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food for the brain

Championing optimum nutrition for the mind


Parkinson's disease

Parkinson’s Disease is a progressive neurological disorder that is caused by a degeneration of cells in the part of the brain that produces the neurotransmitter dopamine (chemical messenger). It is characterised by loss of motor control such as slowness of movement, rigidity, tremor and balance problems as well as non-movement type symptoms including constipation, low mood, fatigue, sleep and memory problems.

Conventional treatment can involve medication which is primarily aimed at increasing dopamine activity. As dopamine is made in the body from amino acids which are the building blocks of protein, diet can play a key part in ensuring that the right nutrients are available to support the body’s ability to produce dopamine. Optimising nutritional status and addressing co-morbidities such as constipation, depression, fatigue, and insomnia is also an area that can benefit through diet.

Key dietary factors discussed below include reducing toxic load, reducing homocysteine with folic acid, vitamins B12 and B6, zinc and tri-methyl-glycine (TMG) and increasing Omega 3 fats, Vitamin D and Magnesium.

Read on for more information on Parkinson’s Disease and how it can be influenced by nutrition. Also see our nutritional action plan for managing Parkinson’s Disease.

If you would like further help, you can visit our clinic the Brain Bio Centre which specialises in optimum nutrition for mental health recovery. We have worked with people with Parkinson’s to create personalised nutritional programmes based upon their health history, symptoms and test results. If you would like to learn more about how we can help you, please click here. 

 

WHAT IS PARKINSON'S DISEASE?

Parkinson’s Disease is a progressive neurological disorder which affects around 120,000 people in the UK. Progressive (or degenerative) means that it typically worsens over time and neurological means that it affects the nervous system (this system includes the brain, spinal cord, and nerves throughout the body). The main symptoms of Parkinson’s are slowness of movement (bradykinesia), rigidity, tremor and postural instability (balance problems). While Parkinson’s is typically described as a ‘movement disorder’, a person with Parkinson’s may experience a range of other symptoms including constipation, low mood, fatigue, sleep and memory problems. Symptoms of Parkinson’s can be grouped into two major categories – motor symptoms (those that affect movement) and non-motor symptoms (those that don’t).

Parkinson’s typically strikes in middle age, with around 80% of cases presenting between ages of 40 and 70, and progression of symptoms is generally slow and continuous. Younger people who develop Parkinson’s are more likely to have a relative with the illness suggesting a stronger genetic component. Symptoms usually begin gradually and motor symptoms are often preceded by non-motor symptoms such as fatigue, loss of smell, depression, constipation and sweating abnormalities.

If you are concerned that you or a friend or family member has symptoms of Parkinson's, you or they should see a GP immediately.

WHAT CAUSES PARKINSON'S DISEASE?

Parkinson’s is caused by the degeneration of brain cells (neurons) in an area of the brain called the substantia nigra. These neurons are responsible for the production of a particular neurotransmitter (chemical messenger in the brain) called dopamine and it is the lack of this neurotransmitter that is responsible for the main Parkinson’s symptoms. The cause of the disease is not known. However, like most degenerative illnesses, it is likely to be due to a range of factors including interactions between genes and environment. Contributory factors may include environmental toxicity, physical trauma, genetics, drugs, disease (including tumours), nutritional deficiency, mitochondrial insufficiency, enzyme deficiency and unremitting stress.

CONVENTIONAL TREATMENT

Conventional treatment may involve medication which is primarily aimed at increasing dopamine activity either by providing the precursor (raw material) in the form of levodopa (L-Dopa), or by stimulating dopamine receptors (essentially mimicking dopamine) through the use of a dopamine agonist drug. Also used are drugs called COMT inhibitors which can help the levodopa to be more effective and MAO-B inhibitors which prevent dopamine from breaking down so the limited supply is longer lasting. Other therapies may include physiotherapy, osteopathy, remedial movement, massage, speech therapy, psychological therapy and in some cases surgery (deep brain stimulation). There is no cure for the condition, but these treatments can relieve symptoms.

NUTRITION AND PARKINSON'S DISEASE

So, what does nutrition have to do with Parkinson’s?

1. The neurotransmitter dopamine is made in the body from amino acids which are the building blocks of protein. Every time we eat a protein rich food (such as meat, fish, eggs, chicken and nuts) we take in protein which the body breaks down into its component amino acids. Two amino acids (L-phenylalanine and L-tyrosine) are converted in the body into L-Dopa, which is then converted into dopamine in the brain.

2. Nutrient co-factors (vitamins and minerals) are required for each stage of this conversion process, so deficiencies of these may reduce dopamine production.

3. L-dopa medication competes for absorption with dietary amino acids, therefore the timing of taking L-dopa and the eating of protein needs to be managed for optimal absorption and effectiveness of the drug and the reduction of side-effects.

Schema

Therefore, the nutritional therapy approach to Parkinson’s includes:

1. Supporting dopamine production by ensuring adequate precursors (amino acids) and co-factors (vitamins and minerals)

2. Considering drug-nutrient interactions (and timing of medication) to enhance effectiveness and reduce side-effects

3. Optimising nutritional status and addressing co-morbidities (symptoms that may not be considered to be due to Parkinson’s but occur alongside it and to which a nutritional factor may be contribution). These co-morbidities include constipation, depression, fatigue, and insomnia.

