Montana Food Products :: Research

Monosodium Glutamate

Monosodium glutamate (MSG) has been used as a flavor enhancer for over a century. In recent years, it has become the subject of some controversy over its safety as a food additive. Critics claim that at the very least there is a segment of the population who are allergic to it. At the worst, it may be a culprit in the obesity epidemic in western countries. Proponents, however, state that MSG is exactly the same as free glutamate that is present in many of the foods we currently eat regularly including tomatoes and parmesan cheese.

Although the FDA has classified MSG as GRAS (generally recognized as safe) in 1959, we have chosen to remove it from the majority of our products. Below is some information and research we have gathered to help you make your own decision about MSG.

+General Information

+History

The History of Monosodium Glutamate

In 1908, Kikunae Ikeda, a Japanese scientist, after being informed that seaweed (Laminaria Japonica) was the secret to his wife’s excellent soups, extracted glutamic acid from the seaweed and discovered its flavor-enhancing properties. And thus MSG was created.

The food additive, monosodium glutamate, was first used in the United States in any quantity in the late 1940s. According to Dr. George Schwartz, author of In Bad Taste: The MSG Syndrome, although considerable effort had been spent to introduce MSG to the USA, little had been accomplished prior to World War II. However, sometime during the war, the use of MSG in Japanese soldiers' rations was noticed. In 1948, a symposium on MSG, presided over by the Chief Quartermaster of the Armed Forces, was held in Chicago for members of the food industry.

By the 1960s, Accent, the leading brand of the flavor enhancer called "monosodium glutamate," had become a household word. Simultaneously, other hydrolyzed protein products such as autolyzed yeast, sodium caseinate, and hydrolyzed vegetable protein gained in popularity. All of these products qualify as MSG.

It is interesting (or coincidental) that the first published report of a reaction to "monosodium glutamate" did not appear until it was being made by bacterial fermentation. The first published report of a reaction to "monosodium glutamate" appeared in 1968 when Robert Ho Man Kwok, M.D., who had emigrated from China, reported that although he never had the problem in China, about 20 minutes into a meal at certain Chinese restaurants, he suffered numbness, tingling, and tightness of the chest that lasted for approximately 2 hours. This reaction was labelled "Chinese Restaurant Syndrome" by the New England Journal of Medicine and thus began the research and controversy over the safety of MSG that is still going on.

+What is Glutamate?

What is Glutamate?

Glutamate is an amino acid, found in all protein-containing foods. Amino acids are the building blocks of proteins. This amino acid is one of the most abundant and important components of proteins. Glutamate occurs naturally in protein-containing foods such as cheese, milk, mushrooms, meat, fish, and many vegetables. Glutamate is also produced by the human body and is vital for metabolism and brain function. However, there are amino acids that aren’t linked and perform vital functions on their own. For example, glutamate is an excitatory amino acid neurotransmitter, that is, a chemical messenger that triggers the nerve cells to fire. Glutamate is naturally made in the human brain and present within the muscle, kidney, and liver.

Foods Higher in Naturally Occurring Glutamate

Glutamate Contents of Foods
	Food Size	Glutamate (mg/serving)
Tomato juice	1 cup	0.827
Tomato	3 slices	0.339
Meat loaf dinner	9 oz.	0.189
Human breast milk	1 cup	0.176
Mushrooms	1/4 cup	0.094
Parmesan cheese	2 Tbsp	0.047
Corn	1/2 cup	0.031
Peas	1/2 cup	0.024
Cow's milk	1 cup	0.016
Canned tuna (in water)	1/2 can	0.008
Source: Food and Drug Administration

Glutamate Contents of Foods
	Mg/100g
Cow's Milk	2
Human Milk	22
Eggs	23
Beef	33
Fish (Mackerel)	36
Chicken	44
Potatoes	102
Corn	130
Oysters	137
Tomatoes	140
Broccoli	176
Mushrooms	180
Peas	200
Grape juice	258
Fresh tomato juice	260
Walnuts	658
Soy Sauce	1090
Parmesan cheese	1200
Roquefort cheese	1280

+What is Monosodium Glutamate?

What is Monosodium Glutamate?

Monosodium glutamate, or MSG, a free amino acid salt with one sodium atom attached to the amino acid glutamate. When MSG is added to foods, it provides a similar flavoring function as the glutamate that occurs naturally in food. As a result, MSG is created by hydrolyzing vegetable protein or by fermenting corn and starchy foods. The final product of MSG is a white crystal that can easily dissolve into foods.

The MSG manufacturers argue that processed MSG is comprised of nothing more than water, sodium and glutamate, a pure salt exactly the same as the glutamate in our bodies. MSG antagonists argue that processed MSG is impure and also contains a different isomerism, a mirror image of glutamate from the ones naturally made in our bodies. Moreover, by hydrolyzing vegetable protein, glutamate becomes “free” and is able to act as a neurotransmitter. Glutamate is not considered to be an essential amino acid since we are able to produce it ourselves, but it is argued that constant excess of glutamate from oral ingestion could lead to other problems. Neuroscientists argue that excess free glutamate can lead to many disease states.

+Monosodium Glutamate Symptom Complex

Monosodium Glutamate Symptom Complex (a.k.a. Chinese Restaurant Syndrome)

What is popularly called the Chinese restaurant syndrome is not a type of chemical food poisoning. Rather, it is a sensitivity to monosodium glutamate (MSG), a flavor enhancer often used in Chinese cooking. In susceptible people, MSG can produce a multitude of reactions including facial pressure, chest pain, and burning sensations throughout the body. Many people feel anxious as well. The amount of MSG that can cause these symptoms varies considerably from person to person.

Many claim that this reaction is an allergic reaction to MSG, but others say that the adverse reaction is a reaction to a toxin, not a reaction to an allergenic substance, and, as such, is not IgE mediated. Traditional allergy tests only identify reactions that are IgE mediated. The only way to determine if a person is sensitive to MSG is to feed MSG to that person and observe him or her for as long a 48 hours after feeding; or to have the person keep a record of food, drug, cosmetic, and dietary supplement use and MSG reactions. Learning to pinpoint MSG as a reaction trigger, recognizing reactions that might be MSG-induced adverse reactions, and understanding where MSG is hidden in food, are essential to recognizing or diagnosing MSG-induced adverse reactions.

MSG-sensitive people report reactions ranging from simple skin rash to severe depression and life-threatening physical conditions. Two or more reactions occurring together, or one following another, are not uncommon. The amount of processed free glutamic acid (MSG) ingested may play a role in the severity and specific nature of a reaction. The intensity or severity of a reaction also appears to be affected by alcohol ingestion and/or exercise just prior to, or immediately following, MSG ingestion, and some women report variations in their reactions at different times in their menstrual cycles.

Diagnosis of MSG sensitivity is extremely difficult.

· None of the symptoms of MSG-toxicity are caused exclusively by MSG. Most, if not all, could be caused by various physical conditions as well as by other food additives.
· Some people eat MSG and react immediately. Some react as late as 48 hours after ingesting MSG. Of help in diagnosis is the fact that for any one person, the time between eating MSG and reacting to it is generally the same.
· Reactions are dose related. Some people can not tolerate even the smallest amount of MSG. Others tolerate single small amounts, but react to MSG when they ingest a gram or more in any one meal. Others can ingest five grams or more, without evidencing a reaction. Canned soups analyzed some time ago, each contained about .6 grams MSG. Five grams or more MSG can, at times, be found in a single meal.
· The adverse effects of MSG ingestion may be cumulative. People have reported eating products containing small amounts of MSG once a week without experiencing reactions, while having reactions when those same products were consumed two or three days in a row.
· MSG is very often hidden in food. Hiding MSG makes recognition of MSG so complex and confusing that people who are sensitive to MSG have a great deal of difficulty pinpointing their sensitivities. If a person reacted after eating something known to contain MSG, he might suspect that MSG was the culprit. But if that person had the same reaction after eating something that contained MSG, but did not disclose that fact on the label, he would very likely question his original suspicion. Until all sources of MSG are easily identifiable, evaluation of possible MSG reactions will be difficult.
· Difficulty in diagnosing MSG-sensitivity is compounded by the industry practice of illegally advertising "No MSG," "No MSG Added," or "No Added MSG" on labels when products do contain MSG.
· Difficulty in diagnosing MSG-sensitivity is also compounded by use of fertilizers, pesticides, pesticides, and plant "growth enhancers" that contain MSG. MSG in that form has been approved by the EPA for spray on fruits, grains, vegetables, and other vegetation.
· Diagnostic tools generally available to physicians are limited to a procedure called "challenge." In a physician's office, an appropriate dose (or doses) of MSG would be given to the patient, and provision would have to be made for both restricting the patient's contact with other potential reaction triggers and observing reactions delayed by as much as 48 hours.

As an alternative, physician and patient working together may be able to identify, or rule out, MSG as a reaction trigger through analysis of a patient food diary. Restricting intake to totally unprocessed food and drink for three weeks, then reintroducing items, one at a time, may help identify offending sources of MSG.

Cardiac Arrhythmia Atrial fibrillation Tachycardia, Rapid heartbeat, Palpitations Slow heartbeat Angina Extreme rise or drop in blood pressure

Circulatory Swelling

Gastrointestinal Diarrhea Nausea/vomiting Stomach cramps Rectal bleeding Bloating

Muscular Flu-like achiness Joint pain Stiffness

Neurological Depression Mood swings Rage reactions Migraine headache Dizziness Light-headedness Loss of balance Disorientation Mental confusion Anxiety Panic attacks Hyperactivity Behavioral problems in children Attention deficit disorders Lethargy Sleepiness Insomnia Numbness or paralysis Seizures Sciatica Slurred speech Chills and shakes Shuddering

Visual Blurred vision Difficulty focusing Pressure around eyes

Respiratory Asthma Shortness of breath Chest pain Tightness in the chest Runny nose Sneezing

Urological / Genital
Bladder pain (with frequency)
Swelling of the prostate
Swelling of the vagina
Vaginal spotting
Frequent urination
Nocturia

Skin
Hives (may be both internal and external)
Rash
Mouth lesions
Temporary tightness or partial paralysis, numbness or tingling of the skin
Flushing
Extreme dryness of the mouth
Face swelling
Tongue swelling
Bags under eyes

Migraine headache is the single most often reported adverse reaction to MSG and as such, it might warrant special attention. However, it is never mentioned by the FDA or the glutamate industry. The subject of migraine headache is simply ignored. The Internet gives wide coverage to the subject of migraine headache and virtually every migraine headache clinic in the country refers to MSG as a migraine headache trigger.

Some information provided by www.truthinlabeling.org

+How Does the Body Process Glutamate and MSG?

How are Glutamate and MSG Handled by the Body?

MSG manufacturers assure us that the human body treats glutamate that is added to foods in the form of MSG the same as the natural glutamate found in food. For instance, the body does not distinguish between free glutamate from tomatoes, cheese or mushrooms and the glutamate from MSG added to foods. Glutamate is glutamate, whether naturally present or from MSG.

