title: Low circulating vitamin B(6) is associated with elevation of the inflammation marker C-reactive protein independently of plasma homocysteine levels.
abstract: BACKGROUND
  Lower vitamin B(6) concentrations are reported to confer an increased and independent risk for cardiovascular disease (CVD). The mechanism underlying this relationship, however, remains to be defined. Other diseases, such as rheumatoid arthritis, are associated with reduced vitamin B(6) levels. Despite a clear distinction in pathophysiology, inflammatory reaction may be the major link between these diseases. We hypothesized a relationship between pyridoxal 5'-phosphate (PLP), the active form of vitamin B(6), and the marker of inflammation C-reactive protein (CRP). We also evaluated whether total plasma homocysteine (tHcy), a well-defined risk factor for CVD and a major determinant of plasma PLP levels, had a possible role as a mediator of this hypothesized relationship.
  
  
  RESULTS
  Data from 891 participants from the population-based Framingham Heart Study cohort were analyzed. Subjects were divided into 2 groups according to normal or elevated CRP values: group 1, CRP <6 mg/L; group 2, CRP >/=6 mg/L. Plasma PLP levels were substantially lower in group 2 than in group 1 (mean values in group 2, 36.5 nmol/L versus 55.8 nmol/L in group 1, P<0.001). In a multiple logistic regression model adjusted for tHcy, the association of PLP with CRP remained highly significant (P=0.003).
  
  
  CONCLUSIONS
  Low plasma PLP is associated with higher CRP levels independently of tHcy. This observation may reflect a vitamin B(6) utilization in the presence of an underlying inflammatory process and represent a possible mechanism to explain the decreased vitamin B(6) levels in CVD.
authors.affiliation: Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
authors.forename: S
authors.initials: S
authors.lastname: Friso
authors.forename: P F
authors.initials: PF
authors.lastname: Jacques
authors.forename: P W
authors.initials: PW
authors.lastname: Wilson
authors.forename: I H
authors.initials: IH
authors.lastname: Rosenberg
authors.forename: J
authors.initials: J
authors.lastname: Selhub
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism*; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D004032:Diet; D005260:Female; D005492:Folic Acid; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000453:epidemiology; D016015:Logistic Models; D008297:Male; D008404:Massachusetts / Q000453:epidemiology; D011732:Pyridoxal Phosphate / Q000097:blood; D011736:Pyridoxine / Q000097:blood*; D012307:Risk Factors; D012709:Serum Albumin / Q000378:metabolism; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D012709:Serum Albumin; D006710:Homocysteine; D011732:Pyridoxal Phosphate; D002097:C-Reactive Protein; D005492:Folic Acid; D003404:Creatinine; D011736:Pyridoxine; D014805:Vitamin B 12