WHAT IS PARKINSON’S DISEASE.
Parkinson’s Disease is a progressive neurodegenerative disease that affects and depletes the nerve cells (neurons) in an area of the brain known as the substantia nigra where the brain produces dopamine, when normally functioning.
Dopamine is a vital brain chemical that serves as a chemical messenger allowing communication between the substantia nigra and another area of the brain called the corpus striatum. This communication allows and coordinates smooth and balanced muscle movement. A lack of dopamine results in abnormal nerve functioning, causing a loss in the ability to control body movements.
Related symptoms include increasingly slow motor function, tremor when at rest, muscle rigidity, and abnormalities in your walk.
Parkinson’s disease is one of several diseases categorized by clinicians as movement disorders.
Parkinson’s disease was first characterized extensively in 1817 by James Parkinson, an English doctor,.
- 10 million people worldwide are living with Parkinson’s disease.
- 1-1.5 million Americans are affected by Parkinson’s.
- 60,000 Americans are diagnosed with Parkinson’s each year, (wihout taking into consideration the thousands of unreported cases).
- Incidence of Parkinson’s increases with age, but an estimated four percent of people with PD are diagnosed before the age of 50. Cases are now being reported regularly in people even under 40 years of age.
- Men are one and a half times more likely to have Parkinson’s than women. Source: pdf.org/parkinson_statistics
PARKINSON’S DISEASE SYMPTHOMS
Parkinson’s disease symptoms are of three orders:
- Primary Motor Symptom
- Secondary Motor Symptoms
- Nonmotor Symptoms
Early stage symptom of the disease common to about 70 percent of people.
It manifests as a slight tremor in the hand or foot on one side of the body, or less commonly in the jaw or face. A typical onset is a tremor in one finger in one side of the body.
It consists of a shaking or oscillating movement in one finger, and it appears when a person’s muscles are at rest, hence the term “resting tremor.”
The affected body part trembles when it is at rest and it usually ceases when a person begins an action. The tremor spreads to the other side of the body as the disease progresses,
Not all people with PD (Parkinson’s Disease) will develop tremor.
Bradykinesia: (slowness of movement)
A defining feature of Parkinson’s, bradykinesia also describes a general reduction of spontaneous movement, which can give the appearance of a decrease in facial expressivity.
The patient will show difficulty with repetitive movements, as well as performing everyday functions, such as buttoning a shirt, cutting food or brushing his or her teeth.
Difficulty walking: they walk with short, shuffling steps.
Difficulty of speech, which becomes less distinct as Parkinson’s progresses.
Rigidity causes stiffness and inflexibility of the limbs, neck and trunk., tightness of the neck, shoulder, and leg.
the muscle tone of an affected limb is always stiff and does not relax, contributing to a decreased range of motion.
It is the tendency to be unstable when standing upright because some of the reflexes needed for maintaining an upright posture have been lost and is likely to topple backward
They may also find difficulty pivoting or making turns or quick movements.
Secondary Motor Symptoms
People who experience freezing step forward hesitantly because they feel as if their feet are glued to the floor.Freezing can be temporary when starting to walk, when pivoting, when crossing a threshold or doorway, and when approaching a chair.
Iit may increase a person’s risk of falling forward.
It is the name for a shrinkage in handwriting. This occurs as a result of bradykinesia, which causes difficulty with repetitive actions.
A person’s face may appear less expressive than usual, it is due to a decrease of the unconscious facial movements.
For some people with Parkinson’s experience movements that are too quick or speech that is top fast. Excessively fast speech, tachyphemia, produce a rapid stammering that is hard to understand. Uncontrollable acceleration in gait, may be at increased risk for falls.
Additional secondary motor symptoms include also:
- Stooped posture, a tendency to lean forward
- Dystonia, disorder in which a person’s muscles contract uncontrollably
- Impaired fine motor dexterity and motor coordination
- Impaired gross motor coordination
- Poverty of movement (decreased arm swing)
- Poverty of movement (decreased arm swing)
- Akathisia, a movement disorder characterized by a feeling of inner restlessness and a compelling need to be in constant motion
- Speech problems, such as softness of voice or slurred speech caused by lack of muscle control
- Difficulty swallowing
- Sexual dysfunction
- Drooling and excess saliva resulting from reduced swallowing movements
but not all people with Parkinson’s will experience all of these.
There are nonmotor symptoms, that is symptoms that do not involve movement, coordination, physical tasks or mobility. These are more difficult to detect for an observer.
Nonmotor symptoms precede motor symptoms by years.
- Loss of sense of smell,
- REM behavior disorder (a sleep disorder)
- Mood disorders
- Orthostatic hypotension (low blood pressure when standing up).
