treated with 2.6 g/kg MSG via injection on

the first day of birth A lesion developed in the hypothalamus that

was quite conspicuous as early as 3 hours following treatment.

* Infant B received the same dose as the first infant but was

seven days old. Its lesion was slightly smaller in terms of the

percentage of the hypothalamus.

* Infant C received the smallest 1 g/kg dose orally and showed

degeneration of about 50 neurons in the hypothalamus.

* Infant D received a 2 g/kg oral dose and showed degeneration of

about 80 neurons in the hypothalamus.

* Infant E received the highest 4 g/kg dose orally and showed

degeneration of about 90 neurons. This infant also experienced

vomiting which decreased the amount of MSG absorbed into the system.

The sixth infant monkey to receive an MSG dose (labeled infant I)

received 4 g/kg via injection and developed severe reactions

including cyanosis, vomiting and convulsions.

 

In concluding remarks, Dr. Olney states,

 

" Our data do not support the view that only subprimates (i.e mice &

rats) are susceptible to MSG-induced neurotoxicity. The lesions in

our primate infants A, B and I following relatively high subcutaneous

doses of MSG were so similar to those consistently observed in mice

treated with high doses of MSG that it seems unrealistic to deny

primate susceptibility to the MSG effect. Since lesions we detected

in infants treated orally with lower doses were also similar in

localization and identical in cytopathological detail to those we

routinely find in infant mice treated orally with low doses of MSG, a

causal link between low oral doses of MSG and necrosis (damage) of

neurons in the infant primate hypothalamus also seems likely.

However, since the lesions in these infants were quite small, careful

consideration should be given to possible explanations other than MSG

toxicity. "

 

 

 

 

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MSG & Aspartate Cause Brain Damage

Following A Single Low Level Dose

 

To determine at what level the food additives MSG and Aspartate could

cause brain lesions, it was

 

MSG damages brain at low doses

 

 

Microscopic photograph at left shows normal brain area called the

arcuate nucleus. Photograph at right shows same area after exposure

to MSG at 1 g/kg.

White areas are dead brain cells resulting from the MSG exposure.

 

given to a group of 75 infant mice starting at the very low " normal

human exposure levels " of .25-.50 g/kg (grams of MSG per kilogram of

animal body weight) upwards to 2 g/kg. In each case only a single

dose of the compound was given. Five hours after MSG and Aspartate

treatment each animal was anaesthetized and examinations were

performed on the brain cells within the hypothalamus using a light

microscope. The results showed that only the very lowest .25 g/kg

level had no harmful observable effect upon the brain cells. Of the

twenty-three animals given .5 g/kg doses of MSG, twelve (52%)

suffered hypothalamic damage; and of sixteen animals treated at .75

g/kg, thirteen (81%) were affected. Nineteen animals (100%) treated

at 1g/kg and seven (100%) treated with 2 g/kg developed lesions in

the part of the hypothalamus known as the arcuate nucleus.

 

It was found that MSG and Aspartate can combine their damage

potential when test animals were fed 0.5 g/kg of each compound

simultaneously that they developed the amount of hypothalamic damage

characteristically seen in animals treated with either agent at 1 g/kg.

 

Dr. John W. Olney

Washington University School of Medicine, St. Louis, Missouri

Nature, 227, August 8, 1970

 

 

 

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Obesity - Shorter Growth - and Reproduction Problems

From MSG Intake

 

To investigate the possibility of long term effects from MSG

ingestion, Dr. Olney followed five litters of Swiss albino mice,

consisting of 38 healthy animals, from birth to nine months of age.

Twenty animals received injections of MSG daily from 1 to 10 days

after birth, 18 control animals received no treatment.

 

The results showed MSG treated animals appeared stunted in growth and

still remained shorter than controls on day 30. Of significant

interest, animals treated with MSG continued to gain weight on

unrestricted diets beyond the age of 5 months. Average weights of the

5 month old animals were 37 grams for the non-MSG treated and 57

grams for the MSG treated animals (see picture at right). It is

important to point out that contrary to expectation, the " obese " MSG

treated animals actually consumed less food than their thinner

control counterparts, implying damage to the brain area responsible

for controlling body weight. Mean per capita food consumption over

the daily 4 hour measuring period was 2.5 grams for the controls and

1.7 grams for the MSG treated animals.

 

Also noted at 5 months, the MSG animals were quite lethargic as

adults, and they lacked the sleekness of body coat seen in the

controls. The reproductive capacity of the MSG females was also

modified in that they repeatedly failed to conceive in spite of

adequate exposure from 5 to 9 months of age.

 

In summary, Dr. Olney writes,

 

" These observations, linking MSG treatment of the neonatal mouse with

a syndrome of manifestations, including skeletal stunting, marked

adiposity, and sterility of the female, coupled with

histopathological findings in several organs associated with

endocrine function, suggest a complex endocrine disturbance. In view

of the additional finding of lesions in regions of the brain thought

to function as neuroendocrine regulatory centers, a unitary

hypothesis might be constructed relating all or most of the findings

to the neonatal disruptions of neuronal development in these

centers.... The assumption that MSG is an entirely innocuous

substance for human consumption has been questioned recently in view

of its role in the Chines Restaurant syndrome. The finding that

neuronal necrosis can be induced in the immature mouse brain by 0.5

mg/kg of MSG raises the more specific question whether there is any

risk to the developing human nervous system by maternal use of MSG

during pregnancy. The primate placenta maintains amino acids in

consistently higher concentrations in the fetal circulation than

those found in the maternal circulation, the ratio of glutamic acid

being grater than 2:1. In fact, when high doses of phenylalanine were

given to a pregnant rhesus monkey, the ratio of mother to fetus for

this amino acid remained unchanged so that exceedingly high fetal

blood levels resulted. The possibility that brain lesions could occur

in the developing primate embryo in response to increased glutamic

acid concentrations in the maternal circulation, therefore, warrants

investigation. "

 

Dr. John W. Olney

Department of Psychiatry, Washington University School Medicine, St.

Louis, Missouri

SCIENCE 164:719-721 (1969)

 

 

 

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ASPARTAME (NUTRASWEET)

 

INTRODUCTION

 

Aspartame is an artificial sweetener that has developed widespread

use in the United States. The compound was originally given FDA

approval in 1974, however, its purported safety was called into

question and approval was suspended pending further investigation. In

fact, final approval for consumer use was not finally given until the

mid 1980's.

 

As with MSG, researchers Reynolds, Butler and Lemkey-Johnson (Journal

of Toxicology and Environmental Health, 2: 471-480, 1976) reported

that 0.5 or 1.0 g/kg of aspartame on Days 6-12 resulted in small

hypothalamic lesions in neonatal mice. These results and the

potentially wide use of a new artificial sweetener suggested a need

for further examination of the neurobehavioral consequences of

aspartame administration. Interest in and concern about aspartame has

been elevated by the fact that its metabolic breakdown will liberate

the amino acids phenylalanine and aspartate.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

End of article - While this is not real current (1997) today we have

an epidemic of birth defects proving the accuracy of this report.

 

Aspartame has a synergistic and additive effect with MSG. Like

pouring gasoline on fire.

 

MSG, www.truthinlabeling.org

Aspartame: www.mpwhi.com, www.dorway.com, www.wnho.net

Aspartame Toxicity Center, www.holisticmed.com/aspartame

 

Dr. Betty Martini, D.Hum, Founder

Mission Possible International

9270 River Club Parkway

Duluth, Georgia 30097

770 242-2599