Nutritional Support for Parkinson’s Disease

According to the NHS website, it is estimated that around 1 in 500 people are affected by Parkinson’s disease, which means approximately 127,000 people in the UK live with the condition.

Parkinson’s is a progressive neurological disorder in which the initial pathology leads to the degeneration of neurons in the substantia nigra, an area of the brain that produces the neurotransmitter dopamine, a critical signalling molecule involved in the control of movement and emotional response. In this week’s blog, we look at nutritional support for Parkinson’s Disease.

Levels of dopamine continue to fall slowly during the disease progression; however, the body appears to continue to function with a reduced availability of dopamine. It is believed that symptoms of Parkinson’s appear when approximately 80% of dopamine has been lost.

Autopsy shows the presence of Lewy bodies within the substantia nigra. Lewy bodies are normal cellular proteins which have been marked for degradation but in Parkinson’s they appear to escape normal degradation processes. Scientists are also exploring the idea that loss of cells in other areas of the brain and body contribute to Parkinson’s. For example, researchers have discovered that Lewy Bodies are found not only in the mid-brain but also in the brain stem and the olfactory bulb.

Symptoms of Parkinson’s

Symptoms of Parkinson’s disease often appear after the age of 50. Although later onset or diagnosis is common (average age is approximately 60). Early onset of Parkinson’s does arise and is referred to in those diagnosed before the age of 40. Juvenile Parkinson’s, diagnosed before the age of 18, is rare. The condition is more common in men than in women.

Often, Parkinson’s is diagnosed by observing a collection of signs and symptoms associated with the disease. However, these can differ greatly from person to person; slow onset, means that symptoms may have been present for some time before a diagnosis is made. Not all symptoms will be present in an individual, although others often develop as the condition progresses.

The tremor of Parkinson’s is perhaps one of the most well-known signs, although not always present. Early appearance of tremor may just involve the arms, legs, head or jaw. The tremor is more noticeable when relaxing and reduced when moving or sleeping.

Bradykinesia, which simply means ‘slowness of movement’, is also a recorded sign: patients have difficulty initiating movement (akinesia), often referred to as freezing, or movement taking longer to perform.

Additional signs and symptoms include:

  • Low mood and/or anxiety
  • Poor memory and reasoning ability
  • Psychotic symptoms such as hallucinations or delusions
  • Gastro-intestinal symptoms particularly constipation
  • ‘Pill-rolling’ – movement between the thumb and forefinger
  • Stooped posture

There is no specific test currently available that can confirm the presence of the condition and NHS National Guidelines advise that Parkinson’s should be suspected in people presenting with tremor, stiffness, slowness and balance or gait problems. Doctors should refer patients prior to treatment to a specialist in differential diagnosis of Parkinson’s disease.

Medical Treatment

Currently, there is no known cure for Parkinson’s disease: treatment focuses on the use of medication to control the symptoms with a variety of drugs including:

  • Drugs that replace dopamine
  • Drugs that mimic the action of dopamine (dopamine agonists)
  • Drugs that prevent the breakdown of dopamine
  • Drugs which inhibit the action of acetylcholine

Patients’ responses to drugs can be variable and it may take time to find the most suitable. Early response to treatment is usually good; as the condition progresses symptoms may be more difficult to resolve and increased dosage and/or additional or different medications are used.

A potential new treatment, Nilotinib, is currently undergoing clinical trials to test its effectiveness. It is primarily a leukaemia treatment but tests undertaken in 2013 show that Nilotinib reverses the loss of dopamine neurons and improves motor behaviour.


It is generally agreed that, as with most chronic conditions, Parkinson’s is a multi-factorial condition with a number of factors exacerbating, contributing or leading to onset with genetic predisposition, toxic exposure and diet playing a part. The cell death within the substantia nigra has been attributed to oxidative stress, inflammation and mitochondrial dysfunction.


Some incidences of Parkinson’s suggest a genetic predisposition, but the majority of cases have no indication of a hereditary link. However, recent studies have demonstrated a potential epigenetic link to Parkinson’s whereby environmental factors have an effect on gene expression.

