Regular consumption of tea and coffee containing caffeine might reduce the risk of Parkinson’s disease in individuals with certain Asian gene variants predisposing them to the condition, according to new research published in The Lancet Regional Health—Western Pacific00195-5/fulltext).
Parkinson’s disease is a neurodegenerative condition characterized by symptoms like resting tremors, slow movement (bradykinesia), and postural instability. Its incidence increases with age, and it poses a growing challenge for societies with aging populations. Previous research has indicated that both genetic and environmental factors play a role in the development of Parkinson’s disease. Notably, some Asian gene variants, specifically those linked to the LRRK2 gene, have been associated with an increased risk of Parkinson’s disease.
Caffeine has previously been studied for its potential protective effects against Parkinson’s disease. Studies have shown that caffeine can reduce the risk of Parkinson’s disease by up to 25%, with a dose-response relationship indicating that higher caffeine intake may offer greater protection.
The neuroprotective mechanism of caffeine is believed to involve blocking adenosine A2A receptors, reducing neuroinflammation, and mitigating excitotoxicity. However, until this study, the interaction between caffeine and Asian-specific Parkinson’s disease gene variants had not been explored comprehensively.
“The vast majority of the global population consumes tea and coffee regularly, and caffeine may have a protective effect on an aging brain,” said study author Eng-King Tan, deputy CEO and senior neurologist at National Neuroscience Institute in Singapore and a professor at Duke NUS Medical School.
The study involved 4,488 participants and employed a case-control design, a type of observational research design used in medical and epidemiological research. Parkinson’s disease cases were diagnosed based on the UK PD Society Brain Bank clinical diagnostic criteria by movement disorder neurologists at two major movement disorders centers in Singapore. Healthy controls without neurodegenerative diseases were recruited from a Community Health Screening Programme.
The researchers administered a standardized questionnaire through clinical interviews to collect data on demographics, family history of movement disorders, and lifetime caffeine consumption. Caffeine intake was assessed based on daily consumption of coffee and tea, as these are the primary sources of caffeine in the Asian population. Individuals who reported zero lifetime caffeine consumption were categorized as non-caffeine drinkers.
Blood samples were collected from participants and subjected to genotyping to identify the presence of specific LRRK2 gene variants associated with Parkinson’s disease risk. Three variants, G2385R, R1628P, and S1647T, were of particular interest in this study.
Individuals carrying these Asian-specific genetic variants were found to have a 1.5 to 2 times higher risk of developing Parkinson’s disease. However, caffeine consumption significantly reduced the risk of Parkinson’s disease in individuals carrying these gene variants. Caffeine drinkers with the Parkinson’s disease gene variants had a risk reduction of four to eight times compared to non-caffeine drinkers with the same genetic makeup.
Tan told PsyPost he was surprised by the “magnitude of risk reduction in high risk genetic variants carriers.”
Interestingly, the protective benefits of caffeine appeared to increase with higher doses. But even those who consumed less than 200mg of caffeine per day — a relatively modest amount, equivalent to about two cups of traditional Singaporean kopi — still experienced a reduced risk of Parkinson’s disease. This is heartening news for those who might be concerned about overindulging in caffeine.
“This research has important implications for the prevention of Parkinson’s disease, especially in countries like Singapore where the Asian gene variants are common,” Tan said in a press release. “Tea and coffee are readily available and culturally accepted in most Asian societies and consuming caffeine within normal limits offers an easy, pleasant and sociable way for people to potentially reduce their risk of Parkinson’s disease.”
However, the researchers acknowledge the study’s limitations, including the relatively small number of non-caffeine drinkers with specific gene variants due to the lower frequency of non-caffeine consumption in the population. Further independent replication of the findings in other Asian populations is necessary to strengthen the credibility of these results.
The exact mechanisms underlying the interaction between caffeine and LRRK2 variants remain unclear, but further research, including in vitro and animal models, could help unravel this relationship. Finally, it’s essential to recognize that case-control studies can establish associations between factors and outcomes but cannot prove causation. Further research, including prospective cohort studies and experimental studies, are needed to confirm causal relationships.
“We do not know if there are any other unknown contributory factors,” Tan said. “An association does not imply a direct cause effect relationship. This needs to be addressed in a prospective longitudinal study.”
The study, “Caffeine intake interacts with Asian gene variants in Parkinson’s disease: a study in 4488 subjects“, was authored by Yi-Lin Ong, Xiao Deng, Hui-Hua Li, K. Narasimhalu, Ling-Ling Chan, Kumar M. Prakash, Wing-Lok Au, Pavanni Ratnagopal, Louis C. S. Tan, and Eng-King Tan.
