Introduction
While many significant health problems, including heart disease, cancer, type 2 diabetes, and hypertension, can be prevented and reversed by plant nutrition and lifestyle change, degenerative neurological diseases are typically viewed as incurable, somewhat hopeless conditions that can barely be managed. The good news is that medical management combined with plant-exclusive nutrition, without added salt, oil and sugar, can significantly decrease the risk, the intensity of symptoms, and the progression of neurodegenerative diseases – including Parkinson’s Disease (PD).
In this article by Dr Frank Sabatino – The CMA’s Science and Research Director, we hope to inspire and empower our readers with the knowledge that a whole-plant diet really can make a difference in preventing the progression – or even the development – of this devastating condition. We are indebted to Dr Sabatino – and the National Health Association who will be publishing a version of this article very soon.
Parkinson’s disease is the second most prevalent neurodegenerative disease, behind Alzheimer’s disease, affecting over 10 million people, including 2-3% of people over the age of 65 worldwide. (1) It is a complex condition associated with a number of classic movement (motor) dysfunctions as well as other physiological and cognitive disturbances.
Even your simplest physical movements require a fine orchestration of multiple brain areas to fashion the activities of daily living into smooth flowing “kinetic melodies”. Think about sitting down for dinner and deciding to use a fork to pick up food from your plate. Your intention activates the firing of brain cells in your highest brain center (cerebral cortex) that signal muscles to extend your arm to reach for your fork, contract your fingers to grab the fork, flex your arm to bring the fork to your mouth and then extend the arm to bring the fork back to your plate. There also has to be an inhibition of any neuromuscular activity that would interfere with the smooth operation of your intended action. Near the middle part of your brain, there are a set of interconnected structures referred to as the basal ganglia that help different parts of the brain work together and manage the signals that promote the smooth operation of routine muscular movement.
Symptoms and evaluation of Parkinson’s Disease
In PD, there is damage and death of nerve cells (neurons) in an important part of the basal ganglia called the substantia nigra pars compacta (SN). The SN is a midbrain community of nerve cells that produce the neurotransmitter dopamine and communicate with an area called the striatum to modulate the intentionality and activity of smooth precise muscular movement. Typically, when the diagnosis of PD is made, there can be more than a 50-60% loss of dopamine containing neurons in the SN. (2) As a result of this loss of brain cells and dopamine, PD may foster early neurological disturbances that include loss of smell, drooling, sleeping problems, constipation, orthostatic hypotension, depression, and trouble thinking and focusing. Most commonly, PD manifests significant disturbances of muscular activity and control including: slow movement (bradykinesia), tremors of muscles at rest, rigidity and stiffness that is constant and unchanging (lead-pipe rigidity) or jerky like a ticking second hand on a mechanical clock (cogwheel stiffness), unstable gait, hunched over posture and stooped stance, short shuffling stride when walking, blinking less, cramped small handwriting, decreased facial expression, difficulty swallowing, and soft speaking voice.
The standard tool for classifying and evaluating the impact of PD is the Unified Parkinson’s Disease Rating Scale (UPDRS). This tool evaluates how PD affects your quality of life related to non-motor conditions including depression, anxiety, bowel function, urinary incontinence as well as all the aforementioned movement difficulties associated with your activities of daily living and the frequency and duration of your symptoms.
Causes and effects of Parkinson’s Disease
The cause(s) of PD are basically unknown. However, routine nutritional choices may play a significant role in the etiology of PD. The excesses and nutritional deficiencies of animal-based, processed food diets often compromise protein utilization, transport and function, lack fiber and critical antioxidants/nutrients, interfere with neurotransmitter production and produce a variety of toxic by-products. As a result, an excess of animal products and lack of whole plant foods may promote the chronic brain inflammation and oxidative stress that destroys neurons in the SN, and other brain areas, decrease production and availability of dopamine, and significantly increase the risk and progression of PD.
In the neurons of the SN, the essential amino acid tyrosine is converted by the enzyme tyrosine hydroxylase to levodopa (L-3,4-dihydroxyphenylalanine) which is then converted to dopamine. The brain modulates the amount of dopamine with the enzyme monoamine oxidase (MAO) that breaks down dopamine. Since there is a deficiency of dopamine in PD, it is crucial for the brain to increase dopamine by maximizing the availability of tyrosine and levodopa, supporting the converting enzymes that produce dopamine, reducing the activity of MAO, and decreasing the damage/death of brain cells in the SN.
