Preliminary trials have suggested that the amino acid, methionine (5 grams per day), may effectively treat some symptoms of Parkinson’s disease.¹

Drug therapy for Parkinson’s disease has been reported to deplete vitamin B3 in humans.² Vitamin B3 may be needed to decrease SAMe levels, and in so doing, may possibly help people with Parkinson’s disease. However, the two main forms of vitamin B3, niacin and niacinamide, when taken in combination with L-dopa, have demonstrated no benefit for people with Parkinson’s disease.³ Nicotinamide adenine dinucleotide (NADH)—the active form of vitamin B3 in the body—effectively raises the level of dopamine in the brain, making it potentially useful in the treatment of people with Parkinson’s disease. In preliminary research, NADH supplementation reduced symptoms and improved brain function in people with Parkinson’s disease.^4,5 One researcher has recommended 5 mg taken twice per day for people with Parkinson’s disease.⁶ However, one small, double-blind, short-term trial using injections of NADH found no significant effects.⁷

In a small, four-week trial, D-phenylalanine (DPA) supplementation improved motor control and tremors in people with Parkinson’s disease.⁸ Additional research is needed before the benefits of this treatment can be considered proven. DPA should not be taken with L-dopa as it may interfere with the transport of L-dopa to the brain.⁹ People with Parkinson’s disease should consult with a physician before using DPA. Some commercially available phenylalanine products contain a 50:50 mixture of DPA and LPA, the form of phenylalanine that occurs naturally in food (these products are known as DLPA). People with Parkinson’s disease should consult a physician before using DPA or DLPA.

In a preliminary study of 31 Brazilian individuals with Parkinson’s disease, all had laboratory evidence of vitamin B2 (riboflavin) deficiency. Nineteen of these individuals received 30 mg of supplemental riboflavin three times a day for six months. After three months, all participants treated with riboflavin demonstrated an improvement in motor capacity, and this improvement was either maintained or greater at six months.¹⁰ The participants in this study also eliminated red meat from their diet, but it is not clear whether that dietary change played any role in the observed improvement.

Some preliminary studies have indicated that high dietary intakes of antioxidant nutrients, especially vitamin E, are associated with a low risk of Parkinson’s disease,^11,12 even though Parkinson’s patients are not deficient in vitamin E.^13,14 The correlation between protection from Parkinson’s and dietary vitamin E may be not be due to the vitamin E itself, however. Legumes (beans and peas) contain relatively high amounts of vitamin E. Independent of their vitamin E content, consumption of legumes has been associated with low risk of Parkinson’s disease.¹⁵ In other words, high vitamin E intake may be a marker for diets high in legumes, and legumes may protect against Parkinson’s disease for reasons unrelated to their vitamin E content.

Interest in the relationship between antioxidants and Parkinson’s disease led to a preliminary trial using high amounts of vitamin C and vitamin E in early Parkinson’s disease¹⁶ and to a large ten-year controlled trial of high amounts of vitamin E combined with the drug deprenyl.¹⁷ In the trial combining vitamins C and E, people with early Parkinson’s disease given 750 mg of vitamin C and 800 IU of vitamin E four times each day (totaling 3,000 mg of vitamin C and 3,200 IU of vitamin E per day) were able to delay the need for drug therapy (i.e., L-dopa or selegiline) by an average of about two and a half years, compared with those not taking the vitamins.¹⁶ The ten-year controlled trial used 2,000 IU of vitamin E per day found no benefit in slowing or improving the disease.¹⁷ The difference in the outcomes between these two trials might be due to the inclusion of vitamin C and/or the higher amount of vitamin E used in the successful trial. However, the difference might also be due to a better study design in the trial that found vitamin E to be ineffective.

The amounts of vitamin E used in the above trials were very high, because raising antioxidant levels in brain tissue is quite difficult to achieve.²⁰ In fact, some researchers have found that even extremely high intakes of vitamin E (4,000 IU per day) failed to increase brain vitamin E levels.²¹ The difficulty in increasing brain vitamin E levels may explain the poor results of the large, controlled trial.

In preliminary research, an extract of Mucuna prurient (HP-200) was studied in people with Parkinson’s disease, 43% of whom were taking Sinemet before HP-200 treatment; the remaining 57% were not medicated.²² Statistically significant reductions in symptom scores were seen from the beginning to the end of the 12-week trial. The amount used in the trial was 7.5 grams of the extract (dissolved in water) three to six times daily.

L-tyrosine is the direct precursor to L-dopa. Theoretically, supplementing L-tyrosine could be an alternative to L-dopa therapy; however, L-tyrosine should not be taken with L-dopa as it may interfere with the transport of L-dopa to the brain.²³ One small preliminary trial demonstrated that some people with Parkinson’s disease who supplemented with L-tyrosine (45 mg per pound of body weight) for three years had better clinical results and fewer side effects than did patients using L-dopa.²⁴ Until these findings are confirmed, L-tyrosine should not be used as a replacement for, or in addition to, L-dopa.

People with Parkinson’s disease treated with L-dopa have been reported to have reduced levels of the neurotransmitter phosphatidylserine.²⁵ In one trial, supplementing with phosphatidylserine (100 mg three times daily) improved the mood and mental function in patients with Parkinson’s disease, but exerted no beneficial effects on muscle control.²⁶ The phosphatidylserine used in this trial was obtained from cow brain. That product is not available in the United States, because of concern that an extract of cow brain could cause Creutzfeld-Jakob disease, the human variant of “mad cow” disease. The phosphatidylserine sold in the United States is manufactured from plant sources and cow-brain phosphatidylserine.²⁷

Vitamin D deficiency is common in Parkinson’s disease. In a double-blind trial, supplementation with 1,200 IU per day of vitamin D for 1 year slowed the progression of Parkinson's disease, compared with a placebo.³²

In people with Parkinson's disease, vitamin D deficiency combined with reduced levels of activity may increase the risk of developing osteoporosis.³³ Low vitamin D levels in Parkinson’s disease have been reported to increase the risk of hip fracture due to osteoporosis.³³ This risk has been significantly reduced with the use of synthetic, activated vitamin D—a prescription drug.³⁵ Whether the same effect could be achieved with supplemental vitamin D remains unknown, though some doctors recommend 400–1,000 IU vitamin D per day. People with Parkinson’s disease may wish to discuss the use of synthetic activated vitamin D with a healthcare professional.