nutrients

Review
The Role of Diet and Dietary Patterns in Parkinson’s Disease
Emily Knight 1 , Thangiah Geetha 1,2 , Donna Burnett 1,2 and Jeganathan Ramesh Babu 1,2, *

1 Department of Nutritional Sciences, Auburn University, Auburn, AL 36849, USA

2 Boshell Metabolic Diseases and Diabetes Program, Auburn University, Auburn, AL 36849, USA
* Correspondence: [email protected]

Abstract: Parkinson’s Disease (PD) is a neurodegenerative disorder associated with diminished

nutrition status and decreased quality of life. While the prevalence of PD is expected to increase, no
preventative or curative therapy for PD exists at this time. Although nutrition and diet represent
modifiable risk factors for reducing chronic disease risk, research on the impact of single nutrients
on PD has yielded mixed results. As a result, this single-nutrient approach may be the driving
force behind the inconsistency, and a holistic dietary approach may overcome this inconsistency by
accounting for the interactions between nutrients. The following review aims to examine the impact
of a generally healthy dietary pattern, the protein-restricted diet (PRD), the ketogenic diet (KD),
the Mediterranean diet (MD), and the Mediterranean-DASH Intervention for Neurodegenerative
Delay (MIND) diet on PD risk, progression, and severity. While most of the included studies
support the role of diet and dietary patterns in reducing the risk of PD or alleviating PD severity, the
inconsistent results and need for further evidence necessitate more research being conducted before
making dietary recommendations. Research on the potential beneficial effects of dietary patterns on
PD should also investigate potential risks.

Keywords: Parkinson’s Disease; diet; dietary patterns; ketogenic diet; Mediterranean diet; MIND diet;
protein-restricted diet

Citation: Knight, E.; Geetha, T.;

Burnett, D.; Babu, J.R. The Role of
Diet and Dietary Patterns in 1. Introduction
Parkinson’s Disease. Nutrients 2022,
With 680,000 men and women ages 45 and older having Parkinson’s Disease (PD)
14, 4472. https://doi.org/10.3390/
in the United States (US) in 2010, PD is the second most prevalent neurodegenerative
nu14214472
disorder following Alzheimer’s Disease [1,2]. While the prevalence of PD correlates with
Academic Editor: Shigeki Furuya geographical region and biological sex, the most significant risk factor is increasing age [1–3].
Received: 6 October 2022
As the number of older adults increases in the US, PD cases will likely exceed 1.2 million by
Accepted: 21 October 2022
2030 [1]. First identified by James Parkinson [4] in 1817, PD is a disorder characterized by its
Published: 25 October 2022
cardinal motor symptoms of bradykinesia, postural instability, rigidity, and tremors, along
with the degeneration of dopaminergic neurons [5–8]. The histopathological hallmarks
Publisher’s Note: MDPI stays neutral
of PD—Lewy bodies and Lewy neurites—result from the intracellular aggregation of
with regard to jurisdictional claims in
α-synuclein [9–11]. In addition, PD includes non-motor symptoms, such as cognitive
published maps and institutional affil-
decline, constipation, depression, hyposmia, and urinary dysfunction [12–14].
iations.
Since several years may pass before neurodegeneration manifests the motor and non-
motor symptoms of PD, the International Parkinson, and Movement Disorder Society
(MDS) broke the definition of PD down into three categories: preclinical PD, prodromal PD,
Copyright: © 2022 by the authors.
and clinical PD [15–17]. These three categories differentiate individuals with PD-related
Licensee MDPI, Basel, Switzerland. neurodegeneration based on the presentation and the type of symptoms. For instance,
This article is an open access article prodromal PD denotes individuals with neurodegeneration between the presymptomatic
distributed under the terms and stage of preclinical PD and the diagnostic stage of clinical PD [16–20]. As a result, the three
conditions of the Creative Commons categories distinguish between PD cases based on progression, but other tools differentiate
Attribution (CC BY) license (https:// PD cases based on severity.
creativecommons.org/licenses/by/ Scientific research has primarily utilized two different tools for measuring PD severity.
4.0/). The first tool was developed by Hoehn & Yahr [21] in 1967. The scale comprises five stages

Nutrients 2022, 14, 4472. https://doi.org/10.3390/nu14214472 https://www.mdpi.com/journal/nutrients

Nutrients 2022, 14, 4472 2 of 20

for categorizing PD patients based on the degree of affected extremities and the severity
of an individual’s disability. The second tool, the Unified Parkinson’s Disease Rating
Scale (UPDRS), was revamped by the MDS in 2008 to create the MDS-UPDRS [22]. The
MDS-UPDRS has four parts: Non-Motor Experiences of Daily Living (Part I), Motor Expe-
riences of Daily Living (Part II), Motor Examination (Part III), and Motor Complications
(Part IV) [22,23]. As a result, the MDS-UPDRS allows for a more thorough examination of
PD severity than the UPDRS, based on the type of symptoms and the impact on activities
of daily living.
Since PD progression is linked to increased disability and caregiver burden, the severity
of PD has a notable impact on an afflicted individual’s quality of life [24–26]. Moreover, the
COVID-19 pandemic may have exacerbated the burden of PD. Recent research indicates
PD patients, regardless of COVID-19 infection history, experienced disrupted healthcare
provision, worsened symptoms, and decreased quality of life [27–29]. As a result, reducing
PD severity is becoming increasingly essential to improving the quality of life of individuals
with PD.
In addition to disease severity, the nutritional status of an individual with PD is directly
related to their quality of life [30–32]. A key indicator of nutrition status, malnutrition
looks past an individual’s body mass index (BMI) and focuses on body composition, energy
intake, and weight changes [33]. Furthermore, malnutrition is a concern for older adults due
to its association with increased healthcare costs, length of stay, mortality, and readmission
among hospitalized patients [34–36]. Notably, between 3 to 60% of individuals with PD
are at malnutrition risk [37]. While malnutrition is a critical measure of nutrition status, an
individual with PD’s motor and non-motor symptoms also influences nutrition status [38].
For instance, a three-year cohort study found a direct relationship between constipation
and body fat loss [39]. Additionally, researchers observed a direct relationship between
an individual’s risk of malnutrition and motor symptom severity [40,41]. Other nutrition-
related symptoms may include dementia, depression, dyskinesia, dysphagia, gastroparesis,
hyposmia, tremors, rigidity, and small bowel dysfunction [38,42–45]. As a result, both an
individual’s motor and non-motor symptoms may impact their nutrition status and quality
of life.
As PD’s exact etiology and pathophysiology remain unclear, researchers experience
difficulty in developing effective preventative and curative strategies. At this time, no
preventative or curative treatment for PD exists, but several pharmacological drugs may
alleviate PD symptoms. Currently, levodopa is the most common pharmacological inter-
vention for improving the motor symptoms of PD [46]. One approach to studying the
development of PD is to explore factors associated with increased PD risk. For instance,
several factors contribute to the risk of developing PD, including genetics, biological sex,
environmental exposures, and lifestyle [47–50]. As a result, modifiable risk factors serve as
potential targets for attenuating an individual’s risk.
Since nutrition and diet represent modifiable risk factors for other chronic diseases,
they are potential areas for reducing PD risk and slowing disease progression. A meta-
analysis observed that caffeine consumption typically from coffee is inversely related to PD
risk and progression [51]. Nevertheless, several studies examining dietary antioxidants—
polyphenols, carotenoids, vitamin A, vitamin C, and vitamin E—have yielded inconsistent
results [52–57]. Likewise, studies on the role of dietary fat in PD yielded mixed results [58].
Thus, several researchers have proposed that the single-nutrient approach used to examine
disease risk may be the driving force behind the inconsistency, arguing that a holistic
approach could account for the synergistic effect [59]. Therefore, this review examined the
impact of diet and dietary patterns on PD.

