Parkinson's disease is a chronic disorder typically affecting people over age 55. The condition is caused by the death of nerve cells in certain parts of the brain, leading to characteristic problems with movement. These include a "pill rolling" tremor in the hands (so called because it appears that the individual is rolling a small object between thumb and forefinger), difficulty initiating walking, a shuffling gait, decreased facial expressiveness, and trouble talking. Thinking ability may become impaired in later stages of the disease, and depression is common.
Although the underlying cause of Parkinson's disease is unknown, many researchers believe that free radicals may play a role in destroying at least some of the nerve cells.
The nerve cells that are affected in Parkinson's disease work by supplying the neurotransmitter dopamine to another part of the brain. Most treatments for Parkinson's disease work by artificially increasing the brain's dopamine levels. Simply taking dopamine pills won't work, however, because the substance cannot travel from the bloodstream into the brain. Instead, most people with Parkinson's disease take levodopa (L-dopa), which can pass into the brain and be converted there into dopamine. Many people take levodopa with carbidopa, a drug that increases the amount of levodopa available to make dopamine.
At first, levodopa produces dramatic improvement in symptoms; however, over time, levodopa becomes less effective and more likely to produce side effects. Other drugs may be useful as well, including bromocriptine, trihexyphenidyl, entacapone, tolcapone, selegiline, and pergolide. There are also surgical treatments that can decrease symptoms, such as pallidotomy and deep brain stimulation.
Short for cytidinediphosphocholine, CDP-choline (sometimes called citicholine) is a substance that occurs naturally in the human body. It is closely related to choline, a nutrient commonly put in the B vitamin family. For reasons that are not completely clear, CDP-choline seems to increase the amount of dopamine in the brain.3,4 On this basis, it has been tried for Parkinson’s disease.
In a 4-week, single-blind study of 74 people with Parkinson's disease, researchers tested whether oral CDP-choline might help levodopa be more effective.5 Researchers divided participants into two groups: one group received their usual levodopa dose, the other received half their usual dose without knowing which dosage they were getting. All the participants took 400 mg of oral CDP-choline 3 times daily.
Even though 50% of the participants were taking only half their usual dose of levodopa, both groups scored equally well on standardized tests designed to evaluate the severity of Parkinson's disease symptoms.
Support for the use of CDP-choline also comes from studies in which the supplement was administered by injection.6-9
In general, CDP-choline appears to be safe.11 The study of oral CDP-choline for Parkinson's disease reported only a few brief, nonspecific side effects such as nausea, dizziness, and fatigue.12 In a study of 2,817 elderly people who took oral CDP-choline for up to 60 days for problems other than Parkinson's disease, side effects were few and mild and reported in only about 5% of participants.13 Two-thirds of these side effects were gastrointestinal (nausea, stomach pain, and diarrhea), and none required stopping CDP-choline. The dose in this study was 550 mg to 650 mg per day, about half the dose used for Parkinson's disease.
The supplement coenzyme Q 10 (CoQ 10) been widely advertised as effective for treating Parkinson's disease. However, there is only minimal evidence that it works, and some evidence that it does not.
A study published in 2002 raised hopes that CoQ 10 might help slow the progression of Parkinson’s disease. In this 16-month, double-blind, placebo-controlled trial, 80 people with Parkinson’s disease were given either CoQ 10 (at a dose of 300 mg, 600 mg, or 1,200 mg daily) or placebo. 44 Participants in this trial had early stages of the disease and did not yet need medication. The results appeared to suggest that the supplement, especially at the highest dose, might have slowed disease progression. However, for a variety of statistical reasons, the results were, in fact, quite inconclusive.
A subsequent double-blind, placebo-controlled study of 28 people with Parkinson’s disease, which was well-controlled by medications, indicated that 360 mg of CoQ 10 daily could produce a mild improvement in some symptoms.45 Based on these results, a more substantial study was undertaken, enrolling 131 people with Parkinson’s disease (again, well-controlled by medications).55 Unfortunately, it didn’t work. While benefits were seen in both the placebo and the CoQ 10 group, the supplement failed to prove more effective than placebo.
For more information, including dosage and safety issues, see the full CoQ10 article.
Several other natural products have been studied for preventing or treating Parkinson’s disease, with mixed results.
