Researchers highlight the sub-avoidance-specific effects of tea, soda and pesticides on Parkinson’s disease, suggesting that prolonged lifestyle and environmental motor symptoms can shape from prolonged diagnosis.

Study: Parkinson’s disease motor severity with a longitudinal evaluation of the association between pesticide risk and lifestyleImage Credit: Pixel-shot / Shutterstock

In a recent article published in the journal NPJ Parkinson’s diseaseResearchers investigated how lifestyle factors and environmental risk affect the severity of motor symptoms in patients with Parkinson’s disease over time.

They found that the consumption of black tea was associated with Miller motor symptoms in a form of disease. At the same time, pesticides and caffeinated soda consumption is implicated in deteriorating motor symptoms in another disease type.

background

Parkinson’s disease is a neurodynative disorder that is currently affecting around 12 million people worldwide, with cases of over 60% of cases from 1990 to 2021. Lack of treatment means that the burden on society continues to increase.

About 15% of Parkinson’s cases are caused by single gene mutation or strong risk factors, the LRRK2 G2019s variant is the most common for autosomal Parkinson’s disease (LRRK2-PD).

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

Environment and lifestyle factors also play an important role in the development and progress of this situation. Pesticide Risk is a well -installed risk factor, which is associated with the onset and rapid progress of earlier disease.

Other environmental risk, such as air pollution, solvents and heavy metals, show mixed results. Drinking coffee and smoking appears continuously protective, delaying the onset in both IPD and LRRK2-PD, while caffeinated soda can begin in LRRK2-PD.

However, the effect of these factors on the severity of the motor over time is not clear, especially for smoking and caffeine intake. Cross-sectional studies indicate that smoking can deteriorate symptoms with post-onset, causing a contradiction where a factor that prevents the disease can be harmful after diagnosis.

Therefore, more strong longitudinal studies using large corrts need to clarify how environmental and lifestyle motor symptoms affect progress, especially the difference between LRRK2-PD and IPD.

About studies

This study used data from two large online corrts. Participants were recruited with Parkinson’s disease and were performed through regular online assessment of non-motor and motor symptoms as well as detailed questionnaires at lifestyle habits and environmental risks.

Ethical approval and informed consent was secured for both colleagues.

To ensure continuity, participants with an age only with an age over 25 years of age, and at least three motor assessments were included. As a result, there were 5,134 IPD patients and 81 LRRK2-PD patients.

Motor symptoms severity was measured using a cumulative score, which was constantly collected in both colleagues. Follow-up lasted up to 35 months for a coert and 60 months for the other, divided into the discrepant period for analysis.

Environment and lifestyle factors, including pesticides, risk, smoking and caffeine intake, were measured using standardized Parkinson’s Risk Caurus Questionnaire.

Over time, linear mixed-effect models were used to assess relationships between these factors and motor symptoms progression. As a random effect, the patient’s identity with the number of the disease, the duration of the disease, the experience of the off episode, and the adjustable models adjusted to the age on sex experience.

The importance to many comparisons in pesticide risk analysis was adjusted to Thresholds; Other analysis were searching. This approach ensured a strong, longitudinal assessment of how environment and lifestyle Parkinson’s disease can affect motor consequences.

major findings

During several assessments, motor symptoms gradually deteriorated in both groups, but IPD patients usually showed more serious progress than LRRK2-PD patients.

In particular, more motor motor in IPD patients in PPMI-online coast in contact with pesticides at work was seriously linked to Fox Insight Cohourt with a similar but non-realized tendency. The association remained after adjusting to sex. No such association was found in LRRK2-PD patients.

Smoking was also associated with increasing motor symptoms severity in IPD patients over time. This effect was important in PPMI-Online Cohort, but only one microscopic trend was observed in Fox Insight Corort. This effect was held after controlling for sex.

Regarding caffeinated drinks, black tea consumption did not affect the severity of the motor in IPD, but LRRK2-PD was associated with milder symptoms in patients. While the authors took care that this subgroup was small, they strengthened this initial discovery by repeating it in each other, independent corket of LRRK2-PD patients.

In contrast, caffeinated soda consumption was associated with more severe motor symptoms in IPD patients and a similar trend in LRRK2-PD, although less strongly. The paper notes that caffeine diet soda, which lacks high sugar material, showed no such association.

Interestingly, caffeine -rich soda intake and worse motor symptoms were stronger in women than men with IPD. Coffee and green tea consumption showed no clear effect on motor symptoms progression in both groups.

conclusion

This study highlights the impact of environment and lifestyle factors on the progression of Parkinson’s disease. It was found that the intake of pesticides exposure and caffeinated soda was associated with worse motor symptoms in IPD, while smoking showed a weak association that both studies did not suit the cohorts.

For LRRK2-PD, the consumption of black tea appeared protective, although this effect was not seen in the IPD, which suggests sub-availability-specific effects. This discovery is notable because it was seen in two independent colleagues, although both were small.

The strength of the study involves the size of its large sample, long follow -up periods and the use of two independent colleagues, supporting strong conclusions. However, small LRRK2-PD samples limit generally, and other monoogenic forms have not been thoroughly examined. The dose of the drug, dietary details (eg sugar intake), and lack of data on potential recall prejudices are additional limitations.

Despite these, the study emphasizes that environmental risk, which is difficult to control compared to lifestyle options, can even spoil the symptoms of Parkinson’s even after the onset of the disease. Conclusions also underlines how factors such as smoking can be protective before the beginning, but potentially can be harmful, and suggests how materials like sugar in soda can play a different role from caffeine.

Future research should confirm these results in large, diverse genetic groups and use the purpose measures of risk. Understanding these relationships can help in tailor prevention and management strategies for various Parkinson’s disease sub -factories.