- Bladder problems
- Sexual problems
- Excessive saliva
- Weight loss or gain
- Vision and dental problems
- Fatigue and loss of energy
- Fear and anxiety
- Skin problems
- Cognitive issues, such as memory difficulties, slowed thinking, confusion and in some cases, dementia
- Medication side effects, such as impulsive behaviors
WHAT CAUSES PARKINSON DISEASE
There have studies and researches that have linked Parkinson’s to:
Insecticides: like permethrin and beta-hexachlorocyclohexane (beta-HCH).
Herbicides: like paraquat and 2,4-dichlorophenoxyacetic acid.
Fungicide: like maneb.
Agent Orange used in the Vietnam War.
MPTP, a synthetic neurotoxin (can cause Parkinsonism)
Pesticides and herbicides like glyphosate now strongly linked to Parkinson’s disease and other neurological disorders.
1 Pesticides, Herbicides And Parkinson’s
Pesticides and herbicides are sprayed so carelessly today, are infiltrating both the chemistry of the food and the air we breathe.
From the Division of Cancer Epidemiology and Genetics at the National Cancer Institute, researchers found that chronic pesticide exposure is linked directly to Parkinson’s disease.
In May 2013, the American Academy of Neurology (AAN) published results of over 100 studies from around the world, showing that increased “exposure to pesticides, herbicides and solvents is “likely associated with a higher risk of developing Parkinson’s disease.” Farmers that work directly with these chemicals suffer the most from neurological disorders, especially Parkinson’s. Pesticide exposure in rural areas was directly linked to a two-fold increased risk of developing Parkinson’s.
Pesticides and herbicides are destroying the body’s natural relationship
Mankind wants to control and manipulate nature by taking chemical shortcuts with agriculture and food production. But we have to understand that thousands of chemicals that have been developed are interfering with the natural, healthy relationship between our organ systems.
Now finally scientists are understanding that the mechanism that the herbicide glyphosate uses to destroy plants, is the same mechanism that kills the good microbes in the human gut. We need these microbes that assist in the proper absorption of nutrients, elimination of waste, detoxification of impurities, and protection of the gut lining and blood. Without a strong microbiome, the human body is slow to initiate immune responses to pathogenic stressors.
Genes are being damaged at a young age as infants are inundated with chemicals
The burden of chemicals is much more devastating on small, developing bodies which are typically 1/30th the weight of a grown adult.
Unfortunately, infants are being introduced to pesticides and herbicides at such a young age. Additionally, the rate at which infants are being injected with vaccine aluminum, antibiotics, formaldehyde, MSG, animal and human body cell lines, and in some cases mercury, suggests that their healthy genes may never see normal conditions to express their innate, healthy disposition.
These chemicals break down the lining of the gut and deplete the body’s intelligent microbiology, the blood is easily infiltrated, allowing chemicals to circulate through the entire system, taxing filtration systems like kidneys, gall bladder, liver, and skin.
If the body is exposed for long enough, the pesticides, heavy metals and other chemicals may even circulate to the brain, causing neuron cell death and interfering with hormones and mental homeostasis.
Many risk factors have been implicated in PD. Since the discovery of MPTP Parkinsonian inducing effects, this arouses the possibility of other similar compounds relevant to MPTP, for example, paraquat to induce PD.
Numerous classes of pesticides were introduced during the twentieth century. Although PD existed long before the introduction of these pesticides, the thought is that pesticide exposure has contributed to the increased incidence of the disease .
In a 2011 study led by researchers at the University of California Los Angeles’s School of Public Health, simple, routine home-and-garden pesticide exposure resulted in three times increased risk of Parkinson’s. In a meta-analysis, 17 out of 19 studies showed that increased duration of exposure to pesticide and herbicide chemicals was directly linked with increased risk of Parkinson’s.
The fumigant class encompasses a variety of agents most commonly used to control insects or fungi in grains, soil, or other various consumables. Fumigants, such as ethylene dibromide, are highly toxic to humans but most adverse actions are nonneuronal. Although there is some evidence that carbon disulfide-based fumigants can induce parkinsonian-like neurotoxicity . This chemical class is not suitable for induction of PD in an animal model.
Fungicides are agents of a wide variety of chemical structures. Maneb, or manganese ethylene-bis-dithiocarbamate, is one type of possible parkinsonian symptoms which may be secondary to exposure to the manganese metal core.
