Dietary management of Parkinson's disease

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Parkinson's disease is the 2nd most prevalent neurological disorder within the United States and Europe, affecting around 1% of the population over the age of 60. [1] While the link connecting the onset of Parkinson's disease to environmental factors is known, the link between dietary patterns and the disease is just beginning to be researched more fully. [2] [3] Additionally, other research has sought to examine the symptoms of the disease and propose methods on how to alleviate these symptoms through changes in diet. Current medications that work to alleviate the symptoms of Parkinson's disease can also be made more effective through changes in diet.

Contents

Background

Parkinson's disease is a degenerative disorder of the central nervous system that results due to the death of dopamine producing cells within the central nervous system. Because of the death of these cells, less dopamine is available within the brain, resulting in tremors and other side effects within motor functions. The reason for the deaths of these cells is a topic of current research, with some theories suggesting a contribution of oxidative stress due to free radicals and inflammation. Currently, there are no treatments to cure Parkinson's disease, yet a variety of treatment options are available to alleviate the symptoms including medication and dietary changes.

Dietary prevention and neuroprotection

Many theories of the cause of Parkinson's Disease symptoms point to the death of dopamine-producing neurons within the central nervous system due to oxidative stress. This oxidative stress is caused by metabolism and the production of molecules known as free radicals. Accumulation of these free radicals within the brain can cause damage to neurons. Additionally, dopamine-producing neurons are particularly vulnerable to oxidative stress due to the relatively high levels of metabolism associated with the production of dopamine, resulting in comparatively higher amounts of free radicals being produced by these dopamine-producing neurons. [4] The effects of dopamine within the brain are widespread, including voluntary motor control. With the death of these dopamine-producing cells within an area of the mid-brain known as the substantia nigra, the central nervous system has less control over the body, resulting in the tremors and rigidity seen in patients with Parkinson's disease.

Mediterranean diet foods in comparison to the typical Western diet Differences between Mediterranean diet and Western diet.png
Mediterranean diet foods in comparison to the typical Western diet

Antioxidants are suggested to be useful in preventing Parkinson's Disease because they scavenge free radicals such as reactive nitrogen and oxygen, preventing their build-up and the destruction of dopamine-producing neurons. [5] Research has attempted to link dietary patterns to the likelihood of developing Parkinson's disease. The MIND and Mediterranean diets are emerging as potentially beneficial diets for people with Parkinson's. People with Parkinson's who maintained the Mediterranean diet were more likely to have symptoms appear 17.4 years earlier than those who closely followed it; while MIND diet participants functioned at a cognitive level 7.5 years younger, and they declined cognitively more slowly. [6] Research shows that a diet consisting of foods typically associated with the Mediterranean diet may act as a preventative measure for the disease due to the high levels of antioxidants found in within these foods such as complex phenols, vitamins C and E, and carotenoids. [7] A typical Mediterranean diet consists of a high intake of vegetables, legumes, fruits, and cereals, olive oil (unsaturated fatty acids), and fish and low to moderate intake of foods such as dairy, meats, poultry. Research by John Hopkins has found that a common compound in fruit, called farnesol, preserves dopaminergic neurons. [8] However, people who consume more dairy products have an increased likelihood of developing Parkinson's disease. [9] It is important to note that the increased risk from consumption of dairy products is slight and dairy provides different nutrients that are beneficial for people with Parkinson's. [9] Additionally, it has been seen that the intake of animal fats may be linked to the development of the disease. [10] It has also been suggested that a diet that results in high plasma urate can result in a reduced risk of developing Parkinson's. [11]

Management of symptoms through diet

Typical symptoms of the disease include bodily shaking, rigidity, slowness of movement, difficulty in movement, as well as other motor related symptoms. As the disease progresses, patients develop cognitive and behavior problems such as dementia, sensory impairment, sleep problems, and emotional issues. PD can have an effect on neurons that control the digestive process, so subjects may experience constipation and gastroparesis due to the disease. [12] PD may also make a subject more tired in the later parts of the day, decreasing the likelihood to want to eat food and leading to further dietary problems.

