House Protects Pizza as a Vegetable

By Lisa Baertlein and Charles Abbott

(Reuters) – The House of Representatives dealt a blow to childhood obesity warriors on Thursday by passing a bill that abandons proposals that threatened to end the reign of pizza and French fries on federally funded school lunch menus.

The scuttled changes, which would have stripped pizza’s status as a vegetable and limited how often French fries could be served, stemmed from a 2010 child nutrition law calling on schools to improve the nutritional quality of lunches served to almost 32 million U.S. school children.

The action is a win for the makers of frozen French fries and pizza and comes just weeks after the deep-pocketed food, beverage and restaurant industries successfully weakened government proposals for voluntary food marketing guidelines to children.

“It’s an important victory,” said Corey Henry, spokesman for the American Frozen Food Institute (AFFI). That trade association lobbied Congress on behalf of frozen pizza sellers like ConAgra Foods Inc and Schwan Food Co and French fry makers McCain Foods Ltd and J.R. Simplot Co, the latter best known as a supplier to fast-food company McDonald’s Corp.

“Our concern is that the standards would force companies in many respects to change their products in a way that would make them unpalatable to students,” Henry said.

Other AFFI members include H.J. Heinz Co, General Mills Inc and Kraft Foods Inc.

The school lunch provisions were a small part of a mammoth bill that provides money for all parts of the federal government. The House sent the bill to the Senate for final Congressional approval.

“They started out with French fries and now they have moved on to pizza,” said Jared Polis, Colorado Democrat, who lamented the government’s subsidy of unhealthy diets through school meals. “Pizza alone (without side dishes) … common sense, it’s not a vegetable.”

Calls to Minnesota-based Schwan and its external public relations firm and ConAgra were not returned.

Mark Dunn, AFFI’s chairman and J.R. Simplot’s main lobbyist, referred requests for comment to a company spokesman, who declined to respond.

PIZZA AS A VEGETABLE

Polis mentioned French fries in reference to a provision in the bill that would have blocked the government from limiting servings of white potatoes to one cup per week in meals served through the roughly $18 billion U.S. school meals program overseen by the U.S. Department of Agriculture.

In addition to potatoes, USDA also proposed limits on starchy vegetables including corn, green peas and lima beans, while requiring lunches to serve a wider variety of fruit and vegetables.

Another provision bars the USDA from changing the way it credits tomato paste, used in pizza. The change would have required pizza to have at least a half-cup of tomato paste to qualify as a vegetable serving. Current rules, which likely will remain in place, require just two tablespoons of tomato paste.

According to a USDA report from November 2007, pizza and French fries were among the most commonly consumed lunch foods by participants in the national school lunch program.

Sam Farr of California, the Democratic leader on the appropriations subcommittee in charge of the USDA, said the interference with USDA rule-writing was “wrong” and “shouldn’t be done”. Still, Farr supported passage of the overall bill.

Agriculture Secretary Tom Vilsack said on Wednesday that U.S. school children would still see more fruit and vegetables, more grains, more low-fat milk and less salt and fat in meals despite the language in the spending bill.

“First of all, we can assure parents of school-age children (that) USDA will do everything it can” to improve the nutritional quality of school meals, as required by the 2010 child nutrition law.

Vilsack was speaking via teleconference from Hanoi during a U.S. trade trip.

Healthier school lunches are a cornerstone of First Lady Michelle Obama’s campaign to end childhood obesity. Nearly one in three children in America is overweight or obese and the numbers are growing.

“Clearly more pizza and French fries in schools is not good for kids, but it’s good for companies that make pizza and French fries,” said Margo Wootan, nutrition policy director at the Center for Science in the Public Interest, a consumer group that advocates better food and nutrition policies.

Wootan said U.S. food makers trumpet products they say are healthy while at the same time lobbying against regulations aimed at improving the nutritional quality of their products.

“A year ago, I was walking the halls of Congress arm-in-arm with the food industry, fighting for healthier school lunches,” Wootan said. “Today, we are on opposite sides, and I’m battling to keep them from weakening school nutrition standards and school marketing guidelines and other provisions.”

(Editing by Martinne Geller)

Soda and Aggression?

Soda and Aggression?

Are your teenagers getting out of control?  What do you do? Who do you blame? Yourself? Violent video games? How about the culprit that is hiding in your fridge!

Before you point fingers at anyone or anything, I want you to consider how much soda your teenager drinks. A new study shows that high school kids who drink more than 5 cans of soft drinks per week are 15% more likely to act violently when compared to their non-soda drinking counterparts. The study included over 1,800 students.  Although more research is needed to prove that soda is the cause, these results sure do raise suspicion.

A key ingredient found in almost every soft drink out there is high-fructose corn syrup (HFCS).  Not only may soda be involved with more violence, it will probably make them fat too! HFCS “is significantly more metabolically detrimental than plain white sugar” Rats that free-fed on HFCS showed a “48% greater weight gain, higher abdominal fat deposition and higher triglycerides than rats free-fed plain sugar water”. With high-fructose corn syrup being in an estimated 40% of all prepared food and beverages consumed in the US, the “sweetener has been implicated as a major contributor” to diabetes, obesity, and now violence!

Eating healthy is critical to having a great brain and keeping a healthy body weight.

Allergy “Season” only finds some bodies

Allergy “Season” only finds some bodies

Sneezing, wheezing, running nose, itchy eyes, blotchy skin — here we go again with allergy season!

Sneezing, wheezing, coughing and itching are commonly considered symptoms of allergies, but joint stiffness, sluggishness, headaches, alternating constipation and diarrhea – these symptoms and others can also be signs of an “allergic reaction,” a “sensitivity,” or an “intolerance” to something entering your body.

Why do some of us suffer every year, others have good years and bad years, while others never suffer allergies??
To answer this, let’s understand how the body works and what you can do to help yourself, your family, friends and coworkers with their symptoms of allergies the natural way, without medications!

The skin is the most important part of the immune system.

It protects us from the outside world. We also have a special “skin” that protects us from our inside world, which is the mucus membrane. This moist tissue covers the inside of your mouth, throat, stomach and intestines. It also lines your nasal passages and lungs. The purpose of these highly specialized tissues is to protect your body from foreign substances. An important principle to understand is that this “skin” is the first defense for your immune system. When your skin allows these foreign substances to “leak” through into your blood stream, that’s when the real trouble begins.

Immune Challenges are met by antibodies
Allergic reactions begin when substances capable of beginning a “reaction” enter through your nose, lungs, skin or intestines. These substances are commonly thought to be pollen and foods, but they can also come from synthetic chemicals in our environment, drinks or foods.

Regardless of the source, all allergic reactions are a response by your body to the foreign substance. The body responds by sending antibodies to the rescue.
Antibodies are an important part of the body’s natural defense system and are produced normally by our white blood cells to help fight infection or toxins. These white blood cells make antibodies to bind with the foreign materials and then eliminate them. This is a great design!

If this antibody system is designed to protect me from bacteria, viruses and parasites, why am I allergic to foods, perfume and cleaning solvents?

Let’s discuss foods first. One way a body can become overly sensitive (allergic) to common foods occurs when poor digestive function sends partially digested foods down the intestines for absorption. The mucus membrane lining your intestine is supposed to absorb the good nutrients and keep out the rest. If that lining is unhealthy and “leaky,” allergic reactions begin. That’s because the “leaky” state of the intestines allows large protein particles from partially digested foods to be absorbed into the blood stream. These particles are recognized as “foreign” by the immune system, and they are removed from the body by the immune system, by binding with antibodies.
Similarly, chemicals in our environment challenge our immune system by irritating the mucus membranes of the nose and lungs, making them “leak,” and thereby allowing foreign substances to enter the tissues. The immune system must respond yet again.
Additionally, the poor quality of the food we eat, poor digestion, and unhealthy bowel flora also contribute to nutritional deficiency. A nutritionally deficient body does not have the necessary nutrients available to build and maintain healthy tissues, including the skin and mucus membranes that form barriers to protect us. In this way symptoms of allergies begin.
One can see how in our world full of pollution, synthetic foods and chemicals of all types, our immune systems are challenged constantly. We often become overly sensitive to common substances. Such a constant demand on the immune system to respond to “challenges” can result from nutritional deficiency and cause nutritional deficiency, creating a vicious cycle, eventually leading to immune system exhaustion.

A natural approach to cause and care of allergies
To summarize the cause of allergies:

  • Nutritional deficiency can be the cause of allergies.
  • Poor digestion can be the cause of allergies.
  • Insufficient healthy bowel flora can be the cause of allergies.
  • Environmental toxins can be the cause of allergies.
  • 
Understanding the non-drug approach to treating the CAUSES of Allergies
.

In previous issues of “Dr. Chapa’s News You Need to Know” we have addressed each of these important principles of HealthBuilding. Please refer to Issue 3 for digestive support, Issue 5 for the importance of bowel flora, Issue 6 for the importance of purification of the body for health, and Issue 7 for simple ways to enhance the immune system. And always take Catalyn to prevent nutritional deficiency.
Even though we eat the right foods, support the body with digestive enzymes, probiotics, organic minerals and vitamin complexes, we may still experience symptoms of ALLERGIES from time to time. Reactions such as sneezing, wheezing, running nose, itchy eyes and many others are caused by the release of histamine in the affected body tissues.

Question: Should I use anti-histamines when I feel allergic symptoms?

