Black tea helps in one Parkinson’s type, but soda and pesticides worsen another

By Priyanjana Pramanik, MSc.Reviewed by Susha Cheriyedath, M.Sc.Jun 16 2025

Researchers uncover subtype-specific effects of tea, soda, and pesticides on Parkinson’s disease, revealing how lifestyle and environment can shape motor symptom severity long after diagnosis.

Study: Longitudinal assessment of the association between pesticide exposure and lifestyle with Parkinson’s disease motor severity. Image Credit: Pixel-Shot / Shutterstock

In a recent article published in the journal npj Parkinson’s Disease, researchers investigated how lifestyle factors and environmental exposures affect the severity of motor symptoms in patients with Parkinson’s disease over time.

They found that the consumption of black tea was linked to milder motor symptoms in one form of the disease. At the same time, pesticide exposure and the consumption of caffeinated soda have been implicated in worsening motor symptoms in another disease type.

Background

Parkinson’s disease is a neurodegenerative disorder currently affecting about 12 million people worldwide, with cases rising by over 60% from 1990 to 2021. The lack of a cure means the burden on society continues to grow.

Around 15% of Parkinson’s cases are caused by single gene mutations or strong risk factors, with the LRRK2 G2019S variant being the most common for autosomal-dominant Parkinson’s disease (LRRK2-PD).

Previous research suggests that LRRK2-PD patients often have more pronounced motor issues but less severe non-motor symptoms compared to idiopathic Parkinson’s disease (iPD) patients.

Environmental and lifestyle factors also play a significant role in the development and progression of this condition. Pesticide exposure is a well-established risk factor, linked to earlier disease onset and faster progression.

Other environmental risks, like air pollution, solvents, and heavy metals, show mixed results. Drinking coffee and smoking consistently appear protective, delaying onset in both iPD and LRRK2-PD, whereas caffeinated soda may hasten onset in LRRK2-PD.

However, the effect of these factors on motor severity over time remains unclear, especially for smoking and caffeine intake. Cross-sectional studies hint that smoking could worsen symptoms post-onset, creating a paradox where a factor that protects against developing the disease might be harmful after diagnosis.

Therefore, more robust longitudinal studies using large cohorts are needed to clarify how environment and lifestyle impact motor symptom progression, particularly distinguishing between LRRK2-PD and iPD.

About the study

This study used data from two large online cohorts. Participants with Parkinson’s disease were recruited and followed through routine online assessments of non-motor and motor symptoms, as well as detailed questionnaires on lifestyle habits and environmental exposures.

Ethical approval and informed consent were secured for both cohorts.

To ensure consistency, only participants with an age at onset of over 25 years, a disease duration of under 50 years, and at least three motor assessments were included. This resulted in 5,134 iPD patients and 81 LRRK2-PD patients.

Motor symptom severity was measured using a cumulative score, consistently collected in both cohorts. Follow-up lasted up to 35 months for one cohort and 60 months for the second, divided into discrete periods for analysis.

Environmental and lifestyle factors, including pesticide exposure, smoking, and caffeine intake, were measured using standardized Parkinson’s disease Risk Factor Questionnaires.

Linear mixed-effects models were used to assess the relationship between these factors and motor symptom progression over time. The models adjusted for age at onset, disease duration, experience of OFF episodes, and sex, with the patient’s identification number as a random effect.

Significance thresholds were adjusted for multiple comparisons in pesticide exposure analyses; other analyses were exploratory. This approach ensured a robust, longitudinal assessment of how environment and lifestyle may influence Parkinson’s disease motor outcomes.

Key findings

Across multiple assessments, motor symptoms worsened gradually in both groups, but iPD patients generally showed more severe progression than LRRK2-PD patients.

Notably, exposure to pesticides at work was linked to greater motor severity in iPD patients in the PPMI-Online cohort, with a similar but non-significant trend observed in the Fox Insight cohort. This association persisted after adjusting for sex. No such association was found in LRRK2-PD patients.

Smoking was also associated with increased motor symptom severity over time in iPD patients. This effect was significant in the PPMI-Online cohort, but only a subtle trend was observed in the Fox Insight cohort. This effect held after controlling for sex.

Regarding caffeinated drinks, black tea consumption did not influence motor severity in iPD but was linked to milder symptoms in LRRK2-PD patients. While the authors caution that this subgroup was small, they strengthened this preliminary finding by replicating it in a second, independent cohort of LRRK2-PD patients.

Conversely, caffeinated soda consumption was associated with more severe motor symptoms in iPD patients and showed a similar trend in LRRK2-PD, though less robustly. The paper notes that caffeinated diet soda, which lacks high sugar content, showed no such association.

Interestingly, the link between caffeinated soda intake and worse motor symptoms was stronger among women than men with iPD. Consumption of coffee and green tea showed no clear impact on motor symptom progression in either group.

Conclusions

This study highlights the impact of environmental and lifestyle factors on the progression of Parkinson’s disease. It found that pesticide exposure and caffeinated soda intake were linked to worse motor symptoms in iPD, while smoking showed a weaker association that was not consistent across both study cohorts.

For LRRK2-PD, black tea consumption appeared protective, though this effect was not seen in iPD, suggesting subtype-specific impacts. This finding is notable because it was observed in two independent cohorts, although both were small.

The study’s strengths include its large sample size, long follow-up period, and use of two independent cohorts, which support robust findings. However, small LRRK2-PD samples limit generalizability, and other monogenic forms have not been thoroughly examined. Lack of data on medication doses, dietary details (such as sugar intake), and potential recall bias are additional limitations.

Despite these, the study emphasizes that environmental exposures, which are harder to control than lifestyle choices, can worsen Parkinson’s symptoms even after disease onset. The findings also underscore how a factor like smoking can be protective before onset but potentially harmful after, and suggest how ingredients like sugar in soda may play a role separate from caffeine.

Future research should confirm these results in larger, diverse genetic groups and use objective measures of exposure. Understanding these relationships may help tailor prevention and management strategies for different Parkinson’s disease subtypes.