Parkinson's Disease

A chronic progressive CNS disorder characterized by slowness of purposeful movement, resting tremors, and muscle rigidity.  Also called "Parkinsonism" and "Paralysis Agitans"

Dorland's Medical Dictionary describes the Parkinsonian complex as "neurologic disorders characterized by hypokinesia, tremors and muscular rigidity. It typically occurs late in life, although juvenile forms have been described."

The diagnosis for their disorder is made from the history and physical examination. Findings upon examinations are mask-like faces, a fenestrating gait, brady-kinesia, muscular weakness, poor balance, palmomental reflex, and a positive globella test. Patients often complain about excessive sweating and leg cramps. They may also experience speech loss, memory loss, and mild depression.

The disease and its symptoms result form an accelerated loss of dopamine (a neurotransmitter) from an area in the brain called the substantia nigra.  It should be noted that everyone, as they age, will lose dopamine to some degree. Parkinson's signs occur when the amount of dopamine being produced is less than 80%.

Conventional treatment of this disorder is only palliative: a cure has yet to be discovered. Medicines are directed towards increasing dopamine in the brain, and others are used to counteract the side effects of the primary drugs. Monoamine oxidase B inhibitors, such as selegiline, have also shown some success.

Surgery has been tried in this disorder: A pallidotomy (a dissection of an area of the brain called the pallium) has been used since the 1940s.  Symptomatic relief is expected; however, side effects, such as blindness and stroke, are possible. A brain pacemaker has been utilized in the attempt to relieve sincere tremors.

The  patient  is  typically middle-aged or elderly when symptoms begin. The disease is extremely gradual in

progression. In the majority of patients it is not a familial disorder, but occurs randomly. Although the syndrome

is well presented in a worldwide distribution and the manifestations often are clearly distinguishable and easily

diagnosed, the disease is idiopathic and the pathophysiology poorly understood.

There is usually a loss of cells in the substantia nigra, locus ceruleus, and in other pigmented cells, as well as

a decrease in the dopamine levels in the axon terminals of cells connecting the substantia nigra to the caudate

nucleus and putamen.

The disease initially presents as a unilateral disorder, but in later stages becomes symmetrical. It has an insidious onset, and may not become incapacitating for many years. After World War I, there was an encephalitis outbreak that led to numerous patients developing symptoms almost exactly like Parkinson's, as the same cells that become disordered in Parkinson's were the same ones to be affected by the encephalitis, which is one of the known causes

of the disease. Generally, however, only the idiopathic version of the disease is termed Parkinsonism.


Parkinson's Disease Signs and Symptoms

May range from a minor flu-like illness to a severe liver disease ending in hepatic failure and death; there are

usually several distinct stages:


Cogwheel rigidity

This describes the rachet-like catches that occur when a sufferer's arm is put through passive movements. It is

due to the hypertonia of muscles that equally affects opposing muscles.


Lead-pipe rigidity

This describes another possible presentation of the muscle rigidity and is a general resistance to movement. With either muscle rigidity, there may be pain, cramping and decreased strength. However, the patient retains normal sensation and reflexes in the limbs. The patient's writing becomes small and hard to read.



The patient exhibits a general slowing of all voluntary movements.



The  patient  exhibits  a  paucity or even an absence of spontaneous movements associated with the typical

animations of a normal individual.


Festinating gait

This term describes the patient's difficult process for initiating walking from a standing position. The patient takes several small, awkward steps and then breaks into a jog or run to prevent himself from falling. The typical patient pose during walking includes small, shuffling steps often dragging the feet, a slightly bent over posture, and having the arms in 90 degree flexion and held tightly at his sides.


Propulsion of Retropulsion

This describes the patient who falls forward or backward, respectively, upon being pushed.


Fixed facial mien

The typical facial expression of the Parkinson patient is one of a fixed, immobile nature, with a monotonous voice.

There may be drooling at the corners of the mouth. The eyes stare and do not blink as often as normal.


