Environmental Toxins Are Very Harmful To The Brain
In 2018, a study named An Emerging Mechanism Translating Environmental Toxicant Exposure Into Neuroinflammation in Parkinsons Disease explained the mechanism behind why environmental toxicity is so harmful to the brain.
As previously mentioned, some pesticides are able to cross the blood-brain barrier. A pesticide called Rotenone, which is used in agriculture and in water management, has been linked to Parkinsons disease. This pesticide causes a cascade of neuroinflammation in the brain by activating a protein called an inflammasome.
The role of neuroinflammation in Parkinsons disease has been validated extensively by several studies. It is characterized by the buildup of toxic metabolites, oxidative stress, and misfolding of proteins in the brain, which are all associated with Parkinsons disease.
Due to our industrialized life, we are constantly exposed to toxins our bodies cannot process. Our bodies have not evolved mechanisms for processing these chemicals, like the mechanisms they have developed to prevent starvation or to ward off pathogens like the flu virus.
Parkinson Disease Incidence In Urban Counties With Metal
The annual age-, race-, and sex-standardized Parkinson disease incidence in urban counties with high reported copper, manganese, or lead release was greater than in urban counties with no or low reported release of all 3 study metals . The risk of Parkinson disease was elevated in counties with high reported manganese release = 1.78, 95% CI: 1.54, 2.07). Counties with high reported copper or lead release did not show an elevation in Parkinson disease risk. Hierarchical regression analysis produced odds ratios that were in the same general direction of the primary analysis but with wide confidence intervals that spanned unity.
Age-, Race-, and Sex-standardized Annual Incidence of Nonmobile Parkinson Disease Cases Living in Urban Counties With No Versus High Reported Copper, Manganese, and Lead Metal Release, US Medicare Beneficiaries, 2003
How Is Parkinsons Disease Diagnosed
Diagnosis is difficult at every stage of the disease, but particularly in the early stages. No single test can provide a diagnosis. A diagnosis will likely involve physical and neurological examinations, conducted over time to assess changes in reflexes, coordination, muscle strength, and mental function. Your doctor might also see how you respond to medicine.
You may need to have brain imaging tests to rule out other conditions that might be causing your symptoms. Such tests could include MRI and CT scans and possibly some other types of scans. Blood tests may also be done to exclude other illnesses.
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Parkinson Causes: Do Genetics Or Environmental Toxins Lead To Parkinson
While Parkinson causes are diverse
Both genetic and environmental causes of Parkinsons Disease are well recognized in the medical literature.
1) Environmental toxins lead to Parkinsons:
Studies, both of large groups of people and experimental studies show that both pesticides and metal toxicity are Parkinson causes.
- These toxins cause a-Syn aggregation which leads to neuro-degenerative diseases including Parkinsons.
2) Genomic defects are among Parkinson Disease causes:
- Yes, family history, or genetics can be a player, but few people get Parkinsons directly from genetic mutation. A number of factors usually combine to trigger the disease.
Which Parkinson Disease Causes Might Affect You?
When Parkinson causes converge either genomic, or environmental factors or both, these lead to abnormalities in the mitochondria of the cells and there is more oxidative stress.
- Toxicity causes inflammation and oxidative stress and eventually the balance of health tips toward disease.
While not a Parkinson cure, we can protect better against toxins, and lower inflammation and oxidative stress.
What Is Body Burden
Heavy metals and other substances can build up in our system and organs. For example, lead can be stored in our bones. As we age and lose bone mass, lead is released into the circulation.
Whether the substance stores or circulates in our body, it contributes to our overall body burden. Body burden is the total amount of toxicants that accumulate in an individuals body. Whether our toxins are stored in our fatty tissue, our brain, our bones or organs, there is a lot we can do to rid our body of these substances.
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Environmental Factors In Parkinsons Disease
Here are environmental factors that may play a role in the development of Parkinsons disease:
Although environmental exposure to these and other toxins is of continued research interest, its hard to determine if any one substance is a culprit. Most often, individual cases of Parkinsons disease result from a complex interplay between genetics and environmental and other factors.
