Parkinson’s disease (PD) is an age-related neurodegenerative disorder characterized by progressive neuronal loss in discrete areas of the brain.

    Parkinson’s affects over 1 million Americans (about 3 percent) and the average age is 60 years and seems to affect men and women equally.  More than 50,000 new cases are being diagnosed each year in the U.S.

    It is manifested as a disturbance of the motor system, with a gradual onset and slow progression to severe disability. PD’s features include tremor, bradykinesia (slowness of movement), muscle rigidity (may involve any of the major limbs), and loss of postural reflexes. PD tremors occur in hands, arms, legs, and jaw; rigidity of the limbs and trunk; slow movement; and impaired balance and coordination. The disease worsens with stress and anxiety. Other parts of the brain are also affected resulting in symptoms such as depression, fear and accelerated dementia.

    While the underlying causes of Parkinson’s Disease remain unknown, three factors are proposed:

    • Genetics probably plays a role in PD development because 15-20 percent of Parkinson’s Disease patients have a close relative with the disorder.
    • Free-radical problems such as environmental toxins (pesticides, insecticides, chemicals, stress, drugs, mining dust, occupational toxins, radiation) are also considered a cause. Glutathione, a critical amino acid of brain chemistry that helps to preserve brain tissue and protect people from free radical destruction, is reduced in the brains of Parkison’s Disease patients.
    • The most common theory is that free radical-mediated degeneration of dopamine-producing cells and oxidative destruction of dopamine causes Parkinson’s.

    The region of the brain that deteriorates with PD, the substantia nigra, is found deep within the brain stem and contains dark pigment cells, which “synapse” to cells of the striatum. The striatum is responsible for balance, control of movements, and walking. Dopamine, produced in the substantia nigra, passes messages between the striatum and the substratia nigra. When the cells of the substantia deteriorate, as in Parkinson’s, there is a corresponding decrease in the amount of dopamine produced between the cells. The decrease in dopamine causes the neurons in the striatum to fire uncontrollably, causing impairment of motor function. There is no cure, but optimum healthy therapy appears to delay the progression of the disease, especially if started in the early stages.

    There also seems to be a liver connection to Parkinson’s Disease. Endotoxin-producing bacteria and fungi proliferate in the liver and the bloodstream. Glutathione is the most important component of detoxifying the liver. Glutathione’s precursor N-Acetyl Cysteine, enhances the body’s production of glutathione. Glutathione also acts to recycle antioxidants (vitamins C and E) and in one study IV supplementation with glutathione improved patients with a 42% decline in disability.

    Currently, the most effective means of treating PD is by replacing dopamine deficiency with L-dopa. Many patients who take L-dopa also take carbidopa, a drug that increases the amount of L-dopa used by neurons to make dopamine. L-dopa reverses Parkison’s Disease symptoms, prolongs a patient’s ability to stay independent, and increases survival time.


    Diet can be an important factor for PD patients, even though potential associations between PD and diet rarely have been assessed in prospective studies. Many studies have shown that a high-fat diet increases the risk of PD, but the reason is not clear.

    If the patient is on L-dopa therapy, eating higher protein foods in the evening is advised so that blood L-dopa levels stay steady during the day. Yet, symptoms such as tremors, tapping, and walking difficulties all were reduced in severity on a lower protein diet. No one specific diet is indicated, but poor digestion and eating habits may produce wastes in the blood stream that can under-nourish nerve cells that use 70% of the food we eat. Muscle rigidity may result because Parkinson’s patients may have difficulty chewing their food, therefore a soft-food diet may be recommended.

    In one European study, high doses of riboflavin (Vitamin B2) and elimination of red meat promoted the recovery of some motor functions in Parkinson’s patients.

    A Chinese study published in Annals of Neurology showed results that suggested that higher intake of dairy products may increase the risk of PD in men; however, this finding needs further evaluation, and the underlying active components need to be identified.

    Try to avoid having these patients get diarrhea or dysbiosis. Eating more fiber is advisable, and ingestion of a very low-protein diet in the morning and afternoon, may enhance the effectiveness of L-dopa therapy. Drink plenty of water and eat 50-75% of the diet with raw foods; nuts, seeds, grains, raw milk, and other whole foods. Include foods high in the amino acid phenylalanine, such as almonds, Brazil nuts, fish, pecans, pumpkin, lima beans, and lentils. “Green” foods and drinks may significantly reduce symptoms (try juicing.) Foods high in L-dopa, the precursor to dopamine are broad beans, especially fava beans and pods.

    Consuming nearly all of the day’s protein in the dinner meal reduces competition with L-dopa utilization. To exert its action in PD, L-dopa must be absorbed from the gastrointestinal tract into the bloodstream. Intake of food, particularly protein can interfere with this process at a number of levels.

    Avoid chemicals, toxins and pesticides on food. There is evidence that drinking coffee, which keeps dopamine levels high, may help prevent PD in the first place. Non-caffeinated coffee worked as well.


    Since vitamin B6 (pyridoxine) is an activating cofactor of an enzyme called AAAD, it is useful for L-dopa overdoses. However, in contrast, patients taking carbidopa/levodopa (Sinenet) should avoid vitamin B6 supplements, because carbidopa inhibits the action of AAAD much better when B6 is present at low concentrations. Long-term use of Sinemet may also result in folic acid and vitamin B12 deficiencies. Supplementation is recommended. Although no cures exist for this debilitating condition, long-term antioxidant intake may offer a protective benefit. Adequate antioxidants via diet and/or supplementation in theory may help reduce the potential toxic side effects of free radical damage that is caused by L-dopa over long-term treatment.

