Conventional Treatment for Parkinson's Disease

By Joel Fuhrman, M.D.

Modest Suppression Of Symptoms Is The Best You Can Hope For!

Conventional treatment of Parkinson’s disease (PD) includes medications that ease the movement-related symptoms of the disease by increasing levels of dopamine in the brain. Sometimes anti-cholinergic drugs, which increase levels of acetylcholine in the brain, are used as well. Unfortunately, none of these medications has been shown to slow the progression of the disease. Often, the dose of medication will need to be increased over time, or different medications will need to be added in order to manage symptoms. 21 Levodopa, a drug that is converted to dopamine in the brain, is the oldest and most effective treatment for Parkinson’s symptoms.

Problems With Levodopa

The problem with levodopa is that it accelerates the loss of the dopamine nerve terminals over the long term. This can cause a very gradual acceleration of the progression of the disease, necessitating periodic increases in the dosage to achieve the same results. In the majority of patients, the chronic intermittent stimulation from dopamine-producing drugs causes changes in the brain that within five years of treatment will worsen the dyskinesia (difficult or distorted voluntary movements). The duration and dose of levodopa treatment are risk factors for developing dyskinesia.

Strategies to improve dyskinesia involve reduced dosage of levodopa, neurosurgery, addition of antidyskinesia drugs, or addition of alternative PD medications called dopamine agonists. Dopamine agonists are designed to deliver dopamine in a more continuous fashion, but patients taking them are still at risk for dyskinesia.

Additional side effects of levodopa and dopamine agonists include nausea, vomiting, loss of effect of the medication, sleep disturbances, and impulsive behaviors. The neurosurgical procedure for PD is called deep brain stimulation. An electrode is inserted into the brain and programmed to deliver a steady frequency of electrical pulses in order to counteract the abnormal brain activity associated with PD.22 This surgery may decrease the dose of medication needed, but, like the medication, it only suppresses symptoms and does not slow or halt progression of PD.21


1. MedlinePlus: Parkinson’s Disease html

2. Parkinson’s Disease Foundation

3. Brown TP, et al. Pesticides and Parkinson’s Disease—Is There a Link? Environ Health Perspect 114:156-164 (2006).

4. Priyadarshi A, et al. A meta-analysis of Parkinson’s disease and exposure to pesticides. Neurotoxicology 2000 Aug;21(4):435-40.

5. Dinis-Oliveira RJ, et al. Paraquat exposure as an etiological factor of Parkinson’s disease. Neurotoxicology 2006 Dec;27(6):1110-22. [Epub 2006 Jul 3.]

6. United States Environmental Protection Agency. Prevention, Pesticides, and Toxic Substances (7508W) EPA-738-F-96-018 August 1997 R.E.D. FACTS Paraquat Dichloride.

7. Uversky VN, et al. Pesticides directly accelerate the rate of alpha-synuclein fibril formation: a possible factor in Parkinson’s disease. FEBS Lett 2001 Jul 6;500 (3):105-8.


9. Elbaz A, et al. Professional exposure to pesticides and Parkinson disease. Ann Neurol 2009 Apr 13;66(4):494-504. [Epub ahead of print.]

10. United States Center for Disease Control Third National Report on Human Exposure to Environmental Chemicals: Organochlorine Pesticides.

11. Fleming L.Parkinson’s disease and brain levels of organochlorine pesticides. Ann Neurol 1994 Jul;36(1):100-3.

12. United States Center for Disease Control Factsheet: Dieldrin.

13. Kanthasamy AG, et al. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Neurotoxicology 2005 Aug;26(4):701-19.

14. Richardson JR. Elevated serum pesticide levels and risk of Parkinson disease. Arch Neurol 2009 Jul;66(7):870-5.

15. Karen DJ, et al. Striatal dopaminergic pathways as a target for the insecticides permethrin and chlorpyrifos. Neurotoxicology 2001 Dec;22(6):811-7.