However, opponents say that while the glutamic acid found in unprocessed, unadulterated food and in the human body is composed of one form of a single amino acid, L-glutamic acid, the processed free glutamic acid used in processed food is always composed of two forms of glutamic acid (L-glutamic acid and D-glutamic acid) and a variety of other chemicals commonly referred to as contaminants. In addition to the D-glutamic acid, contaminants may include, but are not limited to, pyroglutamic acid, mono and dichloro propanols, heterocyclic amines, and peptides. Mono and dichloro propanols and heterocyclic amines are carcinogenic.

Most excess amino acids are not stored as amino acids. The body has elaborate means of changing extra amino acids into other amino acids, and removing nitrogen and changing amino acids into fuel to be stored. There are processes such as ;"transamination" and "deamination" which occur mostly in the liver. Patients with compromised livers, however, may have trouble transaminating cysteine, for example, into taurine, the amino acid that acts counter to glutamate. Also, an excess of the amino acid aspartate (found in Nutrasweet) may result in excess glutamate, since the body can convert aspartate directly to glutamate.Aspartate and glutamate affect some of the same receptors. In a different example, there is an enzyme that the body uses to convert excess glutamate into another neurotransmitter called GABA. In many patients with Type II Diabetes, their bodies view the enzyme responsible for turning MSG into GABA as an enemy and create antibodies to attack it so that it cannot do its job, thus compromising the body’s effectiveness in getting rid of excess glutamate.

+Why Add MSG to Foods

+Manufacturers of MSG

Why Add MSG to Foods – What the Manufacturers of MSG say

Improving Taste

The natural flavor-enhancing level of glutamate in food varies greatly, but is high in foods such as tomatoes, mushrooms and parmesan cheese. MSG enhances many but not all food flavors through the interaction between glutamate and other flavors. It works well with a variety of foods including meats, poultry, seafood and many vegetables. It is used to enhance the flavor of some soups, stews, meat-based sauces and snack foods. MSG harmonizes well with salty and sour tastes, but does little for sweet foods such as cakes, pastries or candies.

MSG manufacturers state that MSG can not improve bad-tasting food or make up for bad cooking. It does not allow a cook to substitute low-quality for high-quality ingredients in a recipe, and does not tenderize meat. It just makes good food taste better.

Improving Nutrition

What most people don't realize is that the importance of taste doesn't stop at simply enjoying the flavor of the foods we eat. Although treating yourself to a meal at a superb restaurant or enjoying a scrumptious dinner at home seems reward enough, taste is actually an integral and important part of nutrition. To a large degree, our taste buds that actually trigger important digestive and metabolic functions allowing us to better use the essential nutrients we get from our diet. When food passes over our taste buds, those wonderful tastes not only trigger pleasure and satisfaction, they also send an important message to our body – nutrition is on its way. Those tiny taste buds are, in essence, telling our bodies to get to work, and metabolize the foods we are eating.

Not only does MSG make good food taste better for consumers, new studies show that MSG may play a role in the overall health and nutrition of people who need it most. Aging, as well as a number of diseases and illnesses, decrease our ability to taste and smell. This decrease in our senses is a major contributor to poor nutritional status in populations like the elderly, making it increasingly difficult for doctors and nutritionists to ensure that their patients get much-needed nutrients. Studies have found that adding MSG to certain foods, such as soup and mashed potatoes, has been successful in increasing the food intake in institutionalized elderly populations.

However, researchers from the Division of Human Nutrition, Wageningen University in the Netherlands found that enhancing the taste of a cooked meal with flavor and/or MSG did not lead to a higher energy intake and body weight among nursing home elderly. They conducted an experiment with four groups (control group (n=23), MSG group (n=19), flavor group (n=19), flavor plus MSG group (n=22)). They measured intake of the cooked meal by weighing back leftovers during 14 days and body weight. Both were measured before and at the end of the intervention period. After 16 weeks, energy intake and body weight did not increase within the control group, the flavor group, the flavor plus MSG group and the MSG group. Between the groups, no differences were found in changes in energy intake and body weight. (Essed NH, van Staveren WA, Kok FJ, de Graaf C. Appetite. 2007 Jan;48(1):29-36. Epub 2006 Aug 17).

Reducing Sodium Intake

MSG is also low in sodium, with about a third of the sodium of table salt. Many Americans add salt to improve the flavor of food; however, this can be problematic for people watching their intake of sodium. By using a small amount of MSG in conjunction with a decreased level of salt, sodium intake can be reduced by as much as 30 to 40 percent while still maintaining flavor.

By way of comparison, MSG contains about 12 percent sodium while table salt contains 39 percent. And, MSG is used at levels lower than salt. Considering all sources of dietary sodium (natural sodium content of foods, table salt, sodium-containing ingredients in processed foods, drinking water and pharmaceuticals), typical use of MSG contributes about 1 to 2 percent of the total sodium contained in the average daily American diet.

+Opponents of MSG

Why Add MSG to Foods – What the Opponents of MSG say

MSG tricks your tongue into making you think a certain food is high in protein and thus nutritious. It is not a "meat tenderizer." It is not a "preservative." The food industry is trying to confuse the issue by focusing on the "fifth" taste sense they call umami (the Japanese word for “savory”). Free glutamic acid is detected by the taste buds as a simple way to signal the presence of protein in a food, just as there are fat receptors to detect fats and receptors that sense carbohydrate or sweet flavors. The purpose is to help us discern real food from inedible matterIt changes your perception of not simply taste but the nutritious qualities of what you put into your mouth. However, it is the very same neurotransmitter that your brain and many organs including your ears, eyes, nervous system and pancreas in your body use to initiate certain processes in your body.

MSG stimulates the pancreas to produce insulin. So many diets these days are concerned about the Glycemic Index of foods and yet none of them address the fact that MSG and free glutamic acid stimulate the pancreas to release insulin when there doesn't even have to be carbohydrates in the food for that insulin to act on. The food industry has found its own "anti-appetite suppressant." It's a convenient way to keep consumers coming back for more. The blood sugar drops because of the insulin flood. And you are hungry an hour later.

The body changes excess glutamate to GABA (gamma aminobutyric acid). Since GABA is inhibitory and glutamate is excitatory, both neurotransmitters work together to control many processes, including the brain's overall level of excitation. Many of the drugs of abuse affect either glutamate or GABA or both to exert tranquilizing or stimulating effects on the brain. For instance, caffeine inhibits GABA release, while increasing glutamate activity, creating an excited state in the brain. Alcohol and valium, on the other hand, inhibits glutamate activity on the brain, while increasing GABA release, creating a calming effect.

Cost. The illusion created by adding MSG to a food product enables the food processor to add LESS real food. The illusion of more protein in a food allows the food producer to put LESS protein in it. The consumer perceives the product - say chicken soup - to have more chicken in it than is actually there.

+Taurine

Taurine

Some MSG sensitive individuals report relief from some MSG symptoms by taking taurine in powder form free of additives or fillers. The rationale behind this approach is that glutamate competes with the amino acid cysteine for uptake in the body. An excess of glutamate will interfere with the body's ability to convert cysteine into taurine, the other free form amino acid which acts as the body's heartbeat regulator. Taurine is the body's water soluble anti-oxidant and inhibitory neurotransmitter. The body also uses taurine to make bile, which aids in the digestion of fats.

The idea of taking taurine for accidental MSG ingestion is that since MSG may inhibit taurine formation, those with irregular heartbeat, digestive problems, epilepsy, vision disturbance, and panic attacks from MSG, may benefit from ingesting taurine instead of waiting for the body to make it.

Unfortunately, most food scientists are not taught about taurine because adults are assumed to be able to make it and shouldn't need to eat it. It isn't even listed in most tables of the amino acids. However, taurine is so important in the body, that since 1986 it has been added to baby formula because it is essential for proper growth and development in humans. Also, studies of people with epilepsy have shown that taurine levels in the brain after a seizure are unusually low.Taurine is now being considered as treatment for diabetes as well as epilepsy.

Foods high in taurine include fresh fish and meat.It is not found in significant amounts in foods of non-meat origin. Heat for long periods of time destroys it. It is interesting that the Japanese use much MSG, but also eat diets high in fish, and raw fish at that.A Japanese meal of sushi contains much taurine, as well as MSG. Chinese food, which often is cooked at high heat and also contains mushrooms, another source of free glutamate, and often mostly vegetables, would contain less protective taurine.

+The FDA and Monosodium Glutamate (MSG)

FDA and Monosodium Glutamate (MSG)

Monosodium glutamate (MSG) is used as a flavor enhancer in a variety of foods prepared at home, in restaurants, and by food processors. Its use has become controversial in the past 30 years because of reports of adverse reactions in people who've eaten foods that contain MSG. Research on the role of glutamate--a group of chemicals that includes MSG--in the nervous system also has raised questions about the chemical's safety.

Studies have shown that the body uses glutamate, an amino acid, as a nerve impulse transmitter in the brain and that there are glutamate-responsive tissues in other parts of the body, as well. Abnormal function of glutamate receptors has been linked with certain neurological diseases, such as Alzheimer's disease and Huntington's chorea. Injections of glutamate in laboratory animals have resulted in damage to nerve cells in the brain. Consumption of glutamate in food, however, does not cause this effect. While people normally consume dietary glutamate in large amounts and the body can make and metabolize glutamate efficiently, the results of animal studies conducted in the 1980s raised a significant question: Can MSG and possibly some other glutamates harm the nervous system?

A 1995 report from the Federation of American Societies for Experimental Biology (FASEB), an independent body of scientists, helps put these safety concerns into perspective and reaffirms the Food and Drug Administration's belief that MSG and related substances are safe food ingredients for most people when eaten at customary levels.

The FASEB report identifies two groups of people who may develop a condition the report refers to as "MSG symptom complex." One group is those who may be intolerant to MSG when eaten in a large quantity. The second is a group of people with severe, poorly controlled asthma. These people, in addition to being prone to MSG symptom complex, may suffer temporary worsening of asthmatic symptoms after consuming MSG. The MSG dosage that produced reactions in these people ranged from 0.5 grams to 2.5 grams.

Although FDA has not fully analyzed the FASEB report, the agency believes that the report provides the basis to require glutamate labeling. FDA will propose that foods containing significant amounts of free glutamate (not bound in protein along with other amino acids) declare glutamate on the label. This would allow consumers to distinguish between foods with insignificant free glutamate levels and those that might contribute to a reaction.

What Is MSG?

MSG is the sodium salt of the amino acid glutamic acid and a form of glutamate. It is sold as a fine white crystal substance, similar in appearance to salt or sugar. It does not have a distinct taste of its own, and how it adds flavor to other foods is not fully understood. Many scientists believe that MSG stimulates glutamate receptors in the tongue to augment meat-like flavors.

Asians originally used a seaweed broth to obtain the flavor- enhancing effects of MSG, but today MSG is made by a fermenting process using starch, sugar beets, sugar cane, or molasses.

