Parkinson's Disease and a Plant Based Diet
Kathrynne Holden, MS, RD
The nature of Parkinson’s disease
Parkinson’s disease (PD) afflicts about one to one and one-half million people in the United States (Tanner 1992). PD is a progressive neurological disorder that results in the death of dopamine-producing cells in the brain. Loss of dopamine affects movement, both of skeletal muscle and the smooth muscle of the gastrointestinal (GI) tract. This can result in slow, shuffling gait, resting tremor, and/or slowed peristalsis. Individuals with PD may experience frequent falls (Dolinis et al., 1997; Northrid ge et al., 1996), d ifficulty handling cooking and eating utensils, and such GI-related problems as slow stomach emptying, gastroesophageal reflux, and chronic constipation (Jost WH, 1997; Edwards et al, 1993; Edwards et al., 1994; Byrne et al., 1994).
Individuals with PD have been found to have a higher incidence of bone thinning and fractures than age-matched control groups (Ishizaki et al., 1993; Kao et al., 1994; Taggart, et al., 1995; Revilla et al., 1996; Koller et al., 1989; Johnell et al., 1992, Sato et al., 1997). Loss of the olfactory sense and sense of taste are frequently present (Huttenbrink, 1995; Hawkes et al., 1997), along with xerostomia (dry mouth) (Clifford and Finnerty, 1995), and sometimes loss of appetite (Starkstein SE, 1990). These, along with other factors, may contribute to the high rate of unplanned weight loss in this population (Markus et al., 1993; Davies et al., 1994; Beyer et al., 1995).
There are also indications that B vitamin deficiencies may be of concern, although the causes are not clearly understood. In 1979, Bender et al. reported the possibility that users of levodopa-carbidopa (Sinemet, Sinemet CR, a medication used to treat the symptoms of PD) could be at risk for both niacin and vitamin B6 deficiencies. Long-time users of levodopa-carbidopa have since been found to have increased levels of serum homocysteine (Kuhn et al., 1998, Muller et al., 1999), implicating vitamins B6, folate, and B12. In attempts to determine the etiology of PD, Hellenbrand et al. compared the dietary habits of patients vs. a control group; patients were found to have consumed significantly less niacin than controls (Hellenbrand et al. 1996). In a more recent Swedish study researchers note that consumption of niacin-containing foods appeared to reduce risk for PD (Fall et al., 1999). Finally, in an unpublished study, pellagra was discovered in several patients using levodopa-carbidopa (Iacono et al.). Thus, patients could have increased risk for vascular disease, pellagra, and other conditions resulting from deficiencies of B vitamins.
Constipation is very common due to the disease and/or to the medications used to treat PD (Jost, 1997; Jost and Schrank, 1998; McIntosh and Holden, 1999). Chronic constipation can raise the risk for fecal impaction (Sonnenberg et al., 1994) and colon cancer (Jacobs and White, 1998; Will et al., 1998), therefore, safe methods of controlling constipation are desirable.
Furthermore, PD brings with it a food-medication interaction that has been generally under-addressed by dietetics professionals. Levodopa, the primary medication used to treat PD, competes with the five large neutral amino acids for carriers, both in the gut and at the blood-brain barrier (Lieberman, 1992). Thus, levodopa absorption is effectively blocked if taken with meals.
How can a vegetarian or plant-based diet be of help to people with PD?
While research has failed to conclusively show a link between diet and PD, nevertheless, fiber, nutrients found particularly in plants, and protein, are excellent reasons to choose among the various vegetarian and plant-based eating plans. Animal foods are often high in protein and lack fiber. Plants in general have a high proportion of carbohydrate, with moderate amounts of protein. Plants also contain fiber and many phytochemicals, which animal products do not.
Fiber. A plant-based diet is generally richer in fiber, which can alleviate constipation, and thereby reduce risk for fecal impaction and colorectal cancer. In a pilot study, McIntosh and Holden found that while 21 out of 24 patients reported frequent constipation, analysis of three-day food diaries showed that 18 patients reported intake of fewer than 25 grams of dietary fiber daily. Education in the need for greater fiber intake, and its benefits to health, is necessary for PD patients. Additionally, a high-fiber eating plan may promote bioavailability of levodopa. Astarloa et al. found a correlation between a diet rich in insoluble fiber and plasma levodopa concentration, and postulate that the improvement of constipation may have a positive effect upon levodopa availability (Astarloa et al., 1992). While there is no research as yet on benefits of a vegetarian diet for people with PD, nevertheless, a vegetarian or plant-based diet may have special significance for people with PD.
Unplanned weight loss. To combat weight loss, patients must consume more calories. Yet delayed stomach emptying, if present, may require moderate use of fatty foods, while those using levodopa may need to control their use of protein. Such restrictions sometimes necessitate small, frequent meals and snacks, and a diet high in carbohydrates. A vegetarian diet adapts very well to such an eating plan, as it can be both high in carbohydrates and low in fat, whereas animal foods are often high in fat.