The typical standard of medical care is to treat PD with levodopa that can be converted to dopamine in the brain. However, levodopa can be converted to dopamine in the body that is not able to enter the brain. So, levodopa is often combined with the drug carbidopa that blocks the body conversion of levodopa making levodopa available for the brain. (2) And since the brain also blocks the entry of carbidopa, this drug can not interfere with the conversion of levodopa in the brain. In addition, a class of drugs called MAO inhibitors are often prescribed to block MAO from breaking down dopamine, so more is available in the brain. As PD progresses, the frequency of levodopa use often needs to be increased to deal with the increase and fluctuation of PD symptoms and may lead to decreased effectiveness of the drug and potential toxic effects.
When a person with PD ingests levodopa and protein, the essential amino acid tyrosine in beans, nuts, seeds, and other plant foods, as well as the levodopa, are absorbed from the intestine into the bloodstream and carried to the brain via a transport protein called the 1-type amino acid transporter. In PD, it is crucial to get the most efficient transport of tyrosine into the brain where it can be converted into dopamine. However, if you consume large amounts of protein, especially at the same time that you take levodopa, other amino acids can compete with tyrosine and levodopa on the transporter and potentially interfere with their access to the brain. This is of special concern when you consider the high protein intake of many people on conventional animal-based diets.
The recommended dietary allowance for protein is .36-.40 grams of protein per pound of body weight depending on gender and age, which translates to approximately 36-80 grams for people between 100 and 200 pounds. However, 40-60 grams is more than adequate to meet the demands of the body and is provided perfectly by a plant-exclusive diet. Unfortunately, many people in industrialised nations are obsessed with high protein animal-based diets, often consuming more than a 100 grams of animal protein a day, potentially decreasing tyrosine availability in the brain and promoting subsequent dopamine deficiency in the SN. Decreasing protein intake to 50 grams a day in PD patients produced a 50% improvement in motor performance. (3) In a Brazilian study, reduction of red meat consumption, showed a 50% improvement in motor skills in 5 months and a 60% improvement in 6 months. (4)
In addition, the modification of a specific protein, alpha-synuclein protein is common in PD. Proteins are complex chains of amino acids that fold and vibrate at certain frequencies to carry out their function. However, in PD the misfolding of alpha-synuclein causes clumps (Lewy bodies) in the memory and thinking areas of the brain. Lewy bodies contribute to a variant of cognitive decline called Lewy body dementia, which represents about 15% of all dementia cases. There are data to suggest that meat and animal products are an exogenous source of alpha-synuclein protein that may contribute to the aberrant aggregations of this protein in PD. (5)
Neuro-inflammation and brain damage
The body responds to tissue damage by initiating the protective process of inflammation. This inflammatory immune response promotes healing and survival. But if irritation continues day in and day out, exacerbated by dangerous excesses of processed oils, salt, animal protein, refined sugar, and toxic by-products of these excesses, inflammation can become more chronic and contribute to cellular damage and death in the brain.
Several factors associated with animal and processed foods may contribute to chronic neuroinflammation and brain damage of PD. Glycation refers to the chemical link between sugar molecules and proteins and fats that can alter the structure and function of proteins to produce advanced glycation end products (AGEs) associated with inflammation and aging. (6) AGEs can be produced in the body in the presence of high blood sugar and protein across time or they can be ingested preformed in foods loaded with processed oils, refined sugar, and animal and dairy products that are baked, broiled, and fried at high temperatures. Simply put, The AGE content of fresh fruits, vegetables, whole grains, and beans is 100-2000 times less than all meat, refined oils, and dairy products.
Several studies suggest that alpha-synuclein protein is prone to glycation (7) and that may lead to dangerous clumping, neurotoxicity, and the increase in Lewy body dementia in PD. (8)(9) The increase of AGEs increases receptors for AGEs in the brain (RAGE) that activate neuroinflammation and damage brain cells. The presence of RAGE in the midbrain may regulate neuroinflammation by activating supporting brain cells called microglia that increase inflammation in response to AGEs. (10) Therefore, the consistent reduction of glycation and AGEs with SOS-free plant exclusive nutrition may reduce the risk, severity and progression of PD.
