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Dietary Supplementation of Polyunsaturated Fatty Acids in Caenorhabditis elegans
Published on: November 29, 2013
Maternal dietary intake of polyunsaturated fatty acids modifies association between prenatal DDT exposure and child
Rafael Ogaz-González1, Ángel Mérida-Ortega1, Luisa Torres-Sánchez1
1Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico.
Background:
Maternal 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) serum levels during pregnancy have been negatively linked to child neurodevelopment in contrast to intake of omega-3 and -6 (ω-3 and ω-6) fatty acids.
Objectives:
To assess whether maternal dietary intake of ω-3 and ω-6 during pregnancy modifies the association between exposure to DDE and child neurodevelopment from age 42-60 months.
Methods:
Prospective cohort study with 142 mother-child pairs performed in Mexico. DDE serum levels were determined by electron capture gas chromatography. Dietary ω-3 and ω-6 intake was estimated by questionnaire. Child neurodevelopment was assessed by McCarthy Scales.
Results:
Docosahexaenoic (DHA) fatty acid intake significantly modified the association between DDE and motor component: increased maternal DDE was associated with lower motor development in children whose mothers had lower DHA intake (βlog2DDE = -1.25; 95% CI: -2.62, 0.12), in contrast to the non-significant increase among children whose mothers had higher DHA intake (βlog2DDE-motor = 0.50; 95% CI: 0.55, 1.56). Likewise, arachidonic fatty acid (ARA) intake modified the association between DDE and memory component: increased maternal DDE was associated with a significantly larger reduction in the memory component in children whose mothers had lower ARA intake (βlog2DDE = -1.31; 95% CI: -2.29, -0.32) than children whose mothers had higher ARA intake (βlog2DDE-memory = 0.17; 95% CI: -0.78, 1.11).
Conclusions:
Dietary intake of DHA and ARA during pregnancy may protect against child neurodevelopment damage associated with prenatal maternal DDE levels.
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