16. National Pesticides Telecommunication Network—Permethrin.


18. Calon F, Cole G. Neuroprotective action of omega-3 polyunsaturated fatty acids against neurodegenerative diseases: evidence from animal studies. Prostaglandins Leukot Essent Fatty Acids 2007;77(5-6):287-93.

19. Bousquet M, et al. Beneficial effects of dietary omega-3 polyunsaturated fatty acid on toxin-induced neuronal degeneration in an animal model of Parkinson’s disease. The FASEB Journal 2008;22:1213-1225.

20. Samadi P, et al. Docosahexaenoic acid reduces levodopa-induced dyskinesias in 1- methyl-4-phenyl-1,2,3,6-tetrahydropyridine monkeys. Ann Neurol 2006;59(2): 282-8.

21. National Parkinson Foundation

22. Encarnacion EV, et al. Levodopa-Induced Dyskinesias in Parkinson’s Disease: Etiology, Impact on Quality of Life, and Treatments. Eur Neurol 2008;60:57-66.

23. Bains JS, Shaw CA. Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death. Brain Res Brain Res Rev 1997 Dec;25(3):335-58.

24. Sullivan PG, Brown MR. Mitochondrial aging and dysfunction in Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry 2005 Mar;29(3):407-10.

25. Kidd PM. Parkinson’s disease as multifactorial oxidative neurodegeneration: implications for integrative management. Altern Med Rev 2000 Dec;5(6):502-29.

26. Kidd PM. Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management. Altern Med Rev 2005 Dec;10(4):268-93.

27. Liu J. The effects and mechanisms of mitochondrial nutrient alpha-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview. Neurochem Res 2008 Jan;33(1):194-203. [Epub 2007 Jun 29.]

28. Packer L, et al. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med 1997;22(1-2):359-78.

29. Maczurek A, et al. Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer’s disease. Adv Drug Deliv Rev 2008 Oct-Nov;60(13-14): 1463-70. Epub 2008 Jul 4.

30. Singh U, Jialal I. Alpha-lipoic acid supplementation and diabetes. Nutr Rev 2008 Nov;66(11):646-57.

31. Zhang H, et al. Combined R-alpha-lipoic acid and acetyl-L-carnitine exerts efficient preventative effects in a cellular model of Parkinson’s disease. J Cell Mol Med 2008 Jun. [Epub ahead of print.]

32. Karunakaran S, et al. Activation of apoptosis signal regulating kinase 1 (ASK1) and translocation of death-associated protein, Daxx, in substantia nigra pars compacta in a mouse model of Parkinson’s disease: protection by alpha-lipoic acid. FASEB J 2007 Jul;21(9):2226-36. [Epub 2007 Mar 16.]

33. Puca FM, et al. Clinical pharmacodynamics of acetyl-L-carnitine in patients with Parkinson’s disease. Int J Clin Pharmacol Res 1990;10(1-2):139-43.

34. Montgomery SA, et al. Meta-analysis of double blind randomized controlled clinical trials of acetyl-L-carnitine versus placebo in the treatment of mild cognitive impairment and mild Alzheimer’s disease. Int Clin Psychopharmacol 2003; 18:61-71.

35. Shults CW, et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol 2002 Oct;59(10):1541-50.

36. Growdon JH, et al. Effects of oral L-tyrosine administration on CSF tyrosine and homovanillic acid levels in patients with Parkinson’s disease. Life Sci 1982 Mar 8; 30(10):827-32.

37. Lemoine P, et al. L-tyrosine: a long term treatment of Parkinson’s disease. C R Acad Sci III 1989;309(2):43-7.

38. Youdim KA, et al. Essential fatty acids and the brain: possible health implications. Int J Dev Neurosci 2000 Jul-Aug;18(4-5):383-99.

39. De Franceschi, et al. Molecular insights into the interaction between alpha-synuclein and docosahexaenoic acid. J Mol Biol 2009 Nov 20;394(1):94-107. [Epub 2009 Sep 8.]

40. Barichella M. Major nutritional issues in the management of Parkinson’s disease. Mov Disord 2009 Oct 15;24(13):1881-92.

