Parkinson’s Disease: What Studies Suggest About Nutritional, Metabolic, Hormonal and Immune Links
- Curtis Baker
- Aug 12
- 6 min read
Quick take: Research is increasingly exploring how everyday biology—nutrients, blood sugar, hormones, inflammation, and even infections—may influence Parkinson’s disease (PD) risk, symptoms, and progression. Our clinic has reviewed 26 studies on these factors and how they may relate to PD. Below, we translate key findings into clear, actionable insights.
As always, none of this replaces individualized medical care. Findings are early or mixed in places, and “may” is the operative word—these are associations and signals that need to be interpreted in your own clinical context.
Why this matters
PD is best known for tremor, stiffness, and slowness, but it often involves whole‑body biology. Studies suggest some people with PD may carry underlying nutritional, metabolic, hormonal, or immune‑related imbalances that could shape risk or day‑to‑day function. Understanding those layers can guide smarter lifestyle and medical decisions.
Nutritional factors
Vitamin B12 (cobalamin)
A nationwide cohort study found that gastric‑cancer patients who underwent total gastrectomy had a lower incidence of PD if they consistently received vitamin B12 afterward; those without B12 had higher risk—hinting that B12 status may matter in PD biology (Choi 2021). Mechanistically, B12 participates in myelin and one‑carbon metabolism; low levels may elevate homocysteine, which has been linked to cognitive decline (see below).
Folate & Homocysteine
People with PD were reported to have lower folic acid levels in a recent analysis, pointing to potential methylation and neuroprotective pathways that might be relevant (Ding 2023).
Separately, in PD, higher homocysteine was associated with faster cognitive decline, suggesting that B‑vitamin status (B12/folate/B6) may influence brain health trajectories (Periñán 2023).
Why it matters: Folate and B12 work together to keep homocysteine in check. Elevated homocysteine may contribute to oxidative stress and vascular injury, which could in turn affect cognition.
Vitamin D
In a randomized trial, vitamin D supplementation was associated with improved mobility and functional test performance in PD—encouraging, practical data for daily living outcomes (Bytowska 2023).
Dietary Antioxidants: Beta‑carotene & Vitamin E
A 2023 systematic review and meta‑analysis reported a lower PD risk among individuals with higher beta‑carotene and vitamin E intake (antioxidants that may help counter oxidative stress) (Niu 2023).
Zinc
Iron balance
While iron is essential for dopamine synthesis, too much may fuel oxidative stress. A prospective study found very high iron intake associated with increased PD risk (Wang 2015). Striking the right balance—not too little, not too much—may be key.
Selenium
Selenium is a cofactor for antioxidant enzymes. A 2024 retrospective cohort analysis linked moderate selenium intake with lower mortality among people with PD, with possible interaction by blood cadmium (heavy‑metal exposure), suggesting a U‑shaped or “balanced‑intake” relationship (Tu 2024).
Metabolic factors
Blood sugar (diabetes & prediabetes)
A meta‑analysis of 15 cohort studies including 29.9 million participants and 86,345 PD cases found diabetes associated with a 27% higher relative risk of developing PD; even prediabetes carried a small but significant increase (Aune 2023).
Why it matters: Insulin signaling intersects with mitochondrial function and neuroinflammation. Over time, glucose dysregulation may amplify oxidative stress pathways implicated in PD.
Uric acid (urate)
Urate is a powerful antioxidant in human plasma. A dose‑response meta‑analysis of 15 studies concluded that higher urate levels were associated with lower PD risk; every 1 mg/dL increase in urate correlated with ~6% lower risk (Chang 2022). This does not mean aiming for gout—rather, it highlights antioxidant pathways that may be relevant.
Immune & inflammatory factors
Systemic inflammation
A 2019 meta‑analysis reported higher inflammatory markers in PD, supporting the idea that neuroinflammation and systemic inflammation may interact (Qiu 2019). Inflammation may be both a driver and a consequence of neurodegeneration, creating a feed‑forward loop.
Anti‑inflammatory medicines (observational)
A 2024 systematic review and meta‑analysis found that non‑aspirin NSAIDs—particularly ibuprofen—were associated with reduced PD risk; aspirin showed no clear association (Badawoud 2024). This is not a treatment recommendation, but it does lend weight to the inflammation‑PD link.
Hormone‑related factors
Thyroid function
A systematic review and meta‑analysis (3 cohort + 6 case‑control studies) found that both hypothyroidism and hyperthyroidism were associated with increased PD risk (Charoenngam 2022). Thyroid hormones influence brain metabolism and neurotransmission, so significant deviation in either direction may matter.
