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Parkinson's Disease

Brief History, Classifications, and Risk Factors

Dr. James Parkinson first described the motor system disorder known today as Parkinson's disease in an 1817 paper entitled "An Essay on the Shaking Palsy."3 In his report, Dr. Parkinson described several characteristic traits, including an abnormal posture and gait, and partial paralysis with muscle weakness; he also described the progression of the disease. The contribution of more clearly defining the condition, theretofore known as paralysis agitans, led to the adoption of Dr. Parkinson's last name as the moniker that remains with us today.

Since 1817, medical advancements have helped us establish a much greater understanding of Parkinson's disease. Today, clustered symptoms like tremor at rest, stiffness, slowed movement, and postural instability are classified, based upon their cause, into different categories.

Parkinson's Disease (Primary Parkinson's)

This is the most common form of the disease; what most of us think of when we hear the term "Parkinson's." Primary Parkinson's disease has no clear external cause, and is therefore classified as idiopathic or without cause (arising spontaneously). Recently, however, several genes directly tied with the development of Parkinson's disease have been identified. This has led to the classification of heritable Parkinson's disease of genetic origin as familial Parkinson's disease, while Parkinson's disease that arises independently of genetic predisposition is referred to as sporadic Parkinson's disease.

Despite the fact that conventional medical dogma holds tightly to the notion that primary Parkinson's disease truly lacks an identifiable cause (other than genetics in familial Parkinson's disease), metabolic phenomena, such as oxidative stress, mitochondrial fatigue, and other age-related abnormalities are linked with the death of dopamine-producing neurons.4

Exposure to pesticides may substantially increase risk for Parkinson's disease.5-10 In one study, higher pesticide exposure increased Parkinson's disease risk three-fold.10 Numerous epidemiological studies have confirmed the association.6,11 Toxin-induced Parkinson's symptoms may be classified as secondary, rather than primary Parkinson's.4,12

Interestingly, pesticides seem to accumulate in the dopaminergic tract, where they inhibit mitochondrial function and lead to neuronal death.7,13 Dopaminergic neurons are particularly susceptible to the pesticide dieldrin, which is no longer in use in the United States, but remains ubiquitous due to environmental contamination.14 In addition to acting as neuronal and mitochondrial toxins, some pesticides also impair the breakdown of protein aggregates, like Lewy bodies.15

Several lines of evidence suggest that a genetic inability to properly detoxify environmental toxicants may predispose some individuals to Parkinson's disease.16,17

In addition, those who experience constipation throughout their lives appear to be at increased risk.18 In one study, constipation documented in medical records as much as 20 years before disease onset was associated with a significantly increased risk.19 Some researchers believe that this may be related to intake of drinking water—lower water intake appears to be a risk factor as well.20 This may be linked to reduced elimination of water-soluble toxins.

Due to the strong association between pesticides, and other environmental toxins, with Parkinson's disease, readers are strongly encouraged to review Life Extension's “Metabolic Detoxification” protocol.

Parkinsonian Syndrome (Secondary Parkinson's)

Other forms of Parkinsonism can occur as a secondary effect of brain tumor, drugs, toxins (eg, carbon monoxide poisoning), post encephalitis (viral infectious disease, "sleeping sickness"). For example, another cause of Parkinsonism is brain damage sustained by repeated blows to the head such as suffered by professional prize fighters and athletes in high-impact sports like football. Traumatic events, infections, use of certain medications, etc. can all damage the dopaminergic cells within the midbrain and lead to the same symptoms as primary Parkinson's disease.

For example, the defining basis for Parkinsonism due to encephalitis (brain inflammation) was a worldwide influenza pandemic in 1917. After recovering from this illness, many patients developed Parkinson's disease years later.21 Acquired immunodeficiency syndrome (AIDS) may also lead to Parkinsonism.22 Resuscitation from cardiac arrest (due to temporary lack of oxygen supply to the brain), and stroke can lead to Parkinsonism as well.23

Several centrally acting drugs, especially those that exert an effect on the dopamine system within the brain, such as antipsychotics, frequently induce secondary Parkinsonism after sustained chronic use. In fact, drug-induced Parkinsonism is a well-documented phenomenon.24-26 Some antidepressants and calcium channel blockers, and the antiarrhythmic drug amiodarone, can lead to Parkinsonian tremors as well.26 Several illicit drugs can cause Parkinsonism as well.

Some diseases or disorders considered to cause Parkinsonian syndromes include multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBGD), and Pick's disease.

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