2. General Dietary Patterns

Dietary pattern is a broad term used to describe an individual or population’s intake
of dietary components over a certain period [60,61]. Over the years, research has supported
the role of a healthy dietary pattern in preventing or alleviating depression, dementia, and
Nutrients 2022, 14, 4472 3 of 20

neurodegeneration [62,63]. Articles were identified using PubMed and Google Scholar,
along with screening the reference sections of included articles. The studies included in this
review were published in or after 2011 to focus on recent research on the effect of dietary
patterns on PD, although older studies were identified in the published literature.

2.1. Defining a Healthy Dietary Pattern

A ‘healthy dietary pattern’ represents any dietary pattern scientifically linked to
reduced mortality and improved health outcomes. As a result, great variety exists in
defining a healthy dietary pattern. A broad range of scoring systems further complicates
the definition of a healthy dietary pattern. For example, the Alternative Healthy Eating
Index (AHEI) is a scoring system that assesses diet quality and adherence to the Dietary
Guidelines for Americans [64,65]. Another scoring system, the Dietary Inflammatory Index
(DII), measures an individual’s consumption of foods associated with inflammation [66].
Like other dietary indexes, the DII is associated with positive health outcomes, including a
reduced risk of cardiovascular disease [66]. Consequently, a healthy dietary pattern links
an eating style to a favorable health outcome.
While healthy dietary patterns generally focus on improving an individual’s overall
health, several dietary patterns are geared toward specific diseases, food groups, or the
timing of meals. First, dietary patterns may target the risk reduction of specific diseases
and conditions. For instance, the Dietary Approaches to Stop Hypertension (DASH) diet
is a dietary pattern characterized by the consumption of fruit, vegetables, and low-fat
dairy products and reduced intake of sodium, saturated fat, and cholesterol [67,68]. As its
name implies, the DASH diet represents a dietary pattern designed to assist individuals in
managing their blood pressure [67,68]. Second, dietary patterns may reflect the composition
of a meal. For example, vegetarian and vegan dietary patterns reflect the consumption of
plant-based foods and beverages instead of animal products [69,70]. Third, dietary patterns
may reflect the timing of meals. Time-restricted diets, like intermittent fasting, restrict
eating to specific time intervals during a day or week [71,72].

2.2. The Impact of General Dietary Patterns on PD

Previous research examined the relationship between PD and an individual’s dietary
intake of specific food groups. A cross-sectional study by Mischley et al. [73] evaluated the
dietary patterns of 1053 US men and women with idiopathic PD. Mischley et al. [73] found a
significant relationship between reduced PD severity and increased consumption of coconut
oil, fish, fresh fruit, fresh vegetables, nuts, olive oil, spices, and wine. Likewise, PD severity
decreased with the diminished consumption of beef, canned fruit, canned vegetables,
cheese, yogurt, ice cream, fried food, and diet soda [73]. As a result, Mischley et al. [73]
concluded that adherence to a plant-based diet with fish might slow the progression of
PD. While other studies support the role of increased vegetable consumption in reducing
PD risk, some studies have found that the type of dairy product consumed affects PD
risk [74–76]. Although Hughes et al. [75] observed increased dairy and milk intake to be
associated with an increased risk for PD, the authors noted that the type of dairy product
could impact PD risk. PD risk increased with an increased intake of low-fat dairy products
but decreased with an increased intake of high-fat dairy products [75]. While the exact
cause of this relationship is unknown, the relationship between dairy and PD risk may be
explained by its effect on serum urate levels (higher serum urate levels are associated with
a lower risk of PD). As a result, Hughes et al. [75] hypothesized that the protein found in
dairy products might decrease serum urate levels, while saturated fat may increase serum
urate levels. The reliance on patient-reported PD diagnosis and disease severity indicators
limits the generalizability of the study by Mischley et al. [73]. Additionally, the primary
author’s ownership of the tool used by patients to report outcomes related to PD severity,
the PRO-PD, increases the study’s risk of bias.
Additionally, examining specific food groups through factor analysis can describe
dietary patterns linked to disease risk. Okubo et al. [77] utilized factor analysis to examine
Nutrients 2022, 14, 4472 4 of 20