In addition, the essential fatty acids, linoleic acid (LA, omega-6) and alpha-linolenic acid (ALA, omega-3), play a major role in modulating healthy inflammatory responses and brain health. Through a series of enzymes, LA is converted to arachidonic acid and then to compounds that promote inflammation, including prostaglandins, thromboxanes and leukotrienes. ALA is converted to longer chain polyunsaturated fatty acids(LC-PUFAs), EPA and DHA , that reduce inflammation. DHA is the most abundant LC-PUFA in the brain, making up 40% of the membranes of all brain cells. DHA is a precursor to a family of bio active metabolites that regulate neurite growth, inflammation and oxidative stress and reductions in DHA have been observed in patients with neurodegenerative and psychiatric disorders. (11)
As herbivore/frugivores, humans have the ability to produce LC-PUFAs (EPA and DHA) from the precursor essential fatty acid ALA provided by plant foods. It is in your best interest to allow the body to use the enzymatic conversion pathways to provide your EPA, DHA, and arachidonic acid rather than obtaining them as preformed compounds in fish, fish oil, algal oil, animal and dairy products. The argument that has been mounted against this approach is that less than 1% of ALA is converted to DHA in red blood cells, suggesting dangerous deficiencies that may compromise the integrity and function of brain cells and increase chronic inflammation.
However, even though blood conversion of ALA to DHA is low, there are data suggesting that this in body tissues is more than 47 times greater than in the blood (12) and is made available on demand for the brain “as needed” to prevent a buildup of DHA in the blood that can increase the production of risky LDL cholesterol, and promote dangerous atrial fibrillation of the heart . So consuming plant foods with the highest ALA content, including walnuts (just a few walnuts a day), hemp, chia and ground flax seeds, and legumes on a regular basis can reduce inflammation and support brain cells. The excessive consumption of meat and dairy products exaggerates preformed arachidonic acid that produces pro-inflammatory Prostaglandins E2 and D and may contribute to the progression of neuroinflammation. (13)
Keep in mind that the excessive saturated and trans-fats found in animal products and processed foods are some of the most inflammatory foods (14) and should be completely avoided for anyone with PD. On the other hand, fiber may be the biggest deficiency in the Western diet and is one of the most important anti-inflammatory components of any diet overall – providing essential prebiotic nutrition for the most healthy anti-inflammatory gut microbiota. Just adding 10 grams of fiber a day to the diet of Parkinson’s patients significantly improved motor function. (15)
Oxidative stress, toxins and plant protection
In the energy factories of all cells (mitochondria), glucose from plant foods, in the presence of the oxygen, is transformed into your essential energy reserves. However, during energy processing, highly reactive forms of oxygen (oxidants, or free radicals) are produced that promote all chronic diseases. You can also be assaulted by free radicals in pesticides/environmental toxins, animal and processed foods, alcohol and tobacco. The body protects itself with antioxidants it creates naturally or consumes from a diverse high antioxidant diet of fresh fruits and vegetables. When the level of free radicals overwhelms the body’s antioxidant protection, you create the dangerous condition of oxidative stress. Oxidative stress is considered to be an important underlying mechanism leading to the death of dopamine producing brain cells. (16) The rigidity and tremors of PD generate more free radicals making people with PD more susceptible to oxidative stress and damage.