Resting tremor

This is the classic tremor of the Parkinson patients. It occurs during rest, and is described as a pill-rolling of the fingers with the hand bent in flexion. It is often unilateral, but may become bilateral. Although it is most pronounced in the hands, it is also seen in the legs, lips, tongue, and eyelids (when they are firmly closed). The tremor disappears upon voluntary movement and during sleep. It worsens with fatigue, emotional stress and embarrassment, and many patients will try to hide the affected hand by keeping it in their pocket, or by covering

it with their unaffected hand during the interview.



About half of Parkinson patients present with or will develop depression.

Parkinson Dietary Consideration

Low protein, low fat (esp. animal fat), antioxidant rich diet (ref #1-5)



Symptoms appear to become less severe when patients are placed on low-protein diets.  In one study, patients taking L-dopa were placed on a high-protein diet of 1.6 g/kg of a low protein diet of 0.8 g/kg, with most of the protein consumed during the evening meal. Symptoms, such as tremors, tapping, and amount of time that a patient had difficulty in walking all were reduced in severity on the lower protein diet.1 Another study that was double-blinded arrived at the same conclusion, i.e., that symptoms become less severe when patients are placed on low-protein diets.  It was also found that these results did not correlate with L-dopa levels. Thus, it was conjectured that high dietary protein influences L-dopa's central nervous system effects, directly or indirectly, as a result of blood-brain barrier interference.2  Closely monitoring and adjusting L-dopa dosage may be necessary because the required therapeutic range may become reduced when the dietary protein is raised.


Predisposing Foods

In one study, there appeared to be an increased risk of Parkinson's disease that manifested in newly diagnosed patients who consumed diets that are high in animal fat. Additionally, consuming foods high in vitamin D may increase the risk of a patient manifesting the disorder. This study also concluded that there appears to be a significant correlation with vitamin A supplementation and an increased risk of contracting Parkinson's disease.3


Antioxidant Rich Diets

There is a growing evidence that diets that are high in antioxidants may help to confer some degree of protection against the neurodegenerative processes involved in the progression of Parkinson's disease. Representative of the growing belief behind this hypothesis, a study, conducted in the Netherlands, demonstrated that a high intake

of dietary vitamin E may protect individuals against the occurrence of Parkinson's disease.5

"Gluten sensitivity is common in patients with neurological disease of unknown cause and may have aetiological significance" Lancet, 347:369-371(1996).


Environmental Factors

(The need to address the detoxification pathway) (ref #6-11)

A leading hypothesis of the pathogenesis of Parkinson's has associated excessive oxidative damage of the substantia  nigra dopamine-containing cells.6      There  are  currently numerous predisposing etiologies under investigation as either triggering or contributing factors to the onset of Parkinson's disease. Among the most commonly held factors are infections, industrial exposure, pesticides, head injuries, low dietary antioxidant intakes, and not smoking.7,8 Although the reason for a greater risk for contracting Parkinson's disease among nonsmokers has yet to be delineated, it may involve differences in premorbid personality traits. Occupational exposures to manganese, copper, lead, and iron have been associated with the development of Parkinson's disease.9 It also appears that organophosphate poisoning can lead to acute, yet reversible parkinsonism.10


This sensitivity most likely represents a genetic susceptibility or another type of predisposition.

There  is  no  question  that  environmental factors play a crucial role in the predisposition, development, and

progression of Parkinson's disease.

Although all the evidence required for the creation of an all-inclusive list of epidemiologic factors has not been created, there is no question that external factors are intimately involved in the etiology of this disease. This is clearly illustrated by a study, conducted in 1992, in southwestern Finland with an urban and rural population of

196,864 subjects as a follow-up to a similar study conducted in the same area in 1971. The conclusions reached were that a significant male and rural predominance was present that was not seen in 1971, suggesting a probable environmental causative factor.11


  • Access need for systemic detox program (ref #6-12)

Suggested Nutritional Supplementation


  • Lumina - 2-4 softgels daily.

Lumina is designed to support healthy mental function and relaxation-issues related to proper focus, attention, learning, and memory-through modulating the metabolism of neurotransmitters such as dopamine, gamma-aminobutyric acid (GABA), and norepinephrine.

  • Ceralin Forte - 3 capsules daily.

