NEURODEGENERATIVE DISEASES AND ASPARTAME

 

CHAPTER FOUR

MULTIPLE SCLEROSIS

The question begs an answer as to why only certain neurons suffer because of these enzyme deficiencies and why others are spared? The hippocampus contains one of the highest concentrations of glutamate receptors in the entire brain and is the most severely damaged in Alzheimer’s disease, whereas there are fewer glutamate sensitive neurons in other areas of the brain. However, it is the overstimulation by glutamate, aspartate, and other excitotoxins that cause the energy deficient neurons to be damaged in the first place.

Aspartame is made up of 10% methanol or wood alcohol. This deadly poison is gradually released in the small intestine when the methyl group of Aspartame encounters the enzyme chymotrypsin, a pancreatic digestive enzyme that catalyzes the hydrolysis of certain proteins in the small intestine into polypeptides and singular free form amino acids. Free methanol is created from Aspartame when it is heated above 86 degrees Fahrenheit or 30 degrees Celsius and its absorption is expedited when ingested. This will occur within a human body that has a temperature above 86 degrees Fahrenheit, or when products containing Aspartame are not refrigerated properly or used in cooking.

Once methanol has been absorbed, it breaks down into formic acid. In nature, formic acid is found in the stings and bites of many insects, including bees and ants. Formic acid is also a precursor of formaldehyde, which is a neurotoxin (DHHS, 1993; Liesivuori, 1991). The U.S. Environmental Protection Agency (EPA) assessment of methanol states that exposure of humans to methanol by inhalation or ingestion may result in visual disturbances, such as blurred or dimness of vision, leading to blindness.  Neurological damage, specifically permanent motor dysfunction, may also result. It is considered a cumulative poison due to the low rate of excretion once it is absorbed (U.S. Environmenal Protection Agency, 2000). Both formic acid and formaldehyde are neurotoxic metabolites (Osterloh & Holmes, 1995).

Low-level exposure to methanol has been shown to cause headaches, dizziness, nausea, tinnitis, gastrointestinal disturbances, weakness, vertigo, chills, memory lapses, numbness, shooting pains, behavioral disturbances, neuritis, misty vision, vision tunneling, blurring of vision, conjunctivitis, insomnia, vision loss, depression, heart problems, diseases of the heart muscle, and pancreatic inflammation. It is important to understand that extremely low-level methanol and formaldehyde exposure mimics multiple sclerosis (MS). Dr. Woodrow C. Monte wrote: "Methanol, one of the breakdown products of Aspartame, has no therapeutic properties and is considered only as a toxicant. The ingestion of two teaspoons is considered lethal in humans" (Monte, 1984, p. 44).

The chronic intake of free methanol in significant amounts account for some of the symptoms associated with neurodegenerative diseases. In 1975, Dr. Herbert S. Posner, who is associated with the National Institute of Environmental Health Sciences, wrote a review entitled, "Biohazards of Methanol in proposed New Uses" six years before the FDA approved Aspartame. He stressed the failure to recognize the delayed and irreversible effects on the nervous system of methanol at widely varying levels of exposure and at rather low levels. (Posner, 1975; Roberts, 2000). The intake of methyl alcohol from natural sources averages less than 10 mg daily; Aspartame beverages, however, contain about 55 mg methanol per liter and nearly twice as much in some carbonated orange sodas in order to preserve the taste. The Methyl ester imparts sweetness to Aspartame (Monte, 1984). Individuals who drink five liters a day therefore can be ingesting over 400 mg of methanol.

Table 2

 One (1) 12oz. can of diet soda contains close to 200 mg of Aspartame (Murray, 2005).

Phenylalanine	=	100mg	=	50%
Aspartic Acid	=	80 mg	=	40%
Methanol	=	13 mg	=	10%

The insulating envelope of myelin that surrounds the core of a nerve fiber or axon and facilitates the transmission of nerve impulses is called the myelin sheath. The loss of the myelin sheath on the nerve fibers characteristic of MS is due to the death of the oligodendroglia cells at the site of the lesions or plaques. Oligodendroglia cells are part of the supportive tissue of the nervous system or neuroglia, consisting of cells similar to but smaller than astrocytes, found in the central nervous system and associated with the formation of myelin.

 

Figure 14. Areas of damaged myelin are known as plaques. These plaques, or sites of damage, can cause MS symptoms.

