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Best neuro-protective foods and supplements.
You may ask us about:
- Supplements scientifically shown to replenish glutathione levels to protect against cell death and toxins
- Glutathione-building supplement for detoxifying metals and pesticides
We hope that you have been inspired for better Parkinson Disease treatments with natural help.
- Knowing that yes, that environmental toxins lead to Parkinson is hopefully less scary, because there are prptective foods and supplements.
- For your best shot at a Parkinson cure, you will want to add the best foods and supplements shown to be neuro-protective.
Metals such as iron are usually high in the brains of Parkinsons patients. Iron can be reduced in the body by:
- not taking iron supplements
- eating less red meat
- drinking green tea and adding curcumin to your food. These contain natural iron-chelating, substances molecules that bind to and remove iron.
Knowing the causes Parkinson Disease will hopefully help live a fuller and longer life!
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1. Int J Mol Sci. Parkinsons Disease: From Pathogenesis to Pharmacogenomics 2017 Mar 18: 551. Published online 2017
2. Front Neurosci. Neurochemical and Behavior Deficits in Rats with Iron and Rotenone Co-treatmen. 2017 Nov 23 11:657. doi: 10.3389/fnins.2017.00657. eCollection 2017.
3. PARKINSONS DISEASE: A SYNDROME NOT ADISEASE Issue: BCMJ, vol. 43 , No. 3, April 2001 , Pages 129-132Clinical Articles By: Donald B. Calne, OC, DM
Evaluate Relationship Between Environmental And Genetic Risk Factors
Gene-environment interaction is often used to describe the majority of idiopathic PD etiology , but most human population studies assess genetic risk for PD without any context of exposure. A few rare highly penetrant genetic mutations such as in the -synuclein gene clearly cause the PD phenotype . In contrast, mutations in the LRRK2 gene, responsible for perhaps 12%of PD, are only 30%penetrant . The much more common genetic variants identified in large GWASs are associated with only minimally increased risk and are not even thought of in terms of their penetrance. These observations clearly suggest and are supported by twin studies that except in very rare circumstances, interactions with the environment are necessary to produce the disease. PD is not unique in this respect. Highly penetrant mutations cause only a small proportion of virtually all late life disorders. The converse of course is also truehighly penetrant environmental exposures are rare causes of late life disorders, perhaps with the exclusion of smoking related disease.
Fig. 3
Number of publications on Parkinsons disease and select topics, 1960-2021. Based on Medline search of Medical Subject Headings and PubMed for keywords or phrases in publications for PD-related topics. Estimates vary depending on search terms and database coverage.
What Causes Parkinsons Disease
Parkinsons disease is a chronic, progressive neurological disease that currently affects about 1 million Americans. Parkinsons disease involves a small, dark-tinged portion of the brain called the substantia nigra. This is where you produce most of the dopamine your brain uses. Dopamine is the chemical messenger that transmits messages between nerves that control muscle movements as well as those involved in the brains pleasure and reward centers. As we age, its normal for cells in the substantia nigra to die. This process happens in most people at a very slow rate.
But for some people, the loss happens rapidly, which is the start of Parkinsons disease. When 50 to 60 percent of the cells are gone, you begin to see the symptoms of Parkinsons.
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Quick Summary If Youre In A Hurry
- Environmental factors such as exposure to certain pesticides and other chemicals, infection, and even brain injury have been found to slightly increase the risk of Parkinsons.
- Some individuals may be more or less susceptible to different risk factors.
- It is almost impossible to identify the exact cause of Parkinsons in most people.
Parkinsons Disease Risk Factors
Although a primary cause for Parkinsons disease is yet to be identified, a number of risk factors are clearly evident.
Advancing age Although there is the occasional case of the disease being developed as a young adult, it generally manifests itself in the middle to late years of life. The risk continues to increase the older one gets. Some researchers assume that people with Parkinsons have neural damage from genetic or environmental factors that get worse as they age.
Sex- Males are more likely to get Parkinsons than females. Possible reasons for this may be that males have greater exposure to other risk factors such as toxin exposure or head trauma. It has been theorised that oestrogen may have neuro-protective effects. Or, in the case of genetic predisposition, a gene predisposing someone to Parkinsons may be linked to the X chromosome.
