title: Significant correlations of plasma homocysteine and serum methylmalonic acid with movement and cognitive performance in elderly subjects but no improvement from short-term vitamin therapy: a placebo-controlled randomized study.
abstract: BACKGROUND
  Deficiencies of vitamin B-12, folic acid, and vitamin B-6-as defined by laboratory measures-occur in 10-20% of elderly subjects. The clinical significance remains unresolved.
  
  
  OBJECTIVE
  The objective was to explore any association between vitamin status and vitamin treatment and movement and cognitive performance in elderly subjects.
  
  
  METHODS
  Community-dwelling subjects (n = 209) with a median age of 76 y were randomly assigned to daily oral treatment with 0.5 mg cyanocobalamin, 0.8 mg folic acid, and 3 mg vitamin B-6 or placebo (double blind) for 4 mo. Movement and cognitive performance tests were performed before and after treatment.
  
  
  RESULTS
  A high plasma total homocysteine (tHcy) concentration (> or =16 micromol/L) was found in 64% of men and in 45% of women, and a high serum methylmalonic acid (MMA) concentration (> or =0.34 micromol/L) was found in 11% of both sexes. Movement time, digit symbol, and block design (adjusted for age, sex, smoking, and creatinine) correlated independently with plasma tHcy (P < 0.01, < 0.05, and < 0.01, respectively); the simultaneity index and block design correlated with serum MMA (P < 0.05 for both). Vitamin therapy significantly decreased plasma tHcy (32%) and serum MMA (14%). No improvements were found in the movement or cognitive tests compared with placebo. Neither vitamin therapy nor changes in plasma tHcy, serum MMA, serum vitamin B-12, plasma folate, or whole-blood folate correlated with changes in movement or cognitive performance.
  
  
  CONCLUSIONS
  High plasma tHcy and serum MMA were prevalent and correlated inversely with movement and cognitive performance. Oral B vitamin treatment normalized plasma tHcy and serum MMA concentrations but did not affect movement or cognitive performance. This might have been due to irreversible or vitamin-independent neurocognitive decline or to an insufficient dose or duration of vitamins.
authors.affiliation: Department of Medicine at the Sahlgrenska Academy, Göteborg University, Göteborg, Sweden. catharina.lewerin@vgregion.se
authors.forename: Catharina
authors.initials: C
authors.lastname: Lewerin
authors.forename: Michael
authors.initials: M
authors.lastname: Matousek
authors.forename: Gunilla
authors.initials: G
authors.lastname: Steen
authors.forename: Boo
authors.initials: B
authors.lastname: Johansson
authors.forename: Bertil
authors.initials: B
authors.lastname: Steen
authors.forename: Herman
authors.initials: H
authors.lastname: Nilsson-Ehle
mesh_terms: D000368:Aged; D003071:Cognition / Q000187:drug effects*; D004311:Double-Blind Method; D005260:Female; D005492:Folic Acid / Q000627:therapeutic use; D005494:Folic Acid Deficiency / Q000188:drug therapy*; D005853:Geriatrics; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008124:Locomotion / Q000187:drug effects; D008297:Male; D008764:Methylmalonic Acid / Q000097:blood*; D011597:Psychomotor Performance / Q000187:drug effects*; D014806:Vitamin B 12 Deficiency / Q000188:drug therapy*; D026681:Vitamin B 6 Deficiency / Q000188:drug therapy*; D014803:Vitamin B Complex / Q000627:therapeutic use*
chemical_list: D006710:Homocysteine; D014803:Vitamin B Complex; D008764:Methylmalonic Acid; D005492:Folic Acid