Histamine is involved in myriad physiological conditions, all with the goal of supporting healing. When antibodies bind with foreign substances, histamine is released to begin a process of flooding the irritated tissue with healing fluids. This inflammatory reaction can be quite uncomfortable, but is a necessary part of the healing process. One does not want to inactivate histamine, although it is ideal to clear the histamine from our tissues efficiently after it has done its job.
Drug forms of antihistamine may interfere with the healing purposes of histamine, and frequently have side effects. More importantly, these drugs may be altogether avoided by supporting normal body processes. What we need is a natural product that helps the body handle the histamine reactions, relieve symptoms, and support healing. For this exact purpose we recommend:

Antronex© which contains Yakriton, a liver fat extract discovered in the 1920’s. Yakriton has been shown to help the liver efficiently filter the blood, removing excess histamine and toxins from the blood.
Protection of the stomach, nasal passages, lungs, liver and kidneys is the ultimate HealthBuilding goal when it comes to strengthening the body to handle allergic reactions. A whole food concentrate product which supports all these body systems is appropriately named Allerplex ©.
Allerplex© is a special combination formula of whole food concentrates containing a wide variety of nutrients effective in helping maintain a healthy immune system. Allerplex is useful in supporting proper acid/alkaline balance, and sustaining healthy liver function. Allerplex has been used by doctors since 1959 for this very purpose.
General Whole Food Guidelines for Allergic People

  1. Live a healthy lifestyle with whole foods and whole food concentrates as outlined in The Nutritional Essentials – Issues.
  2. Take Allerplex 1-3 per day for life .†
  3. When symptoms of allergies are on the rise, take 1-3 Antronex per hour to help the liver clear out histamines until symptoms subside†.

Patients Speak About Allergies
“My entire life I suffered bad allergies. Sneezing, runny nose so bad at times they would lay me out! My nutritional program has entirely cleared this up, AND my chronic cough I have had for over 10 years GONE!!” D.M.M.

What Did you Learn

Herbal Extracts: Beware of Toxic, Un-Natural Processing

Herbal Extracts: Beware of Toxic, Un-Natural Processing

Standardization of Herbs

by Nathan Jaynes, M.H., Student Advisor, School of Natural Healing

A look into the way some plants are standardized should show just how un-natural this whole process is. Below is a common way alkaloids are extracted from raw plant material. This is not a recipe; some of these chemicals are very dangerous.

  1. The plant material is first juiced and blended along with water.
  2. Acetic acid (or some other acid) is added until the solution is around 5 pH. This acidic solution slowly converts the alkaloids into alkaloid salts.
  3. The solution is heated for hours and sometimes days.
  4. The aqueous solution is strained off and saved and the plant material goes through the process sometimes three or four times before the plant matter is finally discarded.
  5. A defatting solvent like methylene chloride (see reverse), ether, chloroform, dichloromethane or naphtha (lighter fluid) is added to the solution. This will take out all fats and waxes from the product.
  6. The mixture will separate into 2 parts the solvent with dissolved fats and oils and the alkaloid solution. The solvent mixture is discarded.
  7. To this solution, a base chemical is added like ammonium hydroxide, sodium hydroxide (lye), ethyl acetate or potassium hydroxide until the pH is about 9 or 10. This un-hooks the salts and transforms the alkaloids into their free base form.
  8. The alkaloids are no longer soluble in water and are extracted as in step 5 by again adding more methylene chloride, ether, chloroform, or naphtha (lighter fluid).
  9. This yellow to brown extract (the color indicates alkaloid content) is allowed to evaporate or is heated and the process may be applied again and again until a final white crystalline product is achieved.
  10. The resulting isolated alkaloid is then added to your herbs just before encapsulation. Even after adding all of these chemicals they market the end product as “all natural”. Ephedrine, extracted in this manner from mahuang is as natural as cocaine from coco leaves or morphine from poppies. When did the herb stop being a natural and safe product and start being a dangerous and powerful chemical?

Answer: When the “inactive” phytochemicals that are usually present in the plant are taken out. These “inactive” phytochemicals work synergistically or as buffers with the so called “active” principles making the whole plant a safer and more effective medicine. The less processing of an herb between harvest and ingestion, the better and more natural it is.

FACT SHEET: Methylene Chloride (Dichloromethane)

Methylene chloride, also known as dichloromethane, is a very widely-used solvent and is commonly used in processing herbs to standardize them. Beware that residues of this toxic solvent may remain in standardized herbs.

Methylene chloride is found in many common products, including:

  • paint and varnish thinners and removers
  • cleaning solutions
  • paints and adhesives
  • metal and plastic cleaners and degreasers
  • aerosols (as a propellant)
  • pesticides, fumigants, insecticides, and herbicides
  • refrigeration and air conditioning equipment.

Health Effects

Overexposure to methylene chloride can cause serious health problems. Like most organic solvents, methylene chloride can damage the brain, as well as the skin, lungs, and other organs. In addition, methylene chloride has been shown to cause cancer in humans and laboratory animals. Most people cannot smell methylene chloride until it reaches a hazardous level — so don’t depend on your sense of smell to warn you of overexposure. If you smell it, your exposure is too high.

How Can Methylene Chloride Get Into Your Body?

Methylene chloride can enter your body when you breathe in vapors. It can also be absorbed through your skin, so proper protective clothing is essential. If you eat, smoke, or drink in your work area, or if you don’t wash your hands, you can also ingest (swallow) methylene chloride and other chemicals that you work with.

Short-Term (Acute) Health Effects

Methylene chloride can irritate the eyes, nose, throat, and skin and cause skin rash, coughing, and shortness of breath. At high levels, exposure to methylene chloride can also affect your central nervous system (brain) and cause the following symptoms: “drunk” behavior, sluggishness, staggering, mental confusion, sleepiness, irritability, lightheadedness, dizziness, and headache. At higher levels, symptoms can include nausea, flushing, confusion, slurred speech, loss of balance and coordination. Exposure can also irritate the lungs, causing a build-up of fluid that can lead to death.

Methylene chloride breaks down in the body to carbon monoxide. Carbon monoxide decreases the blood’s ability to carry oxygen, and reduces the amount of oxygen that gets to your heart, brain, and other organs. This may result in fatigue, shortness of breath, and chest pain. If you are exposed to methylene chloride and carbon monoxide at work, both exposures should be kept to a minimum. Smoking also increases levels of carbon monoxide in the body. If you smoke, you may be more susceptible to the effects of methylene chloride exposure.

Long-Term (Chronic) Health Effects

Methylene chloride causes a variety of cancers in laboratory animals, including cancer of the lung, liver, breast, and salivary glands. Chemicals that cause cancer in animals are assumed to pose cancer risks to humans as well. (The Food and Drug Administration has just banned methylene chloride from hairsprays because of the potential cancer risks faced by hairdressers and consumers.) One study of workers indicated that methylene chloride may pose a risk of cancer of the pancreas.

Long-term exposure to methylene chloride can damage the brain (causing memory loss, blackouts, personality changes, poor coordination, and reduced thinking ability). At higher exposures, methylene chloride can also damage your liver. Methylene chloride also causes kidney damage in animals.

One study has suggested that male workers exposed to methylene chloride may be at greater risk of sterility. Methylene chloride may irritate the lungs, especially when used near heat (furnaces, welding, etc.) Repeated exposures may cause bronchitis with cough, phlegm, and/or shortness of breath. When exposed to heat, methylene chloride breaks down into deadly phosgene gas. Exposure to methylene chloride may cause heart disease or aggravate pre-existing heart disease and cause irregular heartbeat and rapid pulse.

Acrylamides

Acrylamides

World Alert Over Cancer Chemical (Acrylamides) in Cooked Food

Uhlig, Robert, news at Telegraph.Co.Uk, May 18, 2002

A worldwide alert was issued after scientists announced that much of the food we eat contains a chemical [acyrlamide] known to cause cancer, damage the nervous system and affect fertility.

The Food Standards Agency said that its scientists had confirmed recent Swedish findings that “significant levels” of acrylamide occurs in fried, baked and processed foods ranging from biscuits, bread and crisps to chips and possibly meat.

The finding has the potential to change the way certain types of food are viewed, in much the same way that studies in the 1960s changed perception of the health risks of smoking.

Acrylamide causes gene mutations leading to a range of cancers in rats, including breast cancer, uterine cancer and tambours in the adrenal glands and the internal lining of the scrotum.

Among the products tested in the British study – some of which had levels of acrylamide 1,280 times higher than international safety limits – were chipped and fried supermarket potatoes, Walkers crisps, crackers, Kellogg’s Rice Crispies and Pringles crisps.

The results have so alarmed health experts that they have called international meetings to discuss what should be done.

The British and Swedish findings were presented yesterday to the Scientific Committee on Food that advises the European Commission on food safety.

World Health Organization experts will discuss the research at a special meeting in Geneva next month. It is expected to recommend further studies.

According to the findings, acrylamide forms naturally in food when it is fried or baked. The scientists believe it also occurs in roasted, grilled and barbecued food. As a genotoxic carcinogen, acrylamide is classified as a “probable” cancer-causing chemical with no safe dose.

Diane Benford, a toxicologist at the FSA, said: “We cannot define a safe level. We have to assume that at any level of exposure there may be some risk, albeit very small.”

With 30 to 40% of cancers caused by diet, Dr Benford said that it was too early to say whether acrylamide was one of the major causes of cancer.

Dr Benford said: “We are not advising any changes of diet or cooking procedures because we do not know enough yet.”

Steve Wearne, head of contaminants at the FSA, said: “It’s about any food that’s cooked this way. It appears that any of these cooking processes in food production can lead to acrylamide forming. It’s not clear what the factors are that lead to acrylamide formation; it may be due to the type of cooking, temperature, or chemical composition of the food, or other factors.”

Our Comment:

Foods which have been highly heated (i.e. heated over boiling temperature, 212 deg. F.) and thus, contain toxic acrylamides, should avoided for those who want to enjoy excellent health and a long life.

This new evidence further supports the concept of eating some raw (uncooked) food every day as a regular part of your diet. We recommend eating at least 50% of your diet as raw food, such as fresh fruit, raw vegetables (especially raw salads), soaked nuts and seeds (soaking them neutralizes their enzyme inhibitors which can interfere with human digestion), fermented seed cheese, raw homemade kefir, etc.

Boiling Temperature is Safe

When cooked foods are eaten, they should not be cooked over boiling temperature (212 deg. F.) to avoid the formation of acrylamides. Foods heated in a microwave oven or a regular oven (which usually means temperatures between 300 – 450 deg. F.) should be avoided. Examples of highly heated foods (best to avoid) are bread, cakes, cookies, buns, rolls, bagels, pizza, French fries, chips, donuts, etc.

