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Population-based study of baseline ethanol consumption and risk of incident essential tremor
  1. E D Louis1,2,3,4,
  2. J Benito-León5,
  3. F Bermejo-Pareja5
  1. 1
    GH Sergievsky Center, Columbia University, New York, USA
  2. 2
    Department of Neurology, Columbia University, New York, USA
  3. 3
    Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, USA
  4. 4
    Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, USA
  5. 5
    Department of Neurology, University Hospital “12 de Octubre,” Madrid, Spain
  1. Dr E Louis, Unit 198, Neurological Institute, 710 West 168th Street, New York, NY 10032, USA; EDL2{at}columbia.edu

Abstract

Background: Recent postmortem studies have demonstrated pathological changes, including Purkinje cell loss, in the cerebellum in essential tremor (ET). Toxic exposures that compromise cerebellar tissue could lower the threshold for developing ET. Ethanol is a well-established cerebellar toxin, resulting in Purkinje cell loss.

Objective: To test whether higher baseline ethanol consumption is a risk factor for the subsequent development of incident ET.

Methods: Lifetime ethanol consumption was assessed at baseline (1994–1995) in a prospective, population-based study in central Spain of 3285 elderly participants, 76 of whom developed incident ET by follow-up (1997–1998).

Results: In a Cox proportional hazards model adjusting for cigarette pack-years, depressive symptoms and community, the baseline number of drink-years was marginally associated with a higher risk of incident ET (relative risk, RR = 1.003, p = 0.059). In an adjusted Cox model, the highest baseline drink-year quartile doubled the risk of incident ET (RR = 2.29, p = 0.018), while other quartiles were associated with more modest elevations in risk (RR3rd quartile = 1.82 (p = 0.10), RR2nd quartile = 1.75 (p = 0.10), RR1st quartile = 1.43 (p = 0.34) vs non-drinkers (RR = 1.00)). With each higher drink-year quartile, the risk of incident ET increased an average of 23% (p = 0.01, test for trend).

Conclusions: Higher levels of chronic ethanol consumption increased the risk of developing ET. Ethanol is often used for symptomatic relief; studies should explore whether higher consumption levels are a continued source of underlying cerebellar neurotoxicity in patients who already manifest this disease.

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Footnotes

  • An additional figure is published online only at http://jnnp.bmj.com/content/vol80/issue5

  • Funding: NEDICES was supported by the Spanish Health Research Agency and the Spanish Office of Science and Technology. Dr Louis is supported by NIH R01 NS042859, R01 NS039422, and ES P03 09089 from the National Institutes of Health, Bethesda, Maryland.

  • Competing interests: None.

  • Ethics approval: Ethics approval was provided by University Hospital “12 de Octubre.”

  • Patient consent: Obtained.

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