the dietary pattern of 249 PD cases and 368 controls recruited from eleven different hospitals
in Japan. Okubo et al. [77] identified three different dietary patterns (healthy, light meal,
and western) associated with PD risk. The healthy dietary pattern included increased intake
of vegetables, seafood, and tea with a low intake of alcohol [77]. The Western diet was rich
in beef, pork, chicken, vegetable oil, and salt. The light meal dietary pattern was rich in
bread, noodles, dairy products, fruit, soft drinks, and sugar [77]. Overall, Okubo et al. [77]
found that greater adherence to a healthy dietary pattern trended with a reduced risk
of PD among participants. Nevertheless, the study methodology (the inclusion of non-
matched controls and study questionnaires not validated for the study population) limits
the generalizability of the results [77]. While both Mischley et al. [73] and Okubo et al. [77]
examined specific food groups to characterize a dietary pattern associated with positive
PD outcomes, the studies lack comparability to studies examining adherence to previously
defined dietary patterns. Besides examining individual food groups, researchers examine
healthy dietary patterns in terms of diet quality. Molsberry et al. [78] measured diet quality
using the AHEI scoring system among 17,400 participants from the Nurses’ Health Study
and the Health Professionals Follow-up Study. Participants with greater AHEI scores
were less likely to develop symptoms of prodromal PD. In contrast to Molsberry et al. [78],
Sääksjärvi et al. [79] found no relationship between AHEI scores and risk of PD in a cohort of
4524 Finnish men and women. Out of the 4524 participants, 85 PD cases were recorded [79].
Sääksjärvi et al. [79] used a modified version of the AHEI due to the absence of data on
participant intake of multivitamin supplements and alcohol [79]. While the exclusion of
supplement and alcohol intake could account for the difference in the two studies’ results, a
large European cohort study by Peters et al. [80] further observed no relationship between
lifetime alcohol consumption or the type of alcoholic beverage consumed and PD risk.
Furthermore, the difference in the results of the two studies could be related to the different
study populations and the definitions of PD utilized.
In addition to the AHEI, researchers can assess diet quality using the Dietary Screening
Tool (DST)—a questionnaire designed to measure dietary intake and eating behavior [81].
In a cohort study, Liu et al. [81] utilized the DST to examine diet quality and PD risk among
3653 men and women over 65 years old residing in the US. After almost seven years of
follow-up, 47 participants developed PD [81]. Overall, Liu et al. [81] observed a significant
inverse relationship between better diet quality and PD risk. As a result, the study supports
the benefits of adhering to a healthy dietary pattern to reduce the risk of PD. Nevertheless,
more research is needed to explore the impact of diet quality on PD as measured by DST
among different populations and geographic regions.
While the benefits of adhering to a generally healthy diet can be measured using diet
quality indexes, researchers also explore the role of specific dietary patterns, such as the
DASH diet, in PD. Agarwal et al. [82] conducted an observational study in a cohort of
706 US men and women. In the study, Agarwal et al. [82] found no relationship between
adherence to the DASH diet and PD risk. Though this study suggests no association
between the DASH diet and PD, the cohort primarily consisted of elderly females. Thus,
more research is required to examine the DASH diet in larger diverse cohorts.
While the studies discussed so far relied primarily on observational data, Hegel-
maier et al. [83] conducted a cross-sectional study and clinical trial. The study built upon
previous research linking PD to gut microbiome dysbiosis [84]. First, Hegelmaier et al. [83]
examined the gut microbiome of 54 participants with idiopathic PD and 32 healthy controls
in Germany. In agreement with previous research, Hegelmaier et al. [83] found differences
between the microbiome of participants with PD and healthy controls. Second, a subset
of sixteen of the PD patients received an ovo-lacto-vegetarian diet (n = 16) for fourteen
days [83]. Ten of the sixteen participants received the ovo-lacto-vegetarian diet combined
with an enema intervention for eight days [83]. Although both the diet-only and combined
intervention groups had significant improvements in motor symptoms (UPDRS Part III),
the combined intervention group had the most significant score improvements at the end of
the 14 days [83]. Compared to baseline, the combined intervention group’s mean levodopa
Nutrients 2022, 14, 4472 5 of 20

dosage was lower one-year post-intervention, while the diet-only group’s mean dosage had
increased [83]. While the study supports the role of diet in PD, the study’s small sample
size and lack of diversity limit the generalizability of the data. More research needs to
be conducted to solidify the benefits of diet on modifying the gut microbiome in PD and
alleviating motor symptoms.
Overall, the articles mentioned to this point explored the relationship between fol-
lowing a general healthy dietary pattern and PD development and progression. Misch-
ley et al. [73], Okubo et al. [77], Molsberry et al. [78], and Liu et al. [81] support the benefits
of following a general healthy dietary pattern and reduced PD risk or severity. Further-
more, the clinical trial by Hegelmaier et al. [83] provides evidence that a healthy dietary
pattern may modify PD severity. Nevertheless, the comparability and generalizability of
the studies have several limitations, including the different definitions used to measure
adherence to a healthy dietary pattern. The remainder of this review focuses on the evi-
dence for four specific dietary patterns: the protein-restricted diet (PRD), the ketogenic diet
(KD), the Mediterranean diet (MD), and the Mediterranean-DASH Diet Intervention for
Neurodegenerative Delay (MIND).

3. Protein-Restricted Diet
While some dietary patterns focus on the distribution of different food groups in an
individual’s diet, other dietary patterns focus on the distribution of macronutrients, such
as protein. Previous research linked dietary protein to levodopa bioavailability based on
both substances utilizing the same large neutral amino acid transporter for absorption in
the small intestine and transport across the blood–brain barrier [85–87]. The purpose of a
PRD is to improve the bioavailability of levodopa by limiting protein consumption [87,88].
Although previous studies examining the role of a PRD on PD indicated a beneficial impact
on disease management, the studies’ small sample sizes limit the generalizability of the
data [86–89].

3.1. Defining a Protein-Restricted Diet

Since a PRD aims to reduce complications from drug-nutrient interactions, two dif-
ferent definitions predominate scientific literature. First, a low-protein diet is a dietary
pattern that limits daily protein intake to 0.8 g/kg of an individual’s body weight [87,89].
Second, a protein redistributed diet may or may not require participants to adhere to the
maximum daily protein intake of 0.8 g/kg. Instead, the definition of a protein redistributed
diet focuses on the timing of protein intake, limiting protein intake during the morning
and afternoon to 7 g and allowing unlimited protein intake during the evening meal until
bedtime [87].
While the daily protein limit of 0.8 g/kg in the low-protein diet is based on the
Recommended Dietary Allowance (RDA) [89], some studies have raised concerns that
0.8 g/kg/day may not be sufficient to meet the protein needs of individuals with PD. For
example, Silva et al. [90] observed a negative nitrogen balance among seventeen participants
with PD consuming an average of 1.1 g/kg of protein per day. As a result, some studies
have examined the impact of energy- or protein-rich nutrition supplements in PD patients
adhering to a PRD.