Targeting Parkinsons-Linked Protein Could Neutralize 2 of the Diseases Causes
Researchers report they have discovered how two problem proteins known to cause Parkinsons disease are chemically linked, suggesting that someday, both could be neutralized by a single drug designed to target the link.
Cumulative Exposure Tied To Progression Of Symptoms
The new study concerns 886 Midwestern workers at two shipyards and a heavy machinery fabrication shop. At the start of the study, all the participants were examined by neurologists who specialize in movement disorders. After that, 398 of the participants had further follow-up examinations for up to 10 years.
The researchers assessed exposure to manganese from questionnaires filled in by the participants. These included questions about the types of job they had and how long they served in them. The researchers found that the average exposure was a manganese concentration of 0.14 milligrams of manganese per cubic meter.
The results showed that 15 percent of the participants had parkinsonism, with scores of at least 15 on a scale of 0 to 108 points in a movement test known as the Unified Parkinson Disease Rating Scale motor subsection part 3.
The researchers also found that cumulative manganese exposure was linked to a yearly increase in the movement test scores. For every extra milligram of manganese per cubic meter of exposure per year, there was an additional 0.24 points on the test score.
For example, a worker who had been a welder for 20 years before the first examination had an estimated 2.8 milligrams manganese per cubic meter years exposure and would be predicted to have nearly a seven-point increase on the movement test related to that welding fume exposure, explains Prof. Racette.
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Shsy5y Differentiation Into Neuron
SH-SY5Y cells were seeded in the corresponding plates at a density of 10,000 cells/cm2. The next day, 10µM of retinoic acid was added to start the differentiation in EMEN/F12 media supplemented with 10% of FBS and 1% Penicillin-Streptomycin. After 6 days of RA treatment, cells were treated for 4 days with 50ng/mL of BDNF in EMEN/F12 media supplemented only with 1% Penicillin-Streptomycin .
Assessment Of Cell Viability Via Mtt Assay
For the MTT assay, cells were seeded in triplicate in 96 well plates. After heavy metal treatments 10µL of 5mg/mL 3–2,5 diphenyltetrazolium bromide reactive was added to each well containing 100uL of media and incubated for 4h at 37°C. Active mitochondria of living cells can cleave MTT to produce formazan, a purple crystal whose level is directly proportional to the number of living cells. After incubation, formazan crystals were solubilized in 100uL DMSO and absorbance was measure at 595nm.
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Metal Exposure And Parkinson’s Symptoms: Link Explored
- Iowa State University
- A new study describes the biological process that causes Parkinson’s-like symptoms to develop following exposure to the metal manganese. The new research could lead to earlier detection of Parkinson’s disease and better outcomes for patients.
A new study from Iowa State University biomedical researchers illuminates the biological processes by which exposure to some metals can contribute to the onset of Parkinson’s-like symptoms.
The study, published today in the peer-reviewed journal Science Signaling, focuses on the metal manganese, which has a range of industrial uses as an alloy. Anumantha Kanthasamy, a Clarence Hartley Covault Distinguished Professor in veterinary medicine and the Eugene and Linda Lloyd Endowed Chair of Neurotoxicology, said the research details how manganese exposure can lead to misfolded proteins in the brain, which cause a neurological disease. Kanthasamy said the findings could lead to earlier detection of the disease and better outcomes for patients.
Kanthasamy said small amounts of manganese are necessary for the proper functioning of the human body, but too much exposure has been linked with neurological symptoms much like those experienced by patients with Parkinson’s Disease. Links between manganese and neurological disorders have been noted since the 1950s, Kanthasamy said, because of the tendency of manganese to accumulate in brain tissues.