Oxidative Stress

One of the first biochemical changes noted in Parkinson’s is the depletion of glutathione (a major intracellular antioxidant and redox regulator) within the substantia nigra, suggesting that oxidative stress is a significant factor in the onset and progression of Parkinson’s. Glutathione depletion has been linked to the aggregation of defective proteins leading to death of dopaminergic neurons and increased susceptibility to endogenous and exogenous toxins.

Environmental toxins

Studies have identified an association between Parkinson’s and exposure to environmental toxins including:

  • Pesticides (organochlorines, carbamates, paraquat, maneb, rotenone, pyrethroid and diethyldithiocarbamate)
  • Certain trace metals including copper, iron and manganese as well as heavy metals such as lead
  • Solvents

Phase 2 liver detoxification

In addition to identifying and reducing exposure to environmental toxins, it is important to consider the individual’s capacity to biotransform toxins via the detoxification pathways. A reduction in phase 2 liver detoxification is particularly relevant in Parkinson’s. Studies have shown that patients have reduced capacity to detoxify xenobiotics in particular. It is thought that reduced detoxification function can increase susceptibility to neurotoxins.


Research into the aetiology of Parkinson’s has found disrupted iron metabolism together with the presence of increased iron levels within the substantia nigra of some Parkinson’s disease patients. Oxidative damage to cells, resulting from the Fenton reaction of iron and the accumulation of iron in the substantia nigra, is associated with neuronal loss and Lewy body pathology. (The Fenton reaction = the oxidation of organic substrates by iron(II) and hydrogen peroxide).

Intake of dietary iron and supplementation should be considered, as research has identified an association in men between high dietary iron intake and increased risk of Parkinson’s disease via oxidative stress.


Studies have shown that patients with Parkinson’s tend to consume fewer vegetables, more animal fat and protein and have a higher carbohydrate consumption than controls.

A dietary study carried out with both males and females with a follow-up after 16 years found that “Dietary patterns with a high intake of fruit, vegetables, legumes, wholegrains, nuts, fish and poultry, a low intake of saturated fat and moderate alcohol may protect against PD”.

When comparing a “prudent” diet (high intake of fruit, vegetables and fish) with a “Western diet” (high intake of red meat, processed foods, refined grains, desserts and high fat dairy), the prudent diet was inversely associated with the risk of Parkinson’s disease. A similar result was shown when the Mediterranean diet was compared with a Western diet.

Caloric restriction has been indicated for many conditions associated with ageing and could also be useful in prevention and potential therapy for Parkinson’s disease. Research suggests that caloric restriction can extend lifespan and increases resistance of the brain to insults that involve metabolic compromise and excitotoxicity.

Much of the interest in neurological conditions such as Parkinson’s and nutrition has looked at the impact of exposure to free radicals or pro-oxidants and the corresponding lack of antioxidants in the diet. Research has shown certain plant derived antioxidants can inhibit dopamine oxidation.


Flavonoids The benefits of flavonoids as potential antioxidants and anti-inflammatory agents with free radical scavenging abilities have been documented considerably over the years. It is therefore no surprise to discover the potential of flavonoids for conditions such as Parkinson’s disease. Research has identified flavonoids as modulators of brain function and the central nervous system, providing protection for neurons and suppressing neurological inflammation. Specific flavonoids identified in research as beneficial to Parkinson’s disease include:

  • Green Tea; catechins found in green tea have metal chelating, antioxidant and anti-inflammatory activity.
  • Resveratrol and quercetin have been shown to protect dopaminergic neurons, diminishing apoptotic neuronal cell death by acting on the expression of pro-and anti-apoptotic genes.
  • Curcumin has demonstrated the ability to reduce reactive oxygen species and protect cells against apoptosis; curcumin’s ability to cross the blood brain barrier makes it particularly interesting for neurological conditions, with potential therapeutic value for Parkinson’s and other neurodegenerative disease.
  • Flavonoids, particularly polyphenols have demonstrated membrane stabilising properties. It has been shown that restoring the lipid content, and therefore stabilising, the inner mitochondrial membrane is important for protecting both mitochondrial and neural function.
  • In an animal study, researchers identified extracts of tangerine peel (described as ‘rich in polymethoxylated flavones’), cocoa (rich in procyanidins) and red clover (providing isoflavones) as protective of the dopaminergic neurons.

