title: The effect of homocysteine reduction by B-vitamin supplementation on inflammatory markers.
abstract: BACKGROUND
  Hyperhomocysteinemia has been associated with vascular disease in many epidemiological studies. However, the pathophysiology is unclear. It is postulated that increased levels of homocysteine induce an inflammatory response in endothelial cells, mediated by pro-inflammatory cytokines and chemokines. The aim of this study was to investigate whether plasma concentrations of interleukin-6, interleukin-8, C-reactive protein, and monocyte chemoattractant protein-1 are increased with higher plasma homocysteine concentrations and whether decreasing homocysteine by vitamin supplementation decreases the concentration of these markers.
  
  
  METHODS
  Plasma homocysteine, interleukin-6, interleukin-8, C-reactive protein, and monocyte chemoattractant protein-1 concentrations were measured in 230 volunteers before and after 8 weeks of multivitamin supplementation (folic acid, B(6), and B(12)).
  
  
  RESULTS
  At baseline, plasma homocysteine concentration was weakly associated with interleukin-8, but not with interleukin-6, C-reactive protein or monocyte chemoattractant protein-1. Vitamin supplementation resulted in a significant decrease in homocysteine concentration, but no effect on interleukin-6, interleukin-8, C-reactive protein or monocyte chemoattractant protein-1 was observed.
  
  
  CONCLUSIONS
  At baseline homocysteine was only weakly correlated with interleukin-8, but not with interleukin-6, C-reactive protein or monocyte chemoattractant protein-1. Vitamin supplementation affected homocysteine concentration, but not cytokine levels. The hypothesis that hyperhomocysteinemia increases arteriosclerotic or thrombotic risk through vascular inflammation was not supported by this study.
authors.affiliation: Department of Endocrinology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Anita C T M
authors.initials: AC
authors.lastname: Peeters
authors.forename: Benien E
authors.initials: BE
authors.lastname: van Aken
authors.forename: Henk J
authors.initials: HJ
authors.lastname: Blom
authors.forename: Pieter H
authors.initials: PH
authors.lastname: Reitsma
authors.forename: Martin
authors.initials: M
authors.lastname: den Heijer
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000097:blood; D019587:Dietary Supplements; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage*; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000188:drug therapy*; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D014805:Vitamin B 12 / Q000008:administration & dosage*; D025101:Vitamin B 6 / Q000008:administration & dosage*
chemical_list: D015415:Biomarkers; D018932:Chemokine CCL2; D015850:Interleukin-6; D016209:Interleukin-8; D006710:Homocysteine; D025101:Vitamin B 6; D002097:C-Reactive Protein; D005492:Folic Acid; D014805:Vitamin B 12