Glutamate itself is in many living things: It is found naturally in our bodies and in protein-containing foods, such as cheese, milk, meat, peas, and mushrooms.

Some glutamate is in foods in a "free" form. It is only in this free form that glutamate can enhance a food's flavor. Part of the flavor-enhancing effect of tomatoes, certain cheeses, and fermented or hydrolyzed protein products (such as soy sauce) is due to the presence of free glutamate.

Hydrolyzed proteins, or protein hydrolysates, are acid- treated or enzymatically treated proteins from certain foods. They contain salts of free amino acids, such as glutamate, at levels of 5 to 20 percent. Hydrolyzed proteins are used in the same manner as MSG in many foods, such as canned vegetables, soups, and processed meats.

Scientific Review

In 1959, FDA classified MSG as a "generally recognized as safe," or GRAS, substance, along with many other common food ingredients, such as salt, vinegar, and baking powder. This action stemmed from the 1958 Food Additives Amendment to the Federal Food, Drug, and Cosmetic Act, which required premarket approval for new food additives and led FDA to promulgate regulations listing substances, such as MSG, which have a history of safe use or are otherwise GRAS.

Since 1970, FDA has sponsored extensive reviews on the safety of MSG, other glutamates and hydrolyzed proteins, as part of an ongoing review of safety data on GRAS substances used in processed foods.

One such review was by the FASEB Select Committee on GRAS Substances. In 1980, the committee concluded that MSG was safe at current levels of use but recommended additional evaluation to determine MSG's safety at significantly higher levels of consumption. Additional reports attempted to look at this.

In 1986, FDA's Advisory Committee on Hypersensitivity to Food Constituents concluded that MSG poses no threat to the general public but that reactions of brief duration might occur in some people.

Other reports gave similar findings. A 1991 report by the European Communities' (EC) Scientific Committee for Foods reaffirmed MSG's safety and classified its "acceptable daily intake" as "not specified," the most favorable designation for a food ingredient. In addition, the EC Committee said, "Infants, including prematures, have been shown to metabolize glutamate as efficiently as adults and therefore do not display any special susceptibility to elevated oral intakes of glutamate."

A 1992 report from the Council on Scientific Affairs of the American Medical Association stated that glutamate in any form has not been shown to be a "significant health hazard."

Also, the 1987 Joint Expert Committee on Food Additives of the United Nations Food and Agriculture Organization and the World Health Organization have placed MSG in the safest category of food ingredients.

Scientific knowledge about how the body metabolizes glutamate developed rapidly during the 1980s. Studies showed that glutamate in the body plays an important role in normal functioning of the nervous system. Questions then arose on the role glutamate in food plays in these functions and whether or not glutamate in food contributes to certain neurological diseases.

Anecdotal Evidence

Many of these safety assessments were prompted by unconfirmed reports of MSG-related adverse reactions. Between 1980 and 1994, the Adverse Reaction Monitoring System in FDA's Center for Food Safety and Applied Nutrition received 622 reports of complaints about MSG. Headache was the most frequently reported symptom. No severe reactions were documented, but some reports indicated that people with asthma got worse after they consumed MSG. In some of those cases, the asthma didn't get worse until many hours later.

Also, several books and a TV news show have reported widespread and sometimes life-threatening adverse reactions to MSG, claiming that even small amounts of manufactured glutamates may cause adverse reactions.

A problem with these unconfirmed reports is that it is difficult to link the reactions specifically to MSG. Most are cases in which people have had reactions after, but not necessarily because of, eating certain foods containing MSG.

While such reports are helpful in raising issues of concern, they do not provide the kind of information necessary to describe who is most likely to be affected, under what conditions they'll be affected, and with what amounts of MSG. They are not controlled studies done in a scientifically credible manner.

1995 FASEB Report

Prompted by continuing public interest and a flurry of glutamate-related studies in the late 1980s, FDA contracted with FASEB in 1992 to review the available scientific data. The agency asked FASEB to address 18 questions dealing with:

· the possible role of MSG in eliciting MSG symptom complex
· the possible role of dietary glutamates in forming brain lesions and damaging nerve cells in humans
· underlying conditions that may predispose a person to adverse effects from MSG
· the amount consumed and other factors that may affect a person's response to MSG
· the quality of scientific data and previous safety reviews

FASEB held a two-day meeting and convened an expert panel that thoroughly reviewed all the available scientific literature on this issue

FASEB completed the final report, over 350 pages long, and delivered it to FDA on July 31, 1995. While not a new study, the report offers a new safety assessment based on the most comprehensive existing evaluation to date of glutamate safety.

Among the report's key findings:

· An unknown percentage of the population may react to MSG and develop MSG symptom complex, a condition characterized by one or more of the following symptoms:
· burning sensation in the back of the neck, forearms and chest
· numbness in the back of the neck, radiating to the arms and back
· tingling, warmth and weakness in the face, temples, upper back, neck and arms
· facial pressure or tightness
· chest pain
· headache
· nausea
· rapid heartbeat
· bronchospasm (difficulty breathing) in MSG-intolerant people with asthma
· drowsiness
· weakness
· In otherwise healthy MSG-intolerant people, the MSG symptom complex tends to occur within one hour after eating 3 grams or more of MSG on an empty stomach or without other food. A typical serving of glutamate-treated food contains less than 0.5 grams of MSG. A reaction is most likely if the MSG is eaten in a large quantity or in a liquid, such as a clear soup
· Severe, poorly controlled asthma may be a predisposing medical condition for MSG symptom complex
· No evidence exists to suggest that dietary MSG or glutamate contributes to Alzheimer's disease, Huntington's chorea, amyotrophic lateral sclerosis, AIDS dementia complex, or any other long-term or chronic diseases
· No evidence exists to suggest that dietary MSG causes brain lesions or damages nerve cells in humans
· The level of vitamin B6 in a person's body plays a role in glutamate metabolism, and the possible impact of marginal B6 intake should be considered in future research
· There is no scientific evidence that the levels of glutamate in hydrolyzed proteins causes adverse effects or that other manufactured glutamate has effects different from glutamate normally found in foods

Ingredient Listing

Under current FDA regulations, when MSG is added to a food, it must be identified as "monosodium glutamate" in the label's ingredient list. Each ingredient used to make a food must be declared by its name in this list.

While technically MSG is only one of several forms of free glutamate used in foods, consumers frequently use the term MSG to mean all free glutamate. For this reason, FDA considers foods whose labels say "No MSG" or "No Added MSG" to be misleading if the food contains ingredients that are sources of free glutamates, such as hydrolyzed protein.

In 1993, FDA proposed adding the phrase "(contains glutamate)" to the common or usual names of certain protein hydrolysates that contain substantial amounts of glutamate. For example, if the proposal were adopted, hydrolyzed soy protein would have to be declared on food labels as "hydrolyzed soy protein (contains glutamate)." However, if FDA issues a new proposal, it would probably supersede this 1993 one.

In 1994, FDA received a citizen's petition requesting changes in labeling requirements for foods that contain MSG or related substances. The petition asks for mandatory listing of MSG as an ingredient on labels of manufactured and processed foods that contain manufactured free glutamic acid. It further asks that the amount of free glutamic acid or MSG in such products be stated on the label, along with a warning that MSG may be harmful to certain groups of people. FDA has not yet taken action on the petition.

References

· Federal Register, Dec. 4, 1992 (FR 57467) and Federal Register, Jan. 6, 1993 (FR 2950); FDA Consumer, December 1993, "Food Allergies: When Eating is Risky."

+Other Names for Monosodium Glutamate

Hidden Names for MSG

There are many ways in which food packagers can include monosodium glutamate (or free glutamates) in foods without listing the words "monosodium glutamate" in the ingredients.

Foods always contain MSG when these words are on the label:

MSG
Gelatin
Calcium Caseinate
Monosodium Glutamate
Hydrolyzed Vegetable Protein (HVP)
Textured Protein
Monopotassium Glutamate
Hydrolyzed Plant Protein (HPP)
Yeast Extract
Glutamate
Autolyzed Plant Protein
Yeast food or nutrient
Glutamic Acid
Sodium Caseinate
Autolyzed Yeast

Foods made with the following products often contain MSG:

Barley malt, Malted Barley (flavor), Malt Extract or Flavoring
Flavors, Flavoring
Modified food starch
Reaction Flavors
Rice syrup or brown rice syrup
Natural Chicken, Beef, or Pork Flavoring "Seasonings" (often assumed to mean salt, pepper, or spices and herbs, which sometimes it does)
Lipolyzed butter fat
Maltodextrin
Soy Sauce or Extract
"Low" or "No Fat" items
Caramel Flavoring (coloring)
Cornstarch
Corn syrup and corn syrup solids (some companies use another process to make their product, saying it is MSG free)
Soy Protein, Soy Protein Isolate or Concentrate
Citric Acid (when processed from corn)
Stock
Broth
Bouillon
Flowing Agents
Dry Milk Solids
Milk Powder
Carrageenan
Wheat, rice, or oat protein
Whey, Whey Protein or Whey Protein Isolate or Concentrate
Annatto
Enriched or vitamin enriched “anything”
Protein fortified "anything"
Enzyme modified "anything"
Ultra-pasteurized "anything"
Fermented "anything"
Spice
Pectin
Gums
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+A Collection of Research Abstracts

+Behavior

Effects of Monosodium Glutamate on Behavior — A Collection of Research Abstracts

Behavioral and endocrinological effects of single injections of monosodium glutamate in the mouse
Lorden JF, Caudle A., Neurobehav Toxicol Teratol. 1986 Sep-Oct;8(5):509-19

Treatment of neonatal mice with large, repeated doses of monosodium L-glutamate (MSG) produces a syndrome of obesity and endocrinological dysfunction generally attributed to a hypothalamic lesion. We have used single injections of MSG, administered on postnatal day four, to explore the lower end of the dose-response curve for this toxin. Major features of the MSG syndrome including hypophagia (undereating), obesity, hypoactivity (lethargy), reduced pituitary protein content, decreased ovarian weight, delayed puberty and elevated plasma corticosterone levels were obtained at the highest dose. Of the variables measured, feeding disturbances and reduced pituitary and ovarian weights were the most sensitive indicators of damage. The extent of damage produced in the arcuate nucleus of the hypothalamus increased with increasing dose. A prominent lesion was also detected in the medial preoptic area of animals receiving the highest dose. Damage was not evident in other diencephalic structures associated with body weight regulation. Since little is known about the mechanisms underlying MSG obesity, a second study examined the contribution of ovarian hormones to obesity in MSG treated mice. Ovariectomy increased the body weights of animals injected with low but not high doses of MSG, suggesting that a reduction in ovarian function may contribute to the MSG obesity syndrome in the female. Measurement of hypothalamic monoamines and metabolites in these mice indicated that as with repeated doses of MSG, single injections of the toxin reduced hypothalamic dopamine levels. DOPAC levels were unchanged.

