Mercury Exposure and Parkinsons Disease

All of the comments 1 have made concerning Alzheimer's disease also apply to Parkinson's disease. Like Alzheimer's and ALS, Parkinson's disease is associated with free-radical and lipid-peroxidation damage to a very restricted part of the brain called the substantia nigra and its connections. Like the others, excitotoxicity appears to play a central role in the disease process itself. There is strong evidence that iron toxicity is also critical in this disease. Some feel that the free-radical generation caused by mercury is related to the fact that it causes free iron to be released from its binding protein, ferritin.

On top of all this, those destined to get Parkinson's disease seem to possess an inherited weakness in their ability to detoxify toxins, both those formed within the body during metabolism and those ingested or inhaled. A recent study, in which one hundred Parkinson's patients were compared to two hundred matched controls, found that Parkinson's patients had a genetic defect that altered their ability to form conjugating enzymes, a vital method of cellular detoxification,98 and a condition that would make them more susceptible to oxidative stress in the part of the brain causing the disease. Mercury, by increasing free-radical generation (oxidative stress) and poisoning the antioxidant network, would greatly magnify the effects of this inherited weakness.

In one case report, a female dentist, age forty-seven, developed Parkinson's disease within eighteen months of the onset of her first symptoms.99 Her baseline urinary mercury was 46 ug. With chelation using penicillamine, it increased to 79 ug and then continued to fall during the week of treatment. During the period of the treatment, she improved clinically and then stabilized. It was noted that this represented a new possible cause of Parkinson's disease in the absence of other signs of mercury poisoning. Penicillamine is not the best choice for chelating agents, especially for removal from the brain. In addition, the treatment period was too short and should have included a more complete program for mercury toxicity reduction.

In another study, researchers looked at environmental factors such as pesticide exposure, well-water drinking, and heavy metal, solvent, and animal exposures possibly related to Parkinson's disease.100 They discovered a very strong correlation with pesticide exposure, a finding that has been confirmed repeatedly in other studies. Interestingly, they also found that patients with Parkinson's disease had a significantly higher number of dental amalgam fillings than did controls. The study also found that having a relative with the disease compounded all of these factors indicating a genetic sensitivity to these toxins.

I again emphasize, all of the neurodegenerative diseases I have discussed can—and frequently do—overlap, which would indicate a common cause. Why one person would develop Parkinson's disease and another ALS may depend on a multitude of factors such as associated toxins, nutritional factors, associated viral injuries, genetic sensitivities, biochemical differences, and timing of exposure to the toxin. In my previous book, Excitotoxins: The Taste That Kills, I demonstrated how simply altering the dose of a toxin could make the difference between an animal developing ALS or dementia. The same may hold true for mercury.

FIGURE 3.3 This diagram demonstrates the numerous factors that can induce excitotoxi-city, leading to degeneration of various parts of the nervous system. Notice the intimate connection between microglial activation (brain immune activation) and excitotoxicity. Also note the connection between excitotoxicity and free-radical generation. In the real world, many of these factors operate simultaneously.

FIGURE 3.3 This diagram demonstrates the numerous factors that can induce excitotoxi-city, leading to degeneration of various parts of the nervous system. Notice the intimate connection between microglial activation (brain immune activation) and excitotoxicity. Also note the connection between excitotoxicity and free-radical generation. In the real world, many of these factors operate simultaneously.

Mercury is extremely toxic to numerous organs, tissues, and cells, but especially to the brain. Like lead, the medically acceptable definition for mercury toxicity is constantly being revised by health authorities. Levels that we considered safe ten years ago are now known to be quite toxic. The reason for these ongoing revisions is that scientific instrumentation for measuring the toxic effects of these metals has become much more sophisticated. Also, we now know a lot more about the biological systems being affected by the metals. Finally, our ability to test for subtle changes in neurological function has also improved.

In the past, toxicity determinations were based on evaluations of obvious effects. Mercury levels high enough to cause obvious confusion, dementia, or a loss of sensation in the limbs were used to determine safe levels—any level below that needed to cause these effects was considered safe. With our ability to measure biochemical functions in cells and tissues, we can now measure toxicities on a molecular level that occur at concentrations far below these early estimates of safety.

Another problem with setting safe levels for toxic metals is that we have no idea what they do over a very long period of time. Most studies are of short duration, weeks or months at most. Also, we rarely consider the effects of these metals on certain individuals whose sensitivities may be quite different from the majority of individuals tested. There is always a subset of individuals whose biochemistry differs in ways that can produce profound toxic effects not seen in others; often these individuals are lost in statistical analysis involving large numbers of people. No one seems to care about them.

Finally, we simply do not know the effects of combining various toxic metals. While there is some evidence that their toxicities are synergistic, we do not know for sure in many cases. For example, substance A may have no toxicity at low concentrations when used alone. The same may be true of substance B. Yet, when combined they may be very toxic. We are just now beginning to discover the effects of such combinations.

Unraveling Alzheimers Disease

Unraveling Alzheimers Disease

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