3.2. The Impact of a Protein-Restricted Diet on PD

Over the years, several studies have examined the impact of a PRD on PD. In an Italian
observational study, Barichella et al. [91] examined adherence to a protein redistributed diet
on PD severity in 600 PD cases and 600 controls recruited from a single center. Compared
to the age- and gender-matched control group, participants with PD had significantly
lower BMI (26.2 kg/m2 vs. 28.5 kg/m2; p < 0.001), greater energy intake (31.3 kcal/kg vs.
26.7 kcal/kg; p < 0.001), and greater protein intake (1.2 g/kg vs. 1.0 g/kg; p < 0.001) [91].
Barichella et al. [91] observed that PD participants with greater adherence to a protein
redistributed diet received lower levodopa doses and experienced fewer motor symptoms
Nutrients 2022, 14, 4472 6 of 20

fluctuations. Additionally, Barichella et al. [91] found a direct association between increased
protein intake by 10 g—over the RDA of 0.8 g/kg/day—was directly linked to an increase
in levodopa dosage. As a result, the study’s data suggest that adherence to a protein
redistributed diet may assist individuals with PD in managing motor fluctuations linked to
drug-nutrient interactions. While the study did not raise any concerns about the nutritional
safety of adhering to a PRD, the study center includes nutrition services as part of the
disease management of patients receiving diet-related recommendations.
Because restrictive diets may worsen the nutritional status of individuals with neu-
rological disease, Cucca et al. [92] conducted a randomized control trial to examine the
safety of an amino acid supplement in twenty-two men and women receiving levodopa
therapy and following a protein redistributed diet. In the Italian study, participants were
randomized to receive two doses of either an amino acid supplement (4 g of essential polar
amino acids per dose) or a placebo twice a day for six months [92]. While neither group
experienced a significant change in levodopa dosage, motor fluctuations, or UPDRS Part III
score during the study, both groups experienced a significant improvement in nutrition
status as measured by the Mini Nutrition Assessment [92]. As a result, the study indicated
that individuals with PD could safely consume an amino acid supplement to prevent the
adverse effects of a PRD on nutrition status. Nevertheless, the small sample size limits the
generalizability of the study [92]. The strict timing of supplement and levodopa intake
prevents the study results from informing researchers on the safety and effectiveness of sup-
plement consumption at other times of the day. Furthermore, the strict timing contributed
to the study’s high drop-out rate. Two out of the eight participants who withdrew from the
study cited complications such as nausea and early satiety from the amino acid supplement
as their reasoning for withdrawing from the study [92]. Therefore, more research is needed
to confirm the benefits of amino acid supplements in counteracting the adverse effects of
PRD in PD.
Because the drug-nutrient interaction between protein and levodopa is the basis
behind a PRD, Virmani et al. [93] conducted an observational study to examine the impact
of “protein interactions with levodopa (PIL)” on motor fluctuations in 1037 individuals
with PD in the US. The researchers considered PIL to have occurred if participants reported
motor fluctuations following the consumption of a meal containing protein-rich foods,
such as dairy, eggs, and meat [93]. Virmani et al. [93] noted that 5.9% of levodopa therapy
participants reported PIL. As a result, the study’s data indicates that a PRD may not be
necessary for most individuals with PD on levodopa therapy. Virmani et al. [93] also
observed that PIL developed on average 12.9 years after the initial appearance of motor
symptoms and 7.9 years after levodopa therapy initiation. Therefore, the study’s data
indicates that a PRD may not be necessitated during the initial stages of PD and levodopa
therapy. Regardless, the small proportion (n = 52) of participants reporting PIL limits the
generalizability of the study. The study also highlighted concerns about the safety of a PRD,
with 12 out of 20 participants reporting weight loss following diet modification. Given the
small number of participants reporting PIL and the potential for weight loss following a
PRD, the results of Virmani et al. [93] highlight the need for more research on the benefits
and risk of following a PRD among individuals with PD.
Overall, the studies discussed build upon previous research indicating that a PRD may
be beneficial in managing motor fluctuations of individuals with PD on levodopa therapy.
The study by Barichella et al. [91] supports the benefits of a PRD on motor fluctuations in PD
and indicates that future research must explore the impact of regular nutrition services in
preventing the diet’s adverse effects. Additionally, the data by Cucca et al. [92] indicate that
polar amino acids supplements may serve as an effective strategy for maintaining nutrition
status in an individual with PD while on a PRD. Lastly, the study by Virmani et al. [93]
indicates that a PRD may not be necessary for all individuals with PD receiving levodopa
therapy, especially during the initial stages of PD.
Nutrients 2022, 14, 4472 7 of 20

4. Ketogenic Diet
While a PRD diet focuses on the quantity and distribution of protein in an individual’s
diet, other dietary patterns focus on the distribution of dietary carbohydrates and fats. The
KD is a dietary pattern low in carbohydrates and rich in fat [94]. Since 1921, the KD has
served as a potential treatment for epilepsy [94,95]. Recently, research has begun to explore
the potential benefits of the KD on type 2 diabetes [96] and Alzheimer’s Disease [97–100].

4.1. Defining the Ketogenic Diet

According to the Academy of Nutrition and Dietetics [101], the term “ketogenic diet”
refers to any dietary pattern expected to promote a ketogenic state in an individual. From
a physiological perspective, a very-low-carbohydrate diet decreases the body’s supply of
glucose and results in a metabolic shift from using glucose as its primary fuel source to
using fatty acids [97]. As a result, the degree of ketogenesis—the breakdown of fatty acids
into ketone bodies (acetoacetate, acetone, and β-hydroxybutyrate)—increases [98]. During
this time, the body maintains blood glucose levels and synthesizes glucose from either
amino acids or glycerol through a process known as gluconeogenesis [102]. As the level of
ketone bodies in the bloodstream rises, the body enters a state of ketosis.
While the KD broadly encompasses any dietary pattern predicted to induce a keto-
genic state [101], some clinicians and researchers utilize stricter definitions. The “classic”
or ‘traditional’ KD consists of a ratio of 4:1 or 3:1 (dietary fat: dietary protein and carbohy-
drates) [101]. The modified Atkins diet is less restrictive than the classic KD and utilizes a
ratio of 1:1 [103]. Other versions of a KD include the medium-chain triglyceride KD and
low glycemic index treatment, allowing the user to consume slightly more carbohydrates
than the classic KD [104].
Additionally, the KD’s restrictive nature necessitates the involvement of a patient’s
Physician and Registered Dietitian Nutritionist (RDN), particularly when a KD is prescribed
for the treatment of epilepsy [101,104]. Furthermore, compliance with a KD may be
hindered by its associated short- and long-term side effects such as anemia, constipation,
cardiomyopathy, decreased appetite, hepatitis, nausea, vomiting, nephrolithiasis, and
pancreatitis [94,98].

