What Causes Parkinson’s?
Most often it is reported that the causes of Parkinson’s are unknown. What is exceptionally interesting about this is that there have been a tremendous number of studies undertaken over a long period of time to attempt to establish a definite cause, so some potential causes are well known.
Because of the disease's complicated nature, the wide variety of symptoms, progression and different clinical subtypes it is stated that there has been little to no success. The reality of it is that there actually has been a significant amount of success in studying the pathogenesis of Parkinson’s. One of the biggest roadblocks to determining the cause is probably related to the fact that much scientific research fails to consider that this disease does not have one particular cause and there is no one treatment that will cure all of the symptoms. Another notable fact about research is that it often looks more at the resulting pathology of the disease rather than what occurs at inception. Some researchers clearly state that it is a cascading series of events that leads to a diagnosis of Parkinson’s disease which is probably a more accurate assessment.
Parkinson’s is a multi-factoral condition that involves many different systems throughout the body. Although it is considered a brain disease much information points to the possibility that it has an entirely different etiology. There are many changes that occur in the body with Parkinson’s aside from the physical symptoms. Imbalances in minerals, vitamin deficiencies, enzymatic changes, DNA alterations and malfunctions at the cellular level are all noted in the disease. It is known that a depletion of dopamine in the brain is a cardinal clinical feature of the disease. Exactly how this whole process occurs is still not understood. Oxidative stress is strongly suspected to be a causative factor in the disease but again it has not fully been comprehended. It is important to look at all of these factors independently and then review them in summary to better understand what occurs.
There is much reference to possible genetic causes of Parkinson’s. Inherited genetic causes of Parkinson’s are estimated to be less than 2 percent suggesting that it is more a disease of genetic alteration rather than an inherited trait. The term ‘predisposed genetic disposition’ also is frequently used. This is an exceptionally confusing subject because genetics is a very broad and complicated subject that is not easily explained in layman’s terms. We are all born with a set of genes that constitute our physical makeup. This can encompass everything from hair and eye color to thought processes and behaviors. What is important to remember about your gene makeup and DNA is that much of it is not set in stone as an unchanging part of you. DNA must be looked at as a living organism in itself that can undergo changes at any time. To avoid confusion we will not attempt to obtain a full understanding of DNA and its complete structure and makeup but instead focus on the most basic biology and functions of it.
DNA is made up of 4 chemical bases (Adenine, Thymine, Guanine and Cytosine) attached to a sugar phosphate backbone. An important property of DNA is that it can replicate itself. There are two very important features to note here. The fact that replicates itself is a critical feature because it relates to the ability of cells to function properly. When there is an error in the DNA code it allows changes further down the chain at the cellular level. This commonly is due to a type of change in the protein structure that essentially controls the manner in which the cells function.
What is probably more imperative to understand about the DNA replication process is that much if not most of the time when an improper or defective DNA strand is replicated it will continue to duplicate the same defective strand eventually changing its core structure. This is what is known as gene expression. Initially there may be no clinical signs of the error occurring but as time passes and more of the defective strand is duplicated and clinical features will begin to develop. DNA does not distinguish whether or not the duplicate strand is defective or not, it simply duplicates the existing strands. This is frequently a pathway to disease. Probably the best recourse would be to correct the defective strand at inception so that it would once again replicate the correct sequence. Unfortunately it’s not that simple. To correct a defective strand of DNA it must be possible to correct the sequence at the inception of change to allow it to correct itself in the proper pathways. This is where DNA replication gets complicated.
Enzymes created in the body are the primary source for DNA modification. Finding the defective DNA strand is only one part of determining the etiology of disease. It may in fact rely more on modifying the enzyme or enzymes that bring about the change in the first place. This is why stem cell replacement in many diseases only yields a temporary response to the disease. It replaces improperly functioning cells which restore functionality but it does not stop the replication of the improperly coded DNA strands. More importantly it does not correct the defective enzymes that cause the improper coding in the first place. It’s similar to putting out a fire and not extinguishing the coals. The fire will just reignite if there is fuel. In this case, the transplanted cells act as the fuel and the defective DNA represents the coals. This is why it is critical to gain understanding of the pathways rather than focus on the biological changes that take effect after the alteration has occurred.
There are many different things that affect gene expression and enzyme function. Manmade chemicals are probably the most notable for changes in gene expression but natural chemicals such as those contained in plants and foodstuffs can also have a direct effect on DNA structure. Sometimes these natural chemicals are beneficial and other times they can be devastating to the organism, it really depends on the structure of the compound.
