Chronic pain afflicts over 20% of the adult population. Sadly, most MDs have essentially no education in treating pain, beyond offering a few toxic medications. Then they tend to steer people with pain away from those health practitioners who are trained. This puts the acupuncture community on the front lines for addressing this epidemic.
Treating Parkinson's Naturally: Western and TCM Perspectives (Pt. 1)
Parkinson's disease (PD) is the second most common neurodegenerative disease in the world; it has a prevalence rate of 1 percent of adults over the age of 601 and 2 percent of adults ages 70 or older. These numbers will grow larger as the aging population increases. It is the second most common neurodegenerative disease involving movement disorder.2-3
According to the National Parkinson Foundation, there are approximately 1.2 million people with PD in the U.S. and Canada. An estimated 50,000 Americans develop the condition each year. Males are most likely to develop PD (50 percent more men than women), and its incidence in Caucasians seems higher than in other races.4-5 Some studies find a higher incidence rate in developed countries.
Symptoms & Causation
The condition is characterized by cognitive impairment, physical tremors, slowness of movement (brandykinesia), instability, muscular rigidity, and other non-motor symptoms. It is a Lewy body-related dementia. Lewy bodies are abnormal aggregates or protein that accumulate within specific nerve cells, resulting in their death (apoptosis). These neurons are known as "dopaminergetic neurons" because they are responsible for the production of dopamine (DA).6
The primary cause of PD is the lack of dopamine production, primarily due to the aggregation of alpha synuclein in the brain (mostly in the substantia nigra pars compacta part of the brain), resulting in a broad range of symptoms such as poor ability to complete normal daily functions, motor coordination issues and tremors, rigidity, and reduction in cognitive and motivational function.
Alpha synuclein in normal cases has many essential functions such as supporting dopamine synthesis, storing and releasing neurotransmitters (responsible for synapse that determines communication between cells), supporting mitochondria, brain plasticity and more.
Factors that Impact Brain Functioning and Brain Disease
Some of the factors that can cause or contribute to Parkinson's include: exposure to toxins such as mercury, manganese, iron, lead, and arsenic; low levels of antioxidants (glutathione is the antioxidant found in the highest levels in the brain); excessive free-radical activity; poor diet [fried foods, refined carbohydrates, sugary drinks, any artificial sweeteners (Stevia is fine)]; chronic inflammation; mitochondrial dysfunction (mitochondria provide the energy for our cells); excess sugar levels; compromised autography (our brain's clean-up system); brain barrier compromise; and gut imbalances.
A primary factor in Parkinson's is the aggregation and misfolding of alpha synuclein, which result in the build-up of lewy bodies, also found in some patients with Alzheimer's.
The problem with PD Drugs
The traditional approach focuses on drugs that help slow down the progression of PD and reduce motor issues and tremors. Although these drugs do help, they often can have serious side effects as well, including making the symptoms worsen over time.
Ideally, using natural approaches for managing PD while minimizing the dosages of drugs needed could prove much more beneficial to the patient, particularly regarding trying to determine and addressing the underlying causes of PD, some of which are mentioned above.
Dietary Recommendations
Diets should be mostly comprised of vegetables and low-sugar fruits such as berries (by contrast, bananas and melons are very high in sugar). These foods are alkaline oriented and considered anti-inflammatory, while acidic foods which promote inflammation include carbohydrates (particularly refined carbohydrates found in white flour, rice and pasta, as well as all sugars). (Stevia is excellent as an herbal sweetener with no negative side effects, and actually has positive side effects including lowering blood pressure and balancing sugar/insulin).
The following should be completely avoided, as they produce substances that are toxic to the brain: fried foods, sugary drinks including most juices, canned foods and artificial sweeteners (these should be avoided at all costs as they produce phenylalanine, aspartic acid and methanol). Phenylalanine and aspartic acid interfere with the transport of dopamine and serotonin in the brain, increase neuronal hyperexcitability and lead to degeneration in astrocytes and neurons essential for synapses (the passing of information from cell to cell).
Top Nutrients to Protect the Brain
More than 50 nutrients (herbs, vitamins and essential oils) have been shown to reduce the symptoms of PD, including some that reduce alpha synuclein build-up, help prevent apoptosis (cell death), reduce inflammation, depression and anxiety, support better sleep, improve cognitive function, and much more. Below is a brief review of the top nutrients to help protect the brain related to Parkinson's:
Ashwagandha – an ayurvedic herb used commonly as a nerve tonic and adaptogen, helping the body handle stress, boosting the immune system, reducing inflammation and neuronal cell death, reversing behavioral deficits, stimulating dendrite formation and neurite growth, improving synaptic function, reducing anxiety, improving concentration and even reducing beta amyloid build-up related to Alzheimer's disease.
