This just in: caffeine may help prevent Parkinson’s disease:
A new case study published […] in the Archives of Neurology has examined the prevalence of PD, smoking, caffeine, and NSAID usage in 356 patients and 317 of their family members. The study, conducted by a team at Duke University Medical Center, found that although there was no link between PD and NSAID usage, both smoking and caffeine intake were inversely related to PD.
I hven’t bothered to grab the original study off PubMed yet but an Ars Technica reader did post the results from the paper, so I’ve copied them into extended entry if you’re interested.
of course, caffeine might well have long term health effects that make Parkinson’s seem tame; certainly that is the case with smoking. But as a justification for my third cup already this morning, this news works for me.
Results from models examining associations of smoking while controlling for AAE and sex are shown in Table 1.
Individuals with PD were 0.56 times as likely to report ever smoking and 0.30 times as likely to report current smoking compared with unaffected relatives. Dosage, duration, and intensity presented ORs indicative of inverse relationships between PD and smoking with significance at most exposure levels. Dose-response associations were detected with increasing status, dosage, duration, and intensity presented ORs indicative of inverse relationships between PD and smoking with significance at mostexposure levels.
Dose-response associations were detected with increasing status, dosage, duration, and intensity (P .005). Patterns remained significant after truncating exposure at 10 and 20 years before the reference age (Table 1) and adjusting for caffeine and NSAIDs (data not shown). Even after applying the conservative Bonferroni correction for multiple testing, most associations and trends in ORs for smoking remained significant.
Caffeinated coffee associations withPDrelative to never consuming it were assessed while controlling for AAE and sex. When truncating exposure at the reference age, a significant dose response for intensity (trend P=.05) was observed. When truncating exposure at 10 years before the reference age, high dosage ( 2.0 cups/d) was significantly inversely associated with PD (OR=0.64; 95% confidence interval, 0.42-0.99), and increasing dosage showed a significant trend in ORs (P=.05). No significant associations were observed after truncating exposure at 20 years before the reference age or adjusting for smoking and NSAIDs (data not shown).
Overall caffeine associations with PD compared with never consuming it were also assessed while controlling for AAE and sex. These results are presented in Table 2. Case subjects were neither more nor less likely than controls to report ever consuming caffeine. However, a significant inverse association with PD at high dosage and significant inverse gradients for dosage and intensity were detected. The significant inverse gradient for dosage persisted after truncating exposure at 10 and 20 years before the reference age. The trends in ORs for dosage and intensity were nearly significant after adjusting for AAE, sex, smoking, and NSAIDs (trend P=.06 for both), but the significant trends shown in Table 2 did not withstand the conservative Bonferroni correction (trend P=.08 for dosage and trend P=.09 for intensity after Bonferroni correction).