title: Specialty supplement use and biologic measures of oxidative stress and DNA damage.
abstract: BACKGROUND
  Oxidative stress and resulting cellular damage have been suggested to play a role in the etiology of several chronic diseases, including cancer and cardiovascular disease. Identifying factors associated with reduced oxidative stress and resulting damage may guide future disease-prevention strategies.
  
  
  METHODS
  In the VITamins And Lifestyle (VITAL) biomarker study of 209 persons living in the Seattle area, we examined the association between current use of several specialty supplements and oxidative stress, DNA damage, and DNA repair capacity. Use of glucosamine, chondroitin, fish oil, methylsulfonylmethane (MSM), coenzyme Q10 (CoQ10), ginseng, ginkgo, and saw palmetto was ascertained by a supplement inventory/interview, whereas the use of fiber supplements was ascertained by questionnaire. Supplements used by more than 30 persons (glucosamine and chondroitin) were evaluated as the trend across number of pills/week (non-use, <14 pills/week, 14+ pills/week), whereas less commonly used supplements were evaluated as use/non-use. Oxidative stress was measured by urinary 8-isoprostane and PGF2α concentrations using enzyme immunoassays (EIA), whereas lymphocyte DNA damage and DNA repair capacity were measured using the Comet assay. Multivariate-adjusted linear regression was used to model the associations between supplement use and oxidative stress/DNA damage.
  
  
  RESULTS
  Use of glucosamine (Ptrend: 0.01), chondroitin (Ptrend: 0.003), and fiber supplements (P: 0.01) was associated with reduced PGF2α concentrations, whereas CoQ10 supplementation was associated with reduced baseline DNA damage (P: 0.003).
  
  
  CONCLUSIONS
  Use of certain specialty supplements may be associated with reduced oxidative stress and DNA damage.
  
  
  CONCLUSIONS
  Further research is needed to evaluate the association between specialty supplement use and markers of oxidative stress and DNA damage.
authors.affiliation: Authors' Affiliations: Public Health Sciences Division, Clinical Research Division, Fred Hutchinson Cancer Research Center; Departments of Epidemiology, Pharmacy, and Pharmaceutics, University of Washington, Seattle, Washington; Division of Preventive Oncology, National Center for Tumor Diseases; Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center, Heidelberg, Germany.
authors.forename: Elizabeth D
authors.initials: ED
authors.lastname: Kantor
authors.forename: Cornelia M
authors.initials: CM
authors.lastname: Ulrich
authors.forename: Robert W
authors.initials: RW
authors.lastname: Owen
authors.forename: Peter
authors.initials: P
authors.lastname: Schmezer
authors.forename: Marian L
authors.initials: ML
authors.lastname: Neuhouser
authors.forename: Johanna W
authors.initials: JW
authors.lastname: Lampe
authors.forename: Ulrike
authors.initials: U
authors.lastname: Peters
authors.forename: Danny D
authors.initials: DD
authors.lastname: Shen
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Vaughan
authors.forename: Emily
authors.initials: E
authors.lastname: White
mesh_terms: D000368:Aged; D002807:Chondroitin / Q000008:administration & dosage; D004249:DNA Damage; D019587:Dietary Supplements; D005260:Female; D005944:Glucosamine / Q000008:administration & dosage; D006801:Humans; D008019:Life Style; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D012307:Risk Factors; D011795:Surveys and Questionnaires
chemical_list: D002807:Chondroitin; D005944:Glucosamine
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