Estrogen (exploratory)
An earlier clinical study suggested a trend toward reduced motor symptom severity with estrogen use in PD, though results were not definitive (Parkinson Study Group 2011). Hormone evaluation is individualized and should balance potential benefits and risks.
Environmental & infectious factors
Lead
Higher lead exposure was linked to faster cognitive decline in PD, highlighting how heavy metals may add neurotoxic stress on already vulnerable circuits (Weuve 2013).
Helicobacter pylori (stomach bacteria)
A meta‑analysis found H. pylori was more common in PD and that treatment was associated with improvement in PD symptoms in some patients—possibly by enhancing medication absorption or reducing systemic inflammation (Su 2018).
What this means in plain language
Oxidative stress keeps coming up. Antioxidant‑related nutrients (vitamin E, beta‑carotene, selenium, zinc) and metabolites (urate) appear in several studies. Supporting healthy antioxidant capacity may be helpful, but extremes (very high iron, very high selenium) may backfire.
Metabolic health matters. Diabetes/prediabetes were linked to higher PD risk, while urate (an antioxidant end‑product of purine metabolism) tracked with lower risk. Balanced nutrition and blood sugar management aim to reduce oxidative stress and inflammation.
Hormones and immunity are part of the picture. Thyroid imbalances and inflammatory activity may influence PD biology; selective anti‑inflammatory strategies are under study.
Environment & gut can nudge the system. Metals like lead and infections like H. pylori may add stressors that are worth identifying and addressing.
A naturopathic doctor (ND) looks at these layers alongside your neurologist or family physician. Natural therapies are often used as adjuncts—not replacements—to standard care.
How our clinic approaches this
We start with your story and your goals, then consider targeted labs guided by your history, medications, and current symptoms. When indicated, we discuss nutrition and lifestyle strategies that aim to optimize antioxidant capacity, blood sugar balance, hormone health, and gut‑immune interactions. We coordinate with your medical team to keep care integrated and safe.
A note on interpreting blood work
At our clinic, we use personalized ranges to interpret blood work, tailored specifically to each patient and their unique context. Standard blood ranges often lack customization and may not account for individual health needs. By focusing on precise targets, we aim to support specific conditions. Research suggests that certain conditions tend to improve quicker at certain nutritional blood target levels. Similarly, optimal hormone levels are typically found within a narrow, specific range of the standard reference values, ensuring better balance and well‑being.
If appropriate for your care, we can arrange:
A comprehensive nutritional panel (vitamins, minerals, and related markers such as homocysteine) to identify potential shortfalls or excesses.
A metabolic and inflammatory panel (blood sugar control, uric acid context, inflammatory markers) and, when relevant, thyroid testing or stool/breath testing for GI issues such as H. pylori.
We use these results to develop individualized nutrition and lifestyle plans that aim to optimize hormonal and metabolic balance.
Note: The list of tests mentioned in this post covers just a few of the many tests we may consider when evaluating a case and this post is not intended to be comprehensive.
Key studies referenced (linked in‑text)
B12 & PD risk: Choi 2021
Beta‑carotene & vitamin E meta‑analysis: Niu 2023
Homocysteine & cognitive decline in PD: Periñán 2023
Diabetes/prediabetes & PD risk (15 cohorts): Aune 2023
Lead & cognitive decline in PD: Weuve 2013
Vitamin D supplementation & mobility: Bytowska 2023
Zinc (higher intake → lower risk): Sun 2021; Low zinc in PD (meta): Du 2017
High iron intake & PD risk: Wang 2015
Lower folate in PD: Ding 2023
Inflammation markers elevated (meta): Qiu 2019
NSAIDs & PD risk (meta): Badawoud 2024
Urate & PD risk (15 studies): Chang 2022
Thyroid dysfunction & PD risk (3 cohort + 6 case‑control): Charoenngam 2022
Estrogen trend data: Parkinson Study Group 2011
Selenium & PD prognosis: Tu 2024
Bottom line
No single nutrient or lab defines PD—but a pattern of small, testable factors may add up. If you or a loved one is navigating PD, consider a visit with our clinic’s team (including a naturopath) to explore safe, personalized steps that complement your neurologist’s plan.
Disclaimer: This post is for informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your healthcare provider or a qualified medical professional before starting any new treatment or if you have questions about your medical condition. While we aim to provide accurate, research-based information, individual needs and responses to treatments can vary. Our clinic offers personalized consultations to discuss health concerns and develop tailored care plans. Never disregard professional medical advice or delay seeking it because of information you have read on this site.
