Diet’s Role in Parkinson’s Disease
By Jamie Santa Cruz
Today’s Dietitian
Vol. 25 No. 7 P. 32

Evidence suggests key nutrients and dietary patterns may help prevent or lessen signs and symptoms.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that causes unintended or uncontrollable movements. It’s the second-most common neurodegenerative disease after Alzheimer’s. Nearly 1 million people in the United States currently live with the disease, but that number is expected to grow to 1.2 million by 2030.1 What’s more, large numbers of older adults experience Parkinsonian signs (ie, motor symptoms similar to PD), although they haven’t been diagnosed with PD.

Scientists don’t yet know what causes the disease, and while there’s no known cure, diet is emerging as a modifiable risk factor that can slow disease progression and improve symptoms for people who have it.

What Is PD?
The hallmark of PD is the accumulation of abnormal alpha-synuclein neural proteins in the brain that damage dopamine-producing cells. Dopamine is a neurotransmitter that’s essential in movement control, and the loss of dopamine causes the distinctive motor symptoms characteristic of PD.

Although PD symptoms can vary greatly from one person to the next, common motor symptoms include slowness of movement, stiffness, decreased flexibility, tremors, and trouble with balance and coordination. Patients with PD also frequently experience nonmotor symptoms, such as mood changes, cognitive impairments, sleep disturbances, constipation, and difficulties with speech and swallowing.

Role of Diet
There are several avenues through which diet may affect the course of PD, including the following:

• Antioxidant and inflammatory effects: PD is associated with oxidative stress and inflammation, which contribute to the degeneration of dopamine-producing cells. It’s thought that a diet high in antioxidants and anti-inflammatory foods may help protect against this damage to neural cells, slowing disease progression.

• Drug interactions: Levodopa is the main medication used to manage PD, but diet can affect its absorption. In particular, protein-rich foods can be problematic because large neutral amino acids compete with levodopa for the same transporters to cross the gut and enter the brain. Emily Knight, MS, RD, a PhD student in the department of nutritional sciences at Auburn University in Auburn, Alabama, says, “Imagine you have a large group that’s all trying to get into a house but there’s only one door.”

• Alteration of the gut microbiome: As noted above, PD is characterized by the accumulation of abnormal alpha-synuclein neural proteins in the brain. Some evidence suggests these proteins may originate in the gut (as a result of gut dysbiosis) and then migrate to the brain via the vagus nerve.2 Thus, resolving dysbiosis in the gut could, in theory, impact the course of PD. In addition, certain gut microbiota are capable of producing or metabolizing dopamine, so alterations to the gut microbiome also could impact dopamine levels in the brain, influencing motor symptoms of PD via this avenue.3 According to Tracy Lister, DCN, MHS, RD, a functional nutritionist in private practice in Parksville, British Columbia, Canada, research into the gut-brain connection and how diet can impact the brain via the microbiome is currently one of the most promising areas of research on PD. “We’re always thinking about the brain, levodopa, producing dopamine, but we’re not thinking about the gut, and we should be, because it produces dopamine. But if there’s intestinal permeability or dysbiosis, that mechanism is altered.”

There’s now substantial evidence that diet in midlife significantly affects the risk of developing PD. Epidemiologic research shows that a diet high in dairy, meat, refined pastries, and fried food is linked to increased risk of developing the disease, whereas a diet high in fresh fruits and vegetables, whole grains, legumes, nuts, and seeds is associated with lower risk.4

So far, there’s less research available about how diet affects the progression of PD once the disease process is underway. However, early evidence suggests that dietary interventions indeed can have an impact. The research so far seems to suggest that an overall dietary pattern may have a more significant effect on PD progression than individual foods or nutrients. Here’s what dietitians need to know about the impact of individual nutrients and overall dietary patterns.

