[Fwd: Toxins added to our food! Disguised as natural flavoring, SOY protein, spices, yeast extract, textured protein]

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ot Just Another Scare: Toxin Additives in Your Food and Drink

Toxins added to our food! Disguised as natural

flavoring, spices, yeast extract, textured protein, soy protein, Etc.

 

 

- http://www.royalrife.com/blaylock.html

-

This article and more information can be found at http://www.aspartamekills.com

 

Not Just Another Scare: Toxin Additives in Your Food

and Drink

Russell L. Blaylock, M.D.

 

There are a growing number of clinicians

and basic scientists who are convinced that excitotoxins play a

critical role in the development of several neurological disorders,

including migraines, seizures, infections, abnormal neural development,

certain endocrine disorders, specific types of obesity, and especially

the neurodegenerative diseases; a group of diseases which includes:

ALS, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease,

and olivopontocerebellar degeneration.

An enormous amount of both clinical and

experimental evidence has accumulated over the past decade supporting

this basic premise. 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 tastes better. Aspartame is an artificial

sweetener.

The public must be made aware that 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 (below toxic levels) of excitotoxins are given to

animals, they experience full toxicity. 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 amino acids, that react with specialized receptors

in the brain in such a way as to lead to destruction of certain types

of brain cells. 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, is used

by the brain only in very , very small concentrations - no more than 8

to 12ug. 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 cell death.

The brain has several elaborate

mechanisms to prevent accumulation of MSG in the brain. First is the

blood-brain barrier, a system that impedes glutamate entry into the

area of the brain cells. But, this system was intended to protect the

brain against occasional elevation of glutamate of a moderate degree,

as would be found with un-processed food consumption. It was not

designed to eliminate very high concentrations of glutamate and

aspartate consumed daily, several times a day, as we see in modern

society. Several experiments have demonstrated that under such

conditions, glutamate can by-pass this barrier system and enter the

brain in toxic concentrations. In fact, there is some evidence that it

may actually be concentrated within the brain with prolonged exposures.

 

There are also several conditions under

which the blood-brain barrier (BBB) is made incompetent. Before birth,

the BBB is incompetent and will allow glutamate to enter the brain. It

may be that for a considerable period after birth the barrier may also

incompletely developed as well. Hypertension, diabetes, head trauma,

brain tumors, strokes, certain drugs, Alzheimer’s disease, vitamin and

mineral deficiencies, severe hypoglycemia, heat stroke, electromagnetic

radiation, ionizing radiation, multiple sclerosis, and certain

infections can all cause the barrier to fail. In fact, as we age the

barrier system becomes more porous, allowing excitotoxins in the blood

to enter the brain. So there are numerous instances under which

excitotoxin food additives can enter and damage the brain. Finally,

recent experiments have shown that glutamate and aspartate (as in

aspartame) can open the barrier itself. Another system used to protect

the brain against environmental excitotoxins, is a system within the

brain that binds the glutamate molecule (called the glutamate

transporter) and transports it to a special storage cell (the

astrocyte) within a fraction of a second after it is used as a

neurotransmitter. This system can be overwhelmed by high intakes of

MSG, aspartame and other food excitotoxins. It is also known that

excitotoxins themselves can cause the generation of numerous amounts of

free radicals and that during the process of lipid peroxidation

(oxidation of membrane fats) a substance is produced called

4-hydroxynonenal. This chemical inhibits the glutamate transporter,

thus allowing glutamate to accumulate in the brain.

Excitotoxins destroy neurons partly by

stimulating the generation of large numbers of free radicals. Recently,

it has been shown that this occurs not only within the brain, but also

within other tissues and organs as well (liver and red blood cells).

This could, from all available evidence, increase all sorts of

degenerative diseases such as arthritis, coronary heart disease, and

atherosclerosis,as well as induce cancer formation. Certainly, we would

not want to do something that would significantly increase free radical

production in the body. It is known that all of the neurodegenerative

disease, such as Parkinson’s disease, Alzheimer’s disease, and ALS, are

associated with free radical injury of the nervous system.

