title: Consumption of black and green tea had no effect on inflammation, haemostasis and endothelial markers in smoking healthy individuals.
abstract: OBJECTIVE
  Firstly, to study the effect of tea and tea polyphenols on cardiovascular risk indicators of the inflammatory system (IL6, IL1beta and TNF-alpha, CRP), and on haemostasis and endothelial proteins with an acute phase behaviour (fibrinogen, vWF, PAI-1, FVIIa and u-PA). Secondly, to study the relationship between plasma levels of antioxidants (alpha-tocopherol, beta-carotene and vitamin C) and these acute-phase, cardiovascular risk indicators.
  
  
  METHODS
  Randomized study.
  
  
  METHODS
  Sixty-four smoking healthy volunteers were recruited by newspaper advertisements; there were five dropouts.
  
  
  METHODS
  Four-week administration of black tea, green tea, green tea polyphenol isolate and mineral water ( 13-16 per group).
  
  
  METHODS
  Plasma levels of the inflammatory markers IL6, IL1beta, TNF-alpha, CRP, fibrinogen, vWF, PAI-1, FVIIa and u-PA and of the antioxidants alpha-tocopherol, beta-carotene and vitamin C.
  
  
  RESULTS
  Different dosages of tea polyphenols had no effect on inflammation, haemostasis and endothelial markers. There was a significant negative correlation between the levels of the antioxidant beta-carotene and the inflammation markers IL6 and fibrinogen (r = -0.35 and r = -0.37, respectively, P<0.01) in this group of smokers. Remarkably, there was a significant positive correlation between the levels of the antioxidant alpha-tocopherol and the inflammation marker IL6 (r = 0.28, P<0.05).
  
  
  CONCLUSIONS
  Tea drinking had no effect on the levels of the inflammation, haemostasis and endothelial cardiovascular risk factors measured. We did observe a relationship between the antioxidant variables alpha-tocopherol and beta-carotene and inflammation markers in this group of healthy smoking subjects.
authors.affiliation: Division of Vascular and Connective Tissue Research, Gaubius Laboratory, TNO-PG, Leiden, The Netherlands. MPM.deMaat@pg.tno.nl
authors.forename: M P
authors.initials: MP
authors.lastname: de Maat
authors.forename: H
authors.initials: H
authors.lastname: Pijl
authors.forename: C
authors.initials: C
authors.lastname: Kluft
authors.forename: H M
authors.initials: HM
authors.lastname: Princen
mesh_terms: D000210:Acute-Phase Reaction; D000328:Adult; D000975:Antioxidants / Q000032:analysis; D015415:Biomarkers; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005419:Flavonoids; D006487:Hemostasis; D006801:Humans; D007249:Inflammation / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009426:Netherlands; D010636:Phenols / Q000008:administration & dosage; D011108:Polymers / Q000008:administration & dosage; D059808:Polyphenols; D012307:Risk Factors; D012907:Smoking / Q000097:blood / Q000503:physiopathology*; D013662:Tea / Q000737:chemistry
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D005419:Flavonoids; D010636:Phenols; D011108:Polymers; D059808:Polyphenols; D013662:Tea; D005340:Fibrinogen; D002097:C-Reactive Protein