In fact, maneb is one of the toxins used to induce PD in animal models but usually in combination with other agents specially paraquat . The maneb effect has been undoubtedly documented to increase the severity of PD models which make it one of the good candidates in PD research
The possibility that paraquat may damage the nigrostriatal dopaminergic system (one of the major dopamine pathways in the brain, the connection between the susbtantia nigra and corpus striatum) and therefore contribute to the neuropathology of Parkinson’s disease (PD
This theory was first proposed in the mid-1980s following the observation that its chemical structure closely resembles that of MPP+(1-methyl-4-phenylpyridinium ion, is a positively charged toxic molecule. It acts by interfering with oxidative phosphorylation in mitochondria by inhibiting complex I, (an enzyme of the respiratory chains of myriad organisms from bacteria to humans, It catalyzes the transfer of electrons from NADH to coenzyme Q10 (CoQ10) and, in eukaryotes)
Mitochondria in cells treated with MPP+ also display a phenotype indicative of apoptosis: small, round, and fewer in number. It also inhibits the synthesis of catecholamines, reduces levels of dopamine and cardiac norepinephrine, and inactivates tyrosine hydroxylase.
Animal studies confirmed the ability of paraquat to induce selective dopaminergic nigrostriatal degeneration.
Alarming new research published in the journal Neurotoxicology and Teratology supports the emerging connection between glyphosate, the active ingredient in Monsanto’s Roundup herbicide, and neurodegenerative conditions such as Parkinson’s disease and Parkinsonian disorders.
Herbicides have been recognized as the main environmental factor associated with neurodegenerative disorders, such as Parkinson’s disease.
There are several subclasses of insecticides, each with their own subdivisions. Many of the compounds in this class are, by design, neurotoxic. Similarities between the insect and human nervous systems can lead to cross-toxicity of these compounds.
2 Deterioration Of Gut Bacteria (also responsible for chronic fatigue).
Increasingly scientists are connecting the dots and finding that Parkinson’s is truly related to gut bacteria.
In 2015, research from the Department of Neurological Sciences at the University of Helsinki – along with doctors at the University Central Hospital studied the bacteria of 72 Parkinson’s patients and compared them with 72 healthy human control subjects.
The scientists analyzed the feces of each of the subjects and ran sequencing scans in order to determine the genetics of their microbiome (cumulative genetic contents of a person’s intestinal bacteria as gauged through the analysis of feces).
Healthy bacteria are called probiotics, while disease-causing bacteria are called pathobiontic’s, or pathogenic bacteria
The results of the Swedish study were surprising. The scientists found that on average Parkinson’s disease patients had about 23 percent less Prevotella (healthy gut bacteria) and more bacteria in the Enterobacteriaceae family compared with the healthy subjects.
(The Enterobacteriaceae family includes disease-causing bacteria such as Escherichia coli, Yersinia pestis, Klebsiella, Citrobacter, Shigella, Proteus, Salmonella, Enterobacter and Serratia species of bacteria).
The link between guts and Parkinson’s
Parkinson’s damages neutrons in the area of the brain called substantia nigra.
The substantia nigra thus cannot produce enough dopamine.
Lewy bodies are involved in the progression of Parkinson’s.
Lewy bodies are linked with increased pathogenic bacteria in the gut.
Pathogenic bacteria, fight for territory within the gut. If they win this competition, the results is what medical researchers call SIBO – small intestine bacteria overgrowth. which is typical of Parkinson’s patients.
SO IT IS PROVEN THAT PARKINSON’S PATIENTS WITH SILENT CELIAC DISORDER COULD BE TREATED WITH PROBIOTICS (live microorganisms that are believed to provide health benefits when consumed helpful in improving your gut fighting against pathogenic bacteria).
But to what degree will it make a difference?
Probiotic supplementation for a few weeks will not make any significant impact. Some laboratory research using probiotics has shown improved brain tissue protection and decreased inflammation among brain tissues. But long-term clinical studies on human subjects have been limited
And the question is whether a few years of significant probiotic treatment could help decrease the Parkinson’s symptoms – or at least slow the progression of this condition.
At the very least we know that probiotic supplementation will help the Parkinson’s patient improve bowel movement consistency and frequency – and possibly eliminate constipation associated with Parkinson’s.
Said lead researcher Sarkis Mazmanian from the Californian Institute of Technology (Caltech): “Now a new study in mice has shown that the toxic fibers that build up around the nerve cells of Parkinson’s patients can influence the nerves in the brain in a matter of weeks.
“We have discovered for the first time a biological link between the gut microbiome and Parkinson’s disease,”
3 Vitamin D deficiency
Life Extension Magazine reports:
“Previous studies … [suggested] that long-term effects of Parkinson’s disease may contribute to the development of insufficient vitamin D concentrations … Contrary to [the] expectation that vitamin D levels might decrease over time because of disease-related inactivity and reduced sun exposure, vitamin D levels increased over the study period.
These findings are consistent with the possibility that long-term insufficiency is present before the clinical manifestations of Parkinson’s disease and may play a role in the pathogenesis of PD.”