Family history Having one or more close relatives with the disease increases the likelihood that you will get it, but to a minimal degree. This lends support to the idea that there is a genetic link in developing Parkinsons.
Post menopausal who do not use hormone replacement therapy are at greater risk, as are those who have had hysterectomies.
Low levels of B vitamin folate Researchers discovered that mice with a deficiency of this vitamin developed severe Parkinsons symptoms, while those with normal levels did not.
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What Raises Someones Risk For Parkinsons
Its a complex picture, but you may be more likely to get Parkinsons based on:
Age. Since it mostly affects people 60 and older, your risk goes up as the years go by.
Family history. If your parent, brother, or sister has it, youre a little more likely to get it.
Job. Some types of work, like farming or factory jobs, can cause you to have contact with chemicals linked to Parkinsons.
Race. It shows up more often in white people than other groups.
Serious head injury. If you hit your head hard enough to lose consciousness or forget things as a result of it, you may be more likely to get Parkinsons later in life.
Gender. Men get it more than women. Doctors arent sure why.
Where you live. People in rural areas seem to get it more often, which may be tied to chemicals used in farming.
Lack Of Exercise/physical Activities
The idea that exercise might have a role in Parkinsons disease is not new. Researchers have been trying to find a connection between Parkinsons and exercise for many years. They think that those who do regular exercise are less likely affected by the disease than those who dont.
A study published in the Journal of Neurology suggests that higher levels of physical activity may reduce the risk of developing Parkinsons disease. In this study, 125,828 provided information on physical activity in early adulthood. During the follow-up, a total of 387 Parkinsons cases were identified. The study found that the people who didnt develop the disease were mostly involved in some sort of higher levels of physical activity.
Similarly, one meta-analysis that included data from 8 prospective studies has concluded that moderate to vigorous physical activity may have an inverse relationship with a risk of Parkinsons.
Although it is not known how exercise could protect someone from developing Parkinsons, researchers think that it may inhibit abnormal changes in dopamine neurons and contribute to the healthy functioning of brain parts involved in body movement.
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Utilize Expansive New Tools To Consider Gene
All disease phenotype is a result of our genes and our environment . As we predict that gene-environment interaction drives the majority of idiopathic PD cases , preclinical research platforms provide a crucial resource for testing these associations. Transgenic and knock-in animal models, induced pluripotent stem cells and other human derived cells, CRISPR-edited cell lines, zebrafish, drosophila, C. elegans, and yeast, are well-suited to manipulate genetic targets that interact with environmental contaminants. In addition, high-throughput content assays, such as transcriptomics and epigenetics, provide ideal measurements to evaluate toxicity of environmental contaminants linked to PD, and to screen for novel chemicals of concern. In combination, these assays are even more powerful. For example, Parmalee and colleagues have characterized a robust method to perform RNA-Seq in C. elegans exposed to manganese, which could be easily adaptable for any environmental exposure . Combined with the relative ease of genetic manipulation in C. elegans, platforms such as these are ideal for amassing gene-environment information relative to disease mechanisms in PD, like mitochondria and monoamine function .
Parkinson Disease Risks: Correctly Identifying Environmental Factors For A Chronic Disease
Center for Health + Technology and Department of Neurology, University of Rochester Medical Center, Rochester, New York, USA.
Address correspondence to: Karl Kieburtz, 265 Crittenden Boulevard, CU 420694, Rochester, New York 14642, USA. Phone: 585.275.8911 Email: .
Find articles byKieburtz, K.in:JCI |PubMed |
Center for Health + Technology and Department of Neurology, University of Rochester Medical Center, Rochester, New York, USA.
Address correspondence to: Karl Kieburtz, 265 Crittenden Boulevard, CU 420694, Rochester, New York 14642, USA. Phone: 585.275.8911 Email: .
J Clin Invest.
