Natural Flavors/MSG

NATURAL FLAVORS (MSG)

A Hidden Toxin Lurking in Your Food and 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 fmaily, 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 summery 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 neuroendo-crine 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.

References

1. Ikonomidou C and Turski L, Glutamate in Neurodegenerative Disorders , In, Stone TW ( Ed) , 

    Neurotransmitters and Neuromodulators: Glutamate, CRC Press, Boca Raton, 1995, 253-272.
2. Whetsell WO, Shapira NA. Biology of Disease. Neuroexcitation, excitotoxicity and human neurological disease. Lab Invest 68: 372-387, 1993.
3. Lucas DR and Newhouse JP. The toxic effect of sodium L-glutamate on the inner layer of the retina. Arch Opthalmol 58: 193-201, 1957.
4. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate.

    Science 165: 719-721, 1969.
5. Pol ANV, Wuarin J-P, Dudek E. Glutamate, the dominate excitatory transmitter in neuroendocrins  regulation. Science 250: 1276-1278, 1990.
6. Coyle JT, et al. Excitatory Amino Acid Neurotoxins: Selectivity, Specificity, and Mechanisms of Action. Neurosci Reseach Bull 19: #4, 1981.
7. Blackstone CD, Huganir RL. Molecular structure of Glutamate Receptor Channels. In, Stone TW, ed, CNS Neurotransmitters and neuromodulators: Glutamate. CRC Press, Boca Raton, 1995, 53-67.
8. Analysis of Adverse Reactions to Monosodium Glutamate ( MSG). Life Sciences Research Office.

    FASEB, July 1995.
9. Blaylock, RL. Excitotoxins: The Taste That Kills. Health Press, Santa Fe, NM, 1997, 248-254.
10 Olney JW. Glutamate: a neurotoxic transmitter. J Child Neurol 4: 218-226, 1989.
11. Choudhary P, Malik VB, et al. Studies on the effect of monosodium glutamate on hepatic microsomal  lipid peroxidation, calcium, ascorbic acid and glutathione and its dependent enzymes in adult male mice. 
  Toxicol Lett 89: 71-76, 1996.
12. Plaitakis A and Caroscio JT. Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann Neuro 22: 575-579, 1987.
13. Blaylock RL. Neurodegeneration and aging of the central nervous system: Prevention and treatment by

      phytochemicals and metabolic nutrients. Integrative Med 1: 117-133, 1998.
14. Olney JW. Excitotoxic food additives: functional teratological aspects. Prog Brain Res 18: 283-294, 1988.
15. Parsons RB, Waring RH, et al. In vitro effect of the cysteine metabolites homocysteic acid,

      homocysteine and cysteic acid upon human neuronal cell lines. Neurotoxicology 19: 599-603, 1998.
16. Esskes TK. Neural tube defects, vitamins and homocysteine. Eur J Pediatr 157: Suppl 2: S139-S141,

      1998.
17. McCaddon A, Daves G, et al. Total serum homocysteine in senile dementia of Alzheimer type. In J Geriatr Psychiatry 13: 235-239, 1998.
18. Banks JC, et al. Retinal pathology in Alzheimer's disease. I. Ganglion cell loss in foveal/parafoveal retina.

      Neurobiol Aging 17: 377-384, 1996.19. Onanow CW. A radical hypothesis for neurodegeneration. Trends

      in neurosci 16: 439-444, 1993.
20. Aisen PS, Davis KL. Inflammatory mechanisms in Alzheimer's disease: implications for therapy. Am J Psych 151: 1105-1113, 1994.
21. Murphey T, Parikh A, et al. Arachidonic acid metabolism in glutamate neurotoxicity. Ann NY Acad Sci 559: 474-477, 1989.
22. Smith MA, Richey Pl, et al. Widespread peroxynitrite-mediated damage in Alzheimer's disease. J

      Neurosci 17: 2653-2657, 1997.
23. Jenner P, et al. Oxidative stress as a cause of nigral cell death in Parkinson's disease and incidental Lewy body disease. Ann Neurol 32: 282-287, 1992.
24. Griffiths PD, Crossman AR. Distribution of iron in the basal ganglion and neocortex in Parkinson's disease and Alzheimer's disease. Dementia 2: 61-65, 1993.
25. Bolanos JP, Almeida A, et al. Nitric oxide-mediated mitochondrial damage in the brain: mechanisms and implications for neurodegenerative diseases. J Neurochem 68: 2227-2240, 1997.
26. Dexter DT, et al. Increased iron content in post-mortum Parkinsonian brain. Lancet ii: 219-220, 1987.
27. Hirsch EC, Brandel JP, et al. Iron and aluminum increase in the substantia nigra of patients with Parkinson's disease: an X-ray microanalysis. J. Neurochem 56: 446-451, 1991.
28. Logroscino G, Marder K, Graziano J, et al. Altered systemic iron metabolism in Parkinson's Neurology 49: 714-717, 1997.
29. Schapira AHV, et al. Mitochondrial complex I deficiency in Parkinson's disease J. Neurochem 54: 823-827, 1990.
30. Bergerson C. Oxidative stress: Its role in the pathogenesis of amyotrophic lateral sclerosis. Neurol Sci 129: 81-84, 1995. Page 14
31. Gerlach M, Ben-Shachar D, et al. Altered brain metabolism of iron as a cause of neurodegenerative diseases. J Neurochem 63: 793-807, 1994.
32. Dawson VL, Dawson TM, et al. Mechanisms of nitric oxide-mediated neurotoxicity in primary brain cultures. J Neurosci 13: 2651-2661, 1993.
33. Williams LR. Oxidative stress, age-related neurodegeneration, and the potential for neurotrophic treatment. Cerebrovasc Brain Metab Rev 7: 55-73, 1995.
34. Domenico E, Pellegrini-Giampietro, et al. Excitatory amino acid release and free radical formation may cooperate in the genesis of ischemia-induced neuronal damage. J Neurosci 10: 1035-1041, 1990.
35. Mundy WR, Freudenrich TM, Kodavanti PR. Aluminum potentiates glutamate-induced calcium

      accumulation and iron-induced oxygen free radical formation in primary neuronal cultures. Mol Chem Neuropathol 32: 41-57, 1997.
36. Aarala JT, Loikkanen JJ, et al. Lead amplifies glutamate-induced oxidative stress. Free Radical Biol Med 19: 689-693, 1995.
37. Lipton SA, Nicotera P. Calcium, free radicals and excitotoxins in neuronal apoptosis. Cell Calcium 23: 165-171, 1998.
38. Murphey TH, et al. Immature cortical neurons are uniquely sensitive to glutamate toxicity by inhibition of cystine uptake. FASEB 6: 1624-1633, 1990.
39. Fahn S. A pilot trial of high-dose alpha-tocopherol and ascorbate in early Parkinson's disease. Ann Neurol 32: S128-S132, 1992.
40. Niki E. Interactions of ascorbate and alpha-tocopherol. Third Conference of Vitamin C, Burns ET (Ed), NY Acad Sci 498: 186-199, 1987.
41. Beal MF, Hyman BT, Koroschetz W. Do defects in mitochondrial energy metabolism underlie the pathology of neurodegenerative diseases? Trends in Neurosci 16: 125- 131, 1993.
42. Pall HS, Blake DR, et al. Raised cerebrospinal-fluid copper concentration in Parkinson's disease. Lancet

