Response to Baggott and Tamura: "Serum Iron Parameters and Plasma Total Homocysteine Concentrations"

Abstract

In their comment on our article, Baggott and Tamura suggest that plasma total homocysteine concentrations may serve as a marker for excess body iron stores. They refer to a study conducted in five healthy volunteers in which non– protein-bound iron was found to catalyze the conversion of thioethers, such as methionine and S-adenosylmethionine, into homocysteine (1). The authors hypothesize that the association between iron stores and homocysteine concentrations may underlie the apparent lack of any significant effects of B-vitamin supplementation on occlusive vascular disease. In our recently published article, we reported that increased concentrations of serum iron and ferritin were associated, cross-sectionally, with decreased cognitive performance in the folic acid and carotid intima-media thickness (FACIT) population (2). Plasma total homocysteine did not confound the observed associations as results were similar regardless if homocysteine concentrations were included in the analyses. We evaluated the relationship between serum iron parameters, HFE C282Y genotype, and plasma total homocysteine in our study sample. We found that carriers of the HFE C282Y mutation did not differ significantly from non carriers in terms of homocysteine concentrations (t = −.677, p = .499). In addition, the concentrations of serum iron, total iron-binding capacity, transferrin saturation, and non– transferrin-bound iron were not significantly correlated with homocysteine concentrations at baseline (r = −.064, p = .068; r = .005, p = .885; r = −.066, p = .060; and r = –.042, p = .236, respectively). However, serum ferritin, which is an indicator of body iron stores, showed a significant positive correlation with plasma total homocysteine at baseline (Spearman’s rank correlation coefficient = .125, p < .001).