Is It Really That Bad
Lead is a chemical toxicant, which can cause major damage especially in developing brains. Newborns and young children have the greatest health risks and will suffer lifelong problems both intellectually and physically following exposure to the toxin. Studies show that lead exposure leads to reduced IQ in children, and this reduction in IQ carries on into adulthood. It also causes attention deficit disorders and has been linked to both Parkinsons disease and, more recently, Alzheimers. There is consistent literature demonstrating that children are at risk for developing emotional and behavioral problems following even mild exposure. Lead poisoning during childhood undoubtedly poses a significant threat to healthy development.
It is important to note that all levels of lead exposure have adverse effects on the central nervous system. Evidence suggests that if this exposure happens early in life, it can cause neurodegeneration later in life. Like some other types of brain injury, chronic low-level lead exposure is difficult to diagnose. Slightly elevated blood-lead levels often do not produce specific signs or symptoms, and few physicians think to test for toxicity because exposure is generally perceived to be a rarity. Lead has been called a silent toxin in much the same way that traumatic brain injury has been referred to as the silent epidemic.
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Mercury And Neuron Toxicity:
Mercury is highly neurophilic and highly lipophilic .Mercury is initially distributed by the circulatory system and enters nerve endings and travels the central nervous system using a mechanism known as retrograde axonal transport leaving a path of destruction.
How Mercury Causes Brain Neuron Damage – University of Calgary
Effect Of Lead On Neurodevelopment
A childs BPb measurement is estimated to account for 2% to 4% of variance in neurodevelopment measures //. The Agency for Toxic Substances and Disease Registry // cautions, however, that when studying the effects of lead on child development, the influence of multiple factors like treatment by parents or other adult caregivers should be taken into account. A childs family and personal psychosocial experiences are strongly associated with performance on neurodevelopment measures and account for a greater proportion of the explained variance in these measures than BPb levels.
Many studies have examined the effects of lead on childrens development outcomes covering varying ages at which BPb was measured and varying ages over which BPb levels were averaged. Statistically significant associations have been identified between average BPb levels over a specific period and various adverse health outcomes other studies have reported statistically significant associations with a single lead measurement at a specific age or with a peak measurement. In contrast to adults, central nervous system effects are more prominent than peripheral effects in the developing nervous system //. The developmental effects of lead occur during a critical time window .
Low-level BPb and development
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Amalgams And Teeth Bleaching:
Little has been done to warn the public about this very serious hazard.Teeth bleaching with peroxide whiteners will trigger the release of mercury when in contact with silver-mercury amalgam dental fillings.The quantity of peroxide in the whitener and the duration of treatment are important factors which affect amount of mercury released.It has been shown that a silver colored, toxic slurry of mercury can be found in the “trays” after a multi-hour whitening treatment.DON’T DO IT!!!
- “The tested bleaching products significantly elevated the surface mercury levels of amalgam in vitro.”
Safe Mercury Amalgam Removal Technique:
The International Academy of Oral Medicine and Toxicology has developed the Safe Mercury Amalgam Removal Technique protocol recommendations.The IAOMT website also has a searchable worldwide dentist databaseor check out Dr. McGuire’s database for a dentist with skills to meet the IAOMT protocol for removing amalgam fillings.
IAOMT Safe Mercury Amalgam Removal Technique protocol. Ignore the comment about taking chlorella as it is not a good chelator and will move rather than remove mercury.
Amalgam fillings can be replaced with porcelain inlays or onlays bonded to the tooth or with a composite. Be sure to use one of the newer bonding agents which do not contain Bisphenol A which is a bio-accumulative, xenoestrogen endocrine disrupting chemical which has estrogen hormone like properties.This is also true in choosing composite filling materials. Choose materials which are BPA-free.Also be sure to reduce your BPA exposure by choosing glass over canned food products and don’t microwave polycarbonate plastic food containers.Dental materials testing panel: Clifford Consulting and Research
Binders such as activated charcoal can be taken 20 to 30 minutes before the amalgam removal procedure starts for the purpose of attaching to any mercury particles that may be ingested.For more on binders, see below.
Removing dental mercury amalgam using the SMART protocol Dr McBride DDS
For more details and photos see the IAOMT SMART protocol for mercury amalgam removal.