Whether a symptom of the disease or a response to disability, depression affects many people with Parkinson's disease, and long-term use of levodopa may contribute to this problem. Research suggests that levodopa can deplete the brain of a substance called S-adenosylmethionine (SAMe for short).14,15 As SAMe has been found in a number of small studies to have antidepressant effects,16 it is possible that depleting it might trigger depression.
Researchers conducted a trial to determine if taking SAMe supplements could decrease depression in 21 individuals with Parkinson's disease who were taking levodopa.17 In this double-blind study, each participant received either a combination of oral and injected SAMe or placebo daily for 30 days, followed by the alternate treatment for another 30 days. Although other symptoms of Parkinson's didn't change, 72% of people taking SAMe felt that their depression was improved after 2 weeks, while only 30% noted improvement with placebo. It is not yet known if oral SAMe alone would have similar effects.
Although SAMe might appear to be an excellent accompaniment to levodopa, there is another side to the issue. During treatment with levodopa, SAMe participates in breaking it down and gets used up in the process. It is possible that taking extra SAMe could lead to decreased effectiveness of levodopa.18 In the short-term study described above, SAMe did not interfere with levodopa's effects, but longer-term use might do so.
The bottom line: If you have Parkinson's disease, it's safest to use SAMe—if at all—only under the supervision of a physician.
For more information, including dosage and safety issues, see the full SAMe article.
Phosphatidylserine (PS for short) is a major component of cell membranes. Several studies have found PS supplementation effective for improving mental function in individuals with Alzheimer's disease. One trial examined its use in 62 people, all of whom had both Parkinson's disease and Alzheimer's-type dementia. The results appeared to indicate some benefit, but due to the incompleteness of the report on this trial, it is difficult to draw conclusions.23
For more information, including dosage and safety issues, see the full Phosphatidylserine article.
Because of indications that free radicals play a role in causing Parkinson's disease, treatment with high doses of vitamin E has been tried to see if it can slow down the progression of Parkinson's disease. However, a large study yielded disappointing results. In this trial, 800 individuals newly diagnosed with Parkinson's disease took 2,000 IU of tocopherol (synthetic vitamin E) or placebo daily for an average of 14 months.24-26 Vitamin E had no effects in delaying symptoms of the disease—nor did it reduce side effects of levodopa.
For more information, including dosage and safety issues, see the full Vitamin E article.
One problem with levodopa treatment for Parkinson's disease is the so-called "on-off effect," in which a person taking levodopa will move more freely for some hours, followed by sudden "freezing up." Vitamin C has been tried as a remedy for "on-off effects" in a small double-blind study,27 but the results were so minimal that the researchers didn't feel justified in recommending it.
For more information, including dosage and safety issues, see the full Vitamin C article.
The herb Mucuna pruriens contains L-dopa. One very small study reportedly found evidence that use of the herb as an L-dopa source offers advantages over purified L-dopa given as a medication itself.49
Other proposed natural treatments for Parkinson's disease have minimal or conflicting evidence supporting them, including NADH,28-30 glutathione,31 policosanol,32 and the amino acids D-phenylalanine,33 and L-methionine.34,35 Caution is advised with the latter three, as they might affect the function of levodopa.36,37 (See Herbs and Supplements to Use Only with Caution, below.) A two-year study failed to find more than minimal benefits at most with creatine.53
Weak evidence hints that the supplement 5-HTP might be helpful for depression in people with Parkinson’s disease.19 However, 5-HTP should not be combined with the drug carbidopa. (See Herbs and Supplements to Use Only with Caution, below.)
A review of 20 randomized trials with 470 patients found that real rTMS improved motor symptoms more effectively than sham rTMS. Treatment times ranged from 1 day to 12 weeks. In these trials, the most improvement was also seen with high-frequency rTMS.64,58,46,50,57,61 However, a subsequent small, randomized study involving 23 people did not find promising results.63 Compared to placebo, 10 days of transcranial electrostimulation did not improve the symptoms of Parkinson's disease.
