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Parkinson's disease is characterised by impairment of movement, muscle rigidity, and tremor. It was named after an accomplished English doctor called James Parkinson (1755-1824) who after patiently observing and carefully listening to six sufferers with involuntary shaking of the body, differentiated it from other known medical causes at that time. At first he called it the shaking palsy, which later became known as Parkinson's disease. A further distinction is made between true Idiopathic Parkinson's disease when the cause of the disease is unknown, and diseases with similarities to Parkinson's such as hypothyroidism and degenerative diseases of the nervous system, which are often referred to as Parkinsonism.

There are approximately 120,000 people with Parkinson's in the UK. It develops between the ages of 50-80 years but can also affect people younger or older. There doesn't appear to be a pattern regarding whom it affects as it is equally common in males and females, is not related to overwork, stress levels, occupation, pregnancy, social status or lifestyle. However, the process of ageing does tend to increase the risk, as with age the brain naturally shows milder changes similar to those of Parkinson's.

The disease is not fatal but as yet is incurable, and the course of the disease is variable for all sufferers. 1/10 patients, mainly of the younger age group, show little progression with symptoms under control for many years. Others exhibit advancing severity of symptoms to the extent that voluntary and involuntary movements deteriorate, affecting the whole body.

Although Parkinson's disease appears to be a muscular failure, it is in fact a progressive disorder of the central nervous system which affects muscular movement. Specifically, it is a problem of co-ordinating the nervous impulses to the muscles involved in movement.

If the nerve pathways are working, muscles will contract and relax in the correct time and order and with the right force. If this does not happen imperfect movements will occur.

The co-ordination of the nerve messages to muscles is controlled by the dopaminergic neurons in the basal ganglia, which is directly associated with the substantia nigra (a pair of large, darkly pigmented nuclei that control subconscious muscle activities) and corpus striatum (the largest nucleus in the basal ganglia is the corpus striatum) in the brain. These neurons release the inhibitory neurotransmitter dopamine to transmit information via the cortex, thalamus and hypothalamus to the muscles. If a reduced amount of dopamine is released, the patient may know what he or she intends to do, but the messages received by the muscles will be inaccurate. The resulting movements will be tremor, rigidity, dyskinesia, (on-off reactions) dystonia, (muscular spasm), akinesia, (slowness in starting movement), bradyphrenia, (slowness of thinking) bradykinesia, (paucity of movement) and hypokinesia (slowness with decreasing range of movement). These in turn can affect speech, posture, gait, dexterity, memory, bowel function, temperature control, digestion, salivation, swallowing, and facial expression.

Thus, in Parkinson's disease sufferers the basal ganglia are either not able to manufacture dopamine or the dopamine receptors in the brain are blocked in some way, interfering with the action of the brain chemical.[1] Signs of Parkinson's show when 80% of the dopamine is lost from the basal ganglia, directly correlating with the loss of cells in the substantia nigra. A reduction in dopamine also upsets the neurons of the caudate nucleus in the basal ganglia that release the excitatory neurotransmitter acetylcholine causing a stimulatory affect on skeletal muscles.[2]

At present there appears to be no true reason and no definitive cure for the insidiously slow and silent deterioration of the dopaminergic neurons, and ongoing research is being carried out to determine possible causes. These causes should not be overlooked, as they may be vitally important in preventing and slowing down the disease once present.

Figure 1: Diagram showing the metabolic pathways of Dopamine, Adrenaline and Thyroxin.

