Life Extension Magazine June 2004
Natural Prescriptions For Parkinson's Disease
By Bruce Scali
By Bruce Scali
|LE Magazine June 2004|
|Natural Prescriptions For Parkinson's Disease|
By Bruce Scali
After 200 years of investigation, researchers and clinicians have identified neither the cause nor the cure for Parkinson’s disease, the condition first described by James Parkinson in 1817. Yet with the baby-boom generation on the cusp of retirement, the need for definitive answers has never been more urgent.
Neurodegenerative symptoms such as tremor and a shuffling gait, also known as paralysis agitants, have been observed and recorded by physicians since ancient times. Much has been learned since about the characteristics of Parkinson’s disease, but much remains unknown. Not only do the cause and cure of Parkinson’s continue to elude us, but doctors still cannot identify those in early stages of the disease. Consequently, a definitive program for prevention remains uncertain.
On the positive side, much is known about Parkinson’s disease, the factors that contribute to its development, and medical treatments and natural alternatives that relieve its symptoms and may even slow its progression. And avenues of further inquiry have shown great promise.
Parkinson’s disease is correlated with age, and up to 40% of those with the disease experience serious mental decline.1 Diagnostic tools such as the P300 brainwave speed and voltage test can identify early cognitive loss and may help detect early-stage Parkinson’s disease as well.2
According to the National Parkinson Foundation, there are approximately 1.2 million people with Parkinson’s disease in the US and Canada. Parkinson’s disease afflicts 1% of adults aged 60 or older and 2% of adults aged 70 or older.3 As the population ages and the average life span grows, researchers estimate that 1.5 million Americans will be afflicted with Parkinson’s in the near future.
The Pathology of Parkinson's
Epidemiological factors play a part in Parkinson’s disease. Males are more likely to develop the disease than females and its incidence in Caucasians seems higher than in other races.5,6 The prevalence of Parkinson’s disease differs geographically, but when allowances are made for age distribution, diagnostic criteria, and varying access to health care, the results are not conclusive.7,8 It is worthwhile noting, however, that three genes have been identified that give rise to the Parkinsonian phenotype, and Parkinson’s disease occurs more frequently in identical twins.9
Genetic studies involving families, twins, and single genes also have not been definitive.10-12 Data too often have depended on the subjects’ memories, and Parkin-son’s disease could be explained by diet and environmental factors that also are shared by the subjects. Regardless, if Parkinson’s disease were strictly a genetic trait, we would see far more occurrences of it in families than at present.
Toxins such as carbon monoxide, herbicides, methanol, and insecticides have been linked to Parkinson’s disease, so both industrial and farm populations are affected. Exposure to infections such as encephalitis, measles, influenza, and sexually transmitted diseases also has been associated with Parkinson’s.13
Determining cause becomes a question of whether something specific is responsible or whether one’s genetic composition predisposes susceptibility to environmental factors linked to Parkinson’s disease. In the absence of a specific cause, the consensus is that Parkinson’s disease results from both genetic and environmental factors.
Symptoms and Diagnosis
In the absence of clinical certainty, a physician can use meth-ods of exclusion to eliminate Parkinson’s disease as a diagnosis. Blood tests identify toxic poisoning and hypoparathyroidism that could explain symptoms. Magnetic resonance imaging (MRI), computed tomography (CT), positron emission tomography (PET), and single photon emission computed tomography (SPECT) scans uncover structural, vascular, and metabolic abnormalities that cause Parkinson’s disease. Patient history reveals previous infections and drug therapies. Because motor deficits appear and advance gradually in Parkinson’s, rapid onset or progression of symptoms would argue against a diagnosis of the disease. Exclusion also is attributed to non-responsiveness to dopamine therapies.15 Eliminating the possibility of Parkinson’s disease helps physicians to focus on effective treatments for the actual condition presented by patients.
Accurate diagnosis is a significant issue with Parkinson’s disease. A post-mortem study showed that 25% of those diagnosed with Parkinson’s disease had another cause of the symptoms presented.16 Inaccurate diagnoses can lead to wasteful, ineffective, or even harmful treatments for patients, as well as provide faulty data that make finding a cure for Parkinson’s even more difficult.
