(From New Vegetarian and Natural Health, Autumn 2001)

by Roger French


Parkinson’s disease, a degenerative condition of part of the brain, is considered to be of unknown cause and incurable. It may well be ‘incurable’ with orthodox medicine, but we have recently discovered that some people have fully or partially reversed the disease through lifestyle methods.

Their experiences pave the way for other sufferers to apply the same approach. The cause of PD is no longer a mystery. So many studies are pointing to the same causes and mechanisms that we don’t need to wait helplessly for the elusive proof before taking action. This is fiddling while Rome burns.

From the considerable amount of research into PD, it is clearly implied how to prevent the disease in the first place or how to prevent its progression once started. Even if the hypotheses put forward should turn out to be wrong, the only ‘side-effect’ of this approach would be to reduce the risks of cancer, artery disease and some other conditions.


Parkinson’s disease afflicts more than 30,000 Australians. It can affect people at all levels of society. Amongst famous people worldwide who suffer Parkinson’s Disease are the Pope, Muhammad Ali and the actor, Michael J Fox.

In summary, it is a degenerative disease of the central nervous system (CNS) in which a small part of the mid-brain is damaged, involving a massive loss of nerve cells. This results in the classical ‘pill rolling’ muscle tremor, stiffness, loss of coordination, slow movements, shuffling walk and deadpan facial expression.

As explained by neurologist, Dr Harvey Sagar,(1) the disease is named after an English doctor, James Parkinson, who lived between 1755 and 1824. He named it ‘paralysis agitans’ or shaking palsy, but a French neurologist later named it after Dr Parkinson. The disease is often referred to as ‘idiopathic’, meaning the cause is unknown, but, as we shall see, that is debatable. Some drugs, poisons and other diseases produce similar symptoms, described as Parkinsonism, but these are not true PD.

The disease is less common in China and Japan than in the white races of Western countries where it affects anywhere from 1 in every 1500 people to 1 in every 500. Over our whole lifetimes, we Westerners have 1 chance in 40 of developing PD. It is a disease of adults, typically commencing between 50 and 80 years of age, although very rarely it can occur before age 30. It is equally common in men and women.

In some sufferers, the disease shows little progression, but typically it advances slowly with new symptoms developing over the course of years rather than months. The tendency is that the younger the sufferer, the slower the progress.

When we decide to make a particular movement, the thinking part of the brain sends instructions to a part of the mid-brain called the basal ganglia which coordinates a series of messages and sends them down the nerves to the muscles. However, the brain and nervous system consists of cells in series so that nerve impulses have to jump from one ‘wire’ to the next. The body makes chemicals to fill in the gaps and in the brain these are typically dopamine, acetylcholine, and noradrenaline. Within the basal ganglia, dopamine is the major chemical, and if its production is compromised, the basal ganglia cannot get its messages through and so coordination breaks down.

The area of the basal ganglia that is most affected in Parkinson’s Disease is called the substantia nigra (‘nigra’ means black) because in the laboratory it stains a darker colour than the rest of the brain, which is grey. In essence, the cells in the substantia nigra that produce dopamine die off, leading to the nerve control problems that produce the symptoms of PD. The sufferer knows alright what they intend to do, but the muscles fail to respond.

Because there are other diseases with symptoms similar to PD, diagnosis depends on the distinctive appearance of damaged cells in the substantia nigra, called Lewy bodies.

The loss of dopamine produces three principal types of movement problems:

The slowness of movement is due to inability to get nerve messages through to the muscles. Actions take longer and are slower. But why would there be tremor when the limbs are not being used? Besides coordinating messages, the basal ganglia also filters out false messages. When this function is impaired, the latter get through and cause rigidity and the classic ‘pill tolling’ tremor, so-named because it resembles the movements of old-fashioned pill makers who rolled their pills between the thumb and fingers.

In well established PD, the rigidity tends to produce a deadpan facial expression, a characteristic stooped posture, difficulty in getting up from a chair, difficulty in starting walking and in turning, and loss of dexterity. Tremor usually affects the fingers, hands and head, and in more advanced cases, the legs. It is most pronounced at rest and declines when the limb is being used. It increases with emotions such as fear, anxiety, anger or even extreme joy. Usually its worst aspect is the social embarrassment.

The above symptoms are due to problems with motor coordination, ‘motor’ referring to outgoing messages. If damage also occurs in other parts of the brain, this can lead to different kinds of symptoms. They may include memory problems, depression, incontinence and problems with blood pressure control. While memory is not usually a major problem, most sufferers do become depressed at some time or other. Urinary problems can include slowness in starting, dribbling afterwards, frequent urination or incontinence. There can be problems with salivation and libido. Of greater concern is constipation which is more common in PD sufferers because of sluggish bowel muscles.

Recent research has confirmed that parts of the brain other than the mid-brain are likely to be affected. In 1996 the Prince of Wales Medical Research Institute in Sydney found that the volume of the hippocampus had shrunk by an average of one quarter in Parkinson’s sufferers. The hippocampus is crucial for memory processing and was previously thought to be involved only in Alzheimer’s Disease.