An excellent, delicious alternative to eating most breads (typically highly heated) is to make your own homemade flatbread (using a skillet on your stove).

Relief of Fibromyalgia Symptoms

Relief of Fibromyalgia Symptoms

Following Discontinuation of Dietary Excitotoxins

Jerry D. Smith, Chris M. Terpening, Siegfried Schmidt and John G. Gums

The Annals of Pharmacotherapy: Vol. 35, No. 6, pp. 702-206.

Background: Fibromayalgia is a common rheumatologic disorder that is often difficult to treat effectively.

Case Summary: Four patients diagnosed with fibromyalgia syndrome for 2 to 17 years are described. All had undergone multiple treatment modalities with limited success. All had complete, or nearly complete, resolution of their symptoms within months after eliminating monosodium glutamate (MSG) or MSG plus aspartame from their diet. All patients were women with multiple comorbidities prior to elimination of MSG. All have had recurrence of symptoms whenever MSG is ingested.

Discussion: Excitotoxins are molecules, such as MSG and aspartate that act as excitatory neurotransmitters, and can lead to neurotoxicity when used in excess. We propose that these four patients may represent a subset of fibromyalgia syndrome that is induced or exacerbated by excitotoxins or alternatively, may comprise an excitotoxin syndrome that is similar to fibromyalgia. We suggest that identification of similar patients and research with larger numbers of patients must be performed before definitive conclusions can be made.

Conclusions: The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.

Do you have nerve and memory problems?

Do you have nerve and memory problems?

Do your nutritional supplements contain “natural flavors” (a disguised term for MSG)?

Then carefully read below.

A Hidden Toxin Lurking in Your Supplements

The following excellent article by Dr. Russell Blaylock explains how a common additive often found in food and nutritional supplements, listed as “natural flavors”, is not natural at all and is really a disguised term for MSG (monosodium glutamate). It is a known neurotoxin and excitotoxin, which is linked to many nerve disorders, depression and physical degeneration.

But “Natural Flavors” Sounds So Natural

Unbelievably, many nutritional supplements contain MSG (which is not listed under that name). Look on your supplement labels for the term, “natural flavors” (a deceptive name for MSG) — such as “natural vanilla flavor” or “natural chocolate flavor” or “natural lemon flavor.” For the best health of yourself and your patients, stop using products with “natural flavors.” It’s definitely not natural.

So why is MSG put in nutritional products? To enhance the taste (or to cover up the “off taste” of bad-tasting or inferior ingredients).

Excitotoxins, Neurodegeneration, Neurodevelopment,

Migraines, & Seizures

By Russell L. Blaylock, M.D., Author of Excitotoxins: The Taste That Kills

There are a growing number of clinicians and basic scientists who are convinced that a group of compounds called excitotoxins play a critical role in the development of several neurological disorders including migraines, seizures, infections, abnormal neural development, certain endocrine disorders, neuropsychiatric disorders, learning disorders in children, AIDS dementia, episodic violence, lyme borreliosis, hepatic encephalopathy, specific types of obesity, and especially the neurodegenerative diseases, such as ALS, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and olivopontocerebellar degeneration.(1)

An enormous amount of both clinical and experimental evidence has accumulated over the past decade supporting this basic premise.(2) Yet, the FDA still refuses to recognize the immediate and long term danger to the public caused by the practice of allowing various excitotoxins to be added to the food supply, such as MSG, hydrolyzed vegetable protein, and aspartame. The amount of these neurotoxins added to our food has increased enormously since their first introduction. For example, since 1948, the amount of MSG added to foods has doubled every decade. By 1972, 262,000 metric tons were being added to foods. Over 800 million pounds of aspartame have been consumed in various products since it was first approved. Ironically, these food additives have nothing to do with preserving food or protecting its integrity. They are all used to alter the taste of food. MSG, hydrolyzed vegetable protein, and natural flavoring are used to enhance the taste of food so that it taste better. Aspartame is an artificial sweetener.

These toxins (excitotoxins) are not present in just a few foods, but rather in almost all processed foods. In many cases they are being added in disguised forms, such as natural flavoring, spices, yeast extract, textured protein, soy protein extract, etc. Experimentally, we know that when subtoxic levels of excitotoxins are given to animals in divided doses, they experience full toxicity, i.e. they are synergistic. Also, liquid forms of excitotoxins, as occurs in soups, gravies and diet soft drinks are more toxic than that added to solid foods. This is because they are more rapidly absorbed and reach higher blood levels.

So, what is an excitotoxin?

These are substances, usually acidic amino acids, that react with specialized receptors in the brain in such a way as to lead to destruction of certain types of neurons. Glutamate is one of the more commonly known excitotoxins. MSG is the sodium salt of glutamate. This amino acid is a normal neurotransmitter in the brain. In fact, it is the most commonly used neurotransmitter by the brain. Defenders of MSG and aspartame use, usually say: How could a substance that is used normally by the brain cause harm? This is because, glutamate, as a neurotransmitter, exists in the extracellular fluid only in very, very small concentrations – no more than 8 to 12uM. When the concentration of this transmitter rises above this level the neurons begin to fire abnormally. At higher concentrations, the cells undergo a specialized process of delayed cell death known as excitotoxicity, that is, they are excited to death.

It should also be appreciated that the effects of excitotoxin food additives generally are not dramatic. Some individuals may be especially sensitive and develop severe symptoms and even sudden death from cardiac irritability, but in most instances the effects are subtle and develop over a long period of time. While the food additives, MSG and aspartame, are probably not direct causes of the neurodegenerative diseases, such as Alzheimer’s dementia, Parkinson’s disease, or amyotrophic lateral sclerosis, they may well precipitate these disorders and certainly worsen their pathology as we shall see. It may be that many people with a propensity for developing one of these diseases would never develop a full blown disorder had it not been for their exposure to high levels of food borne excitotoxin additives. Some may have had a very mild form of the disease had it not been for the exposure. Likewise, food borne excitotoxins may be harmful to those suffering from strokes, head injury and HIV infection and certainly should not be used in a hospital setting.

How Excitotoxins Were Discovered

In 1957, two opthalmology residents, Lucas and Newhouse, were conducting an experiment on mice to study a particular eye disorder.(3) During the course of this experiment, they fed newborn mice MSG and discovered that all demonstrated widespread destruction of the inner nerve layer of the retina. Similar destruction was also seen in adult mice but not as severe as the newborns. The results of their experiment was published in the Archives of Opthalmology and soon forgotten. For ten years prior to this report, large amounts of MSG were being added not only to adult foods but also to baby foods in doses equal to those of the experimental animals.

Then in 1969, Dr. John Olney, a neuroscientist and neuropathologist working out of the Department of Psychiatry at Washington University in St. Louis, repeated Lucas and Newhouse’s experiment.(4) His lab assistant noticed that the newborn of MSG-exposed mice were grossly obese and short in statue. Further examination also demonstrated hypoplastic organs, including pituitary, thyroid, adrenal as well as reproductive dysfunction. Physiologically, they demonstrated multiple endocrine deficiencies, including TSH, growth hormone, LH, FSH, and ACTH. When Dr. Olney examined the animal’s brain, he discovered discrete lesions of the arcuate nucleus as well as less severe destruction of other hypothalamic nuclei. Recent studies have shown that glutamate is the most important neurotransmitter in the hypothalamus.(5) Since this early observation, monosodium glutamate and other excitatory substances have become the standard tool in studying the function of the hypothalamus. Later studies indicated that the damage by monosodium glutamate was much more widespread, including the hippocampus, circumventricular organs, locus cereulus, amygdala-limbic system, subthalamus, and striatum.(6)

More recent molecular studies have disclosed the mechanism of this destruction in some detail.(7) Early on it was observed that when neurons in vitro were exposed to glutamate and then washed clean, the cells appeared perfectly normal for approximately an hour, at which time they rapidly underwent cell death. It was discovered that when calcium was removed from the medium, the cells continued to survive. Subsequent studies have shown that glutamate, and other excitatory amino acids, attach to a specialized family of receptors (NMDA, kainate, AMPA and metabotrophic) which in turn, either directly or indirectly, opens the calcium channel on the neuron cell membrane, allowing calcium to flood into the cell. If unchecked, this calcium will trigger a cascade of reactions, including free radical generation, eicosanoid production, and lipid peroxidation, which will destroy the cell. With this calcium triggered stimulation, the neuron becomes very excited, firing its impulses repetitively until the point of cell death, hence the name excitotoxin. The activation of the calcium channel via the NMDA type receptors also involves other membrane receptors such as the zinc, magnesium, phencyclidine, and glycine receptors.

In many disorders connected to excitotoxicity, the source of the glutamate and aspartate is indogenous. We know that when brain cells are injured they release large amounts of glutamate from surrounding astrocytes, and this glutamate can further damage surrounding normal neuronal cells. This appears to be the case in strokes, seizures and brain trauma. But, food born excitotoxins can add significantly to this accumulation of toxins.

The FDA’s Response

In July, 1995 the Federation of American Societies for Experimental Biology ( FASEB) conducted a definitive study for the FDA on the question of safety of MSG.(8) The FDA wrote a very deceptive summary of the report in which they implied that, except possibly for asthma patients, MSG was found to be safe by the FASEB reviewers. But, in fact, that is not what the report said at all. I summarized, in detail, my criticism of this widely reported FDA deception in the revised paperback edition of my book, Excitotoxins: The Taste That Kills, by analyzing exactly what the report said, and failed to say.(9) For example, it never said that MSG did not aggravate neurodegenerative diseases. What they said was, there were no studies indicating such a link. Specifically, that no one has conducted any studies, positive or negative, to see if there is a link. A vital difference.

