What is Parkinson’s Disease
Parkinson's disease (PD) is a progressive disorder of the central nervous system. An English physician, Dr. James Parkinson, who called it “Shaking Palsy”, originally described the major symptoms of the disease in 1817. Parkinson’s disease is a chronic, slowly progressing disease, which ultimately affects the mind and personality. Parkinson's disease is caused by the degeneration of the pigmented neurons in the brain, resulting in decreased dopamine availability. Possible risk factors of Parkinson's disease are oxidative stress and metal toxicity (1,2,3,5). People who live in areas where the aluminum content of the drinking water is high have an excessive risk of developing Parkinson's disease (16, 17). Exposure to pesticides and herbicides has also been linked to a significantly higher risk of developing Parkinson's disease (18, 19).
Parkinson’s Disease Symptoms
Four main features clinically characterize Parkinson’s disease:
1)Resting tremor (shaking back and forth when the limb is relaxed)
2)Rigidity (stiffness, or resistance of the limb to passive movement when the limb is relaxed)
3)Bradykinesia (slowness of movement)
4)Postural instability (poor balance)
How is Parkinson’s disease treated
L-dopa (levo-dihydroxy-phenylalanine) is an important treatment for Parkinson’s disease. L-dopa is a dopamine-precursor that can cross the blood- brain barrier and is converted to dopamine in the brain. L-dopa is often used in combination with carbidopa (Sinemet) or benserazide (Madopar) that protects it from breaking down before it reaches the brain tissue. L-dopa becomes less effective with time. When the effects decreased after 4-5 years, the patient will experience unpredictable “on-off” syndromes. There is also evidence that the use of l-dopa medications may lead to a deficiency of B vitamins, especially niacin and vitamin B-6. Most Parkinson's disease experts now recommend that l-dopa therapy be started as late as possible after diagnosis of Parkinson's disease so as to postpone the day when it no longer works and to limit its many serious adverse effects [1,2,3,4,5,6].
Alternative Treatment
Some studies have found that broad beans are an extremely good source of L- dopa. A 100 g serving of broad beans provides about 250 mg of L-dopa and a significant amount of proanthocyanidins, a class of flavonoids and antioxidants. Medication dosage may have to be adjusted if broad beans are consumed on a regular basis [7,8].
Supplementation with vitamin C and E slows the progression of the disease in its early stages. Supplementation with vitamin B complex may also be necessary, especially for patients who take L-dopa medications. The timing of protein intake can markedly increase the effectiveness of L-dopa and thereby lead to reduce dosage requirements. Researchers now recommend that protein intake is kept as low as possible and that protein be included primarily in the evening meal [7,9].
Proteins:
As L-dopa must compete with other amino acids in crossing both from the gut to the blood stream and from the blood stream to the brain, the timing of protein intake can significantly increase the effectiveness of medication. The goals of most dietary therapies have been to facilitate L-dopa's entry into the brain by restricting protein intake and thus decreasing the “on-off” phenomenon. Studies have showed that protein redistribution in the diet can significantly prolong the efficacy of levodopa therapy in many fluctuating "end-stage" PD patients [10]. Studies recommended limiting protein intake in the active hours of the day. As a result, protein intake is displaced to the less active times of the day, usually in the evening [7, 9]. The dietary restriction for protein intake in PD reflects the current recommended daily allowance (RDA) of 0.8g/kg/day but the primary difference is the redistribution of protein intake throughout the day in order to reduce motor fluctuations in response to L-dopa medication [14].
Antioxidants:
Antioxidants slowed down the progression of existing Parkinson's disease as demonstrated by Dr. Stanley Fahn’s pilot study in 1991. Patients with early PD were asked to take 3200 units of vitamin E and 3000 mg of vitamin C a day before starting any other antiparkinsonian therapy. Patients taking the vitamins in early stages of PD were able to delay the standard treatment with L-dopa for 2.5-3 years [11,12]. Researchers at the University of Magdeburg in Germany recently reported that a diet high in vitamin C and beta-carotene provide significant protection against PD [13]. The same study also showed that people with high carbohydrate intake (mono- and disaccharides) increased their risk of developing Parkinson's disease (OR=2.74, 95% CI: 1.30-6.07).
Reference
1. Beal, M. Flint, et al. Parkinson's disease and other extrapyramidal disorders. Harrison's Principles of Internal Medicine, 13th edition, McGraw-Hill, 1994, pp. 2275-80
2. Fahn, Stanley. Parkinsonism. Merritt's Textbook of Neurology, 9th edition, Williams & Wilkins, 1995, pp. 713-30
3.Youdim, Moussa B.H. and Riederer, Peter. Understanding Parkinson's disease. Scientific American, January 1997, pp. 52-59
4. Nadeau, Stephen E. Parkinson's disease. Journal of the American Geriatrics Society, Vol. 45, No. 2, February 1997, pp. 233-40
5. Playfer, J.R. Parkinson's disease. Postgraduate Medicine Journal, Vol. 73, May 1997, pp. 257-64
6. Bender, D.A., et al. Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa. Clinical Science, Vol. 56, January 1979, pp. 89-93
7. Kempster, P.A. and Wahlqvist, M.L. Dietary factors in the management of Parkinson's disease. Nutrition Reviews, Vol. 52, February 1994, pp. 51-58
8. Cansfield, P.E., et al. Condensed proanthocyanidins of fababeans. Journal of the Science of Food and Agriculture, Vol. 31, August 1980, pp. 802-12
9. Rona, Zoltan P. Parkinson's disease. Health Counselor, Vol. 9, February/March 1997, pp. 26-27
10. Karstaedt PJ, Pincus JH. Protein redistribution diet remains effective in patients with fluctuating parkinsonism. Arch Neurol 1992 Feb;49(2):149-51
11.Fahn, Stanley. An open trial of high-dosage antioxidants in early Parkinson's disease. American Journal of Clinical Nutrition, Vol. 53, January 1991, pp. 380S-82S
12.Fahn, Stanley. A pilot trial of high-dose alpha-tocopherol and ascorbate in early Parkinson's disease. Annals of Neurology, Vol. 32, 1992, pp. S128-S32
13. Hellenbrand, W., et al. Diet and Parkinson's disease II: a possible role for the past intake of specific nutrients. Neurology, Vol. 47, September 1996, pp. 644-50
14. Carter JH, Nutt JG, Woodward WR, Hatcher LF, Trotman TL. Amount and distribution of dietary protein affects clinical response to levodopa in Parkinson's disease. Neurology 1989 Apr;39(4):552-6
15. Logroscino, G., et al. Dietary lipids and antioxidants in Parkinson's disease: a population-based, case-control study. Annals of Neurology, Vol. 39, January 1996, pp. 89-94
16. Foster, Harold D. Health, Disease & the Environment, CRC Press, 1992, pp. 370-98
17. Bolla, Karen I., et al. Neurocognitive effects of aluminum. Archives of Neurology, Vol. 49, October 1992, pp. 1021-26
18. Fleming, L., et al. Parkinson's disease and brain levels of organochlorine pesticides. Annals of Neurology, Vol. 36, July 1994, pp. 100-03
19. Golbe, L.I., et al. Follow-up study of early-life protective and risk factors in Parkinson's disease. Movement Disorders, Vol. 5, No. 1, 1990, pp. 66-70