A study of more than 150 Parkinson’s patients found that almost 70 percent had vitamin D insufficiency (defined as levels of less than 30 nanograms per milliliter) at the beginning of the study, and about 26 percent were classified as deficient (levels of less than 20 nanograms per milliliter.)
Now also a deficiency in vitamin D appears to be a prime risk factor for PD.
The new findings refute the previous belief that vitamin D deficiency was a symptom of Parkinson’s and instead clearly indicate the vitamin D deficiency is one of the causes of Parkinson’s:
the Archives of Neurology is offering even further scientific proof that backs this claim up:
“Previous studies in Asian populations reported a higher prevalence of hypovitaminosis D (deficiency or insufficiency) in patients with more advanced disease, suggesting that long-term effects of Parkinson’s disease may contribute to the development of insufficient vitamin D concentrations,” the authors write.
“Contrary to our expectation that vitamin D levels [in Parkinson’s patients] might decrease over time because of disease-related inactivity and reduced sun exposure, vitamin D levels increased over the study period.
These findings are consistent with the possibility that long-term insufficiency is present before the clinical manifestations of Parkinson’s disease and may play a role in the pathogenesis of [Parkinson’s].”
4 Consumption of Gluten Containing Foods
Gluten’s toxicity affects the nervous system, producing symptoms identical to classical Parkinson’s disease. Parkinsonism exacerbates celiac disease
A new case study adds to a growing body of research indicating that wheat’s neurotoxicity is greatly underestimated.
the Journal of Neurology published a new case report describing the recovery of a 75-year-old Parkinson’s disease patient after following a 3-month long gluten free diet.
the report also notes that celiac disease often manifests with only neurological symptoms, even in advanced age.
After the various tests, finall, a duodenal biopsy on the patient revealed intestinal characteristics consistent with celiac disease. As a result, the gastroenterologist prescribed a gluten-free diet.
After only 3 months of abstinence from gluten, the patient was an almost complete remission of parkinsonism symptoms, that was subsequently confirmed by a neurological evaluation. A reexamination 18 months later found that he had improved further.
The published literature on gluten related adverse health effects shows that non intestine related expressions of intolerance to gluten-containing grains are more common than gut-related ones.
The range of mechanisms driving gluten associated neurotoxicity, are many:
• Gluten Acts As A ‘Brain Drug’: In gluten are present pharmacologically active opioid peptides which include four gluten exorphins (a group of opioid peptides formed during digestion of the gluten protein). Gluten has the ability to restrict blood flow to the frontal cortex.
• ‘Gluten Brain’ Autoimmunity: In susceptible individuals wheat increases intestinal permeability (the control of material passing from inside the gastrointestinal tract through the cells lining the gut wall, into the rest of the body.) , and leads to the immune system to misidentify tructures within the neurological tissue as “other,” causing the host immune system to attack its own nervous system.
• Wheat’s “Invisible Thorns” Affect The Brain: the wheat germ agglutinin (WGA) (defensive carbohydrate-binding protein), also know as “wheat lectin,” crosses the blood-brain-barrier and interferes with neurological function in a number of ways (Pro-inflammatory, Immunotoxic, Neurotoxic, Cytotoxic, Endocrine Function Disruptor, Cardiotoxic, Gastrointestinal Function impairment)
• Grains Cause Metabolically Impair Of The Brain: Dr. David Perlmutter in his NY Times bestselling book Grain Brain links cognitive impairments endemic to older populations in Western cultures to the over consumption of carbohydrates (from grains and sugar), and the under consumption of fats.
Considering these factors, it is not surprising that gluten removal from the diet could result in the improvement of the parkinsonism symptoms after the introduction of a gluten-free diet of patients with silent celiac disease.
Similar remarkable recoveries in cases of debilitating dementia, including Alzheimer’s disease, have been noticed optimizing intake of fats like coconut (MCTs is the primary type of fat found within coconut oil)
5 Genetic Inheritance
There is also some evidence that Parkinson’s disease may be passed on genetically from family members).
however the possibility of a genetic cause of Parkinson’s disease is considerably controversial.
Though In a small number of families, specific genetic abnormalities leading to the illness have been identified, the vast majority of people with Parkinson’s disease do not have one of these identified genetic abnormalities.
Only in people who develop Parkinson’s disease early in life (called young-onset Parkinson’s disease) there is a genetic component.
In the past 10 years, researchers have identified a number of rare instances where Parkinson’s disease appears to be caused by a single genetic mutation. In these cases, the mutated gene is passed from generation to generation, resulting in a great number of Parkinson’s disease cases within an extended family. Mutations in the LRRK2 gene are the greatest genetic contributor to Parkinson’s disease discovered to date.