 

Studies have shown that excessive exposure to excitotoxins, like Aspartame, at the site of the lesions can result in the death of these important cells (Blaylock, 2004). These excitotoxins are secreted from microglia immune cells in the central nervous system. This process not only destroys the myelin-producing cells it also breaks down the blood-brain barrier (BBB), allowing excitotoxins in the blood stream to enter the site of damage. The BBB is semi-permeable to allow some materials to cross its wall of capillaries but prevents others. In most parts of the body, the smallest blood vessels and capillaries, are lined with endothelial cells. Endothelial tissue has small spaces between each individual cell so substances can move readily between the inside and the outside of the vessel. However, in the brain, the endothelial cells fit tightly together and substances cannot pass into the bloodstream. With the BBB damaged, as in MS, these excitotoxins can freely enter the site of injury, greatly magnifying the damage (Blaylock, 2004).

A condition called benign MS is diagnosed after a person experiences one or two symptoms with complete recovery. This form of MS does not worsen with time and there is no permanent disability. Benign MS can only be identified when there is minimal disability ten to fifteen years after onset. Benign MS tends to be associated with less severe symptoms at onset. However, continued consumption of Aspartame can convert this benign condition into full-blown, clinical MS (Blaylock, 2004). Methanol is an axon poison and when combined with the toxicity of the aspartate, adds up to considerable brain toxicity. Once MS becomes full-blown, further consumption of excitotoxins can magnify the toxicity, increase the symptoms, and may lead eventually to death (Martini, 2007).

Glia cells or astrocytes form a layer around brain blood vessels and are important in the development of the BBB. Astrocytes, a sub-type of the glia cells in the brain, regulate the internal environment of the brain, especially the fluid surrounding neurons and their synapses, and provide nutrition to nerve cells. Glia have important developmental roles such as producing molecules that modify the growth of axons and dendrites. They are also active participants in the hippocampus and cerebellum in synaptic transmission. They regulate clearance of neurotransmitters from the synaptic cleft and release ATP which modulates presynaptic function (Evangelista & Bowen, 2002). The BBB has several important functions, among them are protecting the brain from foreign substances in the blood that may injure the brain, protecting the brain from hormones and neurotransmitters that exist in the rest of the body, and maintaining a constant environment for the brain.

Several areas of the BBB are weak, allowing substances to cross into the circumventricular organs in the brain somewhat freely. The brain is then able to monitor the composition of the blood as it passes through the pineal, neurohypophysis, area postrema, subfornical organ and the median eminence (Smith, 2000). In general, amino acids are carefully regulated because some also serve as neurotransmitters or transmitter precursors; without strict control of these substances, our brains would be transmitting extraneous impulses.

Chronic elevations of blood excitotoxins can seep through the normal BBB when high concentrations are maintained over a long period of time. This, naturally, would occur when individuals daily consume foods containing excitotoxins such as Aspartame. In nature, aspartate levels are not normally elevated on a daily basis. Sustained elevations of these excitotoxins are attributed to the modern diet in humans who also concentrate MSG in their blood five times higher than mice from a comparable dose, and maintain the higher blood level longer than mice (Blaylock, 1997). In fact, humans concentrate MSG in their blood to a greater degree than any other known animal, including monkeys.  And children are four times more sensitive to a given MSG dose than adults (South, 2003).

Scientists have used excitotoxins to make lesions in the brains of experimental animals because they have the ability to destroy neurons while leaving the fibers of passage alone (Winn, 1990). Recently, findings show that excitotoxins act at different sites within the central nervous system (CNS) not only destroying the neurons, but also stripping the myelin from fibers, and compromising the integrity of the BBB. Excitotoxic lesions of the lateral hypothalamus have shown to produce local demyelination, which is characteristic of MS (Brace, Latimer & Winn, 1997).