Unfortunately, for the consumer, the corporate food processors not only continue to add MSG to our foods but they have gone to great links to disguise these harmful additives. For example, they use such names as hydrolyzed vegetable protein, vegetable protein, textured protein, hydrolyzed plant protein, soy protein extract, caseinate, yeast extract, and natural flavoring. We know experimentally that when these excitotoxin taste enhancers are added together, they become much more toxic than is seen individually.(10) In fact, excitotoxins in subtoxic concentrations can be fully toxic to specialized brain cells when used in combination.

Frequently, I see processed foods on supermarket shelves, especially frozen or diet foods, that contain two, three or even four types of excitotoxins. We also know, as stated, that excitotoxins in liquid forms are much more toxic than solid forms because they are rapidly absorbed and attain high concentration in the blood. This means that many of the commercial soups, sauces, and gravies containing MSG are very dangerous to nervous system health, and should especially be avoided by those either having one of the above mentioned disorders, or who are at a high risk of developing one of them. They should also be avoided by cancer patients and those at high risk for cancer, because of the associated generation of free radicals and lipid peroxidation.(11)

In the case of ALS, amyotrophic lateral sclerosis, we know that consumption of red meats and especially MSG itself, can significantly elevate blood glutamate, much higher than is seen in the normal population.(12) Similar studies, as far as I am aware, have not been conducted in patients with Alzheimer’s disease or Parkinson’s disease. But, as a general rule I would certainly suggest that person’s with either of these diseases avoid MSG containing foods as well as red meats, cheeses, and pureed tomatoes, all of which are known to have higher levels of glutamate.

It must be remembered that it is the glutamate molecule that is toxic in MSG (monosodium glutamate). Glutamate is a naturally occurring amino acid found in varying concentrations in many foods. Defenders of MSG safety allude to this fact in their defense. But, it is free glutamate that is the culprit. Bound glutamate, found naturally in foods, is less dangerous because it is slowly broken down and absorbed by the gut, so that it can be utilized by the tissues, especially muscle, before toxic concentrations can build up. Therefore, a whole tomato is safer than a pureed tomato. The only exception to this as stated, based on present knowledge, is in the case of ALS. Also, the tomato plant contains several powerful antioxidants known to block glutamate toxicity.(13)

Hydrolyzed vegetable protein is a common food additive and may contain at least two excitotoxins, glutamate and cysteic acid. Hydrolyzed vegetable protein is made by a chemical process that breaks down the vegetable’s protein structure to purposefully free the glutamate, as well as aspartate, another excitotoxin. This brown powdery substance is used to enhance the flavor of foods, especially meat dishes, soups, and sauces. Despite the fact that some health food manufacturers have attempted to sell the idea that this flavor enhancer is “all natural” and “safe” because it is made from vegetables, it is not. It is the same substance added to processed foods. Experimentally, one can produce the same brain lesions using hydrolyzed vegetable protein as by using MSG or aspartate.(14)

A growing list of excitotoxins are being discovered, including several that are found naturally. For example, L- cysteine is a very powerful excitotoxin. Recently, it has been added to certain bread dough and is sold in health food stores as a supplement. Homocysteine, a metabolic derivative, is also an excitotoxin.(15) Interestingly, elevated blood levels of homocysteine has recently been shown to be a major, if not the major, indicator of cardiovascular disease and stroke. Equally interesting, is the finding that elevated levels have also been implicated in neurodevelopmental disorders, especially anencephaly and spinal dysraphism (neural tube defects).(16) It is thought that this is the protective mechanism of action associated with the use of the prenatal vitamins B12, B6, and folate when used in combination. It remains to be seen if the toxic effect is excitatory or by some other mechanism. If it is excitatory, then unborn infants would be endangered as well by glutamate, aspartate (part of the aspartame molecule), and the other excitotoxins. Recently, several studies have been done in which it was found that all Alzheimer’s patients examined had elevated levels of homocysteine.(17)

One interesting study found that persons affected by Alzheimer’s disease also have widespread destruction of their retinal ganglion cells.(18) Interestingly, this is the area found to be affected when Lucas and Newhouse first discovered the excitotoxicity of MSG. While this does not prove that dietary glutamate and other excitotoxins cause or aggravate Alzheimer’s disease, it is powerful circumstantial evidence. When all of the information known concerning excitatory food additives is analyzed, it is hard to justify continued approval by the FDA for the widespread use of these food additives.

The Free Radical Connection

It is interesting to note that many of the same neurological diseases associated with excitotoxic injury are also associated with accumulations of toxic free radicals and destructive lipid oxidation products.(19) For example, the brains of Alzheimer’s disease patients have been found to contain high concentration of lipid peroxidation products and evidence of free radical accumulation and damage.(20, 21, 22)

In the case of Parkinson’s disease, we know that one of the early changes is the loss of one of the primary antioxidant defense systems, glutathione, from the neurons of the striate system, and especially in the substantia nigra.(23) It is this nucleus that is primarily affected in this disorder. Accompanying this is an accumulation of free iron, which is one of the most powerful free radical generators known.(24) One of the highest concentrations of iron in the body is within the globus pallidus and the substantia nigra. The neurons within the latter are especially vulnerable to oxidant stress because the catabolic metabolism of the transmitter-dopamine- can proceed to the creation of very powerful free radicals. That is, it can auto-oxidize to peroxide, which is normally detoxified by glutathione. As we have seen, glutathione loss in the substantia nigra is one of the earliest deficiencies seen in Parkinson’s disease. In the presence of high concentrations of free iron, the peroxide is converted into the dangerous and very powerful free radical, hydroxide. As the hydroxide radical diffuses throughout the cell, destruction of the lipid components of the cell takes place, a process called lipid peroxidation. Of equal importance is the generation of the powerful peroxynitrite radical, which has been shown to produce serious injury to cellular proteins and DNA, both mitochondrial and nuclear.(25)

Using a laser microprobe mass analyzer, researchers have recently discovered that iron accumulation in Parkinson’s disease is primarily localized in the neuromelanin granules (which gives the nucleus its black color).(26) It has also been shown that there is dramatic accumulation of aluminum within these granules.(27) Most likely, the aluminum displaces the bound iron, releasing highly reactive free iron. It is known that even low concentrations of aluminum salts can enhance iron-induced lipid peroxidation by almost an order of magnitude. Further, direct infusion of iron into the substantia nigra nucleus in rodents can induce a Parkinsonian syndrome, and a dose related decline in dopamine. Recent studies indicate that individuals having Parkinson’s disease also have defective iron metabolism.(28)

Another early finding in Parkinson’s disease is the reduction in complex I enzymes within the mitochondria of this nucleus.(29) It is well known that the complex I enzymes are particularly sensitive to free radical injury. These enzymes are critical to the production of cellular energy. As we shall see, when cellular energy is decreased, the toxic effect of excitatory amino acids increases dramatically.

In the case of ALS there is growing evidence that similar free radical damage, most likely triggered by toxic concentrations of excitotoxins, plays a major role in the disorder.(30). Several studies have demonstrated lipid peroxidation product accumulation within the spinal cords of ALS victims as well as iron accumulation.(31)

It is now known that glutamate acts on its receptor via a nitric oxide mechanism.(32) Overstimulation of the glutamate receptor can produce an accumulation of reactive nitrogen species, resulting in the generation of several species of dangerous free radicals, including peroxynitrite. There is growing evidence that, at least in part, this is how excess glutamate damages nerve cells.(33) In a multitude of studies, a close link has been demonstrated between excitotoxicity and free radical generation.(34- 37)

Others have shown that certain free radical scavengers (antioxidants), have successfully blocked excitotoxic destruction of neurons. For example, vitamin E is known to completely block glutamate toxicity in vitro.(38) Whether it will be as efficient in vivo is not known. But, it is interesting in light of the recent observations that vitamin E combined with other antioxidant vitamins slows the course of Alzheimer’s disease and has been suggested to reduce the rate of advance in a subgroup Parkinson’s disease patients as well. In the DATATOP study of the effect of alpha- tocopherol alone, no reduction in disease progression was seen. The problem with this study was the low dose that was used and the fact that the DL-alpha-tocopherol used is known to have a much lower antioxidant potency than Dalpha-tocopherol. Stanley Fahn found that a combination of D-alpha-tocopherol and ascorbic acid in high doses reduced progression of the disease by 2.5 years.(39) Tocotrienol may have even greater benefits, especially when used in combination with other antioxidants. There is some clinical evidence, including my own observations, that vitamin E also slows the course of ALS as well, especially in the form of D- alpha-tocopherol. I would caution that antioxidants work best in combination and when use separately can have opposite, harmful, effects. That is, when antioxidants, such as ascorbic acid and alpha tocopherol, become oxidized themselves, such as in the case of dehydroascorbic acid, they no longer protect, but rather act as free radicals themselves. The same is true of alpha- tocopherol.(40)

Again, it should be realized that excessive glutamate stimulation triggers a chain of events that in turn sparks the generation of large numbers of free radical species, both as nitrogen and oxygen species. These free radicals have been shown to damage cellular proteins (protein carbonyl products) and DNA. The most immediate DNA damage is to the mitochondrial DNA, which controls protein expression within that particular cell and its progeny, producing rather profound changes in cellular energy production. It is suspected that at least some of the neurodegenerative diseases, Parkinson’s disease in particular, are affected in this way.(41)

Chronic free radical accumulation would result in an impaired functional reserve of antioxidant vitamins/minerals and enzymes, and thiol compounds necessary for neural protection. Chronic unrelieved stress, chronic infection, free radical generating metals and toxins, and impaired DNA repair enzymes all add to this damage. We know that there are four main endogenous sources of oxidants:

1. Those produced naturally from aerobic metabolism of glucose. 2. Those produced during phagocytic cell attack on bacteria, viruses, and parasites, especially with chronic infections. 3. Those produced during the degradation of fatty acids and other molecules that produce H2O2 as a by-product. (This is important in stress, which has been shown to significantly increase brain levels of free radicals.) And 4. Oxidants produced during the course of p450 degradation of natural toxins. And, as we have seen, one of the major endogenous sources of free radicals is from the exposure of tissues to free iron, especially in the presence of ascorbate. Unfortunately, iron is one mineral heavily promoted by the health industry, and is frequently added to many foods, especially breads and pastas. Copper is also a powerful free radical generator and has been shown to be elevated within the substantia nigra of Parkinsonian brains.(42)

What has been shown in all these studies is a direct connection between excitotoxicity and free radical generation in a multitude of diseases and disorders such as seizures, strokes, brain trauma, viral infections, and neurodegenerative diseases. Interestingly, free radicals have also been shown to prevent glutamate uptake by astrocytes as well, which would significantly increase extracellular glutamate levels.(43) This creates a vicious cycle that will multiply any resulting damage and malfunctioning of neurophysiological systems, such as plasticity.