Chewing/swallowing difficulty. Patients in mid-to-late stages of PD may experience difficulty chewing food, and/or moving the tongue to position food properly for swallowing. The normal esophageal peristalsis may be slowed, resulting in choking. While a swallowing evaluation should be performed, along with education in safe swallowing techniques, it should be noted that plant foods may be easier to chew than many meats; plant foods also can be chopped, mashed, or pureed easily to provide the best consistency for the individual’s needs while retaining valuable fibers and phytochemicals.
Nutrients. Plant foods are rich in magnesium and vitamin K, important to bone health. This should be emphasized, as PD patients, due to the nature of the disease, may be prone to falls (Ishizaki et al., 1993; Kao et al., 1994; Taggart, et al., 1995; Revilla et al., 1996; Koller et al., 1989; Johnell et al., 1992, Sato et al., 1997), and therefore more susceptible to fractures (Dolinis et al., 1997; Northridge et al., 1996). Good sources of calcium and vitamin D must be highlighted, also, as there may be a greater need for these in this population; in a controlled study, Sato et al. found increased incidence of vitamin D deficiency and reduced bone mass in individuals with PD (Sato et al., 1997).
A vegetarian or plant-based diet can provide excellent amounts of the B vitamins (with the possible exception of B12), especially folate; and education regarding need for B vitamins is important. The vegan patient may need to use a supplement of vitamin B12, and in fact, if deficiencies are suspected, a B complex may be required, at least temporarily. It should be noted that large amounts of vitamin B6 (over ten mg per day) may reverse the effects of levodopa; therefore, supplements should be taken with meals, with levodopa taken at least 30 minutes prior to meals, to avoid this food-medication interaction.
Protein-levodopa interactions. As stated before, protein breaks down in the gut to individual amino acids, with which levodopa must compete for carriers across the intestinal wall. For this reason, patients must take levodopa at least 30 minutes prior to meals or snacks. As the disease progresses, individuals often begin to experience fluctuations in their response to levodopa, resulting in the "on-off" phenomenon, a condition wherein a dose of levodopa wears off before the next dose is due. Without levodopa, the individual may be able to move only very slowly, or not at all, and is effectively disabled.
To cope with these motor fluctuations, it has long been advised that patients avoid protein during the day, limiting intake to no more than ten grams prior to the evening meal. The bulk of protein needs is met at the evening meal, allowing the patient optimal use of levodopa during the daytime hours. However, this often means that the patient cannot move all night long, which can be very frustrating and even frightening, as s/he cannot turn over in bed, get up to use the bathroom, or adjust the bedclothes. If diabetes, hypoglycemia or other conditions are present, this protein restriction is even less desirable.
Although less widely understood, a high-carbohydrate eating plan consisting of a ratio of five parts carbohydrate to one part protein, or higher, can be very effective (Berry 1991). Once in the bloodstream, the high ratio of carbohydrates causes an insulin rush that removes amino acids from the blood as well, thus allowing levodopa to reach the blood-brain barrier unobstructed. (See Eriksson et al. 1988; Sanchis et al. 1991.) A plant-based diet is an ideal way to achieve a high-carbohydrate meal plan, as plant proteins are often found in a carbohydrate-to-protein ratio of 3:1 or higher, whereas meats have virtually no carbohydrate. Legumes, seeds, and nuts are excellent foods, and can easily be incorporated into a meal consisting of a 5:1 or higher ratio.
Most patients gain improved "on time" with some form of protein adjustment. Some find they can reduce the amount of levodopa needed. Reduction of levodopa may result in lessened side effects, such as hallucinations and dyskinesia (unwanted twisting or writhing movements). Much more research is needed in this area, to document reduction in medications, improved "on time, lessened dyskinesia, and reduced adverse effects of medications.
It will be important to assess nutrition risk, and a three-day food diary can be of great help in determining whether fiber and nutrient intake is adequate. Information intake via interview is also important, paying particular attention to weight changes and risk for bone thinning. If unplanned weight loss has occurred, determine whether this is due to depression, excessive calorie expenditure because of tremor, dyskinesias, or rigidity, inability to self-feed at a normal pace, chewing or swallowing problems, or other condition. Small, frequent meals and snacks are often preferable to the usual three meals a day. To assess delayed stomach emptying, inquire whether the individual experiences heartburn or acid reflux, often a sign of slowed peristalsis; also find out how long it takes for medications to take effect. If the patient is using levodopa, and taking it at least 30 minutes prior to meals without feeling the onset of antiparkinson effects, delayed stomach emptying is a possible factor. Small plant-based meals and snacks, moderate in fat, may be an effective way to counter delayed stomach emptying.