4.2. The Impact of the Ketogenic Diet on PD

Several studies examined the potential impact of the KD on PD. In an 8-week clinical
trial conducted in New Zealand, Philips et al. [105] randomized participants to follow
either a low-fat diet (n = 23) or a KD (n = 24) [105]. Both diet plans provided participants
with the same amount of protein (1.0 g/kg/day) and included a weekly shopping list,
daily menu sets, and recipes [105]. While both intervention groups experienced significant
improvements in MDS-UPDRS Part I, Part II, and Part III scores, only the KD group
experienced a significant improvement in MDS-UPDRS Part IV scores [105]. As a result,
the study by Philips et al. [105] indicates that short-term use of either a low-fat diet or
KD could alleviate PD symptoms. Because data was not collected on the effect of either
diet post-intervention, more research is needed to examine the long-term implications
of a low-fat diet or KD after diet cessation in PD. The occurrence of weight loss among
participants in both diet groups and exacerbated tremor or rigidity among patients in the
KD group also highlights the need for more research on the safety of long-term adherence
to a KD in individuals with PD [105].
In an 8-week clinical trial in the US, Krikorian et al. [106] examined the impact of
the KD among eighteen participants with PD-mild cognitive impairment (MCI). Par-
ticipants were randomized to follow a low-carbohydrate (ketogenic) diet (n = 10) or a
high-carbohydrate diet (n = 8) [106]. While participants following the KD had signifi-
cant improvements in cognitive performance compared to the high-carbohydrate group,
no difference emerged between the groups in MDS-UPDRS Part III after the interven-
tion [106]. Furthermore, the KD group experienced a significant reduction in body weight,
and Krikorian et al. [106] noted a relationship between weight loss and improvements in
Nutrients 2022, 14, 4472 8 of 20

cognitive function. Therefore, more research is needed to explore the safety of long-term
adherence to the KD and its relationship with weight loss and cognition.
Both Philips et al. [105] and Krikorian et al. [106] examined the potential role of short-
term adherence to a KD among individuals with PD. While both studies indicate that a
low-carbohydrate (ketogenic) diet may alleviate some PD symptoms, the researchers found
conflicting results on the impact of a KD on motor symptoms (MDS-UPDRS Part III). There-
fore, more research is needed to examine this relationship. Furthermore, Philips et al. [105]
and Krikorian et al. [106] reported weight loss among participants following the KD. Be-
cause previous studies have linked weight loss to malnutrition risk and adverse outcomes
for individuals with PD [38], more research is needed to explore the impact of a ketogenic
dietary intervention on the nutrition status of individuals with PD.
In a longer (3-month) clinical trial in Turkey, Koyuncu et al. [107] examined the effect
of the KD on voice quality among 74 men and women with PD who were not receiving
medication for PD treatment. Participants were randomized to follow either a regular
diet (n = 37) or a KD (n = 37) [107]. Unlike the regular diet group, participants in the KD
group had significant improvements in voice quality as measured by the Voice Handicap
Index-10, a scoring system that uses self-reported measures of voice quality [107]. While
the study indicates that a KD may improve voice quality in PD, the lack of information on
participant KD training and the degree of participant adherence limits the generalizability
of the study [107].
While the studies discussed indicate that adherence to a KD may improve various
PD symptoms, the studies’ small sample sizes and short intervention periods limit their
generalizability. Furthermore, Philips et al. [105] and Krikorian et al. [106] reported weight
loss among participants with PD following a KD. Because previous research indicates
that PD patients are at greater risk of developing malnutrition, more research is needed
to explore the long-term implications of adherence to a KD on the nutritional status and
quality of life of PD patients. Additionally, Philips et al. [105] and Krikorian et al. [106]
utilized nutrition education and counseling to prepare participants and their caregivers
for implementing a KD. In light of the role of an RDN in KD therapy in epilepsy, future
research should also examine the role of RDNs in improving KD compliance and safety
among individuals with PD.

5. Mediterranean Diet
The MD may play a beneficial role in disease prevention, and several studies sup-
port its role in reducing all-cause mortality [108,109] along with the risk of cancer [110],
diabetes [111], stroke [112], and cardiovascular disease [112]. Moreover, the MD may
positively influence health-related biomarkers such as high-density lipoproteins [112,113],
triglycerides [112,114], blood pressure [112], waist circumference [112], and insulin resis-
tance [115]. Recently, scientific evidence is emerging to support the beneficial role of the
MD on depression [116–118], Alzheimer’s disease [62], and neurodegeneration.

5.1. Defining the Mediterranean Diet

First identified by Ancel Keys, the definition of the MD has changed over the years [119].
As a result, the definition of the MD varies from study to study—making it difficult to
compare results and draw conclusions [120,121]. Broadly, the MD represents a dietary
pattern rich in fruits, vegetables, legumes, cereals, nuts, fish, and monounsaturated fatty
acids with moderate alcohol intake and low intake of dairy products and red meats [122].
Previously, several studies explored the definition of the MD to clarify its mean-
ing. Davis et al. [122] noted differences across research studies in the number of serving
sizes and the number of grams for different components of the MD. Furthermore, Abdel-
hamid et al. [120] conducted a systematic review of seventy-four primary research articles
and observed considerable variability in the methods for defining food group categories
and calculating the MD score. The observed variation likely stemmed from the MD score’s
reliance on specific population and study food group category means over absolute set-
Nutrients 2022, 14, 4472 9 of 20

points [120]. Zaragoza-Martí et al. [123] evaluated the quality of twenty-eight different
MD scores based on the Scientific Advisory Committee of the Medical Outcomes Trust’s
criteria [123]. The authors noted that several studies considered the method developed
by Trichopoulou et al. [124] in 1995 to be the gold standard because it was developed
first; however, evidence was insufficient for all MD scores with the methods developed by
Panagiotakos et al. [125], Buckland et al. [126], and Sotos-Prieto et al. [127] possessing the
most evidence [123].
Similar to previous studies, variations exist in how studies calculated MD adher-
ence in this review. Five of the studies [78,128–131] used the MD score created by Tri-
chopoulou et al. [132] or a variation of that method, while three studies [82,130,133]
used the MD score created by Parganiotakos et al. [125] or a variant of that method. Tri-
chopoulou et al. [132] MD score builds upon the score created by Trichopoulou et al. [124]
but updated the previous score to include dietary fish intake. The score rewards participants
for consuming more significant amounts of cereal, fish, fruit, legumes, nuts, and vegetables
and lower amounts of dairy products, meat, and poultry [132]. Trichopoulou et al. [132]
observed a positive association between higher MD score and all-cause mortality, coronary
heart disease mortality, and cancer mortality. Furthermore, the results maintained their
significance after controlling for age, sex, education, smoking status, BMI, waist-to-hip
ratio, energy expenditure, energy intake, egg consumption, and potato consumption [132].