The phosphate backbone in DNA is essentially what holds the structure together. This is what the chemical base and proteins bind to. If any portion of this is broken it will cause an error in the genetic sequence leading to immediate faults in gene replication. Organophosphates and Phthalates can directly alter this structure and certainly lead to clinical manifestations of disease. This is not something that is imperative for the average person to fully understand but it is important to understand the simple concept of this in relative terms. Any chemical that is considered an organophosphate has the potential to damage this DNA phosphate backbone. Organophosphates as a cause are listed in their own section with a more detailed explanation.
Certain types of medications or drugs can cause Parkinson’s symptoms. Drug induced Parkinsonism is often symmetrical affecting both sides and pill rolling tremor (a circular movement of the thumb and index finger) is uncommon. Some prescription drugs that can cause Parkinson’s symptoms are tranquilizers, antipsychotics and drugs for gastric disturbances. These drugs have the ability
to block dopamine receptors. Sometimes it can take years for the symptoms to be reversed. MPTP is a byproduct of a street drug produced in the 1980’s and is a known cause of Parkinson’s disease causing severe symptoms. It produces many of the same symptoms quite rapidly. There are some distinct differences between MPTP induced Parkinson’s and idiopathic Parkinson’s, namely the acute nature, lack of Lewy body accumulation and resting tremor. MPTP is used to induce Parkinson’s in rat models of the disease and much research is based around this. This may in fact make it clinically ineffective in the study of Idiopathic Parkinson’s in research although it continues to be used.
Several studies have suggested that depression independently increases the risk of Parkinson’s. Most of these studies are survey based and include little to no pathology to support this theory. To some extent they are relevant, but at the same time they are completely irrelevant and irresponsible in regards to the etiology of Parkinson’s disease.
About 60 percent of people with Parkinson’s disease suffer from depression as well as up to 40 percent of people suffering from other chronic illnesses. Depression is not a causative factor but in fact a resulting factor of the illness. There is definitely pathology associated with depression and chronic disease. Serotonin appears to play a key role in the pathogenesis of depression. Coincidentally serotonin is yet another chemical in the body that has a distinct imbalance in Parkinson’s. There is no conclusive evidence or pathology to date that indicates that depression is either a risk or causative factor for Parkinson’s. It might at best be a clinical
indicator for developing the disease but without extensive workup to examine levels of Serotonin, Norepinephrine or other pathological factors that correlate Parkinson’s disease with depression, there will never be a valid clinical association between depression and the risk of Parkinson’s.
Parkinson’s is often thought of as an age related disease but that school of thought is changing rapidly. It was previously estimated that less than 10 percent of Parkinson’s cases were below the age of 50. In a span of 10 years, that number has changed to 20 percent. This is much more evident when places such as Australia or Nebraska are considered but still is probably not an accurate representation. It is certainly not a relevant factor when the Parkinson’s syndrome of Guam is considered due to the rate documented and short life expectancy. Parkinson’s is more likely related to rate of exposure over time rather than age.
Certain types of chemical exposure can be directly related to Parkinson’s disease. Manganese intoxication is a known etiological cause of Parkinson’s type syndrome. The characteristic features are slightly different with tremor and stiffness being predominant. Manganese poisoning is also evident on MRI’s showing basal ganglia degeneration which is not seen in the early stages of Parkinson’s. Interestingly, elevated manganese levels in the brain are seen in Parkinson’s due to a deficiency of zinc.
Agent Orange is also a highly suspected chemical cause of Parkinson’s disease. Many Vietnam veterans diagnosed with Parkinson’s are told quite directly by their doctors that it is in fact the cause of their Parkinson’s. Agent Orange is a combination of 2,4-D and 2,4,5-T that is a part of the dioxin related class of herbicides which becomes tremendously toxic when overheated as occurred in the 1950’s during production and is cited as possibly one of the most toxic chemicals ever created by man. It was produced by the Monsanto Company which continues nearly unrestricted to this day in its production of toxic chemicals that are in widespread use throughout the world. 2,4-D is one of the most commonly used chemicals worldwide, along with Glyphosate, which is a suspected cause of Parkinson’s and said to be unavoidable in the environment. A more detailed discussion is in the Toxic Means section.