If the individual uses levodopa and motor fluctuations occur, consider protein adjustment. The simplest, and often very effective method, is to estimate individual protein needs, and divide the protein equally among meals. If weight loss or slowed stomach emptying is present, I often suggest small meals with low-protein snacks between meals. This provides the most natural eating plan. If the person is protein-sensitive, it may be helpful to increase carbohydrates. Try a ratio of 5:1 initially, as this provides the most protein and therefore a more natural eating plan. After two to three weeks, the individual should notice improved "on time;" if not, increase the ratio to 6:1 or 7:1. This eating plan is often harder to teach; it may be necessary to provide ready-made menus for meals and snacks. NOTE: it is difficult to provide a 7:1 eating plan having less than 1800 kcal per day. This may be too much food for some people, especially small women. If a 7:1 ratio works well for the person, s/he may wish to use it throughout the day in small meals and snacks, then add additional protein at the evening meal. This will provide for a smaller number of calories and offer sufficient protein, while still allowing for better levodopa absorption during the day.
Some cautions to be aware of are the increased risk for bone thinning, and need for vitamin B12. It may be necessary for patients to use vitamin/mineral supplements, especially of calcium, vitamin D, and vitamin B12. In some cases, a vitamin B complex may be needed as well. Patients who use levodopa should take supplements containing large amounts of vitamin B6 with meals, at least 30 minutes after taking levodopa, in order to avoid the interference of vitamin B6 with levodopa absorption.
Sample high-carbohydrate menu:
1 ½ cups split pea or lentil soup
1 oz whole-grain crackers
1 TB peanut butter
8 oz cranberry juice
½ cup grapes
(694 calories, 122 g carb, 24 g pro, 16 g fiber, 66 mg calcium)
For more information, see Parkinson's Disease: Guidelines for Medical Nutrition Therapy, which includes PD-specific Risk Assessment Tools and Initial Interview Form. The patient-caregiver handbookEat Well, Stay Well With Parkinson’s Disease contains patient education information, including recipes and menus. A two-hour seminar (Level II, 2 CEUs) is available: Nutrition and Parkinson’s disease: What the health professional needs to know.
Astarloa R, Mena MA, Sanchez V, de la Vega L, de Yebenes JG. Clinical and pharmacokinetic effects of a diet rich in insoluble fiber on Parkinson disease. Clin Neuropharmacol. 1992;15 (5): 375-380.
Bender DA, Earl CJ, Lees AJ. Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa. Clin Sci 1979 Jan;56(1):89-93.
Berry EM, Growdon JH, Wurtman JJ, Caballero B, Wurtman RJ: A balanced carbohydrate: protein diet in the management of Parkinson's disease. Neurology 1991 Aug;41(8):1295-1297
Beyer PL, Palarino MY Michalek D, Busenbark K, Koller WC: Weight change and body composition in patients with Parkinson’s disease. J Am Diet Assoc. 1995; 95:979-83.
Byrne KG, Pfeiffer R, Quigley EM: Gastrointestinal dysfunction in Parkinson’s disease. A report of clinical experience at a single center. J Clin Gastroenterol. 1994; 19:11-16.
Clifford T, Finnerty J: The dental awareness and needs of a Parkinson’s disease population. Gerodontology. 1995; 12:99-103.
Davies KN, King D, Davies H: A study of the nutritional status of elderly patients with Parkinson’s disease. Age Ageing. 1994; 23:142-5.
Dolinis J, Harrison JE, Andrews GR: Factors associated with falling in older Adelaide residents. Aust N Z J Public Health. 1997; 21:462-468.
Edwards L, Quigley EM, Hofman R, Pfeiffer RF: Gastrointestinal symptoms in Parkinson disease: 18-month follow-up study. Movement Disorders. 1993; 8:83-6.
Edwards LL, Quigley EM, Harned RD, Hofman R, Pfeiffer RF: Characterization of swallowing and defecation in Parkinson’s disease. Am J Gastroenterol. 1994; 89:15-25.
Eriksson T, Granerus AK, Linde A, Carlsson A: ‘On-off’ phenomenon in Parkinson’s disease: relationship between dopa and other large neutral amino acids in plasma. Neurology. 1988; 38:1245-1248.
Fall PA, Fredrikson M, Axelson O, Granerus AK. Nutritional and occupational factors influencing the risk of Parkinson's disease: a case-control study in southeastern Sweden. Mov Disord 1999 Jan;14(1):28-37.
Hawkes CH, Shephard BC, Daniel SE: Olfactory dysfunctions in Parkinson’s disease. J Neurol Neurosurg Psychiatry. 1997; 62:436-46.