In 1999 the same institute found that still another part of the brain, the thalamus, contains on average 40% less cells in PD sufferers. The thalamus is associated with attention and consciousness and also has a role in physical movement.

These new discoveries confirm that the damage commonly extends beyond the basal ganglia, and hence the variety of symptoms.


The causes of PD include genetics to a small degree and environmental factors, particularly nerve toxins, to a large degree.

The mechanism of nerve cell death almost certainly (although not proven) involves those toxic substances, free radicals, which are now known to account for cancer and many other serious illnesses. It cannot be many years before ‘free radicals’ is a household expression. In brief, free radicals – which are particularly induced by iron (yes, the important nutrient iron) – damage the energy-producing units (mitochondria) in affected cells, causing decreased energy production, which in turn causes the formation of more free radicals. These lead to further mitochondrial damage (including oxidation of mitochondrial DNA, proteins and lipids) and the formation of still more free radicals, forming a vicious cycle which terminates with the death of the nerve cell.

Although protective antioxidant enzymes (particularly one called glutathione) will be produced to combat the radicals and the damage, if the generation of free radicals and oxidation are overwhelming or the body’s defences are down, then it is to be expected that substantial cell death will follow. Because the brain uses a large amount of oxygen, it is particularly prone to oxidation induced by free radicals or iron.(2) Further, the large amount of dopamine in the substantia nigra is particularly prone to oxidation. Hence the chain of events leading to Parkinson’s Disease. The process involves problems caused by iron and certain other metals, while the metabolism of calcium and possibly other minerals is upset.

Is PD In Our Genes?

The fact that two PD genes have recently been matched and that 10% or more of sufferers have a family history of the illness suggests that in some cases it is inherited. An answer is provided by The Parkinson’s Institute, Sunnyvale, California (3) which has concluded that no genetic component is evident when the disease begins after 50 years of age, but before this age genetic factors appear to be important.

As with most conditions, it is probably the case that we can inherit susceptibility to the disease, but not the disease itself. However, people do tend to inherit their parents’ lifestyle, and if lifestyle factors caused the disease in the parents, the similar lifestyle may well do the same in the progeny.

Powerful Oxidative Damage

Oxygen is essential for life, but even oxygen can go wrong and become destructive, the aggressive form being referred to as reactive oxygen species (ROS). These can damage lipids, proteins and nucleic acid (including the DNA in genes).

In a healthy individual, there is a delicate balance between these oxygen free radicals and the body’s free-radical- scavenging systems.

In parallel with oxidative damage is impaired energy production in the mitochondria, but the researchers are not certain whether this causes the disease or is an end result of some other destructive effect.

The brain is particularly susceptible to oxidative damage to its energy-producing units because, while representing only a few percent of body weight, the brain uses approximately 20% of the total oxygen consumed. Brain tissue, therefore, easily generates a lot of oxygen free radicals. Also, because nerve cells don’t reproduce themselves, the damage to DNA, proteins and lipids accumulates. Further, for some reason the brain has relatively low levels of protective antioxidant enzymes and other antioxidants.(4)

In 1999, Austrian researcher, K A Jellinger, reviewed the research(5) and concluded that the key factors in PD are:

The evidence to support this hypothesis is:

In summary, oxidative stress in the brain has been described as ‘the brain on fire’. Oxidation products in nerve mitochondria cause the release of iron which catalyses more free-radical production which damages the nerve cells and produces more products of oxidation. A key part of the oxidative damage is peroxidation of the lipids in the mitochondrial and cellular membranes. As might be expected, the oxidising activity uses up greater amounts of antioxidants such as vitamin E, coenzyme Q10 and lipoic acid.

Some Minerals Have Key Roles

Iron and manganese. When iron is in a free form, it is a powerful pro-oxidant, acting as a catalyst to the formation of highly toxic free radicals. The body knows of this danger and attempts to keep iron safely packaged away attached to proteins in the form of haemoglobin in red blood cells or ferritin in blood plasma and other fluids.

Any increase in iron concentration in the brain increases the potential for free-radical damage. It has, in fact, been observed that in patients with PD there are increased iron concentrations in the substantia nigra (5).

Manganese is somewhat similar to iron and thought to have pro-oxidant properties. However, research at the Unit on Neurodegeneration, Bethesda USA(9) has found that manganese causes neither lipid peroxidation (damage by free-radicals) nor depletion of dopamine. In contrast, it protected neurons in the substantia nigra from iron damage. The results suggest that manganese can in some situations act as an antioxidant and therefore be protective.

The body has other ways of protecting itself against increases in brain iron. Research at Pennsylvania University has found(10) that in the normal case any age- related increase in brain iron concentration is compensated for by conversion to ferritin, in which it is bound to protein and rendered harmless.

Aluminium, Cadmium and Magnesium. In acid soils, aluminium and cadmium are taken up by plants in which they produce toxic effects, the same effects applying to humans who eat those plants. Also in acid soils beneficial minerals like calcium and magnesium are more easily leached away. If the diet is low in calcium, or both calcium and magnesium, it has been found(11) that the aluminium content in central nervous system tissues increases, and if aluminium intake is high, the level of aluminium in the brain will be high and capable of inducing CNS degeneration.

