Q I have recently been diagnosed as having Parkinson’s disease, so I am naturally very interested in anything that may help keep it under control, especially since I resisted all attempts to enlist me for clinical trials of a new drug combination. In fact, I refused to go on drugs at all, since the likely side effects sounded worst than the condition I’m in! I consulted a medically qualified homoeopath and under his guidance take mercurius, which seems to be helping. But if I can also help myself through diet, so much the better.- C J C, Exeter.
A You are wise to be interested in alternative treatments for Parkinson’s. Mainstream medicine is utterly confused by this disease, where the extrapyramidal system controlling movement is disturbed, and consequently has experimented (unsuccessfully) with ever more desperate solutions.
The cornerstone of medical treatment of Parkinson’s disease is levodopa or L-dopa (L-dihydroxyphenylalaline). Autopsy studies on the brain of patients with Parkinson’s show that they have a massive deficiency of dopamine (Fed Proc, 1973; 32: 183-90). A precursor of dopamine, synthetic L-dopa is taken in an attempt to restore the imbalance between dopamine and acetylcholine.
However, L-dopa often causes a load of side effects – abnormal movements of the extremities, face and trunk, short-term memory loss and confusion, and nausea and vomiting – which sound suspiciously like all the symptoms of Parkinson’s that you are attempting to treat. Consequently, most doctors must walk a tightrope in dosage prescribing, providing enough medication to rid the patient of symptoms while not prescribing a dose that is high enough to bring on side effects.
Fortunately, a number of nutritional measures can help you to cut, if not entirely eliminate, the need for medication, according to our panellist Dr Melvyn Werbach, who has exhaustively researched the literature for evidence of nutritional treatments for Parkinson’s (Nutritional Influences on Illness, Tarzana, CA: Third Line, 1993).
Your first port of call should be to rule out heavy metal toxicity, particularly with mercury or aluminium. In one study, 42 patients, compared with a set of matched controls, showed that occupational exposure to aluminium, manganese or iron more than doubled the risk of Parkinson’s disease, and increased it by 13 times after 30 years (Can J Neurol Sci, 1990; 17: 286-91).
High blood mercury levels have also been shown to be present in Parkinson’s patients (Neuroepidemiology, 1989; 8: 128-41).
It’s also wise to make sure that your copper blood levels aren’t too high. Significantly higher levels of copper in the cerebrospinal fluid have been found in Parkinson’s patients; the higher the levels of copper, the worse the patient’s symptoms ( Lancet, 1987; ii: 238-41). If you are on the Pill, it’s important to get off it immediately, since the Pill causes copper levels in the body to soar. (A nutritionist will then help to settle your copper levels back into line.) Excessively high levels of iron, usually acquired occupationally, also contribute to Parkinson’s (Can J Neurol Sci, 1990; 17: 286-91).
If you are on L-dopa, according to Dr Werbach, the mainstay of your nutritional programme should be a diet that is low in protein. L-dopa is a large amino acid that must compete with numerous other amino acids to pass across the blood-brain barrier. Since the object is to get as much L-dopa to your brain as possible, you need to eliminate the competition which, of course, is fed to your body via protein.
In one small study, patients on a high-protein diet were compared with two groups of patients on low-protein diets, one of whom had protein evenly distributed throughout the day and the other of whom consumed 90 per cent of the daily quota of protein solely during the evening meal. Those consuming protein only in the evening enjoyed significant improvement in symptoms, including a lessening of tapping and tremor (Neurology, 1989; 39: 552-6).
Research shows that a low-protein diet can also eliminate the inevitable ‘on-off’ effect of L-dopa, in which its effectiveness fluctuates throughout the day. In another double-blind study, patients on low-protein diets were significantly better on low-protein diets; nevertheless, a patient’s symptoms didn’t correlate with the amount of L-dopa; indeed, three patients on the high-protein diet had the highest peaks of L-dopa and yet the worse performance and greatest number of off hours. This suggests that large quantities of protein somehow block the effectiveness of L-dopa (Neurology, 1989; 39: 549-52).
If you do start on a low-protein diet, it’s important that you are monitored by your doctor, as your levels of L-dopa may have to be reduced. L-dopa itself reduces levels of S-adenosyl methionine (SAMe), an essential sulphur amino acid (J Neurol Neurosurg Psychiatry, 1990; 53: 569-72). Two studies have examined patients taking L-methionine. In one, patients were started with only 1 g per day and gradually increased to 5 g per day). After several months, two-thirds of the patients had improved in most parameters, including ease of movement, a lessening of involuntary movement, muscular strength, and even concentration, mood and sleep (South Med J, 1984; 77: 1577). Another study showed that the benefits of SAMe were similar to those of L-dopa (Rev Neurol, 1982; 138: 297-303).