There have been suggestions of bacterial or viral causes of Parkinson’s. Dr. Lawrence Broxmeyer who is a well known researcher and author of more than 40 books has suggested that tuberculosis type bacteria may in fact be responsible for alterations in brain chemistry and protein aggregation. Unfortunately these studies were largely ignored by the scientific community due to Dr. Broxmeyer’s reclusive nature even though he may very well be correct. It would certainly be prudent to read his articles and investigate his theories in the clinical arena.
Other types of bacterial infection involve the spirochete family of bacteria which are primarily comprised of syphilis and Lyme-causing bacteria along with others yet to be discovered. The bacteria that cause syphilis will cause Parkinson’s symptoms especially in its tertiary (late) stages. Lyme has not been conclusively associated with Parkinson’s symptoms in a pathological manner even though it has been cited numerous times and much conjecture has circulated as to it being the cause. It certainly merits further investigation but the symptoms of late stage Lyme are rather inconsistent with the disease as is H. Pylori infection which is a spirochete bacteria found in cat feces.
There is a certain amount of merit to bacterial causes because clinical studies have initially shown that Rifamyacin may be effective in the treatment of Multiple System Atrophy which is an incurable and fatal Parkinson’s plus syndrome. It has many of the same symptoms but it also has a very short course of illness and affects the autonomic nervous system very early on.
There have been known incidences of neurological presentations of Celiac disease that resemble Parkinson’s. Some pathology can be associated with this but it is difficult to tie Celiac clinically to Parkinson’s symptoms. Gluten intolerance is a subject that also merits further investigation but receives little attention from the scientific community and is frequently dismissed. Part of this is because insurance companies are quite hesitant to pay for testing for Celiac, as it is costly and there is limited mainstream evidence supporting the need for testing on this ailment even though conclusive tests would lead to a very simple and cost effective solution. It is certainly not something that should be overlooked when neurological problems are present and contrary to many loosely written articles, it does in fact exist. Testing should be conducted on a wider basis to assess the true extent of Celiac.
Low Testosterone levels:
A recent study noted that low Testosterone levels have been found in male Parkinson’s patients. It is possible that there is relevance to this but it is clinically insignificant and not likely causative in any way. Considering that the age group associated with Parkinson’s is typically between 40 and 60 years old. Concluding that testosterone levels in men within this age group are low would be quite simple if not obvious. This is backed by significant clinical evidence. If you were to undertake a small study of only men with Parkinson’s in this age group the expected results are obvious.
Another thing important to note is that testosterone levels in women tend to increase in this age group so they should be included in these types of studies as well. When these facts are considered, testosterone levels almost can be eliminated as irrelevant by virtue of nature.
Metal toxicity invariably is a factor in Parkinson’s and many other neurological disorders. It is clinically noted and has supporting pathology. The biochemical reactions caused by metal toxicity are well known and quite relevant. Metal toxicity is not what it sounds like. It is not necessarily related to ingestion of metals but more to how liver enzymes and other factors influence the balance and excretion of metals in the body through the proper channels.
Defining heavy metals is the first step in understanding this pathogenesis. Whether it is related to atomic weight or specific gravity may have no relevance at all. It is an uncommon diagnosis with the exception of iron and lead. Most of the following relevant items regarding acute and chronic effects are taken from Adefris Adal’s citation ‘Heavy Metal Toxicity’. Only neurologic conditions are included.
-Arsenic – encephalopathy, painful neuropathy
-Bismuth – encephalopathy
-Copper – Wilson’s disease, hepatic and basal ganglia degeneration
-Iron – hepatic cirrhosis, Parkinson’s
- Lead – encephalopathy, foot drop, wrist drop
-Manganese–Parkinson’s like syndrome, Neuropsychiatric conditions
-Mercury – tremor
-Nickel – encephalopathy
-Thallium – neurologic syndromes
-Zinc – Neurological degeneration
This is certainly only a glance at metal toxicity. Aluminum is another metal that must be kept under consideration. Excessive copper (or the inability to metabolize copper) is a known factor in the genetically inherited Wilson’s disease. Mercury is a definite cause of tremor as noted in many studies. Something interesting about tremor and Parkinson’s is the fact that presentations that begin with tremor have a much slower progress of degeneration. This form of Parkinson’s could potentially be a simple case of poisoning rather than a classic case of the disease. This stresses the importance of finding an accurate clinical diagnosis for all etiologies of the disease.