Hellenbrand W, Boeing H, Robra BP, Seidler A, Vieregge P, Nischan P, Joerg J, Oertel WH, Schneider E, Ulm G. Diet and Parkinson's disease. II: A possible role for the past intake of specific nutrients. Results from a self-administered food-frequency questionnaire in a case-control study. Neurology 1996 Sep;47(3):644-50.
Huttenbrink KB: Disorders of the sense of smell and taste. Ther Umsch.1995; 52:732-737.
Iacono RP, Radulescu T, Schoonenberg T, Kuniyoshe S, Hubbard RW. Pellagra manifesting during Parkinson’s treatment [Unpublished study]. Neuroscience and Movement Disorders Center, Loma Linda University, Loma Linda CA 92350.
Ishizaki F, Harada T, Katayama S, Abe H, Nakamura S: Relationship between osteopenia and clinical characteristics of Parkinson’s disease. Mov Disord. 1993; 8:507-511.
Jacobs EJ, White E. Constipation, laxative use, and colon cancer among middle-aged adults. Epidemiology. 1998; 9(4):385-391.
Johnell O, Melton LJ 3d, Atkinson EF, O’Fallon WM, Kurland LT: Fracture risk in patients with parkinsonism: a population-based study in Olmstead County, Minnesota. Age Ageing. 1992; 21:32-38.
Jost WH: Gastrointestinal motility problems in patients with Parkinson’s disease. Effects of antiparkinsonian treatment and guidelines for management. Drugs Aging. 1997; 10:249-258.
Jost WH, Schrank B. Defecatory disorders in de novo Parkinsonians--colonic transit and electromyogram of the external anal sphincter. Wien Klin Wochenschr 1998 Aug 21;110(15):535-7.
Kao, CH, Chen CC, Wang SJ, Chia LG,Yeh SH: Bone mineral density in patients with Parkinson’s disease measured by dual photon absorptiometry. Nucl Med Commun. 1994; 15:173-177.
Koller WC, Glatt S, Vetere-Overfield B, Hassanein R: Falls and Parkinson’s disease. Clin Neuropharmacol. 1989; 12:98-105.
Kuhn W, Roebroek R, Blom H, van Oppenraaij D, Przuntek H, Kretschmer A, Buttner T, Woitalla D, Muller T – Elevated plasma levels of homocysteine in Parkinson's disease.. Eur Neurol 1998 Nov;40(4):225-7.
Lieberman A: An integrated approach to patient management in Parkinson’s disease. Neurol Clin 1992; 10:553-556.
Markus HS, Tomkins AM, Stern GM: Increased prevalence of undernutrition in Parkinson’s disease and its relationship to clinical disease parameters. J Neural Transm Park Dis Dement Sect. 1993; 5:117-25.
McIntosh GC and Holden, KE Risk for malnutrition and bone fracture in Parkinson's disease: a pilot study. J Nutr Elderly. 1999;18(3) 21-31.
Muller T, Werne B, Fowler B, Kuhn W: Nigral endothelial dysfunction, homocysteine, and Parkinson’s disease. Lancet. 1999; 354.
Northridge ME, Nevitt MC, Kelsey JL: Non-syncopal falls in the elderly in relation to home environments. Osteoporos Int. 1996; 6:249-255.
Revilla M, de la Sierra G, Aguado F, Varela L, Jimenez-Jimenez FJ, Rico H: Bone Mass in Parkinson’s Disease: A Study with Three Methods. Calcif Tissue Int. 1996; 58:311-315.
Sanchis G, Mena MA, Martin del Rio R, Morales B, Casarejo MJ, de Yebenes MJ, Tabernero C, Jimenez A, de Yebenes JG: Effect of a controlled low-protein diet on the pharmacological response to levodopa and on the plasma levels of L-dopa and amino acids in patients with Parkinson’s disease. Arch Neurobiol (Madr). 1991; 54:296-302.
Sato Y, Kikuyama M, Oizumi K: High prevalence of vitamin D deficiency and reduced bone mass in Parkinson’s disease. Neurology. 1997; 49:1273-1278.
Sonnenberg A, Tsou VT, Muller AD. The "institutional colon": a frequent colonic dysmotility in psychiatric and neurologic disease. Am J Gastroenterol 1994 Jan;89(1):62-66.
Starkstein SE, Preziosi TJ, Forrester AW, Robinson RG: Specificity of affective and autonomic symptoms of depression in Parkinson’s disease. J Neurol Neurosurg Psychiatry. 1990; 53:869-873.
Taggart H, Crawford V: Reduced bone density of the hip in elderly patients with Parkinson’s disease. Age Ageing. 1995; 24:326-8.
Tanner CM: Epidemiology of Parkinson's disease. Neurol Clin.1992:10:317-329.
Will JC, Galuska DA, Vinicor F, Calle EE. Colorectal cancer: another complication of diabetes mellitus? Am J Epidemiol 1998;1:147:816-825