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Updated on Tuesday 18th March 2008.

 

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Antioxidants and Free Radicals; What ARE they - and how can they be involved in so many health issues?

Nutritional supplements and Parkinson's Disease.
Below is an overview of Parkinson's Disease, followed by summaries of a selection of papers concerned mainly with free radical damage and the possible role of anti-oxidants in this disease.  Although it is thought that free radical damage contributes to the symptoms of Parkinson's, there isn't any clear evidence that anti-oxidant treatment helps.  This may be because the main area of damage is the substantia nigra which is within the brain and probably inaccessible to most anti-oxidant vitamins.  One anti-oxidant preparation which can get into the brain, and has been used to treat Alzheimers disease with some success, is Ginkgo biloba.  My opinion is that research on the effect of Ginkgo biloba on Parkinson's would be worthwhile, but, as yet none has been published.
 

 

Overview of Parkinson's Disease.

[The following is a summary of the characteristics of Parkinson's Disease taken from the online medical encyclopaedia on the Medline website.  The full text can be viewed by clicking here:  http://www.nlm.nih.gov/medlineplus/ency/article/000755.htm .]

 
Parkinson's disease is a disorder of the brain characterized by shaking (tremor) and difficulty with walking, movement, and coordination. The disease is associated with damage to a part of the brain that is involved with movement.

The disease affects approximately 2 of every 1,000 people and most often develops after age 50. Sometimes Parkinson's disease occurs in younger adults and is rarely seen in children. It affects both men and women and is one of the most common neurologic disorders of the elderly.

In some cases the disease occurs within families, especially when it affects young people. Most late onset cases have no known cause. The term "parkinsonism" refers to any condition that involves a combination of the types of changes in movement seen in Parkinson's disease, which is the most common cause of these symptoms. Parkinsonism may be caused by other disorders or by external factors like certain medications used to treat schizophrenia.

Parkinson's disease is caused by progressive deterioration of the nerve cells of the part of the brain that controls muscle movement (the basal ganglia and the extrapyramidal area). Dopamine, which is one of the substances used by cells to transmit impulses, is normally produced in this area. Deterioration of this area of the brain reduces the amount of dopamine available to the body.

Insufficient dopamine disturbs the balance between dopamine and other transmitters, such as acetylcholine. Without dopamine, the nerve cells cannot properly transmit messages, and this results in the loss of muscle function.

The exact reason that the cells of the brain deteriorate is unknown. The disorder may affect one or both sides of the body, with varying degrees of loss of function.

In addition to the loss of muscle control, some people with Parkinson's disease become severely depressed. This may be due to loss of dopamine in certain brain areas involved with pleasure and mood. Lack of dopamine can also affect motivation and the ability to initiate voluntary movements.

Although early loss of mental capacities is uncommon, with severe Parkinson's, the person may exhibit overall mental deterioration (including dementia and hallucinations). Dementia can also be a side effect of some of the medications used to treat the disorder.

Although rare, when Parkinson's is found in children, it appears to be due to decreased sensitivity of the nerves (post-synaptic) to dopamine rather than deterioration of the area of the brain that produces dopamine.
The following are a short selection of summaries of papers investigating the role of nutritional supplements in treatment of Parkinson's disease.
 

 

1. J Am Coll Nutr 1999 Oct;18(5):413-23
Multiple antioxidants in the prevention and treatment of Parkinson's disease.

Prasad KN, Cole WC, Kumar B.

Center for Vitamins and Cancer Research, Department of Radiology, University of Colorado Health Sciences Center, Denver 80262, USA.

