Abstract
IntroductionBreastfeeding effects on cognition are attributed to long-chain polyunsaturated fatty acids (LC-PUFAs), but controversy persists. Genetic variation in fatty acid desaturase (FADS) and elongase (ELOVL) enzymes has been overlooked when studying the effects of LC-PUFAs supply on cognition. We aimed to: 1) to determine whether maternal genetic variants in the FADS cluster and ELOVL genes contribute to differences in LC-PUFA levels in colostrum; 2) to analyze whether these maternal variants are related to child cognition; and 3) to assess whether children's variants modify breastfeeding effects on cognition.MethodsData come from two population-based birth cohorts (n = 400 mother-child pairs from INMA-Sabadell; and n = 340 children from INMA-Menorca). LC-PUFAs were measured in 270 colostrum samples from INMA-Sabadell. Tag SNPs were genotyped both in mothers and children (13 in the FADS cluster, 6 in ELOVL2, and 7 in ELOVL5). Child cognition was assessed at 14 mo and 4 y using the Bayley Scales of Infant Development and the McCarthy Scales of Children's Abilities, respectively.ResultsChildren of mothers carrying genetic variants associated with lower FADS1 activity (regulating AA and EPA synthesis), higher FADS2 activity (regulating DHA synthesis), and with higher EPA/AA and DHA/AA ratios in colostrum showed a significant advantage in cognition at 14 mo (3.5 to 5.3 points). Not being breastfed conferred an 8- to 9-point disadvantage in cognition among children GG homozygote for rs174468 (low FADS1 activity) but not among those with the A allele. Moreover, not being breastfed resulted in a disadvantage in cognition (5 to 8 points) among children CC homozygote for rs2397142 (low ELOVL5 activity), but not among those carrying the G allele.ConclusionGenetically determined maternal supplies of LC-PUFAs during pregnancy and lactation appear to be crucial for child cognition. Breastfeeding effects on cognition are modified by child genetic variation in fatty acid desaturase and elongase enzymes.
Highlights
Breastfeeding effects on cognition are attributed to long-chain polyunsaturated fatty acids (LC-PUFAs), but controversy persists
After birth breast milk provides a unique supply of crucial LC-PUFAs including eicosapentaenoic acid (EPA), arachidonic acid (AA) and docosahexanoic acid (DHA), which support the accretion of LC-PUFA in the brain growth spurt that takes place during the third trimester of pregnancy and the first two years of life [8,9]
The rs174602-G, and 174464-T in the FADS cluster were associated with lower levels of DHA, and other SNPs in the cluster showed a trend to be associated with DHA levels in the same direction as the observed for AA (Table S2)
Summary
Breastfeeding effects on cognition are attributed to long-chain polyunsaturated fatty acids (LC-PUFAs), but controversy persists. Higher concentrations of DHA and AA, rapidly incorporated in the developing brain, are found in infants who are breastfed in comparison with infants fed with unsupplemented formulas [10]. It remains controversial whether breastfeeding provides a direct nutritional advantage for child cognition– attributed in part to the high levels and range of LCPUFAs– or reflects more favorable socio-environmental factors– no fully controlled in statistical analysis– among women who breast feed [11,12,13,14]
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