No special diet is required for subjects with PD, yet a well balanced diet is beneficial due to the effects of increased energy and improved effectiveness of drugs. Additional, in research it has been shown that nutritionally healthy, balanced meals enable the most effective use of symptom reducing drugs. [13] In order to cope with the decrease in energy that many patients express, smaller meals are recommended for such cases. A good diet includes high fiber foods (such as vegetables, dried peas, beans, whole grain foods, pasta, rice, and fresh fruit) in order to reduce constipation, low saturated fats and cholesterol, low sugar and salt intake, plenty of water, and limited alcohol intake. Although this needs to be further elucidated, recent studies have shown that curcumin, a chemical in turmeric which is highly consumed by the South Asian population, can have protective roles in PD.

Dietary considerations with medications

Treatments are only effective in moderating the symptoms of the disease, mainly with drugs including levodopa (L-DOPA) and dopamine agonists. Once too many dopamine producing cells have been lost however, the effects of L-DOPA become less effective. Once this occurs, a complication known as dyskinesia commonly occurs in which subjects undergo involuntary writhing movements despite the use of L-DOPA. The effects of dyskinesia vary between periods of high symptoms and low symptoms. In order to limit the onset of dyskinesia, typical L-DOPA dosages are kept as low as possible while still achieving desired results. Lastly, in cases in which drugs are ineffective, deep brain stimulation and surgery can be used to reduce symptoms. [14]

Levodopa is taken orally and is absorbed through the small intestines into the blood, competing for access with natural proteins. Additionally, once the drug has entered the blood stream, L-DOPA utilizes the same pathways to cross the blood brain barrier as natural protein. [15] [16] Only about 5 – 10% of levodopa crosses the blood brain barrier, while the remaining is metabolized elsewhere in the body. The metabolism of medications elsewhere is known to cause side effects such as nausea, dyskinesias, and stiffness. [17]

In order to improve the effectiveness of PD drugs such as L-DOPA, a diet low in excessive protein is recommended since L-DOPA competes with these dietary proteins for access to the blood and brain. It is therefore recommended that the drug be taken so that it is not affected by digestion. It is recommended to take L-DOPA ideally 30 minutes before eating or at least 1 hour afterwards. A protein redistribution diet is sometimes recommended in which most protein should be eaten in the afternoon. [18] However, with the development of dyskinesias the protein redistribution diet need not apply because slowing the absorption of L-DOPA may be beneficial. [19] Plenty of water with the intake of L-DOPA ensures that the drug will be absorbed more quickly. L-DOPA can cause nausea in some subjects when taken on an empty stomach. Methods to reduce nausea include taking carbidopa (Sinemet), sugary drinks to calm the stomach, and avoidance of orange and grapefruit juices due to high acidity. Some PD medications are known to cause the subject to become thirsty, and methods to reduce thirst include drinking plenty of water as well as limiting caffeine uptake because it may interfere with medication or increase thirst. [20]

Related Research Articles

<span class="mw-page-title-main">Substantia nigra</span> Structure in the basal ganglia of the brain

The substantia nigra (SN) is a basal ganglia structure located in the midbrain that plays an important role in reward and movement. Substantia nigra is Latin for "black substance", reflecting the fact that parts of the substantia nigra appear darker than neighboring areas due to high levels of neuromelanin in dopaminergic neurons. Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta.

<small>L</small>-DOPA Chemical compound

l-DOPA, also known as levodopa and l-3,4-dihydroxyphenylalanine, is made and used as part of the normal biology of some plants and animals, including humans. Humans, as well as a portion of the other animals that utilize l-DOPA, make it via biosynthesis from the amino acid l-tyrosine. l-DOPA is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), which are collectively known as catecholamines. Furthermore, l-DOPA itself mediates neurotrophic factor release by the brain and CNS. In some plant families, l-DOPA is the central precursor of a biosynthetic pathway that produces a class of pigments called betalains. l-DOPA can be manufactured and in its pure form is sold as a psychoactive drug with the INN levodopa; trade names include Sinemet, Pharmacopa, Atamet, and Stalevo. As a drug, it is used in the clinical treatment of Parkinson's disease and dopamine-responsive dystonia.