6 Oxidative Stress.
Also, it is believed that oxidative stress can cause Parkinson’s disease. Oxidation causes free radicals which, in an attempt to replace the missing electron, react with other molecules
Oxidation is caused by Free radicals which normally forme in the brain and body, and usually the brain and body have mechanisms to get rid of them but In people with Parkinson’s disease, the mechanisms may not work and produce too many free radicals.
Oxidation cause damage to tissues, including neurons.
One reason to intake antioxidants is that they protect cells from free radical damage.
A small proportion of PD cases have a toxic cause as the sole or a partial cause of Parkinson’s Disease.
The toxic exposure usually has to be acute or chronic. Symptoms normally develop when the toxic exposure occurs or soon after, or gradually increase over time when the exposure persists. Symptoms do not develop years later as is sometimes claimed. Avoidance of the source of toxicity can lead, in most cases, to a reduction in the symptoms but with some toxins this can take years.
Toxicity can be cause by:
Annonaceae is a family of flowering plants that is also called the custard apple family. Some annonaceae species produce edible fruits. Annonaceae contain acetogenins. In Guadeloupe, Annonaceae are consumed as herbal teas and fruits, especially soursop. Annonacin, which is the most abundant acetogenin, is toxic to dopaminergic neurons in nanomolar concentrations. Acetogenins are potent mitochondrial toxins, like other Parkinsonism inducing compounds. The concentrations of annonacin, the major acetogenin in Annona Muricata, are so high that one fruit or can of nectar per day is more in a year than induced brain lesions in rats receiving purified annonacin by intravenous infusion.
Carbon disulfide is a colourless, flammable, and poisonous liquid with the chemical formula CS2. Carbon disulfide is in pesticides used as fumigants, disulfiram, which is a drug used in the treatment of chronic alcoholism, industrial solvents, and solvents used in the production of viscose rayon and cellophane film. Carbon disulfide interferes with the enzyme pyridoxal 5-phosphate, which is essential for the formation of dopamine from L-dopa. So carbon disulfide might cause Parkinson’s Disease symptoms by reducing the formation of L-dopa.
Copper, whose chemical symbol is Cu, is a chemical element that is required as an essential nutrient, but which can be toxic in large quantities. Common causes of copper toxicity include Wilson’s Disease in which there is a genetic accumulation of copper, copper mines, copper cooking pots, copper plumbing, extreme consumption of nutritional supplements that contain copper. Excessive copper can cause the formation of a copper-dopamine complex, which leads to the oxidation of dopamine to aminochrome.
Cycad seeds of the Cycas micronesica contain ss-methylamino-L-alanine (BMAA), which have been implicated as the cause of toxicity due to the involvement of a product of BMAA and a beta-carbamate. Cycad seeds, by different means, can cause Amyotrophic lateral sclerosis (ALS) and Parkinsonism-dementia complex (PDC). This occurs in Guam, which is in the Mariana islands in the Pacific Ocean, the Kii peninsula of Japan, and New Guinea, which is divided between Indonesia and Papua New Guinea.
Dieldrin is used as a pesticide. Dieldrin was the most frequently detected Organochlorine pesticide in people with Parkinson’s Disease thereby suggesting that dieldrin may be associated with Parkinson’s Disease.
Dieldrin levels were above normal in brains of people with Parkinson’s Disease.
Dieldrin adversely affects cellular processes associated with Parkinson’s Disease including mitochondrial function and reactive oxygen species production. Dieldrin showed inhibitory effects on proteasome activities at low concentrations. Dieldrin induces apoptosis in dopaminergic neurons via caspase-3-dependent proteolytic activation of protein kinase C delta.
Hydrocarbons are organic compounds consisting entirely of hydrogen and carbon. Common sources are : hydrocarbon poisoning such as that of benzene and petroleum usually occurs accidentally by their inhalation or ingestion. Sources of hydrocarbons include : natural gas, cooking gas, petrol, gasoline.
People that have been subjected to exposure to petroleum products, especially when working with petroleum products, increase the likelihood of developing Parkinson’s Disease. Working in a gas station (petrol station) increased the risk of Parkinson’s Disease by 2.6 times.
Lead is a chemical element that is toxic in humans. Common sources are : lead contaminated soil, ingestion of lead dust or chips from deteriorating lead-based paints, air pollution from the processing of lead, food grown in contaminated soil, drinking water from plumbing and fixtures that are either made of lead or have trace amounts of lead in them. Lead can also be found in cosmetics in some countries, some herbal remedies, and in toys such as many from China. Serious and chronic exposure to lead can more than double the likelihood of developing Parkinson’s Disease. Milder exposure to lead did not increase the likelihood of Parkinson’s Disease.
The main active element of Maneb is manganese ethylene-bis-dithiocarbamate. Maneb is used as a fungicide. There is a greatly increased likelihood of developing symptoms by people involved in horticulture and agriculture.