Ceralin Forte is formulated to provide well-rounded support for brain and nerve protection, addressing multiple pathways involved in neurological health.

  • CoQ10 200 mg - 1-6 softgels daily.

Stablized Coenzyme Q10 with Natural Vitamin E

Although the research is preliminary, animal models have shown that Co Q10 may be useful in the treatment of Parkinson's disease. The effects appear to arise form Co Q10's ability to protect against neurotoxicity.14, 33, 35

  • Benesom - 1-3 tablets at bedtime.

Benesom is formulated to promote a restful, relaxed state and relieve occasional sleeplessness by beneficially modulating the metabolism of melatonin and GABA.

Melatonin is known to scavenge several highly toxic free radicals and has been shown to reduce the oxidative damage that occurs in Parkinson's disease. In one study, mice with neural injuries that were given melatonin experienced reduced damage and fewer tremors and seizures.  Another study tested melatonin's ability in the laboratory to rescue dopamine neurons from free-radical damage and found that treatment effectively rescued nearly all dying cells.

  • Wellness EssentialsTM - 1 packet twice daily.

Base nutrition with essential fatty acids and detox support.

  • GLA Forte - 1-2 softgels daily.

Administration of essential fatty acids (EFAs), such as omega 6 has been show to help in controlling tremors.16  It is believed that, through regulation of prostaglandin pathways and displacement of harmful fatty acids, EFAs support overall neurologic health.

  • Mucuna Pruriens Extract - 6-8 capsules daily at bedtime. (3 months on then 1 month off)

Research reports mention that levodopa derived from mucuna pruriens could be two to three times more effective than synthetic levodopa. Also, the natural levodopa was better tolerated than synthetic and

in summary, recent clinical studies support the safety and efficacy of mucuna pruriens in Parkinson's


NOTE: Do not use Mucuna Pruriens Extract if on levadopa.

Additional Considerations

SAMe (s-adenosyl-methionine) and or Methionine

Treatment with L-dopa reduces S-adenosyl-methionine (SAMe) levels, yet supplementation with L-methionine,

an essential amino acid, can cross the blood-brain barrier and be converted into SAMe.17  A large majority of patients treated with 1 g and working up to 5 g of methionine experienced a dramatic reduction in symptom severity.18  Responses seen included increased activity levels, less rigidity, and improvements in attention span, concentration, voice control, muscular strength, and sleep and mood.


Treatment with L-dopa, when given with carbidopa or other decarboxylase inhibitors, may increase the risk for the

development of niacin deficiency.19  In turn, supplementation with niacin may extend the elevation of dopamine levels that result from the treatment with l-dopa.20  In addition to niacin, 1-N-methylnicotinamide and the reduced form of nicotinamide adenine dinucleotide can also help to maintain dopamine levels.


Use of this amino acid may reduce the severity of some symptoms of Parkinson's disease without helping to control tremors. Phenylalanine should not be taken with, or near the time of, consumption of L-dopa because phenylalanine will compete for absorption with the therapeutic agent. In one study, after suspending the conventional medication  regimen,  15  patients were given diphenylanine, 100-250 mg, 2 times per day.  Four  weeks  later reexamination revealed significant improvements in speech and ability to walk as well as significant reduction in depression and rigidity.21


Supplementation with this mood-enhancing amino acid, when given at different intervals than when L-dopa is administered, to avoid competitive absorption interference, can help to control Parkinson's disease-associated depressions and may improve functional ability.22,23



There is a strong correlation in animal models between dietary intake of iron and brain iron concentrations. In addition, there is a significant increase in oxidized glutathione and a decrease in total glutathione levels. Iron alone does not appear to have a causative effect on triggering Parkinson's disease. However, this supplement appears to set the stage for future oxidative insults that could trigger neurodegeneration that may, in turn, ultimately manifest  as  degenerative  disease.24,25   There  may  be a synergistic relationship between the consumption of dietary animal fat and a systemic defect in iron metabolism with regard to the progression of lipid peroxidation

in Parkinson's disease.30



Evidences suggests that a localized reduction in the caudate nucleus occurs in patients who are suffering form

Parkinson's and other neurodegenerative diseases.26  Because only 1 percent of all body magnesium is found

in the serum, a standard chemistry panel with magnesium will not give an accurate physiologic read on true available levels.  Instead, a cellular magnesium level test may provide a more accurate benchmark for checking supplementation efficacy.



