A great deal of research over the past decade has linked heavy metal exposure with brain and neurological disease. Alzheimer’s, Parkinson"s, Huntington"s, MS, Autism and learning disabilities of all ages have been thought to be related to exposure to Aluminum, Mercury, Lead, Copper, Arsenic and a variety of metals.
At first glance the average person would never think that they are at risk, but when we look at common sources of exposure, the picture becomes much less rosy. Over many years I have seen patients with heavy metal exposure that would never have thought of it. Some had mild cognitive changes, yet others have had significant disability.
Exposure can come from dental fillings, water, pipes in the home, smoking, pots and pans, fish consumption, chicken and meat consumption, and vaccines.
Typical symptoms can be mild or severe, and include memory loss, problems with concentration, word retrieval, fatigue, indigestion, muscle weakness, apathy, depression, visual changes, hair changes, and things ranging all over the body.
Heavy metals are extreme free radicals and can damage any areas of there body, including heart, lungs, immune function, hormone production, and bones.
Unfortunately testing for these villains is rarely done unless a physician is well educated or cutting edge with the latest research.
Occasionally a doctor will do blood levels for the metals, but this is actually a waste of time, because these substances don"t stay in the blood, but migrate to the soft and neurological tissues.
In my practice I have been testing for these for almost 20 years, and do a specialized protocol to evaluate and treat them.
A chelation treatment is done to attract and carry metals out of the body to the urine, and a 24 hour urine test will tell what is there.
The first urine test will usually reveal abnormality if these substances are there. But interestingly those who have metal exposure after doing some chelation treatment will feel much better, and second 24 hour urine will tell us the extent of exposure. The second urine might show even higher levels of toxins, this just means that there were a lot in the body at the time.
The 24 hr. urine tests determine how much treatment is needed.
Please see the articles below.
Thanks,
Dr, Chris Calapai
Public Health and Economic Consequences of Methyl Mercury Toxicity to the Developing Brain
Methyl mercury is a developmental neurotoxicant. Exposure results principally from consumption by pregnant women of seafood contaminated by mercury from anthropogenic (70%) and natural (30%) sources.
Throughout the 1990s, the U.S. Environmental Protection Agency (EPA) made steady progress in reducing mercury emissions from anthropogenic sources, especially from power plants, which account for 41% of anthropogenic emissions. However, the U.S. EPA recently proposed to slow this progress, citing high costs of pollution abatement.
To put into perspective the costs of controlling emissions from American power plants, we have estimated the economic costs of methyl mercury toxicity attributable to mercury from these plants. We used an environmentally attributable fraction model and limited our analysis to the neurodevelopmental impacts—specifically loss of intelligence.
Using national blood mercury prevalence data from the Centers for Disease Control and Prevention, we found that between 316,588 and 637,233 children each year have cord blood mercury levels > 5.8 μg/L, a level associated with loss of IQ.
The resulting loss of intelligence causes diminished economic productivity that persists over the entire lifetime of these children. This lost productivity is the major cost of methyl mercury toxicity, and it amounts to $8.7 billion annually (range, $2.2–43.8 billion; all costs are in 2000 US$).
Of this total, $1.3 billion (range, $0.1–6.5 billion) each year is attributable to mercury emissions from American power plants. This significant toll threatens the economic health and security of the United States and should be considered in the debate on mercury pollution controls.
The Relevance of Iron in the Pathogenesis of Parkinson"s Disease
Investigations that revealed increased levels of iron in postmortembrains from patients with Parkinson"s disease (PD) as comparedto those from individuals not suffering from neurological disordersare reported. The chemical natures in which iron predominatesin the brain and the relevance of neuromelanin for neuronaliron binding are discussed.
Major findings have been that ironlevels increase with the severity of neuropathological changesin PD, presumably due to increased transport through the blood-brainbarrier in late stages of parkinsonism. Glial iron is mainlystored as ferric iron in ferritin, while neuronal iron is predominantlybound to neuromelanin.
Iron overload may induce progressivedegeneration of nigrostriatal neurons by facilitating the formationof reactive biological intermediates, including reactive oxygenspecies, and the formation of cytotoxic protein aggregates.There are indications that iron-mediated neuronal death in PDproceeds retrogradely.
These results are also discussed withrespect to their relevance for disease progression in relationto cytotoxic -synuclein protofibril formation.
Chronic exposure to aluminum in drinking water increases inflammatory parameters selectively in the brain
A link between aluminum (Al) exposure and age-related neurological disorders has long been proposed. Although the exact mechanism by which the metal may influence disease processes is unknown, there is evidence that exposure to Al causes an increase in both oxidative stress and inflammatory events.
These processes have also been suggested to play a role in Alzheimer"s disease (AD), and exposure to the metal may contribute to the disorder by potentiating these events. Al lactate (0.01, 0.1, and 1 mM) in drinking water for 10 weeks increased inflammatory processes in the brains of mice. The lowest of these levels is in the range found to increase the prevalence of AD in regions where the concentrations of the metal are elevated in residential drinking water (Flaten [2001] Brain Res. Bull. 55:187-196).
Nuclear factor- B as well as tumor necrosis factor- (TNF- ) and interleukin 1 (IL-1 ) levels were increased in the brains of treated animals. The mRNA for TNF- was also up-regulated following treatment. Enhancement of glial fibrillary acidic protein levels and reactive microglia was seen in the striatum of Al-treated animals.
The level of amyloid beta (A 40) was not significantly altered in the brains of exposed animals. Insofar as no parallel changes were observed in the serum or liver of treated animals, the proinflammatory effects of the metal may be selective to the brain.
Al exposure may not be sufficient to cause abnormal production of the principal component of senile plaques directly but does exacerbate underlying events associated with brain aging and thus could contribute to progression of neurodegeneration.
The role of aluminum and copper on neuroinflammation and Alzheimer"s disease
Metals such as aluminum (Al), copper (Cu), zinc and iron have been implicated in the pathogenesis of Alzheimer"s disease (AD). Because trace amounts of metals are present in the drinking water, there is a possibility for low-dose chronic exposure. Since the presence of Al and Cu in drinking water has been shown to adversely affect the progression of AD, these two metals may aggravate some of the events associated with the disease process.
The main focus of this review will be on the effects of Al and Cu in initiating or propagating an inflammatory response within the aging brain. Since inflammatory events are reported to be upregulated in the AD brain, this may be one of the mechanisms by which the metals potentiate neurodegeneration.