Glutathione  An important antioxidant produced in the body, the levels are known to fall with ageing and have been shown to be reduced within the substantia nigra in patients with Parkinson’s. Nutrients such as N-acetylcysteine and alpha-lipoic acid are precursors for glutathione and may increase levels. Glutathione is also available as a supplement. Other antioxidants may help to conserve glutathione, particularly high dose vitamin C.

Coenzyme Q10  In a double-blind trial CoQ10 slowed functional decline in Parkinson’s disease. Patients selected were those in the early stages of disease, not requiring treatment for their condition. At follow-up, less disability was found to have developed in those receiving CoQ10, with the greatest benefits linked to the higher doses of 1200mg/day.

Vitamin B6, folate and B12 A review on dietary intake of vitamins and the incidence of Parkinson’s disease indicated a low intake of B6 being independently associated with an increased risk of the disease. This was via the potential for accelerated dopaminergic cell death resulting from increased homocysteine. Increased homocysteine levels are also associated with insufficient levels of folate and B12.

Vitamin E  Research identified that the risk of Parkinson’s disease was significantly reduced among men and women with high dietary intake of vitamin E from foods. However, results did not concur when vitamin E supplementation was taken; the researchers considered that other constituents in vitamin E rich food may be protective. We should, of course, consider the form of delivery for the vitamin E used; vitamin E occurs in nature as tocopherols and tocotrienols of which there are 4 of each. Most supplements only include alpha-tocopherol i.e. one of the 8 constituents. In addition, in food vitamin E is naturally complexed with additional support nutrients such as bioflavonoids, carotenoids, lipids and more. The form of nutrient and/or additional co-factors would appear of relevance to these study results.

Vitamin D  Studies of vitamin D levels have shown them to be insufficient in 55% of patients with Parkinson’s disease in comparison to ‘healthy people’. The substantia nigra contains high levels of vitamin D receptors; further research is required to establish at what stage the deficiency occurs and if supplementation or increased exposure to sunlight may be beneficial.

Gingko biloba  Research, both in vitro and in vivo, has shown Gingko biloba to have a protective effect on Parkinson’s disease models. It has been shown to inhibit lipid peroxidation of cell membranes, enhance energy utilisation and have membrane stabilising and antioxidant effects.

Kapikacchu  This is a herb that has been used in several studies on Parkinson’s disease. It is a powerful antioxidant and natural source of L-dopa which increases dopamine. However, it should not be taken at the same time as prescription drugs, such as Levodopa, that increase dopamine.

If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Clare) by phone or email at any time., 01684 310099

Clare Daley and the Cytoplan Editorial Team

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Phytoshield – Phytoshield is a very potent and powerful phyto-antioxidant nutrient formula containing high levels of flavonoids and carotenoids.

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R-Omega – R-Omega is a phospholipid rich DHA and EPA omega 3 supplement from herring roe.

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Mixed Tocopherols & Tocotrienols – Containing the full spectrum of vitamin E as it occurs in nature; alpha, beta, delta, gamma tocopherol and alpha, beta, delta, gamma tocotrienol.

Last updated on 26th July 2017 by cytoffice


4 thoughts on “Nutritional Support for Parkinson’s Disease

    1. Dear Dee,

      Thank you for your question. The product we recommend is our CoQ10 Multi which combines multivitamins and minerals at optimal levels, including B-Complex vitamins, specifically B12. Taking this product daily will help boost your vitamin B intake to optimal levels. However, everyone is different and people with neurological problems should be assessed individually so that their needs are met.

      All the best,

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