Etiologic roles of beverages in narcolepsy are unknown, although excessive alcohol has been described.1 We conducted a case-control study to assess whether alcohol and caffeinated drinks are associated with narcolepsy among those with human leukocyte antigen (HLA) DQB1*0602. Recruitment methods for cases and controls are detailed elsewhere.2,3 Briefly, we enrolled 67 cases and 95 controls between 18 and 50 years of age, all of whom carried HLA DQB1*0602. Subjects were asked about their consumption of alcohol and caffeinated coffee, tea, and soft drinks before age 21. We examined the associations of narcolepsy with duration, frequency, and consumption before age of onset for cases and before a corresponding index date for controls. Information on demographic factors was obtained during the interview. The University of Washington's institutional review board approved the study, and all participants provided written informed consent. We used logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs). As done previously,2,3 we multiply imputed missing income, and adjusted all models for African American race and income. Models for coffee were additionally adjusted for smoking. We restricted cases to those with cataplexy in secondary analyses.
Among cases, average age of onset was 13.8 years (SD = 6.6), and cataplexy was present in 82%. Coffee consumption before age 21 was significantly associated with narcolepsy (OR = 3.5; 95% CI: 1.5, 8.1). However, when assessed in relation to age of onset, a significant association existed only among those who started drinking coffee after age of onset (OR = 5.0; 95% CI: 2.0, 12.8) compared to non-drinkers, and was not observed for those who drank before the age of onset (OR = 2.2; 95% CI: 0.8, 6.0). Current drinkers of alcohol had a 70% decreased likelihood of having narcolepsy (OR = 0.3; 95% CI: 0.1, 0.7). For caffeinated soft drinks, we observed a significant decreasing trend in the odds ratios for narcolepsy with increasing frequency of consumption (p = 0.03). Estimates of association for those who started consuming soft drinks before age of onset were decreased, although not statistically different from nondrinkers (OR = 0.3; 95% CI: 0.1, 1.4). Associations were not observed for current consumers of caffeinated soft drinks or tea. Restricting cases to those with cataplexy did not change our results.
Our results do not support etiologic roles for coffee, alcohol, or tea. Reverse causality likely explains our findings - that is, cases avoided alcohol and self-medicated with coffee as a result of symptoms or treatments. Results of an inverse association for soft drinks require further exploration. Future epidemiologic studies can build on these initial efforts to provide greater understanding of etiology and thus, prevention of narcolepsy.
DISCLOSURE STATEMENT
The authors have indicated no financial conflicts of interest.
REFERENCES
- 1.Esther M, Fredrickson PA, Richardson J. Association of possible or probable alcoholism in patients with narcolepsy (abstract) Sleep Res. 1990;19:222. [Google Scholar]
- 2.Koepsell TD, Longstreth WT, Ton TG. Medical exposures in youth and the frequency of narcolepsy with cataplexy: a population-based case-control study in genetically predisposed people. J Sleep Res. 2010;19:80–86. doi: 10.1111/j.1365-2869.2009.00756.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Ton TG, Longstreth WT, Koepsell TD. Active and passive smoking and risk of narcolepsy in people with HLA DQB1*0602: a population-based case-control study. Neuroepidemiology. 2009;32:114–21. doi: 10.1159/000177037. [DOI] [PMC free article] [PubMed] [Google Scholar]