A postural training method called Alexander technique has shown some promise.47
A small placebo-controlled study found that use of bright lights, best known as a treatment for seasonal affective disorder, may also help relieve various symptoms of Parkinson’s disease, possibly by reducing levels of melatonin in the brain.56
In two studies, acupuncture failed to provide much benefit for Parkinson’s disease.48,52 And, in two comprehensive reviews of multiple clinical trials, independent sets of researchers concluded that there was currently no well-established evidence for acupuncture’s effectiveness in Parkinson’s.59,60
In a randomized trial of 95 patients with Parkinson's disease, Tai Chi improved symptoms, like balance, gait, and strength, compared to other forms of treatment (ie, resistance training, stretching).62
If you have Parkinson's disease, it is best to avoid taking the herb kava. Preliminary reports suggest that kava may counter the effects of dopamine and possibly reduce the effectiveness of medications for Parkinson's.38
Other substances may also interact with Parkinson's drugs. Iron supplements can interfere with absorption of levodopa and carbidopa and should not be taken within 2 hours of either medication.39 Amino acid supplements, such as branched-chain amino acids (BCAAs), can temporarily decrease levodopa's effectiveness, as may methionine and phenylalanine, two amino acids studied for treatment of Parkinson's disease.40,41
Vitamin B6 in doses higher than 5 mg per day might also impair the effectiveness of levodopa and should be avoided.42 However, if you take levodopa-carbidopa combinations, this restriction may not necessarily apply. Talk with your physician about an appropriate dose of vitamin B 6.
The supplement 5-HTP has a potentially dangerous interaction with carbidopa. Using the two substances together may increase your chance of developing symptoms resembling those of the disease scleroderma.20-22
As noted above, SAMe could conceivably impair the effectiveness of levodopa.
1. Cerhan JR, Wallace RB, Folsom AR. Antioxidant intake and risk of Parkinson's disease (PD) in older women [abstract]. Am J Epidemiol. 1994;139:S65.
2. de Rijk MG, Breteler MB, den Breeijen JH, et al. Dietary antioxidants and Parkinson disease: the Rotterdam study. Arch Neurol. 1997;54:762-765.
3. Garcia-Mas A, Rossinol A, Roca M, et al. Effects of citicholine in subcortical dementia associated with Parkinson's disease assessed by quantified electroencephalography. Clin Ther. 1992;14:718-729.
4. Secades JJ, Frontera G. CDP-choline: pharmacological and clinical review. Methods Find Exp Clin Pharmacol. 1995;17(suppl B):1-54.
5. Eberhardt R, Birbamer G, Gerstenbrand F, et al. Citicoline in the treatment of Parkinson's disease. Clin Ther. 1990;12:489-495.
6. Birbamer G, Gerstenbrand F, Rainer J, et al. CDP-choline in the treatment of Parkinson syndrome. New Trends in Clin Neuropharmacology. 1990;4:29-34.
7. Secades JJ, Frontera G. CDP-choline: pharmacological and clinical review. Methods Find Exp Clin Pharmacol. 1995;17(suppl B):1-54.
8. Agnoli A, Ruggieri S, Denaro A, et al. New strategies in the management of Parkinson's disease: a biological approach using a phospholipid precursor (CDP-choline). Neuropsychobiology. 1982;8:289-296.
9. Ruggieri S, Zamponi A, Casacchia M, et al. Therapeutic effects of cyticholine (cytidine-diphospho-choline) in Parkinsonian syndrome [in Italian]. Clin Ther. 1976;78:515-525.
10. Eberhardt R, Birbamer G, Gerstenbrand F, et al. Citicoline in the treatment of Parkinson's disease. Clin Ther. 1990;12:489-495.
11. Secades JJ, Frontera G. CDP-choline: pharmacological and clinical review. Methods Find Exp Clin Pharmacol. 1995;17(suppl B):1-54.
12. Eberhardt R, Birbamer G, Gerstenbrand F, et al. Citicoline in the treatment of Parkinson's disease. Clin Ther. 1990;12:489-495.
13. Lozano Fernndez R. Efficacy and safety of oral CDP-choline: drug surveillance study in 2817 cases. Arzneimittelforschung. 1983;33:1073-1080.
14. Liu X, Lamango N, Charlton C. L-dopa depletes S-adenosylmethionine and increases S-adenosyl homocysteine: relationship to the wearing-off effects [abstract]. Abstr Soc Neurosci. 1998;24:1469.
15. Bottiglieri T, Hyland K, Reynolds EH, et al. The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. Drugs. 1994;48:137-152.
16. Bressa GM. S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies. Acta Neurol Scand Suppl. 1994;154:7-14.
17. Carrieri PB, Indaco A, Gentile S, et al. S-adenosylmethionine treatment of depression in patients with Parkinson's disease: a double-blind, crossover study versus placebo. Curr Ther Res. 1990;48:154-160.
18. Liu X, Lamango N, Charlton C. L-dopa depletes S-adenosylmethionine and increases S-adenosyl homocysteine: relationship to the wearing-off effects [abstract]. Abstr Soc Neurosci. 1998;24:1469.