It should also be appreciated that the

effects of excitotoxin food additives generally is 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 MSG

and aspartame are probably not 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 effects. 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.

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. 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. 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. In other

words it has not been looked at. 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 a hydrolyzed vegetable protein, vegetable

protein, hydrolyzed plant protein, caseinate, yeast extract, and

natural flavoring. We know experimentally, as stated, when these

excitotoxin taste enhancers are added together they become much more

toxic. 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 of diet

food, that contain two, three or even four types of excitotoxins. We

also know that excitotoxins in a liquid form 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 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.

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. 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 high 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, based on present knowledge, is in the case

of ALS. Also, in the case of tomatoes, the plant contains several

powerful antioxidants known to block glutamate toxicity.

Hydrolyzed vegetable protein should not

be confused with hydrolyzed vegetable oil. The oil does not contain

appreciable concentration of glutamate, it is an oil. 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.

A growing list of excitotoxins is 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.

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). It

is thought that this is the protective mechanism of action 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.

Recent studies have shown that persons

affected by Alzheimer’s disease also have widespread destruction of

their retinal ganglion cells. 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 makes one very

suspicious. One could argue a common intrinsic etiology for central

nervous system neuronal damage and retinal ganglion cell damage, but

these findings are disconcerting enough to warrant further

investigations.

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 enzymes. For example, the brains of Alzheimer’s

disease patients have been found to contain high concentration of

lipolytic enzymes, which seems to indicate accelerated membrane lipid

peroxidation, again caused by free radical generation.

In the case of Parkinson’s disease, we

know that one of the early changes is the loss of glutathione from the

neurons of the striate system, especially in a nucleus called the

substantia nigra. 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. 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 oxidant 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.

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). It has also been shown that

there is dramatic accumulation of aluminum within these granules. 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.

Another early finding in Parkinson’s

disease is the reduction in complex I enzymes within the mitochondria

of this nucleus. 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. When cellular energy is

decreased, the toxic effect of excitatory amino acids increases

dramatically, by as much as 200 fold. In fact, when energy production

is very low, even normal concentrations of extracellular glutamate and

aspartate can kill neurons.

One of the terribly debilitating effects

of Parkinson’s disease is a condition called " freezing up", a state

where the muscle are literally frozen in place. There is recent

evidence that this effect is due to the unopposed firing of a special

nucleus in the brain (the subthalamic nucleus). Interestingly, this

nucleus uses glutamate for its transmitter. Neuroscientist are

exploring the use of glutamate blocking drugs to prevent this disorder.

 

And finally, there is growing evidence

that similar free radical damage, most likely triggered by toxic

concentrations of excitotoxins, causes ALS. Several studies have

demonstrated lipid peroxidation product accumulation within the spinal

cords of ALS victims. Iron accumulation has also been seen in the

spinal cords of ALS victims.

Besides the well known reactive oxygen

species, such as super oxide, hydroxyl ion, hydrogen peroxide, and

singlet oxygen, there exist a whole spectrum of reactive nitrogen

species derived from nitric oxide, the most important of which is

peroxynitrate. These free radicals can attack proteins, membrane lipids

and DNA, both nuclear and mitochondrial, which makes these radicals

very dangerous.

It is now known that glutamate acts on

its receptor via a nitric oxide mechanism.Overstimulation of the

glutamate receptor can result in accumulation of reactive nitrogen

species, resulting in the concentration of several species of dangerous

free radicals. There is growing evidence that, at least in part, this

is how excess glutamate damages nerve cells. In a multitude of studies,

a close link has been demonstrated between excitotoxity and free

radical generation. Others have shown that certain free radical

scavengers (anti-oxidants), have successfully blocked excitotoxic

destruction of neurons. For example, vitamin E is known to completely

block glutamate toxicity in vitro (in culture). Whether it will be as

efficient in vivo (in a living animal) is not known. But, it is

interesting in light of the recent observations that vitamin E slows

the course of Alzheimer’s disease, as had already been demonstrated in

the case of Parkinson’s disease. 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 anti-oxidants 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.

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 exposure to free iron.

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 nucleus of

Parkinsonian brains.