      Aug 1: 238- 241,1987.
43. Sorg O, Horn TF, et al. Inhibition of astrocyte glutamate uptake by reactive oxygen species: role of antioxidant enzymes. Mol Med 7: 431-440, 1997.
44. Toth E and Lajtha A. Elevation of cerebral levels of nonessential amino acids in vivo by administration of large doses. Neurochem Res 6: 1309-1317, 1981.
45. Dowling P, Husar W, et al. Cell death and birth in multiple sclerosis brain. J Neurol Sci 149: 1-11, 1997.
46. Bennow K, et al. Blood-brain barrier disturbance in patients with Alzheimer's disease is related to vascular factors. Acta Neuro Scand 81: 323-326, 1990.
47. Zuccarello M, Anderson DK. Interactions between free radicals and excitatory amino acids in the blood brain barrier disruption after iron injury in the rat. J Neurotrauma 10: 397- 481, 1993.
48. Koenig H, et al. Capillary NMDA receptors regulate blood-brain barrier function and breakdown. 588: 297-303, 1992.
49. Novelli A, Reilly JA, et al. Glutamate becomes neurotoxic via the N-methyl-D aspartate receptor when intracellular energy levels are reduced. Brain Res 451: 205-207, 1988
50. Greenemyer JT. Neuronal bioenergetics defects, excitotoxicity and Alzheimer's disease: Use it or lose it. Neurobiol Aging 12: 334-336, 1991.
51. Parker WD, Boyson SJ, Parks JK. Abnormalities of the electron transport chain in idiopathic Parkinson's disease. Ann Neurol 26: 719-723, 1989.
52. Schapira AHV, Mann VM, et al. Mitochondrial function in Parkinson's disease. Ann Neurol 32: S116-S124,1992.
53. Beal MF, et al. Coenzyme Q10 and niacinamide are protective against mitochondrial toxins in vivo. Neuro 44 (Supp2) April 1994, A177.
54. Calvani M, Koverech A, Carurso G. Treatment of mitochondrial diseases. In, DiMauro S, Wallace DC, eds. Mitochondrial DNA in Human Pathology. Raven Press, New York,1993, 173-198.
55. Bucht G, et al. Changes in blood glucose and insulin secretion in patients with senile dementia of Alzheimer's type. Acta Medica Scand 213: 387-392, 1983. 56 Bucht,G, et al. Acta Medica Scand 213: 387-392, 1983.
57. Fujiasawa Y, Saki K, Akiyama K. Increased insulin levels after OGTT load in peripheral blood and cerebrospinal fluid of patients with dementia of the Alzheimer's type. Bio Psych 30: 1219-1228, 1991.
58. Gotoh F, Kitamura A, et al. Abnormal insulin secretion in amyotrophic lateral sclerosis. J Neurol Sci 16: 201-207, 1972.
59. Pettgrew JW, et al. The role of membranes and energetics in Alzheimer's disease. In, Terry RD, et al (Eds) Alzheimer's Disease, Raven Press, New York, 1994.
60. Leibson CL, Rocca WA, et al. Risk of dementia among persons with diabetes mellitus: a population- based cohart study. Am J Epidemiol. 145: 301-308, 1997.
61. Kalaria RN, Harik SI. Reduced glucose transporter at the blood-brain barrier and in the cerebral cortex in Alzheimer's disease. J Neurochem 53: 1083-1088, 1989
62. Kaleria RN, et al.The glucose transporter of the human brain and blood brain barrier. Ann Neurol 24: 757-764, 1988.
63. Tannaka M, Kovalenko SA, et al. Accumulation of deletions and point mutations in mitochondrial genome in degenerative diseases. Ann NY Acad Sci 15: 102-111, 1996.
64. Spencer JP, Jenner A, et al. Intense oxidative DNA damage promoted by L-dopa and its metabolites.

      Implications for neurodegenerative disease. FEBS Lett 353: 246-250, 1994. 65.Ames BN, Shigenaga MK,Hagen TM. Oxidants, antioxidants, and the degenerative diseases of aging. Proc Natl Acad Sci 90: 7915-7922, 1993.
66. Raos KS. DNA-damage & DNA-repair in aging brain. Indian J Med Res 106: 423-437, 1997.
67. Boerrigter ME, Wei JY, Vijg J. DNA repair and Alzheimer's disease. J Gerontol 47: B177-B184, 1992.
68. Lyras L, Cairns NJ, et al. An assessment of oxidative damage to proteins, lipids and DNA in the brain from patients with Alzheimer's disease. J Neurochem 68: 2061-2069, 1997.
69. Mattson MP. Antigenic changes to those seen in neurofibrillary tangles are elicited by glutamate and Ca+2 influx in cultured hippocampal neurons. Neuron 2: 105-117, 1990.
70. Markey SP. MPTP: a new tool for understanding Parkinson's disease. Disc Neurosci 4: 1986
71. Olney JW, Wozniak DF, Farber NB. Excitotoxic neurodegeneration in Alzheimer's disease. New

      hypothesis and new therapeutic strategies. Arch Neurol 54: 1234-1240, 1997.
72. Gruenewald RA. Ascorbic acid distribution patterns in human brain. A comparison with nonhuman mammalian species. Ann NY Acad Sci 498: 1-12, 1987.
73. Grunewald RA. Ascorbic acid in the brain. Brain Res Rev 18: 123-133, 1993.
74. Boutelle MG, Svensson L, Fillenz M. Effect of diazepam on behavior and associated changes in

      ascorbate concentration in rat brain areas: striatum, N. Accumbens and hippocampus.

      Psychopharmacology 100: 230-236, 1990.75. Tolbert LC, Thomas NT, et al. Ascorbate blocks

      amphetamine-induced turning behavior in rats with unilateral nigrostriatal lesions. Brain Res Bull. 4: 43-48, 1979.
76. Den Hartog Jager WA. Experminental amyotrophic lateral sclerosis in Guinea-pig. J Neurol Sci 67: 133-142, 1985.
77. Svenson L, Wu C, et al. Effect of aging on extracellular ascorbate concentration in rat brain. Brain Res 309: 36-40, 1993.
78. Suzuki K, Martin PM. Neurotoxicants and developing brain. In, Harry GJ, Ed, Developmental

      Neurotoxicology. CRC Press, Boca Raton, 1994, 9-32.
79. Hirsch SR, Garey LJ, Belleroche J. A pivotal role for glutamate in the pathogenesis of schizophrenia, and its cognitive dysfunction. Pharmacol Biochem Behavior 56: 797-802, 1997.
80. Gong SL, Xia FQ, et al. Harmful effects of MSG on function of hypothalamus-pituitary-target gland system. Biomed Environ 8: 310-317, 1995.
81. Trocho C, Rardo R, et al. Formaldehyde derived from dietary aspartame binds to tissue components in vivo. Life Sci 63: 337-349, 1998.
82. Kenessey A, Yen S-H, et al. Detection of D-aspartate in tau proteins associated with Alzheimer paired helical filaments. Brain Res 675: 183-189,1995 83.Fisher GH, D'Aniello AD, et al. Quantification of D-asparate in normal and Alzheimer brains. Neurosci Lett 143: 215-218, 1992) 84. Suzuki K, Martin PM,

      Neurotoxicants and The Developing Brain, In, Harry GT, ed, Developmental Neurotoxicology, CRC Press, Baco Raton, 1994, 9-32.
85.Olney JW. Excitotoxic food additives: functional teratological aspects. Progress Brain Res 73: 283-294, 1988 86.Brody JR, et al. Effect of micro-injections of L-glutamate into the hypothalamus on attack and flight behavior in cats. Nature 224: 1330, 1969
87. Wong PT, Neo LH, et al. Deficits in water escape performance and alterations in hippocampal

      cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice. Pharmacol Biochem Behav 57: 383-388, 1997.
88. Klingberg H, Brankack J, Klingberg F. Long-term effects on behavior after post-natal treatment with monosodium L-glutamate. Biomed Biochem ACTA 46: 705-711, 1987.
89. Freider B, Grimm VE. Prenatal monosodium glutamate (MSG) treatment given through the mother's diet causes behavioral deficits in rat offspring. Intern J Neurisci 23: 117-126, 1984.
90. Frieder B, Grimm VE. Prenatal monosodium glutamate causes long-lasting cholinergic and adrenergic

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; changes in various brain regions. J Neurochem 48: 1359-1365, 1987<br>91. Kubo T, Kohira R, et al. Neonatal glutamate can destroy the hippocampal CA1 structure and impair discrimination learning in rats. Brain Res 616: 311-314, 1993.<br>92. Bakke JL, Lawrence J, et al. Late endocrine effects of administering monosodium glutamate to neonatal rats. Neuroendocrinology 26: 220-228, 1978.<br>93. Maiter D, Underwood LE, et al. Neonatal treatment with monosodium glutamate: effects of prolonged growth hormone (GH)-releasing hormone deficiency on pulsatile GH secretion and growth in female rats.Endocrinology 128: 1100-1106, 1991.<br>94. Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway for neurologic disorders. New Eng J Med 330: 613-622, 1994.<br>95. Rodriguez MC, Obeso JA, Olanow CW. Subthalamic nucleus-mediated excitotoxicity in Parkinson's disease: a target for neuroprotection. Ann Neurol 44: ( Supp 1) S175-S188, 1998.<br><br><br>__________

Doors of Perception

DOORS OF PERCEPTION

The Doors of Perception

 

Why Americans Will Believe Almost Anything

 

by Dr. Timothy O'Shea, medical researcher

We are the most conditioned, programmed beings the world has ever known. Not only are our thoughts and attitudes continually being shaped and molded; our very awareness of the whole design seems like it is being subtly and inexorably erased.

The doors of our perception are carefully and precisely regulated. Who cares, right?

It is an exhausting and endless task to keep explaining to people how most issues of conventional wisdom are scientifically implanted in the public consciousness by a thousand media clips per day. In an effort to save time, I would like to provide just a little background on the handling of information in this country.

