Low serum caffeine level may be an early biomarker of Parkinson's

By John Murphy, MDLinx
Published January 3, 2018

Key Takeaways

A low serum level of caffeine may be an early diagnostic biomarker of Parkinson’s disease (PD), according to results of a new study published online in Neurology.

In this study, patients with Parkinson’s disease had significantly lower absolute serum concentrations of caffeine and nine caffeine-related metabolites than subjects without the disease, despite consuming the same amount of caffeine.

When the researchers analyzed these data, they correctly identified Parkinson’s disease patients from controls with very high accuracy (area under the curve: 0.98).

“Caffeine metabolite profiles may be reliable diagnostic biomarkers for early Parkinson’s disease,” the authors concluded.

“If these results can be confirmed, they would point to an easy test for early diagnosis of Parkinson’s, possibly even before symptoms are appearing,” said neuropathologist David G. Munoz, MD, MSc, University of Toronto, Canada, who wrote an editorial accompanying the study. “This is important because Parkinson’s disease is difficult to diagnose, especially at the early stages.”

This research suggests that the decrease in caffeine metabolites occurs in the earliest stages of Parkinson’s, Dr. Munoz noted, because serum levels of caffeine weren’t lower in patients with more severe stages of the disease.

Metabolism of caffeine

Other researchers have suggested that daily caffeine consumption has a neuroprotective effect against Parkinson’s disease.

“Previous studies have shown a link between caffeine and a lower risk of developing Parkinson’s disease, but we haven’t known much about how caffeine metabolizes within the people with the disease,” said study author Shinji Saiki, MD, PhD, Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.

To that end, Dr. Saiki and fellow researchers recruited 108 patients who had Parkinson’s disease for an average of 6 years, as well as 31 age-matched participants without the disease, and tested their blood samples for caffeine and 11 of its metabolites. They also tested patients for mutations in caffeine-associated genes.

Subjects in both groups consumed about the same amount of caffeine, equivalent to nearly two cups of coffee per day. Upon genetic analysis, researchers found no differences in caffeine-related genes between the two groups.

However, serum levels of caffeine and almost all its downstream metabolites were lower in Parkinson’s disease patients than in controls. For instance, Parkinson’s disease patients had serum levels of caffeine—and its three main metabolites—that were less than half of the levels found in control participants. Dr. Saiki and colleagues concluded that patients with Parkinson’s disease didn’t absorb caffeine as well as the control subjects.

A notable limitation of the study: Nearly all the Parkinson’s disease patients were on antiparkinsonian medications, which may affect caffeine metabolism, the investigators noted.

“The authors address this issue by finding no association between levels of caffeine metabolites and levodopa equivalent doses, but it is obvious that the validity of the study hangs on this point,” Dr. Munoz wrote in his accompanying editorial. “If a future study were to demonstrate similar decreases in caffeine in untreated patients with PD…the implications of the current study would take enormous importance.”

Such studies in drug-free patients are urgently needed, he added.

This study was supported by the Japan Agency for Medical Research and Development, Japan Society for the Promotion of Science, and the Japanese Ministry of Education, Culture, Sports, Science and Technology.

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