Heavy coffee consumption results in lower dopamine activity in the striatum, a brain region affected in Parkinsons disease, and does not ease motor symptoms in early diagnosed patients who have not yet been treated for the neurological disease, a study has found.
However, coffee consumption before brain imaging was seen to influence results, with a temporary enhancement of dopamine activity in the brain.
Clinicians should consider caffeines potential influence on [dopamine] imaging results and incorporate appropriate guidelines for caffeine abstinence prior to imaging, researchers wrote in the study Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease, which was published in the journal Annals of Neurology.
While the reduced dopamine activity in high coffee drinkers may not be harmful, these findings do not support advocating caffeine treatment or increased coffee intake for newly diagnosed PD [Parkinsons disease] patients, the researchers wrote.
Parkinsons is marked by the loss of dopaminergic neurons, those responsible for the production of dopamine, in a brain region called thesubstantia nigra. This causes a deficit of dopamine in the striatum, a region involved in motor control. Dopamine is a signaling molecule that plays a role in controlling movement.
Caffeine has been reported to protect nerve cells from damage, with studies suggesting that its regular intake is associated with a lower risk of developing Parkinsons. Few studies have assessed the effects of caffeine on disease progression in people diagnosed with Parkinsons.
The association between high caffeine consumption and a reduced risk for Parkinsons disease has been observed in epidemiological studies, Valtteri Kaasinen, MD, PhD, a professor of neurology at the University of Turku and the studys lead scientist, said in a university press release. However, our study is the first to focus on the effects of caffeine on disease progression and symptoms in relation to dopamine function in Parkinsons disease.
The researchers at the University of Turku and Turku University Hospital, in Finland, evaluated the effects of caffeine on brain dopamine function in 163 patients with early Parkinsons as well as 40 healthy individuals, who served as controls.
Dopamine activity in the brain was measured using an imaging technology called DaT-SPECT, or dopamine transporter single-photon emission computed tomography. The technology uses X-rays and an injected dye to visualize the levels of dopamine transporter in the brain. This transporter regulates the flow of dopamine between nerve cells, and its steady decrease is found in the brain affected by Parkinsons.
Patients received their first brain scan as part of an observational clinical study (NCT02650843) at Turku University Hospital, and all of them had lower dopamine activity according to their DaT-SPECT scans.
The majority (115 patients) were treatment-nave, meaning they had not yet received any treatment for Parkinsons, with the remaining 47 patients having received dopamine medications at the time of the brain scan.
A total of 44 patients volunteered to participate in the longitudinal analysis where they repeated the brain scans after a mean of 6.1 years (range of 2.3-7.6 years). Of the 44 patients, 29 had been treatment-nave at the start of the study.
During data analysis, patients were grouped according to their daily coffee and therefore caffeine consumption. This was evaluated by a questionnaire and by determining concentrations of caffeine and its metabolites in the blood.
Patients consuming up to three cups of coffee per day were considered low caffeine consumers, and those consuming more were deemed high consumers.
The results from the studys first scan showed treatment-nave patients with a high caffeine intake had lower dopamine activity compared with those with low caffeine consumption, after accounting for several factors, including age, gender, and motor symptom severity.
In the striatum, the levels of dopamine activity were significantly reduced, from 8.3% to 15.4%, in the high versus low coffee drinkers. The highest difference (15.4%) was seen in one of the subregions of the striatum, called the right caudate. No significant differences were found in patients treated with dopaminergic medications or in healthy controls.
After a mean of 6.1 years, dopamine activity was still significantly lower in the striatum of the 29 patients who were initially treatment-nave and high coffee drinkers. This decrease remained statistically significant after accounting for age at the start of the study, gender, and annual change in motor function.
No significant effects of caffeine on motor function were observed.
While caffeine may offer certain benefits in reducing risk of Parkinsons disease, our study suggests that high caffeine intake has no benefit on the dopamine systems in already diagnosed patients. A high caffeine intake did not result in reduced symptoms of the disease, such as improved motor function, Kaasinen said.
Metabolite analysis using blood samples revealed, however, that caffeine intake before brain scan imaging led to a significant, temporary increase of dopamine activity in the brain. The analysis showed a positive correlation between caffeines main metabolite paraxanthine and dopamine activity.
This effect was present for at least 7.5 hours after no more caffeine was consumed. These findings suggest it may be necessary to refrain from caffeine-containing products for at least 24 hours before DAT imaging, the researchers wrote.
Further research encompassing longitudinal [long-term] studies of the acute and long-term effects of caffeine consumption on [dopamine activity] in healthy subjects and individuals at risk for PD is warranted, they concluded.
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Coffee before brain scans may influence results in early Parkinson's - Parkinson's News Today
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