Polyphenols are antioxidant compounds found in dark colored fruits and veggies. Flavonoids, the most abundant polyphenols, are found in a diverse assortment of plant foods including berries, beans, apples, oranges, kiwi, mangos, kale, onions, and leafy greens and significantly reduce oxidative stress. People consuming foods with the highest flavonoid content over a 20-year period decreased their risk of developing PD by 20-40%. (17) Foods rich in flavonoids suppress the oxidation of fats in brain cell membranes (lipid peroxidation) thereby reducing oxidative stress and potential cell death of dopamine-producing neurons. Elevated levels of oxidized fats have been discovered in the SN and in red blood cells of people with PD. Anthocyanins, in the dark red, purple and blue pigments in berries, beans and grapes decrease cell death of dopamine-containing neurons in the SN and alleviate the slow movement of PD. One cup of berries a day delayed PD related dementia by an average of 2 years. (17) Soy isoflavones have anti-oxidant and anti-inflammatory properties that enhance the ability of tyrosine hydroxylase to produce levodopa, and decrease the inflammatory activity of supporting neurons (microglia) to protect dopamine-producing brain cells. (18). Sesame seeds in tahini contain antioxidants sesamin and sesamolin that may promote the genetic expression of the enzyme that converts tyrosine to levodopa, and along with walnuts contains gamma-tocopherol Vitamin E which is the most brain protective, anti-oxidant form of this vitamin. (2)
The excessive consumption of animal products also increases dangerous concentrations of toxic compounds that may significantly increase the risk and progression of PD. The beta-carboline, harmane, is a heterocyclic amine found in cooked meat that is a potent tremor producing neurotoxin in PD with adverse effects on learning and memory. (19) The heme iron in the blood of animal meat is absorbed too quickly and causes a rapid elevation of iron that fosters oxidative stress and lipid peroxidation that can damage cells, mitochondria and DNA. This rapid increase in iron levels causes the liver to release a chemical called hepcidin that slows down and blocks iron absorption causing it to build up in the digestive tract triggering toxic and carcinogenic effects.
Plant iron is bound to the antioxidant phytic acid (inositol hexaphosphate) that slows down iron absorption and inhibits the formation of iron mediated free radicals and oxidative stress. (20) The body safely controls the absorption of iron it needs by signaling the gut microbiota to cleave off phytic acid and release iron more slowly across time. This is especially important in PD because elevated iron deposits are more prevalent in the PD brain (21), and MRI studies have highlighted the imbalanced accumulation of iron in the SN (22) that is also associated with the generation of tremors (23). A direct relationship between iron deposits and misfolded alpha-synuclein has also been implicated in the progression of PD. (24)
There are also fat-soluble environmental toxins that accumulate in the fat tissue of animals and have a significant impact on the risk and progression of PD. Multiple studies suggest that consistent exposure to pesticides can damage dopamine producing neurons, and increase the risk and progression of PD. (25) The organochlorine PCB, in the dye of fish feed that colors fish-farmed salmon pink to resemble wild salmon, is found in fish but also other foods of animal origin including meat, cheese, eggs and dairy products. PCBs are neurotoxic and can damage brain cells, increase oxidative stress and even inhibit the action of the enzymes that convert tyrosine to levodopa and dopamine. Mercury contamination in fish is ubiquitous and extremely neurotoxic and may promote damage and death of brain cells in the SN. (2) There is also danger from indoor toxins – and you might find this article – of interest too: The Hidden Dangers of Indoor Toxins and How to Eliminate The Naturally.
It is important to note that as a result of difficulty swallowing, loss of appetite and the increased energy needed to maintain the tight, rigid muscles of PD, 52-65% of people with PD demonstrate significant weight loss and are appreciably underweight within one year of PD diagnosis. (26) This research indicated that in over 40% of underweight PD patients the mechanism for this condition was mediated by 5 different genera of organisms in the microbiome that increased the pro-inflammatory state, decreased the production of short chain fatty acids that help regulate appetite and satiety, and disturbed metabolism.(26) These weight changes are associated with an increased risk of dependency, dementia and death, requiring help with the activities of daily living. (27)
Lifestyle Interventions – Including Nutritional Change Point to an Optimistic Outlook
PD is a relentless condition of brain cell death and dopamine deficiency that cannot typically be reversed. However, there is hope in food choices that will optimize the function of the remaining dopamine containing brain cells. By combining dopamine enhancing medication and a diverse, organic, plant-exclusive, SOS-free diet, containing high fiber to support the healthiest microbiota, moderate protein, more calorie dense nuts, seeds, avocados and starches, a rainbow of fruits and vegetables, whole grains, beans, herbs and spices, you may reduce the symptoms and progression of PD, and potentially enhance motor function, performance, and quality of life.
This article has kindly been supplied by Dr Frank Sabatino – The CMA’s Science and Research Director. Please see his website for more outstanding in-depth articles on a wide variety of health topics. DrFrankSabatino.com
References
1. Pajares et al. Inflammation in Parkinson’s Disease: mechanisms and therapeutic implications. Cells 2020, July 14; 9(7): 1687.
2. Blake. Parkinson’s Disease: Dietary Regulation of Dopamine. Lifelong Press, Second Edition, 2017 (ebook @ Dr SteveBlake.com).