Zinc. This valuable nutrient can reduce oxidative stress and, in particular, is a potent inhibitor of nitric oxide synthesis. It has been found(12) that in PD cerebrospinal-fluid levels of zinc are significantly decreased, and it was concluded that low zinc levels may increase the risk of the disease.

Mercury. This is another heavy metal that appears to be involved in PD. National University of Singapore researchers found a clear relationship between blood mercury levels and PD.(13) They said that the factors that could contribute to the body burden of mercury include fish, over-the- counter medications, environmental exposures and dental-amalgam fillings.

The Hormone, Melatonin, a Rescuer

Melatonin, a hormone produced by the pineal gland, has recently been discovered to be a free-radical scavenger and antioxidant – in fact, one of the most potent scavengers of toxic radicals.(14) Philadelphia research found that it possesses a remarkable ability to rescue neurons from cell death caused by oxidative stress.

A review by the University of Texas Health Science Centre(15) concluded that, besides being an antioxidant, melatonin also stimulates the production of antioxidative enzymes, inhibits the synthesis of nitric oxide and reduces lipid peroxidation and oxidative damage to DNA. Since body-made melatonin levels fall markedly with advanced age, the researcher deduced that its loss may contribute to Parkinson’s and similar diseases.

Bleached Flour

Chemicals in bleached flour can damage nerve cells. Researchers at the University of British Columbia in Vancouver have explained(16) that the ‘agene process’, used to bleach as much as 80% of all flour from around 1900 to 1950, employed a chlorine compound, nitrogen trichloride. This produced a bi-product, methionine sulphoxinine (MSO) which inhibits the production of glutathione, a key free-radical scavenger, and glutamine, lack of which increases levels of ammonia. The researches concluded that cells in the nervous system are particularly sensitive to these effects, and the result could be nerve cell death.

Cycad Seeds

The amyotrophic lateral sclerosis and Parkinson’s dementia complex of the Chamorro natives of Guam may be due to an amino acid in cycad seeds which are indigenous in the area and extensively eaten. This was explained in the Spring 2000 issue of New Vegetarian and Natural Health, pages 50 – 53.


Sufferers of PD tend to lose weight in spite of increased calorie intake. The loss is due to fat loss rather than muscle loss. Whether the investigators suspect malnutrition is not clear, but a London group found that blood serum levels of a number of nutrients were significantly lower – the protein albumen, vitamin A, vitamin E and zinc.(17) The last three are important antioxidant nutrients.

Environmental Chemicals

Numerous studies have reported that a large number, if not the majority, of PD sufferers have histories of significant exposure to toxic synthetic chemicals. Considering the potential of many such chemicals for free-radical generation, this is not surprising.

A review in 1989(18) associated early-onset PD in North America and Europe with vegetable farming, well-water drinking, and the wood pulp, paper and steel industries. In China(19) PD was associated with exposure to industrial chemicals, printing plants and quarries. In contrast, simple rural village life was associated with a low risk of PD. In Israel, drinking water and agricultural chemicals were the most likely environmental factors.

Other studies have found that lifetime exposure to herbicides in field crop and grain farming was a significant predictor of PD,(20) that in British Columbia pesticides used in fruit growing were significantly associated with PD,(21) and in Taiwan the risk was greatest among people exposed to herbicides and pesticides, in particular paraquat. (22) Frequent use of pesticides has also shown up in other studies.

Along with agricultural chemicals, industrial chemicals are significantly associated with PD. These include organic solvents(23); a strong association with ethylene oxide used in the production of industrial chemicals(24); a stabiliser employed universally in the production of plastics that damages the dopamine cells of the substantia nigra(25); and coal-tar extracts as would be liberated in the burning or refining of coal(26).


Surprisingly, non-smokers are at greater risk of PD than smokers – a consistent finding suggesting there may be something in cigarette smoke that protects the dopamine nerve cells against death.

Dr Harvey Sagar(1) puts it the other way around, “People with Parkinson’s Disease smoke on average less through their life than do non-Parkinsonians.” However, he says, people would be well advised not to start smoking to protect against PD because the harm in other ways would far outweigh the benefits. Further, it may not be that smoking protects against the disease, but rather that the personality type that is prone to PD tends not to smoke.

Personality Type

Dr Sagar(1) reports that the personality type that is more likely to develop PD is introverted, mentally inflexible, prone to depression, and also more likely to exhibit shyness.

Researchers have considered the possibility that these personality traits are the result of early deterioration in the brain. On the other hand, it is possible that certain types of people are more susceptible.

Other Factors

There are still a few other factors mentioned by the researchers that increase the risk of PD. They include head injuries and environmental stresses such as ionising radiation and heat shock.


Minimise Free Radical Damage

Dealing with the underlying causes is far superior to drug therapy aimed at restoring dopamine levels. As one researcher points out,(27) the standard drug used, Levodopa, may in some circumstances accelerate the rate of nerve degeneration.