When free radicals are generated, the

first site of damage is to the cell membranes, since they are composed

of polyunsaturated fatty acid molecules known to be highly susceptible

to such attack. The process of membrane lipid oxidation is known as

lipid peroxidation and is usually initiated by the hydroxal radical. We

know that one’s diet can significantly alter this susceptibility. For

example, diets high in omega 3-polyunsaturated fatty acids (fish oils

and flax seed oils) can increase the risk of lipid peroxidation

experimentally. Contrawise, diets high in olive oil, a monounsaturtated

oil, significantly lowers lipid peroxidation risk. From the available

research.The beneficial effects of omega 3-fatty acid oils in the case

of strokes and heart attacks probably arises from the anticoagulant

effect of these oils and possibly the inhibition of release of

arachidonic acid from the cell membrane. But, olive oil has the same

antithrombosis effect and anticancer effect but also significantly

lowers lipid peroxidation.

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. Interestingly, it has recently been found that

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 can easily

increase hypothalamic levels as well. One of the earliest and most

consistent findings with exposure to MSG is damage to an area known as

the arcuate nucleus. This small hypothalamic nucleus controls a

multitude of neuroendocrine functions, as well as being intimately

connected to several other hypothalamic nuclei. It has also been

demonstrated that high concentrations of blood glutamate and aspartate

(from foods) can enter the so-called "protected brain" by seeping

through the unprotected areas, such as the hypothalamus or

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. This, naturally, would be the situation seen

when individuals consume, on a daily basis, foods high in the

excitotoxins - MSG, aspartame and 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 daily 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, ministrokes, 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. But, not only is

the adjacent brain vulnerable, but the openings act as a points of

entry, eventually exposing the entire brain to potentially toxic levels

of glutamate. Several clinicians have remarked on seeing MS patients

who 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.

Recently, it has been shown that not

only can free radicals open the blood-brain barrier, but excitotoxins

can as well. In fact, glutamate receptors have been demonstrated on the

barrier itself. 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, sort of a vicious cycle.

Relation to Cellular Energy Production

Excitotoxin damage is heavily dependent

on the energy state of the cell. Cells with a normal energy generation

systems that are efficiently producing adequate amounts of cellular

energy, 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. In fact, 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. 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 from the mitochondria of the

substantia nigra. (Part of the Electron Transport System.)

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 (Those involved in Parkinson’s and Huntington’s

diseases.) are exposed to microinjected excitotoxins there is a

dramatic, and rapid fall in energy production by these neurons.

CoEnzyme Q10 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. I would recommend for those with neurodegenerative disorders, a

combination of CoQ10, 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. 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. Phosphotidyl 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. For example, approximately one third of

Americans suffer from what is known as reactive hypoglycemia. That is,

they respond to a meal composed of either simple sugars or

carbohydrates that are quickly broken down into simple sugars (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 burn 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.

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". 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. 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. 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. 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.

Again, it should be realized that

excessive glutamate stimulation triggers a chain of events that in turn

triggers the generation of large numbers of free radical species, both

as nitrogen species and oxygen species. Once this occurs, especially

with the accumulation of the hydroxyl ion, destruction of the lipid

components of the membranes occurs, as lipid peroxidation. In addition,

these free radicals damage proteins and DNA as well. The most immediate

DNA damage is to the mitochondrial DNA, which controls protein

expression within that particular cell and its progeny. It is suspected

that at least some of the neurodegenerative diseases, Parkinson’s

disease in particular, are inherited in this way. But more importantly,

it may be that accumulated damage to the mitochondrial DNA secondary to

progressive free radical attack (somatic mitochondrial injury) is the

cause of most of the neurodegenerative diseases that are not inherited.

This would result from an impaired reserve of antioxidant

vitamins/minerals and enzymes, increased cellular stress, chronic

infection, free radical generating metals and toxins, and impaired DNA

repair enzymes.

It is estimated that the number of

oxidative free radical injuries to DNA number about 10,000 a day in

humans. Normally, these injuries are repaired by special repair

enzymes. It is known that as we age these repair enzymes decrease or

become less efficient. 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. 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 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. 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.