The Blood-Brain Barrier

One of the MSG industry’s chief arguments for the safety of their product is that glutamate in the blood cannot enter the brain because of the blood-brain barrier (BBB), a system of specialized capillary structures designed to exclude toxic substance from entering the brain. There are several criticisms of their defense. For example, it is known that the brain, even in the adult, has several areas that normally do not have a barrier system, called the circumventricular organs. These include the hypothalamus, the subfornical organ, organium vasculosum, area postrema, pineal gland, and the subcommisural organ. Of these, the most important is the hypothalamus, since it is the controlling center for all neuroendocrine regulation, sleep wake cycles, emotional control, caloric intake regulation, immune system regulation and regulation of the autonomic nervous system. As stated, glutamate is the most important neurotransmitter in the hypothalamus.

Therefore, careful regulation of blood levels of glutamate is very important, since high blood concentrations of glutamate would be expected to increase hypothalamic levels as well. One of the earliest and most consistent findings with exposure to MSG is damage to an area of the hypothalamus known as the arcuate nucleus.This small hypothalamic nucleus controls a multitude of neuroendocrine functions, as well as being intimately connected to several other hypothalamic nuclei. It has also been demonstrated that high concentrations of blood glutamate and aspartate (from foods) can enter the so-called “protected brain” by seeping through the unprotected areas, such as the hypothalamus or other circumventricular organs.

Another interesting observation is that chronic elevations of blood glutamate can even seep through the normal blood-brain barrier when these high concentrations are maintained over a long period of time.(44) This would be the situation seen when individuals consume, on a daily basis, foods high in the excitotoxins – MSG, aspartame and L-cysteine. Most experiments cited by the defenders of MSG safety were conducted to test the efficiency of the BBB acutely. In nature, except in the case of metabolic dysfunction (such as with ALS), glutamate and aspartate levels are not normally elevated on a continuous basis. Sustained elevations of these excitotoxins are peculiar to the modern diet. (and in the ancient diets of the Orientals, but not in as high a concentration.)

An additional critical factor ignored by the defenders of excitotoxin food safety is the fact that many people in a large population have disorders known to alter the permeability of the blood-brain barrier. The list of condition associated with barrier disruption include: hypertension, diabetes, mini-strokes, major strokes, head trauma, multiple sclerosis, brain tumors, chemotherapy, radiation treatments to the nervous system, collagen-vascular diseases (lupus), AIDS, brain infections, certain drugs, Alzheimer’s disease, and as a consequence of natural aging. There may be many other conditions also associated with barrier disruption that are as yet not known.

When the barrier is dysfunctional due to one of these conditions, brain levels of glutamate and aspartate reflect blood levels. That is, foods containing high concentrations of these excitotoxins will increase brain concentrations to toxic levels as well. Take for example, multiple sclerosis. We know that when a person with MS has an exacerbation of symptoms, the blood-brain barrier near the lesions breaks down, leaving the surrounding brain vulnerable to excitotoxin entry from the blood, i.e. the diet.(45) But, not only is the adjacent brain vulnerable, but the openings act as points of entry, eventually exposing the entire brain to potentially toxic levels of glutamate. Several clinicians have remarked that their MS patients were made worse following exposure to dietary excitotoxins. I have seen this myself. It is logical to assume that patients with the other neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, and ALS will be made worse on diets high in excitotoxins. Barrier disruption has been demonstrated in the case of Alzheimer’s disease.(46)

Recently, it has been shown that not only can free radicals open the blood-brain barrier, but excitotoxins can as well.(47) In fact, glutamate receptors have been demonstrated on the barrier itself.(48) In a carefully designed experiment, researchers produced opening of the blood-brain barrier using injected iron as a free radical generator. When a powerful free radical scavenger (U-74006F) was used in this model, opening of the barrier was significantly blocked. But, the glutamate blocker MK-801 acted even more effectively to protect the barrier. The authors of this study concluded that glutamate appears to be an important regulator of brain capillary transport and stability, and that overstimulation of NMDA (glutamate) receptors on the blood-brain barrier appears to play an important role in breakdown of the barrier system. What this also means is that high levels of dietary glutamate or aspartate may very well disrupt the normal blood-brain barrier, thus allowing more glutamate to enter the brain, creating a vicious cycle.

Relation to Cellular Energy Production

Excitotoxin damage is heavily dependent on the energy state of the cell.(49) Cells with a normal energy generation systems are very resistant to such toxicity. When cells are energy deficient, no matter the cause – hypoxia, starvation, metabolic poisons, hypoglycemia – they become infinitely more susceptible to excitotoxic injury or death. Even normal concentrations of glutamate are toxic to energy deficient cells.

It is known that in many of the neurodegenerative disorders, neuron energy deficiency often precedes the clinical onset of the disease by years, if not decades.(50) This has been demonstrated in the case of Huntington disease and Alzheimer’s disease using the PET scanner, which measures brain metabolism. In the case of Parkinson’s disease, several groups have demonstrated that one of the early deficits of the disorder is an impaired energy production by the complex I group of enzymes within the mitochondria of the substantia nigra.(51, 52) Interestingly, it is known that the complex I system is very sensitive to free radical damage.

Recently, it has been shown that when striatal neurons are exposed to microinjected excitotoxins there is a dramatic, and rapid fall in energy production by these neurons. CoEnzyme Q-10 has been shown, in this model, to restore energy production but not to prevent cellular death. But when combined with niacinamide, both cellular energy production and neuron protection is seen.(53) I recommend for those with neurodegenerative disorders, a combination of CoQ-10, acetyl-L carnitine, niacinamide, riboflavin, methylcobalamin and thiamine.

One of the newer revelation of modern molecular biology, is the discovery of mitochondrial diseases, of which cellular energy deficiency is a hallmark. In many of these disorders, significant clinical improvement has been seen following a similar regimen of vitamins combined with CoQ10 and L-carnitine.(54) Acetyl L-carnitine enters the brain in higher concentrations and also increases brain acetylcholine, necessary for normal memory function. While these particular substances have been found to significantly boost brain energy function they are not alone in this important property. phosphatidyl serine, ginkgo biloba, vitamin B12, folate, magnesium, vitamin K and several others are also being shown to be important.

While mitochrondial dysfunction is important in explaining why some are more vulnerable to excitotoxin damage than others, it does not explain injury in those with normal cellular metabolism. There are several conditions under which energy metabolism is impaired. We know, for example, approximately one third of Americans suffer from reactive hypoglycemia. That is, they respond to a meal composed of either simple sugars or carbohydrates (that are quickly broken down into simple sugars, i.e. a high glycemic index.) by secreting excessive amounts of insulin. This causes a dramatic lowering of the blood sugar.

When the blood sugar falls, the body responds by releasing a burst of epinephrine from the adrenal glands, in an effort to raise the blood sugar. We feel this release as nervousness, palpitations of our heart, tremulousness, and profuse sweating. Occasionally, one can have a slower fall in the blood sugar that will not produce a reactive release of epinephrine, thereby producing few symptoms. This can be more dangerous, since we are unaware that our glucose reserve is falling until we develop obvious neurological symptoms, such as difficulty thinking and a sensation of lightheadedness.

The brain is one of the most glucose dependent organs known, since it has a limited ability to metabolize other substrates such as fats. There is some evidence that several of the neurodegenerative diseases are related to either excessive insulin release, as with Alzheimer’s disease, or impaired glucose utilization, as we have seen in the case of Parkinson’s disease and Huntington’s disease.(55)

It is my firm belief, based on clinical experience and physiological principles, that many of these diseases occur primarily in the face of either reactive hypoglycemia or “brain hypoglycemia”, a condition where the blood sugar is normal and the brain is hypoglycemic in isolation. In at least two well conducted studies it was found that pure Alzheimer’s dementia was rare in those with normal blood sugar profiles, and that in most cases Alzheimer’s patients had low blood sugars, and high CSF (cerebrospinal fluid) insulin levels.(56, 57) In my own limited experience with Parkinson’s and ALS patients, I have found a disproportionately high number suffering from reactive hypoglycemia.

I found it interesting that several ALS patients have observed an association between their symptoms and gluten. That is, when they adhere to a gluten free diet they improve clinically. It may be that by avoiding gluten containing products, such as bread, crackers, cereal, pasta ,etc, they are also avoiding products that are high on the glycemic index, i.e. that produce reactive hypoglycemia. Also, all of these food items are high in free iron. Clinically, hypoglycemia will worsen the symptoms of most neurological disorders. We know that severe hypoglycemia can, in fact, mimic ALS both clinically and pathologically.(58) It is also known that many of the symptoms of Alzheimer’s disease resemble hypoglycemia, as if the brain is hypoglycemic in isolation.

In studies of animals exposed to repeated mild episodes of hypoxia (lack of brain oxygenation), it was found that such accumulated injuries can trigger biochemical changes that resemble those seen in Alzheimer’s patients.(59) One of the effects of hypoxia is a massive release of glutamate into the space around the neuron. This results in rapid death of these sensitized cells. As we age, the blood supply to the brain is frequently impaired, either because of atherosclerosis or repeated syncopal episodes, leading to short periods of hypoxia. Hypoglycemia produces lesions very similar to hypoxia and via the same glutamate excitotoxic mechanism. In fact, recent studies of diabetics suffering from repeated episodes of hypoglycemia associated with over medication with insulin, demonstrate brain atrophy and dementia.(60)

Another cause of isolated cerebral hypoglycemia is impaired transport of glucose into the brain across the blood-brain barrier. It is known that glucose enters the brain by way of a glucose transporter, and that in several conditions this transporter is impaired. This includes aging, arteriosclerosis, and Alzheimer’s disease.(61, 62) This is especially important in the diabetic since prolonged elevation of the blood sugar produces a down-regulation of the glucose transporter and a concomitant “brain hypoglycemia” that is exacerbated by repeated spells of peripheral hypoglycemia common to type I diabetics.