Role of Nutrients in Parkinson's

Nutrient deficiencies and excesses can contribute to Parkinson's. As can be seen from the diagram of the metabolic pathway of dopamine (see Figure 1), vitamins B3, B6, B12, C, E, folic acid, copper and iron are important in the correct amounts, along with digestion and assimilation of protein foods. Evidence suggests that the disease is associated with a low intake of foods rich in vitamin E and folic acid deficiency early in life.[3] Excess manganese in the basal ganglia can cause a similar condition to Parkinson's and as manganese competes with iron for absorption it is also able to deplete iron levels.[4] Iron is needed for the enzyme that converts the amino acid L tyrosine to L-Dopa; however excess iron can damage the dopaminergic cells of the substantia nigra as can an overabundance of copper.[5] Vitamin B6 is vitally important, as it is needed to catalyse the conversion of L-Dopa to dopamine, but care has to be taken when used with L-Dopa medication as it may counteract the effects unless taken with the drug carbidopa.[6]

Defective neuronal mitochondria, which have a role in energy production and cellular support, may also predispose people to neurodegenerative diseases. Exhausted mitochondria damages dopaminergic neurons, and mutations in mitochondrial DNA affect the ageing process contributing to Parkinson's disease. Investigators suggest that mitochondrial dysfunction may result from the accumulated effect of environmental toxins, neurotoxins and oxidative stress in genetically predisposed individuals.[7-8] Nutrition could aid in providing the necessary nutrients for mitochondrial function, which are carbohydrates, CoQ10, NADH, iron, biotin, B vitamins, magnesium, manganese and oxygen. Of these NADH, nicotinamide adenine dinucleotide, a metabolite of niacinamide, the active co-enzyme form of vitamin B3, is of interest. Studies by the Birkmayer Institute show that not only does NADH aid energy production, but it also stimulates the body to produce its own L-Dopa, the precursor to dopamine.[9] Essential fatty acids and vitamin E are also important for cell membrane integrity and thus mitochondrial function.

Defects in the liver's enzyme detoxification systems may also play a role in the aetiology of Parkinson's Disease. Steventon and Waring have reported faulty metabolism of sulfur amino acids in patients with Parkinson's.[10] Genetic predisposition is indicated as a cause, as well as dietary constituents like red wine, coffee, certain cheeses, and chocolate, which are known inhibitors of sulphation. Cysteine, methionine and molybdenum aid in detoxifying sulphates. Food additives and preservatives, as well as environmental factors such as mercury, lead, and aluminium also overburden the liver.[11-12] Nutritional approaches to regulate dysfunctional liver enzyme systems have been used with some success. In 1992 Jeffrey Bland described a nutritional intervention program using a supplement called 'Ultra Clear Plus', which contains nutrients to aid liver function. In studies it increased the effectiveness of drugs, reduced symptoms and increased energy levels in those suffering from the early stages of Parkinson's.[13,13a] Other useful aids for liver function are cruciferous vegetables: cauliflower, cabbage and broccoli; bioflavonoids: catechin and hesperidin; liver herbs: burdock root, dandelion, ginger root and silymarin; and juices: carrot and beetroot.

Role of Toxins in Parkinson's

Toxic substances can also produce symptoms of Parkinson's Disease. One in particular is synthetic meperidine (MPTP), which was discovered in 1982 when addicts in California were making their own drugs using MPTP as a cheap alternative to heroin.[14] One 23-year-old student taking MPTP developed akinesia, tremor and rigidity, and improved when he was treated with anti-Parkinson drugs. Some time later he died and the post mortem indicated severe damage to the dopaminergic cells in the substantia nigra. The neurotoxic effects induced by MPTP can be prevented in mice when treated with a Chinese herb called Ginkgo biloba.[15]

Medical drugs are also implicated in Parkinson's Disease. Research by Jerry Avorn MD and colleagues at the Harvard Medical School found that elderly people prescribed Reglan for gastroesophageal reflux (chronic heartburn) had high chances of being diagnosed with Parkinson's.[16] Reglan's side effects can include Parkinson like symptoms such as difficulty with speaking, trembling, muscle spasm and limb stiffness. Anti-psychotic and butyrophenone drugs are also associated with Parkinson's.[17]

A further theory posed in 1991 by Jenner concerns free radical damage in the presence of excess iron, which destroy cell membranes and nerve cells in the substantia nigra.[18] Antioxidants help to prevent free radical damage and slow the progression of the disease. In one seven-year pilot study twenty-one patients with early Parkinson's were treated with daily doses of the antioxidants, vitamin C (3,000mg) and vitamin E (3200iu). The results showed that the use of drug therapy for Parkinson's was delayed up to 2-3 years compared to matched groups who did not receive the antioxidants.[19]

The nerve cells of the substantia nigra can also be destroyed by a build up of a protein substance within the cells. The damage shows up as Lewy bodies, named after Lewy who first noted their appearance in the brains of Parkinson's sufferers in 1912. Lewy bodies look like darkened circles with a light halo around them, and when present in large numbers in the brain provide definite medical evidence that the brain is damaged.