Eicosanoids and

Excitotoxins

It is known that one of the destructive

effects triggered by excitotoxins is the release of arachidonic acid

from the cell membrane and the initiation of the eicosanoid reactions.

Remember, glutamate primarily acts by opening the calcium pore,

allowing calcium to pour into the cell’s interior. Intracellular

calcium in high concentrations initiates the enzymatic release of

arachidonic acid from the cell membrane, where it is then attacked by

two enzymes systems, the cyclooxygenase system and the lipooxgenase

system. These in turn produce a series of compounds that can damage

cell membranes, proteins and DNA, primarily by free radical production,

but also directly by the "harmful eicosanoids."

Biochemically, we know that high

glycemic carbohydrate diets, known to stimulate the excess release of

insulin, can trigger the production of "harmful eicosanoids." We should

also recognize that simple sugars are not the only substances that can

trigger the release of insulin. One of the more powerful triggers

includes certain amino acids, including leucine, alanine, and taurine.

Glutamine, while not acting as an insulin trigger itself, markedly

potentiates insulin release by leucine. This is why, except under

certain situations, individual "free" amino acids should be avoided.

It is known that excitotoxins can also

stimulate the release of these "harmful eicosanoids." So that in the

situation of a hypoglycemic individual, they would be subjected to

production of harmful eicosanoids directly by the high insulin levels,

as well as by elevated glutamate levels. Importantly, both of these

events significantly increase free radical production and hence, lipid

peroxidation of cellular membranes. It should be remembered that diets

high in arachidonic acid, such as egg yellows, organs meats, and liver,

may be harmful to those subjected to excessive excitotoxin exposure.

And finally, in one carefully conducted

experiment, it was shown that insulin significantly increases glutamate

toxicity in cortical cell cultures and that this magnifying effect was

not due to insulin’s effect on glucose metabolism. That is, the effect

was directly related to insulin interaction with cell membranes.

Interestingly, insulin increased toxic sensitivity to other

excitotoxins as well.

The Special Role of Flavanoids

Flavonoids are diphenylpropanoids found

in all plant foods. They are known to be strong antioxidants and free

radical scavengers. There are three major flavonols - quercetin,

Kaempferol, and myricetin, and two major flavones - luteolin and

apigenin. Seventy percent of the flavonoid intake in the average diet

consist of quercetin, the main source of which is tea (49%), onions

(29%), and apples (7%). Fortunately, flavonoids are heat stable, that

is, they are not destroyed during cooking. Other important flavonoids

include catechin, leucoanthocyanidins, anthocyanins, hesperedin and

naringenin.

Most interest in the flavonoids stemmed

from their ability to inhibit tumor initiation and growth. This was

especially true of quercetin and naringenin, but also seen with

hesperetin and the isoflavone, genistein. There appears to be a strong

correlation between their anticarcinogenic potential and their ability

to squelch free radicals. But, in the case of genistein and quercetin,

it also has to do with their ability to inhibit tyrosine kinase and

phosphoinositide phosphorylase, both necessary for mammary cancer and

glioblastoma (a highly malignant brain tumor) growth and development.

As we have seen, there is a close

correlation between insulin, excitotoxins, free radicals and eicosanoid

production. Of particular interest, is the finding that most of the

flavonoids, especially quercetin, are potent and selective inhibitors

of delta-5-lipooxygenase enzyme which initiates the production of

eicosanods. Flavones are also potent and selective inhibitors of the

enzyme cyclooxygenase (COX) which is responsible for the production of

thromboxane A2, one of the "harmful eicosanoids". The COX-2 enzymes is

associated only with excitatory type neurons in the brain and appears

to play a major role in neurodegeneration.

One of the critical steps in the

production of eicosanoids is the liberation of arachidonic acid from

the cell membrane by phospholipase A2. Flavonones such as naringenin

(from grapefruits) and hesperetin (citrus fruits) produce a dose

related inhibition of phospholipase A2 (80% inhibition), thereby

inhibiting the release of arachidonic acid. The non-steroidal

anti-inflammatory drugs act similarly to block the production of

inflammatory eicosanoids.