41. Håglin L, Selander B. Diet in Parkinson disease. Tidsskr Nor Laegeforen 2000 Feb 20;120(5):576-8.

42. Riley D, et al. Practical application of a low-protein diet for Parkinson’s disease. Neurology 1988 Jul;38(7):1026-31.

43. Tsui JK, et al. The effect of dietary protein on the efficacy of L-dopa: a double-blind study. Neurology 1989 Apr;39(4):549-52.

44. Bracco F, et al. Protein redistribution diet and antiparkinsonian response to levodopa. Eur Neurol 1991;31(2):68-71.

45. Karstaedt PJ, et al. Protein redistribution diet remains effective in patients with fluctuating parkinsonism. Arch Neurol 1992 Feb;49(2):149-51.

46. Hirata H, et al. Influence of protein-restricted diet on motor response fluctuations in Parkinson’s disease. Rinsho Shinkeigaku 1992 Sep;32(9):973-8.

47. Ueki A, et al. Life style risks of Parkinson’s disease: association between decreased water intake and constipation. J Neurol 2004 Oct;251 Suppl 7:vII18-23.

48. Gao X, et al. Prospective study of dietary pattern and risk of Parkinson Disease. Am J Clin Nutr 2007 November;86(5):1486-1494.

49. Johnson CC, et al. Adult nutrient intake as a risk factor for Parkinson’s disease. Int J Epidemiol 1999 Dec;28(6):1102-9.

50. Chen H, et al. Dairy products and risk of Parkinson’s disease. Am J Epidemiol 2007 May 1;165(9):998-1006.

51. Perez CA, et al. Iron Chelators as Potential Therapeutic Agents for Parkinson’s Disease. Curr Bioact Compd 2008 Oct 1;4(3):150-158.

52. Fillit H. Cardiovascular disease risk factors and cognitive impairment. Am J Cardiol 2006;97(8)1262-5.

53. Notkola I, et al. Serum total cholesterol, apolipoprotein E epsilon 4 allela, and Alzheimer’s disease. Neuroepidemiology 1998;17:14-20.

54. Scarmeas N, et al. Mediterranean diet, Alzheimer’s disease, and vascular mediation. Arch Neurol 2006;63:1709-17.

55. Morris MC, et al. Dietary fats and the risk of incident Alzheimer’s disease. Arch Neurol 2003;60:194-200.

56. Morris MC, et al. Dietary copper and high saturated and trans fat intakes associated with cognitive decline. Arch Neurol 2006;63:1085-8.

57. Puglielli L, et al. Alzheimer’s disease B-amyloid activity mimics cholesterol oxidase. J Clin Invest 2005;115:2556-63. University of Rochester Medical Center (2007, November 8). Copper Damages Protein That Defends Against Alzheimer’s. ScienceDaily Retrieved January 25, 2010, from /releases/2007/11/071107074329.htm

58. Bartzokis G, et al. In vivo evaluation of brain iron in Alzheimer’s disease using magnetic resonance imaging. Arch Gen Psychiatry 2000;57:47-53.

59. Joseph JA, et al Grape juice, berries, and walnuts affect brain aging and behavior. J Nutr 2009 Sep;139(9);1813S-7S. [Epub 2009 Jul 29.]

60. Sato Y, et al. High prevalence of vitamin D deficiency and reduced bone mass in Parkinson’s disease. Neurology 1997 Nov;49(5):1273-8.

61. Grant WB. Does vitamin D reduce the risk of dementia? J Alzheimers Dis 2009 May;17(1):151-9.

62. van Praag H. Exercise and the brain: something to chew on. Trends Neurosci 2009 May; 32(5):283-290.

63. Hamer M, Chida Y. Physical activity and risk of neurodegenerative disease: a systematic review of prospective evidence. Psychol Med 2009 Jan;39(1):3-11. [Epub 2008 Jun 23.]

64. Dai Q, et al. Fruit and vegetable juices and Alzheimer’s disease: the Kame Project. Am J Med 2006:119(9):751-9.

Become a Member of Christian Care Ministry and explore the benefits of Medi-Share!