Bacopa Monniera – known to have neuroprotective and cognition-enhancing effects. Importantly, it helps prevent dopaminergic neurodegeneration. Bacopa monniera addresses a cause of the loss of neuron brain cells responsible for dopamine production (alpha-synuclein aggregation).
Baicalein – a flavonoid used as an antioxidant and anti-inflammatory agent without side effects. Baicalein reduces alpha-synuclein naturally and has neuroprotective properties.
Curcumin – some of the benefits of curcumin or turmeric include reducing oxidation and the free radicals that cause the deterioration of neurons. This yellow spice reduces age-related mental decline and inflammation. Curcumin increases neurogenesis and regulates enzymes essential for enzyme disbursement. It also improves mitochondrial regulation, gene expression, oxidative stress and more.
DHA – crosses all the major brain health categories, with benefits that include supporting neuron communication, helping prevent neuron cell death, reducing inflammation, and improving memory and cognition. Low DHA levels are also known to lower brain and cellular growth factors, such as brain-derived neurotrophic factor (growth factor). BDNF plays an important role in neuronal survival and growth.
Gingko biloba – has neuroprotective properties due to its potent free-radical scavenging and antioxidant properties; improves working memory, circulation and overall brain function.
Ginseng – has many wonderful benefits that include improving learning and memory, reducing apoptosis (cell death), inhibiting neuroinflammation, improving neuroplasticity, potentiating neuronal growth, repairing damaged neuronal networks, and reducing depression and anxiety. Ginseng may also reduce amyloid and neurofibrillary fiber build-up related to Alzheimer's.
Glutathione – the antioxidant found in highest amounts in the brain. Levels tend to be low in Parkinson's patients. Glutathione is an essential part of neutralizing ROS (reactive oxygen species) and other free-radical activity in the brain.
Lutein – its content in neural tissue has been positively correlated with cognitive function and has been found to accumulate in the brain. Lutein has been found to be significantly related to multiple measures of temporal processing speed, an important aspect of sensory and cognitive function.
In animal studies, lutein has been found to reverse the loss of nigra dopaminergic neurons by increasing dopamine levels and decreasing mitochondrial dysfunction and oxidative stress, resulting in decreased cell death and improved motor function.
Phopshatidylersine – essential for proper brain function, and has been found to be in low levels in PD patients. It helps improve mood and general brain function.
Pyrroloquinoline Quinone (PQQ) – a quinone compound reported to improve learning ability. It may also enhance working memory, as well as improve cerebral blood flow that can help protect against cognitive decline and dementia in the elderly.
PQQ may have neuroprotective properties against Alzheimer's, Parkinson's and cognitive injuries, and is critical in supporting healthy mitochondrial function.
Sage – contains over 160 distinct polyphenols: plant-based chemical compounds that act as potent antioxidants and have been shown to buffer one's brain defense system. It appears to halt the breakdown of the chemical messenger acetylcholine (ACH) that plays an essential role in memory, promotes neurogenesis (production of new brain cells), and is one of the nutrients found to be deficient in the brains of Alzheimer's patients.
Vitamins B1, B6, B9, B12, D3, and E – are all essential in supporting brain health and cognitive functioning. Deficiencies can mimic symptoms of Parkinson's and dementia. Seniors have less efficient digestion and may need supplementation.
Editor's Note: Part 2 discusses potential Chinese medicine treatment strategies for Parkinson's.
References
- de Lau LM, Breteler MM. Epidemiology of Parkinson's disease. Lancet Neuro, 2006;5;6:525-535.
- Malek N, Grosset DG. Medication adherence in patients with Parkinson's disease. CNS Drugs, 2015;29:47-53.
- Ding H, et al. Identification of a panel of five serum miRNAs as a biomarker for Parkinson's disease. Parkinsonism Relat Disord, 2016;22:68-73.
- Kessler II. Epidemiologic studies of Parkinson's disease: II. A hospital-based survey. Am J Epidemiol, 1972 Apr;95(4):308-18.
- Schoenberg BS, et al. Comparison of the prevalence of Parkinson's disease in the biracial population of Copiah County, Mississippi. Neur,1985;35:841-845.
- Poewe W. The natural history of Parkinson's disease. J Neurol, 2006;253;7(supp):2-6.