What makes all of this especially

interesting is that recently, two major studies have found that not

only can non-steroidal anti- inflammatories slow the course of

Alzheimer’s disease, but they may prevent it as well. But, these drugs

can have significant side effects, such as GI bleeding, liver and

kidney damage. In high doses, the flavonoids have shown a similar

ability to reduce "harmful eicosanoid" production and should have the

same beneficial effect on the neurodegenerative diseases without the

side effects. Also, these compounds are powerful free radical

scavengers and would be expected to reduce excitotoxicity as well.

But, there is another beneficial effect.

There is experimental, as well as clinical evidence, that the

flavonoids can reduce capillary leakage and strengthen the blood brain

barrier. This has been shown to be true for rutin, hesperedin and some

chalcones. Rutin and hesperedin have also been shown to strengthen

capillary walls. In the form of hesperetin methyl chalcone, the

hesperedin molecule is readily soluble in water, significantly

increasing its absorbability. Black currents have the highest

concentration of hesperetin of any fresh fruit, and in a puree form, is

even more potent.

The importance of these compounds again

emphasizes the need for high intakes of fruits and vegetables in the

diet, and may explain the low incidence of many of these disorders in

strict vegetarians, since this would supply a high concentration of

flavonoids, carotenoids, vitamins, minerals, and other antioxidants to

the body. Normally, the flavonoids from fruits and vegetables are only

incompletely absorbed, so that relatively high concentrations would be

needed to attain the same therapeutic levels seen in these experiments.

Juice Plus allows us to absorb high, therapeutic concentrations of

these flavonoids by a process called cryodehydration. This process

removes the water and sugar from fruits and vegetable but retains their

flavonoids in a fully functional state. Also the process allows one to

consume large amounts of fruits and vegetables that would be impossible

with the whole plant.

Iron and Health

For decades we, especially women, have

been told that we need extra iron for health -that it builds healthy

blood. But, recent evidence indicates that iron and copper may be doing

more harm than good in most cases. It has been well demonstrated that

iron and copper are two of the most powerful generators of free

radicals. This is because they catalyze the conversion of hydrogen

peroxide into the very powerful and destructive hydroxyl radical. It is

this radical that does so much damage to membrane lipids and DNA bases

within the cell. It also plays a major role in the oxidation of

LDL-cholesterol, leading to heart attacks and strokes.

Males begin to accumulate iron shortly

after puberty and by middle age have 1000mg of stored iron in their

bodies. Women, by contrast, because of menstruation, have only 300 mg

of stored iron. But, after menopause they begin to rapidly accumulate

iron so that by middle age they have about 1500 mg of stored iron. It

is also known that the brain begins to accumulate iron with aging.

Elevated iron levels are seen with all of the neurodegenerative

diseases, such as Alzheimer’s dementia, Parkinson’s disease, and ALS.

It is thought that this iron triggers free radical production within

the areas of the brain destroyed by these diseases. For example, the

part of the brain destroyed by Parkinson’s disease, the substantia

nigra, has very high levels of free iron.

Normally, the body goes to great trouble

to make sure all iron and copper in the body is combined to a special

protein for transport and storage. But, with several of these diseases,

we see a loss of these transport and storage proteins. This is where

flavonoids come into play. We know that many of the flavonoids

(especially quercitin, rutin, hesperidin, and naringenin) are strong

chelators of iron and copper. In fact, drinking iced tea with a meal

can reduce iron absorption by as much as 87%. But, flavonoids in the

diet will not make you iron deficient.

Phosphotidyl serine and Excitotoxity

Recent clinical studies indicate that

phophotidyl serine can significantly improve the mental functioning of

a significant number of Alzheimer’s patients, especially during the

early stages of the disease. We know that the brain normally contains a

large concentration of phosphotidyl serine. Interestingly, this

compound has a chemical structure similar to L-glutamate, the main

excitatory neurotransmitter in the brain. Binding studies show that

phosphotidyl serine competes with L-glutamate for the NMDA type

glutamate receptor. What this means is that phosphotidyl serine is a

very effective protectant against glutamate toxicity. Unfortunately, it

is also very expensive.