Parkinson's disease (PD) is one of the major progressive neurological disorders for which no preventative or long-term effective treatment strategies are available. Epidemiologic studies have failed to identify specific environmental, dietary or lifestyle risk factors for PD except for toxic exposure to manganese, meperidine (Demerol, the "designer drug" version of which often contains a toxic byproduct of the synthesis, 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine [MPTP]), and some herbicides and pesticides. The search for genetic risk factors such as mutation, overexpression or underexpression of nuclear genes in DA neurons in idiopathic PD has not been successful as yet. Polymorphism in certain genes appears to be a risk factor, but there is no direct evidence for the causal relationship between polymorphism and increased risk of PD. In familial PD, mutation in the alpha-synuclein gene is associated with the disease, but a direct role of this gene in degeneration of DA neurons remains to be established. Although mutations in the Parkin gene has been associated with autosomal recessive juvenile Parkinson's disease, the role of this gene mutation in causing degeneration of DA neurons has not been defined. We have reported that in hereditary PD, a mutation in the alpha-synuclein gene may increase the sensitivity of DA neurons to neurotoxins. We hypothesize that, in idiopathic PD, epigenetic (mitochondria, membranes, protein modifications) rather than genetic events are primary targets which, when impaired, initiate degeneration in DA neurons, eventually leading to cell death. Although the nature of neurotoxins that cause degeneration in DA neurons in PD is not well understood, oxidative stress is one of the intermediary risk factors that could initiate and/or promote degeneration of DA neurons. Therefore, supplementation with antioxidants may prevent or reduce the rate of progression of this disease. Supplementation with multiple antioxidants at appropriate doses is essential because various types of free radicals are produced, antioxidants vary in their ability to quench different free radicals and cellular environments vary with respect to their lipid and aqueous phases. L-dihydroxyphenylalanine (L-dopa) is one of the agents used in the treatment of PD. Since L-dopa is known to produce free radicals during its normal metabolism, the combination of L-dopa with high levels of multiple antioxidants may improve the efficacy of L-dopa therapy.

 

 
2. Free Radic Biol Med 2000 Dec 15;29(12):1222-33  
Phenolic antioxidants attenuate neuronal cell death following uptake of oxidized low-density lipoprotein.

Schroeter H, Williams RJ, Matin R, Iversen L, Rice-Evans CA.

Wolfson Centre for Age-Related Diseases, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College, Guy's Campus, London, England.

Oxidative stress is implicated in neuronal loss associated with neurodegeneration such as in Parkinson's disease, Alzheimer's disease and age-related cognitive decline. Recent reports indicate that the consumption of flavonoid-rich fruits partly reverses the age-related neuronal and cognitive decline. In this study, cultured striatal neurons were exposed to oxidized lipids in the form of low-density lipoprotein (oxLDL) as a model for the induction of oxidative injury, and the abilities of phenolic antioxidants, flavonoids and hydroxycinnamic acid derivatives, to attenuate this neuronal damage were examined. OxLDL was demonstrated to enter neuronal cells and to be capable of eliciting neurotoxicity in a dose- and time-dependent manner, inducing DNA fragmentation and cell lysis. Flavonoids exert protective effects, which appear to be related to specific structural characteristics, particularly relevant being those defining their reduction potentials and partition coefficients. In summary, these data suggest a possible role for flavonoids in reducing neurodegeneration associated with chronic disorders in which oxidative stress is implicated.
 

 
Vitamin E is an anti-oxidant which is of benefit for many conditions (notably heart disease) but this paper is one of several which indicates that it has no effect on Parkinson's Disease.  This is probably because it is unable to cross the blood-brain barrier into the brain where nerve cell deterioration occurs.
3. Arch Gerontol Geriatr 2001 Aug;33(1):7-12  
Plasma levels of vitamin E in Parkinson's disease.

Nicoletti G, Crescibene L, Scornaienchi M, Bastone L, Bagala A, Napoli ID, Caracciolo M, Quattrone A.

Institute of Experimental Medicine and Biotechnology, National Research Council, Contrada Burga, I-87050 Piano Lago di Mangone, Cosenza, Italy

Oxidative stress has been implicated as a major contributor to selective neuronal death in Parkinson's disease (PD). Vitamin E is an antioxidant that may protect the brain from free radical-induced oxidative damage. It is, therefore, reasonable to hypothesize that low levels of vitamin E concentrations may increase the risk of developing PD. To elucidate the possible role of vitamin E in the pathogenesis of PD, we assessed the plasma levels of vitamin E, measured by high-performance liquid chromatography (HPLC), in 54 patients with PD. Vitamin E concentrations were also assessed in 93 age and sex matched normal individuals. The mean plasma levels of vitamin E did not differ significantly between these two groups (22.5+/-8.15 &mgr;mol/l for PD patients and 21.0+/-7.9 &mgr;mol/l for controls). The results of our study suggest that plasma vitamin E concentrations do not play a major role in the pathogenesis of PD.
 

 
The next paper points out that the areas of the brain most affected are exquisitely sensitive to oxidative damage (another term for damage by free radicals).  Several suggestions for dietary control of symptoms, including an antioxidant-rich diet, are made at the end of the summary.
 

 
4. Altern Med Rev. 2000 Dec;5(6):501 Click here to read
Parkinson's disease as multifactorial oxidative neurodegeneration: implications for integrative management.

Kidd PM.