3. Baroni et al. Pilot dietary study with normoproteic protein-redistributed plant-food diet and motor performance in patients with Parkinson’s disease. Nutritional Neuroscience 2011 Vol. 14 No.1.
4. Riley et al. Practical application of a low-protein diet for Parkinson’s disease. Neurology 1988; 38:1026-31
5. Killinger and Labrie. Vertebrate food products as a potential source of prion-like alpha-synuclein. npj Parkinson’s Disease 2017, 3;33.
6. Reddy et al. Advanced glycation end products in health and disease. Microorganisms 2022; 10(9):1848.
7. Iannuzzi et al. Differential effects of glycation on protein aggregation and amyloid formation. Front Mol Biosci. 2014; 1:9.
8. Munch et al. Crosslinking of alpha-synuclein by advanced glycation end products- an early pathophysiological step in Lewy body formation. Chem Neuro Anat. 2000; 20:253-257.
9. Vicente et al. Glycation potentiates alpha-synuclein associated neurodegeneration of synucleinopathies. Brain 2017;140:1399-1419.
10. Gelain et al. RAGE against the glycation machinein synucleiopathies: time to explore new questions. J Parkinson’s Dis. 2023; 13(5):717-728.
11. Brinley et al. Measuring brain docosahexaenoic acid turnover as a marker of metabolic consumption. Pharmacology and Therapeutics 2023, August; 248:108437.
12. Domenichiello et al. Is Docosahexaenoic acid synthesis from alpha-linolenic acid sufficient to supply the adult brain. Prog Lipid Res. 2015 JUL; 59:54-66.
13. Thomas et al. Dietary arachidonic acid increases deleterious effects of amyloid-beta oligomers on learning abilities and expression of AMPA receptors: putative role of ACSL4-cPLA2 balance. Alzheimer’s Research and Therapy 2017, 9,69.
14. Lopez-Garcia et al. Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. Nutr. 2005; 135:562-566.
15. Fernandez-Martinez et al. A randomized clinical trial to evaluate the effects of Plantago ovata husk in Parkinson’s patients: changes in levodopa pharmacokinetics and biochemical parameters. BMC Complementary and Alternative Medicine 2014; 14:296.
16. Hauser et al. Mitochondrial dysfunction and oxidative stress in Parkinson’s disease and monogenic parkinsonism. Neurobiology of Disease, 2013 march; 51:35-42.
17. Devore et al. Duetary intake of berries and flavonoids in relation to cognitive decline. Annals of Neurology, 2012 July; 72(1): 135-143.
18. Seidl et al. The emerging role of nutrition in Parkinson’s disease. Frontiers in Aging Neuroscience, 2014, March: Volume 6, Article 36.
19. Khan et al. Pharmacological and toxicological profile of harmane-beta carboline alkaloid: friend or foe. Curr Drug Metab. 2017; 18(9): 853-857.
21. Abeyawardhane and Lucas. Iron redox chemistry and implications in Parkinson’s disease brain. Oxidative Medicine and Cellular Longevity, 2019 Article ID 4609702, 11 pages.
21. Costa-Mallon et al. Brain iron concentration in regions of interest and relation with serum iron levels in Parkinson’s disease. Journal of Neurological Sciences, 2017; 378:38-44.
22. Lee and Lee. Brain iron accumulation in atypical parkinsonian syndromes: in vivo MRI evidence for distinctive patterns. Frontier in Neurology, 2017 Volume 10.
23. Homayoon et al. Nigral iron deposition in common tremor disorders. Movement Disorders 2019; 34(1): 129-132.
24. Hare et al. Iron and dopamine: toxic couple. Brain, 2016;139(4): 1026-1035.
25. Van der Mark et al. Is pesticide use related to Parkinson’s disease? Some clues to heterogeneity in study results. Environmental Health Perspectives, 2012; 120:340-347.
26. Shih et al. Unraveling the mechanisms of underweight in Parkinson;s disease by investigating into the role of gut micobiome. npj Parkinson’s Dis. 2024, 10 Article number: 28.
27. Cumming et al. Early weight loss in parkinsonism predicts poor outcomes: evidence from an incident cohort study. Neurology, 2017; 89: 2254-2261.