The Many Functions of

Ascorbic Acid

The brain contains one of the highest

concentrations of ascorbic acid in the body. Most are aware of its

function in connective tissue synthesis and as a free radical

scavenger. But, ascorbic acid has other functions that make it rather

unique. Ascorbic acid in solution is a powerful reducing agent where it

undergoes rapid oxidation to form dehydroascorbic acid. Oxidation of

this compound is accelerated by high ph, temperature and some

transitional metals, such as iron and copper. The oxidized form of

ascorbic acid can promote lipid peroxidation and protein damage. This

is why it is vital that you take antioxidants together, since several,

such as vitamin E (as D- alpha-tocopherol) and alpha-lipoic acid, act

to regenerate the reduced form of the vitamin.

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. 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.

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. It also attenuates the behavioral response of

rats exposed to amphetamine, which is known to act through an

excitatory mechanism. 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.

It is known that as we age there is a

decline in brain levels of ascorbic acid. 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.

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 was

consumed faster during oxidative stress than the vitamin E. Once the

vitamin C was totally consumed, the vitamin E began 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. Recent experiments

have shown that such combinations can produce widespread destruction

within the striate areas of the brain. This is because the free iron

oxidizes the ascorbate to produce the powerful free radical

hydroxyascorbate. 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.

Conclusion

In this discussion, I tried to highlight

some of the more pertinent of the recent findings related to

excitotoxicity in general and neurodegenerative diseases specifically.

In no way is this an all inclusive discussion of this topic. There are

many areas I had to omit because of space, such as alpha-lipoic acid,

an antioxidant that holds great promise in combatting many of these

diseases. Also, I did not go into detail concerning the metabolic

stimulants, the relationship between exercise and degenerative nervous

system diseases, the protective effect of methycobalamin, and the

various disorders related to excitotoxins.

I also purposely omitted discussions of

magnesium to keep this paper short. It is my experience, that magnesium

is one of the most important neuroprotectants known. I would encourage

those who suffer from one of the excitotoxin related disorders to

avoid, as much as possible, food borne excitotoxin additives and to

utilize the substances discussed above. The fields of excitotoxin

research, in combination with research on free radicals and

eicosanoids, are growing very rapidly and new information arises daily.

Great promise exist in the field of flavonoid research as regards many

of these neurodegenerative diseases as well as in our efforts to

prevent neurodegeneration itself.

A recent study has demonstrated that

aspartame feeding to animals results in an accumulation of formaldehyde

within the cells, with evidence of significant damage to cellular

proteins and DNA. In fact, the formaldehyde accumulated with prolonged

use of aspartame. With this damning evidence, one would have to be

suicidal to continue the use of aspartame sweetened foods, drinks and

medicines. The use of foods containing excitotoxin additives is

especially harmful to the unborn and small children. By age 4 the brain

is only 80% formed. By age 8, 90% and by age 16 it is fully formed, but

still undergoing changes and rewiring (plasticity). We know that the

excitotoxins have a devastating effect on formation of the brain

(wiring of the brain) and that such exposure can cause the brain to be

"miswired." This may explain the significant, almost explosive increase

in ADD and ADHD. Glutamate feeding to pregnant animals produces a

syndrome almost identical to ADD. It has also been shown that a single

feeding of MSG after birth can increase free radicals in the

offspring’s brain that last until adolescence. Experimentally, we known

that infants are 4X more sensitive to the toxicity of excitotoxins than

are adults. And, of all the species studied, cats, dogs, primates,

chickens, guinea pigs, and rats, humans are by far the most sensitive

to glutamate toxicity. In fact, they are 5x more sensitive than rats

and 20x more sensitive than non-human primates.

I have been impressed with the dramatic

improvement in children with ADD and ADHD following abstention from

excitotoxin use. It requires care monitoring of these children. Each

time they are exposed to these substances, they literally go bonkers.

It is ludicrous, with all we know about the destructive effects of

excitotoxins, to allow our children and ourselves to continue on this

destructive path.

Index