Parkinson's Disease, a Preventable Epidemic?

Overview

If it seems like you're hearing more about people getting Parkinson's disease, you're not imagining it. Between 1990 and 2016, global Parkinson's disease (PD) cases surged from 2.5 million to 6.1 million, and by 2019, this number reached approximately 8.5 million. More striking: age-standardized prevalence increased by 21.7% during this period, meaning the rise isn't simply because people are living longer.

Parkinson's disease occurs when neurons in a brain region called the substantia nigra progressively die, depleting dopamine—the neurotransmitter essential for smooth, coordinated movement. By the time tremor and other motor symptoms appear, more than half of these neurons are already gone.

Over five reports, this series will translate the latest Parkinson's prevention research into practical guidance. We'll cover: (1) potentially modifiable environmental risk factors, (2) the early warning signs that appear years before motor symptoms—plus breakthrough diagnostic tests, (3) exercise as disease-modifying medicine, (4) brain-protective nutrition, and (5) the gut-brain connection.

The 85% Mystery

Only 15% of people with PD have a family history of the disease. That means 85% of cases may be driven by environmental and lifestyle factors—things we can potentially modify. The evidence increasingly points to a crisis shaped by modern living, industrialization, and environmental exposures. Neurodegenerative processes likely begin at least 10-15 years before symptoms develop. Being mindful of environmental exposures earlier in life may have a profound impact on whether this disease ever develops.

The Environmental Culprits

Golf Course Proximity, a Novel Discovery

In May 2025, a landmark study published in JAMA Network Open revealed an unexpected risk factor: living within one mile of a golf course is associated with a 126% increased risk of developing Parkinson's disease compared to living six or more miles away. The mechanism? U.S. golf courses use pesticides at levels up to 15 times higher than European courses, and these chemicals leach into drinking water through groundwater contamination.

The study examined 419 PD cases and 5,113 matched controls from 1991-2015, controlling for age, sex, income, and urban/rural location. People whose municipal water systems draw from groundwater areas with golf courses had nearly double the odds of PD, and risk was even higher in regions with vulnerable groundwater (shallow aquifers, permeable soil).

Pesticides and Agricultural Chemicals

The association between pesticides and Parkinson's disease is among the most robust findings in environmental neurology. Paraquat and rotenone have shown the strongest associations, with meta-analyses demonstrating approximately 2-fold increased risk with exposure. The landmark Agricultural Health Study found that occupational exposure to paraquat increased PD risk substantially. In rural areas, PD prevalence is strongly correlated with pesticide use; even drinking well water and working in agriculture are associated with increased risk.

For those concerned about pesticide exposure through drinking water, a 2024 study in Environmental Pollution offers reassurance: researchers tested nine residential water treatment methods and found that activated carbon filters and reverse osmosis systems demonstrated 100% efficiency in removing the 13 pesticides tested. For families living near golf courses or in agricultural areas, quality water filtration represents a practical, immediate risk-reduction strategy.

Occupational Exposures

In addition to those working in the agricultural sector, several other occupations carry elevated Parkinson's risk due to chemical exposures.

Trichloroethylene (TCE), once ubiquitous in dry cleaning, manufacturing, and aviation, has been identified as a likely contributor to Parkinson's disease. TCE was widely used to degrease jet engines and aircraft parts, clean electronics, and strip paint—putting military personnel, aircraft mechanics, machinists, and workers across dozens of trades at elevated risk. A 2023 study of Marines stationed at Camp Lejeune—where drinking water was heavily contaminated with TCE—found a 70% higher risk of developing Parkinson's disease decades later compared with veterans who trained elsewhere.

TCE affects mitochondrial function in dopaminergic neurons, and animal studies show it causes selective loss of dopamine-producing cells. Perchloroethylene (used in dry cleaning) is also implicated. In 2024, the EPA declared that TCE presents an "unreasonable risk of injury to human health" and issued a ban on consumer and commercial uses, though aviation and defense industries have a decade to phase it out.

Micro- and Nanoplastics: An Emerging Concern

A November 2023 study in Science Advances revealed a potential mechanism linking plastic pollution to Parkinson's pathology. Anionic polystyrene nanoplastics—commonly found in single-use cups and cutlery—bind to alpha-synuclein protein, a key protein in the pathology of PD. In mouse models, nanoplastics exacerbated the spread of alpha-synuclein pathology across brain regions, including dopaminergic neurons in the substantia nigra. A 2025 study further demonstrated that polystyrene nanoplastics can travel via the gut-brain axis to exacerbate Parkinson's pathology. If you needed another reason to reduce your use of single-use plastics, here it is.

Brain Iron Accumulation

In people with PD, iron levels in the substantia nigra—the brain region where dopamine-producing neurons die—are significantly elevated compared to healthy aging. The mechanism is well understood: excess iron generates oxidative stress through the Fenton reaction, promoting neuronal death. Iron also accelerates the aggregation of alpha-synuclein, the misfolded protein central to PD pathology.

A 2024 study in Science Advances revealed a striking finding: brain iron levels show a U-shaped relationship with Parkinson's risk, with individuals at the high end of iron accumulation showing threefold increased risk. The same study found that men homozygous for the C282Y mutation—the primary cause of hereditary hemochromatosis, a genetic disorder of iron overload affecting 1 in 200 people of Northern European descent—had approximately twofold increased risk of movement disorders.

Early-Life Iron Exposure: A Provocative Hypothesis

One emerging theory may help explain why Parkinson's rates are rising faster in high-income countries: early-life iron fortification. In the U.S. and Europe, infant cereals and formulas have been heavily fortified with iron for decades. A hypothesis published in npj Parkinson's Disease proposes that this increased early-life iron exposure—combined with genetic factors affecting iron regulation—may predispose individuals to accelerated brain iron accumulation later in life.

Practical Implications of Brain Iron Levels

The iron-PD connection is complex. Certainly, individuals with hemochromatosis or known iron-related gene mutations should discuss neurological monitoring with their physicians. Beyond this, it must be emphasized that the relationship between brain iron and body iron levels is by no means completely understood. A Mendelian randomization study found that higher blood iron may in fact be somewhat protective for PD risk. Certainly more study is needed in this area before any recommendations about iron consumption or supplementation can be made.

Stay Tuned

Understanding environmental risks is foundational. Genetics cannot be changed. But environment, activity level, diet, and gut health may be modifiable. Our next report covers the early warning signs—including a sleep disorder that predicts Parkinson's with greater than 80% certainty over extended follow-up—plus breakthrough diagnostic tests that can detect the disease before motor symptoms appear.