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Basic Science: Conclusions And A Path Forward
The etiology of PD is influenced by environmental exposures . Thus, while not exhaustive, incorporating one or several environmentally focused components into basic PD research will ultimately improve our ability to prevent PD. Many of these efforts will require collaborative, cross-disciplinary groups and emerging technology combined with basic toxicological principles such as those that have been applied in other fields , but less frequently for PD.
One tool that has been specifically designed to do just this, is the Human Health Exposure Analysis Resource , a program sponsored by multiple NIH entities . HHEAR uses an eligibility and feasibility-based application for access to data analysis services that will incorporate exposure data into human health studies. With both laboratory and data analysis support, the incorporation of biomarkers, transcriptomics or metabolomics, and gene-environment interaction for a specific project would be an ideal mechanism for PD studies, both in the pre-clinical and clinical areas. However, one of the strengths of the HHEAR program is also a limitation. The very rigorous analysis approach may reduce the discovery of unknown associations as the bulk of the program targets already known environmental factors.
The Search For Environmental Causes Of Parkinsons Disease: Moving Forward
Issue title: The Times They Are a-Changin: Parkinsons Disease 20 Years from Now
Guest editors: Patrik Brundin, J. William Langston and Bastiaan R. Bloem
Article type: Review Article
Authors: Chen, Hongleia* | Ritz, Beateb
Affiliations: Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing, MI, USA | Department of Epidemiology and Environmental Health Sciences, Fielding School of Public Health, University of California Los Angeles, Los Angeles, CA, USA
Correspondence: Correspondence to: Honglei Chen, MD, PhD, Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, 909 Wilson Rd, East Lansing, MI 48824, USA. Tel.: +1 517 884 3990 E-mail: .
Keywords: Parkinsons disease, etiology, progression, environmental risk factors, prodromal symptoms
DOI: 10.3233/JPD-181493
Journal: Journal of Parkinsons Disease, vol. 8, no. s1, pp. S9-S17, 2018
Abstract
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Reasons Why Parkinsons Disease Occurs
The scientific reason given for Parkinsons disease is that the patient has lost nerve cells in the part of the brain called the substantia nigra. A very important chemical called dopamine is produced by the substantia nigra. The loss of the ability to produce dopamine contributes to the early stages of Parkinsons disease.
Leading Possible Risk Factors For Parkinsons
Genetic factors
Scientists estimate that less than 10% of cases of Parkinsons disease are primarily due to genetic causes. The most common genetic effect that triggers Parkinsons disease is mutation in a gene called LRRK2. The LRRK2 defect is particularly frequent in families of North African or Jewish descent. Mutations in alpha-synuclein have also been found to trigger Parkinsons, but these are quite rare. In most cases, no primary genetic cause can be found.
Other risk factors
There are other things that put an individual at higher risk for developing Parkinsons. The main risk factor is age, because Parkinsons disease is most commonly found in adults over the age of 50 . Men also have a higher risk of Parkinsons disease than women. The actual links between any of these factors and Parkinsons disease are not completely understood.
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Model Combined Environmental Exposures
Environmental contaminants are rarely, if ever, encountered in isolation. Toward this end, modeling combined exposures is critical for assessing PD risk in a basic research setting. Such an approach should also consider lifestyle factors, much the way epidemiology studies stratify PD risk based on smoking . This is a difficult task regulatory agencies have struggled with how to deal with chemical mixtures. Besides the challenges of interpreting the scientific findings, the regulations are not designed to address mixtures. However, from a scientific perspective we must try to study the real-life norm of combined exposures.
An example of this strategy was employed to measure the combined toxicity of trichloroethylene with traumatic brain injury , both of which are independently implicated in PD risk, on mitochondrial function in the nigrostriatial tract . In an acute treatment model in male Fisher 344 rats, neither TCE nor TBI alone caused significant reduction in striatal mitochondrial complex I activity, but together produced approximately a 50%reduction in this brain region . As TCE was heavily used by the military until 2007 , exposure to the organic solvent plus combat or training injury are realistic combined exposures that may contribute to PD risk in military personnel . In addition, TCE is substantially metabolized in the body resulting in numerous byproducts that may contribute to toxicity of combined phyiological stressors .