Once the basic principles are illustrated about how our current system of media control arose historically, the reader might be more apt to question any given story in today's news.

If everybody believes something, it's probably wrong. We call that Conventional Wisdom.

In America, conventional wisdom that has mass acceptance is usually contrived: somebody paid for it. Examples:

  • Pharmaceuticals restore health.
  • Vaccination brings immunity.
  • The cure for cancer is just around the corner.
  • When a child is sick, he needs immediate antibiotics.
  • When a child has a fever, he needs Tylenol.
  • Hospitals are safe and clean.
  • America has the best health care in the world.
  • And many, many more

This is a list of illusions that have cost billions and billions to conjure up. Did you ever wonder why you never see the President speaking publicly unless he is reading? Or why most people in this country think generally the same about most of the above issues?

 

How This Set-Up Got Started

In Trust Us, We're Experts, Stauber and Rampton pull together some compelling data describing the science of creating public opinion in America.

They trace modern public influence back to the early part of the last century, highlighting the work of guys like Edward L. Bernays, the Father of Spin. From his own amazing chronicle, Propaganda, we learn how Edward L. Bernays took the ideas of his famous uncle, Sigmund Freud himself, and applied them to the emerging science of mass persuasion.

The only difference was that instead of using these principles to uncover hidden themes in the human unconscious, the way Freudian psychology does, Bernays used these same ideas to mask agendas and to create illusions that deceive and misrepresent, for marketing purposes.

 

The Father Of Spin

Bernays dominated the PR industry until the 1940s, and was a significant force for another 40 years after that. (Tye) During all that time, Bernays took on hundreds of diverse assignments to create a public perception about some idea or product. A few examples:

As a neophyte with the Committee on Public Information, one of Bernays' first assignments was to help sell the First World War to the American public with the idea to "Make the World Safe for Democracy." (Ewen)

A few years later, Bernays set up a stunt to popularize the notion of women smoking cigarettes. In organizing the 1929 Easter Parade in New York City, Bernays showed himself as a force to be reckoned with.

He organized the Torches of Liberty Brigade in which suffragettes marched in the parade smoking cigarettes as a mark of women's liberation. Such publicity followed from that one event that from then on women have felt secure about destroying their own lungs in public, the same way that men have always done.

Bernays popularized the idea of bacon for breakfast.

Not one to turn down a challenge, he set up the advertising format along with the AMA that lasted for nearly 50 years proving that cigarettes are beneficial to health. Just look at ads in issues of Life or Time from the 40s and 50s.

 

Smoke And Mirrors

Bernay's job was to reframe an issue; to create a desired image that would put a particular product or concept in a desirable light. Bernays described the public as a 'herd that needed to be led.' And this herdlike thinking makes people "susceptible to leadership."

Bernays never deviated from his fundamental axiom to "control the masses without their knowing it." The best PR happens with the people unaware that they are being manipulated.

Stauber describes Bernays' rationale like this: "the scientific manipulation of public opinion was necessary to overcome chaos and conflict in a democratic society." (Trust Us, p42)

These early mass persuaders postured themselves as performing a moral service for humanity in general - democracy was too good for people; they needed to be told what to think, because they were incapable of rational thought by themselves. Here's a paragraph from Bernays' Propaganda:

"Those who manipulate the unseen mechanism of society constitute an invisible government which is the true ruling power of our country. We are governed, our minds molded, our tastes formed, our ideas suggested largely by men we have never heard of. "

This is a logical result of the way in which our democratic society is organized. Vast numbers of human beings must cooperate in this manner if they are to live together as a smoothly functioning society.

In almost every act of our lives whether in the sphere of politics or business in our social conduct or our ethical thinking, we are dominated by the relatively small number of persons who understand the mental processes and social patterns of the masses. It is they who pull the wires that control the public mind."

 

Here Comes The Money

Once the possibilities of applying Freudian psychology to mass media were glimpsed, Bernays soon had more corporate clients than he could handle. Global corporations fell all over themselves courting the new Image Makers. There were dozens of goods and services and ideas to be sold to a susceptible public. Over the years, these players have had the money to make their images happen. A few examples:

 

Philip Morris

Allstate

Coors

Shell Oil

Boeing

General Mills

Pfizer

Monsanto

Ciba Geigy

DuPont

Standard Oil

General Motors

Goodyear

Union Carbide

Eli Lilly

Chlorox

Protector & Gamble

Dow Chemical

 

The Players

Though world-famous within the PR industry, the companies have names we don't know, and for good reason.

 

The best PR goes unnoticed

 

For decades they have created the opinions that most of us were raised with, on virtually any issue which has the remotest commercial value, including:

 

 

pharmaceutical drugs

vaccines

medicine as a profession

alternative medicine

fluoridation of city water

chlorine

household cleaning products

tobacco

dioxin

global warming

leaded gasoline

cancer research and treatment

pollution of the oceans

forests and lumber

images of celebrities, including damage control

crisis and disaster management

genetically modified foods

aspartame

food additives; processed foods

dental amalgams

 

 

Lesson #1

Bernays learned early on that the most effective way to create credibility for a product or an image was by "independent third-party" endorsement.

For example, if General Motors were to come out and say that global warming is a hoax thought up by some liberal tree-huggers, people would suspect GM's motives, since GM's fortune is made by selling automobiles.

If however some independent research institute with a very credible sounding name like the Global Climate Coalition comes out with a scientific report that says global warming is really a fiction, people begin to get confused and to have doubts about the original issue.

So that's exactly what Bernays did. With a policy inspired by genius, he set up "more institutes and foundations than Rockefeller and Carnegie combined." (Stauber p 45)

Quietly financed by the industries whose products were being evaluated, these "independent" research agencies would churn out "scientific" studies and press materials that could create any image their handlers wanted. Such front groups are given high-sounding names like:

Temperature Research Foundation

Manhattan Institute

International Food Information Council

Center for Produce Quality

Consumer Alert

Tobacco Institute Research Council

The Advancement of Sound Science Coalition

Cato Institute

Air Hygiene Foundation

American Council on Science and Health

Industrial Health Federation

Global Climate Coalition

International Food Information Council

Alliance for Better Foods

Sound pretty legit, don't they?

 

Canned News Releases

As Stauber explains, these organizations and hundreds of others like them are front groups whose sole mission is to advance the image of the global corporations who fund them, like those listed on page 2 above.

This is accomplished in part by an endless stream of 'press releases' announcing "breakthrough" research to every radio station and newspaper in the country. (Robbins) Many of these canned reports read like straight news, and indeed are purposely molded in the news format.

This saves journalists the trouble of researching the subjects on their own, especially on topics about which they know very little. Entire sections of the release or in the case of video news releases, the whole thing can be just lifted intact, with no editing, given the byline of the reporter or newspaper or TV station - and voilá! Instant news - copy and paste. Written by corporate PR firms.

Does this really happen? Every single day, since the 1920s when the idea of the News Release was first invented by Ivy Lee. (Stauber, p 22) Sometimes as many as half the stories appearing in an issue of the Wall St. Journal are based solely on such PR press releases. (22)

These types of stories are mixed right in with legitimately researched stories. Unless you have done the research yourself, you won't be able to tell the difference.

 

The Language Of Spin

As 1920s spin pioneers like Ivy Lee and Edward Bernays gained more experience, they began to formulate rules and guidelines for creating public opinion. They learned quickly that mob psychology must focus on emotion, not facts. Since the mob is incapable of rational thought, motivation must be based not on logic but on presentation.

Here are some of the axioms of the new science of PR:

  • technology is a religion unto itself
  • if people are incapable of rational thought, real democracy is dangerous
  • important decisions should be left to experts
  • when reframing issues, stay away from substance; create images
  • never state a clearly demonstrable lie

Words are very carefully chosen for their emotional impact. Here's an example. A front group called the International Food Information Council handles the public's natural aversion to genetically modified foods.