Impact of Foods and Nutrients

A 2020 meta-analysis found that caffeine intake is linked to slower disease progression among individuals with PD.5 Another review article published the same year came to a similar conclusion, arguing that caffeine appears to protect against the degeneration of dopamine cells and that it has benefits for motor and cognitive function in PD.6

However, the evidence isn’t uniform. A large multicenter clinical trial of a caffeine intervention in patients with PD found that caffeine intake didn’t produce any clinically significant improvements in motor function.7 Although there appears to be a clear correlation between caffeine intake and PD progression, some researchers have suggested that the relationship may not be causal. It may be that people who are predisposed to PD are less likely to consume caffeine, rather than caffeine having a protective effect.8 It’s also possible that the impact of caffeine on PD is affected by genes.9 The theory, according to Lister, is that some people have a genetic mutation that impacts the metabolism of caffeine, and for them, caffeine is aversive to their health. For those who can metabolize caffeine, on the other hand, the antioxidants have health benefits.

Currently, the main treatment for PD is levodopa, which is the precursor to dopamine. 10 Several varieties of beans contain levodopa, suggesting that consumption of beans could help improve PD symptoms. Two varieties of beans that have received attention for their potential benefits in PD are fava beans (vicia faba), which contain 0.5% levodopa, and velvet beans (mucuna pruriens), which contain the highest levodopa concentration of any bean—up to 6% levodopa when the beans are dried and roasted.8

Unfortunately, with respect to fava beans, the clinical evidence supporting a benefit for PD symptoms is limited to anecdotal reports; no rigorous studies have examined their utility for treating PD.8 On the other hand, the evidence is more promising with respect to velvet beans. In fact, a velvet bean extract preparation currently is approved for the treatment of PD in India.8

One consideration regarding the value of naturally occurring levodopa in beans is that levodopa can’t be given as a standalone medication. “In pharmaceutical preparations, levodopa has to be combined always with an enzyme-inhibitor to prevent the breakdown of levodopa in the blood,” says Michel Rijntjes, MD, a professor of neurology at the University of Freiburg in Germany. According to Rijntjes, some reports suggest that certain components in velvet beans may work similarly to the enzyme inhibitors in pharmaceutical levodopa, but additional evidence is needed. “This would be very interesting, because it may better explain the effect of [velvet beans] and also lead to new pharmaceutical products,” Rijntjes says.

Coenzyme Q10, Vitamin D, and Other Antioxidants
Coenzyme Q10 is a powerful antioxidant, and supplementation with this nutrient initially was thought to hold great promise for staving off damage to dopamine-producing cells in PD. In fact, animal studies and early human trials supported its benefits for PD.11 Unfortunately, larger, more recent studies tell a different story.12 A large multicenter, randomized, double-blinded, placebo-controlled clinical trial found that supplementation with coenzyme Q10 didn’t affect PD progression.13 Similarly, a meta-analysis of randomized controlled trials found no evidence that coenzyme Q10 impacts motor symptoms of PD.14

Another antioxidant that’s received attention in PD is vitamin D. Several studies have shown that low serum levels of this vitamin are linked with PD progression. However, the nature of the link is unclear. It’s possible that low vitamin D spurs PD progression, but it’s also possible that as PD progresses, individuals with the disease spend more time inside and get less exposure to sunshine, so their vitamin D levels fall.15 Two small clinical trials have examined vitamin D supplementation to determine whether it can slow disease progression, but the results of these trials were conflicting. Thus, it’s not yet clear whether vitamin D supplementation impacts PD progression—and if it does, at what dose.15

One point of note is that dietary intake of antioxidants may have different effects than supplementation. A 2022 longitudinal study of 682 participants found that intake of dietary sources of vitamin E and vitamin C are linked to slower progression of Parkinsonian signs.16 However, lead study author Puja Agarwal, PhD, an assistant professor of nutrition and nutritional epidemiology at the Rush Alzheimer’s Disease Center at Rush University in Chicago, says, “What we found was that the association of vitamin E and vitamin C with slower progression of Parkinsonian signs was significant only when these nutrients were coming from a dietary source, not from supplements.”

Multiple studies have observed that the gut microbiota of healthy adults differs from the gut microbiota of people with PD.17,18 There’s also increasing awareness that the gut microbiome appears to play a significant role in the pathology of PD. Therefore, there’s growing interest in the potential of probiotics to influence symptoms of the disease as well as the disease course.