Measuring the body for elevated levels of manganese can offer insights regarding the presence of this possible causative, and promoting, metal in patients with Parkinson's disease. Elevated manganese levels have been attributed to neurodegeneration. When toxic levels arise from inhalation, accumulation occurs in the nasal ganglia.27

It appears that the neurotoxicity leads to dopamine depletion and the production of neurotoxins.28



Supplementation with copper should probably be avoided, including the copper that may be found in multivitamins. There is evidence that copper levels in the cerebrospinal fluid may become elevated in patients with Parkinson's disease, leading to increased oxidative damage.29



It may be worth actively avoiding supplements, including multivitamins, with zinc unless there are definitive signs

of zinc deficiency. Research has shown that zinc levels are often elevated in the caudate nucleus, lateral putamen, and substantia nigra in Parkinson's disease. Until further evidence about the role that elevated zinc levels play

is discovered, cautious use is highly warranted.

Possible Interactions

There are three important interactions with L-dopa that should be avoided.



Limiting  the  intake  of  alcohol is important because it can antagonize the effects  of  dopamine  and  result in

diminished control of symptoms.



Known as Piper methysticum, this popular treatment for anxiety and mild depression may decrease the effectiveness

of L-dopa as a result of a dopamine antagonistic action.31



Consumption of large quantities of protein containing foods can compete with L-dopa, an amino acid for transport through the intestine, and blood-brain barrier. A diet that varies greatly in protein content can result in difficulty

in controlling symptoms.

Although other significant interactions are likely to exist, these examples serve as  reminders that vitamins, minerals, herbs and food can alter the effectiveness of conventional treatments significantly at times and must

be considered when determining therapeutic doses.



As with so many degenerative conditions, often, the difference between the manifestation of a disease or its symptoms is largely dependent on a person's overall wellness and total physical burdens. Examining risk factors of patients with strong family histories of Parkinson's disease or with early signs of the disorder can allow meaningful changes in one's exposure risks and greatly improve prognosis. Once dietary and environmental variables have been controlled, nutritional and supplementation intervention protocols can improve the quality of life and clinical outcomes for patients who are suffering from   Parkinson's disease and other progressive neurodegenerative conditions.



1.        Carter, J., et al. Amount and distribution of dietary protein affects clinical response to levodopa in Pardinson's disease. Neurology 39:552-556, 1989

2.        Tsui, J., et al. The effect of dietary protein on the efficacy of L-dopa: A double blind study. Neurology 39:549-552, 1989

3.        Anderson, C., et at. Dietary factors in Parkinson's disease: The role of food groups and specific foods. Mov Disord 14(1):21-21, 1999

4.        Bruce-Keller, A.J., et al. Food restriction reduces brain damage and improves behavioral outcome following excitotoxic and metabolic insults. Ann Neurol 45 (1):8-15, 1999.

5.        De Rijk, M.C., et al. Dietary antioxidants and Parkinson's disease: The Rotterdam Study. Arch Neurol 54(6): 762-765, 1997.

6.        Fahn, S., et al. Experience with tranylcypromine in early Parkinson's disease. J Neural Transm 52(suppl.):49-61, 1998.

7.        Ben-Shlomo, Y. The epidemiology of Parkinson's disease. Baillieres Clin Neurol 6(1): 55-68, 1997.

8.        Checkoway, H. Epidemiologic approaches to the study of Parkinson's disease etiology. Epidemiology 10(3): 327-336, 1999.

9.        Gorell, J.M., et al. Occupational exposure to manganese, copper, lead, iron, mercury, and zinc and the risk of Parkinson's disease. Neurotoxicology 20(2-3):239-247, 1999.

10.      Bhatt, M.H., et al. Acute and reversible parkinsonism due to organophosphate pestilcide intoxification: Five cases. Neurology 52(7): 1467-1471, 1999.