Iron metabolism is now becoming a significant clinical feature of Parkinson’s. There are many studies implicating the role of iron in this disease. Many studies have indicated that Lewy bodies and Alpha Synuclein aggregation both have significant levels of Fe3 which is the oxidized form of Iron in the body. Iron is an essential nutrient in the body and is regulated by ferritin and transferrin in the liver. It is very important that these enzymes operate efficiently in the body. When these processes are interrupted or impeded through enzymatic activity it leads to the molecular series of events that lead to certain types of neurodegeneration. Fe2 is important in the body and is readily obtained in many types of foods. The body must properly process this form of Iron to maintain proper cellular functions. The failure that occurs in Parkinson’s is when Fe2 is converted into the oxidative form of Fe3 and creates a toxic reaction in the body at the molecular level. This is becoming evident as a cardinal feature of Parkinson’s. It is also very relative to oxidative stress.
Lipid Peroxidation/Oxidative Stress:
Lipids make up a large portion of our bodies and are the building blocks for cells. They store and release energy and combine with carbohydrates and protein to form the majority of all cells. Lipid peroxidation occurs when types of oxygen and nitrogen are generated at higher than normal rates in the body. It involves the production of reactive oxygen, such as O2 and H2O2. The ability of the liver to detoxify the body is where the primary pathology of oxidative stress reactions in the body occurs. It is a complex process that essentially damages cell membranes and creates a set of dysfunctional mitochondria. Cytochromes are a type of protein-containing compound defined as a protein belonging to a group that contains iron and plays a role in cell respiration. Cytochrome P-450 which is a group of enzymes that plays a role in the catalyzation of oxygen is of specific interest in oxidative stress. These groups of enzymes play a key role in the cell detoxification and transport process. Inhibition of these enzymes is known to occur when exposed to certain chemicals or biological constituents and is often cited as a pathway to disease. Identifying the specific enzymes and correcting their function may be primary means of curing many diseases.
Immune System Reactions:
There is some suggestion that an overactive immune system may play a role in the pathogenesis of Parkinson’s. It is suspected that neuroinflammation may play a role in the development of the disease. This is a logical assumption because inflammation in and of itself is the body's natural reaction to many types of external and internal stimulus. This may have some value as a resulting factor of the disease but is not likely to produce significant results in the etiology of the disease unless the specific causes of the inflammation are identified.
Vitamin and Mineral Deficiencies:
Numerous deficiencies are associated with Parkinson’s. In fact they are sometimes so widespread in the disease that it may be impossible to determine if they are causative factors or if they occur in the course of the disease. Although these deficiencies are widely noted, there is little evidence that supplementation has any prolonged effect on treatment or reversal of the disease.
Folate (B9) deficiencies are often noted in Parkinson’s but it is unclear if increased homocysteine levels cause this deficiency. This is especially noticeable after the administration of Levodopa as it elevates homocysteine. Other B vitamins are noted to be deficient also and independent deficiencies can mimic neurologic symptoms. A complicating factor in B vitamin supplementation is the fact that several B vitamins and certain amino acids must work in a complimentary fashion to be properly absorbed in the digestive tract. As an example, taking B12 for a B12 deficiency may increase plasma levels of the vitamin but not be effectively absorbed by the body to have any complimentary effect. It is very relative to how the body metabolizes multiple different compounds to correct a single deficiency.
Mineral deficiencies are often noted also. Zinc is one of the primary deficiencies being studied currently. There is belief that zinc may play a key role in maintaining the shape of proteins, essentially aiding in the prevention of clumping within the cells. Another known feature of zinc deficiency is that it may increase manganese levels in the basal ganglia resulting in toxicity.
Iron is another key player in understanding Parkinson’s. Iron is known to be deficient in many patients but it is abundant in the protein deposits that have been considered a hallmark of the disease. It is a double edged sword because the two most common forms of iron have different reactive states. Fe2 (ferrous oxide) is a stable from of Iron and is an essential nutrient. Fe3 (ferric oxide) is highly reactive with oxygen and is toxic to a variety of mechanisms in the body. To complicate the matter even further, it is not necessarily a matter of ingesting bad iron or exposure to it that leads to oxidative stress, nor is it a matter of lacking good iron in the diet. Iron is stored, released and regulated by a protein called ferritin. A defective process in the protein can lead to improper conversion and storage of iron and the generation of Fe3 which consequently can bind with proteins and lead to oxidative damage. Fe3 deposits are known to be present in Lewy bodies and the Alpha Synuclein protein. This was what appeared to be an obvious pathway to the disease and received much attention and research. There has been hypothesis that breaking up and removing the Iron deposits from this protein or removing the protein entirely would reverse the path of the disease. In clinical trial this theory ultimately failed and actually exacerbated the symptoms of the disease. It was necessary research to prove or disprove this mechanism as a cause of the disease. Iron imbalance must therefore be a resulting clinical feature, not a pathway to the illness. Iron regulation is controlled in the liver and digestive system and the mechanisms leading to the imbalance must be focused on that particular pathology and its initial effect on protein and DNA structure rather than attempting to reconfigure the protein at its endpoint. Changing the pathway of a protein or eliminating it is entirely ineffective unless the function of that protein is completely understood.