5.2. Impact of the Mediterranean Diet on PD

Currently, studies examining the role of the MD on PD have yielded mixed results. In a
study of 41,715 middle-aged Swedish women, Yin et al. [131] observed a significant inverse
relationship between MD adherence and risk of PD and noted an 11% reduction in PD
risk per unit increase in MD score. Agarwal et al. [82] observed a 3% reduction in PD risk
per unit increase in MD score. Additionally, greater adherence to the MD was associated
with slower PD progression as measured by the UPDRS [82]. The differences in per unit
risk reduction may be accounted for by differences in participant gender, geographical
location, and mean follow-up period [82]. Compared to the incidence of 101 PD cases
in Yin et al. [131], Agarwal et al. [82] documented 302 PD cases. The difference in PD
incidence may be explained by Agarwal et al. [82] using trained clinicians to diagnose
PD and Yin et al. [131] utilizing hospital records to confirm PD diagnosis. In contrast to
Yin et al. [131] and Agarwal et al. [82], Maraki et al. [133] found no relationship between MD
adherence and PD risk among the 1765 participants (34 PD cases) enrolled in the Hellenic
Longitudinal Investigation of Aging and Diet in Greece. Nevertheless, Maraki et al. [133]
noted that their analysis might be underpowered by the documentation of only thirty-four
PD cases.
When examining the probability of prodromal PD instead of clinical PD, Maraki et al. [133]
found an inverse relationship between MD score and the probability of prodromal PD.
Similarly, Molsberry et al. [78] observed a reduced risk of prodromal PD with greater MD
adherence. Studies examining the role of the MD on the age of onset of PD have yielded
mixed results. In a US case–control study of 257 cases and 198 controls, Alcalay et al. [128]
observed that greater adherence to the MD was associated with later onset of PD. Con-
versely, Cassani et al. [129] found no relationship between MD adherence and age at onset
of PD when examining 600 cases and 600 controls in Italy [129]. While both studies calcu-
lated MD scores using the method established by Trichopoulou et al. [132], they occurred
in different geographical regions, and local food availability and food preferences could
have confounded results [128,129]. Additionally, Cassani et al. [129] observed significantly
greater potato consumption among the PD group, but it is unclear how potato consumption
affected MD score calculation. For instance, if potato consumption were factored into the
vegetable intake, PD patients would have received higher MD scores for increased potato
consumption despite Trichopoulou et al. [132] excluding potato intake from the MD score
and associating it with a greater risk of all-cause mortality.
Nutrients 2022, 14, 4472 10 of 20

Metcalfe-Roach et al. [130] examined the role of the MD on the age of onset of
PD among Canadian men and women using the original MD score developed by Tri-
chopoulou et al. [132] and the “Greek” MD score developed by Panagiotakos et al. [134].
Compared to the “original” MD score, greater adherence to the “Greek” MD score was
more strongly associated with later age at onset among 167 PD cases and 119 controls [130].
Interestingly, the MD score developed by Panagiotakos et al. [134] rewards participants
for the consumption of potatoes, limiting the comparability of studies using the different
scoring methods. Furthermore, the exact impact of potato consumption on health outcomes
is unclear [135]. Overall, the results of Metcalfe-Roach et al. [130] highlight the importance
of using consistent definitions of the MD to increase the comparability of study results.
Furthermore, two articles examined the MD in a single-center, 10-week randomized
control trial (RCT) of eighty idiopathic PD patients in Iran [136,137]. The first article
examined cognitive function and randomized participants to follow the MD (n = 40) or
healthy dietary recommendations (n = 40) [136]. At the end of the study, 35 participants
remained in each group [136]. Compared to the control group, participants following
the MD had significantly improved scores for executive function, language, attention,
concentration, and active memory [136]. The second article examined disease severity
using the MDS-UPDRS and randomized participants to follow either an MD (n = 40) or the
traditional Iranian diet (n = 40) [137]. At the end of the study, 36 participants remained in the
intervention group, and 34 participants remained in the control group [137]. Compared to
the control group, the MD group experienced greater serum total antioxidant capacity and
decreased disease severity [137]. While both studies support the benefits of the MD in PD
patients, the inclusion of PD patients from a single center limits the studies’ generalizability
to other parts of Iran and the world.
In summary, the seven case–control and cohort studies [78,82,128–131,133] yielded
mixed results on the benefits of the MD in PD prevention and progression. The MD
was associated with a reduced risk of clinical PD in two studies [82,131] (compared to
one [133]), reduced risk of prodromal PD in two studies [78,133], later age of onset in two
studies [128,130] (compared to one [129]). Differences in mean population dietary patterns
and methods of calculating MD scores could account for these discrepancies. Additionally,
the recruitment of participants from a single center limits the positive results obtained in
the two RCT articles’ [136,137]. Therefore, more research is needed to examine the benefits
of the MD in PD.

6. MIND Diet
Developed to protect against neurodegeneration, the MIND diet combines the MD
and DASH dietary patterns into a single dietary pattern [138]. Previous research indicates
that greater adherence to the MIND diet is associated with a reduced risk of all-cause mor-
tality [139], psychological disorders [140,141], and cognitive decline [142,143]. Additionally,
the MIND diet may play a beneficial role in reducing the risk of another neurodegenerative
disease, Alzheimer’s Disease [144]. While the protective role of the MIND diet in cognitive
decline and Alzheimer’s Disease makes it of interest in PD, the MIND diet’s potential
impact on PD symptoms and an individual’s physical function increases its relevance to
PD. For instance, a recent study by Talegawkar et al. [145] observed that greater adherence
to the MIND diet was associated with better physical function and grip strength in US
adults over 60 years old. This portion of the review will examine the impact of the MIND
diet on PD.