Besides SAMe, it might be prudent to take supplements of several other amino acids, which are often deficient in Parkinson’s patients. These deficiencies may be responsible for the ‘on-off’ fluctuation of L-dopa’s effectiveness in patients. Perhaps the most significant is L-tryptophan, which helps to regulate mood. Parkinson’s patients are often deficient in this vital amino acid because L-dopa competes with L-tryptophan. Regular L-dopa supplementation can lead to malabsorption of L-tryptophan, which can in turn lead to depression and a number of other symptoms which are usually categorised as side effects of the drug.
In one case study of a small number of patients, supplementing with tryptophan improved the mental disturbances which had been observed in them (Acta Med Scand, 1973; 194: 181-9). Supplementing with tryptophan (2 g three times per day) can also help the physical symptoms of Parkinson’s. In one study where patients all received L-dopa, but only half were also given tryptophan, all improved on various motor skills, but only those receiving the tryptophan also improved in functional ability, mood and drive (Lancet, 1972; I: 654-7).
Besides tryptophan, Parkinson’s patients also may need supplements of D-phenylalanine, which is also often diminished (Arzneim Forsch, 1973; 23: 884-5) in this disease, and L-tyrosine, levels of which can drop because of the low-protein diet. In fact, studies have shown that L-tyrosine, a precursor of L-dopa, on its own can work better than L-dopa and with fewer side effects (C R Acad Sci III, 1989; 309: 43-7; Life Sci, 1982; 30: 627-32).
Just make sure not to take any of the amino acids at the same time you are taking L-dopa because they compete for movement across the blood-brain barrier. Taking them simultaneously could increase fluctuations in your response to L-dopa.
Numerous vitamins and minerals can help with symptoms. Perhaps most important are a number of the B vitamins. High levels of thiamine are thought to prevent Parkinson’s; in one laboratory study, thiamine was one of the best inhibitors of dopamine oxidation (Lancet, 1988; i: 363). A deficiency of folic acid is also associated with developing Parkinson’s (J Neurol Neurosurg Psychiatry, 1986; 49: 920-7).
The other vitamin intimately associated with L-dopa absorption is vitamin B6. An enzyme which converts L-dopa to dopamine is dependent upon vitamin B6; treatment with L-dopa on its own can raise blood concentrations of pyridoxal-5-phosphate, the precursor of vitamin B6, while treatment with L-dopa plus a decarboxylase inhibitor may cause a vitamin B6 deficiency (Clin Sci, 1979; 56: 89-93).
Parkinson’s patients can benefit from taking vitamin B6 supplements, although results are mixed, with some studies showing improvement in numerous symptoms (Soy Med, 1979; 7: 14-9; JAMA, 1941; 116: 2484-7) and some showing no improvement (Bull Johns Hopkins Hosp, 1941; 69: 266-75; JAMA, 1941; 116: 2148). Those patients who most benefit receive large doses (100-400 mg per dose). Note: patients with heart conditions, specifically angina or coronary insufficiency, should not receive vitamin B6.
Good results have been achieved by intraspinal injection of 5-10 mg of thiamine and vitamin B6 (5-25 mg) in helping with rigidity (Dis New Sys, 1950; 11: 131-8).
Patients who are on constant doses of L-dopa may be deficient in niacin, says Werbach, since decarboxylase inhibitors also appear to reduce the sythesis of this vitamin. Niacin is also helpful in extending the levels of brain dopamine in patients taking L-dopa (Biochem Med Metabol Biol, 1986; 36: 244-51). In patients who have already developed Parkinson’s, nicotinamide adenine dinucleotide (NADH), a coenzyme made from niacin, helps to convert tyrosine to L-dopa; in one small study, 62 per cent of patients receiving NADH intravenously improved in symptoms by at least 30 per cent. The optimum dosage was 25-30 mg per day (Ann Clin Lab Sci, 1989; 19: 38-43).
Other vital nutrients include vitamin C, which can counteract the adverse side effects of L-dopa (Adv Neurol, 1983; 37: 51-60); 400-3200 IU of vitamin E (SA Factor, presented at Vitamin E: Biochemistry and Health Implications, NY Academy of Sciences Meeting, NY, November 1988); magnesium (Can J Neurol Sci, 1989; 16: 310-4); and omega-6 fatty acids in evening primrose oil, which can reduce tremors (EMR Critchley in DF Horrobin, ed. Clinical Uses of Essential Fatty Acids, Montreal: Eden Press, 1982: 205-8).