    Because there are no definitive tests for PD, people with hypoglycemia are sometimes misdiagnosed with this condition.

    Supplement Protocol

      B vitamins are important nutrients that help regenerate nerve cells, brain cells, energy cells and immune function. VITAMIN B6 may enhance the effectiveness of patients taking L-dopa/carbidopa (thus limit use of vitamin for patients taking Sinemet or generic equivalent.) Dosage: one capsule twice a day. NIACIN plays a role in dopamine production. CHOLINE, a nutrient in the B-vitamin family, may enhance the effects of L-dopa, possibly by increasing dopamine levels in the brain. FOLIC ACID deficiency may be associated with PD. High doses of VITAMIN B2 (Riboflavin) was helpful in recovery of motor skills in some patients. Dosage: 50-150 mg daily.
    2. COENZYME Q-10
      CoQ is an important antioxidant that drives ATP, the energy producing part of the cell called the mitochondria. CoQ decrease oxidative stress by quenching free radicals. Parkinson patients show a profound deficiency of CoQ, which may explain why brains produce an inadequate supply of dopamine. A recent clinical study published in a medical journal determined that people with Parkinson’s have reduced activity of Complex I in the electron transport chain. Complex I interferes with the brain-signaling chemical dopamine, which when depleted causes nerve cell degeneration. Supplementation with CoQ10, while not a cure, is the first intervention that showed a slowing in the progressive deterioration of function associated with this disease. Dosage: 100-1,200 mg a day.
      A very potent antioxidant that enhances energy and provides for the formation of the neurotransmitter acetylcholine. Abnormal acetylcholine metabolism in the brain, may lead to age-related dementias and PD. Its action is similar to Coenzyme-Q10 and NADH. Dosage: 500-2,000 mg daily.
      Glutathione is a potent antioxidant antioxidant that is a free radical scavenger (a main theory as to the cause of PD).  Glutathione is mainly found in the liver, and it is known that Parkinson’s patients have low levels, sometimes reduced as much as 40%. According to Dr. David Perlmutter, glutathione is a safe and inexpensive way to dramatically improve functioning of PD patients. Glutathione doesn’t raise dopamine levels, but it allows the dopamine in the brain to be more effective. Since it also increases serotonin, it also is useful in improving the depressed moods of most PD patients. GSH may administer intravenously by a qualified practitioner.
      A key component of neuronal membranes- the site where brain cells both receive and transmit chemical messages. PS may enhance the effectiveness of the little dopamine remaining- helping to preserve brain function. Dosage: 800-2,400 mg daily.
      NAC is a derivative of the protein amino acid (L-Cysteine) that directly encourages brain GLUTATHIONE production. Glutathione is rapidly digested when given orally, so IV dosage is suggested.  However, when IV glutathione is unavailable, oral NAC should be considered. NAC has anti-oxidant activity and its action is enhanced in the presence of vitamins C and E. Dosage: 600 mg 1-3 times a day.
      NADH is an enzyme with a pivotal role in energy production of all living cells, particularly brain cells. Since Parkinson’s is a failure of cellular energy production, it’s reasonable to look at NADH as a potential therapeutic agent. Some patients show 80% improvement. Dosage up to 5 mg a day.
    8. VITAMIN C
      A potent antioxidant that has been reported (along with vitamin E) to slow the progression of Parkinson’s disease. Dosage: 1,000-3,000 mg daily.
      There are reported low levels of Vitamin D, an important antioxidant, and magnesium in 71% of Parkinson’s patients. Dosage: 1,000-1,500 mg of calcium, 400-600mg of magnesium, and 400-600 IU vitamin D.
      This potent antioxidant serves as a metal chelator that binds to potentially toxic metals in the body, including cadmium and free iron. Parkinson patients show increased free iron in brains. Dosage: 300-600 mg daily.
    11. TYROSINE
      A non-essential amino acid, synthesized from phenylalanine, is also a precursor of several neurotransmitters including L-dopa and dopamine. Tyrosine may have a positive effect on PD patients, especially those suffering with depression and dementia. Dosage: As directed on package.
      This herb is vital in supporting liver function. Parkinson patients, especially those taking prescription drugs, have an increased risk of high liver enzymes. Milk thistle has been shown to cause retention of glutathione, so it should be given with IV doses of glutathione. Dosage: 1-2 doses daily.
      These quality fats have internal anti-inflammatory action and are helpful in balancing hormones in the body. EVENING PRIMROSE OIL (an omega 6 fatty acid) has been shown to be helpful in controlling tremors.. Dosage: 1-3 grams daily.
      Probiotics are important for balancing the good bacteria and maintaining the integrity of bowel flora. Dosage: 1-2 capsules between meals 2-3 times a day.
      An Ayurvedic herbal treatment that contains natural levodopa and MAO inhibitor activity. The plant is indigenous to India. Dosage: As directed.
      This ancient Chinese herb has profound brain antioxidant activity and has proven value to increase mental acuity. Dosage: 60-180 mg daily.
    17. MACA ROOT
      A Peruvian food/herb that speeds healing, increases virility and balances glucose.

    There may be severe interactions with L-dopa and alcohol (antagonizes the effects of dopamine), Kava-kava (may increase the effectiveness of L-dopa), goldenseal should not be taken by PD patients, and protein should be limited as described above (large consumption can compete with L-dopa and may cause more difficulty in controlling symptoms.)

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