<span class="mw-page-title-main">Carbidopa</span> Chemical compound

Carbidopa (Lodosyn) is a drug given to people with Parkinson's disease in order to inhibit peripheral metabolism of levodopa. This property is significant in that it allows a greater proportion of administered levodopa to cross the blood–brain barrier for central nervous system effect, instead of being peripherally metabolised into substances unable to cross said barrier.

Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle movements, including movements similar to tics or chorea and diminished voluntary movements. Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the upper body or lower extremities. Discoordination can also occur internally especially with the respiratory muscles and it often goes unrecognized. Dyskinesia is a symptom of several medical disorders that are distinguished by their underlying cause.

<span class="mw-page-title-main">Amantadine</span> Medication used to treat dyskinesia

Amantadine, sold under the brand name Gocovri among others, is a medication used to treat dyskinesia associated with parkinsonism and influenza caused by type A influenzavirus, though its use for the latter is no longer recommended because of widespread drug resistance. It acts as a nicotinic antagonist, dopamine agonist, and noncompetitive NMDA antagonist. The antiviral mechanism of action is antagonism of the influenzavirus A M2 proton channel, which prevents endosomal escape.

Neuropharmacology is the study of how drugs affect function in the nervous system, and the neural mechanisms through which they influence behavior. There are two main branches of neuropharmacology: behavioral and molecular. Behavioral neuropharmacology focuses on the study of how drugs affect human behavior (neuropsychopharmacology), including the study of how drug dependence and addiction affect the human brain. Molecular neuropharmacology involves the study of neurons and their neurochemical interactions, with the overall goal of developing drugs that have beneficial effects on neurological function. Both of these fields are closely connected, since both are concerned with the interactions of neurotransmitters, neuropeptides, neurohormones, neuromodulators, enzymes, second messengers, co-transporters, ion channels, and receptor proteins in the central and peripheral nervous systems. Studying these interactions, researchers are developing drugs to treat many different neurological disorders, including pain, neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease, psychological disorders, addiction, and many others.

Carbidopa/levodopa, also known as levocarb and co-careldopa, is the combination of the two medications carbidopa and levodopa. It is primarily used to manage the symptoms of Parkinson's disease, but it does not slow down the disease or stop it from getting worse. It is taken by mouth. It can take two to three weeks of treatment before benefits are seen. Each dose then begins working in about ten minutes to two hours with a duration of effect of about five hours.

<span class="mw-page-title-main">Dopaminergic</span> Substance related to dopamine functions

Dopaminergic means "related to dopamine" (literally, "working on dopamine"), dopamine being a common neurotransmitter. Dopaminergic substances or actions increase dopamine-related activity in the brain. Dopaminergic brain pathways facilitate dopamine-related activity. For example, certain proteins such as the dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT2), and dopamine receptors can be classified as dopaminergic, and neurons that synthesize or contain dopamine and synapses with dopamine receptors in them may also be labeled as dopaminergic. Enzymes that regulate the biosynthesis or metabolism of dopamine such as aromatic L-amino acid decarboxylase or DOPA decarboxylase, monoamine oxidase (MAO), and catechol O-methyl transferase (COMT) may be referred to as dopaminergic as well. Also, any endogenous or exogenous chemical substance that acts to affect dopamine receptors or dopamine release through indirect actions (for example, on neurons that synapse onto neurons that release dopamine or express dopamine receptors) can also be said to have dopaminergic effects, two prominent examples being opioids, which enhance dopamine release indirectly in the reward pathways, and some substituted amphetamines, which enhance dopamine release directly by binding to and inhibiting VMAT2.

<span class="mw-page-title-main">Entacapone</span> Chemical compound

Entacapone, sold under the brand name Comtan among others, is a medication commonly used in combination with other medications for the treatment of Parkinson's disease. Entacapone together with levodopa and carbidopa allows levodopa to have a longer effect in the brain and reduces Parkinson's disease signs and symptoms for a greater length of time than levodopa and carbidopa therapy alone.

