Connection to Amyotrophic Lateral Sclerosis

In ALS the motor neuron cells in the spinal cord and motor neuron cells of the brain stem are primarily affected. The mystery has always been why these cells are singled out in this disease and why the disease suddenly appears later in life after so many years of normal function. The answer may be an environmental toxin, or even a combination of toxins. Several studies have shown, for instance, that mercury is selectively taken up by motor neurons in the spinal cord.

In one study, Wister rats were exposed to mercury vapor at a concentration of 50 ug/M3 for six hours a day, five days a week, extending from one to eight weeks.79 A special automet-allographical technique was used to identify the mercury in tissue sections taken from the animals and was quantified using cold atomic absorption spectroscopy. At the end of the selected time periods, sections were made of the spinal nerve ganglion (dorsal root ganglion) and the spinal cord. Representative sections were made from the cervical, thoracic, and lumbar spinal cord. After two weeks of mercury vapor exposure, mercury granules had accumulated heavily in all motor neurons in each of the areas of the spinal cord. Electron microscope analysis showed that the mercury was localized primarily in the large motor nerve cells.80

Human studies of mercury's relation to ALS have not made the same strong connection. For example, in a fairly recent examination of fifty-three ALS patients using provocative testing with the mercury chelator DMSA, researchers found no difference between ALS patients and controls in either lead or mercury excretion.81 In truth, this still leaves us short of an answer, since some have suggested that those who are unable to excrete mercury on provocative testing may be at a greater risk of neurological disease than those who secrete greater amounts. We have already seen that the nervous system holds onto mercury much tighter than other tissues and organs, and there is some question as to the ability of even chelation drugs, such as DMSA, to remove mercury from the nervous system.

Confirmation of a potential link to ALS comes from several other studies. In one study of persons suffering from ALS, researchers found several metal-related problems when other internal organs were examined.82 The ALS patients had significantly elevated levels of iron in their kidneys and liver as compared to controls. They also had mercury levels two times higher in their kidneys and 17 percent higher in their liver than did controls. Despite this, the differences were not statistically different than the controls because of the wide variations in mercury levels among people.

This might mean that the mercury was tightly bound in these patients, preventing its removal by such chelators as DMPS and DMSA. Despite the fact that some ALS patients possess the same mercury levels as those free of the disease, it may be that ALS patients have several contributing factors that make them much more sensitive to mercury. For example, they may have a weakened antioxidant defense network in their motor neurons, genetic differences in metabolism, impaired detoxification mechanisms, nutritionally impaired cellular energy production, lower selenium levels, an altered blood-spinal cord barrier, associated toxins (such as other toxic metals, pesticides and herbicides), low magnesium levels, or different levels of metallothionein in the affected neurons. Metallothioneins, found throughout the body, are low-molecular-weight proteins and polypeptides of extremely high metal and sulfur content; they are thought to be necessary for intracellular fixation of the essential trace elements zinc and copper, in controlling concentrations of the free ions of these elements, in regulating their flow to their cellular destinations, in neutralizing the harmful influences of exposure to toxic elements such as cadmium and mercury, and in the protection from a variety of stress conditions. There are numerous reasons for a differential effect with similar exposures to toxins, all of which have been well documented in the scientific literature.

A final study deserves examination. In this study, mercury chloride was injected into the abdominal cavities of test mice to see if mercury accumulated in the motor neurons of the spinal cord.83 Researchers used an extremely low dose of mercury (.05-.2 ug/g of body weight). When examined five days later mercury granules were detected in the cell bodies of the spinal and brain stem motor neurons. The mercury still persisted in the motor neurons eleven months later, indicating that this type of neuron in the spinal cord and brain stem acts as a sink for mercury and then holds onto the mercury tenaciously. This would also explain why it would be so difficult to chelate the mercury out of the nervous system of ALS patients.

It may also explain why the disease does not manifest until later in life. First, the mercury accumulates slowly, over many years. This would include all sources of mercury from seafood and dental amalgams, as well as any other environmental exposure. In the case of dental amalgams, we have seen that accumulation can occur at a rate of 2-17 ug per day. At this rate, it would take many years for the body to accumulate enough mercury to actually kill neurons, but during this time the cells are being damaged by the mercury, impairing their ability to produce energy and dramatically increasing free-radical generation while at the same time depleting neurons of their antioxidants. There is overwhelming evidence that free-radical generation by excitotoxins is a central process in this disease.

Mercury also damages cellular DNA and RNA, two factors founds in ALS. Progressive disruption of the cell's homeostatic mechanisms would necessarily lead to eventual cell death (by apoptosis and necrosis). A final piece of the puzzle has recently been supplied, and that is the connection between mercury poisoning and excitotoxicity. There is growing evidence that excitotoxicity plays a major role as the final destructive event in all neurodegenerative diseases; when the neurotransmitter glutamate cannot be removed from the body safely, the nervous system is eventually damaged.

Recent studies have shown that deactivating the transport proteins necessary to safely eliminate glutamate from the body causes the substance to accumulate. Soon afterwards neurons begin to die off. ALS can actually be induced in experimental animals by this process. Mercury, even in extremely low concentrations, acts as a powerful inhibitor of these glutamate transport proteins. In fact, levels that do not affect other cellular functions can inhibit the glutamate transport protein.84 Once the excitotoxic process begins, enormous numbers of free radicals are produced, further injuring the cells.

It should be noted that mercury is not the only substance that can deactivate the glutamate transporter molecule, inflammatory cytokines and infectious agents may do so as well. For example, we know that certain viruses can also hinder these glutamate transport proteins.

FIGURE 3.2 Midsection view of the head demonstrating how mercury can saturate and pass up the olfactory nerve filaments in the nose and the trigeminal nerve filaments in the mouth to reach the brain.



Als Brain Inflammatory Cytokines

FIGURE 3.2 Midsection view of the head demonstrating how mercury can saturate and pass up the olfactory nerve filaments in the nose and the trigeminal nerve filaments in the mouth to reach the brain.


Further research should be done on this possible connection, especially in light of the occasional case of ALS that resolves with amalgam removal.

We have good experimental and human pathological evidence that prolonged free-radical injury to neurons and astrocytes precedes most neurodegenerative diseases by decades. We also have overwhelming evidence that neural energy impairment plays a pivotal role in these diseases. Autopsy studies of large numbers of Alzheimer's victims have consistently shown elevations of mercury, as well as other toxic metals, within the parts of the brain characteristically damaged by the disease. So, I think those who dismiss these concerns out of hand are themselves not using good science and certainly are not using common sense.

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