Prenatal monosodium glutamate (MSG) treatment given through the mother's diet causes behavioral deficits in rat offspring
Frieder B. Grimm VE., Int J Neurosci. 1984 Apr;23(2):117-26

The present study reports various developmental and behavioral changes in the offspring of rat dams that received monosodium glutamate (MSG) in the drinking water all through the second and third trimesters of pregnancy. Three main effects were observed in the MSG exposed offspring: (1) juvenile obesity; (2) reduced general activity levels; (3) a specific type of learning disability in discrimination learning involving choice between simultaneously present positive and negative stimuli.

Neonatal exposure to monosodium glutamate alters the neurobehavioral performance of adult rats
Squibb RE, Tilson HA, Meyer OA, Lamartiniere CA. Neurotoxicology. 1981 Nov;2(3):471-84

On days 1-15 postpartum male and female Sprague-Dawley derived CD strain pups were dosed sc with either L-glutamic acid (MSG) (2-3.5 mg/g), 13% or 0.85% saline and tested at 67 and 102 days of age. At both periods, the body weights of MSG exposed males were less than the 13% exposed isosmotic controls. MSG exposed females, however, appeared to be obese compared to their controls at 102 days and exhibited a 50% incidence of tail-automutilation. Exposure to MSG did not affect the startle responsiveness of males or females to an acoustic startle stimulus. The startle responsiveness of females to a tactile air puff stimulus was significantly depressed in amplitude at 67 and 102 days; the response on the males at 67 days of age was also decreased, but the effect was not statistically significant. Fore- and hindlimb grip strength assessments indicated that MSG exposed females, at 102 days, had greater hindlimb grip strength. Forelimb grip strength was not affected in either sex. Tail flick latencies to a thermal stimulus were significantly elevated at 67 and 102 days of age in both MSG exposed sexes. Relative to the isosmotic control group, spontaneous motor activity of MSG exposed animals was found to be consistently lower. Exposure to MSG did not, however, change the responsiveness of either sex to the motor activity stimulating effects of a d-amphetamine challenge (0.3-3 mg/kg). These results indicate that postnatal exposure to MSG produced measurable, long-term behavioral and somatic alterations in female and, to a lesser degree, male rats.

+Brain Lesions

Effects of Monosodium Glutamate on Brain Lesions — A Collection of Research Abstracts

Brain lesions in an infant rhesus monkey treated with monosodium glutamate
Olney JW, Sharpe LG., Science. 1969 Oct 17;166(903):386-8.

In an infant rhesus monkey brain damage resulted from subcutaneously administered monosodium glutamate. Although a relatively high dose of monosodium glutamate was used, the infant was asymptomatic for a 3-hour observation period during which time hypothalamic neurons were undergoing a process of acute cell death. With the electron microscope it was observed that dendrites and cell bodies of neurons are the tissue components primarily affected in brain damage induced by monosodium glutamate.

Monosodium L-glutamate-induced convulsions: temporary alteration in blood-brain barrier permeability to plasma proteins.
Nemeroff CB, Crisley FD. Environ Physiol Biochem. 1975;5(6):389-95.

Monosodium L-glutamate (MSG), a commonly used food additive, induces convulsive disorders in rats. A reversible change in the cerebrovascular permeability of plasma proteins occurs during convulsions induced by the intraperitoneal administration of 4.0 g/kg of MSG to the neonatal rat. During MSG-induced seizures, but not before or after, trypan blue dye enters into the brain tissues, whereas no dye penetration occurs in control rats receiving saline. The frequency of the incidence of MSG-induced convulsions is inversely proportional to the age of the animal. It decreases with the age of the rat. By 42 days of age no substantial seizure activity of dye penetration into the brain tissue occurs in MSG-treated rats. Histological examination indicates that seizure activity is not correlated with characteristic periventricular-arcuate area lesions known to be induced in neonates by parenteral MSG administration. No hypothalamic damage was observed in MSG-treated rats older than 10 days of age.

Effect of neonatal exposure to monosodium L-glutamate on regional GABA release during postnatal development.
Beas-Zárate C, Sánchez-Ruíz MY, Ureña-Guerrero ME, Feria-Velasco A. Neurochem Int. 1998 Sep;33(3):217-32.

Monosodium L-glutamate (MSG) causes neuronal lesions in certain brain regions when systemically given to young animals. Also, when glutamate (Glu) builds up in the intersynaptic space, it induces neuroexcitatory and neurocytotoxic effects, events mediated by several Glu receptors. Some of these receptors such as NMDA and AMPA receptors are present in the very earliest developmental stages of the central nervous system and play a major role in neuronal plasticity during synaptogenesis. In this paper, the GABAergic system vulnerability was determined in terms of [3H]-GABA release during postnatal development. [3H]-GABA release on days 14, 21, 30, and 60 days after birth was assessed for the cerebral cortex (CC), hippocampus (Hp) and striatum (S) in rats perinatally treated at days 1, 3, 5, and 7 after birth with MSG. The results show a major decrease in baseline [3H]-GABA release in the CC (30 and 60 days after birth) and the Hp (beginning day 21 after birth) vs the control groups [intact rats and rats given a NaCl solution equimolar to that of MSG (eqNaCl)] while in the S baseline release remained unchanged. Stimulated [3H]-GABA release was decreased in the CC on days 14 and 21 after birth and significantly increased on day 60 after birth vs the controls. In the Hp, a decrease was seen on days 14, 21, and 60 after birth vs the controls while stimulated [3H]-GABA release was decreased in the S vs the controls at all ages studied. No significant differences in stimulated [3H]-GABA release were found between the intact group and the group treated with eqNaCl on days 30 and 60 after birth. Results show that CC, Hp and S GABAergic neurones are a major target for the effect of perinatally given MSG and suggest a possible decrease in the number of Hp GABAergic neurones while these results in CC and S suggest a modified neuronal plasticity. NMDA receptor and calcium involvement are discussed as significant mediators of these events.

+Cholesterol

Effects of Monosodium Glutamate on Cholesterol — A Collection of Research Abstracts

Effects of monosodium glutamate (MSG) on serum lipids, blood glucose and cholesterol in adult male mice
Ahluwalia P, Malik VB.Toxicol Lett. 1989 Feb;45(2-3):195-8

Monosodium glutamate (MSG) was administered to adult male mice for 6 d at dose levels of 2, 4 and 8 mg/g b.w. Dose levels of 4 and 8 mg/g MSG resulted in significant changes in serum total lipids, triglycerides, phospholipids, free fatty acids and blood glucose 31 d after cessation of exposure. Administration of 2 mg/g MSG resulted in a decrease in blood glucose concentration but had no effect on the other measured end-points. No change in serum cholesterol was observed, either in free or esterified form or in different fractions of lipoproteins.

Studies on effect of monosodium glutamate (MSG) on various fractions of lipids and certain carbohydrate metabolic enzymes in liver and blood of adult male mice.
Malik VB, Ahluwalia P. Toxicol Lett.1994 Oct;74(1):69-77.

Monosodium glutamate (MSG) was administered subcutaneously to adult male mice for 6 days at dose levels of 2, 4, and 8 mg/g body wt. Dose levels above 4 mg/g body wt. showed significant increase in content of liver total lipids, phospholipids, triglycerides and free fatty acids, 31 days after the last injection. Blood glutamate level was significantly increased in all the groups but blood glutamine was increased in 4 and 8 mg/g body wt. groups (Groups III and IV) only. Blood pyruvate and glucose was significantly increased whereas liver glycogen and blood lactate was decreased in group III and IV. Activity of lactate dehydrogenase was significantly reduced both in serum and liver but the activity of glucose-6-phosphate dehydrogenase was significantly increased in RBC and liver at dose levels of 4 and 8 mg/g body wt. All these observations are suggestive of the fact that carbohydrate metabolism is shifted towards lipogenesis and hence leads to hyperlipidemia.

+Diabetes

Effects of Monosodium Glutamate on Diabetes — A Collection of Research Abstracts

Effects of monosodium glutamate administration in the neonatal period on the diabetic syndrome in KK mice
Cameron DP, Poon TK, Smith GC. iabetologia. 1976 Dec;12(6):621-6.

Administration of monosodium glutamate (MSG) to KK mice during the neonatal period resulted in a syndrome of obesity, stunting and hypogonadism. In some animals the genetic predisposition to diabetes was unmasked with the development of marked hyperglycaemia and or hyperinsulinaemia. Food intake was not increased compared to controls. The elevated plasma glucose and insulin in fed MSG treated mice fell rapidly with food deprivation. Glucose disposal was comparable in MSG treated and control mice after IP glucose, but after oral glucose MSG treated mice showed impaired glucose tolerance. Insulin secretion was defective in MSG treated mice after IP but not after oral glucose.

Decreased incidence of diabetes mellitus by monosodium glutamate in the non-obese diabetic (NOD) mouse
Nakajima H, Tochino Y, Fujino-Kurihara H, Yamada K, Gomi M, Tajima K, Kanaya T, Miyazaki A, Miyagawa J, Hanafusa T, et al., Res Commun Chem Pathol Pharmacol. 1985 Nov;50(2):251-7

Subcutaneous administration of monosodium glutamate (MSG) to neonatal female non-obese diabetic (NOD) mice resulted in obesity associated with stunting and hyperinsulinemia. However, the cumulative incidence of diabetes mellitus at 25 weeks of age in the MSG group was significantly lower than in the control group (10.3% vs. 43.6%, P less than 0.005). The immunoreactive insulin content of the pancreas from the 13- to 20-week-old MSG-treated mice was higher than that of the control mice (P less than 0.005).

Immunohistochemistry showed that the number of pancreatic B-cells was well preserved and insulitis was attenuated in the MSG-treated mice. Plasma corticosterone and 3, 5, 3'-triiodothyronine levels were elevated in the MSG group. These results suggested that, by the MSG treatment, the B-cell functions were maintained through the modification of the degenerative process of the islets in the NOD mouse.

+Obesity

Effects of Monosodium Glutamate on Obesity — A Collection of Research Abstracts

The induction of obesity in rodents by means of monosodium glutamate
Bunyan J, Murrell EA, Shah PP., Br J Nutr. 1976 Jan;35(1):25-39

In 1976, these researchers discovered that administration of MSG could induce obesity in mice and rats. Ever since, researchers have been using MSG to create obese mice and rats in the laboratory to study diseases related to obesity.

