In a new cross-sectional and longitudinal study, researchers from the University of Turku and Turku University Hospital investigated the effect of dietary caffeine intake on dopamine function and clinical symptoms in Parkinson’s disease.
Chronic caffeine intake promotes compensatory and cumulative downregulation of dopamine transporters, consistent with caffeine’s reported reduced risk of Parkinson’s disease. Image courtesy of Department of Clinical Neuroscience, University of Turku.
Caffeine is the most widely consumed psychostimulant worldwide.
Previous studies have shown that regular caffeine consumption may lower the risk of developing Parkinson’s disease.
However, there is limited research on the effect of caffeine on disease progression in patients who have already been diagnosed.
In a new study, Professor Valtteri Karsinen from the University of Turku and his colleagues investigated how caffeine consumption affects the brain’s dopamine function over the long term in patients diagnosed with Parkinson’s disease.
Brain dopamine function was assessed with single-photon emission computed tomography (SPECT) to measure dopamine transporter (DAT) binding.
“An association between high caffeine intake and a reduced risk of Parkinson’s disease has been observed in epidemiological studies,” Professor Karsinen said.
“However, our study is the first to focus on the impact of caffeine on disease progression and symptoms in relation to dopamine function in Parkinson’s disease.”
The authors compared 163 patients with early-stage Parkinson’s disease with 40 healthy controls.
Examination and imaging were performed twice for a subsample, with a mean interval between the first and second imaging sessions being 6 years.
Changes in brain dopamine transporter binding were compared with patients’ caffeine intake, which was assessed using a validated questionnaire and by measuring concentrations of caffeine and its metabolites in blood samples.
Findings revealed that patients with higher caffeine intake had an 8.3-15.4% greater reduction in dopamine transporter binding compared to patients with lower caffeine intake.
However, the observed decrease in dopamine function is unlikely to be due to a significant reduction in dopamine neurons following caffeine ingestion.
Rather, it is more likely a downregulatory compensatory mechanism in the brain that has also been observed in healthy individuals after the use of caffeine and other stimulants.
“While caffeine may have some effect in reducing the risk of Parkinson’s disease, our study suggests that high doses of caffeine have no benefit on the dopamine system in patients already diagnosed with Parkinson’s disease,” Professor Karsinen said.
“Consuming large amounts of caffeine did not result in any reduction in symptoms of the disease, such as improved motor function.”
“Another important finding of this study was the observation that consuming caffeine, for example the morning of an imaging session, temporarily increased a person’s DAT binding levels.”
“This can complicate the interpretation of brain DAT imaging results, which are commonly used clinically.”
“Study results suggest that patients should abstain from coffee and caffeine consumption for 24 hours prior to undergoing a diagnostic DAT imaging procedure.”
a paper A paper explaining the findings was published Annals of Neurology.
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Emi K. Saarinen othersDietary caffeine and brain dopamine function in Parkinson’s disease. Annals of NeurologyPublished online May 20, 2024; doi: 10.1002/ana.26957
Source: www.sci.news