Trigger words are repeated all through the text. Now in the case of GM foods, the public is instinctively afraid of these experimental new creations which have suddenly popped up on our grocery shelves which are said to have DNA alterations. The IFIC wants to reassure the public of the safety of GM foods, so it avoids words like:

 

Frankenfoods

Hitler

biotech

chemical

DNA

experiments

manipulate

 

 

money

 

safety

scientists

radiation roulette

gene-splicing

gene gun

random

 

Instead, good PR for GM foods contains words like:

hybrids

natural order

beauty

choice

bounty

cross-breeding

diversity

earth

farmer

organic

wholesome

 

It's basic Freudian/Tony Robbins word association. The fact that GM foods are not hybrids that have been subjected to the slow and careful scientific methods of real crossbreeding doesn't really matter. This is pseudoscience, not science. Form is everything and substance just a passing myth. (Trevanian)

Who do you think funds the International Food Information Council? Take a wild guess. Right - Monsanto, DuPont, Frito-Lay, Coca Cola, Nutrasweet - those in a position to make fortunes from GM foods.(Stauber,p20)

 

Characteristics Of Good Propaganda

As the science of mass control evolved, PR firms developed further guidelines for effective copy. Here are some of the gems:

  • dehumanize the attacked party by labeling and name calling
  • speak in glittering generalities using emotionally positive words
  • when covering something up, don't use plain English; stall for time; distract
  • get endorsements from celebrities, churches, sports figures, street people - anyone who has no expertise in the subject at hand
  • the 'plain folks' ruse: us billionaires are just like you
  • when minimizing outrage, don't say anything memorable, point out the benefits of what just happened, and avoid moral issues

Keep this list. Start watching for these techniques. Not hard to find - look at today's paper or tonight's TV news. See what they're doing; these guys are good!

 

Science For Hire

PR firms have become very sophisticated in the preparation of news releases. They have learned how to attach the names of famous scientists to research that those scientists have not even looked at. (Stauber, p 201)

This is a common occurrence. In this way the editors of newspapers and TV news shows are often not even aware that an individual release is a total PR fabrication. Or at least they have "deniability," right?

Stauber tells the amazing story of how leaded gas came into the picture. In 1922, General Motors discovered that adding lead to gasoline gave cars more horsepower.

When there was some concern about safety, GM paid the Bureau of Mines to do some fake "testing" and publish spurious research that 'proved' that inhalation of lead was harmless. Enter Charles Kettering.

Founder of the world famous Sloan-Kettering Memorial Institute for medical research, Charles Kettering also happened to be an executive with General Motors.

By some strange coincidence, we soon have the Sloan Kettering institute issuing reports stating that lead occurs naturally in the body and that the body has a way of eliminating low level exposure.

Through its association with The Industrial Hygiene Foundation and PR giant Hill & Knowlton, Sloane Kettering opposed all anti-lead research for years. (Stauber p 92). Without organized scientific opposition, for the next 60 years more and more gasoline became leaded, until by the 1970s, 90% of our gasoline was leaded.

Finally it became too obvious to hide that lead was a major carcinogen, and leaded gas was phased out in the late 1980s. But during those 60 years, it is estimated that some 30 million tons of lead were released in vapor form onto American streets and highways. 30 million tons.

That is PR, my friends.

 

Junk Science

In 1993, a guy named Peter Huber wrote a new book and coined a new term. The book was Galileo's Revenge and the term was junk science. Huber's shallow thesis was that real science supports technology, industry, and progress.

Anything else was suddenly junk science. Not surprisingly, Stauber explains how Huber's book was supported by the industry-backed Manhattan Institute.

 

Huber's book was generally dismissed not only because it was so poorly written, but because it failed to realize one fact: true scientific research begins with no conclusions. Real scientists are seeking the truth becausethey do not yet know what the truth is.

True scientific method goes like this:

1.     Form a hypothesis.

2.     Make predictions for that hypothesis.

3.     Test the predictions.

4.     Reject or revise the hypothesis based on the research findings.

Boston University scientist Dr. David Ozonoff explains that ideas in science are themselves like "living organisms, that must be nourished, supported, and cultivated with resources for making them grow and flourish." (Stauber p 205)

Great ideas that don't get this financial support because the commercial angles are not immediately obvious - these ideas wither and die.

Another way you can often distinguish real science from phony is that real science points out flaws in its own research. Phony science pretends there were no flaws.

 

The Real Junk Science

Contrast this with modern PR and its constant pretensions to sound science. Corporate sponsored research, whether it's in the area of drugs, GM foods, or chemistry begins with predetermined conclusions.

It is the job of the scientists then to prove that these conclusions are true, because of the economic upside that proof will bring to the industries paying for that research. This invidious approach to science has shifted the entire focus of research in America during the past 50 years, as any true scientist is likely to admit.

Stauber documents the increasing amount of corporate sponsorship of university research. (206) This has nothing to do with the pursuit of knowledge. Scientists lament that research has become just another commodity, something bought and sold. (Crossen)

 

The Two Main Targets Of "Sound Science"

It is shocking when Stauber shows how the vast majority of corporate PR today opposes any research that seeks to protect:

1.     public health

2.     the environment

It's a funny thing that most of the time when we see the phrase "junk science," it is in a context of defending something that may threaten either the environment or our health.

This makes sense when one realizes that money changes hands only by selling the illusion of health and the illusion of environmental protection. True public health and real preservation of the earth's environment have very low market value.

Stauber thinks it ironic that industry's self-proclaimed debunkers of junk science are usually non-scientists themselves. (255) Here again they can do this because the issue is not science, but the creation of images.

 

The Language Of Attack

When PR firms attack legitimate environmental groups and alternative medicine people, they again use special words which will carry an emotional punch:

outraged

junk science

sound science

scaremongering

responsible

phobia

hoax

alarmist

hysteria

sensible

 

 

The next time you are reading a newspaper article about an environmental or health issue, note how the author shows bias by using the above terms. This is the result of very specialized training.

Another standard PR tactic is to use the rhetoric of the environmentalists themselves to defend a dangerous and untested product that poses an actual threat to the environment. This we see constantly in the PR smokescreen that surrounds genetically modified foods.

They talk about how GM foods are necessary to grow more food and to end world hunger, when the reality is that GM foods actually have lower yields per acre than natural crops. (Stauber, p173)

The grand design sort of comes into focus once you realize that almost all GM foods have been created by the sellers of herbicides and pesticides so that those plants can withstand greater amounts of herbicides and pesticides. (The Magic Bean)

Kill Your TV?

Hope this chapter has given you a hint to start reading newspaper and magazine articles a little differently, and perhaps start watching TV news shows with a slightly different attitude than you had before.

 

Always ask, what are they selling here, and who's selling it? And if you actually follow up on Stauber & Rampton's book and check out some of the other resources below, you might even glimpse the possibility of advancing your life one quantum simply by ceasing to subject your brain to mass media.

That's right - no more newspapers, no more TV news, no more Time magazine or Newsweek. You could actually do that. Just think what you could do with the extra time alone.

Really feel like you need to "relax" or find out "what's going on in the world" for a few hours every day? Think about the news of the past couple of years for a minute.

Do you really suppose the major stories that have dominated headlines and TV news have been "what is going on in the world?" Do you actually think there's been nothing going on besides the contrived tech slump, the contrived power shortages, the re-filtered accounts of foreign violence and disaster, and all the other non-stories that the puppeteers dangle before us every day?

What about when they get a big one, like with OJ or Monica Lewinsky or the Oklahoma City bombing? Do we really need to know all that detail, day after day? Do we have any way of verifying all that detail, even if we wanted to? What is the purpose of news?

To inform the public? Hardly. The sole purpose of news is to keep the public in a state of fear and uncertainty so that they'll watch again tomorrow and be subjected to the same advertising.

 

Oversimplification? Of course. That's the mark of mass media mastery - simplicity. The invisible hand. Like Edward Bernays said, the people must be controlled without them knowing it.

Consider this: what was really going on in the world all that time they were distracting us with all that stupid vexatious daily smokescreen? Fear and uncertainty -- that's what keeps people coming back for more.

If this seems like a radical outlook, let's take it one step further: What would you lose from your life if you stopped watching TV and stopped reading newspapers altogether?

Would your life really suffer any financial, moral, intellectual or academic loss from such a decision?

Do you really need to have your family continually absorbing the illiterate, amoral, phony, uncultivated, desperately brainless values of the people featured in the average nightly TV program? Are these fake, programmed robots "normal"?

Do you need to have your life values constantly spoon-fed to you?

Are those shows really amusing, or just a necessary distraction to keep you from looking at reality, or trying to figure things out yourself by doing a little independent reading?

Name one example of how your life is improved by watching TV news and reading the evening paper. 

What measurable gain is there for you?

 

Planet of the Apes?

There's no question that as a nation, we're getting dumber year by year. Look at the presidents we've been choosing lately. Ever notice the blatant grammar mistakes so ubiquitous in today's advertising and billboards?

Literacy is marginal in most American secondary schools. Three fourths of California high school seniors can't read well enough to pass their exit exams. (SJ Mercury 20 Jul 01)

If you think other parts of the country are smarter, try this one: hand any high school senior a book by Dumas or Jane Austen, and ask them to open to any random page and just read one paragraph out loud. Go ahead, do it. S.A.T. scales are arbitrarily shifted lower and lower to disguise how dumb kids are getting year by year.