 

CHAPTER FIVE

SIEZURES

In 1987, H.A. Tilson, a neurotoxicologist at the Laboratory of Behavioral and Neurological Toxicology within the National Institute of Environmental Health Sciences in North Carolina, found phenylalanine, a major constituent of Aspartame, a possible cause for an amino acid imbalance resulting in behavioral alterations. He noted that shortly after approval for usage in humans, several reports of Aspartame-associated neurological effects were reported, including headaches, dizziness, and mood alterations (Massachusetts Medical Society, 1984). In the same year, Dr. Wurtman and Dr. Maher noted that the disproportionate elevation of brain phenylalanine concentrations after Aspartame or phenylalanine used in animal studies diminished the dopamine released from the brain (Wurtman & Maher, 1985). They attempted to compare the doses of Aspartame producing neurochemical effects in rodents and humans. Their data shows that 15-20 mg/kg administered to rodents diminishes catecholamine release, which are associated with lower seizure thresholds in genetically epilepsy-prone rats and suggested that exposure to large amounts of Aspartame may ultimately decrease brain levels of norepinephrine and adversely affect some people predisposed to seizures (Tilson, 1985).

Seizures are caused by abnormal electrical discharges from brain cells, often in the cerebral cortex. Their occurrences are not considered a distinct disease. Normally, nerve transmission in the brain occurs in an orderly way, allowing a smooth flow of electrical activity. A seizure occurs when neurons generate uncoordinated electrical discharges that spread throughout the brain. This can occur with both normal and abnormal nerve cells. However, in some cases, overactivity of excitatory neurotransmitters or underactivity of inhibitory neurotransmitters may lead to seizure activity by allowing an uncoordinated flow of electrical activity in the brain (Neurological Channel, 2007).

A seizure reflects the results of too much excitation, too little inhibition or neurons that are too sensitive to the neurotransmitters. During a seizure, certain cells begin to fire repeatedly and spread this behavior to other cells. A normal brain responds with enough inhibitory neurotransmitters to stop the spread. However, if a group of neurons "runs away," firing repeatedly, and the brain cannot inhibit them, a seizure results. Seizures are often self-limiting as the renegade neurons exhaust themselves and eventually stop firing. The period after the seizure may reflect lower than normal activity among the neurons. How and why these "renegade" neurons cause a seizures is still a matter of investigation.

Interestingly, certain areas of the brain are more likely than others to be the source of a seizure. These areas include the motor cortex, (responsible for the initiation of body movement) and the temporal lobes, which includes the hippocampus and involves memory. The reason for this probability may be that nerve cells in these areas are particularly sensitive to certain situations that can provoke abnormal electrical transmission, such as changes in brain biochemistry and communication between brain cells. These basic functions of the neurons that become altered and abnormal can produce seizures or prolonged seizures that will cause injury to the brain. Seizures that last longer than 20 to 30 minutes can permanently damage the brain’s neurons.

Recently, scientists have discovered a link between inflammation of the neurons and various disease conditions that man has been facing (Wyss-Coray & Mucke, 2002). Aspartame is an excitotoxin that creates an enormous inflammation in its repetitive action. Dr. Soffritti and his research team at The European Foundation of Oncology and Environmental Sciences "B. Ramazzini" in Bologna, Italy stated clearly in their recent study that, "inflammation was observed in both animals who were treated with Aspartame as well as in the control group" (Soffritti, 2005, p. 16). What was recently discovered was how radiation creates inflammation in the brain, which leads to Alzheimer’s. Most children who have radiation therapy to eradicate brain tumors may come through the treatment with the tumor destroyed, but will go on to develop learning and memory problems similar to those seen in Alzheimer's patients. The decline of brain cells begins many months or years after the treatment and is currently irreversible. Scientists are starting to understand why. Theo D. Palmer of the Department of Neurosurgery at Stanford University stated, "It's very sad because these children survive the cancer but later on develop cognitive problems and often end up in special education or are institutionalized" (Winstead, 2003, on-line article).

In an effort to understand why radiation to the brain causes cognitive decline, Dr. Palmer and two colleagues conducted experiments in rats and learned that inflammation caused by radiation blocks the production of new neurons in the hippocampus, which usually generates thousands of neurons every day. This region is critical for learning and creating new memories. Individuals who continue to consume Aspartame are creating the same kind of inflammation to their neurons in the hippocampus and possibly destroying their chances in the future of maintaining memory function. They found that rats exposed to radiation stopped producing neurons (Winstead, 2003). Part of the reason they stopped was inflammation, and Swedish researchers working independently made the same discovery concurrently.

