PARKINSONS'S DISEASE AND DIET
PARKINSONS'S DISEASE AND DIET
Vitamins E and C
Since the original description of the disorder by James Parkinson in 1817, much has been learned about Parkinson's disease (PD). PD, characterized chiefly by resting tremor and the disturbance of voluntary movement, has probably always afflicted mankind, but was only specifically identified as recently as the last century. PD is a neurodegenerative disease in which there is a loss of substantia nigra dopaminergic neurons. Symptoms include resting tremors, stiffness of muscles, slowness of movement, tiredness, depression, dribbling, constipation, disturbance of balance, and mental confusion. Some studies point out that patients, with idiopathic PD, are more likely than controls to have used well water and to have lived in the proximity of industrial chemical plants as well as areas of heavy pesticide use. The recent increase in our knowledge of the pharmacokinetics of levodopa and other antiparkinson agents has led to an improved understanding of approaches to treatment of PD patients. For more information on Parkinson's Disease, link to the following sites:
One approach for treatment of PD is through exercise, diet, and nutrition
management. Diet was identified as a potentially important variable in the
management of PD in the late 1960s when 1-3,4-dihydroxy-phenylalanine (L-dopa)
was first used to treat PD. L-dopa is the precursor amino acid of dopamine, the
deficient neurotransmitter in PD. It is a large neutral amino acid (LNAA) which
along with other LNAA's produced during normal dietary protein breakdown,
competes for active transport across the blood brain barrier (BBB). Chronic
L-dopa administration in PD is associated with the gradual development of motor
fluctuation called the "on-of" phenomenon.
The goal of most dietary therapies have been to facilitate L-dopa's entry into the brain by restricting protein intake and thus decreasing the on-off phenomenon. The dietary restriction for protein intake in PD reflects the current recommended daily allowance (RDA) of 0.8g/kg/day but the primary difference is the redistribution of protein intake throughout the day. The basic strategy of these diets is to decrease circulating plasma LNAA's levels by limiting protein intake in the active hours of the day. As a result protein intake is displaced to the less active times of the day, usually in the evening. The resulting loss of L-dopa's antiparkinsonian effect will be less disruptive in the evening. Also many studies indicate that the ideal carbohydrate to protein ratio is 7:1 in order to reduce motor fluctuations in response to L-dopa medication. Basically a meal high in protein may reduce the absorption of L-dopa, and thereby reduce the benefit of treatment.
Not only have high levels of dietary protein been shown to inhibit the function of L-dopa, but vitamin B6 has also been found to interfere with the action of L-dopa. Vitamin B6, which is abundant in sweet potatoes, bananas, spinach, broccoli, raisins, and beef tends to block the use by the brain of L-dopa. Vitamin B6 is a cofactor of LAAD, the rate limiting enzyme in the conversion of L-dopa to dopamine. Large doses of vitamin B6 have been reported to counteract the beneficial effect of L-dopa through a presumed increase in LAAD activity. Increased enzyme activity would drive the conversion of L-dopa to dopamine in the periphery, preventing L-dopa from entering the brain. Although diets should be modified so as to decrease B6 intake, vitamin B6 should not be omitted from the diet. Vitamin B6 is essential for metabolizing all amino acids, synthesis of neurotransmitters, and other key metabolic functions. A deficiency in vitamin B6 may cause headache, anemia, nausea, and vomiting. Having said this, it should also be noted that vitamin B6 does not play a significant role in clinical settings today because LAAD inhibitors have been part of commercial L-dopa preparations.
Vitamins E and C:
Dr. Stanley Fahn, in 1979, began a pilot study in which patients with early PD were asked to take 3200 units a day of vitamin E and 3000 mg a day of vitamin C a day prior to starting any other antiparkinsonian therapy. Patients taking the vitamins in early stages of PD were able to delay the standard treatment with L-dopa for 2.5-3 years. Vitamin E is one of the most important antioxidant. Free radical accumulation is thought to mediate tissue injury, particularly in diseases of aging, and vitamin E is essential in retarding these destructive processes. Basically the role of vitamin E in PD is to slow the gradual progression of the disease and allow patients afflicted with the disease to live a longer and fuller life. Vitamin C is also an effective scavenger of oxidative free radicals. It has been shown to reduce the dopamine depleting effects of MPTP and to facilitate L-dopa's transport across the BBB. However, vitamin C's potentially beneficial effects in PD contrast with potentially negative effects such as vitamin C's ability to inhibit the dopamine-sensitive enzyme adenylate cyclase, thus making it hard to predict what its ultimate effect in PD might be. Those patients who, on their own, are taking in excess of 2g/day should be cautioned against the potential for renal caliculi (renal stones) and hemolysis.
Iron replacement therapy may be occasionally necessary in parkinsonian patients
suffering from a variety of medical problems leading to blood loss. A combination
of soluble iron with vitamin C (which presumably helps iron cross the BBB),
result in a significant short-term improvement in akinesia in various patients
Aspartame has become a popular artificial sweetener in food products and
carbonated diet beverages. In the rat, oral administration of large quantities of
aspartame will increase the plasma and brain concentration of several LNAA's,
including phenylalanine and tyrosine. Because phenylalanine and tyrosine are the
precursor amino acids of dopamine and norepinepherine, similar changes in man may
have clinical consequences in the management of PD. Although no study has looked
at the possible effects of aspartame on antiparkinsonian therapy, there does seem
to be some correlation.
In conclusion, the benefits of protein restriction/redistribution diets in individual patients with PD can be as variable as the disease itself. The mechanism for the beneficial effects of diet in PD are not completely understood. It appears that protein restriction benefits PD by improving the flux of L-dopa across the BBB. Multiple vitamins and minerals also effect the treatment of PD although their mechanisms are not clearly understood either. It is important to point out that in almost every case, the therapeutic effects of nutrition in PD works in either enhancing or reducing the efficacy of the drug L-dopa. There is no evidence showing that nutritional management can in any way effect the disease itself. Future research should address this issue with special emphasis on the mechanism nutrition may have on disease itself. For more information, telephone numbers, and addresses on Parkinson's Disease support groups or research techniques link to:
The preceding information was based on Diet and Related Variables in the
Management of Parkinson's Disease ,by Jorge L. Juncos, and Current Concepts in
Parkinson's Disease Research, editors Jay S. Schneider and Madia Gupta.
This information was compiled by Zareh Baghoomian at the University of Southern
California, School of Gerontology. If you have any questions or comments please
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