At least 10% have documented "learning disabilities," which are reinforced and rewarded by special treatment and special drugs. Ever hear of anyone failing a grade any more?

Or observe the intellectual level of the average movie which these days may only last one or two weeks in the theatres, especially if it has insufficient explosions, chase scenes, silicone, fake martial arts, and cretinesque dialogue.

Radio? Consider the low mental qualifications of the falsely animated corporate simians they hire as DJs -- they're only allowed to have 50 thoughts, which they just repeat at random.

And at what point did popular music cease to require the study of any musical instrument or theory whatsoever, not to mention lyric? Perhaps we just don't understand this emerging art form, right? The Darwinism of MTV - apes descended from man.

Ever notice how most articles in any of the glossy magazines sound like they were all written by the same guy? And this guy just graduated from junior college? And yet he has all the correct opinions on social issues, no original ideas, and that shallow, smug, homogenized corporate omniscience, which enables him to assure us that everything is going to be fine...

 

All this is great news for the PR industry - makes their job that much easier. Not only are very few paying attention to the process of conditioning; fewer are capable of understanding it even if somebody explained it to them.

 

Tea In the Cafeteria

Let's say you're in a crowded cafeteria, and you buy a cup of tea. And as you're about to sit down you see your friend way across the room. So you put the tea down and walk across the room and talk to your friend for a few minutes.

Now, coming back to your tea, are you just going to pick it up and drink it? Remember, this is a crowded place and you've just left your tea unattended for several minutes. You've given anybody in that room access to your tea.

Why should your mind be any different? Turning on the TV, or uncritically absorbing mass publications every day - these activities allow access to our minds by "just anyone" - anyone who has an agenda, anyone with the resources to create a public image via popular media.

As we've seen above, just because we read something or see something on TV doesn't mean it's true or worth knowing. So the idea here is, like the tea, the mind is also worth guarding, worth limiting access to it.

This is the only life we get. Time is our total capital. Why waste it allowing our potential, our personality, our values to be shaped, crafted, and limited according to the whims of the mass panderers?

There are many important issues that are crucial to our physical, mental, and spiritual well-being. If it's an issue where money is involved, objective data won't be so easy to obtain. Remember, if everybody knows something, that image has been bought and paid for.

Real knowledge takes a little effort, a little excavation down at least one level below what "everybody knows."  

Our Comment:

 

Dr. O’Shea’s comments help explain the details of how the media deceives you through the manipulation of PR by the large corporations who do not have your best interest at heart.

Together, we can change the entire system. By passing this article on to as many of your friends and relatives as possible, you can play a major role in helping to lift the veil of deceit that these corporations try to hide the truth with. Together, we can lift the veil of deceit for everyone and help save hundreds of thousands of people from agonizing, premature death and disability.

 

References

  • Stauber & Rampton, Trust Us, We're Experts, Tarcher/Putnam, 2001.
  • Ewen, Stuart, PR!: A Social History of Spin, 1996, ISBN: 0-465-06168-0, Published by Basic Books, A Division of Harper Collins. Tye, Larry, The Father of Spin: Edward L. Bernays and the Birth of Public Relations, Crown Publishers, Inc. 2001.
  • King, R., “Medical journals rarely disclose researchers' ties,” Wall St. Journal, 2 Feb 99.
  • Engler, R et al. “Misrepresentation and Responsibility in Medical Research,” New England Journal of Medicine, v 317 p 1383, 26   Nov 1987.
  • Black, D. PhD, Health At the Crossroads Tapestry, 1988. Revanian Shibumi, 1983. Crossen, C., Tainted Truth: The Manipulation of Fact in America, 1996.
  • Robbins, J., Reclaiming Our Health, Kramer, 1996.
  • O'Shea T., The Magic Bean 2000, www.thedoctorwithin.com.
  • “Inhibitory effect of conjugated dienoic derivatives of linoleic acid and beta-carotene on the in vitro growth of human cancer cells,” Cancer Lett. (Ireland), 1992, 63/2 (125-133).
  • Inhibition of Listeria monocytogenes by fatty acids and monoglycerides Appl. Environ. Microbiol. (USA), 1992, 58/2 (624-629)

Mycoplasma

Common Mycoplasmas - Now Weaponized, Pathogenic & Deadly


By Donald W. Scott, MA, MSc © 2001; 12-30-1

Mycoplasma - The Linking Pathogen in Neuro-systemic Diseases


Several strains of mycoplasma have been "engineered" to become more dangerous. They are now
being blamed for AIDS, cancer, CFS, MS, CJD and other neuro-systemic diseases.


Extracted from Nexus Magazine, Volume 8, Number 5 (August-September, 2001)
www.nexusmagazine.com

PATHOGENIC MYCOPLASMA


A Common Disease Agent Weaponized

There are 200 species of Mycoplasma. Most are innocuous and do no harm; only four or five are pathogenic.
Mycoplasma fermentans (incognitos strain) probably comes from the nucleus of the Brucella bacterium. This disease agent is not a bacterium and not a virus; it is a mutated form of the Brucella bacterium, combined with a visna virus, from which the mycoplasma is extracted.


The pathogenic Mycoplasma used to be very innocuous, but biological warfare research conducted between 1942 and the present time has resulted in the creation of more deadly and infectious forms of Mycoplasma. Researchers extracted this mycoplasma from the Brucella bacterium and actually reduced the disease to a crystalline form. They "weaponized" it and tested it on an unsuspecting public in North America.


Dr. Maurice Hilleman, chief virologist for the pharmaceutical company Merck, Sharp & Dohme, stated that this disease agent is now carried by everybody in North America and possibly most people throughout the world.


Despite reporting flaws, there has clearly been an increased incidence of all the neuro/systemic degenerative diseases since World War II and especially since the 1970s with the arrival of previously unheard-of diseases like chronic fatigue syndrome and AIDS.


According to Dr. Shyh-Ching Lo, senior researcher at The Armed Forces Institute of Pathology and one of America's top mycoplasma researchers, this disease agent causes many illnesses including AIDS, cancer, chronic fatigue syndrome, Crohn's colitis, Type I diabetes, multiple sclerosis, Parkinson's disease, Wegener's disease and collagenvascular diseases such as rheumatoid arthritis and Alzheimer's.


Dr. Charles Engel, who is with the US National Institutes of Health, Bethesda, Maryland, stated the following at an NIH meeting on February 7, 2000: "I am now of the view that the probable cause of chronic fatigue syndrome and fibromyalgia is the mycoplasma..."


I have all the official documents to prove that mycoplasma is the disease agent in chronic fatigue syndrome/
fibromyalgia as well as in AIDS, multiple sclerosis and many other illnesses. Of these, 80% are US or Canadian official government documents, and 20% are articles from peer-reviewed journals such as the Journal of the American Medical Association, New England Journal of Medicine and the Canadian Medical Association Journal. The journal articles and government documents complement each other.

How the Mycoplasma Works
The mycoplasma acts by entering into the individual cells of the body, depending upon your genetic predisposition. You may develop neurological diseases if the pathogen destroys certain cells in your brain, or you may develop Crohn's colitis if the pathogen invades and destroys cells in the lower bowel.

Once the mycoplasma gets into the cell, it can lie there doing nothing sometimes for 10, 20 or 30 years, but if a trauma occurs like an accident or a vaccination that doesn't take, the mycoplasma can become triggered.


Because it is only the DNA particle of the bacterium, it doesn't have any organelles to process its own nutrients, so it grows by uptaking pre-formed sterols from its host cell and it literally kills the cell; the cell ruptures and what is left gets dumped into the bloodstream.


CREATION OF THE MYCOPLASMA
A Laboratory-Made Disease Agent


Many doctors don't know about this mycoplasma disease agent because it was developed by the US military in biological warfare experimentation and it was not made public. This pathogen was patented by the United States military and Dr Shyh-Ching Lo. I have a copy of the documented patent from the US Patent Office.(1)


All the countries at war were experimenting with biological weapons. In 1942, the governments of the United States, Canada and Britain entered into a secret agreement to create two types of biological weapons (one that would kill, and one that was disabling) for use in the war against Germany and Japan, who were also developing biological weapons. While they researched a number of disease pathogens, they primarily focused on the Brucella bacterium and began to weaponize it.


From its inception, the bio-warfare program was characterized by continuing in-depth review and participation by the most eminent scientists, medical consultants, industrial experts and government officials, and it was classified Top Secret.


The US Public Health Service also closely followed the progress of biological warfare research and development from the very start of the program, and the Centers for Disease Control (CDC) and the National Institutes of Health (NIH) in the United States were working with the military in weaponizing these diseases. These are diseases that have existed for thousands of years, but they have been weaponized—which means they've been made more contagious and more effective. And they are spreading.