19. Mayeux R, Stern Y, Sano M, et al. The relationship of serotonin to depression in Parkinson's disease. Mov Disord. 1988;3:237-244.
20. Sternberg EM, Van Woert MH, Young SN, et al. Development of a scleroderma-like illness during therapy with L-5-hydroxytryptophan and carbidopa. N Engl J Med. 1980;303:782-787.
21. Joly P, Lampert A, Thomine E, et al. Development of pseudobullous morphea and scleroderma-like illness during therapy with L-5-hydroxytryptophan and carbidopa. J Am Acad Dermatol. 1991;25(2 pt 1):332-333.
22. Auffranc JC, Berbis P, Fabre JF, et al. Sclerodermiform and poikilodermal syndrome observed during treatment with carbidopa and 5-hydroxytryptophan [translated from French]. Ann Dermatol Venereol. 1985;112:691-692.
23. Funfgeld EW, Baggen M, Nedwidek P, et al. Double-blind study with phosphatidylserine (PS) in parkinsonian patients with senile dementia of Alzheimer's type (SDAT). Prog Clin Biol Res. 1989;317:1235-1246.
24. Parkinson Study Group. Effects of tocopherol and deprenyl on the progression of disability in early Parkinson's disease. N Engl J Med. 1993;328:176-183.
25. Parkinson Study Group. Impact of deprenyl and tocopherol treatment on Parkinson's disease in DATATOP patients requiring levodopa. Ann Neurol. 1996;39:37-45.
26. Kieburtz K, McDermott M, Como P, et al. The effect of deprenyl and tocopherol on cognitive performance in early untreated Parkinson's disease. Parkinson's Study Group. Neurology. 1994;44:1756-1759.
27. Reilly DK, Hershey L, Rivera-Calimlim L, et al. On-off effects in Parkinson's disease: a controlled investigation of ascorbic acid therapy. Adv Neurol. 1983;37:51-60.
28. Dizdar N, Kgedal B, Lindvall B. Treatment of Parkinson's disease with NADH. Acta Neurol Scand. 1994;90:345-347.
29. Kuhn W, Mller T, Winkel R, et al. Parenteral application of NADH in Parkinson's disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis. J Neural Transm. 1996;103:1187-1193.
30. Birkmayer JGD, Vrecko C, Volc D, et al. Nicotinamide adenine dinucleotide (NADH)—a new therapeutic approach to Parkinson's disease. Acta Neurol Scand. 1993;87(suppl 146):32-35.
31. Sechi G, Deledda MG, Bua G, et al. Reduced intravenous glutathione in the treatment of early Parkinson's disease. Prog Neuropsychopharmacol Biol Psychiatry. 1996;20:1159-1170.
32. Snider SR. Octacosanol in parkinsonism [letter]. Ann Neurol. 1984;16:723.
33. Heller B, Fischer E, Martin R. Therapeutic action of D-phenylalanine in Parkinson's disease. Arzneimittelforschung. 1976;26:577-579.
34. Smythies JR, Halsey JH. Treatment of Parkinson's disease with L-methionine. South Med J. 1984;77:1577.
35. Meininger V, Flamier A, Phan T, et al. L-methionine treatment of Parkinson's disease: preliminary results [in French]. Rev Neurol (Paris). 1982;138:297-303.
36. Snider SR. Octacosanol in parkinsonism [letter]. Ann Neurol. 1984;16:723.
37. Nutt JG, Woodward WR, Hammerstad JP, et al. The "on-off" phenomenon in Parkinson's disease. Relation to levodopa absorption and transport. N Engl J Med. 1984;310:483-488.
38. Schelosky L, Raffauf C, Jendroska K, et al. Kava and dopamine antagonism [letter]. J Neurol Neurosurg Psychiatry. 1995;58:639-640.
39. Campbell NRC, Hasinoff BB. Iron supplements: a common cause of drug interactions. Br J Clin Pharmacol. 1991;31:251-255.
40. Goodman LS, Gilman A. In: Hardman JG, Limbird LE, et al., eds. Goodman & Gilman's the Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, Health Professions Division; 1996:510.
41. Nutt JG, Woodward WR, Hammerstad JP, et al. The "on-off" phenomenon in Parkinson's disease. Relation to levodopa absorption and transport. N Engl J Med. 1984;310:483-488.