Oxidative stress results when an excess of free radicals overwhelms the body’s defenses. In their search for an electron to pair with a free radical, molecules cause damage to the donor molecules. The resulting chain reactions damage lipids, protein, DNA, and, ultimately, cells.18 Free radicals also can increase intracellular calcium, causing apoptosis (slow cell death, as opposed to necrosis, a more rapid cell death). Metals such as iron, copper, and aluminum catalyze free radical reactions, and studies have shown an excess of these metals in the brains of Parkinson’s disease patients.19
The exploration of mitochondrial abnormalities in Parkinson’s disease patients resulted from the discovery of the effect of MPTP (a toxin found in heroin and pesticides) on mitochondria exclusively in the SNc region of the brain.20 This finding was not duplicated in patients with other neurodegenerative conditions. It is not known how mitochondrial damage contributes to neuron degeneration, but research is concentrating on a malfunctioning immune system, increased free radical reactions, and how this damage might initiate apoptosis.21
Excitatory amino acids such as glutamate also have been shown to cause cell damage.22 The mechanism is the mediation of an influx of calcium across cell membranes causing damage to proteins, membrane lipids, and DNA.
Inadequate trophic (nutritional) factors contribute to cell death.23 Experiments have shown that neurons die when they are disconnected from target tissue such as muscle.24
Finally, cytokines are small proteins produced as a result of microglia brain cells reacting to damaged neurons. Cytokines produce other cytokines, starting a cascade of events that causes harmful inflammation in brain tissue. In some cases, however, the inflammation causes further damage. Cytokines’ contribution to cell death is not fully understood, but a large number of glial cells have been observed post-mortem in the brains of Parkinson’s victims.13
These complex cellular processes are both challenging and exciting. New information complicates the discovery of a cure for Parkinson’s disease, but also has led to effective strategies for mitigating Parkinson’s symptoms and slowing the disease’s relentless progression.
Disease Onset Strategy
Doctors usually concentrate on treating motor disorders that are disturbing to a person who has never experienced tremors, slow limb movements, or rigidity. While the focus is on treating these symptoms, mention must be made of the cognitive issues that arise with Parkinson’s disease.
For Parkinson’s patients, cognitive degeneration is a serious issue, with a profound impact on their quality of life. A thorough assessment of cognitive status is necessary whenever Parkinson’s disease is first diagnosed. This includes memory, attention, intelligence quotient (IQ), and psychological testing for normative comparisons and baselines, which can be used later to quantify declines and indicate treatment.
While Parkinson’s disease itself does not have an early-warning marker, dementia does. Cognitive assessments and functional tests such as a quantitative electroencephalograph (QEEG) can pinpoint a deficit early enough to allow the use of therapies proven to preserve mental faculties.
Diet is paramount at every stage of Parkinson’s. A certified nutritionist should be an early recruit in the battle. Organic fruits, vegetables, and poultry, wild salmon, red beets, green beans, carrots, turnips, spinach, and red onions are especially beneficial in avoiding toxins. Unheated extra-virgin olive oil and herbs for flavoring should be used. Coffee has been associated with a lower risk of Parkinson’s disease, likely as a result of caffeine’s dopaminergic properties.28 Sugars and fats must be avoided, as high-sugar diets have been correlated with a threefold risk for developing Parkinson’s, and high-fat diets with a fivefold risk.29,30 Others to avoid include dairy, wheat, and gluten products, margarine, fried foods, polyunsaturated oils (especially canola), sweetened foods, artificial sweeteners, processed food (such as deli meats), monosodium glutamate (MSG), alcohol (except red wine), chlorinated and fluoridated water, and microwaved foods.
Finally, weight-bearing exercise has been associated with an increase in testosterone that raises dopamine levels. Combined with the inherent benefit of improved body tone and coordination, an exercise program is indispensable in treating Parkinson’s disease.