No abstract

Some FADS alleles are associated with lower DHA and ARA status assessed by the relative amount of arachidonic acid (ARA) and docosahexaenoic acid (DHA) in plasma and red blood cell (RBC) phospholipids (PL). We determined two FADS single nucleotide polymorphisms (SNPs) in a cohort of pregnant women and examined the relationship of FADS1rs174533 and FADS2rs174575 to DHA and ARA status before and after supplementation with 600 mg per day of DHA. The 205 pregnant women studied were randomly assigned to placebo (mixed soy and corn oil) (n= 96) or 600 mg algal DHA (n=109) in 3 capsules per day for the last two trimesters of pregnancy. Women homozygous for the minor allele of FADS1rs174533 (but not FADS2rs174575) had lower DHA and ARA status at baseline. At delivery, minor allele homozygotes of FADS1rs174533 in the placebo group had lower RBC-DHA compared to major-allele carriers (P = 0.031), while in the DHA-supplemented group, all genotypes had higher DHA status compared to baseline (P = 0.001) and status did not differ by genotype (P = 0.941). Surprisingly, DHA but not the placebo decreased ARA status of minor allele homozygotes of both FADS SNPs but not major allele homozygotes at delivery. Any physiological effects of changing the DHA to ARA ratio by increasing DHA intake appears to be greater in minor allele homozygotes of some FADS SNPs.

No abstract

Human milk compared with infant formulas contains considerably more sialic acid (SA) and cholesterol. Because both compounds accumulate rapidly in the frontal cortex in infancy, it has been suggested these compounds may be conditionally essential nutrients for brain development. A limited number of animal studies demonstrate that dietary cholesterol and SA increase cortical cholesterol and SA concentrations, respectively, and enhance learning. No study to our knowledge has examined the effects of simultaneously increasing cholesterol and SA intake on brain cortex composition. Rats were provided with cholesterol (0 or 0.5% of diet weight) from conception until they were killed on postnatal day (P) 32. Litters were culled (P1) to 8 pups, weaned early (P17), and fed a diet (P17-32) with the same amount of cholesterol as the dam for that litter with 1 of 4 amounts of SA from casein glycomacropeptide estimated to provide 0, 20, 40, or 80 mg · kg⁻¹ · d⁻¹ SA. The brain cortex from 10-12 pups (all from different litters) was analyzed for each of the 8 cholesterol-SA groups. SA, cholesterol, and protein concentrations were measured in cortex. Cholesterol exposure from conception to P32 increased cortex weight (P = 0.003) and the concentrations of cortical cholesterol (P = 0.006), protein (P = 0.034), and ganglioside SA (P = 0.02). Independent of cholesterol feeding, SA fed from P17 to P32 increased the cortical ganglioside SA concentration (P-trend = 0.007). Dietary cholesterol and SA independently contribute to brain cortex composition during early brain development.