Polyunsaturated fatty acid status and methylmercury exposure are not associated with leukocyte telomere length in mothers or their children in the Seychelles Child Development Study

ABSTRACTBackground Leukocyte telomere length (TL) is associated with age-related diseases and early mortality, but there is a lack of data on determinants of TL in early life. Evidence suggests that dietary intake of marine n-3 polyunsaturated fatty acids (PUFA) is protective of telomere attrition. Yet the effect of methylmercury (MeHg) exposure, also found in fish, on TL is unknown. Objective The aim of this study was to investigate associations between prenatal PUFA status, MeHg exposure and TL in mothers and children in the Seychelles, where fish consumption is high. Methods Blood samples collected from 229 mothers (at 28wk gestation and delivery) and children (at 5y of age) in the Seychelles Child Development Study Nutrition Cohort 1 were analyzed for PUFA concentrations. Prenatal Hg was measured in maternal hair collected at delivery. Postnatal Hg was also measured in children’s hair samples, using a cumulative metric derived from values obtained at 3-5y of age. Relative TL was measured in blood obtained from mothers at delivery, in cord blood, and in children at 5y of age by quantitative PCR. Linear regression models were used to investigate associations between PUFA status, MeHg exposure and TL.Results Neither prenatal PUFA status or MeHg exposure were associated with TL of the mother or child, nor with TL attrition rate. However a higher prenatal n-6/n-3 PUFA ratio was significantly associated with longer TL in the mothers (β= 0.001, P= 0.048). Child PUFA status and MeHg exposure were not associated with child TL. However greater values of family Hollingshead socioeconomic status (SES) at 9mo of age were significantly associated with longer TL in cord blood (β=0.005, P= 0.03). Conclusions We found no evidence that PUFA status or MeHg exposure are determinants of TL, in either the mother or child. However, our results support the hypothesis that family SES may be associated with child TL.