Excitotoxins and the Elderly

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While we are never completely safe from excitotoxic damage at any age, the two periods when we are most vulnerable are infancy/early childhood, and during our elderly years.

There is overwhelming evidence that aging is the result of destruction caused by free radicals, which damage cell membranes, DNA, and proteins. Of particular importance is damage to proteins, which make up enzymes, structural proteins, information molecules, and cell membranes. Damage to enzymes interferes with metabolism, particularly energy production, and growing evidence suggests that damage to DNA-repair enzymes increases risk for developing numerous degenerative diseases including cancer.

Injury to the membranes of the cell is particularly important as well, especially those that surround the mitochondria. These membranes are more than coverings used to contain the contents of the cell: they are very active metabolically, shifting information in and out of the cell and its many components. Loss of the membrane's natural fluid quality is associated with aging, and means that information molecules embedded in the membranes can no longer function efficiently. In addition, the various channels that normally control the flow of ions in and out of the cell are also sluggish.

In the case of the mitochondria, a loss of membrane fluidity means that the cell can no longer generate the energy it needs. As a result, the cell's many metabolic and functional processes that depend heavily on this energy begin to slow down or even fail. This is the basic process of aging. As we have seen earlier, when energy supplies fail in the brain, glutamate begins to accumulate outside the neurons. This initiates excitotoxicity, with a rapid, sustained flow of calcium into the cell, which then triggers numerous destructive reactions.

Once the calcium channel gets stuck open, the cell is in real danger. Free radicals of every sort begin to accumulate inside and outside the cell, triggering the release of even more glutamate. Recent evidence indicates that when glutamate begins to accumulate outside the cell, the brain's immune system is activated. The brain's immune cells, microglia, then begin to secrete a host of immune-activating chemicals called cytokines, which stimulate inflammation of the brain, in turn generating more free radicals and a greater release of glutamate.

As if this were not enough, the microglia secrete two excitotoxins, glutamate and quinolinic acid.265 The whole process speeds up, and we have a brain that's in real trouble. This is the probable scenario of Alzheimer's disease, Parkinson's disease, Lou Gehrig's disease, and possibly autism. Early on in this process, one sees damage to the mitochondria with reduced cellular energy production.266 The more glutamate, the greater the damage, and the more rapid the progression to severe dementia.

When the elderly eat foods containing excitotoxic food additives, they increase their brain levels of glutamate.267 But, what about the protection afforded by the blood-brain barrier, you say? In the last decade, we have learned that one effect of aging is a gradual loss of the gatekeeper's ability to keep harmful substances out of the brain, in addition, many elderly have been exposed to one or more conditions known to impair the barrier, such as hypertension, head injuries, certain medications, diabetes, autoimmune diseases (lupus and rheumatoid arthritis), strokes, and chronic infections.

In fact, there is evidence that glutamate and free radicals can themselves impair the blood-brain barrier. Stress is also another common cause of barrier breakdown. So we see that as we age our brain is less and less protected from what we eat. If we consume diets high in free glutamate or aspartate, we risk serious brain damage. And if we happen to carry the gene for a high risk of Alzheimer's disease, elevated levels of blood glutamate from a bad diet may be just the trigger that is needed to initiate the disease. The same is true for Parkinson's disease and ALS.

Aging makes us susceptible to other threats, as well. Our brain depends on a steady supply of glucose to function. While it can use other fuels to a limited extent, glucose is its main fuel. Unfortunately, glucose cannot just enter the brain, it has to get past the blood brain barrier. To control its glucose supply, the brain has a special carrier molecule sitting at the blood-brain barrier whose job it is to escort glucose into the brain. So why have an escort system? Because in high concentrations glucose is toxic to the brain, especially when the brain is injured.

This glucose carrier system begins to fail as we age, making it difficult to control glucose entry.268 As a result, the brain becomes starved for glucose, creating a very strange situation where blood can have high levels of glucose while the brain is starved for it. The result is an isolated hypoglycemic brain. If you suffer from this condition, a doctor testing your blood would find normal or possibly elevated glucose levels. As a result, the doctor would assure you that all was well, and that your memory loss is just the result of normal aging. It has been noted that Alzheimer's disease resembles hypoglycemia in many ways, the only difference being that you cannot recover by eating something sweet.269

As a result of all these problems, we see that the neurons in the brain are unable to make enough energy from what little glucose they can get. Because of this unrelenting damage, the brain begins generating a product, called beta-amyloid protein, that slowly condenses, forming an insoluble lump outside the cell.

