ArticleJournal of neurology, neurosurgery, and psychiatry2009
Population-based study of baseline ethanol consumption and risk of incident essential tremor.
Article in Journal of neurology, neurosurgery, and psychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- An Exploratory Analysis of Essential Tremor and Associated Phenotypes.Tremor and other hyperkinetic movements (New York, N.Y.) · 2026Article
- [Alcohol as a rescue treatment for essential tremor: too risky to recommend].Revista de neurologia · 2022Article
- Review
- Essential tremor.Nature reviews. Disease primers · 2021Review
- Etiologic links between environmental and lifestyle factors and Essential tremor.Annals of clinical and translational neurology · 2019Review
- Essential tremor then and now: How views of the most common tremor diathesis have changed over time.Parkinsonism & related disorders · 2018Review
- Conditions Associated with Essential Tremor in Veterans: A Potential Role for Chronic Stress.Tremor and other hyperkinetic movements (New York, N.Y.) · 2018Article
- Semi-quantitative data on ethanol consumption in 354 ET cases and 370 controls.Journal of the neurological sciences · 2014Article
- Understanding essential tremor: progress on the biological front.Current neurology and neuroscience reports · 2014Review
- Were James Bond's drinks shaken because of alcohol induced tremor?BMJ (Clinical research ed.) · 2013Article
- Biomarkers demonstrate increased consumption, but not abuse, of ethanol in essential tremor.Journal of neurology · 2012Article
- Essential tremor is not a neurodegenerative disease.Neurodegenerative disease management · 2012Article
- The NEDICES Study: Recent Advances in the Understanding of the Epidemiology of Essential Tremor.Tremor and other hyperkinetic movements (New York, N.Y.) · 2012Article
- Methods and design of the baseline survey of the neurological disorders in Salamanca (NEDISA) cohort: a population-based study in Central-Western Spain.Neuroepidemiology · 2011Article
- Treatment of Essential Tremor: Are there Issues We are Overlooking?Frontiers in neurology · 2011Article
- Epidemiology and management of essential tremor in children.Paediatric drugs · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundRecent 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.
objectiveTo test whether higher baseline ethanol consumption is a risk factor for the subsequent development of incident ET.
methodsLifetime 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).
resultsIn 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 (RR(3rd quartile) = 1.82 (p = 0.10), RR(2nd quartile) = 1.75 (p = 0.10), RR(1st 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).
conclusionsHigher 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.