Theories About What Causes Parkinsons
The cause of Parkinsons disease is still unknown, although there is some evidence for the role of genetics, environmental factors, or a combination of both. It is also possible that there may be more than one cause of the disease. Scientists generally believe that both genetics and environment interact to cause Parkinsons disease in most people who have it.
Currently, there is an enormous amount of research directed at producing more answers about what causes Parkinsons disease and how it might be prevented or cured. When physicians diagnose Parkinsons, they often describe it as idiopathic . This simply means that the cause of the disease is not known.
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Environmental Causes Of Parkinsons Disease
Parkinsons Disease causes are classified as environmental causes due to the fact that they occur through exposure to certain drugs which has been proven in scientific studies.
The most common sign of parkinsonism is a resting tremor, which causes shaking when the individual assumes or is forced into certain positions.
Other less frequent symptoms are impaired movement and balance problems due to changes in muscle stiffness, slow movements, rigidity, sleep disturbances, mood changes, and difficulty speaking or swallowing.
Symptoms worsen with time as the disease progresses to its final stages where it causes an inability to walk, talk, swallow properly, stay awake for a long period of time.
Include Populations With High Exposure Burden
The current and projected global growth of PD in populous nations cannot alone be attributed to increased lifespan. Areas of the world that have seen the greatest growth of modern industrialization, such as China and India, have had the highest increase in age-adjusted prevalence estimates for PD . Some of the increased prevalence in PD among these nations may be a result of better characterization and diagnosis of PD by neurologists or reductions in smoking, which is widely accepted to be protective against PD risk . However, other critical factors are the products and by-products of industrialization. In the case of pesticides, China greatly outpaces the rest of the world in annual usage, estimated at over 1,800,000 tons, followed by the U.S. with approximately 55,000 tons . In the last few decades, South American pesticide usage has risen sharply . As regulations for chemical usage vary widely between nations, the risks for their harms may be especially high in certain parts of the world.
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An Environmental Research Agenda For Preventing Pd
To prevent PD, our basic and clinical research activities must expand substantially. We present 10 key areas that could help accelerate disease prevention .
Fig. 1
Parkinsons disease Prevention Agenda. Preclinical and clinical research areas of focus to better characterize environmental influence and prevent Parkinsons disease.
What Is Parkinsons Disease
Parkinsons disease is a motor system disorder resulting from the loss of dopamine-producing cells in the brain.1 PD mostly affects people over 60 years of age, but in rare cases can start as early as your 20s. The rate at which it progresses is different for different people, and early symptoms are difficult to catch.
PD affects your movements in a way that you cannot control it. It starts out with tremors, stiffness, and slow movements and gradually progresses into difficulty swallowing, speaking, sleeping, and even thinking. The most unfortunate part is that daily activities that youve been doing for years become not so doable, affecting relationships and your basic quality of life.
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Interplay Of Aging Genetics And Environment: What Animal Models Show
Aging is recognized to be the primary risk factor for PD with incidence rising exponentially with advancing age. Nevertheless, most elderly over 85years do not have PD. Familial PD due to monogenic causes account for about 5% of all PD but the majority of known mutations have incomplete and variable penetrance. It is hypothesized that genetic risk factors may render the individual more sensitive to the pathologic influence of other factors. For example, the cumulative risk of PD in carriers of LRRK2 p.G2019S, the most common LRRK2 mutation in PD, rises exponentially from the age of 50 onwards , suggesting that aging interacts with LRRK2 mutations to initiate disease. This observation is corroborated in a LRRK2 G2019S knock-in mouse model which showed dysfunctions in plasma membrane and vesicular DA transporters, and accumulation of serine129-phosphorylated -synuclein, the predominant form of -synuclein in Lewy bodies, in 12-month-old KI mice compared to age-matched wild-type mice. These changes were not present in young 3-month-old KI mice, suggesting a progressive response relying on the interaction of the mutation and aging . Similarly, another LRRK2 KI mouse model, LRRK2 R1441G, showed a progressive, age-dependent accumulation of oligomeric -synuclein in the striatum and cortex compared with age-matched WT mice this higher rate of oligomeric -synuclein accumulation in KI than WT mice was first apparent at 15months and became significant at 18months of age .