The Special Virus Cancer Program, created by the CIA and NIH to develop a deadly pathogen for which humanity had no natural immunity (AIDS), was disguised as a war on cancer but was actually part of MKNAOMI.(2)


Many members of the Senate and House of Representatives do not know what has been going on. For example, the US Senate Committee on Government Reform had searched the archives in Washington and other places for the document titled "The Special Virus Cancer Program: Progress Report No. 8", and couldn't find it.


Somehow they heard I had it, called me and asked me to mail it to them. Imagine: a retired school teacher being called by the United States Senate and asked for one of their secret documents! The US Senate, through the Government Reform Committee, is trying to stop this type of government research.


Crystalline Brucella
The title page of a genuine US Senate Study, declassified on February 24, 1977, shows that George Merck, of the pharmaceutical company, Merck, Sharp & Dohme (which now makes cures for diseases that at one time it created), reported in 1946 to the US Secretary of War that his researchers had managed "for the first time" to "isolate the disease agent in crystalline form".(3)


They had produced a crystalline bacterial toxin extracted from the Brucella bacterium. The bacterial toxin could be removed in crystalline form and stored, transported and deployed without deteriorating. It could be delivered by other vectors such as insects, aerosol or the food chain (in nature it is delivered within the bacterium). But the factor that is working in the Brucella is the mycoplasma.

Brucella is a disease agent that doesn't kill people; it disables them. But, according to Dr Donald MacArthur of the Pentagon, appearing before a congressional committee in 1969,(4) researchers found that if they had mycoplasma at a certain strength -- actually, 10 to the 10th power (10-10) -- it would develop into AIDS, and the person would die from it within a reasonable period of time because it could bypass the natural human defenses. If the strength was 10 to the 8th, the person would manifest with chronic fatigue syndrome or fibromyalgia. If it was 10 to the 7th, they would present as wasting; they wouldn't die and they wouldn't be disabled, but they would not be very interested in life; they would waste away.


One salt shaker of the pure brucella disease agent in a crystalline form could sicken the entire population of Canada. It is absolutely deadly, not so much in terms of killing the body but disabling it.


Because the crystalline disease agent goes into solution in the blood, ordinary blood and tissue tests will not reveal its presence. The mycoplasma will only crystallize at 8.1 pH, and the blood has a pH of 7.4 pH. So the doctor thinks your complaint is "all in your head".


Crystalline Brucella and Multiple Sclerosis
In 1998 in Rochester, New York, I met a former military man, PFC Donald Bentley, who gave me a document and told me: "I was in the US Army, and I was trained in bacteriological warfare. We were handling a bomb filled with brucellosis, only it wasn't brucellosis; it was a Brucella toxin in crystalline form. We were spraying it on the Chinese and North Koreans."


He showed me his certificate listing his training in chemical, biological and radiological warfare. Then he showed me 16 pages of documents given to him by the US military when he was discharged from the service. They linked brucellosis with multiple sclerosis, and stated in one section: "Veterans with multiple sclerosis, a kind of creeping paralysis developing to a degree of 10% or more disability within two years after separation from active service, may be presumed to be service-connected for disability compensation.


Compensation is payable to eligible veterans whose disabilities are due to service." In other words: "If you become ill with multiple sclerosis, it is because you were handling this Brucella, and we will give you a pension. Don't go raising any fuss about it." In these documents, the government of the United States revealed evidence of the cause of multiple sclerosis, but they didn't make it known to the public--or to your doctor.


In a 1949 report, Drs. Kyger and Haden suggested "the possibility that multiple sclerosis might be a central nervous system manifestation of chronic brucellosis". Testing approximately 113 MS patients, they found that almost 95% also tested positive for Brucella.(5) We have a document from a medical journal, which concludes that one out of 500 people who had brucellosis would develop what they call neuro-brucellosis; in other words, brucellosis in the brain, where the Brucella settles in the lateral ventricles -- where the disease multiple sclerosis is basically located.(6)


Contamination of Camp Detrick Lab Workers
A 1948 New England Journal of Medicine report titled "Acute Brucellosis Among Laboratory Workers" shows us how actively dangerous this agent is.(7) The laboratory workers were from Camp Detrick, Frederick, Maryland, where they were developing biological weapons. Even though these workers had been vaccinated, wore rubberized suits and masks and worked through holes in the compartment, many of them came down with this awful disease because it is so absolutely and terrifyingly infectious.


The article was written by Lt. Calderone Howell, Marine Corps, Captain Edward Miller, Marine Corps, Lt. Emily Kelly, United States Naval Reserve, and Captain Henry Bookman. They were all military personnel engaged in making the disease agent Brucella into a more effective biological weapon.


COVERT TESTING OF MYCOPLASMA
Testing the Dispersal Methods


Documented evidence proves that the biological weapons they were developing were tested on the public in various communities without their knowledge or consent.

The government knew that crystalline Brucella would cause disease in humans. Now they needed to determine how it would spread and the best way to disperse it. They tested dispersal methods for Brucella suis and Brucella melitensis at Dugway Proving Ground, Utah, in June and September 1952. Probably, 100% of us now are infected with Brucella suis and Brucella melitensis.(8)


Another government document recommended the genesis of open-air vulnerability tests and covert research and development programs to be conducted by the Army and supported by the Central Intelligence Agency.


At that time, the Government of Canada was asked by the U.S. Government to cooperate in testing weaponized Brucella, and Canada cooperated fully with the United States. The US Government wanted to determine whether mosquitoes would carry the disease and also if the air would carry it. A government report stated that "open-air testing of infectious biological agents is considered essential to an ultimate understanding of biological warfare potentialities because of the many unknown factors affecting the degradation of micro-organisms in the atmosphere".(9)


Testing via Mosquito Vector in Punta Gorda, Florida
The Government of Canada had established the Dominion Parasite Laboratory in Belleville, Ontario, where it raised 100 million mosquitoes a month. These were shipped to Queen's University and certain other facilities to be infected with this crystalline disease agent. The mosquitoes were then let loose in certain communities in the middle of the night, so that the researchers could determine how many people would become ill with chronic fatigue syndrome or fibromyalgia, which was the first disease to show.


One of the communities they tested it on was the St Lawrence Seaway valley, all the way from Kingston to Cornwall, in 1984. They let out hundreds of millions of infected mosquitoes. Over 700 people in the next four or five weeks developed myalgic encephalomyelitis, or chronic fatigue syndrome.


COVERT TESTING OF OTHER DISEASE AGENTS
Mad Cow Disease/Kuru/CJD in the Fore Tribe


Before and during World War II, at the infamous Camp 731 in Manchuria, the Japanese military contaminated prisoners of war with certain disease agents. They also established a research camp in New Guinea in 1942. There they experimented upon the Fore Indian tribe and innoculated them with a minced-up version of the brains of diseased sheep containing the visna virus which causes "mad cow disease" or Creutzfeldt & Jakob disease.


About five or six years later, after the Japanese had been driven out, the poor people of the Fore tribe developed what they called kuru, which was their word for "wasting", and they began to shake, lose their appetites and die. The autopsies revealed that their brains had literally turned to mush. They had contracted "mad cow disease" from the Japanese experiments.


When World War II ended, Dr. Ishii Shiro--the medical doctor who was commissioned as a General in the Japanese Army so he could take command of Japan's biological warfare development, testing and deployment—was captured. He was given the choice of a job with the United States Army or execution as a war criminal. Not surprisingly, Dr. Ishii Shiro chose to work with the US military to demonstrate how the Japanese had created mad cow disease in the Fore Indian tribe.


In 1957, when the disease was beginning to blossom in full among the Fore people, Dr. Carleton Gajdusek of the US National Institutes of Health headed to New Guinea to determine how the minced-up brains of the visna-infected sheep affected them. He spent a couple of years there, studying the Fore people, and wrote an extensive report. He won the Nobel Prize for "discovering" kuru disease in the Fore tribe.


Testing Carcinogens over Winnipeg, Manitoba
In 1953, the US Government asked the Canadian Government if it could test a chemical over the city of Winnipeg. It was a big city with 500,000 people, miles from anywhere. The American military sprayed this carcinogenic chemical in a 1,000%-attenuated form, which they said would be so watered down that nobody would get very sick; however, if people came to clinics with a sniffle, a sore throat or ringing in their ears, the researchers would be able to determine what percentage would have developed cancer if the chemical had been used at full strength.

We located evidence that the Americans had indeed tested this carcinogenic chemical -- zinc cadmium sulphide -- over Winnipeg in 1953. We wrote to the Government of Canada, explaining that we had solid evidence of the spraying and asking that we be informed as to how high up in the government the request for permission to spray had gone. We did not receive a reply.