As Maneb contains manganese it is possible that it causes Parkinson’s Disease symptoms via the same means as manganese, which is by inhibiting tyrosine hydroxylation. Tyrosine hydroxylation is essential for the formation of dopamine. It would thereby lower dopamine levels. The effects of Maneb are potentiated when there is simultaneous exposure to the pesticide Paraquat.
Manganese is a chemical element that is required as a nutrient but can be toxic in large quantities.
Occupational exposures occur in welding, when highly exposed, miining as miners are surrounded by manganese dust and airborne manganese particles, alloy production, processing, ferro-manganese operations especially in which manganese ore or manganese compounds are turned into steel, and work with agrochemicals.
Areas surrounding manganese heavy industry could also become affected by exposure to manganese. It could occur with very excessive use of manganese supplements. Manganese can cause Manganism, which is a medical disorder that is virtually no different in its symptoms from Parkinson’s Disease.
Mercury is a chemical element that is toxic in humans.
Common sources are : dietary fish intake, ethnic over-the-counter medications, occupational exposures to mercury vapour, possession of dental amalgam fillings, gold production, skin ointment, and some soaps. One of the chief means of toxicity is via the enzyme pyruvate dehydrogenase (PDH), which is irreversibly inhibited by several mercury compounds.
However, the cause of the symptoms of Parkinson’s Disease is likely to be due to the fact that mercury potently causes the release of dopamine, thereby lowering dopamine levels.
MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine) is a chemical that may be produced accidentally during illicit manufacture of the recreational drug MPPP, which is a synthetic heroin substitute. The most common source is the recreational drug MPPP (Desmethylprodine). It was also developed but unused as a herbicide. It is also an industrial toxin. MPTP inhibits tyrosine hydroxylation, which is essential for the formation of dopamine. So MPTP causes Parkinson’s Disease by lowering dopamine levels.
Nitrogen dioxide is an intermediate in the industrial synthesis of nitric acid, millions of tons of which are produced each year.
At higher temperatures it is a reddish-brown gas that has a characteristic sharp, biting odour and is a prominent air pollutant. Exposure of nitrogen dioxide to tyrosine hydroxylase results in the nitration of its tyrosine residues. High exposure to nitrogen dioxide, largely because of pollution, trebled the risk of Parkinson’s Disease. Lower exposures did not significantly increase the risk.
Octenol, which is commonly known as mushroom alcohol, is produced by several plants and fungi. Octenol can often be inhaled by humans after being produced in damp, mouldy or water damaged buildings. Octenol interferes with two genes involved in the creation of dopamine : the human plasma membrane dopamine transporter (DAT) and the human VMAT ortholog (VMAT2). This demonstrates that 1-octen-3-ol exerts toxicity via disruption of dopamine homeostasis.
Organophosphorous pesticides are used primarily in pest control as alternatives to chlorinated hydrocarbons that can persist in the environment. Organophosphorous pesticides are used in agriculture. Organophosphorus chemicals have also been used as active ingredients in household pesticides for several decades. Organophosphorus pesticides are significantly associated with Parkinson’s Disease. The frequent use of household pesticides that contain organophosphorus chemicals increased the chances of developing Parkinson’s Disease by 71% .
Paraquat is used as a herbicide.
There is a greatly increased likelihood of developing symptoms by people involved in horticulture and agriculture.
People with Parkinson’s Disease are more than twice as likely to report heavy exposure to pesticides over their lifetime as family members without Parkinson’s Disease. Those people affected were usually those who used a lot of pesticides in their homes and in their hobbies rather than those who routinely used pesticides for their occupation. Pesticides are also known to affect well water. However, it is claimed that Paraquat only potentiates the effect of Maneb, and that it has no effect on humans on its own.
Rotenone is used as an insecticide.
There is a greatly increased likelihood of developing symptoms by people involved in horticulture and agriculture.
People with Parkinson’s Disease are more than twice as likely to report heavy exposure to pesticides over their lifetime as family members without Parkinson’s Disease.
Those affected were usually those who used a lot of pesticides in their homes, rather than those who routinely used pesticides for their occupation. Insecticides are also known to affect well water. Rotenone is commonly used to treat parasitic mites on chickens and other fowl, and so can be found in poultry. Rotenone inhibits tyrosine hydroxylation, which is essential for the formation of dopamine.
Toluene is used as an octane booster in fuel, as a solvent in paints, paint thinners, chemical reactions, rubber, printing, adhesives, lacquers, leather tanning, disinfectants, producing phenol and TNT. Toluene is also used as a raw material for toluene diisocyanate, which is used in the manufacture of polyurethane foams. Toluene is also used in the manufacture of dyes. Dyes are highly associated with the symptoms of Parkinson’s Disease.