Many cases of Parkinson’s have been directly related to injury, more specifically repeated head injury. These mechanisms are almost completely misunderstood. It is known as Chronic Traumatic Encephalopathy and has been documented fairly extensively. Obviously the mechanisms involved must be related to particular types of tissue damage. Other types of injuries such as neck or back injuries have also received consideration. One plausible possibility is that some types of tissue damage may perhaps open a pathway that allows toxins normally circulated in the blood to enter parts of the brain or cerebral spinal fluid and cause direct cellular damage resulting in severe neurological deficits. There is little to no research to support this idea.
Certain food additives:
Food additives are unfortunately just a part of daily life. Many additives are suspected of leading to many types of illness. In the United States it is believed that 80 percent of packaged foods have dangerous additives that are outlawed in many other parts of the world. Preservatives, artificial sweeteners, hydrogenated oils, benzoates, bleaching agents and growth hormones. BPA is a chemical that has been banned as an additive but is routinely used in many types of packaging. Studies have shown that BPA levels in people that eat canned goods are elevated to very high levels as evidenced in urine samples over a period of less than a week. BPA is a suspected endocrine disruptor. The list of additives is extensive and the health effects of a majority of them are unknown to the public. The EPA and the FDA allow manufacturers to conduct and submit their own scientific studies on additives. This is a very flawed system because the profit potential of using a less costly additive could certainly influence the outcome of the research conducted. The best policy is probably to avoid additives and preservatives as much as possible even if there are claims that question their safety.
There is evidence of neurological disorders caused by occupational exposure to chemicals in many different industries. Industrial and agricultural occupations are often cited. Some chemicals are known to produce an immediate effect on the CNS whereas others may be caused by long term exposure to chemicals such as pesticides and herbicides (listed separately).
Industrial chemicals related to neurological diseases include but is not limited to the following:
-Inorganic Mercury – tremor, convulsion, dysarthria, anxiety, cognitive dysfunction, pain, peripheral neuritis and abnormal MRI imaging.
-Carbon Disulfide – dysarthria, hemiparesis, polyneuropathy, organic brain syndrome and psychiatric disorders.
-Trichloroethylene and other industrial solvents – chronic toxic encephalopathy, cerebellar syndrome and severe ataxia.
-Methyl Bromide – gait disturbance, polyneuropathy, and brain lesions.
-Organotin - mental and behavioral changes, metabolic acidosis, hypokalemia and coma.
-Acetonitrile – stiffness, dizziness, severe fatigue nausea, vomiting and delirium.
-Carbon Monoxide - unconsciousness, cognitive loss, motor dysfunction, and delayed hypoxic encephalopathy.
-Hexane - peripheral neuritis.
-Mixed solvents – anosmia, cranial nerve palsy, reflex sympathetic dystrophy.
-Manganese – Parkinson’s type syndrome, ALS.
There is no real surprise that these chemicals cause neurological problems. Much research has been conducted on these agents and the mechanisms of some but not all of them are fairly well understood. Most of these chemicals if not all are still used in industrial applications or are a byproduct of production. Even though there is documented evidence of toxicity, the EPA continues to remain lax in their regulation and periodically reviews them for relabeling often without actually reviewing them or considering current scientific evidence.
Pesticides and Herbicides:
Pesticides and herbicides are at the leading edge of research into the cause of Parkinson’s disease. Several have already been directly implicated in the etiology of the disease. Organophosphates are known to cause DNA damage and have been implicated in Parkinson’s disease, neurologic dysfunction, Gulf War Illness, and depression in chronic low doses through their binding with the amino acid Tyrosine which is a precursor to dopamine.