DIET AND NUTRITION...KEY FACTORS

Optimise your diet, reduce your toxic load

While the cause of Parkinson’s is not known, environmental toxins such as pesticides and herbicides are implicated. Researchers have found levels of these chemicals to be higher in the brains of Parkinson’s sufferers and incidence of Parkinson’s is higher in areas with greater use of these chemicals. It makes sense to avoid any environmental toxins that you can. Also, consider your intake of dietary toxins such as alcohol and caffeine – avoiding or reducing these may reduce the load on your body’s detoxification pathways.

Ensuring that you take in plenty of antioxidants from fresh fruits and vegetables is recommended. These nutrients may help to combat inflammation (a feature of Parkinson’s) and support your body’s detoxification pathways too.

It also makes sense to optimise your nutrient intake and ensure that your digestive system is working well so that your absorption of nutrients is maximised. Identify any food intolerances and avoid these foods, or you could avoid some of the key culprits (gluten, dairy, soya, yeast) for a trial period of 2-3 weeks to see if this makes a difference to how you feel. Any significant changes to your diet should not be pursued in the long-term without consulting your GP or a nutritional therapist, to ensure that your diet remains balanced.

Keep your blood sugar levels balanced. Eating sugar and refined carbohydrates will give you peaks and troughs in the amount of glucose in your blood; symptoms that this is going on include fatigue, irritability, dizziness, insomnia, depression, excessive sweating (especially at night), poor concentration and forgetfulness. In addition, excess glucose in the blood contributes to inflammation, which is a feature of Parkinson’s.

See action plan for our recommendations.

Homocysteine

Homocysteine is an amino acid which is toxic if elevated, and some studies have found that it is elevated in people with Parkinson’s. At this stage it isn’t known whether higher levels of homocysteine contribute to the development of Parkinson’s or whether the Parkinson’s (or Parkinson’s medications) contributes to higher levels of homocysteine, or both. Either way, reducing homocysteine to a healthy level is a good idea. The nutrients needed to reduce homocysteine include folic acid, vitamins B12 and B6, zinc and tri-methyl-glycine (TMG). Some of these nutrients are co-factors for dopamine production too.

See action plan for our recommendations.

Increase your omega-3 fats

The omega-3’s are anti-inflammatory which may be beneficial as neuro-inflammation is a feature of Parkinson’s. Mood problems are also a common feature and there has been a lot of research into the mood-boosting properties of the omega-3 essential fats. A small placebo-controlled pilot trial reported significantly greater improvement of depression in Parkinson’s patients treated with omega-3 fatty-acid supplementation versus placebo. The richest dietary source is from fish such as salmon, mackerel, herring, sardines, trout, pilchards and anchovies.

See action plan for our recommendations.

Vitamin D

Vitamin D is a hot topic for research since it was discovered that we have receptors for this vitamin in the brain, and that it enhances brain-derived neurotrophic factor (BDNF – think of this as akin to a growth hormone for neurons), and is anti-inflammatory. This nutrient is mainly provided by the action of sunlight on the skin.

In a small pilot study, bright light therapy was found to be superior to placebo (less bright light) in Parkinson’s patients. Since vitamin D deficiency is increasingly likely as we get older (and it has a number of implications for health), it makes sense to ensure you have a good level.

See action plan for our recommendations.

Up your magnesium

Magnesium is a mineral that acts as a natural relaxant. Some indications of deficiency are: muscle tremors or spasm, muscle weakness, insomnia or nervousness, high blood pressure, irregular heartbeat, constipation, hyperactivity, depression. Magnesium’s role in supporting good sleep may also be quite important here, since many people with Parkinson’s experience poor sleep patterns.

Research on any link between magnesium and Parkinson’s is lacking, however patients at the Brain Bio Centre are routinely tested and found to be magnesium deficient. Given its role as a relaxant it is certainly worthy of consideration to reduce spasms and anxiety, and improve sleep.

See action plan for our recommendations.

References

Optimise your diet and reduce your toxic load

Fleming L. et al., ‘Parkinson’s disease and brain levels of organochlorine pesticides’, Ann Neurol, Vol 36(1), 1994, pp.100-3

Thiruchevlvam M. et al., ‘The Nigrostriatal Dopaminergic System as a preferential target of repeated exposures to combined paraquat and maneb: implications for Parkinson’s Disease’, Journal of Neuroscience, Vol 20(24), 2000, pp.9207-14

Corell J. et al., ‘The risk of Parkinson’s disease with exposure to pesticides, farming, well water and rural living’, Neurology, Vol 67, 1998, pp.1210-18

Homocysteine

Martignoni E et al., (2007) Homocysteine and Parkinson's disease: a dangerous liaison? J Neurol Sci. 257:31-7.

Hassin-Baer S. et al., ‘Plasma homocysteine levels and Parkinson’s disease: Disease progression, carotid intima-media thickness and neuropsychiatric complications’, Clin Neuropharmacol, Vol 29(6), 2006, pp. 305-11

Postuma R.B. et al., ‘Vitamins and entacapone in levodopa-induced hyperhomocysteinemia: A randomized controlled study’, Neurology, Vol 66(12), 2006, pp. 1941-3

de Lau L. M. et al., ‘Dietary folate, vitamin B12, and vitamin B6 and the risk of Parkinson’s disease’, Neurology, Vol 67(2), 2006, pp. 315-8

Omega-3

da Silva TM et al., (2008) Depression in Parkinson's disease: a double-blind, randomized, placebo-controlled pilot study of omega-3 fatty-acid supplementation. J Affect Disord. 111:351-9

Vitmain D

Bright light therapy has been reported to be slightly superior to placebo (with less bright light) in a trial

Paus S et al., (2007) Bright light therapy in Parkinson's disease: a pilot study. Mov Disord. 22:1495-8