Parkinson's Disease (PD)

Parkinson's disease (PD) is a neurodegenerative disorder that causes unintended movements of the body and behavioral changes

PD occurs as a result of progressive damage or death to nerve cells (neurons)

PD activity begins in a crescent-shaped area of the midbrain called the substantia nigra pars compacta, which produces Dopamine. (Substantia nigra is Latin for dark substance, so named for this darker colored area of the brain). Dopamine is a neurotransmitter used to control movement and motor function (visual, auditory and movement), mood / emotions, behaviors, and cognitive functions, including memory. A decrease in Dopamine leads to a disruption of signals regulating these functions.
The neurotransmitter Dopamine. This chemical messenger transmits signals between the par compacta (a subdivision of the substantia nigra of the mid-brain) and the corpus striatum (largest part of the subcortical basal ganglia). This is a critical component of motor and action planning, decision making, motivation, and reward systems, serving as primary input to the rest of the basal ganglia, and therefore has a key role in the choices of which movement or behaviors to execute.

Damage to neurons occurs via oxidative stress. This damaging process occurs due to an imbalanced presence of reactive oxygen species (ROS) resulting from, for example, normal ROS byproducts of cellular processes uncontrolled by a sufficiency of antioxidants, or as an immune response to a microbial infection.

Oxidative stress promotes amyloidosis. Involved in over 50 human diseases, including PD, Alzheimer’s disease and Type II diabetes. Amyloidosis is an aggregation of abnormal α-synuclein (α-Syn) (a protein abundant in the brain involved in release of neurotransmitters). αSyn proteins become misfolded and clump together – losing their normal function as they form long, fibrous structures called amyloid fibrils, which become plaque deposits that can disrupt normal cellular function – and are considered core pathological markers of neurodegenerative diseases.

Who gets PD?

Worldwide, Parkinson’s is the 2nd fastest growing age-related neurological disease after Alzheimer’s. A Parkinson’s Foundation study reports that there are currently over 1.1 million Americans and over 11 million in the world.

  • Age is the highest risk factor. Incidence estimates increasing over 65 years old), although an estimated 4% of cases are diagnosed before 50.
  • Men are at higher risk than women.
  • Living in a high pollution area. The so-called “Rust Belt” (U.S. industrial manufacturing areas, S. California, Florida, S.E. Texas, Central Pennsylvania) have higher incidence rates. Study
  • Those not consuming enough antioxidants (naturally present in organic, unprocessed fruits and vegetables). Autopsy samples of those with PD indicate increased oxidative damage of substantia nigra.  PubMed   PubMed  Antioxidants and oxidants have a yin-yang complementary balancing effect.

Lifespan expectations with PD

Interestingly, the destruction of Dopamine cells does not directly reduce lifespan, but the effect of PD-related falls or infections does impact life-length.

Symptoms

  • Tremors. Usually beginning in the hand, sometimes the foot or jaw. PD tremor is characterized by a back-and-forth shaking. Predominant when hand at rest or person is stressed. A particular symptom is that the affected person rubs their thumb and forefinger together. Shaking does not usually occur during sleep.
  • Rigidity. Muscle tightness resists movement
  • Slowness of movement (bradykinesia). Can make simple tasks take longer
  • Poor balance / postural changes. Increases risk of falling. Leaning forward whilst walking, reduced arm-swinging.
  • Speech and swallowing difficulties.  Forming words, speaking quietly, hesitation, slurring, talking too fast, excess saliva. 
  • Other symptoms may develop. These include problems sleeping, oilier or drier skin, bladder / bowel / sexual dysfunction, dementia, cognitive problems (such as dementia, memory, slow thought-process), dizziness due to sudden drop of blood pressure getting up or down, fatigue, muscle pain / contractions.

Causes / Risk factors

General risks

  • Most cases do not run in families, but some cases may involve genetics
  • Affect men more than women
  • Most likely cause is environmental exposure to toxins
  • Researchers have detected damage from oxidative stress
  • Viral infections are a substantial risk factor and possible trigger or potential cause of PD. A common, normally considered harmless virus, human pegivirus (HPgV), brain infection was found (in post-mortem analysis) in 50% of people with Parkinson’s disease, but not in those without the condition.  2025 study. Parkinsonism was observed after the 1918 epidemic of Encephalitis lethargica (“Sleeping SIckness”), also after flaviviral encephalitis (caused by West Nile virus), St. Louis Encephalitis virus, Japanese Encephalitis B virus, and HIV (worsened on progression to AIDS and alleviated with antiretroviral therapy).