Excitotoxins found in foods are also implicated in the premature death of brain cells. Glutamate and aspartate are two examples, and excessive amounts can lead to neuronal excitability, particularly if there are deficiencies in Vitamins C, E and magnesium. Both of these molecules naturally occur in protein foods as well as in the food additives monosodium glutamate, a flavour enhancer and aspartame, an artificial sweetener.[20]

A viral infection in the brain is another possible cause of Parkinson's, but no specific virus has yet been identified. This theory is derived from patients who suffered post encephalitic Parkinson's after waking up from the epidemic of encephalitis lethargica (sleeping sickness), caused by influenza, after the first world war. Oliver Sacks wrote about these patients and the effects of introducing the new drug L-Dopa for Parkinson's in his incredible book Awakenings.[21] This epidemic has not happened since and medically it is said to be no longer of significance.[22]

Finally, severe head injuries can produce brain damage and superficial features of Parkinson's disease, and it is thought that the famous boxer Mohammed Ali suffers from Parkinson's from this cause.

Medical and Complementary Treatments

Diagnosis is based on a full case history, neurological examination, and evaluation of symptoms. X rays, CT scans (computerised tomography) MRI scans (magnetic resonance imaging) and PET (positron emission tomography) brain scans are used both to diagnose and to eliminate other similar diseases. Surgical procedures, such as implanting adrenal medullary or foetal tissue to manufacture dopamine have also been carried out with limited success.

Since the 1960s the main area of treatment is daily medication to raise dopamine levels or to inhibit neurotransmitters whose activities become enhanced by dopamine's deficiency such as acetylcholine.

Less attention has been focussed on the treatment for the progressive degeneration of the dopaminergic neurons. The most popular drug is levadopa (L-Dopa), which unlike dopamine can cross the blood brain barrier and act as the precursor for dopamine. Other drugs such as carbidopa have been introduced alongside levadopa to increase its effectiveness and counteract the side effects. Anticholinergic drugs block the action of acetylcholine, which works in balance with dopamine to co-ordinate movement; selegiline helps to metabolise levadopa making it more effective and Catechol-O-Methyl Transferase inhibitors increase the availability of levadopa. Medication neither cures nor limits the progression of the disease and all the drugs have significant side effects.

Alongside medication, complementary treatments focus on controlling the symptoms and maintaining quality of life through stress control, nutrition, exercise and relaxation.

Stress and depression are often associated with Parkinson's Disease. Apart from the obvious reasons of coping with such an illness and the side effects of the medication, research shows that sufferers have low levels of the neurotransmitter serotonin in the brain.

Experimental therapy is being carried out to replace the correct amount of serotonin by using 5-HTP (5-ydroxytryptophan), the intermediate between tryptophan and serotonin. It has proved to be beneficial if used in combination with the drugs levadopa and carbidopa as it counteracts the drugs' negative effects on mood and sleep.[23] Useful anti-stress herbs with the ability to nourish the nervous system are black cohosh, catnip, lemon balm, passionflower, skullcap and valerian root. Kava extracts like St. John's Wort, used for stress and depression, may interfere with dopamine causing a worsening of Parkinson's symptoms, and should not be used unless further research proves its safety.[24] Relaxation techniques, visualization, aromatherapy massages using chamomile, jasmine, lavender, neroli and rose oils will help to relieve stress and tension as well as sharing problems with others. Gentle exercises to stretch, strengthen and tone the muscles along with soft tissue manipulation will help musculoskeletal difficulties and aid mobility.

