By Kathy J. Shattler, BS, MS, RDN
Parkinson’s disease is an irreversible neurological disorder resulting from lowered levels of the neurotransmitter, dopamine, at the basal ganglia of the brain and typically results in trembling, rigidity, slowness of gain, insomnia, incoordination, constipation, cognitive decline and other systemic symptoms. Approximately 1.5 million people in the US have Parkinson’s syndrome. There is no cure, only symptomatic relief of which L-Dopa, the precursor to dopamine and product of tyrosine metabolism, is administered along with other supportive medications such as anti-depressants or MAO Inhibitors.
Although there is a strong genetic component to Parkinson’s Disease (PD), only about 10% are truly genetic. The remainder of the cases are thought to be results of long-term exposure to manganese, lead, iron, pesticides, herbicides, contaminated well water or even medications such as major tranquilizers and benzodiazepines. Other predisposing factors are head trauma/injury, high intake of red meat and heme iron, low caffeine intakes (in women, but not men), & vitamin D deficiency (but not directly). Genetic aberrations in how iron is handled have been found with alterations in transferrin and the hemochromatosis gene meaning that iron metabolism is deregulated which may account for the iron deposits found in the brains of PD patients.
Neuroprotection is being studied as a means of protecting the nervous system and brain from the ravages of PD as L-Dopa, the primary treatment of choice, grows less effective as time wears on. Nutritionists are looking at dietary factors that can prevent oxidation, provide neuroprotection and offer supportive functions where the metabolic pathways have become ineffectual. (1)
The Role of Macronutrients
Macronutrients refers to proteins, fats, carbohydrates and fibers in the diet. The amounts, types and distribution of each of these nutrients play a key supportive and therapeutic role in the nutritional treatment of PD. If an overall diet plan were to be chosen, the Mediterranean Diet eating plan would be the template for any dietary modifications since it is consistently favored in the literature as a preventative dietary approach for PD.
L-Dopa, the major therapeutic treatment for PD, competes with the amino acids from protein fragments for absorption. Consequently, low protein diets, either .5g/kg or a straight 40 g protein diet, are therapeutically recommended to enhance the effectiveness of L-Dopa absorption at its lowest possible dose for the longest period of time possible. The protein limit prior to the last meal of the day is 7 grams according to one study (2). Generally, protein loads are advised for the evening meal with mostly carbohydrates, fiber, fats and fluids throughout the day. This means the daily diet should consist of fruits, vegetables, some grains, water, juice, limited nuts and nut butter and low protein medical foods. While dairy is important, do not take it with medications or within 40 minutes after L-Dopa as it, too, contains proteins.
Fats are classified as either saturated, polyunsaturated or monounsaturated. Early studies in rats showed a detrimental effect of total fat on PD progression. Later studies in humans showed more of a negative relationship to animal fats in PD progression. Saturated fat theoretically alters the cell membrane adversely affecting the lipid membrane and promoting oxidative stress. (2)
Neuroprotection has been found with diets high in polyunsaturated fats(PUFA), particularly with the omega-3 fatty acids. It has also been consistently shown that diets high in PUFA and low in saturated fats reduce the risk of PD and protect from the toxic effects of neurotoxins.
Saturated fats, found abundantly in meats, are loaded with the “heme” protein, a protein some PD patients are genetically programmed not to metabolize correctly, thus aggravating symptoms and possibly accounting for the negative associations between meat consumption and PD development. (2)
Carbohydrates may play a more positive role in decreasing progression of PD. Carbohydrates are full of polyphenols, fibers and increase the release of insulin-induced dopamine in the brain. Since a high consumption of carbohydrates is not necessarily beneficial for everyone, particularly those with diabetes, emphasis should be placed on fiber containing carbohydrates rather than simple sugars.
Constipation is a common complaint in patients with PD as is adequate fluid intake. Getting enough fiber will help to avoid constipation and straining, but an increase should be gradual to avoid gas and bloating and should be accompanied by an intake of 8-10 glasses of fluids per day. Twenty-five grams of fiber a day is the current daily recommendation.
Some nutrients have been identified to have a supportive role in PD preventing oxidation and neurodegeneration thus delaying or mitigating symptoms associated with the demise associated with this disorder.
Omega 3 Fatty Acids
Omega 3's have proven to be a protective factor in many neurodegenerative diseases. (2) Oral administration of docosahexaenoic acid (DHA), an omega 3 fatty acid, increases dopaminergic neurotransmission, synaptic membrane formation as well as the density of dendrite spines. In the first study of its kind, DHA supplementation in rats was shown to have neurorestorative and disease-modifying properties. (3) Supplements of 1,000 mg of DHA/EPA omega 3 fatty acids may be supportive in the prevention of the ravages of PD.
Of all supplements studied, only fish oil (a source of omega 3’s and coenzyme Q10 showed significant associations with PD progression. (4)
Both folic acid and B12 have commonly been supplemented in PD. Both are known to lower the neurotoxin homocysteine and are often low in PD patients.
Patients on L-Dopa must frequently limit their B6 intake to 15 mg so as to not interfere with L-Dopa.