Nutritional and lifestyle factors

  • A diet rich in fruit. vegetables, beans, whole grains, nuts, fish and poultry, low in saturated fat and moderating alcohol intake may lower risk for PD.  According to a study of 130,000 people over 16 years. The high antioxidant intake would counter oxidative damage.   The Role of Vitamins in the Course of Parkinson’s Disease
  • Caffeine intake 

Mainstream treatments

Mainstream medicine offers no cure for Parkinson’s – with treatments focusing on:

  • Replacing missing Dopamine in the brain with:
  1. Dopamine precursors, mainly Carbidopa-Levodopa (L-dopa) which converts to Dopamine only when in the brain and unlike Dopamine, L-dopa can cross the blood brain barrier but does have unpleasant side-effects). A high protein diet reduces its effectiveness. Choose vegetables and beans over animal products.
  2. Dopamine agonists. Drugs that mimic Dopamine, such as apomorphine, pramipexole, ropinirole, and rotigotine.
  3. MAO-B inhibitors. Block breakdown of Dopamine in the brain. E.g. selegiline and rasagiline
  4. COMT inhibitors. Also block Dopamine breakdown, prolonging L-dopa effects.
  • Controlling abnormal movements using drugs. E.g. drugs that reduce production or uptake of the neurotransmitter acetylcholine. However, these treatments to not replace damaged neurons or stop progression of PD.

Alternative treatments for Parkinson's disease

 

Vitamin

The treatment goals are:

  1. Destroy the likely microbial infection that has entered the brain and is damaging the dopamine-production area (substantia nigra pars compacta). Dopamine is a necessary neurotransmitter in the CNS for motor function, mood and cognitive functions
  2. Attempt to repair the damage
  3. Replace the missing Dopamine.
  4. Reduce inflammation

DMSO

DMSO has many studies supporting its healing abilities in the CNS. Most research has been with animals; here are a few of them:

  • DMSO shown to counteract neuronal damage in rats, induced to have Parkinson’s.  Study
  • DMSO increased blood flow to brain and prevented neuronal damage / loss of memory in rats surgically modified to reduce blood to their brain (took 3 months). Study
  • IV DMSO (2 weeks) counteracted chemically induced memory impairment in rats.  Study.
  • Oral administration of DMSO is an effective treatment for amyloid A amyloidosis for gastrointestinal involvement.

HOWEVER – although DMSO is a healing modality in its own right (anti-inflammatory, antioxidant, and somewhat anti-microbial), its main attribute is its ability to penetrate cell membranes and tissues.  DMSO can also combine with and ferry some healing substances with it – even through the blood brain barrier (BBB), since DMSO can open the tight junctions of the BBB and enter the CNS. This enables an anti-microbial / anti-toxin substance to gain access to the brain, where it can remove whatever is causing damage to the Dopamine-producing cells of the substantia nigra. HOWEVER, since DMSO opens a door to the brain for itself and the therapeutic substance it is carrying, it could also possibly allow passage of microbes and toxins currently in the blood. It is therefore necessary to first detox the blood using one of several methods available, The Beck Protocol and Chlorine dioxide therapy (CDT) are two very effective methods.

Anti-microbials / Anti-toxins that can cross the blood-brain barrier

Vitamin C.  Its antioxidant role can neutralize oxidants toxic to nerve cells. Readily crosses the BBB and enters cells. It inhibits alpha-synuclein aggregation and microglial inflammation response.

Could Vitamins Have a Positive Impact on the Treatment of Parkinson’s Disease? PubMed

The Role of Vitamins in the Course of Parkinson’s Disease.  PubMed

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References

Gao, X., …, (2007), Prospective study of dietary pattern and risk of Parkinson’s disease, The American Journal of Clinical Nutrition, 86(5):1486-1494. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2225168/

Barnham KJ, Masters CL, Bush AI. Neurodegenerative diseases and oxidative stress. Nat Rev Drug Discov. 2004;3:205–14. doi: 10.1038/nrd1330. PubMed

Rao AV, Balachandran B. Role of oxidative stress and antioxidants in neurodegenerative diseases. Nutr Neurosci. 2002;5:291–309. doi: 10.1080/1028415021000033767. PubMed

 

Chronic low-level inflammation

  • Detoxifies
  • Boosts immune system / cellular energy
  • Anti-inflammatory / Pain-relief
  • Aids sleep / Reduces stress
  • Accelerates healing of tissue, bone, muscles, scars
  • Improves circulation +++

Successful electrotherapies

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