Multiple human trials have found that probiotic supplementation can help relieve constipation in PD (constipation is a very common symptom of the disease and underscores the involvement of the gut in the disease pathology).19 Thus far, there’s limited evidence about the effect of probiotics on other aspects of the disease, such as motor symptoms or cognitive function. However, several studies in animal models of PD suggest that probiotics stave off the loss of dopamine-producing neurons and also reduce motor impairments.20 In addition, one small randomized, double-blinded, placebo-controlled human trial by Iranian researchers found that a multistrain probiotic administered over the course of 12 weeks resulted in improved motor function in patients with PD.21 A 2023 meta-analysis found that probiotics can significantly improve motor symptoms as well as gastrointestinal, anxiety, and depressive symptoms in people with PD. That said, the researchers note that the quality of the evidence was low or very low and that further research is needed in larger trials.22

Dietary Patterns and PD
To date, much of the research on individual nutrients and their potential as treatments for PD has proven inconclusive. Some researchers have suggested that it’s more promising to examine the impact of holistic diets rather than individual nutrients. Here’s what research shows thus far:

Protein-Restricted Diet
As noted previously, protein consumption can impact absorption of levodopa, the primary treatment for PD. For this reason, individuals with PD are sometimes encouraged to follow a protein-restricted diet.

In an observational study of 600 people with PD and 600 controls, Italian researchers found that people with PD who had greater adherence to a protein-restricted diet received lower levodopa doses and had fewer fluctuations in motor symptoms than those with lower adherence to a protein-restricted diet. The same study also found that increased intake of protein (10 g per day over the RDA recommendation) was directly linked to increased levodopa usage.23

However, there’s a caveat: Any diet that restricts intake of certain foods can promote weight loss, which is already a significant concern in PD. Furthermore, only 6% of patients with PD have protein interactions with levodopa, meaning that protein consumption can hinder levodopa absorption.24 According to Knight, this means that protein restriction shouldn’t be recommended to the majority of people with PD. “If they aren’t experiencing protein interactions with levodopa, you would be putting them at risk of malnutrition,” she says.

Mediterranean Diet
A Mediterranean dietary pattern has been associated with reduced risk of various diseases, including neurodegenerative diseases like Alzheimer’s.25 Although the specific definition of the diet varies from study to study, the Mediterranean diet generally means a diet rich in fruits, vegetables, legumes, cereals, nuts, fish, and monounsaturated fatty acids. The diet incorporates moderate alcohol intake but low intake of dairy products and red meats.26

A range of large observational studies have looked at the impact of the Mediterranean diet on PD risk, and most—though not all—have found its link with reduced risk and/or later age of onset.27 By contrast, only a few studies have examined the impact of the Mediterranean diet on PD progression, and those appear promising.

A 2017 cross-sectional study of 1,053 people with self-reported PD looked at the relationship between dietary pattern and disease severity. The study found that greater consumption of coconut oil, fish, fresh fruit, fresh vegetables, nuts, olive oil, spices, and wine were all linked to reduced PD severity. Meanwhile, consumption of beef, canned fruit, canned vegetables, cheese, yogurt, ice cream, fried food, and diet soda were all associated with increased severity. The authors note that the foods linked to lower severity largely constitute the Mediterranean diet and suggest that this diet might slow PD progression.28

Two large observational studies have found that the Mediterranean diet was associated with a slower rate of progression of Parkinsonian signs in older adults.4,29 In addition, two small randomized clinical trials of patients with PD in Iran also found a benefit of following the Mediterranean diet.30,31 The first study found that participants following the Mediterranean diet had significantly better cognitive function at the end of the intervention than those in the control group. The other study found that participants following the Mediterranean diet had lower disease severity. More research is needed to confirm these benefits, but the evidence to date is encouraging.

The MIND Diet
The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet is a combination of the Mediterranean and DASH diets into a single diet that’s specifically targeted to promote brain health. Like both of the diets from which it draws, the MIND diet is a plant-based eating pattern, but its uniqueness is that it places a special emphasis on consumption of green leafy vegetables and berries.32 “Both of these food groups are very rich in different antioxidant nutrients, including phytonutrients like flavonoids, which help lower oxidative stress and inflammation,” Agarwal says.