Shortly after, the Pentagon held a press conference on May 14, 1997, where they admitted what they had done. Robert Russo, writing for the Toronto Star (11) from Washington, DC, reported the Pentagon's admission that in 1953 it had obtained permission from the Canadian Government to fly over the city of Winnipeg and spray out this chemical--which sifted down on kids going to school, housewives hanging out their laundry and people going to work. U.S. Army planes and trucks released the chemical 36 times between July and August 1953. The Pentagon got its statistics, which indicated that if the chemical released had been full strength, approximately a third of the population of Winnipeg would have developed cancers over the next five years.


One professor, Dr. Hugh Fudenberg, MD, twice nominated for the Nobel Prize, wrote a magazine article stating that the Pentagon came clean on this because two researchers in Sudbury, Ontario -- Don Scott and his son, Bill Scott -- had been revealing this to the public. However, the legwork was done by other researchers!


The US Army actually conducted a series of simulated germ warfare tests over Winnipeg. The Pentagon lied about the tests to the mayor, saying that they were testing a chemical fog over the city, which would protect Winnipeg in the event of a nuclear attack.


A report commissioned by US Congress, chaired by Dr. Rogene Henderson, lists 32 American towns and cities used as test sites as well.


Brucella Mycoplasma And Disease
AIDS
The AIDS pathogen was created out of a Brucella bacterium mutated with a visna virus; then the toxin was removed as a DNA particle called a mycoplasma. They used the same mycoplasma to develop disabling diseases like MS, Crohn's colitis, Lyme disease, etc.


In the previously mentioned US congressional document of a meeting held on June 9, 1969,(12) the Pentagon delivered a report to Congress about biological weapons. The Pentagon stated: "We are continuing to develop disabling weapons." Dr. MacArthur, who was in charge of the research, said: "We are developing a new lethal weapon, a synthetic biological agent that does not naturally exist, and for which no natural immunity could have been acquired."


Think about it. If you have a deficiency of acquired immunity, you have an acquired immunity deficiency. Plain as that. AIDS.


In laboratories throughout the United States and in a certain number in Canada including at the University of Alberta, the US Government provided the leadership for the development of AIDS for the purpose of population control. After the scientists had perfected it, the government sent medical teams from the Centers for Disease Control--under the direction of Dr. Donald A. Henderson, their investigator into the 1957 chronic fatigue epidemic in Punta Gorda--during 1969 to 1971 to Africa and some countries such as India, Nepal and Pakistan where they thought the population was becoming too large(13) They gave them all a free vaccination against smallpox; but five years after receiving this vaccination, 60% of those innoculated were suffering from AIDS. They tried to blame it on a monkey, which is nonsense.


A professor at the University of Arkansas made the claim that while studying the tissues of a dead chimpanzee she found traces of HIV. The chimpanzee that she had tested was born in the United States 23 years earlier. It had lived its entire life in a US military laboratory where it was used as an experimental animal in the development of these diseases. When it died, its body was shipped to a storage place where it was deep-frozen and stored in case they wanted to analyze it later.

Then they decided that they didn't have enough space for it, so they said, "Anybody want this dead chimpanzee?" and this researcher from Arkansas said: "Yes. Send it down to the University of Arkansas. We are happy to get anything that we can get." They shipped it down and she found HIV in it. That virus was acquired by that chimpanzee in the laboratories where it was tested.(14)


Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis
Chronic fatigue syndrome is more accurately called myalgic encephalomyelitis. The chronic fatigue syndrome nomenclature was given by the US National Institutes of Health because it wanted to downgrade and belittle the disease.


An MRI scan of the brain of a teenage girl with chronic fatigue syndrome displayed a great many scars or punctate lesions in the left frontal lobe area where portions of the brain had literally dissolved and been replaced by scar tissue. This caused cognitive impairment, memory impairment, etc. And what was the cause of the scarring? The mycoplasma. So there is very concrete physical evidence of these tragic diseases, even though doctors continue to say they don't know where it comes from or what they can do about it.


Many people with chronic fatigue syndrome, myalgic encephalomyelitis and fibromyalgia who apply to the Canada Pensions Plan Review Tribunal will be turned down because they cannot prove that they are ill. During 1999, I conducted several appeals to Canada Pensions and the Workers Compensation Board (WCB, now the Workplace Safety and Insurance Board) on behalf of people who have been turned down. I provided documented evidence of these illnesses, and these people were all granted their pensions on the basis of the evidence that I provided.


In March 1999, for example, I appealed to the WCB on behalf of a lady with fibromyalgia who had been denied her pension back in 1993. The vice-chairman of the board came to Sudbury to hear the appeal, and I showed him a number of documents which proved that this lady was physically ill with fibromyalgia. It was a disease that caused physical damage, and the disease agent was a mycoplasma. The guy listened for three hours, and then he said to me: "Mr. Scott, how is it I have never heard of any of this before? I said: "We brought a top authority in this area into Sudbury to speak on this subject and not a single solitary doctor came to that presentation."


TESTING FOR MYCOPLASMA IN YOUR BODY
Polymerase Chain Reaction Test


Information is not generally available about this agent because, first of all, the mycoplasma is such a minutely small disease agent. A hundred years ago, certain medical theoreticians conceived that there must be a form of disease agent smaller than bacteria and viruses. This pathogenic organism, the mycoplasma, is so minute that normal blood and tissue tests will not reveal its presence as the source of the disease.


Your doctor may diagnose you with Alzheimer's disease, and he will say: "Golly, we don't know where Alzheimer's comes from. All we know is that your brain begins to deteriorate, cells rupture, the myelin sheath around the nerves dissolves, and so on." Or if you have chronic fatigue syndrome, the doctor will not be able to find any cause for your illness with ordinary blood and tissue tests.


This mycoplasma couldn't be detected until about 30 years ago when the polymerase chain reaction (PCR) test was developed, in which a sample of your blood is examined and damaged particles are removed and subjected to a polymerase chain reaction. This causes the DNA in the particles to break down. The particles are then placed in a nutrient, which causes the DNA to grow back into its original form. If enough of the substance is produced, the form can be recognised, so it can be determined whether Brucella or another kind of agent is behind that particular mycoplasma.


Blood Test
If you or anybody in your family has myalgic encephalomyelitis, fibromyalgia, multiple sclerosis or Alzheimer's, you can send a blood sample to Dr. Les Simpson in New Zealand for testing.

If you are ill with these diseases, your red blood cells will not be normal doughnut-shaped blood cells capable of being compressed and squeezed through the capillaries, but will swell up like cherry-filled doughnuts which cannot be compressed. The blood cells become enlarged and distended because the only way the mycoplasma can exist is by uptaking pre-formed sterols from the host cell. One of the best sources of pre-formed sterols is cholesterol, and cholesterol is what gives your blood cells flexibility. If the cholesterol is taken out by the mycoplasma, the red blood cell swells up and doesn't go through, and the person begins to feel all the aches and pains and all the damage it causes to the brain, the heart, the stomach, the feet and the whole body because blood and oxygen are cut off.


And that is why people with fibromyalgia and chronic fatigue syndrome have such a terrible time. When the blood is cut off from the brain, punctate lesions appear because those parts of the brain die. The mycoplasma will get into portions of the heart muscle, especially the left ventricle, and those cells will die. Certain people have cells in the lateral ventricles of the brain that have a genetic predisposition to admit the mycoplasma, and this causes the lateral ventricles to deteriorate and die. This leads to multiple sclerosis, which will progress until these people are totally disabled; frequently, they die prematurely. The mycoplasma will get into the lower bowel, parts of which will die, thus causing colitis. All of these diseases are caused by the degenerating properties of the mycoplasma.


In early 2000, a gentleman in Sudbury phoned me and told me he had fibromyalgia. He applied for a pension and was turned down because his doctor said it was all in his head and there was no external evidence. I gave him the proper form and a vial, and he sent his blood to Dr. Simpson to be tested. He did this with his family doctor's approval, and the results from Dr. Simpson showed that only 4% of his red blood cells were functioning normally and carrying the appropriate amount of oxygen to his poor body, whereas 83% were distended, enlarged and hardened, and wouldn't go through the capillaries without an awful lot of pressure and trouble. This is the physical evidence of the damage that is done.