6.1. Defining the MIND Diet

Morris et al. [138] developed the MIND diet and its scoring method to reward par-
ticipants for consuming foods associated explicitly with neuroprotection. As a result, the
MIND diet retains the focus of the MD and DASH on plant-based foods while additionally
emphasizing the consumption of green leafy vegetables and berries [138].
Nutrients 2022, 14, 4472 11 of 20

6.2. Impact of the MIND Diet on PD

Both studies [82,130] examining the MIND diet observed a decreased risk of develop-
ing PD. Agarwal et al. [82] observed a 13% reduction in PD risk among men and women
with greater adherence to the MIND diet. Likewise, Metcalfe-Roach et al. [130] observed
an association between greater adherence to the MIND diet and later age at onset of PD;
however, the relationship was most substantial in the female subgroup. The more substan-
tial reduction in PD risk among females could be related to the “berry” component of the
MIND diet score. Sääksjärvi et al. [79] observed that the increased intake of berries was
associated with an increased risk of PD in men but a decreased risk in women. Furthermore,
both Agarwal et al. [82] and Metcalfe-Roach et al. [130] observed a greater adherence to
the MIND diet to be more protective against PD than the MD. Overall, both the work
by Agarwal et al. [82] and Metcalfe-Roach et al. [130] highlight the benefits of greater
adherence to the MIND diet in PD prevention; however, more research is needed to confirm
the relationship.

7. Summary
In summary, this review examined the role of diet and dietary patterns in PD in five
different categories: general, PRD, KD, MD, and MIND. Table 1 provides a summary of the
results of the observational studies and Table 2 provides a summary of the clinical trials
included in this review. The potential benefits of different dietary patterns for individuals
with PD are highlighted in Figure 1. Four observational studies [73,77,78,81] and one clinical
trial [83] support the benefits of following a general healthy dietary pattern in reducing PD
risk or severity. While the three PRD studies [91–93] support the beneficial role of a PRD in
managing motor fluctuations of individuals with PD on levodopa therapy, more research
is needed to clarify when a PRD is appropriate for alleviating motor fluctuations among
individuals with PD. Similarly, the three KD studies [105–107] indicate that adherence to
a KD may improve various PD symptoms. Nevertheless, the small sample sizes, short
periods, and diet’s adverse effects require more research on the role of PRD and KD in
PD. Eight articles [78,82,128–131,133,136,137] indicate that the MD may prevent PD and
progression. Lastly, both MIND diet studies [82,130] support the role of the MIND diet in
PD prevention. While most of the included studies support the role of diet and dietary
patterns in reducing PD risk, progression, or severity, inconsistent results and small sample
sizes highlight the need for further research before making nutritional recommendations.
Therefore, more research is needed to explore the impact of specific dietary patterns on PD
along and their potential benefits and risks.

Table 1. Summary of Observational Study Results on the Impact of Diet and Dietary Patterns on PD.

Citation Year Published Study Type Diet Type n Location Key Results
Greater adherence to the MD was
Alcalay et al. 257 cases
2012 Case-Control MD United States associated with a reduced risk of PD and
[128] 198 controls
later age-at-onset of PD.
The healthy dietary pattern was associated
Healthy with a reduced risk of PD, but not
Okubo et al. 249 cases
2012 Case-Control Western Japan statistically significant (p = 0.06).
[77] 368 controls
Light Meal The light meal and Western dietary
patterns were not associated with PD risk.
Adherence to the AHEI was not associated
with PD risk.
Sääksjärvi 4524 (85 Greater intake of berries was associated
2012 Cohort AHEI Finland
et al. [79] cases) with a reduced risk of PD in women but
was associated with an increased risk
among men.
Only 5.9% of participants on levodopa
Virmani et al. 1037 (1037 reported PIL.
2016 Cohort PRD United States
[93] cases) Only 20 participants reported following a
PRD.
Nutrients 2022, 14, 4472 12 of 20

Table 1. Cont.

Citation Year Published Study Type Diet Type n Location Key Results
Adherence to a PRD was associated with a
lower levodopa dosage.
Protein intake was not associated with
Barichella 600 cases
2017 Case-Control PRD Italy levodopa-related motor complications.
et al. [91] 600 controls
An intake of 10 g protein over 0.8
g/kg/day was associated with an increase
in levodopa dosage by 0.7 mg/kg.
No difference in adherence to the MD
Cassani et al. 600 cases existed between cases and controls.
2017 Case-Control MD Italy
[129] 600 controls Adherence to the MD was not associated
with disease duration, or age-at-onset.
A plant/fish based dietary pattern was
associated with a reduced rate of PD
progression.
Foods associated with a reduced rate: fresh
Mischley et al. Cross- 1053 (1053
2017 General United States vegetables, fresh fruit, nuts, seeds, fish,
[73] Sectional cases)
olive oil, coconut oil, and wine.
Foods associated with an increased rate:
canned vegetables, canned fruit, beef, fried
food, cheese, yogurt, ice cream, and soda.
The DASH Diet was not associated with
PD risk.
Both the MIND diet and the MD were
DASH associated with a reduced risk of PD, with
Agarwal et al. 706 (302
2018 Cohort MD United States the MIND diet having the strongest
[82] cases)
MIND relationship to PD risk.
Each unit increase in the MIND diet score
was associated with a 13% reduction in PD
risk.
Adherence to the MD was associated with
a lower probability of prodromal PD.
Maraki et al. 1765 (34
2018 Cohort MD Greece The study’s results remained unchanged
[133] cases)
after excluding constipation as a feature of
prodromal PD.
3653 (47 Greater diet quality was associated with a
Liu et al. [81] 2020 Cohort DST United States
cases) significantly reduced risk of PD.
Greater adherence to both the MD and
Molsberry MD
2020 Cohort 17,400 United States AHEI was associated with a reduced risk
et al. [78] AHEI
of developing features of prodromal PD.
Greater adherence to the MIND diet or the
Greek MD was associated with later age of
onset of PD. The relationship was stronger
Metcalfe- for the MIND diet than the MD.
MD 167 cases
Roach et al. 2021 Case-Control Canada The relationship between the MIND diet
MIND 119 controls
[130] and age of onset was strongest among
women, while the relationship between the
MD (Panagiotakos et al. [134]) was
strongest among men.
Greater adherence to the MD was
associated with a reduced risk of PD.
Yin et al. 41,715 (101
2021 Cohort MD Sweden Each unit increase in MD score was
[131] cases)
associated with an 11% reduction in PD
risk.
Note: Table abbreviations include Dietary Approaches to Stop Hypertension (DASH); Dietary Screening Tool
(DST); Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND); Mediterranean Diet (MD);
Parkinson’s Disease (PD); Protein Interactions with Levodopa (PIL); Protein Restricted Diet (PRD); Sample
Size (n).
Nutrients 2022, 14, 4472 13 of 20

Table 2. Summary of Clinical Study Results on the Impact of Diet and Dietary Patterns on PD.