<span class="mw-page-title-main">Dopamine agonist</span> Compound that activates dopamine receptors

A dopamine agonist(DA) is a compound that activates dopamine receptors. There are two families of dopamine receptors, D1-like and D2-like. They are all G protein-coupled receptors. D1- and D5-receptors belong to the D1-like family and the D2-like family includes D2, D3 and D4 receptors. Dopamine agonists are primarily used in the treatment of Parkinson's disease, and to a lesser extent, in hyperprolactinemia and restless legs syndrome. They are also used off-label in the treatment of clinical depression. The use of dopamine agonists is associated with impulse control disorders and dopamine agonist withdrawal syndrome (DAWS).

In the management of Parkinson's disease, due to the chronic nature of Parkinson's disease (PD), a broad-based program is needed that includes patient and family education, support-group services, general wellness maintenance, exercise, and nutrition. At present, no cure for the disease is known, but medications or surgery can provide relief from the symptoms.

<span class="mw-page-title-main">Dihydroergocryptine</span> Chemical compound

Dihydroergocryptine (DHEC), sold under the brand names Almirid and Cripar among others, is a dopamine agonist of the ergoline group that is used as an antiparkinson agent in the treatment of Parkinson's disease. It is taken by mouth.

<span class="mw-page-title-main">Istradefylline</span> Chemical compound

Istradefylline, sold under the brand name Nourianz, is a medication used as an add-on treatment to levodopa/carbidopa in adults with Parkinson's disease (PD) experiencing "off" episodes. Istradefylline reduces "off" periods resulting from long-term treatment with the antiparkinson drug levodopa. An "off" episode is a time when a patient's medications are not working well, causing an increase in PD symptoms, such as tremor and difficulty walking.

<span class="mw-page-title-main">Dopamine dysregulation syndrome</span> Medical condition

Dopamine dysregulation syndrome (DDS) is a dysfunction of the reward system observed in some individuals taking dopaminergic medications for an extended length of time. It typically occurs in people with Parkinson's disease (PD) who have taken dopamine agonist medications for an extended period of time. It is characterized by problems such as addiction to medication, gambling, or sexual behavior.

<span class="mw-page-title-main">Parkinson's disease</span> Long-term degenerative neurological disorder

Parkinson's disease (PD), or simply Parkinson's, is a long-term neurodegenerative disease of the central nervous system that affects both the motor system and non-motor systems. The symptoms usually emerge slowly, and as the disease progresses, non-motor symptoms become more common. Usual symptoms are tremor, rigidity, slowness of movement, and difficulty with walking, collectively known as parkinsonism. Parkinson's disease dementia, falls and neuropsychiatric problems such as sleep abnormalities, psychosis, mood swings or behavioral changes may arise in advanced stages.

Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and athetosis.

Gene therapy in Parkinson's disease consists of the creation of new cells that produce a specific neurotransmitter (dopamine), protect the neural system, or the modification of genes that are related to the disease. Then these cells are transplanted to a patient with the disease. There are different kinds of treatments that focus on reducing the symptoms of the disease but currently there is no cure.

3-<i>O</i>-Methyldopa Chemical compound

3-O-Methyldopa (3-OMD) is one of the most important metabolites of L-DOPA, a drug used in the treatment of the Parkinson's disease.

<span class="mw-page-title-main">Opicapone</span> Chemical compound

Opicapone, sold under the brand name Ongentys, is a medication which is administered together with levodopa in people with Parkinson's disease. Opicapone is a catechol-O-methyltransferase (COMT) inhibitor.

Parkinson's disease (PD), the second most common neurodegenerative disease after Alzheimer's disease, affects 1% of people over 60 years of age. In the past three decades, the number of PD cases has doubled globally from 2.5 million in 1990 to 6.1 million in 2016. As of 2022, there are ~10 million PD cases globally. In the United States, the estimated prevalence of PD by 2030 is estimated will be ~1.24 million. These numbers are expected to increase as life expectancy and the age of the general population increase. PD is considered to be a multisystem and multifactorial disease, where many factors, such as the environment, gut, lifestyle and genetics, play a significant role in the onset and progression of the disease.