From the large body of evidence summarized above, it is clear that taking steps to limit free radical production and oxidative damage could be expected to prevent PD in the first place or slow its progression if already established.

First and foremost:

Unfortunately, there is a scarcity of studies investigating whether antioxidant nutrients prevent free-radical damage, because, as one researcher says,(28) “Interest is hampered by the limited financial return for drug companies in this field.” However, the same researcher points out that there seems to be no reason to discourage older people taking extra vitamin C and vitamin E along with adequate vegetables and fruits for their betacarotene and other carotenoids.

A number of antioxidants protect the nervous system from free-radical oxidative damage.(29, 30) These include:

The anti-dementia properties of ginkgo have been demonstrated by research. Also, co-enzyme Q10 shows particular promise, because, in addition to having free- radical-scavenging properties, it plays a key role in energy production in the mitochondria.

Reflecting the difficulty in determining whether particular nutrients or other substances protect against diseases that develop over many years, the vitamin likely to be most protective, vitamin E, has produced conflicting results. Research at the University of Hawaii in 1996 did not conclusively find a beneficial effect of vitamin E on PD, although legumes, which are high in vitamin E, have been found to be significantly protective.(31) On the other hand, Erasmus University Medical School, Rotterdam, found in 1997 that a high intake of dietary vitamin E may protect against PD, and the association was dose dependent, that is, the more the better within limits.(32) Previous studies had already suggested that early-life intake of vitamin E- rich foods does decrease the risk.

Vitamin B3 in both its common forms appears to be protective. In one study, nicotinamide was able to prevent damage to DNA,(33) while niacin was associated with reduced incidence.

Long-Term Dietary Protection

It is now well established that free-radical damage is increased by high intakes of the major nutrients, protein, carbohydrate and fat, and by low intakes of antioxidant nutrients.

An adequate but not excessive supply of protein, carbohydrate and fat is the basis of Natural Health Dietary guidelines, which are spelled out in the Spring 1999 issue of New Vegetarian and Natural Health, pages 54 – 60. For the prevention and repair of free-radical damage in the body as a whole, the key antioxidants are the carotenoids, vitamin A, vitamin C, vitamin E and the minerals zinc and selenium.

Carotenoids (about 500 of them including beta-carotene) and vitamin C are found only in green, yellow and red vegetables and fresh fruits. This is why a person of average size needs to consume something of the order of three-quarters to one kilogram daily of fresh vegetables and fruits, being sure to include plenty of the former. There are also hundreds of other antioxidants in these foods.

Vitamin A can be made in the body from carotenoids, so having plenty of these should ensure adequate vitamin A.

Vitamin E is richer in wheat-germ oil than in any other food. It may also be at modest levels in the oils of soya beans, corn, safflower seeds, sesame seeds, peanuts and so on, provided it has not all been refined away. In order to avoid a high fat intake, it is better to consume the whole food than the extracted oil. In any case, a supplement of vitamin E in its natural form is readily available as wheat-germ- oil capsules. Because vitamin E tends to be sacrificed in protecting extracted oil from rancidity, it is probably a good idea to take this supplement regularly.

Zinc is found – in descending order of content – in Brazil nuts, cashews, (lean beef), cheddar cheese, hazelnuts, chick peas, almonds, wholemeal flour, walnuts and brown rice. Because Australian soils are low in zinc, there is a good case for routinely taking a zinc supplement – in the form of chelated zinc.

Selenium is abundant in Brazil nuts. As Australian soils are low in selenium, other sources like wholemeal bread are well down in content compared to Brazil nuts. Apart from a couple of products, selenium supplements in Australia require a medical prescription.


As will be seen in the next section, exercise is good therapy for PD, and therefore it would be reasonable to assume that regular exercise on a long-term basis would also tend to be preventative.



When it was discovered that lack of dopamine is the main problem in PD, attempts were made to administer it as a drug. However, dopamine does not pass from the bloodstream into the brain, so the problem was solved by developing levodopa which does pass into the brain and is then converted to dopamine.(1)

Levodopa taken orally is the most effective drug for the disease, although tremor does not respond as well as akinesia for rigidity. Sometimes all symptoms will disappear.

Other drugs act like dopamine but bypass the dopamine-containing cells and are called dopamine agonists. The commonest are bromocriptine and pergolide.(1)

A review of current drug practices was given by the Department of Neuropsychology of the University of Regensburg in Germany.(34) Early in the disease, dopamine can be used alone. If agonists are used alone, they do produce a response but their efficacy quickly wanes. Starting early with a combination of levodopa and dopamine agonists appears to reduce the severity and delay the appearance of the side effects associated with long-term use of levodopa.

Many people with advanced PD develop an unstable pattern of response to L-dopa because of fluctuating delivery of the drug to the brain. For advanced patients experiencing fluctuations, dopamine plus agonists are most commonly used.

Another drug commonly used in combination with L-dopa is selegiline, particularly where there are fluctuations in symptoms.(1) Normally the body will break down dopamine after it has been produced, but selegiline delays this process so that more dopamine is available to the brain for a longer period.