With aging, one sees several of these energy deficiency syndromes, such as mitochondrial injury, impaired cerebral blood flow, enzyme dysfunction, and impaired glucose transportation, develop simultaneously. This greatly magnifies excitotoxicity, leading to accelerated free radical injury and a progressively rapid loss of cerebral function and profound changes in cellular energy production.(63) It is suspected that at least in some of the neurodegenerative diseases, Alzheimer’s dementia and Parkinson’s disease in particular, this series of events plays a major pathogenic role.(64) Chronic free radical accumulation would also result in an impaired functional reserve of antioxidant vitamins/minerals, antioxidant enzymes ( SOD, catalase, and glutathione peroxidase) and thiol compounds necessary for neural protection. Chronic unrelieved stress, chronic infection, free radical generating metals and toxins, and impaired DNA repair enzymes all add to this damage.

It is estimated that the number of oxidative free radical injuries to DNA number about 10,000 a day in humans.(65) Under conditions of cellular stress this may reach several hundred thousand. Normally, these injuries are repaired by special DNA repair enzymes. It is known that as we age these repair enzymes decrease or become less efficient.(66) Also, some individuals are born with deficient repair enzymes from birth as, for example, in the case of xeroderma pigmentosum. Recent studies of Alzheimer’s patients also demonstrate a significant deficiency in DNA repair enzymes and high levels of lipid peroxidation products in the affected parts of the brain.(67, 68) It is also important to realize that the hippocampus of the brain, most severely damaged in Alzheimer’s dementia, is one of the most vulnerable areas of the brain to low glucose supply as well as low oxygen supply. That also makes it very susceptible to glutamate/ free radical toxicity.

Another interesting finding is that when cells are exposed to glutamate they develop certain inclusions (cellular debris) that not only resembles the characteristic neurofibrillary tangles of Alzheimer’s dementia, but are immunologically identical as well.(69) Similarly, when experimental animals are exposed to the chemical MPTP, they not only develop Parkinson’s disorder, but the older animals develop the same inclusions (Lewy bodies) as see in human Parkinson’s.(70) There is growing evidence that protracted glutamate toxicity leads to a condition of receptor loss characteristic of neurodegeneration.(71) This receptor loss produces a state of disinhibition that magnifies excitotoxicity during the later stage of the neurodegenerative process.

Special Functions of Ascorbic Acid

The brain contains one of the highest concentrations of ascorbic acid in the body. Most are aware of ascorbic acid’s function in connective tissue synthesis and as a free radical scavenger. But, ascorbic acid has other functions that make it rather unique.

In man, we know that certain areas of the brain have very high concentrations of ascorbic acid, such as the nucleus accumbens and hippocampus. The lowest levels are seen in the substantia nigra.(72) These levels seem to fluctuate with the electrical activity of the brain. Amphetamine acts to increase ascorbic acid concentration in the corpus striatum (basal ganglion area) and decrease it in the hippocampus, the memory imprint area of the brain. Ascorbic acid is known to play a vital role in dopamine production as well.

One of the more interesting links has been between the secretion of the glutamate neurotransmitter by the brain and the release of ascorbic acid into the extracellular space.(73) This release of ascorbate can also be induced by systemic administration of glutamate or aspartate, as would be seen in diets high in these excitotoxins. The other neurotransmitters do not have a similar effect on ascorbic acid release. This effect appears to be an exchange mechanism. That is, the ascorbic acid and glutamate exchange places. Theoretically, high concentration of ascorbic acid in the diet could inhibit glutamate release, lessening the risk of excitotoxic damage. Of equal importance is the free radical neutralizing effect of ascorbic acid.

There is now substantial evidence that ascorbic acid modulates the electrophysiological as well as behavioral functioning of the brain.(74) It also attenuates the behavioral response of rats exposed to amphetamine, which is known to act through an excitatory mechanism.(75) In part, this is due to the observed binding of ascorbic acid to the glutamate receptor. This could mean that ascorbic acid holds great potential in treating disease related to excitotoxic damage. Thus far, there are no studies relating ascorbate metabolism in neurodegenerative diseases. There is at least one report of ascorbic acid deficiency in guineas pigs producing histopathological changes similar to ALS.(76)

It is known that as we age there is a decline in brain levels of ascorbate. When accompanied by a similar decrease in glutathione peroxidase, we see an accumulation of H202 and hence, elevated levels of free radicals and lipid peroxidation. In one study, it was found that with age not only does the extracellular concentration of ascorbic acid decrease but the capacity of the brain ascorbic acid system to respond to oxidative stress is impaired as well.(77)

In terms of its antioxidant activity, vitamin C and E interact in such a way as to restore each others active antioxidant state. Vitamin C scavenges oxygen radicals in the aqueous phase and vitamin E in the lipid, chain breaking, phase. The addition of vitamin C suppresses the oxidative consumption of vitamin E almost totally, probably because in the living organism the vitamin C in the aqueous phase is adjacent to the lipid membrane layer containing the vitamin E.

When combined, the vitamin C is consumed faster during oxidative stress than vitamin E. Once the vitamin C is totally consumed, vitamin E begins to be depleted at an accelerated rate. N-acetyl-L-cysteine and glutathione can reduce vitamin E consumption as well, but less effectively than vitamin C. The real danger is when vitamin C is combined with iron. This is because the free iron oxidizes the ascorbate to produce the free radical dehydroxyascorbate. Alpha-lipoic acid acts powerfully to keep the ascorbate and tocopherol in the reduced state (antioxidant state). As we age, we produce less of the transferrin transport protein that normally binds free iron. As a result, older individuals have higher levels of free iron within their tissues, including brain, and are therefore at greater risk of widespread free radical injury.

Neurodevelopment

Recent studies have shown that glutamate plays a vital role in the development of the nervous system, especially as regards neuronal survival, growth and differentiation, development of circuits and cytoarchitecture.(78) For example, it is known that deficiencies of glutamate in the brain during neurogenesis can result in maldevelopment of the visual cortices and may play a role in the development of schizophrenia.(79) Likewise, excess glutamate can cause neural pathways to produce improper connections, a process I call “mis-wiring of the brain”. Excess glutamate during embryogenesis has been shown to reduce dendritic length and suppress axonal outgrowth in hippocampal neurons. It is interesting to note that glutamate can produce classic toxicity in the immature brain even before the glutamate receptors develop. High glutamate levels can also affect astroglial proliferation as well as neuronal differentiation. It appears to act via the phosphoinositide protein kinase C pathway.

It has been shown that during brain development there is an overgrowth of neuronal connections and cellularity, and that at this stage there is a peak in brain glutamate levels whose function it is to remove excess connections and neuronal over-expression. This has been referred to as “pruning”. Importantly, glutamate excess during synaptogenesis and pathway development has been shown to cause abnormal connections in the hypothalamus that can lead to later endocrinopathies.(80)

In general, toxicological injury in the developing fetus carries the greatest risk during the first two trimesters. But, this is not so for the brain, which undergoes a spurt of growth that begins during the third trimester and continues at least two years after birth. Dendritic growth is maximal in the late fetal period to one year of age, but may continue at a slower pace for several more years. Neurotransmitter development also begins during the late fetal period but continues for as long as four years after birth. This means that alterations in dietary glutamate and aspartate are especially dangerous to the fetus during pregnancy and for several years after birth. The developing brain’s succeptability to excitotoxicity varies, since each brain region has a distinct developmental profile. The type of excitotoxin also appears to matter. For example, kianate is non-toxic to the immature brain but extremely toxic to the mature brain. The glutamate agonist, NMDA, is especially toxic up to postnatal day seven while quisqualate and AMPA have peak toxicity from postnatal day seven through fourteen. L-cysteine is a powerful excitotoxin on the immature brain.

Myelination can also be affected by neurotoxins. In general, excitotoxic substances affect dendrites and neurons more than axons but axon demyelination has been demonstrated. During the myelination process, each fiber tract has its own spatiotemporal pattern of development, accompanied by significant biochemical changes, especially in lipid metabolism. More recent studies have shown an even more complicated pattern of CNS myelination than previously thought. This is of importance especially as regards the widespread use of aspartame, because of this triple toxin’s effects on neuronal proteins and DNA. Of special concern is aspartame’s methanol component and its breakdown product, formaldehyde.(81) Also, it is known that the aspartate moiety undergoes spontanous racemization in hot liquids to form D-aspartate, which has been associated with tau proteins in Alzheimer’s disease.(82, 83)

As you can see, the development of the brain is a very complex process that occurs in a spatial and temporal sequence that is carefully controlled by biochemical, structural, as well as neurophysiological events. Even subtle changes in these parameters can produce ultimate changes in brain function that may vary from subtle alteration in behavior and learning to autism, attention deficit disorder and violence dyscontrol.(84, 85, 86)

Experiments in which infant animals were exposed to MSG, have demonstrated significant neurobehavioral deficits.(87, 88) Other studies have shown that when pregnant female animals were fed MSG their offspring demonstrated normal simple learning but showed significant deficits in complex learning, accompanied by profound reductions in several forebrain neurotransmitters.(89, 90) In human this would mean that during infancy and early adolescence learning would appear normal, but with entry into a more advance education level, learning would be significantly impaired. In several ways, this animal model resembles ADD and ADHD in humans. Kubo and coworkers found that neonatal glutamate could severely injure hippocampal CA1 neurons and dendrites and, as a result, impair discriminative learning in rats.(91)

It is also important to note that neonatal exposure to MSG has been shown to cause significant alterations in neuroendocrine function that can be prolonged.(92, 93) By acting on the hypothalamus and its connections to the remainder of the limbic connections, excitotoxins can profoundly affect behavior.