References

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  2. ↑ Tanner CM (2010). “Advances in environmental epidemiology”. Movement Disorders25(1). S58-S62.
  3. ↑ Tanner CM, Ottman R, Goldman SM, et al. (1999). “Parkinson's disease in twins: an etiological study”. JAMA28(1) 341-346.
  4. ↑ Taulous A, Sullivan A (2008). “Progress in Parkinson's Disease—Where Do We Stand?” Progress in Neurobiology85. 376-392.
  5. ↑ Ames BN, Cathcart R, Schwiers E, et al. (1981). “Uric acid provides an antioxidant defense in humans against oxidant-and radical- caused aging and cancer: a hypothesis”. Proc Natl Academy Sciences USA78. 6858-62.
  6. ↑ Ph.D, Rebecca Gilbert, MD (2021-05-04). "MIND & Mediterranean Diets for Parkinson's Disease | APDA". American Parkinson Disease Association. Retrieved 2024-04-02.{{cite web}}: CS1 maint: multiple names: authors list (link)
  7. ↑ Joshipura KJ, Hu FB, Manson JE, et al. (2001). “The effect of fruit and vegetable intake on risk for coronary heart disease”. Ann Intern Med134. 1106-1114.
  8. ↑ "Fruit Compound May Have Potential to Prevent and Treat Parkinson's Disease, Mouse Study Suggests". www.hopkinsmedicine.org. Retrieved 2024-04-13.
  9. 1 2 Ph.D, Rebecca Gilbert, MD (2019-04-22). "Avoiding Foods & Supplements for Parkinson's disease | APDA". American Parkinson Disease Association. Retrieved 2024-04-02.{{cite web}}: CS1 maint: multiple names: authors list (link)
  10. ↑ Logroscino G, Marder K, Cote L, Tang MX, Shea S, Mayeux R (1996). “Dietary lipids and antioxidants in Parkinson's disease: a population-based, case-control study” Ann Neuro39. 89–94
  11. ↑ Gao X, Chen H, Choi HK, Curhan G, Schwarschild M, Ascherio A (2007). “Diet, Urate, and Parkinson's Disease Risk in Men”. American Journal of Epidemiology167(7). 831–838.
  12. ↑ Barichella M, Cereda E, Pezzoli G (October 2009). "Major nutritional issues in the management of Parkinson's disease". Mov. Disord. 24(13): 1881–92.
  13. ↑ Berry EM, Growdon JH, Wurtman JJ, Caballero B, Wurtman RJ (1991). "A balanced carbohydrate protein diet in the management of Parkinson's disease" Neurology41(8). 1295.
  14. ↑ Bronstein JM, Tagliati M, Alterman RL, et al. (February 2011). "Deep brain stimulation for Parkinson disease: an expert consensus and review of key issues". Arch. Neurol.68(2): 165.
  15. ↑ Pincus JH, Barry KM (1987). "Plasma levels of amino acids correlate with motor fluctuations in parkinsonism". Arch Neurol44:1006-9.
  16. ↑ Berry EM, Growdon JH, Wurtman JJ, Caballero B, Wurtman RJ (1991). "A balanced carbohydrate: protein diet in the management of Parkinson's disease". Neurology411295-7.
  17. ↑ The National Collaborating Centre for Chronic Conditions, ed. (2006). "Symptomatic pharmacological therapy in Parkinson's disease". Parkinson's Disease. London: Royal College of Physicians. pp. 59–100. ISBN   1-86016-283-5.
  18. ↑ Leader G, Leader L, Findley L (January 2006). "Parkinson's Disease: Reducing Symptoms with Nutrition and Drugs". Denor Press. London, England.
  19. ↑ Marczewska A, De Notaris R, Sieri S, Barichella M, Fusconi E, Pezzoli G (August 2006). “Protein intake in Parkinsonian patients using the EPIC food frequency questionnaire”. Movement Disorder21(8). 1229-31.
  20. ↑ "Parkinson's Disease and Eating Right: Tips to Stay Healthy".
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