This lump is quite caustic and can generate some nasty free radicals of its own, in particular, hydrogen peroxide. This further aggravates the damage already started in the brain. It is so irritating that it will also activate microglial immune cells in the brain, which significantly increases the inflammation within the parts already affected by Alzheimer's disease, such as the frontal, temporal, and inferior parietal lobes. These areas of the brain control attention, concentration, recent memory, and our orientation in the world: damage to the inferior parietal lobe causes Grandpa to get lost on the way to the store.

Inflammation is known to play a major role in Alzheimer's disease.270 In fact, people who regularly take arthritis medication significantly decrease their risk of developing Alzheimer's. Interestingly, the types of cells destroyed with Alzheimer's disease are not only glutamate-type neurons but are also the only ones having the COX-II enzymes associated with inflammation. It is this enzyme that arthritis medications inhibit to block inflammation, thereby protecting these neurons from degenerating.

This same central mechanism explains the relationship to other features of Alzheimer's disease. For example, elevations of brain iron, mercury, and aluminum, combined with low magnesium levels, all act to increase free-radical generation, activation of the COX-II enzyme, and activation of the brain's immune system by way of the microglia. They also all increase the level of glutamate in the extracellular space.

The final piece of the puzzle is another microscopic change in the brains of Alzheimer's patients, the neurofibrillary tangle. This intracellular clump of tangled material appears to be the remnant of neurofibrils, a special conducting system within neurons. The neurofibrillary tangle is a twisted structure composed of tau proteins, and develops when the tau binds with too many phosphate molecules (excessively phosphorylated). Many substances can contribute to the creation of these tangles: one is a lipid-peroxidation product called 4-hydroxynonenal, others are mercury, aluminum, and MSG.

It has also been noted that the brains of Alzheimer's victims are severely deficient in many essential antioxidants, including carotenoids, vitamin C, magnesium, and glutathione.271 It may be that people with these particular antioxidant deficiencies early in life are the ones most at risk for developing the disease later, especially if combined with free-radical-gener-ating factors, such as excessive iron, mercury, aluminum and MSG in their systems.

As I mentioned before, low levels of magnesium in tissues can dramatically increase free-radical generation, reduce energy production, and enhance excitotoxicity. Several studies have found that people with Alzheimer's disease also have low brain magnesium levels, but only in the parts of the brain affected by the disease.

It has also been determined that people with this dementing disorder have very low levels of vitamin B6 (pyridoxine), folate, and vitamin B12 (methylcobalamin) in their tissues as well. Vitamin B6 plays a major role in protecting the brain against excitotoxicity. Methylcobalamin can directly block excitotoxicity, and folate plays a critical role in the production of acetylcholine, brain phospholipids, and DNA.

One of the metabolic products produced in the series of reactions utilizing these vitamins is called S-adenosyl methionine (SAMe), the molecule that actually performs all of the functions attributed to these vitamins. Not too surprisingly, studies have shown that Alzheimer's brains have very low levels of s-adenosylmethionine.

In the past, doctors frequently gave their elderly patients a B12 shot to boost their energy. Soon, we became too scientifically sophisticated to do such a stupid and wasteful thing. After all, large studies had been conducted on the elderly demonstrating that very few healthy elderly people were deficient in this vitamin.

Unfortunately, these studies were based on measuring blood levels of vitamin B12, and recent research has shown that this is not an accurate measure for this substance. One such study compared the blood levels of vitamin B6, folate, and B12 in groups of healthy and hospitalized elderly, matched for all the variables. At the same time, researchers also drew metabolic studies that more accurately determined if the vitamins were actually in the tissues doing their job. What they found was shocking.

Using only blood levels, it appeared that only 8-9 percent of the healthy elderly, and 19 percent of the hospitalized, had low vitamin levels for one or more of the vitamins. Yet metabolic studies demonstrated that 43 percent of the healthy elderly and 86 percent of the hospitalized elderly had low levels of one or more of the vitamins! It would seem that if we continue to listen to leaders in the medical establishment, a great number of us will end up very sick. Obviously, much evidence-based medicine isn't concentrating on the right evidence.

It is very likely that the "unscientific" doctors of the past, who routinely gave their patients B12 shots, saved millions of older people from lives in nursing homes or early deaths from cancer. Our evidence-based leaders have learned nothing: they continue to snub their noses at nutrition-based doctors who are saving lives.

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