1) Monosodium glutamate (MSG) was administered by various methods to mice and rats of various ages and the incidence of obesity was later measured.
2) Newborn mice were injected subcutaneously with 3 mg MSG/g body-weight at 1, 2, 3, 6, 7, and 8 d of age; 16% died before weaning. Of the survivors, 90% or more became markedly obese. Mean carcass lipid content was increased by about 120% in both sexes at 20-30 weeks old. In male mice, MSG treatment increased body-weight and epididymal fat pad weight, and greatly decreased adrenaline-stimulated lipolysis in isolated fat cells. Body-weight of females was not increased significantly. Food intake was not increased in either sex from weeks 13 to 15. Blood glucose level was not generally increased by MSG but some of the male mice had abnormally high values.
3) Obesity was not detected in the offspring of female mice that had received 100 g MSG/kg diet, either from 3 weeks before mating until weaning, or from the 14th day of pregnancy until weaning.
4) Intraperitoneal injection of 10 mg MSG/g body-weight (in two doses) at weaning increased carcass lipid content in female mice by 34% by 23 weeks of age, but female rats were not affected.
5) The addition of 20 g MSG/l to the drinking-water from weaning onwards did not increase carcass lipid content in female rats or mice.
6) The addition of 20 g MSG/kg diet from weaning onwards did not alter body-weight or carcass lipid content in male and female rats by 14 weeks of age.
7) The obesity induced in mice by MSG was not associated with hyperphagia [overeating], unlike genetic obesity and obesity induced by gold thioglucose (GTG).
8) All types of mouse studied, obese and lean, had essentially the same linear relationship between carcass water content and carcass lipid content.
9) Although MSG-obese mice could not readily be differentiated from normal mice by the increase in body-weight, which was only about 10% compared to 50-120% for genetic and GTG-induced obesity, the proposed schedule of injections in the newborn was almost 100% reliable in inducing a high extent of adiposity.

Effects of monosodium glutamate on somatic development, obesity and activity in the mouse
Pizzi WJ, Barnhart JE, Pharmacol Biochem Behav. 1976 Nov;5(5):551-7

Neonatal mice 1 and 5 days of age and older mice 25 days of age were injected with an increasing dose of monosodium glutamate (MSG) for a ten-day period and observed for at least 150 days. Both male and female animals in the 1- and 5-day age group treated with MSG showed large increases in weight over controls along with a shortened body length. The MSG group also showed decreases in locomotor and exploratory behavior. The 25-day animals took much longer to show effects or failed to show any effects, indicating that the MSG-induced changes studied are age dependent.

Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate
Olney JW. Science. 1969 May 9;164(880):719-21

In newborn mice subcutaneous injections of monosodium glutamate induced acute neuronal necrosis in several regions of developing brain including the hypothalamus. As adults, treated animals showed stunted skeletal development, marked obesity, and female sterility. Pathological changes were also found in several organs associated with endocrine function. Studies of food consumption failed to demonstrate hyperphagia to explain the obesity. It is postulated that the adults’ syndrome represents a multifaceted neuroendocrine disturbance arising from the disruption of developing neural centers concerned in the mediation of endocrine function.

A more in-depth explanation of the study provided by www.chem-tox.com 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. 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 Chinese 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."

Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate
Olney JW. Science. 1969 May 9;164(880):719-21

Components of hypothalamic obesity: bipiperidyl-mustard lesions add hyperphagia to monosodium glutamate-induced hyperinsulinemia
Scallet AC, Olney JW. Brain Res. 1986 May 28;374(2):380-4

Rats with bilateral electrolytic lesions in the general region of the ventromedial hypothalamic (VMH) nucleus develop hyperinsulinemia, excessive food intake and obesity. Monosodium glutamate (MSG) destroys neurons of the arcuate hypothalamic (AH) nucleus and produces hyperinsulinemic but hypophagic obesity. Bipiperidyl mustard (BPM) primarily destroys VMH neurons, but has produced only a slight obesity even when rats were maintained on high-fat diets. In the present study, rats treated with MSG (AH lesion) were hyperinsulinemic, moderately obese and hypophagic; BPM rats (primarily VMH lesion) were not different from controls when fed standard chow diets. However, MSG/BPM rats (AH + VMH lesion) were hyperinsulinemic, massively obese and hyperphagic. Thus, two components of the electrolytic lesion syndrome previously attributed to VMH damage (hyperinsulinemia and obesity) were reproduced simply by MSG treatment alone. The third component (hyperphagia) occurred only when both AH and VMH were lesioned, suggesting that neurons in both nuclei may perform a satiety function and may be able to substitute for one another in this respect. Since MSG treatment is required for all components of both obesity syndromes described here, this underscores the importance of MSG-sensitive neurons in mechanisms of obesity. The combined treatment approach also represents the first rat model of hyperinsulinemic, hyperphagic obesity that can be entirely produced by systemic administration of neurotoxins.

Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite.
Hermanussen M, García AP, Sunder M, Voigt M, Salazar V, Tresguerres JA., Aschauhof Altenhof Germany. hermanussen.aschauhof@t-online.de

BACKGROUND: World-wide obesity has risen to alarming levels. We present experimental support for a new and very challenging hypothesis linking obesity, voracity, and growth hormone (GH) deficiency, to the consumption of elevated amounts of the amino-acid glutamate (GLU). Supraphysiological doses of GLU are toxic for neuronal cells.

METHODS: Human data were obtained from 807,592 German conscripts born between 1974 and 1978, and from 1,432,368 women of the German birth statistics (deutsche Perinatalerhebung) 1995-1997. The effects of orally administered monosodium glutamate (MSG) were investigated in 30 pregnant Wistar rats and their offspring. Pregnant animals either received no extra MSG, or 2.5 g MSG, or 5 g MSG per day, up to the end of the weaning period. In all, 2.5 g, respectively 5 g, MSG accounted for some 10%, respectively 20%, of dry weight of the average daily food ration. After weaning, MSG feeding was continued in the offspring.

FINDINGS: Morbid obesity associates with short stature. Average stature of conscripts progressively declines when body mass index increases above 38 kg/m2. Also morbidly obese young women are shorter than average though to a lesser extent than conscripts. Oral administration of MSG to pregnant rats affects birth weight of the offspring. Maternal feeding with 5 g MSG per day results in severe birth weight reduction (P<0.01). Weight increments remain subnormal when MSG feeding to the mothers is maintained during weaning (P < 0.01). GH serum levels are affected in animals that received MSG during prenatal life via maternal feeding. Animals that are kept on high MSG diet (5 g MSG per day) continue to show serum GH levels that are as low or even lower than those of MSG injected animals (P < 0.05), both at day 30 and at day 90 of life. Animals that were kept on medium MSG diet (2.5 g MSG per day) showed low serum GH levels at day 30 of life (P < 0.01), but seemed to partially recover before day 90. Almost identical results were observed in IGF-1 serum levels. Oral MSG resulted in dose dependent voracity. The animals fed 5 g MSG per day increased water uptake by threefold (P < 0.01), and food uptake by almost two-fold (P < 0.01). The influence of MSG is in general more marked in males than in females.

INTERPRETATION: GLU is a widely used nutritional substance that potentially exhibits significant neuronal toxicity. Voracity, and impaired GH secretion are the two major characteristics of parenterally administered GLU-induced neuronal damage. GLU maintains its toxicity in animals even when administered orally. Males appear to be more sensitive than females. The present study for the first time demonstrates that a widely used nutritional monosubstance--the flavouring agent MSG--at concentrations that only slightly surpass those found in everyday human food, exhibits significant potential for damaging the hypothalamic regulation of appetite, and thereby determines the propensity of world-wide obesity. We suggest to reconsider the recommended daily allowances of amino acids and nutritional protein, and to abstain from the popular protein-rich diets, and particularly from adding the flavoring agents MSG.

Effect of monosodium glutamate given orally on appetite control (a new theory for the obesity epidemic)
Fernandez-Tresguerres Hernández JA, An R Acad Nac Med (Madr). 2005;122(2):341-55; discussion 355-60

Monosodium glutamate is a substance widely used as flavouring agent in the whole world. It is considered to be innocuos by the health agencies of North America and Europe. The effects of the oral administration of two dosages of MSG during the second half of pregnancy and all The developmental process of pups on appetite control and various hormones has been analysed in rats. Effects have been compared with the neonatal parenteral administration of the same compound. The structure of the arcuate nucleus of the hypothalamus has been investigated as well as plasma levels of GH, IGF-1 and leptin and its influence on food consumption. Measurements were performed at 30 and 90 days of life. A nearly total destruction of the arcuate nucleus can be observed with the parenteral administration of MSG but also with the highest oral dose. Significant reductions can be seen in plasma GH and IGF 1 levels at 30 days of life, that are partially recovered at 90 days. Plasma leptin levels are significantly reduced at 90 days of life with the two oral doses together with a significant increase in food intake. In conclussion, oral administration of MSG during pregnancy and development in rats is able to significantly affect hypothalamic control of various hormones and increases appetite.

+Reproduction

Effects of Monosodium Glutamate on Reproduction — A Collection of Research Abstracts

Long-term effect of neonatal monosodium glutamate (MSG) treatment on reproductive system of the female rat
Mi[kowiak B, Kesa B, Limanowski A, Partyka M, Filipiak B., Folia Morphol (Warsz). 1999;58(2):105-13.

The study aimed at determining effects of monosodium glutamate (MSG), introduced in the perinatal period, on the reproductive system of sexually mature female rats. In days 2, 4, 6, 8, 10 the newborns received s.c. injections of MSG (4 mg/g body weight) or 2% NaCl solution. When the animals reached the age of 6, 12 or 18 months, their ovaries and uteri were isolated for histological and morphometric studies while in their sera estradiol level was estimated by the RIA technique. The perinatal injection of MSG was found to decrease relative weights of ovaries and uteri. In the ovaries increased numbers of primordial follicles and decreased numbers of graafian follicles were detected. Also the thickness of endometrium and of the epithelium, which lined the endometrium, was lowered in females, which received perinatal injections of MSG, as compared to the controls. Serum estradiol level in MSG injected females was lowered at the age of 12 and 18 months. In 12 and 18 month old females the alterations were accompanied by obesity and a decreased body length.

Effect of perinatal administration of monosodium glutamate (MSG) on the reproductive system of the male rat
Mi[kowiak B, Limanowski A, Partyka M .Endokrynol Pol. 1993;44(4):497-505.

The study was aimed at investigating the effect of monosodium glutamate administered during the perinatal period on the reproductive system of sexually mature male rats. Monosodium glutamate (at a dose of 4 mg/g of body weight) or hypertonic saline was administered subcutaneously to newborn rats at 2--nd, 4-th, 6-th, 8-th and 10-th day of life. At the age of four months the rats were killed and histological and morphometric examinations of testes, epididymis, seminal vesicles and ventral prostate were carried out. Blood serum levels of LH, FSH, testosterone and 17-beta-estradiol were determined by radioimmunoassay. The administration of monosodium glutamate caused inhibition of growth, obesity and decrease in weight of pituitary glands and testes. Blood serum levels of and FSH as well as the height of epithelial cells of accessory sexual glands remained unchanged, whereas testosterone level was lowered.

In 1969, Olney (143) found hypothalamic lesions, and 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 glutamic acid as neonates. Longitudinal studies, including feeding studies, in which neonatal/infant animals were given doses of monosodium glutamate and then observed over a period of months or years before being sacrificed for brain examination, repeatedly supported Olney's early findings.