Levodopa therapy is considered to have brought great benefits to Parkinson's disease sufferers since its introduction in the 1960s. Unfortunately, most drugs have side-effects and this applies to L-dopa. Recent Japanese research has raised the possibility that long-term L-dopa treatment could accelerate the degeneration of the dopamine neurons.(35)

The only way to avoid the side-effects is to use natural therapies, provided they will achieve the desired result.

Natural Therapies

A number of herbal remedies can be used with PD. Three herbs that may ease the tremor, rigidity and akinesia are skullcap, passion flower and valerian(36). These are anti-convulsive and anti-spasmodic and have sedative properties as well as supporting the nervous system generally. Such remedies should be prescribed by a professional herbalist.

Other natural therapies may be helpful, including acupuncture to relieve pain if it is of concern, hypnosis to relax a highly-strung person, yoga for relaxation and as a form of exercise, and reflexology which is therapeutic massage applied to particular areas on the feet.

As we will see in the case stories that follow, specific natural remedies and therapies are being used successfully to restore normal health with PD. They include Aqua Hydration Formulas, Bowen therapy and flower essences, accompanied by meditation, spiritual development and counselling. The Aquas, a commercially- produced combination designed to re-hydrate bodily cells, are composed of homeopathics, flower essences, herbs and vitamins.


Physical exercise has been tested in a number of studies to determine if it has therapeutic effects with PD. The results have been very positive.

In 1986, two different exercise programs were tested, one developed by the United Parkinson’s Foundation and the other involving upper-body karate training. Both programs brought about an improvement in gait, tremor, grip strength and coordination in tasks requiring fine control.(37)

Another study involved a weekly home-exercise regime for PD patients who were capable of walking.(38) Compared to the controls, those exercising showed significant improvement in recent memory, reduced nausea, improved feeding ability and less urinary retention and incontinence.

A recent Swedish study found that a week of daily walks in the mountains brought improved muscle control, both immediately after the walk and for up to three months later.(39)

The question of whether people with mild to moderate PD are capable of exercising normally was investigated by the University of Sydney in 1997.(40) It was found that peak oxygen consumption and peak workloads were similar to normal values, despite evidence of respiratory and gait abnormalities. It was concluded that the sufferers had the capacity for normal, regular aerobic exercise.

Being Hopeful Helps

A University of New Jersey researcher wondered if an attitude of hope could help Parkinson’s Disease. It was found that sufferers with a high level of hope had a healthier lifestyle, greater spiritual growth and fared better in personal relationships.(41) The aspects of lifestyle most strongly related to hope were personal relationships and nutrition, while the weakest was physical activity.


1. Sagar H, Parkinson’s Disease, 1996. Vermilion/Ebury Press, London.

2. Cassarino DS, Bennet JP, Evaluation of the role of mitochondria in neurodegenerative diseases, Brain Res Rev, 1999 Jan; 29(1): 1-25

3. Tanner CM et al. PD in twins: etiologic study, JAMA, 1999 Jan 27; 281(4): 341-6

4. Functional therapeutics in neurodegenerative disease; unpublished paper by F.I.T. Sales Pty Ltd.

5. Jellinger KA, The role of iron in neurodegeneration, Drugs Aging, 1999 Feb; 14(2): 115-40

6. Logroscino G et al, Dietary lipids and antioxidants in PD, Ann Neural, 1996 Jan; 39(1): 89-94

7. The nitric oxide and hydroxyl radical connection to neurotoxicity; unpublished paper by F.I.T. Sales Pty Ltd

8. Heales SJ et al, Nitric oxide, mitochondria and neurological disease, Biochem Biophys Acta, 1999 Feb

9; 1410(2): 215-28 9. Sziraki I, Manganese: a transition metal protects neurons from oxidative stress …, Neuroscience, 1998 Aug; 85(4): 1101-11

10. Focht SJ et al. Regional distribution of iron, transferrin, ferritin …, Neuroscience 1997 Jul; 79(1): 255-61

11. Yasui M et al, Effects of calcium-deficient diets on manganese deposition in the CNS, Neurotoxicology 1995 Fall; 16(3): 511-7

12. Jimenez-Jimenez FJ et al, Cerebrospinal fluid levels of transition metals in patients with PD, J Neurol Transm, 1998; 105(4-5): 497-505

13. Ngim CH, Devathason G, Epidemiologic study on the association between ….mercury level and PD, Neuroepidemiology, 1989; 8(3): 128-4.

14. Iacovitti L et al, Melatonin rescues dopamine neurons from cell death …, Brain Res, 1997 Sep 12; 768(1-2): 317-26

15. Reiter RJ, Oxidative damage in the CNS: protection by melatonin, Prog Neurobiol, 1998 Oct; 56(3): 359-84

16. Shaw CA, Bains JS, Did consumption of bleached flour … contribute to neurological disease? Med Hypotheses, 1998 Dec; 51(6): 477-81.