Conclusion

In this brief discussion of a most complicated and evolving subject I have had to omit several important pieces of the puzzle. For example, I have said little about the functional components of the receptor systems, the glutamate transporter and its relation to ALS and Alzheimer’s dementia, receptor decay with aging and disease, membrane effects of lipid peroxidation products, membrane fluidity, effects of chronic inflammation on the glutamate/free radical cycle, stress hormones and excitotoxicity, the role of insulin excess on the eicosanoid system, or the detailed physiology of the glutamatergic system. I have also only briefly alluded to the toxicity of aspartame and omitted its strong connection to brain tumor induction.

But, I have tried to show the reader that there is a strong connection between dietary and endogenous excitotoxin excess and neurological dysfunction and disease. Many of the arguments by the food processing industry has been shown to be false. For example, that dietary glutamate does not enter the brain because of exclusion by the blood-brain barrier, has been shown to be wrong, since glutamate can enter by way of the unprotected areas of the brain such as the circumventricular organs. Also, as we have seen, chronic elevations of blood glutamate can breech the intact blood-brain barrier. In addition, there are numerous conditions under which the barrier is made incompetent.

As our knowledge of the pathophysiology and biochemistry of the neurodegenerative diseases increases, the connection to excitotoxicity has become stronger.(94) This is especially so with the interrelationship between excitotoxicity and free radical generation and declining energy production with aging. Several factors of aging have been shown to magnify this process. For example, as the brain ages its iron content increases, making it more susceptible to free radical generation. Also, aging changes in the blood brain barrier, microvascular changes leading to impaired blood flow, free radical mitochondrial injury to energy generating enzymes, DNA adduct formation, alterations in glucose and glutamate transporters and free radical and lipid peroxidation induced alterations in the neuronal membranes all act to make the aging brain increasingly susceptible to excitotoxic injury.

Over a lifetime of free radical injury due to chronic stress, infections, trauma, impaired blood flow, hypoglycemia, hypoxia and poor antioxidant defenses secondary to poor nutritional intake, the nervous system is significantly weakened and made more susceptible to further excitotoxic injury. We know that a loss of neuronal energy generation is one of the early changes seen with the neurodegenerative diseases. This occurs long before clinical disease develops. But, even earlier is a loss of neuronal glutathione functional levels.

I included the material about the special function of ascorbic acid because few are aware of the importance of adequate ascorbate levels for CNS function and neural protection against excitotoxicity. As we have seen, it plays a vital role in neurobehavioral regulation and the dopaminergic system as well, which may link ascorbate supplementation to improvements in schizophrenia.

Our knowledge of this process opens up new avenues for treatment as well as prevention of excitotoxic injury to the nervous system. For example, there are many nutritional ways to improve CNS antioxidant defenses and boost neuronal energy generation, as well as improve membrane fluidity and receptor integrity. By using selective glutamate blocking drugs or nutrients, one may be able to alter some of the more devastating effects of Parkinson’s disease. For example, there is evidence that dopamine deficiency causes a disinhibition (overactivity) of the subthalamic nucleus and that this may result in excitotoxic injury to the substantia nigra.(95) By blocking the glutamatergic neurons in this nucleus, one may be able to reduce this damage. There is also evidence that several nutrients can significantly reduce excitotoxicity. For example, combinations of coenzyme Q10 and niacinamide have been shown to protect against striatal excitotoxic lesions. Methylcobolamine, phosphatidylserine, pycnogenol and acetyl-L-carnitine all protect against excitotoxicity as well.

Of particular concern is the toxic effects of these excitotoxic compounds on the developing brain. It is well recognized that the immature brain is four times more sensitive to the toxic effects of the excitatory amino acids as is the mature brain. This means that excitotoxic injury is of special concern from the fetal stage to adolescence. There is evidence that the placenta concentrates several of these toxic amino acids on the fetal side of the placenta. Consumption of aspartame and MSG containing products by pregnant women during this critical period of brain formation is of special concern and should be discouraged. Many of the effects, such as endocrine dysfunction and complex learning, are subtle and may not appear until the child is older. Other hypothalamic syndromes associated with early excitotoxic lesions include immune alterations and violence dyscontrol.

Over 100 million American now consume aspartame products and a greater number consume products containing one or more excitotoxins. There is sufficient medical literature documenting serious injury by these additives in the concentrations presently in our food supply to justify warning the public of these dangers. The case against aspartame is especially strong.

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Fructose is No Answer For a Sweetener

Fructose is No Answer For a Sweetener

By Nancy Appleton, Ph.D.

The consumption of fructose (corn syrup) has risen considerably in the general population within recent years. In 1980 the average person ate 39 pounds of fructose and 84 pounds of sucrose. In 1994, the average person ate 66 pounds of sucrose and 83 pounds of fructose. These 149 pounds are approximately 19% of the average person’s diet.

This increase is due to several factors. There was a decreased use of cane and beet sugar (sucrose) in processed foods and a wide spread use of corn syrup due to economics. Corn is much cheaper and twice as sweet as table sugar. It is absorbed only 40% as quickly as glucose and causes only a modest rise in blood sugar.

A few years ago the medical community revealed that there was good news for diabetics. Many people had previously known that table sugar (sucrose) was not a healthy food for diabetics because it raised their blood sugar levels above normal.

Since diabetics have a hard time maintaining healthy blood sugar levels, doctors counseled diabetics not to eat sugar. The new revelation was that diabetics could eat fructose because fructose did not raise their blood sugar level extremely high. So far, so good, but there is more.

Many doctors were recommending fructose instead of glucose. Today fructose is not only being used by some diabetics but it is used for a variety of foods, drinks and confectionery around the world. It is used for candies for diabetics, desserts for weight watchers, drinks for the sportsman and jelly for the health conscious.

The medical community recommended it because of a low increase in glucose in the blood. The scientists did not look at other factors in the body when a person eats sugar. Let’s look at some of these factors now.

Fructose: The Facts

1.) Robs the Body of Micronutrients. Fructose has no enzymes, vitamins, and minerals and robs the body of its micronutrient treasures in order to assimilate itself for physiological use.

Fructose browns food more readily (Maillard reaction) than with glucose. This may seem like a good idea, but it is not.

The Maillard reaction, a browning reaction, happens with any sugar. With fructose it happens seven times faster with than glucose, results in a decrease in protein quality and a toxicity of protein in the body.

This is due to the loss of amino acid residues and decreased protein digestibility. Maillard products can inhibit the uptake and metabolism of free amino acids and other nutrients such as zinc and some advanced Maillard products have mutagenic and/or carcinogenic properties. The Maillard reactions between proteins and fructose, glucose, and other sugars may play a role in aging and in some clinical complications of diabetes.

2.) May Increase LDL and Heart Disease Risk. Research showed that in subjects that had healthy glucose tolerance and those that had unhealthy glucose tolerance, fructose caused a general increase in both the total serum cholesterol and in the low density lipoproteins (LDL) in most of the subjects. This puts a person at risk for heart disease.

3.) May Increase VLDL. Another study showed that the very low density lipoproteins (VLDL) increased without an apparent change in high density lipoproteins (HDL). The VLDL and the LDL should be as low as possible and the HDL should be as high as possible.

4.) May Increase Uric Acid. There is a significant increase in the concentration of uric acid that is dependent on the amount of fructose digested. After glucose no significant change occurs. An increase in uric acid can be an indicator of heart disease.

5.) May Increase Lactic Acid and Acidosis. Fructose ingestion in humans results in increases in blood lactic acid, especially in patients with pre-existing acidotic conditions such as diabetes, postoperative stress, or uremia. The significance to human health is that extreme elevations cause metabolic acidosis and can result in death.

6.) May Create Liver Stress And Diarrhea. Fructose is absorbed primarily in the jejunum and metabolized in the liver. Fructose is converted to fatty acids by the liver at a greater rate than is glucose. When consumed in excess of dietary glucose, the liver cannot convert all of the excess of fructose in the system and it may be malabsorbed. What escapes conversion and being absorbed into the cells may be thrown out in the urine. Diarrhea can be a consequence.

7.) May Interact with Oral Contraceptives; Elevate Insulin. Fructose interacts with oral contraceptives and elevates insulin levels in women on “the pill.”

8.) May Create Insulin Resistance. Fructose reduced the affinity of insulin for its receptor. This is the first step for glucose to enter a cell and be metabolized. As a result, the body needs to pump out more insulin, to handle the same amount of glucose.

9.) May Create Kidney Imbalances. Fructose consistently produced higher kidney calcium concentrations than did glucose in a study with rats. Fructose generally induced greater urinary concentrations of phosphorus and magnesium and lowered urinary pH compared with glucose.

The balance of minerals in the body is very important for the function of vitamins, enzymes and other body function. When the minerals are out of the right relationship, the body chemistry suffers. The presence of diarrhea might be the cause of decreased absorption of minerals.

10.) May Create Mineral Loss. Fructose-fed subjects lose minerals. They had higher fecal excretions of iron and magnesium than did subjects fed sucrose. Apparent iron, magnesium, calcium, and zinc balances tended to be more negative during the fructose feeding period as compared to balances during the sucrose feeding period.

11.) May Create Bowel Distress. A study of 25 patients with functional bowel disease showed that pronounced gastrointestinal distress may be provoked by malabsorption of small amounts of fructose.

12.) May Aggravate Herditary Fructose Intolerance. Many times fructose and sorbitol are substituted for glucose in parenteral nutrition (intervenous feeding, IV). This can have severe consequences with people with hereditary fructose intolerance, a congenital disorder affecting one in 21,000. A European doctor declared: “Fructose and sorbitol containing infusion fluids have no further place in our hospital pharmacies.”

13.) May Accelerate Aging. There is significant evidence that high sucrose diets may alter intracellular metabolism, which in turn facilitates accelerated aging through oxidative damage. Scientists found that the rats given fructose had more undesirable cross-linking changes in the collagen of their skin than in the other groups.