Monosodium glutamate disruption of behavioral and endocrine function in the female rat
Rodriguez-Sierra JF, Sridaran R, Blake CA, Neuroendocrinology. 1980 Sep;31(3):228-35

Experiments were conducted to determine the effects of neonatal administration of L-monosodium glutamate (MSG) on behavioral and endocrine function in the female rat. Administration of MSG (4 mg/kg body weight) at days 1, 3, 5, 7 and 9 in neonates results in a delay of vaginal opening (VO) and the absence of ovulation at the time of VO. However, some rats were observed to ovulate after VO if they were subjected to sequential laparotomies. MSG-treated rats also fail to exhibit compensatory ovarian hypertrophy. Ovariectomized MSG-treated rats injected with estradiol benzoate (EB) followed by a progesterone injected 2 days later did not exhibit sexual beahvior to male rats, while all the control rats displayed lordosis. Chronic treatment with EB for 12 days, followed by a progesterone injection on the 12th day, resulted in a marked improvement of the sexual receptivity of the MSG-treated rats. The body weight of the MSG-treated animals was lower than that of the controls during development although the MSG animals looked obese. Food intake is normal in the MSG-treated rats, but when expressed as intake/100 g body weight, the MSG-treated rats appeared slightly hyperphagic, MSG-treated rats respond with increased food intake after ovariectomy and EB treatment suppresses the increased food intake. Thus, the control of food intake by estrogen does not seem to be affected by the MSG treatment; in fact, these animals seem to be more sensitive than control rats to the anorectic effects of EB. Neonatal MSG treatment appears to affect the neural control for the tonic secretion of gonadotropins by destroying arcuate nuclei. This undoubtedly reduces the reproductive capacity of the animals by impeding the growth and secretions of their ovaries. The findings that chronic estrogen followed by progesterone treatment can reinstate sexual receptivity in MSG-treated animals suggests that the arcuate nuclei are not needed for the expression of sexual behavior and that estrogens might remedy the fertility problems of MSG-treated animals.

Monosodium glutamate administration to the newborn reduces reproductive ability in female and male mice
Pizzi WJ, Barnhart JE, Fanslow DJ., Science. 1977 Apr 22;196(4288):452-4

Monosodium glutamate (MSG) administered during the neonatal period (days 2 to 11) resulted in a sequence of events that were manifested in adulthood. Reproductive dysfunction was seen in both female and male animals. Females treated with MSG had fewer pregnancies and smaller litters, while males treated with MSG showed reduced fertility. The MSG-treated mice showed increased body weight and decreased pituitary, thyroid, ovary, or testis weights.

+Additional Resources and Articles

+If MSG is so bad for you, why doesn't everyone in Asia have a headache? -by Alex Renton

If MSG is so bad for you, why doesn't everyone in Asia have a headache?
Alex Renton, Sunday July 10, 2005, Observer

In the port city of Yokohama, south of Tokyo, there is a museum devoted entirely to noodle soup. It may be Japan's favorite foodie day out: one and a half million ramen fans visit the museum every year, and even on the wintry morning that I went the queue wound 50 yards down the street - young couples, mainly: cold, hungry and excited.

Inside the Yokohama Ramen Museum and Amusement Park they meet exhibitions on the evolution of soup bowls and instant noodle packets - more fascinating than you'd think, but these are not the main event. That's deep in the basement, where there's an entire street, done up to look like a raucous 1950s Yokohama harbor-front. Every shop houses a different noodle restaurant, each a clone of one of the best noodle shops of Japan. It's a culinary Madame Tussauds.

The Japanese are sentimental about their noodle soup - it's the working-class food that nourished the nation in the bleak days after World War Two. Ramen chefs are TV celebs, in a country that devotes more broadcast time to cookery than even we do. I asked the young pilgrims just what they valued above all in ramen. They sniffed the tangy air, Bisto-kid style: 'The basis of the experience is the broth,' was the consensus. In the great Japanese cod-Western Tampopo - the only movie to take noodle soup, sex and death with equal seriousness - a ramen guru announces that the key to Japan's national dish is that 'the soup must animate the noodles'.

What does chiefly animate Japanese soups and broths is an amino acid called glutamate. In the best ramen shops it's made naturally from boiling dried kombu seaweed; it can also come from dried shrimp or bonito flakes, or from fermented soy. More cheaply and easily, you get it from a tin, where it is stabilized with ordinary salt and is thus monosodium glutamate.

This last fact is of little interest to the Japanese - like most Asians, they have no fear of MSG. And there lies one of the world's great food scare conundrums. If MSG is bad for you - as Jeffrey Steingarten, the great American Vogue food writer once put it - why doesn't everyone in China have a headache?

To begin to answer this we must go back to Japan a century ago. Professor Kidunae Ikeda comes home from the physics faculty at the Tokyo Imperial University and sits down to eat a broth of vegetables and tofu prepared by his wife. It is - as usual - delicious. The professor, a mild, bespectacled biochemistry specialist, turns to Mrs. Ikeda and asks - as spouses occasionally will - what is the secret of her wonderful soup. Mrs. Ikeda points to the strips of dried seaweed she keeps in the store cupboard. This is kombu, a heavy kelp. Soak it in hot water and you get the essence of dashi, the stock base of the tangy broths and consommés the Japanese love.

This is the professor's 'Eureka!' moment. Mrs. Ikeda's kombu is to lead him to a discovery that will make his fortune and change the nature of 20th-century food. In time, it would bring about the world's longest-lasting food scare, and as a result, kick-start the age of the rebel consumer. It was an important piece of seaweed. Professor Ikeda was one of many scientists at the turn of the century working on the biochemical mechanics which inform our perception of the world. By 1901 they had drawn a map of the tongue, showing, crudely, the whereabouts of the different nerve endings that identify the four accepted primary tastes, sweet, sour, bitter and salty.

But Ikeda thought this matrix missed something. 'There is,' he said, 'a taste which is common to asparagus, tomatoes, cheese and meat but which is not one of the four well-known tastes.' He decided to call the fifth taste 'umami' - a common Japanese word that is usually translated as 'savory' - or, with more magic, as 'deliciousness'. By isolating umami, Ikeda - who had picked up some liberal notions while studying in Germany - hoped he might be able to improve the standard of living of Japan's rural poor. And so he and his researchers began their quest to isolate deliciousness.

By 1909 the work on kombu was complete. Ikeda made his great announcement in the august pages of the Journal of the Chemical Society of Tokyo. He had isolated, he wrote, a chemical with the molecular formula C5H9NO4. This and the substance's other properties were exactly the same as those of glutamic acid, an amino acid produced by the human body and present in many foodstuffs. When the protein containing glutamic acid is broken down - by cooking, fermentation or ripening - it becomes glutamate.

'This study,' concluded Professor Ikeda in triumph, 'has discovered two facts: one is that the broth of seaweed contains glutamate and the other that glutamate causes the taste sensation "umami".'

The next step was to stabilize the chemical. This was easy: mixing it with ordinary salt and water made monosodium glutamate - a white crystal soluble in water and easy to store. By the time he published his paper, the professor had, wisely, already patented MSG. He began to market it as a table condiment called Aji-no-moto ('essence of taste') that same year.

It was an instant success, and when Kidunae Ikeda died in 1936 he was a rich man: he remains, as every Japanese schoolchild knows, one of Japan's 10 greatest inventors. The food chemicals giant Ajinomoto Corp, now owned by General Foods, pumps out a third of the 1.5 million tons of monosodium glutamate we eat every year - from India to Indonesia 'Ajinomoto' means MSG.

Ikeda's original paper muses a little about MSG and why it should excite the taste buds so, without arriving at any convincing conclusion. Much more work has been done since. We now know that glutamate is present in almost every food stuff, and that the protein is so vital to our functioning that our own bodies produce 40 grams of it a day. Probably the most significant discovery in explaining human interest in umami is that human milk contains large amounts of glutamate (at about 10 times the levels present in cow's milk). Babies have very basic taste buds: it's believed that mother's milk offers two taste enhancements - sugar (as lactose) and umami (as glutamate) in the hope that one or other will get the little blighters drinking. Which means mothers' milk and a packet of cheese'n'onion crisps have rather more in common than you'd think.

When you next grate parmesan cheese onto some dull spaghetti, what you will have done in essence is add a shed-load of glutamate to stimulate your tongue's umami receptors, thus sending a message to the brain which signals (as one neuro-researcher puts it) 'Joy and happiness!' Supper is rescued - and your system has added some protein and fats to a meal that was all carbohydrate.

Ripe cheese is full of glutamate, as are tomatoes. Parmesan, with 1200mg per 100 grams, is the substance with more free glutamate in it than any other natural foodstuff on the planet. Almost all foods have some naturally occurring glutamate in them but the ones with most are obvious: ripe tomatoes, cured meats, dried mushrooms, soy sauce, Bovril and of course Worcester sauce, nam pla (with 950mg per 100g) and the other fermented fish sauces of Asia.

Your mate, Marmite, with 1750mg per 100g, has more glutamate in it than any other manufactured product on the planet - except a jar of Gourmet Powder straight from the Ajinomoto MSG factory. On the label, Marmite calls it 'yeast extract'. Nowhere in all their literature does the word 'glutamate' appear. I asked Unilever why they were so shy about their spread's key ingredient, and their PR told me that it was because it was 'naturally occurring ... the glutamate occurs naturally in the yeast'.

As they put monosodium glutamate into production, Professor Ikeda and his commercial partners found that making stable glutamate from the traditional seaweed and salt was unnecessary. They developed a much simpler and cheaper process using fermented molasses or wheat - eventually manufacturers realized that almost any protein can be broken down to produce it.

The product took off, immediately, and within a few years Ajinomoto (which was now the company's name) was selling MSG across Asia. The breakthrough to America came in the aftermath of World War Two. Like pizza and vermouth, MSG was a taste American soldiers brought home with them. They weren't aware that MSG was what they'd liked in Japan - but the US Army catering staff noticed that their men enjoyed the leftover ration packs of the demobilized Japanese Army much more than they did their own, and began to ask why. MSG arrived in America at a key moment. Mass production of processed food was booming. But canning, freezing and pre-cooking have a grave technical problem in common - loss of flavor. And MSG was a cheap and simple additive that made everything taste better. It went into tinned soups, salad dressings, processed meats, carbohydrate-based snacks, ice cream, bread, canned tuna, chewing gum, baby food and soft drinks. As the industry progressed, it was used in frozen, chilled and dehydrated ready meals. MSG is crucial in no-fat or low-fat food, where natural flavor is lost with the extraction of oils. It's now found in cosmetics, pharmaceuticals, and dietary supplements.

Ajinomoto Corp started manufacturing in the States in 1956 and in 1962 allied itself with Kellogg's. MSG sells in the States in supermarkets, under the brand Ac'cent. In Britain you will have to visit a Chinese supermarket for a supply of pure Gourmet Powder, but MSG plays a role - often in secret - in products on almost every shelf of the supermarket.

