Slow or Prevent the Damaging Effects of Parkinson's Disease
Brought to you from the NEEDS Wellness Team

Parkinson's disease is a neurodegenerative disease of the motor and sensory neurons. The first noticeable sign of the disease is usually a tremor in a limb which can progress into slowness of movement, rigidity, and posture instability with impaired walking. Thirty-five percent of those with Parkinson's disease also develop dementia, a loss of cognitive function due to changes in the brain caused by disease or trauma. The progress of the Parkinson's disease is slow, yet unrelenting. In addition, by the time any clinical symptoms are present, there has already been a significant amount of damage to the cells in the brain. However, recent understanding of the actual mechanisms of Parkinson's has generated effective therapies that can slow progression and reduce symptoms of the disease.

All cells in our body have energy powerhouses called mitochondria. A sideeffect of energy production within the mitochondria is the manufacture of free radicals—reactive molecules that can damage the cell and surrounding tissue. Normally, our bodies have antioxidant mechanisms to defend itself against free radicals and prevent damage. However, Parkinson's disease damages the mitochondria, allowing more free radicals to escape. This may also lead to insufficient production of antioxidants. This can further damage the mitochondria, resulting in less energy production and, eventually, cell death. With Parkinson's, this cell death happens to neurons in a particular part of the brain that is responsible for producing dopamine, a molecule that helps coordinate muscular movements.

So, how is the mitochondria damaged in the first place? It may be the result of a genetic problem with the mitochondria or with detoxifying enzymes in the liver or brain. Or, environmental toxins such as pesticides, herbicides, drugs, and heavy metals, may have overwhelmed the body's antioxidant capacity. Also, as we age, our bodies naturally produce less protective antioxidants.

The goals of therapy are to stop, or at least slow, the progression of the disease and to enhance mitochondria function. This is accomplished by optimizing detoxification systems, supplying antioxidants, and helping to rebuild the structure of the mitochondria.

CoQ10 is an antioxidant and also assists in the mitochondria's energy production. A recent study showed that a daily dose of 300 to 1200 mg of a special form of CoQ10 (from Vitaline) reduced the progression of Parkinson's significantly, the greatest benefit being at 1200 mg.

A combination of vitamin C (3 grams per day) and vitamin E (3200 i.u. per day) has proven to delay the need for drugs by 25 to 35 months (monitor your bleeding times with your doctor at this dosage of vitamin E). Other antioxidants shown to be of benefit include N-Acetyl Cysteine (NAC), Alpha-Lipoic Acid and Ginkgo Biloba.

NADH effectively raises the level of dopamine in the brain, reducing symptoms and improving brain function in people with Parkinson's. One researcher has recommended 5 mg two times per day.

Acetyl-L-Carnitine also helps rebuild and protect the mitochondria while increasing its ability to produce energy.

Phosphatidylserine, a component of the mitochondrial membrane, has been shown to improve energy flow in the brain, especially supporting mood and mental function.

Also showing promise is Creatine—helping energy production in the mitochondria and also providing antioxidant support. Some doctors have recommended 3 to 5 grams one to two times per day.

While Parkinson's disease is most often a slowly progressive disease, the appropriate therapies can slow the process and even provide significant symptom relief. The fact that clinical symptoms of Parkinson's disease appear after much damage has already occurred is just one more reason to focus on prevention. Identifying and avoiding environmental triggers and protecting ourselves through the use of antioxidants, detoxification nutrients, and a variety of other nutrients, will protect and enhance our neurological performance.