All Science News articles summarize a research study and are not an official opinion, endorsement or position of the Parkinson’s Foundation’s.
For years, drinking coffee has been associated with having a reduced risk of developing Parkinson's disease (PD). In fact, a 1968 study suggested that coffee drinkers were less like to get PD (Nefzger, Quadfasel, & Karl, 1968). Since then, multiple epidemiologic studies have confirmed the PD/coffee connection (Ascherio et al., 2003; Ascherio et al., 2004; Fujimaki et al., 2018). Researchers have mostly attributed the protective effect to the caffeine component (Lee et al., 2013).
However, coffee is more than a caffeine delivery system. Coffee has more than 1,000 different compounds, including organic acids, sugars, amino acids and fatty acids. One such fatty acid called Eicosanoyl-5-hydroxytryptamide (EHT) has been getting quite a bit of buzz in the PD research community; and, for good reason. A recently published study titled, “Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson’s disease and DLB” (Yan et al., 2018), provides some compelling insights into the possible biochemical protective mechanisms of our cup of joe.A recently published study in the journal, Neuropsychopharmacology, sought to determine if having ADHD and/or its treatment, increases the risk of having basal ganglia and cerebellar diseases. In this 20-year follow-up retrospective cohort study, a total of 190,586 patient records (31,796 with ADHD and 158,790 without ADHD) from Utah were examined. People with no prior PD diagnosis or symptoms, no basal ganglia/cerebellar disease and those with a history of substance abuse were excluded from participating in the study.
Here’s what the researchers did: over a six-month period, they treated groups of two different PD model mice with various combinations of caffeine and EHT (caffeine alone, EHT alone, or caffeine and EHT together) to study their effects on both brain and behavior. There was also a group of mice that received no treatment. Then they performed several behavioral tests to study their movement, as well as study their brains for signs of alpha-synuclein clumps (which result in Lewy bodies, the pathological hallmark of PD), neurodegeneration and inflammation. The study found that the untreated mice had significant amounts of clumped α-synuclein in their brains, increased inflammation and loss of neurons, as well as significant deficits on three different behavioral tests. In general, the mice treated with EHT or caffeine alone showed either no or minimal improvement in any of these measures. However, the mice treated with the combination of EHT and caffeine together showed significant improvements in all of these measures.
- More specifically, mice treated with both EHT and caffeine together:
- Had less alpha-synuclein clumping in the brain
- Maintained better neuron integrity and function
- Had less brain inflammation
- Displayed less movement symptoms
What Does This Mean?
In this study, a synergistic combination of EHT and caffeine was shown to slow down the progression of the neurodegeneration associated with PD in mice — which has potentially readily available therapeutic implications. In addition, previous research has demonstrated that caffeine enhances dopamine signaling in the brain (Volkow et al., 2015); and, it’s the death of dopamine-producing cells that results in movement symptoms of PD (and why dopamine replacement medication is the gold standard treating PD symptoms).
For years, coffee consumption has been suggested to play a protective role in developing PD. However, it was never clear what exactly in coffee had this effect. This study suggests that two compounds, caffeine and the fatty acid EHT, work together to protect against alpha- synuclein clumps and dopamine neuron loss in two different PD models of mice. Interestingly, these effects were seen even using very low doses of the compounds. If the results of this study can be replicated by other researchers, then identifying that delicate balance of safety and effectiveness for humans is likely an essential step that researchers will be investigating in the future.
The Parkinson’s Foundation believes in empowering the Parkinson’s community through education. Learn more about the connection between dopamine, caffeine, Lewy bodies and alpha-synuclein and Parkinson’s in the below Parkinson’s Foundation resources or by calling our free Helpline at 1-800-4PD-INFO (473-4636).
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Ascherio, A., Chen, H., Schwarzschild, M. A., Zhang, S. M., Colditz, G. A., & Speizer, F. E. (2003). Caffeine, postmenopausal estrogen, and risk of Parkinson's disease. Neurology, 60(5), 790-795.
Ascherio, A., Weisskopf, M. G., O'Reilly, E. J., McCullough, M. L., Calle, E. E., Rodriguez, C., & Thun, M. J. (2004). Coffee consumption, gender, and Parkinson's disease mortality in the cancer prevention study II cohort: the modifying effects of estrogen. Am J Epidemiol, 160(10), 977-984. doi:10.1093/aje/kwh312
Chang, K. L., & Ho, P. C. (2014). Gas chromatography time-of-flight mass spectrometry (GC-TOF-MS)-based metabolomics for comparison of caffeinated and decaffeinated coffee and its implications for Alzheimer's disease. PLoS One, 9(8), e104621. doi:10.1371/journal.pone.0104621
Collaborators, G. B. D. P. s. D. (2018). Global, regional, and national burden of Parkinson's disease, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol, 17(11), 939-953. doi:10.1016/S1474-4422(18)30295-3
Fujimaki, M., Saiki, S., Li, Y., Kaga, N., Taka, H., Hatano, T., . . . Hattori, N. (2018). Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology, 90(5), e404-e411. doi:10.1212/WNL.0000000000004888
Lee, K. W., Im, J. Y., Woo, J. M., Grosso, H., Kim, Y. S., Cristovao, A. C., . . . Mouradian, M. M. (2013). Neuroprotective and anti-inflammatory properties of a coffee component in the MPTP model of Parkinson's disease. Neurotherapeutics, 10(1), 143-153. doi:10.1007/s13311-012-0165-2
Nefzger, M. D., Quadfasel, F. A., & Karl, V. C. (1968). A retrospective study of smoking in Parkinson's disease. Am J Epidemiol, 88(2), 149-158.
Vicente, S. J., Ishimoto, E. Y., & Torres, E. A. (2014). Coffee modulates transcription factor Nrf2 and highly increases the activity of antioxidant enzymes in rats. J Agric Food Chem, 62(1), 116-122. doi:10.1021/jf401777m
Volkow, N. D., Wang, G. J., Logan, J., Alexoff, D., Fowler, J. S., Thanos, P. K., . . . Tomasi, D. (2015). Caffeine increases striatal dopamine D2/D3 receptor availability in the human brain. Transl Psychiatry, 5, e549. doi:10.1038/tp.2015.46
Yan, R., Zhang, J., Park, H.-J., Park, E. S., Oh, S., Zheng, H., . . . Mouradian, M. M. (2018). Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson's disease and DLB. Proceedings of the National Academy of Sciences, 115(51), E12053-E12062. doi:10.1073/pnas.1813365115