17. Abbott RA et al, Diet, body size and micronutrient status in PD, Eur J Clin Nutr 1992 Dec; 46(12): 879-84

18. Tanner CM, The role of environmental toxins in PD, Trends Neurosci 1989 Feb; 12(2): 49-54.

19. Tanner CM et al, Environmental factors and PD – a study in China, Neurology, 1989 May; 39(5): 660-4

20. Semchuk KM, PD and exposure to agricultural work and pesticide chemicals, Neurology 1992 Jul; 42(7): 1328-35

21. Hertzman C et al, A study of PD in … British Columbia, Mov Disord, 1994 Jan; 9(1): 69-75

22. Lioutt H et al, Environmental risk factors and PD, Neurology, 1997 Jan; 48(6): 1583-8

23. Smorgiassi A et al, A … study of occupational and environmental risk factors for PD … in Italy, Neurotoxicology, 1998 Aug-Oct; 19(4-5): 709-12

24. Barbosa ER et al, Parkinsonism secondary to ethylene oxide exposure, Arq Neuropsiquiatr, 1992 Dec; 50(4): 531-3

25. Masalha R et al, Selective dopamine toxicity by an industrial chemical, Brain Res, 1997 Nov 7; 774(1-2): 260-4

26. Pinsky C, Bose R, Pyridine and other coal tar constituents as free-radical gen- erating environmental neurotoxicants, Moll Cell Biochem, 1988 Dec; 84(2): 217-22

27. Olanow CW, Attempts to obtain neuroprotection in PD, Neurology, 1997 Jul; 49(1 Suppl 1): S26-33

28. Ward J, Free radicals, antioxidants and preventative geriatrics, Aust Fam Physician, 1994 Jul; 23(7): 1297-301

29. Vatassey GT, Vitamin E and other endogenous antioxidants in the CNS, Geriatrics, 1998 Sep; 53 Suppl 1: S25-7

30. Antioxidants as neuroprotectors, unpublished paper by F.I.T. Sales Pty Ltd

31. Morens DM et al, Case-control study of idiopathic PD and dietary vitamin E intake, Neurology, 1996 May; 46(5): 1270-4

32. de Rijk MC et al, Dietary antioxidants and PD, Arch Neurol, 1997 Jan; 54(6): 762- 5

33. Mukherjee SK and Adams JD, The effects of aging and neurodegeneration … and the benefits of nicotinamide, Mol Chem Neuropathol, 1997 Sep-Dec; 32(1-3): 59- 74

34. Lange KW, Clinical pharmacology of dopamine agonists in PD, Drugs Aging, 1998 Nov; 13(5): 381-9

35. Nakao N et al, Metabolic inhibition enhances selective toxicity of L-Dopa …., Brain Res, 1997 Nov 28; 777(1-2): 202-9

36. Setright R, Get Well for Women, 1993, pub. Atrand Pty Ltd., Crows Nest NSW

37. Palmer SS et al, Exercise therapy for PD, Arch Phys Med Rehabil, 1986 Oct; 67(10): 741-5

38. Hurwitz A, The benefit of a home exercise regimen for ambulatory PD patients, J Neurosci Nurs 1989 Jun; 21(3): 180-4

39. Sunvisson H et al, Changes in motor performance in persons with PD after exercise in a mountain area, J Neurosci Nurs, 1997 Aug; 29(4): 255-60

40. Canning CG et al, PD: an investigation of exercise capacity, respiratory function and gait. Arch Phys Med Rehabil, 1997 Feb; 78(2): 199-207

41. Fowler SB, Hope and a health-promoting lifestyle in persons with PD, J Neurosci Nurs, 1997 Apr; 29(2): 111-6


Returning to Stillness – the Success Stories of John Coleman

The following is a condensed version of the encouraging experiences of Melbourne naturopath, John Coleman, written December 2000.


The telephone woke me from a restless sleep at 9:30 am on Sunday 5th August 1995. I had suffered back and neck pain for many years and was finding it increasingly difficult to walk without shuffling and dragging my right leg; gaining restful sleep had become almost impossible as time went on. I lifted the receiver to greet my caller, but was horrified to hear gibberish coming from my mouth. My mind knew I was saying “Good morning, John Coleman speaking”, but all I could manage was an incoherent stammer. My hands and head shook, I broke into a sweat and stumbled out of bed confused and frightened. Had I suffered a stroke overnight? Was there a brain tumour starting to affect me? Was I going mad?

I had, in fact, suffered the rapid onset of Parkinson’s disease symptoms after giving up smoking in April of 1995. Within four months, my condition had deteriorated from back pain, dragging right leg and great fatigue, to a complete picture of Stage IV Parkinson’s disease with some multi-system atrophy symptoms.

While modern medical therapy, compassionately managed, can prolong active life and ease the burden for patients and carers, all common medical treatments have limited effective life spans. None address the need to rejuvenate and reactivate dopamine-producing cells in the brain, therefore the therapy is provided to an ever-decreasing dopamine supply system.(1) All modern drugs have adverse side-effects (mild or distressing to quite dangerous),(2) and there is some evidence to suggest
that the breakdown of dopamine in the brain can lead to a further destruction of dopamine producing cells.