But MSG's conquest of the planet hit a major bump in April 1968, when, in the New England Journal of Medicine, a Dr Ho Man Kwok wrote a chatty article, not specifically about MSG, whose knock-on effects were to panic the food industry. 'I have experienced a strange syndrome whenever I have eaten out in a Chinese restaurant, especially one that served northern Chinese food. The syndrome, which usually begins 15 to 20 minutes after I have eaten the first dish, lasts for about two hours, without hangover effect. The most prominent symptoms are numbness at the back of the neck, gradually radiating to both arms and the back, general weakness and palpitations...'

And so was born Chinese restaurant syndrome (CRS) and a medico-academic industry dedicated to the researching and publicizing of the dangers of MSG - the foreign migrant contaminating American kitchens. Shortly after Dr Ho came, Dr John Olney at Washington University, who in 1969 injected and force-fed newborn mice with huge doses of up to four grams/kg bodyweight of MSG. He reported that they suffered brain lesions and claimed that the MSG found in just one bowl of tinned soup would do the same to the brain of a two-year-old.

Other scientists were testing MSG and finding no evidence of harm - in one 1970 study 11 humans ate up to 147 grams of the stuff every day for six weeks without any adverse reactions. At the University of Western Sydney the researchers concluded, tersely: 'Chinese restaurant syndrome is an anecdote applied to a variety of postprandial illnesses; rigorous and realistic scientific evidence linking the syndrome to MSG could not be found.'

Science has still not found a convincing explanation for CRS: indeed, some researchers suggest it may well be to do with the other things diners have imbibed there - peanuts, shellfish, large amounts of lager. Others say that fear of MSG is a form of mass psychosis - you suffer the symptoms you've been told to worry about. The fact is that, since the eighties, mainstream science has got bored of MSG. Some research continues; in 2002, for example, New Scientist got very excited over a report that MSG might damage your eyesight, after Japanese scientists announced that they had produced retinal thinning in baby rats fed with MSG. It turned out they were putting 20 grams of MSG in every 100g of rat food - an amazing amount, given that, in the UK, we adults consume about four grams of it each a week. (One project took people who were convinced their asthma was caused by MSG and fed them up to six grams of it a day, without ill-effects). However, at no time has any official body, governmental or academic, ever found it necessary to warn humans against consuming MSG.

But popular opinion has traveled - spectacularly - in the opposite direction to science. By the early eighties, fuelled by books like Russell Blaylock's Excitotoxins - The Taste That Kills, MSG's name was utter mud. Google MSG today, and you'll find it blamed for causing asthma attacks, migraines, hypertension and heart disease, dehydration, chest pains, depression, attention deficit disorder, anaphylactic shock, Alzheimer's and Parkinson's diseases and a host of diverse allergies.

Thus since 1968 the processed food industry has had its own nasty headache as a result of MSG. Hundreds of processed products would have to be withdrawn if amino-acid based flavor-enhancers could not be used. They would become, simply, tasteless. By the 1980s a third of all Americans believed it was actively harmful. Crisp-buying teenagers thought MSG made them stupid and spotty. Mothers read that MSG could put holes in their children's brains.

So the food industry employed its usual tactic in the face of consumer criticism: MSG was buried by giving it new names. The industry came up with a fabulous range of euphemisms for monosodium glutamate - the most cheeky of all is 'natural flavorings' (however, the industry did remove MSG from high-end baby foods). Nowadays the industry's PR beats a big drum. 'Natural, Tasty, Safe' is the slogan. 'Many people believe that monosodium glutamate is made from chemicals. Monosodium glutamate is a chemical in the same way that the water we drink and the oxygen we breathe are chemicals,' explains an MSG website. MSG manufacturers are now pushing it as actively useful for health - a way to eat less salt - and they have pursued the celebrity route too. Heston Blumenthal, of the Fat Duck in Bray, is among the eminent chefs the industry has enlisted for promotion of the umami principle at conferences across the world - although he uses traditional sources like kombu.

It's not surprising that the MSG-makers are so busy on their product's image, because MSG-phobia still shows no signs of subsiding. This despite the fact that every concerned public body that ever investigated it has given it a clean bill of health, including the EU, the United Nations food agencies (which in 1988 put MSG on the list of 'safest food additives'), and the British, Japanese and Australian governments.

In fact, every government across the world that has a food licensing and testing system gives MSG - 'at normal levels in the diet' - the thumbs-up. The US Food and Drug Administration has three times, in 1958, 1991 and 1998, reviewed the evidence, tested the chemical and pronounced it 'genuinely recognized as safe. However, there remains a body of respected nutritionists who are sure MSG causes problems - especially in children. And parents listen. Most doctors who offer guides to parents qualify their warnings about MSG - it may cause problems, it has been anecdotally linked with disorders. But public figures like the best-selling nutrition guru Patrick Holford are powerful advocates against MSG. He's sure the science shows that MSG causes migraines and he is convinced of the dangers of the substance to children, particularly in the child-grabber snacks like Monster Munch and Cheesy Wotsits.

'I'm a practitioner and there's no doubt that kids with behavioral problems react to MSG,' he says. 'I've given them the foods, and seen the different reactions. Glutamate is a brain stimulant in the way that it is given, because it enhances sensory perception in the sense that things taste much better - and some kids become very hyperactive.'

Holford admits that he has not measured this hyperactivity, or tested MSG by itself on children - his statements are based on anecdotal comparison of the effects of plain crisps versus flavored ones. But there is some justice in his complaint that in all the acres of research on MSG, 'most is directed at the possible physiological effects, not the behavioral ones'.

Eric Taylor, professor of child and adolescent psychiatry at King's College in London, is among the leading British experts on food additives and children's behavior. He was a pioneer of 'elimination tests' that examined food additives and their effect on children - establishing, for one, that the coloring tartrazine did contribute to hyperactivity.

Yet he does not think MSG is a culprit and he has never tested it. Why? 'There are so many substances, and there's not much funding. And, with MSG, there's no reasonable physiological theorem to justify the research.' The only investigation he has seen on children's brains and MSG, conducted in the seventies, suggested that the substance might improve reading ability.

Patrick Holford, like many of MSG's foes, also talks of its possible addictive properties and he cannot explain why 'natural' glutamate, say in cheese or parma ham, should be any less addictive, or harmful, than glutamate that's been industrially produced and stabilized with salt.

The anti-additive movement (check out the excellent and informative www.truthinlabeling.org) admits that 'natural' and 'industrially produced' glutamate are chemically the same, and treated by the body similarly. So why doesn't anyone ever complain of a headache or hyperactivity after a four cheese and tomato pizza (where there's easily as much glutamate as in an MSG-enhanced chicken chow mein)?

Their answer is that the industrial fermentation process introduces contaminants. This is possible, of course, but it ignores the fact that whole swaths of the planet - including East Asia, where I live - do not have any problem with MSG. Here in Thailand, the phong chu rot sits on the table with the fish sauce and the chili powder where you would have the salt and pepper.

MSG has had one unarguable effect on us - and it is a benign one. It has made consumers look at the small print. In turn this kick-started the organic food movement and other, more militant consumer power groups. 1968 was a good year for rebels, and the dawn of MSG-phobia coincides with the beginning of a great shift in middle-class consumers' thinking - a withdrawal of our faith in the vast corporations that fed and medicated us. After 1968 we began to question them and their motives. Friends of the Earth and Greenpeace came next. It is now 37 years since Dr Ho Man Kwok named Chinese restaurant syndrome, and it's plain that the case against MSG remains unproven. So either you conclude, as some will, that government, science and the mega-corporates of the food industry really are all in league with each other to poison us for profit. Or, like me, you make a different decision.

Now, I have little faith in the food industry and I'm as suspicious of food additives as the next person - I spend many hours fighting the grim battle to keep them from my children's mouths. But until new evidence emerges I am going to give MSG a conditional discharge. But would I have it in the kitchen? Well, I did. I bought a little bag of Ajinomoto from the corner shop on our Bangkok street and tried it, a gram (the tip of a teaspoon) at a time.

By itself it tasted of almost nothing. So I beat up and fried two eggs, and tried one with MSG, one without. The MSG one had more egg flavor, and didn't need any salting. I tried the crystals on my son's leftover pieces of chicken breast (definitely more chickeny). I tried it in a peanut butter sandwich (nothing). On Weetabix with milk (interesting, sort of malty) and on Weetabix with milk and sugar (thought I was going to be sick). My friend Nic came round. He told me about a Japanese restaurant he'd been to that gave him headaches and a 'weird tingling in the cheeks' - until he told them to stop with the MSG. Then he was fine, he said. I nodded and I served him two tomato and chive salads; both were made using the very same ingredients but I told him one plate of tomatoes was 'organic', the other 'factory-farmed'. The organic tomatoes were far better, we agreed. These, of course, were the tomatoes doused with mono sodium glutamate.

Then we ate mascarpone, parma ham and tomato pizza. Nic felt fine. So did I. I had ingested, I reckoned, a good six grams of MSG over the day, and probably the same again in free glutamate from the food - the equivalent of eating two 250g jars of Marmite.

I've thrown the Ajinomoto out now. It works, but it was embarrassing - a bit like having a packet of Bisto in the cupboard. There is no need to have MSG in the kitchen. If I want extra glutamate in my food I'll use parmesan, or tomato purée, or soy sauce. Or like Mrs. Ikeda, boil up some kelp.

So you think you don't eat MSG? Think again...
· Some of the names MSG goes under
· monopotassium glutamate
· glutavene
· glutacyl
· glutamic acid
· autolyzed yeast extract
· calcium caseinate
· sodium caseinate
· E621 (E620-625 are all glutamates)
· Ajinomoto, Ac'cent
· Gourmet Powder

The following may also contain MSG natural flavours or seasonings
· natural beef or chicken flavouring
· hydrolyzed milk or plant protein
· textured protein
· seasonings
· soy sauce
· bouillon
· broth
· spices

Free glutamate content of foods (mg per 100g)
· roquefort cheese 1280
· parmesan cheese 1200
· soy sauce 1090
· walnuts 658
· fresh tomato juice 260
· grape juice 258
· peas 200
· mushrooms 180
· broccoli 176
· tomatoes 140
· mushrooms 140
· oysters 137
· corn 130
· potatoes 102
· chicken 44
· mackerel 36
· beef 33
· eggs 23
· human milk 22

For more on the MSG debate visit: www.truthinlabeling.org, www.msgmyth.com, www.msgtruth.org or www.food.gov.uk.
Guardian Unlimited © Guardian News and Media Limited 2007

+The Link between Monosodium Glutamate (MSG) and Obesity -by Dani Veracity, NewsTarget.com

The Link between Monosodium Glutamate (MSG) and Obesity
by Dani Veracity, NewsTarget.com, July 9, 2005

If fried snack chips had a warning printed right on the bag that said, "Warning: these chips will make you obese," would you still buy them? Would you still eat them? Well, in a sense, you do see that warning on chips; just read the ingredient list. Research suggests that monosodium glutamate causes obesity, making unhealthy snacks even unhealthier than you may have suspected.

