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Neurodegenerative disorders

Coffee and Parkinson’s disease

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Neurodegenerative disorders
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Effects of coffee consumption

Global Incidence

The World Health Organisation reported that the prevalence of Parkinson’s disease (PD) doubled in the past 25 years. Global estimates in 2019 showed over 8.5 million individuals with PD. Current estimates suggest that, in 2019, PD resulted in 5.8 million disability adjusted life years (DALYs), an increase of 81% since 2000, and caused 329,000 deaths (an increase of over 100% since 2000)23.

PD is a debilitating neurodegenerative disorder. The cardinal features of PD are the slowing down of motor function, resting tremor, muscular rigidity, gait disturbances, and postural reflex impairment, associated with the destruction of neurons in the midbrain. There is currently no available treatment to either prevent or slow down this neuronal loss. Experimental and epidemiological research has focused on lifestyle, dietary and environmental risk factors, including coffee consumption.

Coffee, caffeine and risk of Parkinson’s disease

A large number of epidemiological studies reported an inverse, dose-responsive relationship between coffee/caffeine consumption and the risk of developing PD. Coffee consumption appears to reduce or delay the development of PD and caffeine is most likely the causal factor. However, in women the interaction between caffeine and hormonal therapy still needs further clarification.

A number of meta-analyses and reviews have been undertaken, which support the view that coffee consumption is associated with a reduced risk of PD.

  • A 2017 literature review suggested that most reports indicate that moderate coffee consumption may lower the risk for common neurodegenerative conditions, including PD18.
  • A 2020 meta-analysis concluded that caffeine modified both disease risk among a healthy population and progression of the disease in those diagnosed with PD24.

A 2023 review reinforced the suggestion that caffeine delays the onset of PD in a dose-dependent manner, particularly in men. The authors also suggest that other compounds in coffee may be important in addition to caffeine25.

In women, the data is more equivocal. The same review concludes that some studies have found the difference to be sex-dependent; coffee consumption in men was associated with a lower risk of PD, but not women. However, the authors suggest that coffee consumption is not associated with a reduced risk of PD in women undergoing hormone replacement therapy (HRT)25. Further work supported previous findings that increased caffeine intake may be associated with a decreased PD risk in men and also in women who have never used hormone replacement26.

Mechanism of action

Experimental studies have suggested a potential mechanism of action for caffeine’s preventative role in the development of PD.

A 2021 review of coffee bioactive compounds suggested that trigonelline may be a promising neuroprotective agent mainly due to its antioxidant, anti-inflammatory, and anti-apoptotic properties. However, the exact molecular mechanisms underlying the neuroprotective effects of trigonelline need to be established22.

A 2022 review, suggested that the Mediterranean diet may be involved in modulating both PD onset and its progression, particularly factors such as intakes of polyphenols, polyunsaturated fatty acids, and coffee27.

The role of genetic polymorphisms has been considered in a number of areas. One assessment of PD incidence and prevalence suggested that associations with daily coffee consumption were strongest among carriers of variant alleles in both ADORA2A and CYP1A228. However, a further study of interactions between GRIN2A and CYP1A2 polymorphisms did not show an interaction with caffeine intake in determining PD risk29.

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