title: Serum cholesterol and the progression of Parkinson's disease: results from DATATOP.
abstract: BACKGROUND
  Recent studies have suggested that higher serum cholesterol may be associated with lower occurrence of Parkinson's disease (PD). This study is to test the hypothesis that higher serum cholesterol correlates with slower PD progression.
  
  
  METHODS
  Baseline non-fasting serum total cholesterol was measured in 774 of the 800 subjects with early PD enrolled between 1987 and 1988 in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) trial. Participants were followed for up to two years, with clinical disability requiring levodopa therapy as the primary endpoint. Hazard ratios (HRs) and 95% confidence intervals (CI) were determined for increasing serum cholesterol concentration (in quintiles) for clinical disability requiring levodopa therapy, after adjusting for confounders. At baseline, only nine subjects reported use of cholesterol-lowering agents (two with statins).
  
  
  RESULTS
  The overall mean cholesterol level was 216 mg/dL (range 100-355). The HR of progressing to the primary endpoint decreased with increasing serum cholesterol concentrations. Compared to the lowest quintile, the HRs (95%CI), for each higher quintile (in ascending order) are 0.83 (0.59-1.16); 0.86 (0.61-1.20); 0.84 (0.60-1.18); and 0.75 (0.52-1.09). The HR for one standard deviation (SD) increase = 0.90 [(0.80-1.01), p for trend = 0.09]. This trend was found in males (HR per SD = 0.88 [(0.77-1.00), p for trend = 0.05], but not in females [HR = 1.03 (0.81-1.32)].
  
  
  CONCLUSIONS
  This secondary analysis of the DATATOP trial provides preliminary evidence that higher total serum cholesterol concentrations may be associated with a modest slower clinical progression of PD, and this preliminary finding needs confirmation from larger prospective studies.
authors.affiliation: Department of Neurology, Pennsylvania State University-Milton Hershey Medical Center, Hershey, Pennsylvania, United States of America. Xuemei@psu.edu
authors.forename: Xuemei
authors.initials: X
authors.lastname: Huang
authors.forename: Peggy
authors.initials: P
authors.lastname: Auinger
authors.forename: Shirley
authors.initials: S
authors.lastname: Eberly
authors.forename: David
authors.initials: D
authors.lastname: Oakes
authors.forename: Michael
authors.initials: M
authors.lastname: Schwarzschild
authors.forename: Alberto
authors.initials: A
authors.lastname: Ascherio
authors.forename: Richard
authors.initials: R
authors.lastname: Mailman
authors.forename: Honglei
authors.initials: H
authors.lastname: Chen
mesh_terms: D000975:Antioxidants / Q000627:therapeutic use; D002784:Cholesterol / Q000097:blood*; D018450:Disease Progression; D023381:Endpoint Determination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000097:blood* / Q000188:drug therapy / Q000473:pathology*; D016016:Proportional Hazards Models; D016032:Randomized Controlled Trials as Topic; D012642:Selegiline / Q000627:therapeutic use; D024505:Tocopherols / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D012642:Selegiline; D002784:Cholesterol; D024505:Tocopherols