Nutritional Advice

A full range of nutrients for the functioning of the nervous, muscular, digestive and detoxification systems are vitally important. The endocrine system, particularly the thyroid and adrenal glands, may also need support as tyrosine is not only biochemically converted to dopamine, but is also used to make thyroxine and adrenaline. (See Figure 1)

Nutrients derive mainly from a good quality wholefood diet, high in fibre from grains: millet, rice, corn and quinoa; fruits: apples, pears, kiwi and mangos, and vegetables: cabbage, cauliflower, carrots and broccoli. L-Dopa is actually found in some leguminosae plants of the Vicia fava (broad bean), and researchers are reporting that this plant can replenish brain deficits of L-Dopa more quickly and for longer than synthetic medication without any side effects.[25] Cold pressed oils of safflower, sunflower and olive must be taken daily as well as fresh vegetable juices for their high nutrient content.

Proteins should be obtained mainly from vegetarian sources of rice, millet, quinoa, beans, peas and lentils with smaller amounts from soya, eggs, oily and white fish. Quantity and timing of proteins are important for anyone taking medication, particularly levadopa, as protein constituents of amino acids can prevent Parkinson's drugs from reaching the brain. In several studies protein restriction has made the drugs more effective and lessened dyskinesia. Most of the day's protein, particularly from soya, fish and eggs are best taken with the evening meal away from medication.[26]

Anti-nutrients such as sugar, processed foods, additives and preservatives, in particular aspartame and monosodium glutamate should be avoided. It would also be wise to replace stimulants of coffee, tea and alcohol with alternative beverages such as chamomile, nettle, peppermint and melissa herb teas, rooibosch and filtered water. Care should be taken to avoid gluten grains such as wheat, rye oats and barley as they can prevent absorption of nutrients and medication, and too many foods containing vitamin B6 such as peanuts, bananas, and potatoes may interfere with levadopa medication. Advice from a qualified practitioner should be taken with regard to a nutrition and supplement programme.

If you suffer from Parkinson's disease it makes sense to give yourself every chance to delay the progression of the disease by avoiding all the possible causes mentioned, particularly environmental and food toxins. Nutrient deficiencies should be addressed as well as any malfunctioning of the body's systems such as digestion, detoxification and endocrine. An individualized nutrition, exercise and relaxation programme, and finding ways to cope with stressful issues will also enhance the quality of your life.

Further help can be obtained from the Parkinson's Disease society, which has been set up to research and give welfare support for patients and carers.[27]