"Both studies found that new neurons are very sensitive to inflammation," says Olle Lindvall, of Lund University Hospital in Sweden, who expressed surprise at how detrimental inflammation is to the production of new neurons. The studies suggest a link between inflammation and the suppression of new neurons that may contribute to cognitive decline in people with brain diseases (Winstead, 2003). If the neurons are being constantly excited by excitotoxins, then they will become inflamed and new neurons will not be generated.

Another study done on type I diabetes mellitus (TIDM) shows us that it is not an autoimmune disease, but one of a neuron inflammation to the islet cell (Dosch, 2006). Individuals who are constantly worrying about their weight will fall victim to the high pressured ads on television, internet, or magazines today about Aspartame being safe and sound for them, especially if they have diabetes.

In Canada, Scientists cured twenty-one mice with diabetes over night. It appears the nervous system and inflammation play an enormous key role in diabetes. When diabetic mice were injected with a substance to counteract the effect of malfunctioning pain neurons in the pancreas to restore proper function they became healthy virtually overnight (Dosch, 2006).

When inflammation occurs it contributes to the eventual death of insulin-producing islet cells in the pancreas. Dr. Hans Michael Dosch, an immunologist at the hospital and a leader of the studies, had concluded in a 2000 paper that there were surprising similarities between diabetes and multiple sclerosis (Dosch & Becker, 2000). He noted that there was an "enormous'' number of nerves around the beta-cells and pain neurons primarily used to signal the brain that tissue has been damaged. It turns out the nerves secrete neuropeptides that are instrumental in the proper functioning of the islets. Further study by the team, which also involved the University of Calgary and the Jackson Laboratory in Maine, found the nerves in diabetic mice were releasing too little of the neuropeptides, resulting in a "vicious cycle'' of stress on the islets (Dosch, 2006).

Dr. Russell Blaylock wrote, "With the public concern over childhood obesity and diabetes, few are being told of the overwhelming evidence that early exposure to excitotoxins as found in Aspartame consistently produce gross obesity and insulin resistant diabetes, just as we are seeing in our youth" (Martini, 2005). All these connections are showing us that the axon of the neuron reaches out to many other areas of the body to mimic and create diseases that are associated with these neurons being destroyed by neurotoxins that are exciting neurons to death.

 

Figure 15. Axons are in effect the primary transmission lines of the nervous system and as bundles they help make up up nevers. The longest axons in the human body, for example, are those of the sciatic nerve, which run from the base of the spine to the big toe of each foot. Illustration from Bipolar Disorders: A Guide to Helping Children by Mitzi Waltz.

Excitotoxins lead to neurological inflammation. Glutamate and aspartate are the most abundant neurotransmitters in the CNS (Yasko, 2003). They are also the most toxic, and because of this, they must be highly regulated.

When Protein kinase C activates phospholipase A2 (PLA2) within the neuron membrane, it brings about the release of arachidonic acid into the cytoplasm. PLA2 is a principal phospholipase that cleaves off fatty acids, primarily arachidonic acid. After arachidonic acid is acted on by lipoxygenase and COX, which produce a series of potentially destructive eicosanoids, it is the cyclooxygenase 2 (COX II) enzyme that brings about the accumulation of prostaglandin E2 (PGE2) and Prostaglandin D2 (PGD2). Both PGE2 and PGD2 are pro-inflammatory molecules (Nairn, 1985). Interestingly, only glutamatergic or glutamate receptor-related signal neurons contain COX II enzymes, which are located on distal dendrites and are concentrated in dendritic spines (Blaylock, 1997).

 

Figure 16. Dendrite spines are any of various outgrowths of certain nerve-cell dendrites, ranging in shape from small knobs to thornlike processes that are preferential sites of synaptic axodendritic contact.

 

It is the accumulation of inflammatory eicosanoids that leads to the production of free radicals, including the destructive hydroxyl radical. As free radical production accelerates they interact with the neuron’s numerous membrane structures, which including the nuclear membrane, inner and outer mitochondrial membranes and plasma membranes (Gough, Kyriakides & Hechtman, 2006). Once this cascade of destruction begins, a chain reaction within the membrane’s polyunsaturated fatty acids is initiated. This process is called lipid peroxidation (LPO). There is a close relationship between excitotoxicity and free radical generation. Free radicals speed up the release of glutamate in the brain, and excitotoxins trigger the production of large number of free radicals creating positive-feedback (Blaylock, 1997).

 

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