Parkinson's disease (PD) is the most common movement pathology, severely afflicting dopaminergic neurons within the substantia nigra (SN) along with non-dopaminergic, extra-nigral projection bundles that control circuits for sensory, associative, premotor, and motor pathways. Clinical, experimental, microanatomic, and biochemical evidence suggests PD involves multifactorial, oxidative neurodegeneration, and that levodopa therapy adds to the oxidative burden. The SN is uniquely vulnerable to oxidative damage, having high content of oxidizable dopamine, neuromelanin, polyunsaturated fatty acids, and iron, and relatively low antioxidant complement with high metabolic rate. Oxidative phosphorylation abnormalities impair energetics in the SN mitochondria, also intensifying oxygen free radical generation. These pro-oxidative factors combine within the SN dopaminergic neurons to create extreme vulnerability to oxidative challenge. Epidemiologic studies and long-term tracking of victims of MPTP (1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine) poisoning, suggest oxidative stress compounded by exogenous toxins may trigger the neurodegenerative progression of PD. Rational, integrative management of PD requires: (1) dietary revision, especially to lower calories; (2) rebalancing of essential fatty acid intake away from pro-inflammatory and toward anti-inflammatory prostaglandins; (3) aggressive repletion of glutathione and other nutrient antioxidants and cofactors; (4) energy nutrients acetyl L-carnitine, coenzyme Q10, NADH, and the membrane phospholipid phosphatidylserine (PS), (5) chelation as necessary for heavy metals; and (6) liver P450 detoxification support.
 

 
Another publication dealing with diet for patients with Parkinson's Disease.
 

 

5. Neurosci Biobehav Rev 1988 Fall-Winter;12(3-4):307-9

Nursing care of patients with Parkinson's disease.

Szigeti E.

Department of Adult Health and Anesthesia Nursing, College of Nursing, University of North Dakota, Grand Forks 58202.

Nursing interventions for each of the symptoms of Parkinson's disease, muscle rigidity, bradykinesia, tremors at rest and postural reflex abnormalities, are designed to increase the patient's quality of life by minimizing symptoms. Nurses are responsible for planning patient medication schedules to maximize drug effectiveness. Dietary implications include a low-protein regimen for the patient during the day, eliminating foods high in Vitamin B6, high caloric foods, and soft-solid foods offered at frequent feedings. Constipation is addressed by increasing the patient's fiber and fluid intake and by increasing the patient's mobility. Patient mobility is increased when the patient is taught purposeful activities and to concentrate on the way he walks. Communication is facilitated if the patient takes deep breaths before speaking and uses diaphragmatic speech. A telephone receiver which amplifies the patient's voice is also available. Interventions are good only if the patient chooses to implement them; he is the head of the health team planning his care.

 

 
To present the other side of the picture, and show how researchers can disagree, this paper studied levels of free-radical producing (pro-oxidant) and anti-oxidant substances in both Parkinson's and healthy subjects and found no difference for those studied.  In the case of vitamin E (alpha tocopherol) at least, this could be because it can't get into the brain and thus would be unable to have any effect on the disease.
 

 

6. Rev Neurol 1999 Jul 1-15;29(1):12-5

[Serum pro-oxidant and antioxidant factors and risk of Parkinson's disease: population study]

[Article in Spanish]

Molina-Arjona JA, de Bustos F, Benito-Leon J, Jimenez-Jimenez FJ, Rodriguez J, Trincado R, Porta-Etessan J, Vega S, Bermejo F.

Servicio de Neurologia, Hospital 12 de Octubre, Madrid.

INTRODUCTION: Several studies suggested a role of 'oxidative stress' (increased production of prooxidants, antioxidants deficiencies or both) in the pathogenesis of Parkinson's disease. In this study we have measured the serum levels of a number of prooxidant and antioxidant substances to evaluate their possible relation with the risk for Parkinson's disease. PATIENTS AND METHODS: We assessed the serum levels of iron, ferritin, ansferrin, ceruloplasmine, vitamin A, alpha-carotene, beta-carotene, and alpha-tocopherol, in 28 patients with Parkinson's disease and 85 matched controls. All of them were recruited from a population study. RESULTS: None of the values studied differed significantly between the two study groups, and none of them were correlated with age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale or the Hoehn and Yahr staging in the Parkinson's disease group. CONCLUSIONS: These results confirm the previous findings of classic case-control studies, suggesting the absence of relationship of the studied values with the risk for Parkinson's disease.

 

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