References

1. Ehringer Hornykiewicz. Verteilung von noradrenalin und Dopamine in Gehrin des Menschen and ihr Verbalten bei Erkrankungen des extrapyramidalen Systems. Klin Wochenschr 38: 1236-9 1960.
2. Tortora and Grabowski. Principles of Anatomy and Physiology. John Wiley and Sons, Inc USA. ISBN 0 471 36692 7. 2000.
3. Clayton P et al. Subacute combined degeneration of the cord, dementia and parkinsonism due to inborn error of folate metabolism. J. Neurol Neurosurg Psychiatry 49: 920-7. 1986.
4. Mena Bronner Coburn. Disorders of mineral metabolism – Trace Minerals. NY Academic Press pp 233-70. 1981.
5. Pall HS et al. Raised cerebrospinal fluid copper concentration in Parkinson's Disease. Lancet 2: 238-41. 1987.
6. American Medical Association Drug Evaluations. Fifth Edition. Chicago. 1983.
7. Jeffrey S Bland. Clinical Nutrition A Functional Approach. The Institute of Functional Medicine p. 231. 1999. Available from Nutri Ltd Buxton Road New Mills High Peak SK22 3JU. Tel 01663 746559.
8. Mizuno Y, Ikebe S, Hattorik N, et al. Mitochondrial energy crisis in Parkinson's Disease. Adv Neurol 60: 282-287. 1993.
9. Birkmayer W, Birkmayer JGD, Vrecko C, Paletta B, Reschenhofer E, Ott E. Nicotinamide adenine dinucleotide (NADH) as education for Parkinson's Disease. Experience with 415 patients. New Trends in Clinical Neuropharmacology 4(1): 7-24. 1990.
10. Steventon GB, Waring RH, Heafield MT, et al. Plasma cysteine and sulphate levels in patients with motor neurone, Parkinson's and Alzheimer's Disease. Neurosci Letts. 110: 216-220. 1990.
11. Zayed J et al. Environmental factors in the etiology of Parkinson's disease. Can J Neurol Sci 17(3): 286-91. 1990.
12. Ngim CH, Devathasan G. Epidemiologic study on the association between body burden mercury level and Idiopathic Parkinson's Disease. Neuroepidemiology 8(3): 128-41. 1989.
13. Bland JS and Bralley JA. Nutritional up-regulation of hepatic detoxification enzymes. Journal of Applied Nutrition No 4: 3-15. 1992.
13a. 'Ultra Clear Plus' is available from Nutri Ltd Buxton Road New Mills High Peak SK22 3JU.
Tel: 01663 746559.
14. Ballard TA, et al. Permanent human Parkinsonism due to Meperidine I Methyl 4 Phenyl 1 2 3 6 Tetrahydropyridine(MPTP): Seven cases. Neurology 35: 949-956. 1985.
15. Ramassamy C et al. In vivo Ginkgo biloba extract protects against neurotoxic effects induced by MPTP: Investigations into its mechanism(s) of action. In Effects of Ginkgo biloba extract on the central nervous system. Y Christin Elsevier Press. Paris. 1992.
16. Maryann Napoli. Drug side effects mistaken for Parkinson's. Health Facts. V.XX1: No.202 P.6. 31 March 1996.
17. British National Formulary. Bath Press. ISBN 0 85369 251 3. 1991.
18. Jenner P. Oxidative stress as a cause of Parkinson's Disease. Acta Neurol Scand Suppl136: 6-15. 1991.
19. Fahn S. A pilot trial of high dose alpha-tocopherol and ascorbate in early Parkinson's Disease. Ann Neurol 32(S): 128-132. 1992.
20. Russell L, Blaylock MD. Excitotoxins: The taste that kills. Health Press Santa Fe New Mexico. ISBN 0 929173 14 7. 1995.
21. Oliver Sacks. Awakenings. Macmillan Publishers Ltd (5th Edition). ISBN 0 330 32091 2. 1990.
22. Cotran Kumar. Robbins Pathologic Basis of Disease. p 332. W.B. Saunders Company. (5th. Edition). ISBN 0 7216 5032 5. 1994.
23. Chase TN, Ng LK, Watnaabe AM. Parkinson's Disease. Modification by 5-hydroxytryptophan. Neurology 22: 479-484. 1972.
24. Schelosky L, Raffauf C, Jendroska K, Kava and dopamine antagonism (letter). J Neurol Neurosurg Psychiatry 58: 639-40. 1995.
25. Dan Beth-El. Magic beans? Natural sources of L-Dopa in the treatment of Parkinson's Disease. International J of Comp Med: 11-13. September 1992.
26. Melvyn Werbach MD. Nutritional Influences on Illness. Thorson Publishing Group. ISBN 0 7225 1726 2. 1989.
27. Parkinson's Disease Society, 215 Vauxhall Bridge Road, London SW1V 1EJ. Tel: 020 7931 8080.
Other Reference Books
Dr Geoffrey Leader and Lucille Leader. Parkinson's Disease The New Nutrition Handbook. Bath Press. ISBN 0 952605 1 9. 1997.
James F Balch MD, Phyllis A Balch. CNC Prescriptions for Nutritional Healing. Avery Publishing Group. ISBN 0 89529 727 2. 1997.
Dr Harvey Sagar. Parkinson's Disease. Vermillion Publishers. ISBN 0 09 181310 7. 1996.
Joseph E Pizzorno Jr, Michael T Murray. Textbook of Natural Medicine (2nd Edition). ISBN 0 443 05945 4. 1999.
Gilham Papachristodoulou. Thomas Wills' Biochemical Basis of Medicine. Reed Educational and Professional Publishing Ltd. ISBN 0 7506 2013 7. 1997.