The means of toxicity is unknown. Toluene has been shown to cause Parkinson’s Disease or has been associated with people with Parkinson’s Disease.
Trichloroethylene is a solvent with a sweet smell that is a clear non-flammable liquid. Trichloroethylene is a solvent that is used in industry and the military and is a common environmental contaminant.
It has been used to extract vegetable oils, in coffee decaffeination, and the preparation of flavouring extracts from hops and spices. The means of toxicity is unknown. Workers with workstations adjacent to the source of trichloroethylene and who were subjected to chronic inhalation and dermal exposure from handling trichloroethylene-soaked metal parts all had Parkinson’s Disease.
ALUMINUM FOIL AND PARKINSON’S
Almost everyone has aluminum foil in their kitchens, by the BBQ, or taken with us to the camp site to use on the fire or afterwards to store our cooked food. It has so many uses.
However when it comes to using aluminum in food preparation and storage, what has science informed us? Aluminum foil is safe when used cold, like wrapping a sandwich for the fridge; however, using it hot, or even warm, the foil is degraded and seeps into the food.
When hot or heated, the levels of aluminum that leak into the food are considerably higher if the food actually touches the foil, if seasonings are added, or if the food is acidic. The hotter the foil is heated, the more seepage occurs. This result occurs no matter which side of the foil is next to the food.
Aluminum impedes the digestion of calcium, phosphorus, and fluoride, which can even result in osteoporosis. It harms the kidneys and impairs the liver. It is linked to neurodegenerative diseases like Parkinson’s and Alzheimer’s. It can lead to sleep disturbance, and speech problems.
There are lots of sources of aluminum in our day to day lives; antacids, vaccines, antiperspirants, even drinking water. So we’re already getting a heavy dose of aluminum. Cooking in aluminum foil or aluminum pans increase exposure.
The decision to add fluoride to most public drinking water systems as a way to fight tooth decay has perhaps had the most insidious and widespread effect on the brains of people across North America.
The Fluoride Action Network (FAN) has reported on a study which found that fluoride is linked to lower IQ, even at the ranges added to U.S. water supplies. In all, FAN said that 34 studies now link fluoride to lower IQ levels in humans, while many other studies link fluoride to learning and memory impairment, fetal brain damage and altered neurobehavioral function.
One study sponsored by UNICEF found that IQ was reduced at just 0.88 mg/l of fluoride, a level that is considered within optimal range and is added to U.S. drinking water systems that serve over 200 million Americans every day.
Heavy metals are especially sinister toxins that are not easily removed but are commonplace in the bodies and brains of millions thanks to vaccines, dental procedures, agricultural chemicals, industrial pollution, fish, chicken and more.
Those most susceptible to traumatic brain damage due to mercury are newborn babies who have yet to properly develop their blood-brain barrier and are generally subjected to an intense vaccination schedule that injects mercury directly into their body.
In babies with a genetic susceptibility, such as a defect in enzymes responsible for detoxifying heavy metals, prenatal and early postnatal exposure to mercury leads to neurological damage resulting in autistic symptoms.
Robert Nash, M.D., also suggests that the toxic effects of mercury can cause a broad spectrum of brain-related diseases including autism, Alzheimer’s, amyotrophic lateral sclerosis, multiple sclerosis, Parkinson’s disease and neurodevelopmental diseases.
Avoid the flu shot, mercury fillings and chemicals, and take safety precautions when consuming seafood.
Their negative effects on the brain have been well documented. They are found in sodas, yogurt, chewing gum, cooking sauces, tabletop sweeteners, flavored water, cereals and sugar-free products.
Aspartame is a combination of chemicals, namely aspartic acid (an amino acid with excitatory effects on brain cells), methanol and phenylalanine, and scientists are placing it at the higher end of the range of what is considered toxic. When aspartame breaks down, it produces a compound that is a powerful brain-tumor-causing chemical.
Ninety different symptoms have been documented as a result of aspartame consumption, including anxiety attacks, slurred speech, depression and migraines.
Avoid artificial sweeteners by reading ingredients and avoiding the products above. The FDA also recently approved of calling aspartame AminoSweet, so beware of that ingredient as well.
MONOSODIUM GLUTAMMATE (MSG)
MSG is a form of concentrated salt added to foods to enhance flavor. It was first used in military rations to give them a better taste, but it was soon adopted by the entire food industry.
Dr. Blaylock, a noted neurosurgeon and authority on excitotoxins such as MSG, discovered that there was silent damage to the brain, and over time he saw destruction of major portions of the brain that could cause Parkinson’s, Alzheimer’s disease, and other brain ailments.
The best way to avoid it is to stop eating processed food, or look for it in the ingredients, mainly as monosodium glutamate or yeast extract.