Citation Year Published Diet Manipulation Length Location Key Results

General Dietary Patterns
Compared to baseline:
Individuals with PD were • Compared to the diet only group,
randomized to receive either the combined treatment group had
Hegelmaier
2020 an enema for 8 days and an 2 weeks Germany significant improvements in UP-
et al. [83]
ovo-lacto-vegetarian diet DRS III and daily levodopa dose
(n = 10) or diet only (n = 6). a year after the intervention.

PRD
Compared to baseline:
• Neither group experienced a signif-
icant change in body weight, hand-
grip strength, levodopa dosage, or
Individuals with PD on a motor performance (UPDRS III)
PRD were randomized to • Both groups experienced a signifi-
Cucca et al.
2015 consume either 16 g amino 6 months Italy cant improvement in nutrition sta-
[92]
acid supplement (n = 12) or a tus
placebo (n = 10) daily. • Both groups experienced a de-
crease in insulin sensitivity, with
the greatest decrease occurring in
the placebo group

KD
Compared to baseline:
• Both the KD and low-fat groups
experienced a significant improve-
ment in UPDRS Part I, II, and III.
Individuals with PD were Furthermore, the KD group ex-
Phillips randomized to follow either a New perienced a greater improvement
2018 8 weeks
et al. [105] low-fat diet (n = 23) or a KD Zealand in UPDRS Part I than the low-fat
(n = 24). group.
• Only the KD group experienced
a significant improvement in UP-
DRS Part IV.

Compared to baseline:
• The low carbohydrate group expe-
rienced a significant reduction in
body weight, waist circumference,
and fasting insulin along with
an increase in β-hydroxybutyrate.
Individuals with PD The high carbohydrate group also
randomized to follow either a experienced a decrease in fasting
Krikorian insulin.
2019 low carbohydrate (n = 10) or a 8 weeks United States
et al. [106] • Compared to the high carbohy-
high carbohydrate (n = 8)
diet. drate group, the low carbohydrate
group experienced a significant
improvement in cognitive perfor-
mance.
• Neither group experienced a
change in motor function (UPDRS
Part III).

Compared to baseline:
• The KD group experienced a signif-
Individuals with PD were icant improvement voice quality as
Koyuncu randomized to follow either a measured by all ten components of
2020 3 months Turkey
et al. [107] KD (n = 37) or their regular the Voice Handicap Index-10.
diet (n = 37). • The control group experienced no
change in voice quality.
Nutrients 2022, 14, 4472 14 of 20

Table 2. Cont.

Citation Year Published Diet Manipulation Length Location Key Results

MD
Compared to baseline:
• The MD group experienced an in-
crease in total antioxidant capac-
ity, while the control group experi-
enced no significant change.
Individuals with PD were • The MD group also experienced a
Paknabad randomized to follow either a significant improvement in menta-
2020 10 weeks Iran
et al. [137] MD (n = 40) or the traditional tion, behavior, and mood; activi-
Iranian diet (n = 40). ties of daily living; and complica-
tions of therapy as measured by
the MDS-UPDRS. This improve-
ment remained significant when
compared to the control group.

Compared to baseline:
• The MD group significantly in-
creased their intake of protein and
eicosapentanoic acid, while their
intake of total energy, carbohy-
Individuals with PD were drates, and saturated fatty acids
Paknahad randomized to follow either a decreased
2020 10 weeks Iran • The MD group also experienced
et al. [136] MD (n = 40) or their regular
diet (n = 40). improvements in components of
the Montreal Cognitive Assess-
ment (aspects of executive func-
tion; language score; attention, con-
centration, and working memory;
total cognitive score)

Nutrients 2022, 14,Note:

x FOR PEER
TableREVIEW 16 of 22
abbreviations include International Parkinson and Movement Disorder Society (MDS); Ketogenic
Diet (KD); Sample Size (n); Unified Parkinson’s Disease Rating Scale (UPDRS).

• ⬇ PD risk
General Healthy
• ⬇ levodopa dosage
Dietary Patterns
• ⬆ motor function

Protein • ⬇ levodopa dosage

Restricted Diet • ⬆ nutrition status

• ⬆ UPDRS Parts I, II, III, & IV

• ⬆ cognitive performance
Ketogenic Diet
• ⬇ fasting insulin
• ⬆ voice quality

• ⬇ probability of prodromal PD
Mediteranian
• ⬇ PD risk
Diet
• ⬆ age-at-onset
• ⬇ PD risk
• ⬆ age-at-onset
MIND Diet
• ⬆ cognitive function
• ⬆ total antioxidant capacity

Figure 1. Potential
Figurebenefits of different
1. Potential benefits ofdietary
differentpatterns for individuals
dietary patterns withwith
for individuals PD.PD.
Upward
Upward arrows
arrows(↑)
(⬆)increased
indicate the diet indicate thethe
dietfollowing
increased the following
variable, variable,
while while downward
downward arrows arrows (⬇) indicate
(↓) indicate that diet
that the the
diet decreased the following variable.
decreased the following variable.
8. Conclusions
Overall, PD is a neurodegenerative disorder associated with diminished nutrition
status and quality of life. Since no preventative or curative therapy for PD exists currently,
nutrition and diet represent modifiable risk factors for reducing disease risk. As the single-
nutrient approach yields inconsistent results on the role of diet in PD, this review analyzed
Nutrients 2022, 14, 4472 15 of 20

8. Conclusions
Overall, PD is a neurodegenerative disorder associated with diminished nutrition
status and quality of life. Since no preventative or curative therapy for PD exists currently,
nutrition and diet represent modifiable risk factors for reducing disease risk. As the single-
nutrient approach yields inconsistent results on the role of diet in PD, this review analyzed
studies investigating the role of diet from a holistic approach. Although research on a
general healthy dietary pattern, a PRD, a KD, an MD, and a MIND diet yielded mixed
results, most studies examined in this paper support the role of diet and dietary patterns in
reducing the risk of PD or alleviating PD severity. Nevertheless, more research is needed to
examine the relationship and explore the impact of specific dietary patterns.

Author Contributions: E.K.: Writing—original draft preparation, review and editing. D.B.: review
and editing. T.G.: review and editing, funding acquisition. J.R.B.: Funding acquisition, Supervision,
review and editing. All authors have read and agreed to the published version of the manuscript.
Funding: This work was supported by the Alabama Agricultural Experimental Station (AAES),
Hatch/Multistate Funding Program and AAES Award for Interdisciplinary Research (AAES-AIR) to
J.R.B. and T.G.
Institutional Review Board Statement: Not applicable.
Informed Consent Statement: Not applicable.
Data Availability Statement: Not applicable.
Conflicts of Interest: The authors declare that they have no known competing interest regarding the
publication of this article.

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