These changes are also thought to be markers for aging. The scientists say that it is the fructose molecule in the sucrose, not the glucose, which plays the larger problem.

14.) Converts to Fat. Fructose is not metabolized the same as other sugars. Instead of being converted to glucose which the body uses, it is removed by the liver.

Because it is metabolized by the liver, fructose does not cause the pancreas to release insulin the way it normally does. Fructose converts to fat more than any other sugar. This may be one of the reasons Americans continue to get fatter.

15.) Raises Serum Triglycerides. Fructose raises serum triglycerides significantly. As a left-handed sugar, fructose digestion is very low. For complete internal conversion of fructose into glucose and acetates, it must rob ATP energy stores from the liver.

16.) Inhibits Copper Metabolism. Fructose inhibits copper metabolism. A deficiency in copper leads to bone fragility, anemia, defects of the connective tissue, arteries, and bone, infertility, heart arrhythmias, high cholesterol levels, heart attacks, and an inability to control blood sugar levels.

It seems that the magnitude of the deleterious effects varies depending on such factors as age, sex, baseline glucose, insulin, and triglyceride concentrations, the presence of insulin resistance, and the amount of dietary fructose consumed.

Some people are more sensitive to fructose. They include hypertensive, hyperinsulinemic, hypertrigly-ceridemic, non-insulin dependent diabetic people, people with functional bowel disease and postmenopausal women.

There is a continuing increase in sugar consumption in the United States. We now eat 153 pounds of sugar per person per year. This increase is mostly in the form of fructose. From the research presented, it seems that this increase is going to have a negative influence on our health.

Nancy Appleton, Ph.D. is a clinical nutritionist, researcher, lecturer, and author of “Lick the Sugar”, “Healthy Bones”, “Heal Yourself With Natural Foods” and “The Curse Of Louis Pasteur” and “Lick the Sugar Habit Sugar Counter”.

Note: The 16 short-title headings (not the author’s) were added to provide emphasis for each main point.

ALERT: Do not be fooled by claims that fructose is a “safe” or “natural” sugar and can be eaten without harm. Read labels carefully to avoid many so-called “health foods” which claim to have “natural sweeteners” but which really contain fructose.

References

  1. Beatrice Trum Hunter, “Confusing Consumers About Sugar Intake,” Consumers Research, 78, no 1 (January 1995): 14-17. 2. Judith Hallfrisch, “Metabolic Effects of Dietary Fructose,” FASEB Journal, 4 (June 1990): 2652-2660.
  2. H. F. Bunn and P. J. Higgins, “Reaction of Nonosaccharides with Proteins; Possible Evolutionary Significance.” Science, 213 (1981):2222-2244.
  3. William L Dills Jr., “Protein Fructosylation: Fructose and the Maillard Reaction,” American Journal of Clinical Nutrition, 58 (suppl) (1993): 779S-787S.
  4. J. Hallfrisch et al., “The Effects of Fructose on Blood Lipid Levels,” American Journal of Clinical Nutrition, 37, no, 3 (1983): 740-748.
  5. Claire B. Hollenbeck, “Dietary Fructose Effects on Lipoprotein Metabolism and Risk for Coronary Artery Disease,” American Journal of Clinical Nutrition, 58 (suppl), (1993): 800S-807S.
  6. Hallfrisch, 1990.
  7. J. Macdonald, Anne Keyser, and Deborah Pacy, “Some Effects, in Man, of Varying the Load of Glucose, Sucrose, Fructose, or Sorbitol on Various Metabolites in Blood,” American Journal of Clinical Nutrition, 31 (August 1978)): 1305-1311.
  8. D. Zakim and R. H. Herman, Fructose Metabolism II, American Journal of Clinical Nutrition, 21: 315-319, 1968.
  9. A. E. Bender and K. B. Damji, “Some Effects of Dietary Sucrose,” World Review of Nutrition and Dietetics, 15 (1972): 104-155.
  10. Hunter
  11. Hunter
  12. A. E. Bergstra, A. G. Lemmens, and A. C. Beynens, “Dietary Fructose vs. Glucose Stimulates Nephrocalcinogenesis in Female Rats,” Journal of Nutrition, 123, no. 7 (July 1993): 1320-1327.
  13. R. Ivaturi and C. Kies, “Mineral Balances in Humans as Affected by Fructose, High Fructose Corn Syrup and Sucrose,” Plant Foods For Human Nutrition, 42, no. 2 (1992): 143-151.
  14. J. J. Rumessen and E. Gudmand-Hoyer, “Functional Bowel Disease: Malabsorption and Abdominal Distress After Ingestion of Fructose, Sorbitol, and Fructose-Sorbitol Mixtures,” Gastroenterology, 95, no. 3 (September 1988): 694-700.
  15. Roger B. Mc Donald, “Influence of Dietary Sucrose on Biological Aging,” American Journal of Clinical Nutrition, 62 (suppl), (1995): 284s-293s.
  16. www.NutritionNewsFocus.com, May 25, 2000.
  17. H. Hallfrisch, et al., The Effects of Fructose on Blood Lipid Levels, American Journal of Clinical Nutrition, 37: 5, 1983, 740-748.
  18. Klevay, Leslie, acting director of the U.S. Agriculture Department’s Human Nutrition Research Center, Grand Forks, N.D.
  19. Hollenback
  20. Hallfrisch
  21. Hunter

Three Ingredients You Should NEVER Consume

1. “Natural Flavors”

We continue to be surprised at how many so-called natural products are formulated with “natural flavors”. “Natural flavors” is nice-sounding term for toxic MSG (monosodium glutamate) — a powerful neurotoxin that has the ability to damage and burst brain cells as well as create global body symptoms, especially brain, memory, hormonal, and nervous system distress and damage.

We often feel like a lone wolf trying to lead the health pack away from MSG. But “natural flavors” is such a great flavor enhancer and works so well to disguise any off-tastes, that it is just tThese three food ingredients can cause damage to your healthoo tempting for most manufacturers not to use MSG in their products.

You’ll see MSG listed as “natural flavors” on almost every health bar and protein powder. It’s hard to believe, but MSG lurks everywhere in many health products. Buyer beware. One exception is “natural flavors” listed in products from Europe which may refer to either MSG or actually be natural-source ingredients to flavor a product.

2. Aspartame

Aspartame (brand names: NutraSweet, Equal, NutraSweet Spoonful, Nutra Taste, etc.) is a toxic chemical sweetener contained in numerous consumer products (such as health bars, protein drinks, soft drinks, soup mixes, etc). It is a powerful neurotoxin with the ability to disrupt normal cardiovascular, hormone, and nervous system pathways.

You may want to think twice about consuming foods with aspartame consumption if you have any of the following symptoms: headaches, back pain, memory problems, hormonal concerns, depression, cardiovascular abnormalities, inability to think well or make decisions, fatigue, dizziness, chest pain, blood sugar problems, allergic reactions, allergies, weight gain, sexual problems, etc.

Aspartame Reactions

The following is list of adverse effects from short-term and/or long-term use of aspartame:

  • seizures and convulsions
  • dizziness
  • tremors
  • migraines and severe headaches (can trigger or cause them from chronic intake)
  • memory loss
  • slurring of speech
  • confusion
  • numbness or tingling of extremities
  • chronic fatigue
  • depression
  • insomnia
  • irritability
  • panic attacks (common aspartame toxicity reaction)
  • marked personality changes
  • phobias
  • rapid heart beat, tachycardia (another frequent reaction)
  • asthma
  • chest pains
  • hypertension (high blood pressure)
  • nausea or vomiting
  • diarrhea
  • abdominal pain
  • swallowing pain
  • itching
  • hives / urticaria and other allergic reactions
  • blood sugar control problems (e.g., hypoglycemia or hyperglycemia)
  • menstrual cramps and other menstrual problems or changes
  • impotency and sexual problems
  • food cravings
  • weight gain
  • hair loss / baldness or thinning of hair
  • burning urination & other urination problems
  • excessive thirst or excessive hunger
  • bloating, edema (fluid retention)
  • infection susceptibility
  • joint pain
  • brain cancer (studies in animals)
  • death

Aspartame consumption mimics symptoms or may worsen the following diseases:

  • Fibromyalgia
  • arthritis
  • multiple sclerosis (MS)
  • Parkinson’s disease
  • lupus
  • multiple chemical sensitivities (MCS)
  • diabetes and diabetic complications
  • epilepsy
  • Alzheimer’s disease
  • birth defects
  • chronic fatigue syndrome
  • lymphoma
  • Lyme disease
  • Attention Deficit Disorder (ADD and ADHD)
  • panic disorder
  • depression and other psychological disorders

3. Fructose

Fructose is a refined sugar that has no enzymes, vitamins, or minerals, and robs the body of its own micronutrients in order to be assimilated. Beware of this toxic sweetener contained in many so-called health foods (i.e. health bars, protein drinks, nutritional snacks, children’s vitamins, cookies, etc.)

Research shows that fructose may help cause the following:

  • Create insulin resistance and diabetes risk
  • Increase fat weight gain
  • Increase LDL, VLDL, triglycerides and heart disease risk
  • Create mineral losses, especially iron and magnesium
  • Inhibit copper metabolism
  • Increase uric acid
  • Increase acidosis
  • Increase liver stress and diarrhea
  • Create kidney imbalances
  • Accelerate aging (increases cross-linkage of collagen in skin)

References

  1. Blaylock, Russell, “Excitotoxins: The Taste That Kills,” Health Press, Sante Fe, New Mexico, 1995.
  2. Two former FDA scientists, Jacqueline Verrett and Adrian Gross, spent 3 months at Searle laboratories, discovering serious irregularities in research studies. Verrett called FDA’s final decision to approve aspartame “a giant cover-up.” Food Magazine, Vol 1 No.9, April/June 1990. (England)
  3. Judith Hallfrisch, “Metabolic Effects of Dietary Fructose,” FASEB JOURNAL 4 (June 1990): 2652-2660.