In a groundbreaking revelation, the complex relationship between caffeine consumption and Parkinson's disease (PD) risk has been unveiled, particularly in the context of specific genetic variants. The pivotal study offered profound insights into PD prevention where individuals carrying certain risk variants who abstain from caffeine face dramatically increased odds of PD.
The study results were published in the journal The Lancet Regional Health, Western Pacific.

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Parkinson's disease (PD) continues to be a significant health concern globally. Intriguingly, studies have suggested a potential shield against PD in the form of caffeine intake, although the nuances of this relationship, especially concerning specific genetic variants, have remained veiled. Addressing this gap in knowledge, a recent investigation delved into the intricate interaction between caffeine consumption and genetic variants associated with PD risk, particularly focusing on the LRRK2 gene, in a cohort of Asian subjects.
The study encompassed 5100 participants, a blend of PD patients and controls without neurological disorders. Caffeine intake was meticulously assessed using a validated evaluation tool. Genotyping was conducted to identify the presence of Leucine-rich repeat kinase 2 (LRRK2) risk variants, a significant genetic factor linked to PD susceptibility. Advanced statistical analyses, employing logistic regression models, were utilized to explore these gene-caffeine interactions. The study's unique approach included quantifying these interactions through the attributable proportion (AP) due to interaction, with a positive interaction being defined as AP >0.
Key findings:
Among the 4488 subjects with genetic data for at least one LRRK2 variant, compelling patterns emerged.
Risk-variant carriers, who refrained from caffeine consumption, exhibited a stark increase in PD odds in comparison to wild-type carriers who embraced caffeine.
Noteworthy risk variants, namely G2385R, R1628P, and S1647T, showcased a considerable elevation in PD risk for non-caffeine-drinkers.
The odds ratios for these variants were 8.6, 4.6, and 4.0 respectively, underlining a substantial risk amplification.
Moreover, the attributable proportion (AP) values, quantifying the impact of gene-caffeine interaction, substantiated these findings, further emphasizing the protective role of caffeine in specific genetic contexts.
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Thus, this study illuminates a vital connection between caffeine intake and PD risk among carriers of specific LRRK2 genetic variants. These findings not only shed light on the potential preventive aspects of caffeine but also suggest a promising avenue for lifestyle modifications in individuals at risk for Parkinson's disease. The study's insights hold significant implications for both the scientific understanding of PD and the development of targeted preventive strategies in the Asian population.
Further reading: Caffeine intake interacts with Asian gene variants in Parkinson's disease: a study in 4488 subjects. https://doi.org/10.1016/j.lanwpc.2023.10087