42. Drug Evaluations Annual. Chicago, IL: American Medical Association, Division of Drugs and Toxicology; 1992:12.
43. Snider SR. Octacosanol in parkinsonism [letter]. Ann Neurol. 1984;16:723.
44. Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q 10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. 2002;59:1541-1550.
45. Muller T, Buttner T, Gholipour AF, et al. Coenzyme Q 10 supplementation provides mild symptomatic benefit in patients with Parkinson's disease. Neurosci Lett. 2003;341:201-204.
46. Shimamoto H, Takasaki K, Shigemori M, et al. Therapeutic effect and mechanism of repetitive transcranial magnetic stimulation in Parkinson's disease. J Neurol. 2001;248(suppl 3):III48-III52.
47. Stallibrass C, Sissons P, Chalmers C. Randomized controlled trial of the Alexander technique for idiopathic Parkinson's disease. Clin Rehabil. 2002;16:695-708.
48. Shulman LM, Wen X, Weiner WJ, et al. Acupuncture therapy for the symptoms of Parkinson’s disease. Mov Disord. 2002;17:799-802.
49. Katzenschlager R, Evans A, Manson A, et al. Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study. J Neurol Neurosurg Psychiatry. 2004;75:1672-1677.
50. Khedr EM, Farweez HM, Islam H. Therapeutic effect of repetitive transcranial magnetic stimulation on motor function in Parkinson's disease patients. Eur J Neurol. 2003;10:567-72.
51. Powers KM, Smith-Weller T, Franklin GM, et al. Parkinson's disease risks associated with dietary iron, manganese, and other nutrient intakes. Neurology. 2003;60:1761-1766.
52. Cristian A, Katz M, Cutrone E et al. Evaluation of acupuncture in the treatment of Parkinson's disease: A double-blind pilot study. Mov Disord. 2005 May 9. [Epub ahead of print]
53. Bender A, Koch W, Elstner M, et al. Creatine supplementation in Parkinson disease: a placebo-controlled randomized pilot trial. Neurology. 2006;67:1262-1264.
54. Sunagane N, Aikawa M, Ohta T, et al. Possibility of interactions between prescription drugs and OTC drugs (2nd Report)—interaction between levodopa preparation and OTC kampo medicines for upset stomach. Yakugaku Zasshi. 2006;126:1191-1196.
55. Storch A, Jost WH, Vieregge P, et al. Randomized, double-blind, placebo-controlled trial on symptomatic effects of coenzyme Q 10 in Parkinson disease. Arch Neurol. 2007 May 14. [Epub ahead of print]
56. Paus S, Schmitz-Hubsch T, Wullner U, et al. Bright light therapy in Parkinson's disease: a pilot study. Mov Disord. 2007 May 21. [Epub ahead of print]
57. Lomarev MP, Kanchana S, Bara-Jimenez W, et al. Placebo-controlled study of rTMS for the treatment of Parkinson's disease. Mov Disord. 2005 Oct 6.
58. Hamada M, Ugawa Y, Tsuji S. High-frequency rTMS over the supplementary motor area for treatment of Parkinson's disease. Mov Disord. 2008 Jun 11.
59. Lee MS, Shin BC, Kong JC, et al. Effectiveness of acupuncture for Parkinson's disease: A systematic review. Mov Disord. 2008 Jul 10.
60. Lam YC, Kum WF, Durairajan SS, et al. Efficacy and safety of acupuncture for idiopathic Parkinson's disease: a systematic review. J Altern Complement Med. 2008;14:663-671.
61. Elahi B, Elahi B, Chen R. Effect of transcranial magnetic stimulation on Parkinson motor function-Systematic review of controlled clinical trials. Mov Disord. 2008 Oct 29.
62. Li F, Harmer P, Fitzgerald K, et al. Tai chi and postural stability in patients with Parkinson's disease. N Engl J Med. 2012;366(6):511-519.
63. Shill HA, Obradov S, Katsnelson Y, Pizinger R. A randomized, double-blind trial of transcranial electrostimulation in early Parkinson's disease. Mov Disord. 2011;26(8):1477-1480.
64. Chou YH, Hickey PT, et al. Effects of repetitive transcranial magnetic stimulation on motor symptoms in Parkinson's disease: A systematic review and meta-analysis. JAMA Neurol. 2015 Feb 16 [Epub ahead of print].
Last reviewed December 2015 by EBSCO CAM Review Board
Last Updated: 12/15/2015