Coenzyme Q10 is a naturally occurring, fat-soluble, vitamin-like enzyme found in a variety of foods and synthesized in the body. At levels of 300,600 and 1200 mg/day over a six-month period, patients showed decreasing symptoms over placebo with the best effects achieved at the 1200 mg supplementation level.(5,6)
While black tea is a no-no due to its high manganese level, green tea has shown beneficial effects at about 3 cups per day. Green tea has both anti-oxidant and anti-inflammatory properties and has been shown to have neuroprotective qualities (7). It is thought that the polyphenols and, specifically, epigallocatechin gallate (EGCG), a catechin, are responsible for the beneficial effects.
Melatonin is a hormone synthesized by several tissues other than the pineal gland in the brain that exerts neuroprotective, anti-inflammatory, antioxidant and regulatory effects on the body. Melatonin has been shown to improve motor derangement, non—motor symptoms, sleep and anxiety disorders as well as improving memory and decreasing depression in PD patients. Current research suggests its use in preventing the neurodegeneration in PD. (8) Melatonin is also known to decrease homocysteine, a chemical that is neurotoxic to dopaminergic neurons in PD patients and is a known cardiovascular risk indicator (9).
Because, theoretically, melatonin can cause a decrease in dopamine secretion, it is suggested that therapy begin low and slow at 1 mg in the evening before bed and increasing up to 5 mg if tolerated.
All patients with PD should have their vitamin D checked and repleted if low. Much debate exists over the optimum blood level of this pro-hormone, but its importance in multiple system disease management can no longer be questioned. Since the intake of milk and vitamin D fortified products is often low in PD patients, supplementation is often needed and required for optimum prevention of future neurological demise. Repletion therapy involves high doses of 10,000 IU/day for 5 days per week for six weeks and then retest. Maintenance dose can be anywhere from 400 - 1000 IU/day after repletion therapy.
Additional Supportive Practices
In cases of heavy metal poisoning, eating foods high in sulfur may assist the detoxification process. Foods such as onions, garlic, and foods high in water soluble fibers from guar gum, pectin, oats, oat bran and psyllium seeds. Maintaining a high antioxidant intake of vitamin C and bioflavonoids from vegetables and fruits are helpful as well as lowering meat intake.
In the initial stages of PD, caloric restriction of up to 25% of estimated needs may help alleviate some symptoms, but over time weight loss and adequate caloric intake become of paramount importance to prevent malnutrition. Hydration and choking may become issues of concern. Food may then need to be blenderized and ways to increase calories may need to be implemented to prevent excess weight loss. A weight loss of greater than 10% in six months is high risk for malnutrition and should be addressed by a Dietitian.
Multivitamins with added iron or manganese should be avoided. Caffeine is acceptable and may provide some benefit to brain and energy function. Kava kava, Ephedra, Ma Huang, Ginseng and St. Johns Wort should be avoided as should cooking in aluminum pans.
PD is not curable, but is manageable through diet and medications. Education of the patient and caregivers is of paramount importance in working with the prescribed diet and medications.
1. Agim ZS, Cannon JR. Dietary factors in the etiology of Parkinson’s Disease. Biomed Research International. 2015; http://dx.doi.org/10.1155/2015/672838.
2. Perez-Pardo P, Kliest T, Dodiya HB, et al. The gut-brain axis in Parkinson’s disease: possibilities for food-based therapies. European Journal of Pharmacology. 2017; 817:86-87. http.//dx.doi.org/10.1016/j.ejphar.2017.05.042.
3. Seidl S E, Santiago JA, Bilyk H, Potashkin J.A. The emerging role of nutrition in Parkinson’s disease. Frontiers in aging neuroscience. 2014; 6(36):1-14. Doi.10.3389/fnagi.2014.00036.
4. Pardo P, deJong E, Broersen L M, et al. Promising neurorestorative and gastrointestinal dysfunction after symptom development in the mouse model. Frontiers in Aging Neuroscience. 2017;9(57): 1-12.doi:10.3389/fnagi.2017. 00057.
5.Mischley LK, Lau RC, Bennett RD. Role of diet and nutritional supplements in Parkinson’s disease progression. Oxidative Medicine and Cellular Longevity. 2017. https://doi.org/10.115512017/6405278.
6. Pizzorno JE, Murray MT, Joiner-Bey H, eds. Parkinson’s Disease. In: The Clinician’s Handbook of natural Medicine. 3rd ed St. Louis, Missouri: Elsevier Press; 2016:749-765.
7. Pinto NB, Alexandre B, Neves KR, et al. Neuroprotective properties from Camellia sinensis (Green Tea) and is main bioactive components, epicatechin and epigallocatechin gallate, in the 6-OHDA model of Parkinson’s disease. Evidence based complementary and Alternative Medicine 2015. http://dx.doiorg/10.1155/2015/161092.
8. Mack, JM, Schamne MG, Samoaio Tb, et al. Melatoninergic system in Parkinson’s disease from neuroprotection. Oxidative Medicine and Cellular Longevity. 2016:1-31.
9. Paul R, Phukan BC, Thenmozhi AJ, et al. Melatonin protects against behavioral deficits, dopamine loss and oxidative stress in homocysteine model of Parkinson’s disease. Life Sciences. 2018; 192:238-245. https://doi.org/10.1016/jlfs.2017.11.016.