The orthodox treatment for Parkinson’s disease is L-Dopa, an amino acid. But for this to work, a co-enzyme called NADH is essential. NADH is formed from one of the B vitamins called niacin, or vitamin B3 (Biochem Med Metab Biol, 1986; 36(2): 244-51).
Many Parkinsonian patients have benefited from taking niacin.Oddly enough, Parkinsonian patients being treated with L-Dopa, particularly those also given benserazide or carbidopa, run a risk of developing a niacin deficiency. Taking the two drugs can also produce deficiency of vitamin B6. Besides niacin, you may need vitamin B6 supplements, but this can cancel out the effects of L-Dopa, unless you are taking it concurrently with carbidopa (AMA Drug Evaluations, 5th ed, 1983, American Medical Association, Chicago, 1983).
A common problem with conventional L-Dopa therapy is the so called “on off” effect, where L-Dopa works better at particular times of the day than others. These fluctuations, which have been linked to the consumption of proteins, can be effectively reduced when almost all of the day’s protein is taken with the evening meal (Neurology, 1989; 39: 549-52).
There’s evidence that Parkinsonism is associated with a low intake of foods rich in vitamin E early in life (Arch Neurol, 1988; 45:1350-3); occasionally, a folic acid deficiency may cause Parkinson’s disease (J Neurol Neurosurg Psychiatry, 1986; 49: 920-7), as can a magnesium deficiency (Can J Neurol Sci, 1989, 16 (3) 310-4).
Taking an excessive amount of manganese as a nutritional supplement may lead to Parkinson’s, as can too high levels of mercury or aluminium (Neuroepidem, 1989; 8(3):128-41).
Copper concentrations in the cerebrospinal fluid are often significantly higher in sufferers than in the normal population. In one study, copper concentrations related both to the severity and the rate of progression (Lancet, 1987, ii: 238-41). (Homoeopathic drainage, pioneered in France, can be used to quickly reduce copper concentrations.)
The enzyme that converts the amino acid L-tyrosine to L-Dopa is less active in Parkinsonian patients. As iron activates this enzyme, taking iron supplementation has had impressive results in at least one study (J Neurol Trans, 1986; 67:287-92). But to confuse matters further, Parkinsonian patients are known to have raised iron levels in a portion of their brains, which appears to aggravate the disease process (Can J Neurol Sci, 1990; 17(3): 286-91).
The most successful herbal treatment by far is the root of the deadly nightshade (Atropa belladonna). Used in the treatment of post encephalitic and post influenzal Parkinsonism after the great influenza epidemic in the early part of this century, the treatment was closely investigated and the astonishing results published (R F Weiss, Herbal Medicine, Ab Arcanum, Gothenburg, 1988). More recent research has shown that the total extract of the Belladonna root has significant benefits (Arzneimittel Forschung, 1971, 21(4):528). In the former USSR one successful study was conducted on the treatment of Parkinsonism with Bulgarian Belladonna root preparations (Zhurnal Nevro patologii i Psikhiatrii Imeni S S-Kors-akova, 1966; 66 (5): 698-703).
In Ayruvedic Medicine, material derived from the plant Macuna pruriens is often used on patients with Parkinson’s disease, and one study of 60 patients found it to be effective. Adverse effects, mainly affecting the gut, were very mild (J Alt & Comp Med: Res on Paradigm Pract & Policy, 1995; 1 (3): 249-55).
The most impressive research on non orthodox treatment of Parkinson’s concerns the use of L-methionine. WDDTY panel list Melvyn Werbach knows of several studies showing that L-methionine is as effective as L-Dopa after three weeks in people with previously untreated Parkinson’s disease (Rev Neurol [Paris],1982; 138 (4): 297-303). It also brought about further improvement in Parkinsonian patients who’d reached a plateau in their orthodox treatment (South Med J, 1984; 77: 1577).