To date, just two studies have examined the impact of the MIND diet on progression of Parkinsonian signs, but both have been positive. In 2018, Agarwal’s research team looked at a sample of more than 700 older adults and found that adherence to the MIND diet was associated with a reduced risk of developing Parkinsonian signs as well as a slower rate of progression of those signs.30 Separately, a 2022 observational study of 1,205 adults also found that the MIND diet was linked to a reduced likelihood of developing Parkinsonian signs and a slower rate of progression.29 (Note that in both studies, the researchers were investigating signs of Parkinson’s, not diagnosed Parkinson’s per se.)

Significantly, both of these studies examining the impact of the MIND diet compared the MIND diet with the Mediterranean diet. The two diets were linked with slower progression of Parkinsonian signs, but in both studies, the benefit of the MIND diet was greater than the Mediterranean diet. There are limitations to studies of overall dietary patterns because it’s difficult to control for confounding factors; however, the existing research is promising.

Takeaways for Dietitians
The research on how diet impacts the progression of PD and the severity of symptoms is still early, which means dietitians should refrain from making recommendations to clients and patients. “The evidence supports that there’s a potential for a healthy dietary pattern to reduce PD severity,”27 Knight says. “But evidence isn’t strong enough to recommend a particular dietary pattern.”

Lister agrees with the need for caution. For most dietary interventions, she says, the evidence is still a “mishmash” as to how they impact PD. Nevertheless, Lister’s main message to dietitians is a hopeful one because diet represents a promising strategy for managing a disease that’s currently very burdensome. “I really want dietitians to be aware that we can do something for this population of patients,” she says.

— Jamie Santa Cruz is a writer based in Parker, Colorado.


1. Who has Parkinson's? Parkinson’s Foundation website. Accessed May 29, 2023.

2. Fitzgerald E, Murphy S, Martinson HA. Alpha-synuclein pathology and the role of the microbiota in Parkinson's disease. Front Neurosci. 2019;13:369.

3. Hamamah S, Aghazarian A, Nazaryan A, Hajnal A, Covasa M. Role of microbiota-gut-brain axis in regulating dopaminergic signaling. Biomedicines. 2022;10(2):436.

4. Fox DJ, Park SJ, Mischley LK. Comparison of associations between MIND and Mediterranean diet scores with patient-reported outcomes in Parkinson's disease. Nutrients. 2022;14(23):5185.

5. Hong CT, Chan L, Bai CH. The effect of caffeine on the risk and progression of Parkinson's disease: a meta-analysis. Nutrients. 2020;12(6):1860.

6. Ren X, Chen JF. Caffeine and Parkinson's disease: multiple benefits and emerging mechanisms. Front Neurosci. 2020;14:602697.

7. Postuma RB, Anang J, Pelletier A, et al. Caffeine as symptomatic treatment for Parkinson disease (Café-PD): a randomized trial. Neurology. 2017;89(17):1795-1803.

8. Rijntjes M. Knowing your beans in Parkinson's disease: a critical assessment of current knowledge about different beans and their compounds in the treatment of Parkinson's disease and in animal models. Parkinsons Dis. 2019;2019:1349509.

9. Mahdavi S, Palatini P, El-Sohemy A. CYP1A2 genetic variation, coffee intake, and kidney dysfunction. JAMA Netw Open. 2023;6(1):e2247868.

10. Drugs and supplements carbidopa and levodopa (oral route). Mayo Clinic website. Updated February 1, 2023. Accessed May 29, 2023.

11. Seet RC, Lim EC, Tan JJ, et al. Does high-dose coenzyme Q10 improve oxidative damage and clinical outcomes in Parkinson's disease? Antioxid Redox Signal. 2014;21(2):211-217.

12. Rauchová H. Coenzyme Q10 effects in neurological diseases. Physiol Res. 2021;70(Suppl4):S683-S714.

13. Parkinson Study Group QE3 Investigators, Beal MF, Oakes D, et al. A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. JAMA Neurol. 2014;71(5):543-552.