ECG Test
You can also ask your doctor to give you a 24-hour Holter ECG. You know, of course, that an electrocardiogram is a measure of your heartbeat and shows what is going on in the right ventricle, the left ventricle and so on. Tests show that 100% of patients with chronic fatigue syndrome and fibromyalgia have an irregular heartbeat. At various periods during the 24 hours, the heart, instead of working happily away going "bump-BUMP, bump-BUMP", every now and again goes "buhbuhbuh-buhbuhbuhbuhbuhbuh". The T-wave (the waves are called P, Q, R, S and T) is normally a peak, and then the wave levels off and starts with the P-wave again. In chronic fatigue and fibromyalgia patients, the T-wave flattens off, or actually inverts. That means the blood in the left ventricle is not being squeezed up through the aorta and around through the body.


My client from Sudbury had this test done and, lo and behold, the results stated: "The shape of T and S-T suggests left ventricle strain pattern, although voltage and so on is normal." The doctor had no clue as to why the T-wave was not working properly. I analyzed the report of this patient who had been turned down by Canada Pensions and sent it back to them. They wrote back, saying: "It looks like we may have made a mistake. We are going to give you a hearing and you can explain this to us in more detail."


So it is not all in your imagination. There is actual physical damage to the heart. The left ventricle muscles do show scarring. That is why many people are diagnosed with a heart condition when they first develop fibromyalgia, but it's only one of several problems because the mycoplasma can do all kinds of damage.


Blood Volume Test
You can also ask your doctor for a blood volume test. Every human being requires a certain amount of blood per pound of body weight, and it has been observed that people with fibromyalgia, chronic fatigue syndrome, multiple sclerosis and other illnesses do not have the normal blood volume their body needs to function properly. Doctors aren't normally aware of this.


This test measures the amount of blood in the human body by taking out 5 cc, putting a tracer in it and then putting it back into the body. One hour later, take out 5 cc again and look for the tracer. The thicker the blood and the lower the blood volume, the more tracer you will find.

The analysis of one of my clients stated: "This patient was referred for red cell mass study. The red cell volume is 16.9 ml per kg of body weight. The normal range is 25 to 35 ml per kg. This guy has 36% less blood in his body than the body needs to function." And the doctor hadn't even known the test existed.


If you lost 36% of your blood in an accident, do you think your doctor would tell you that you are alright and should just take up line dancing and get over it? They would rush you to the nearest hospital and start transfusing you with blood. These tragic people with these awful diseases are functioning with anywhere from 7% to 50% less blood than their body needs to function.


Undoing The Damage
The body undoes the damage itself. The scarring in the brain of people with chronic fatigue and fibromyalgia will be repaired. There is cellular repair going on all the time. But the mycoplasma has moved on to the next cell.


In the early stages of a disease, doxycycline may reverse that disease process. It is one of the tetracycline antibiotics, but it is not bactericidal; it is bacteriostatic -- it stops the growth of the mycoplasma. And if the mycoplasma growth can be stopped for long enough, then the immune system takes over.


Doxycycline treatment is discussed in a paper by mycoplasma expert Professor Garth Nicholson, PhD, of the Institute for Molecular Medicine.(15) Dr. Nicholson is involved in a US$8-million mycoplasma research program funded by the US military and headed by Dr. Charles Engel of the NIH. The program is studying Gulf War veterans, 450 of them, because there is evidence to suggest that Gulf War syndrome is another illness (or set of illnesses) caused by mycoplasma.

Endnotes:

  1. "Pathogenic Mycoplasma", U.S. Patent No. 5,242,820, issued September 7, 1993. Dr. Lo is listed as the  "Inventor" and the American Registry of Pathology, Washington, DC, is listed as the "Assignee".
  2. "Special Virus Cancer Program: Progress Report No. 8", prepared by the National Cancer Institute, Viral Oncology, Etiology Area, July 1971, submitted to NIH Annual Report in May 1971 and updated July 1971.
  3. U.S. Senate, Ninety-fifth Congress, Hearings before the Subcommittee on Health and Scientific Research of the Committee on Human Resources, Biological Testing Involving Human Subjects by the Department of Defense, 1977; released as US Army Activities in the U.S. Biological Warfare Programs, Volumes One and Two, 24 February, 1977.
  4. Dr. Donald MacArthur, Pentagon, Department of Defense Appropriations for 1970, Hearings before Subcommittee of the Committee on Appropriations, House of Representatives, Ninety-First Congress, First Session, Monday June 9, 1969, pp 105-144, esp. pp. 114, 129.
  5. Kyger, E. R. and Russell L. Haden, "Brucellosis and Multiple Sclerosis", American Journal of Medical Sciences, 1949:689-693.
  6. Colmonero et al., "Complications Associated with Brucella melitensis Infection: A Study of 530 Cases", Medicine 1996;75(4).
  7. Howell, Miller, Kelly and Bookman, "Acute Brucellosis Among Laboratory Workers", New England Journal of Medicine 1948;236:741.
  8. "Special Virus Cancer Program: Progress Report No. 8", ibid., table 4, p. 135.
  9. US Senate, Hearings before the Subcommittee on Health and Scientific Research of the Committee on Human Resources, March 8 and May 23, 1977, ibid.
  10. New England Journal of Medicine, August 22, 1957, p. 362.
  11. Toronto Star, May 15, 1997.
  12. Dr Donald MacArthur, Pentagon, Department of Defense Appropriations for 1970, Hearings, Monday June 9, 1969, ibid., p.129.
  13. Henderson, Donald A., "Smallpox: Epitaph for a Killer", National Geographic, December 1978, p. 804.
  14. Blum, Deborah, The Monkey Wars, Oxford University Press, New York, 1994.
  15. Nicholson, G. L., "Doxycycline treatment and Desert Storm", JAMA 1995;273:618-619.

 


Recommended Reading:
Horowitz, Leonard, Emerging Viruses: Aids and Ebola, Tetrahedron Publishing, USA, 1996.
Johnson, Hillary, Osler's Web, Crown Publishers, New York, 1996.


Scott, Donald W. and William L. C. Scott, The Brucellosis Triangle, The Chelmsford Publishers (Box 133, Stat. B., Sudbury, Ontario P3E 4N5), Canada, 1998 (US$21.95 + $3 s&h in US).


Scott, Donald W. and William L. C. Scott, The Extremely Unfortunate Skull Valley Incident, The Chelmsford Publishers, Canada, 1996 (revised, extended edition available from mid-September 2001; US$16.00 pre-pub. price + US$3 s&h in US).


The Journal of Degenerative Diseases (Donald W. Scott, Editor), The Common Cause Medical Research Foundation (Box 133, Stat B., Sudbury, Ontario, P3E 4N5), Canada (quarterly journal; annual subscription: US$25.00 in USA, $30 foreign).


Additional Contacts:
Ms Jennie Burke, Australian Biologics, Level 6, 383 Pitt Street, Sydney NSW 2000, Australia tel +61 (0)2 9283 0807, fax +61 (0)2 9283 0910. Australian Biologics does tests for mycoplasma.


Consumer Health Organization of Canada, 1220 Sheppard Avenue East #412, Toronto, Ontario, Canada M2K 2S5, tel +1 (416) 490 0986, website www.consumerhealth.org/.


Professor Garth Nicholson, PhD, Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA, 92649-1401, USA, tel +1 (714) 903 2900.


Dr Les Simpson, Red Blood Cell Research Ltd, 31 Bath Street, Dunedin, 9001, New Zealand, tel +64 (0)3 471 8540, email rbc.research.limited@xtra.co.nz. (Note: Dr Simpson directs his study to red cell shape analysis, not the mycoplasma hypothesis.)


The Mycoplasma Registry for Gulf War Illness, S. & L. Dudley, 303 47th St, J-10 San Diego, CA 92102-5961, tel/fax +1 (619) 266 1116, fax (619) 266 1116, email mycoreg@juno.com.


About the Author:
Donald Scott, MA, MSc, is a retired high school teacher and university professor. He is also a veteran of WWII and was awarded the North Atlantic Star, the Burma Star with Clasp, the 1939&endash; 1945 Volunteer Service Medal and the Victory Medal. He is currently President of The Common Cause Medical Research Foundation, a not-for-profit organization devoted to research into neurosystemic degenerative diseases. He is also Adjunct Professor with the Institute for Molecular Medicine and he produces and
edits the Journal of Degenerative Diseases. He has extensively researched neuro-systemic degenerative diseases over the past five years and has authored many documents on the relationship between degenerative diseases and a pathogenic mycoplasma called Mycoplasma fermentans. His research is based upon solid government evidence.


Nexus Magazine, PO Box 30, Mapleton Qld 4560 Australia; editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381; www.nexusmagazine.com


Donald W. Scott, MA, MSc, President - The Common Cause Medical Research Foundation
190 Mountain Street, Suite 405 Sudbury, Ontario, Canada P3B 4G2; Tel/fax: +1 (705) 670 0180