Toxins, Toxins, Toxins seem to be the main cause if not “the” cause of Parkinson’s Dis-ease.
Whether the toxin comes from a pesticide, a vaccine, aluminum foil , artificial sweeteners, MSG or medications, we find ourselves looking at “toxins” again as the cause of this avoidable dis-ease! Avoid the toxins and you probably won’t EVER get this dis-ease of the body. What is nice is that the G2 Sacraments can detox the body of heavy metals, chemicals and pathogens!
8 Drug-induced Parkinsonism
About 7% of people with parkinsonism have developed their symptoms following treatment with particular medications mainly neuroleptic antipsychotics, and rarely, antidepressants..This form of parkinsonism is called ‘drug-induced parkinsonism’.
Drug-induced parkinsonism tends to remain at its presenting level, not progress like Parkinson’s disease.
What drugs cause drug-induced parkinsonism?
Any drug that blocks the action of dopamine (referred to as a dopamine antagonist) is likely to cause parkinsonism.
Drugs used to treat schizophrenia and other psychotic disorders such as behaviour disturbances in people with dementia, known asneuroleptic drugs, are possibly the major cause of drug-induced parkinsonism worldwide.
Parkinsonism can occur from the use of any of the various classes of neuroleptics.
The atypical neuroleptics – clozapine (Clozaril) and quetiapine (Seroquel), and to a lesser extent olanzapine (Zyprexa) and risperidone (Risperdal) – appear to have a lower incidence of extrapyramidal side effects, including parkinsonism. These drugs are generally best avoided by people with Parkinson’s, although some may be used by specialists to treat symptoms such as hallucinations occurring with Parkinson’s.
For people with Parkinson’s, anti-sickness drugs such as domperidone (Motilium) or ondansetron (Zofran) are the drugs of choice for nausea and vomiting.
As well as neuroleptics, some other drugs can cause drug-induced parkinsonism.
These include some medications for dizziness and nausea such as prochlorperazine (Stemetil); and metoclopromide (Maxalon), which is used to stop sickness and in the treatment of indigestion.
Calcium channel blocking drugs used to treat high blood pressure, abnormal heart rhythm, angina pectoris, panic attacks, manic depression and migraine may occasionally cause drug-induced parkinsonism.
Calcium channel blocking drugs are, however, widely used to treat angina and high blood pressure, and it is important to note that most common agents in clinical use probably do not have this side effect. These drugs should never be stopped abruptly without discussion with your doctor.
A number of other agents have been reported to cause drug-induced parkinsonism, but clear proof of cause and effect is often lacking. Amiodarone, used to treat heart problems, causes tremor and some people have been reported to develop Parkinson’s-like symptoms. Sodium valproate, used to treat epilepsy, and lithium, used in depression, both commonly cause tremor which may be mistaken for Parkinson’s.
What are the characteristics of drug-induced
parkinsonism and how does it differ from idiopathic Parkinson’s?
Drug-induced parkinsonism is more likely to be symmetrical (on both sides of the body) and less likely to be associated with tremor, although it can sometimes present asymmetrically and with a tremor.
Akinesia (lacking of movement) with loss of arm swing can be the earliest feature.
Bradykinesia (slowness of movement) can be an early common symptom, causing expressionless face, slow initiation of movement and speech difficulties.
If the offending drug is stopped, will the drug-induced parkinsonism improve and if so, how long will this take?
Generally, the majority of people will recover within two months, and often within hours or days, of stopping the offending drug. However, some people may take as long as two years.
Currently Prescribed Parkinson’s Drugs May Actually Make You WORSE
Dopamine agonists currently used to treat Parkinson’s. They appear to curb some of the side effects of the disease, but they may lead to some disturbing side effects. These have been reported :
- Dizziness, drowsiness, lightheadedness, or fainting
- Weight loss
- Pathological addiction (gambling, shopping, internet pornography, hypersexuality)
- Unusual tiredness or weakness
- Increased orgasmic intensity
- Twitching, twisting, body movements
9 A Combination Of Genetic And Environmental Causes.
For most Parkinson’s patients, the cause lies somewhere in the middle. While many Parkinson’s patients report one or more family members with the disease, it is not always clear that one or several genes are the cause. Similarly, while some patients suspect that exposure to one or another chemical or environmental toxin caused their Parkinson’s disease, this also cannot be conclusively proved.
Scientists currently believe that in the majority of cases, genetic and environmental factors interact to cause Parkinson’s disease. Research into this subject continues aggressively every day. Unfortunately, however, it is generally impossible to determine what specifically caused an individual’s Parkinson’s disease.
BUT There are a few things you can do to treat this disease.
We will see them on the next post.
Until next time.