14. Zhu ZG, Sun MX, Zhang WL, Wang WW, Jin YM, Xie CL. The efficacy and safety of coenzyme Q10 in Parkinson's disease: a meta-analysis of randomized controlled trials. Neurol Sci. 2017;38(2):215-224.

15. Fullard ME, Duda JE. A review of the relationship between vitamin D and Parkinson disease symptoms. Front Neurol. 2020;11:454.

16. Agarwal P, Wang Y, Buchman AS, Holland TM, Bennett DA, Morris MC. Dietary antioxidants associated with slower progression of parkinsonian signs in older adults. Nutr Neurosci. 2022;25(3):550-557.

17. Nuzum ND, Loughman A, Szymlek-Gay EA, Hendy A, Teo WP, Macpherson H. Gut microbiota differences between healthy older adults and individuals with Parkinson's disease: a systematic review. Neurosci Biobehav Rev. 2020;112:227-241.

18. Zhang F, Yue L, Fang X, et al. Altered gut microbiota in Parkinson's disease patients/healthy spouses and its association with clinical features. Parkinsonism Relat Disord. 2020;81:84-88.

19. Tan AH, Hor JW, Chong CW, Lim SY. Probiotics for Parkinson's disease: current evidence and future directions. JGH Open. 2020;5(4):414-419.

20. Leta V, Ray Chaudhuri K, Milner O, et al. Neurogenic and anti-inflammatory effects of probiotics in Parkinson's disease: a systematic review of preclinical and clinical evidence. Brain Behav Immun. 2021;98:59-73.

21. Tamtaji OR, Taghizadeh M, Daneshvar Kakhaki R, et al. Clinical and metabolic response to probiotic administration in people with Parkinson's disease: a randomized, double-blind, placebo-controlled trial. Clin Nutr. 2019;38(3):1031-1035.

22. Chu C, Yu L, Li Y, et al. Meta-analysis of randomized controlled trials of the effects of probiotics in Parkinson's disease. Food Funct. 2023;14(8):3406-3422.

23. Barichella M, Cereda E, Cassani E, et al. Dietary habits and neurological features of Parkinson’s disease patients: implications for practice. Clin Nutr. 2017;36:1054-1061.

24. Virmani T, Tazan S, Mazzoni P, Ford B, Greene PE. Motor fluctuations due to interaction between dietary protein and levodopa in Parkinson's disease. J Clin Mov Disord. 2016;3:8.

25. Van de Rest O, Berendsen AA, Haveman-Nies A, de Groot LC. Dietary patterns, cognitive decline, and dementia: a systematic review. Adv Nutr. 2015;6(2):154-168.

26. Davis C, Bryan J, Hodgson J, Murphy K. Definition of the Mediterranean diet; a literature review. Nutrients. 2015;7(11):9139-9153.

27. Knight E, Geetha T, Burnett D, Babu JR. The role of diet and dietary patterns in Parkinson's disease. Nutrients. 2022;14(21):4472.

28. Mischley LK, Lau RC, Bennett RD. Role of diet and nutritional supplements in Parkinson's disease progression. Oxid Med Cell Longev. 2017;2017:6405278.

29. Agarwal P, Wang Y, Buchman AS, Holland TM, Bennett DA, Morris MC. MIND diet associated with reduced incidence and delayed progression of ParkinsonismA in old age. J Nutr Health Aging. 2018;22(10):1211-1215.

30. Paknahad Z, Sheklabadi E, Derakhshan Y, Bagherniya M, Chitsaz A. The effect of the Mediterranean diet on cognitive function in patients with Parkinson's disease: a randomized clinical controlled trial. Complement Ther Med. 2020;50:102366.

31. Paknahad Z, Sheklabadi E, Moravejolahkami AR, Chitsaz A, Hassanzadeh A. The effects of Mediterranean diet on severity of disease and serum total antioxidant capacity (TAC) in patients with Parkinson's disease: a single center, randomized controlled trial. Nutr Neurosci. 2022;25(2):313-320.

32. Morris MC, Tangney CC, Wang Y, et al. MIND diet slows cognitive decline with aging. Alzheimers Dement. 2015;11(9):1015-1022.