Living with severe Parkinson’s disease is being trapped behind a one-way mirror. We see the world going on as usual. The people we know do all the things they used to do, and we long to be doing them together. Our minds and spirits reach out to experience the wonderful adventures this world offers: to run and jump, ride our bikes, talk over coffee and cake, make love, mow the lawns and tidy the garden, walk along a cliff top. But, behind the mirror, our desires and aspirations are trapped in a body which will not respond. When others look at us, they see only someone with a shaking body and hesitant speech who spills drinks, drops food on their shirt, soils their trousers when they urinate and dribbles during conversation.

The predominant feeling with PD is increasing isolation from the rest of the world as our activities become more labored, our face loses the ability to express emotion, we become too tired to assert ourselves and sense our lives slipping away.

People confined to wheel chairs – quadriplegics for instance – have spoken to me about being treated “as if they are not there” or are intellectually handicapped. Many with Parkinson’s disease have similar experiences. We may be ignored in shops, spoken to as if we are young children, or shouted at as if deaf. My brother visited me when I was first diagnosed, and shouted at me in childish sentences as if my stammer and tremor were the result of intellectual retardation. My replies were ignored.

It is this sort of treatment that makes us nervous, or even fearful, of mixing in normal society. Our anxiety inevitably increases our symptoms when we do venture out, so we drop things, spill food and drink, or become incontinent even though we are managing very well in the safe environment of our home.

Living behind the mirror of Parkinson’s disease is isolating, frightening, frustrating, debilitating, exhausting and depressing. We long to reach out with warmth and excitement, but our mask of disease prevents us. We turn inwards and become obsessed with trivia or our condition. We appear sullen and disinterested, but that is just our mask. We cry for help, but are told we can’t be helped. We long for energy and vitality, but are told we must live with crumbling, aching bodies and dreadful fatigue. We are treated with anti-depressant drugs, yet the cause of our depressed
emotions, our lack of hope, is not addressed.

When you meet someone with PD, remember that they are fragile, anxious, desperate and have been given no hope. Please treat them as delicate buds about to bloom.



Eleven days after my loss of speech, I collapsed at work. I could no longer force my body to continue with ordinary activities while my symptoms escalated. I trembled, sweated, became confused, ‘froze’ when changing direction, had problems initiating actions and suffered awful fatigue. I felt that every movement was made against the current of a chest high river.

My experiences with neurologists are too disturbing and lengthy to tell here, but served to convince me that Western medicine was not interested in me as a person, nor in trying to reverse my condition. I was prescribed anti-depressants and rest. The rest was good, the drugs ridiculous. Certainly I was downcast; I couldn’t speak coherently, could hardly walk, I had been in pain for thirty years – long before being diagnosed with Parkinson’s disease. I was trying to care for myself and fast running out of money. Of course I was depressed, but anti-depressants wouldn’t help, and
the one prescribed (Doxepin) tended to exacerbate PD symptoms.(2,3) Eventually, three medical practitioners and two complementary therapists diagnosed what I already knew to be Parkinson’s disease.

I decided to find other ways to alleviate my symptoms and, perhaps, move toward health. Over the following two years, I worked with a craniosacral therapist, flower-essence counselor and homoeopath . Each contributed enormously to my physical and emotional wellbeing. With their guidance and skill, my mobility improved, pain decreased and energy increased. At the same time, I worked on my spiritual health with meditation and a spiritual development circle. I also set achievable goals like walking to the front gate without support, cooking a meal once a week and dressing myself in half an hour instead of one and a half hours.(3)
During the two years between August 1995 and September 1997, I tried many other therapies in the hope of finding the one magic remedy to ‘cure’ my Parkinson’s disease. Some helped me, some did nothing, others set me back. My health continued to fluctuate frustratingly, with times of great hope and others of hopelessness.

In September 1997, I heard a lecture on Aqua Hydration Formulas and decided that this could be my ‘magic medicine’. I began enthusiastically, taking the maximum recommended dose. Within three weeks, my symptoms had increased dramatically, I was in excruciating pain and decided to end my life. Fortunately, I was given help to reduce the pain and realised that I had aggravated due to being on the Aquas. These formulas are very powerful medicine and must be treated with respect.(3,4)

The Aquas were developed by a neuro-endocrinologist and a naturopath to increase the absorption and utilisation of water by athletes and people recovering from illness. We need efficient water flow through all our cells to transport nutrients in, allow the production of hormones, neuro-transmitters and other chemicals, and transport those chemicals to where they are needed.

Because of diet, pollution, air-conditioning, stress and other factors, many people are unable to absorb and use water efficiently.

The Aquas are composed of homeopathics, flower essences, herbs and vitamins in combinations to trigger the brain into developing the required absorption and utilisation activity. There are four formulae designed for the specific needs of women and men, morning and evening.

People with robust bodies, such as athletes, can use high doses of Aquas to increase their hydration rapidly. People with Parkinson’s disease are fragile and need changes to take place slowly and gently. The Aquas are available from some health food stores but, in the case of chronically ill people, supervision by an experienced health practitioner is advisable to prevent unfortunate experiences like mine.

