Summary: A new study examined the impact of caffeine on brain dopamine function in patients with Parkinson’s disease, finding no benefit on disease progression. High caffeine intake was linked to a greater decrease in dopamine transporter binding, likely due to a compensatory mechanism rather than neuron loss.
The study also noted that recent caffeine consumption can affect diagnostic imaging results, suggesting patients avoid caffeine before testing.
Highlights:
- No improvement in symptoms: High caffeine consumption did not improve the symptoms of Parkinson’s disease.
- Dopaminergic function: Greater decrease in dopamine transporter binding with high caffeine.
- Imaging results: Recent caffeine consumption may affect brain imaging results.
Source: University of Turku
Previous research has shown that regular caffeine consumption is associated with a reduced risk of developing Parkinson’s disease. However, research into the effects of caffeine on disease progression in already diagnosed patients is limited.
A follow-up study conducted by the University of Turku and Turku University Hospital (Tyks) in Finland examined how caffeine consumption affects brain dopamine function over a prolonged period in patients diagnosed with Parkinson’s disease.
Brain dopaminergic function was assessed by single photon emission computed tomography (SPECT) to measure dopamine transporter (DAT) binding.
“The association between high caffeine consumption and reduced risk of Parkinson’s disease has been observed in epidemiological studies.
“However, our study is the first to focus on the effects of caffeine on disease progression and symptoms in relation to dopaminergic function in Parkinson’s disease,” explains Valtteri Kaasinen, professor of neurology at the University from Turku and principal investigator of the study.
Caffeine consumption had no effect on Parkinson’s disease symptoms
A clinical study compared 163 patients with early-stage Parkinson’s disease to 40 healthy controls. Examinations and imaging were performed twice for a subsample, with an average interval of six years between the first and second imaging sessions.
Changes in brain dopamine transporter binding were compared to patients’ caffeine intake, which was assessed both by a validated questionnaire and by determining concentrations of caffeine and its metabolites in blood samples.
The results revealed that patients with high caffeine intake had an 8.3% to 15.4% greater decrease in dopamine transporter binding compared to those with low caffeine intake.
However, it is unlikely that the observed decline in dopamine function is due to a greater reduction in dopamine neurons following caffeine consumption. Rather, it is a compensatory down-regulation mechanism in the brain that has also been observed in healthy individuals after the consumption of caffeine and other stimulants.
“Although caffeine may offer some benefits in reducing the risk of Parkinson’s disease, our study suggests that high caffeine consumption has no beneficial effects on the dopamine system in already diagnosed patients.
“High caffeine consumption did not lead to a reduction in disease symptoms, such as improved motor function,” says Kaasinen.
Another important finding of the study was the observation that a recent dose of caffeine, for example on the morning of the imaging session, temporarily increases the person’s DAT binding values.
This could potentially complicate the interpretation of brain DAT imaging results commonly used in the clinic.
Research findings suggest that patients should abstain from coffee and caffeine for 24 hours before undergoing DAT diagnostic imaging.
About this Parkinson’s research news
Author: Tuomas Koivula
Source: University of Turku
Contact: Tuomas Koivula – University of Turku
Picture: Image is credited to Neuroscience News
Original research: Free access.
“Dietary caffeine and brain dopaminergic function in Parkinson’s disease” by Valtteri Kaasinen et al. Annals of Neurology
Abstract
Dietary Caffeine and Brain Dopaminergic Function in Parkinson’s Disease
Objective
This study was undertaken to investigate the effects of dietary caffeine consumption on striatal dopaminergic function and clinical symptoms of Parkinson’s disease in a cross-sectional and longitudinal context.
Methods
One hundred and sixty-three patients with early Parkinson’s disease and 40 healthy controls were studied with (123I) FP-CIT single photon emission computed tomography and striatal dopamine transporter binding were assessed in association with daily coffee consumption level and clinical measures. After a median interval of 6.1 years, 44 patients with varying levels of caffeine consumption underwent clinical and imaging re-examination, including profiling of caffeine blood metabolites.
Results
Unmedicated early Parkinson’s disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all striatal regions studied than low consumers, after taking taking into account age, sex and severity of motor symptoms. Higher caffeine consumption was further associated with a progressive decrease in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood tests demonstrated a positive correlation between caffeine metabolites after recent caffeine consumption and dopamine transporter binding in the ipsilateral putamen.
Interpretation
Chronic caffeine consumption results in compensatory and cumulative downregulation of dopamine transporters, consistent with caffeine’s reported risk reduction in Parkinson’s disease. However, this reduction is not manifested by changes in symptoms. The transient increase in dopamine transporter binding after recent caffeine consumption has implications for dopamine imaging guidelines.