title: Consumption of a dark roast coffee decreases the level of spontaneous DNA strand breaks: a randomized controlled trial.
abstract: OBJECTIVE
  Coffee consumption has been reported to decrease oxidative damage in peripheral white blood cells (WBC). However, effects on the level of spontaneous DNA strand breaks, a well established marker of health risk, have not been specifically reported yet. We analyzed the impact of consuming a dark roast coffee blend on the level of spontaneous DNA strand breaks.
  
  
  METHODS
  Healthy men (n = 84) were randomized to consume daily for 4 weeks either 750 ml of fresh coffee brew or 750 ml of water, subsequent to a run in washout phase of 4 weeks. The study coffee was a blend providing high amounts of both caffeoylquinic acids (10.18 ± 0.33 mg/g) and the roast product N-methylpyridinium (1.10 ± 0.05 mg/g). Before and after the coffee/water consumption phase, spontaneous strand breaks were determined by comet assay.
  
  
  RESULTS
  At baseline, both groups exhibited a similar level of spontaneous DNA strand breaks. In the intervention phase, spontaneous DNA strand breaks slightly increased in the control (water only) group whereas they significantly decreased in the coffee group, leading to a 27% difference within both arms (p = 0.0002). Food frequency questionnaires indicated no differences in the overall diet between groups, and mean body weight during the intervention phases remained stable. The consumption of the study coffee substantially lowered the level of spontaneous DNA strand breaks in WBC.
  
  
  CONCLUSIONS
  We conclude that regular coffee consumption contributes to DNA integrity.
authors.affiliation: Division of Food Chemistry, Toxicology, and Molecular Nutrition, Department of Chemistry, University of Kaiserslautern, Erwin-Schroedinger-Str. 52, 67663, Kaiserslautern, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Bakuradze
authors.forename: R
authors.initials: R
authors.lastname: Lang
authors.forename: T
authors.initials: T
authors.lastname: Hofmann
authors.forename: G
authors.initials: G
authors.lastname: Eisenbrand
authors.forename: D
authors.initials: D
authors.lastname: Schipp
authors.forename: J
authors.initials: J
authors.lastname: Galan
authors.forename: E
authors.initials: E
authors.lastname: Richling
mesh_terms: D000328:Adult; D000470:Alkaloids / Q000008:administration & dosage / Q000032:analysis / Q000652:urine; D000975:Antioxidants / Q000008:administration & dosage* / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D002110:Caffeine / Q000008:administration & dosage / Q000032:analysis; D040503:Coffea / Q000737:chemistry; D003069:Coffee / Q000737:chemistry; D015331:Cohort Studies; D020552:Comet Assay; D053960:DNA Breaks; D005511:Food Handling; D005858:Germany; D006358:Hot Temperature; D006801:Humans; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D010349:Patient Compliance; D011726:Pyridinium Compounds / Q000008:administration & dosage / Q000032:analysis / Q000652:urine; D011801:Quinic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000032:analysis; D012639:Seeds / Q000737:chemistry
chemical_list: D000470:Alkaloids; D000975:Antioxidants; D015415:Biomarkers; D003069:Coffee; D011726:Pyridinium Compounds; C472707:caffeoylquinic acid; D011801:Quinic Acid; D002110:Caffeine; C009560:trigonelline; C014677:1-methylpyridinium
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