Ratio NBMI:Hg is 1:1
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Focused Reviewiron And Other Metals In The Pathogenesis Of Parkinson’s Disease: Toxic Effects And Possible Detoxification
Environmental factors often appear to play a pathogenic role in Parkinson’s disease .
Research has shown a connection between PD and metal exposures including Fe, Hg, Mn, and Pb.
Elevated iron levels have been found in the substantia nigra of PD patients.
Reactive oxygen species and loosely chelated Fe cause neurotransmitter dysfunction in PD.
Treatment with metal chelators can inhibit PD progression and exert protection.
Strongest Link To Flux Core Arc Welding In Confined Space
The researchers found little change in the results when they took into account other factors known to affect risk of developing movement disorders, such as smoking, alcohol consumption, and exposure to pesticides.
They found that the strongest link between increased parkinsonism symptoms and cumulative manganese exposure was in workers who did flux core arc welding in a confined space.
They also found that the links were strongest in workers who had their first follow-up exam within 5 years after they started welding. Prof. Racette suggests that this could be because workers with higher exposure may develop parkinsonism and then move to other jobs.
The symptoms that progressed the most as the welders exposure to manganese accumulated over time were stiffness in the arms and legs, slowness of arms and hands, speech problems, and reduced facial expression.
This study suggests that we need more stringent workplace monitoring of manganese exposure, greater use of protective equipment and monitoring and systematic assessment of workers to prevent this disabling disease.
Prof. Brad A. Racette
Prof. Racette points out that the study has some limitations. For instance, it did not use a direct measure of cumulative manganese exposure but derived it from information provided by the workers. Also, the researchers could not rule out the effect of other metals in the fumes, or those that may have come from other sources such as paints and degreasers.
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Exposure To Chromium And Nickel Induced Neuronal Death In Ipsc
Since both genetic and environmental risk factors contribute to the development of neurodegenerative diseases,, a highly relevant model for testing the neurotoxic effects of heavy metals is the use of iPSC-differentiated neurons carrying PSP-associated mutations. Therefore, we used an iPSC line generated from an individual carrying a heterozygous mutation in the MAPT gene , which has been implicated in PSP and other tauopathies,,. Since one of the limitations of using of patient-derived iPSCs is the lack of genetically paired controls, we used the CRISPR/Cas9 genome editing technology, to generate an isogenic control iPSC line . We validated the successful genetic correction of the mutation by Sanger sequencing , and confirmed the pluripotency status of both R406W tau mutant and isogenic control iPSC lines by qPCR measuring the expression LIN28A, NANOG, PODXL, POU5F1, SOX2 genes . Furthermore, using G-band karyotyping we confirmed that no chromosomal aberrations were introduced during the iPSC generation and the gene editing process .
Together, these results demonstrate that Cr and Ni exposure induces intrinsic/mitochondrial apoptosis and that the differentiation of SH-SY5Y cells affects the neurotoxicity induced by Cr and Ni.
The Function Of The Metals In Regulating Epigenetics During Parkinsons Disease
- 1Department of Biological Sciences, Xian Jiaotong-Liverpool University, Suzhou, China
- 2Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China
- 3Department of Biological Sciences, Shaoxing University, Shaoxing, China
Parkinsons means Parkinsons disease, a chronic degenerative disease of central nervous system. The main area which is affected by this disease is motor system. Since it firstly founded by James Parkinson in his 1817 publication, nowadays, people still have lots of questions about this disease. This review mainly summarizes the epigenetics of Parkinsons. DNA methylation is one of the epigenetic mechanisms of Parkinsons. During the development of disease, global hypomethylation, and hypermethylation happen in different areas of patients. Another epigenetic mechanism is histone modification. People believe that some metals can induce Parkinsons disease by modulating epigenetic mechanisms. This review summarizes the relationships between different metals and Parkinsons disease. However, the specific roles of most metals in epigenetics are still unknown, which need further research.
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