I'm sure you already know that tortilla and potato chips aren't health foods, right? They're made with fried fats, they almost always harbor hidden toxic chemicals (acrylamides), and if they're flavored, they usually contain monosodium glutamate (MSG). This is basically a recipe for obesity.

But how does MSG cause obesity? Like aspartame, MSG is an excitotoxin, a substance that overexcites neurons to the point of cell damage and, eventually, cell death. Humans lack a blood-brain barrier in the hypothalamus, which allows excitotoxins to enter the brain and cause damage, according to Dr. Russell L. Blaylock in his book Excitotoxins. According to animal studies, MSG creates a lesion in the hypothalamus that correlates with abnormal development, including obesity, short stature and sexual reproduction problems.

Based on this evidence, Dr. Blaylock makes an interesting point about the American obesity epidemic, especially among young people: "One can only wonder if the large number of people having difficulty with obesity in the United States is related to early exposure to food additive excitotoxins, since this obesity is one of the most consistent features of the syndrome. One characteristic of the obesity induced by excitotoxins is that it doesn't appear to depend on food intake. This could explain why some people cannot diet away their obesity." As an increasing number of elementary school students bring snack-size bags of chips to school in their lunch boxes, the MSG-obesity link demands parental caution.

Instead of passively watching modern society become obese and then commenting on it, we need to change it at the start. That begins with you, the consumer. By avoiding foods with MSG, you are not only protecting your health and your family's health, you are also protecting society's health by not supporting companies that use MSG. Use your buying power to show that you don't accept manufactured foods that use MSG or any of the other hidden forms of MSG such as yeast extract, hydrolyzed vegetable proteins and autolyzed proteins.

The Experts Speak on MSG and Obesity

Olney, J.W. "Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium glutamate." Sci. 165(1969): 719-271. Humans also lack a blood-brain barrier in the hypothalamus, even as adults. It is for this reason that Dr. Olney and other neuroscientists are so concerned about the widespread and heavy use of excitotoxins, such as MSG, hydrolyzed vegetable protein, and cysteine, as food additives. In his experiments Dr. Olney found that high-dose exposure to MSG caused hypoplasia of the adenohypophysis of the pituitary and of the gonads, in conjunction with low hypothalamic, pituitary, and plasma levels of LH, growth hormone, and prolactin. When doses below toxic levels for hypothalamic cells were used, he found a rapid elevation of LH and a depression of the pulsatile output of growth hormone. In essence, these excitotoxins can cause severe pathophysiological changes in the central endocrine control system. Many of these dysfunctional changes can occur with subtoxic doses of MSG. One can speculate that chronic exposure to these neurotoxins could cause significant alterations in the function of the hypothalamus, including its non-endocrine portions.
Excitotoxins by Russell L Blaylock MD, page 263

"Consuming MSG leads to obesity"

Early exposure in life to high doses of glutamate, or the other excitotoxins, could theoretically produce a whole array of disorders much later in life, such as obesity, impaired growth, endocrine problems, sleep difficulties, emotional problems including episodic anger, and sexual psycho-pathology.
Excitotoxins by Russell L Blaylock MD, page 89

The stress-induced abnormalities in blood-brain barrier permeability suggest differing MSG effects dependent on existing states of relaxation or stresses. The suggestive evidence for MSG-induced neuroendocrine effects is substantial, coupled with the observation of increased obesity in children.
In Bad Taste by George R Schwartz MD, page 39

With this enormous consumption of foods laced with MSG additives, it is no wonder that we have an obesity problem in this country, especially when you combine the hypothalamic lesion caused by MSG to the high-fat and -carbohydrate diets of young people. Of particular concern is the suggestion that MSG ingested by pregnant women may actually cause this lesion in children while they are still in the womb.
Health and Nutrition Secrets by Russell L Blaylock MD, page 180

This also means that, while pregnant, mothers of diabetic children also consumed very large amounts of these excitotoxin-containing foods. Also, many parents feed their babies table food from an early age—food often laced with large amounts of MSG. In addition, large numbers of babies are also fed formula, and many formulas are known to be high in excitotoxins such as caseinate. I have already cited studies showing that gross obesity is frequently linked to excessive MSG consumption in test animals.
Health and Nutrition Secrets by Russell L Blaylock MD, page 182

Particularly disturbing is the later obesity after MSG exposure during the neonatal and infant period even after only a short or limited exposure.
In Bad Taste by George R Schwartz MD, page 22

With all of these endocrine malfunctions you would expect these mice to develop abnormally, and they do. Consistently, the animals exposed to MSG were found to be short, grossly obese, and had difficulty with sexual reproduction. One can only wonder if the large number of people having difficulty with obesity in the United States is related to early exposure to food additive excitotoxins since this obesity is one of the most consistent features of the syndrome. One characteristic of the obesity induced by excitotoxins is that it doesn't appear to depend on food intake. This could explain why some people cannot diet away their obesity. It is ironic that so many people drink soft drinks sweetened with NutraSweet® when aspartate can produce the exact same lesions as glutamate, resulting in gross obesity. The actual extent of MSG induced obesity in the human population is unknown.
Excitotoxins by Russell L Blaylock MD, page 81

"Animal studies demonstrate link between MSG and obesity"
The obesity effect of MSG in animals requires evaluation since unexplained obesity is increasing in our population, along with hypertension and diabetes. MSG-induced obesity in animals may carry long-term significance for humans.
In Bad Taste by George R Schwartz MD, page 22

Since his early observation, other studies have confirmed that MSG causes gross obesity in animals. At an international neuroscience meeting, Dr. Olney was asked if he thought the reason Americans were so obese was, in fact, due to their high consumption of MSG additives. The question was never answered, but since that conference in the 1970s, America has undergone this virtual epidemic of gross obesity, especially among its youth.
Health and Nutrition Secrets by Russell L Blaylock MD, page 180

This MSG-induced obesity was characterized by a preference for carbohydrates and an aversion for more nutritious foods, just as we are now witnessing in our youth. Also, excess weight was extremely difficult to exercise off or diet off in these experimental animals.
Health and Nutrition Secrets by Russell L Blaylock MD, page 182

Courtesy of www.NewsTarget.com

+Largest Ever Autism Study Identifies Two Genetic Culprits

Largest Ever Autism Study Identifies Two Genetic Culprits
New regions of the genome can now be plumbed in the search for new therapies for the mysterious mental disorder
By Nikhil Swaminathan

New regions of the genome can now be plumbed in the search for new therapies for the mysterious mental disorder.

The largest genome scan ever conducted to get to the bottom of autism has pinpointed two locations in the human genetic makeup that may trigger the mysterious mental condition. The Autism Genome Project, a collaboration of 120 scientists representing 19 countries and 50 institutions, compared the genomes of 1,168 families that each had at least two autism sufferers in them to try to track down the regions. The consortium reports its findings in this week's issue of Nature Genetics.

Autism is a mental disorder characterized by behavioral problems that may include a lack of social and communications skills, such as failure to respond to one's own name, intense tantrums and general detachment. In the last decade the diagnosis of autism has increased 10-fold. It is now believed to affect one in 166 children born in the U.S. and four boys for every girl.

"Although we know autism is highly inheritable, complex gene interactions and submicroscopic anomalies create a din of statistical noise that drowns out detection of signals from linked sites in the genome," says study co-author Bernie Devlin, a human geneticist at the University of Pittsburgh. "To amplify these signals, we brought to bear gene chip technology with a huge sample, and also screened for these fine-level anomalies, factoring them into the analysis."

Using a DNA microarray, or gene chip, the team was able to scan large stretches of sequence for tiny deletions common within the study families. They also sought out copy number variations and large-scale insertions or deletions of genetic material. In the two-fold analysis, the researchers implicated the gene neurexin 1, located on chromosome 2, as well as a swath of sequence on chromosome 11.

Neurexin 1 is part of a three-member family of genes coding for proteins involved in communication between neurons. It is associated with glutamate, the neurotransmitter known to elevate neuronal activity and play a role in wiring the brain during early development. Glutamate functioning has been implicated in other syndromes involving mental retardation of which autism is often a symptom, such as fragile X syndrome and tuberous sclerosis. Neurexin 1 is specifically believed to be involved in building glutamate synapses, the links through which glutamate neurons send and receive electrical signals.

"Often you don't have any idea of what a gene does, but in this case we know neurexin 1 is involved at sites where the neurotransmitter glutamate is released," says study coauthor Gerard Schellenberg, a medical researcher at the University of Washington. "As for the chromosome 11 location, we think there is another susceptibility gene there and we are actively pursuing it. We are in the neighborhood and have a plan to find it. The section of chromosome 11 identified in the study has been linked to proteins that ferry glutamate across synapses.

Genetic anomalies, from tiny deletions or substitutions of single bases to large stretches of missing code or even multiple copies of the same code, often crop up in the human genome and, occasionally, can create a disposition to a particular type of disorder. Among the variations found in the Autism Genome Project subjects was the deletion of the neurexin 1 gene. Much of the autism research community believes there may be roughly six major genes involved in autism, and maybe 30 others that may confer some risk. A combination of mutations in any of these genes could contribute to the likelihood of being born with autism. Because a number of different genetic factors may contribute to this disease, identifying these markers is made very difficult and large sample sizes are needed to get significant results.

"These findings are a piece of the puzzle," says Geraldine Dawson, director of the University of Washington's Autism Center. "As we identify these genes we will be able to screen young children for autism at an early age and begin interventions earlier, which can have a dramatic effect for some children."

These results are the culmination of phase 1 of the Autism Genome Project, which began in 2002 with the sharing of samples and data from labs around the world. Phase 2 will follow up on the leads discovered in the first phase. The $14.5 million project will receive funding from various institutions such as the National Institutes of Health and Autism Speaks, an organization dedicated to increasing the awareness of and finding a cure for autism spectrum disorders.

"Autism is a very difficult condition for families—communication is taken for granted by parents of healthy children but is so greatly missed by those with autistic children," says study co-author, Jonathan Green, a child psychiatrist at the University of Manchester in England. "We hope that these exciting results may represent a step on the way to further new treatments in the future."

courtesy of www.scientificamerican.com

Note: While this article does not specifically name MSG as a cause, opponents of MSG have pointed out that both genes identified in this study are associated with glutamate. Is there a connection?

Consider that rates in autism have risen from 5 in 10,000 to 1 in 150. New Jersey is reporting rates of 1 in 96. Based on statistics from the U.S. Department of Education and other governmental agencies, autism is growing at a startling rate of 10-17 percent per year.

According to officials at the National Institutes of Health, while there is most likely a genetic predisposition, there must also be an environmental component to autism. The rapid rise in the rate of autism over the last 15 years cannot be attributed solely to genetics.

Autism is no longer considered a heritable, genetic disorder. It is an environmentally triggered disease, therefore preventable and treatable. Environmental research holds the key to finding the cause and developing effective treatments for those affected.

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Research - MSG