Other suspected pesticides or herbicides linked to Parkinson’s disease include but are not limited to paraquat, diquat, maneb, dicamba, mancozeb, rotenone, dioxin, 2,4-D, glyphosate, carbamates and organophosphates including fertilizers.
Many of these inhibit liver enzymes and the action of Cytochrome P-450 while others are known to directly damage the phosphate backbone of DNA altering the sequence. Some are also endocrine disruptors. Much of this is known science, not suggested theory. In fact some of these chemicals are specifically designed to inhibit P-450 enzymes in plants. Manufacturers such as Monsanto and Dow Agribusiness actively deny the link to disease and spend tremendous amounts of money producing their own studies that back the safety of the products. The EPA openly accepts these companies own research and so relicenses and allows increased use of these chemicals almost without question. Monsanto has invested huge sums into the use of GMO seeds which are resistant to certain herbicides, namely Glyphosate and 2,4-D to allow for heavier use on food crops. The distribution and use of the chemicals is a very lucrative and political business. There is a tremendous amount of public outcry in this arena along with lawsuits and ballot initiatives. It is a continuing battle involving corporations, scientists, politicians, farmers and the general public. There is an entire chapter dedicated to toxins because it is so significant.
There are estimations that up to 50 percent of Parkinson’s cases are misdiagnosed. There are many variables that must be considered in the clinical diagnosis of Parkinson’s disease. Being that Parkinson’s is diagnosed by committee, it is critical that many specific tests are conducted to exclude other conditions. It is most often diagnosed by Levodopa responsiveness which is helpful but not always entirely accurate because the medication can effectively mask other underlying causes and often alleviates the resulting symptoms of those causes.
Conditions often diagnosed as Parkinson’s include Multiple System Atrophy, Supranuclear Palsy, Benign Essential Tremor, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Normal Pressure Hydrocephalus, Striato-Nigral Degeneration, Wilson’s disease, Hallevorden Spatz Disease, Olivopontocerebellar Degeneration, and Huntington’s disease. Other considerations include Spinocerebellar Ataxia, Cervical Myelopathy, Encephalitis, Meningitis and other forms of neurological syndromes. Each one of these must be closely investigated to ensure proper treatment.
Other illnesses often result in what is known as Parkinsonism. The clinical manifestations can be strikingly similar and must be considered and eliminated through competent testing and evaluation before a diagnosis of Idiopathic Parkinson’s can be given. Illnesses that must be ruled out are AIDS, Encephalitis, Meningitis, Stroke, Cancer, Diffuse Lewy body disease, Multiple System Atrophy, Progressive Supranuclear Palsy, Neurosyphilis, Chronic Lyme Disease, Hepatic Encephalopathy, Vascular Disease, Pineal Cysts, Hydrocephalus, Celiac Disease, Spinal cord infections or damage, brain damage caused by anesthesia, carbon monoxide poisoning, Mercury or other chemical poisonings, narcotics or use of other medications that may cause Parkinsonism.
The list is not exhaustive by any means and certainly emphasizes the need for a complete diagnostic workup prior to giving a diagnosis of Parkinson’s. The average time for diagnosis in Parkinson’s is one to five years. This is because there is no accurate clinical test or single biomarker that can determine if a patient actually has Parkinson’s. Conclusive tests can only be performed after death.
This is the core feature of Parkinson’s disease as well as some other neurological conditions. It is a complex and confusing condition that is the root of the etiology of this disease. It has been considered in many scientific studies dating back to 1970 and was even noted as far back as 1941. Understanding the enzymatic processes involved in the liver that lead to this disorder are complex and elusive. There is a dramatic imbalance of the amino acids in the body in Parkinson’s. It lends credence to reports of diet and exercise having a positive effect on the symptomatic treatment of the disease as detoxification and respiration are important to the body’s overall well being. Certainly diet and exercise alone will not cure this illness but it does provide clues for research that will aid in understanding the root causes of the disease. Another chapter is dedicated to diet and foods that aid in Parkinson’s and the biochemical means in which they are effective along with descriptions of different foods and their basic biological effects. Alkaloids are of particular interest as well as phytosterols and other components of diet. An additional point to make here is that a majority of the studies produced on causes of Parkinson’s indicate a rate of 2-3 percent of those studied almost regardless of what is being studied. This is directly coincidental to the rate of Parkinson’s in the population as a whole lending little credence to their viability. Studies associated with the liver indicate that 50 percent or more of Parkinson’s patients involved in these studies have abnormal liver function.