When I stopped taking the Aquas, my pain reduced, but a painfully frozen shoulder plagued me. Having been trained as a Bowen therapist, I decided it was time to try it for myself. After just a few treatments, my shoulder was freed and my energy improved. I then started back on the Aquas at a very reduced dosage.

By April 1998, I was completely free of all PD symptoms. My wellness did not arrive with great fanfare; my symptoms faded gradually so that it was several weeks before I was prepared to declare that I no longer had Parkinson’s disease.



Millions of dollars are spent on research to find drugs which will control symptoms better and on procedures holding some hope of a ‘cure’. Parkinson’s disease takes twenty or more years to develop,(3,5) so it seems unreasonable to expect that a ‘magic medicine’ will take it away in a few days or weeks. However, there are enough recovered Parkinsonians around to let us know that recovery is possible. Two Australians, including myself, have fully recovered , plus several
in the United States.
Before Parkinson’s disease symptoms appear, we may lose the use of up to 80% of our dopamine-producing cells.(6) Inevitably, there are many more deficiencies in our bodies that developed over the long period before the appearance of diagnosable symptoms, as dopamine is involved in many functions. We must, therefore, look for ways of assisting the whole person to move towards a state of total health.

There are now two centres in the world guiding people back from neuro-degenerative disorders towards control of their lives and buoyant health. The Parkinson’s Disease Recovery Project in California promotes acupuncture and tuina (an ancient Chinese therapy that pre-dates acupuncture), while the Return To Stillness centre in Melbourne uses hydration, Bowen therapy, self-empowerment and homeopathics.

Physically, the hydration and Bowen restore fluid balance at cellular level, creating an aqueous environment conducive to the regeneration of brain cells and the restoration of normal function. As health improves and we add homeopathic dopamine, new or reactivated dopamine-producing cells generate more dopamine within the brain.

Self-empowerment, including meditation, spiritual development and counseling, assist in dealing with long-suppressed traumas (invariably present in those I see), and maintaining a determined focus on the long journey to wellness. Exercise, nutrition and home environment are all important during this adventure.



Laurie was diagnosed with Parkinson’s disease in 1997, at 76 years of age, and prescribed 1500 mcg Permax daily with Domperidone as needed for subsequent nausea. By January 1999, he suffered extreme muscle rigidity, was unable to walk without a walking stick plus his wife’s help, and needed great assistance to climb onto and turn on my massage table. Laurie fell frequently, could not turn his head at all, experienced severe cramps in his neck and legs, had uncontrollable tremor in both arms and one leg, could not turn over in bed, fell out of bed often, was incontinent and chronically constipated. He was withdrawn, tired and found communication difficult.

Laurie commenced Aqua Hydration Formulas, Bowen therapy and flower essences. At first, progress was frustratingly slow, but over several months he began to walk without assistance, then without his stick. He gained movement in his neck, slept better and took a much more active part in life.

At the end of year 2000, Laurie was walking almost normally, is very active, free from cramps, sleeps normally and has resolved his incontinence and constipation. His tremor is greatly reduced and continues to improve. Laurie now takes no standard medication at all.

It will be some months yet before we can say that Laurie has fully recovered from Parkinson’s disease, but his progress has been remarkable in a short time. It has not always been easy. There have been setbacks when his symptoms worsened, and times when it seemed nothing was happening. But he persisted and is winning. It took me two and a half years to recover – Laurie, like many others, is moving more quickly than I did.



There are many funds and foundations set up to look for a ‘magic cure’ for Parkinsonian people. However, we already know that people can recover from Parkinson’s disease, and urgently need funds to research the current recovery programmes and look for ways to enhance recovery.

I believe that much will happen over the next few years. There will be Return To Stillness centres working with all types of neuro-degenerative disorders, and offering a wide range of therapies and self-empowerment programmes. Practitioners will be trained to assist to people all over Australia – and the world. I don’t know how this will be funded, but I know it is needed, so it will happen.

We can recover from Parkinson’s disease. I know – I did and others are.



Parkinson’s sufferers wishing to contact John Coleman can do so as follows:
Phone:  03 5429 1737 and 03 9576 3110
email:  [email protected]
Address:  12 Bennett Close, Lancefield Vic 3435



1. E-MIMS Disease Index; CD ROM; Published MediMedia, St. Leonards, NSW,
Australia; Year 2000 Edition.
2. MIMS Annual; CD ROM; Published MediMedia, St. Leonards NSW Australia;
February 2000.
3. Coleman, John C, Parkinson’s Disease – Aetiology, Prognosis and Treatment from Medical and Naturopathic Perspectives; published by Return To Stillness, Melbourne, 1998: 49 – 58.
4. Coleman, John C, Parkinson’s Disease – Aetiology, Prognosis and Treatment from Medical and Naturopathic Perspectives; published by Return To Stillness, Melbourne, 1998: 74 – 75.
5. Parkinson’s Australia Magazine, Winter 1998, No. 9.
6. Parkinson’s Australia Magazine, Spring 1999, No. 14: 4 – 5.