Parkinson’s Disease: Nutritional Considerations

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Parkinson’s Disease: Nutritional Considerations

Nutritional links to Parkinson’s disease have been identified, although the mechanisms explaining these associations are not entirely clear.

Nutritional Factors in Prevention

In epidemiologic studies, the following factors have been associated with reduced risk of developing Parkinson’s disease:

Low–fat diets. The prevalence of Parkinson’s disease correlates with intake of animal fat,1,2 and with total and saturated fat.3

Minimizing dairy intake. The Health Professionals Follow–Up Study found a higher risk for Parkinson’s disease in men with high intakes of dairy products (roughly 3 servings per day).4 Positive associations between dairy products and Parkinson’s were found for dairy protein, dairy calcium, dairy vitamin D, and lactose, and not for other sources of these nutrients. Researchers suggest that tetrahydroisoquinolines found in dairy products may be a potential cause of this disease, due to their ability to cross the blood–brain barrier and induce degeneration of dopaminergic neurons in experimental models. The presence of dopaminergic neurotoxins, including beta–carbolines and their derivatives, pesticides, and polychlorinated biphenyls found in dairy products, may also be involved.4

Caffeinated beverages. Observational studies have found protective effects of frequent consumption of coffee or tea,5–7 although some evidence suggests that benefits are limited to men, and to women who do not use postmenopausal hormone–replacement therapy.

Nutritional Factors in Treatment

The most immediate nutritional concerns in Parkinson’s disease treatment include changes in the absorption rate, blood levels, and CNS uptake of L–dopa. The protein content of meals, and particularly the distribution of protein intake throughout the day, has emerged as an important consideration in the effectiveness of L–dopa for many patients.8–11

Patients with PD have a 4–fold increase in risk for weight loss of 10 lbs or more compared to age–matched controls for a variety of reasons, including dysphagia, dyskinesias, depression, and cognitive impairment; conversely, excess weight gain may occur due to an increase in sedentary behavior.12Individuals with chewing or swallowing difficulties should be referred to a speech therapist for appropriate changes in diet texture. A registered dietitian can help families plan meals that are also adequate in fluid and fiber (particularly insoluble fiber), an important concern to prevent constipation.12

Timing of protein intake

The first evidence of a role for protein in modulating treatment response to L–dopa came from patient reports of deterioration of drug benefit (the ‘on/off’ phenomenon) after high–protein meals.10,11 The beneficial effects of a protein–reduced diet, or the redistribution of almost all protein to evening meals on L–dopa availability (and subsequent control of dyskinesias) have been subsequently documented in patients who experience erratic responses to levodopa therapy.8–11 In these studies, reducing protein intake to amounts as low as 10 grams/day (or 0.5g/kg body weight) resulted in an improved therapeutic response in many (though not all) individuals. Low–protein diets resulted in improvements in neurologic scoring.10

Similarly, redistributing all but 7 grams of protein intake to the evening meal resulted in improvement in the Northwest Disability and AIMS Dyskinesia Scale.9 Both low–protein diet and diets reserving protein for evening meals were associated with significant reductions in the need for L–dopa.9,10 A more recent study that both decreased protein intake to the Recommended Daily Allowance (ie, 0.8 g/kg body weight) and distributed almost all protein to the evening meal (through the use of special low–protein starches) demonstrated a similar benefit. Specifically, postprandial and total ‘off’ phases (consisting of dyskinesias and complaints of pain, parasthesias, sweating, constipation or shortness of breath) were reduced from a mean of 79 to 49 minutes, while total ‘off’ time was decreased from a mean of 271 to 164 minutes by the protein redistribution diet, reductions of 38% and 39% in ‘off’ time, respectively.8 In addition, the mid–day dosage of L–dopa was reduced in one –third patients by an average of 9%. Caution may be required because the results of protein redistribution can be so effective that an excess of L–dopa may enter the brain and trigger dyskinesia.13

A protein restriction–induced decrease in requirement for L–dopa may offer more than symptomatic benefit. It is well known that oxidative stress is central to the pathology of PD, and autoxidation of L–dopa increases oxidative stress in the substantia nigra.14 Therefore, any measures that reduce the effective dose of L–dopa may prolong the period during which patients benefit from drug therapy. In addition, high–protein meals raise blood levels of homocysteine,15 a possible risk factor for vascular disease known to be elevated in PD patients as a side–effect of L–dopa.16 Due to the risk of nutrient insufficiencies on such diets,17 multiple–vitamin–mineral supplementation has been suggested.12 Physicians interested in referring patients for a protein redistribution diet that meets both energy and micronutrient needs should contact a registered dietitian who can help patients and families to plan appropriate meals.


The seed powder of the plant Mucuna pruriens contains significant amounts of L–dopa, and has long been used in Ayurvedic (East Indian) medicine for the treatment of movement disorders.18 Although several open trials and one double blind, placebo–controlled trial demonstrated effectiveness, a report by the American Academy of Neurology concluded that there is currently insufficient evidence to support or refute the use of Mucuna pruriens.19However, considering the commercial availability of Mucuna pruriens, in addition to the growing number of East Indian immigrants to the US,20 it is not unlikely physicians may encounter patients who are using this product.

Oxidative stress and Parkinson’s disease

Several factors have led to the theory that oxidative stress contributes to the risk for development of Parkinson’s disease,21 possibly by causing mitochondrial decay.22 This has resulted in trials of both medications that inhibit oxidation as well as of supplements that scavenge free radicals.

Vitamin E. There is good evidence that dietary vitamin E intake is inversely correlated with risk of developing Parkinson’s disease, and lower levels of vitamin E have been found in the cerebrospinal fluid of patients with the condition, when compared with patients with other neurological diseases.23However, vitamin E supplements have not been shown to be effective, either in preventing or slowing the progression of the condition.24

Coenzyme Q10. The neuroprotective effects of coenzyme Q10 (300, 600, or 100 mg/day) are under investigation for a potential role in Parkinson’s disease treatment, but statistically significant benefits have not yet been demonstrated.19


See Basic Diet Orders chapter.

A nutrition consultation would be appropriate to assist the patient in restricting protein prior to the evening hours, and restricting foods rich in vitamin B6.

What to Tell the Family

To minimize deconditioning, patients should maintain an active lifestyle to the extent possible. Also, patients should be aware that Parkinson’s disease often causes weight loss. Family members can help reduce severe weight loss risk by providing breakfast, lunch, and between–meal snacks that are high in calories from whole grains (100% whole oats, oat bran, bulgur, barley, brown rice), fruits, 100% fruit juices, and vegetables. The family should ensure proper nutrient intake and be advised that protein deficiency is unlikely if adequate calories are consumed. Family members can improve the effectiveness of L–dopa therapy by reserving high–protein foods for evening meals. A qualified nutrition professional (eg, registered dietitian) may be helpful in accomplishing these aims.



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