11.      Kuopio, A.M., et al. Changing epidemiology of Parkinson's disease is southwestern Finland. Neurology 52(2): 302-308, 1999.

12.      Ghen, M.J. D.O, Ph.D., and Melindez M., N.D. Protocol for Parkinson's Disease. American Journal of Natural Medicine Vol.5, No. 9, November 1998.

13.      Werbach, M. Nutrktional Influences on Illness. Tarzana: Third Line Press, 1993.

14.      Beal, M.F., et al. Coenzyme Q10 attenuates the 1-methyl-4-phenyl-1,2,3-tetrahydropyridine (MPTP) induced loss of striatal dopamine and dopaminergic axons in aged mice. Brain Res 783(1):109-114, 1998.

15.      Fahn, S. An open trial of high dosage antioxidants in early Parkinson's disease. Am J Clin Nutr 53:380-381, 1991.

16.      Critchley, E.M.R. Everning primrose oil (Efamol) in parkinsonism and other tremors: A preliminary study. In: Horrobin, D.F. (ed.) Clinical Uses of Essential Fatty Acids. Montreal: Eden Press, 1992, pp. 205-208.

17.      Surtess, r, et al. L-3,4,-dihydroxyphenylalanine lowers central nervous system S-adenosyl-methionine concentrations in humans. J Neurol Neurosurg Psychaitry 53(7): 569-572, 1990.

18.      mythies, J.R., et al. Treatment of Parkinson's disease with L-methionine. South Med J 77:1577, 1984.]

19.      Bender, D.A., et al. Niacin depletion in parkinsonian patients treated with L-dopa, benserazide and carbidopa. Clin Sci 56910: 89-93, 1979.

20.      Black, M.J., et al. Nicotinic acid or N-methyl nicotinamide prolongs elevated brain dopa and dopamine in L-dopa treatment. Biochem Med Metab Biol 36(2): 244-251, 1986.

21.      Heller, B., et al. Therpeutic action of D-phenylalanine in Parkinson's disease. Arzeim Forsch 26:577-579, 1976

22.      Sandyk, R., at al, L-tryptoplan supplementation in Parkinson's disease. Int j Neurosci 45(3-4): 215-219, 1989.

23.      Coppen, A.., et al. Levodopa an L-tryptophan therapy in Parkinson's. Lancet 1:654-657, 1972.

24.      Lan, J., et al. Excessive iron accumulation in the brain: A possible potential risk of neurodegeneration in Parkinson's disease. J Neural Transm 104(6-7): 649-660, 1997.

25.      Logroscine, g., et al. dietary iron, animal fat, and risk of Parkinson's disease. Mov Disord 13(1): 13-16, 1998.

26.      Utti, R.J., et al. Regional metal concentrations in Parkinson's disease, other chronic neurological diseases and control brains. Can J Neurol Sci 16(3): 310-314, 1989.

27.      Zayed, J., et al. enviromental factors in the etiology of Parkinson's disease. Can J Neurol Sci 17(3):286-291, 1990.

28.      Florence, T.M., et al. Neurotoxicity of manganese [letter]. Lancet i:363, 1988.

29.      Pall, H.S., et al. Raised cerebrospinal-fluid copper concentrations in Parkinson's desease. Lancet ii:238-241, 1987.

30.      Dexter, D.T., et al. Increased nigral iron content and alterations in other metal ions occurring in brain in Parkinson's disease. J Neurochem 52(6):1830-1836, 1989.

31.      Schelosky, L., et al. Kava and dopamine antagonism. J Neurol Neurosurg Psychiatry, 58(5):639-640, 1995.

32.      Steventon, G.B. et al. Xenobiotic Metabolism in Parkinson's Disease. Neurology 39: 893-887, July 1989.

33.      Botz, ME. Gesstner, A. Harth, R et al "Altered Redox State of Platelet Coenzyme Q10 in Parkinson's Disease" Journal of Neural Transmitters (2000) 107: 41-48.

34.      Natelson BH. Beans a Source of L-Dopa. Lancet 1969; 1:640-641

35.      Effects of Coenzyme Q10 in Early Parkinson Disease ARCH NEUROL 2002:59:1541-50.

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