Premature infants are deprived of prenatal accumulation of brain docosahexaenoic acid [DHA (22:6n-3)], an omega-3 fatty acid [ω-3 FA (n-3 FA)] important for proper development of cognitive function. The resulting brain DHA deficit can be reversed by ω-3 FA supplementation. The objective was to test whether there is a critical period for providing ω-3 FA to correct cognitive deficits caused by developmental ω-3 FA deprivation in mice. Twelve timed-pregnant mice [embryonic day 14 (E14), C57/BL6NCr] were fed an ω-3 FA-deficient diet containing 0.04% α-linolenic acid [ALA (18:3n-3)], and their offspring were fed the same deficient diet (Def group) or changed to an ω-3 FA-adequate diet containing 3.1% ALA at 3 wk, 2 mo, or 4 mo of age. In parallel, 3 E14 pregnant mice were fed the adequate diet and their offspring were fed the same diet (Adeq group) throughout the experiment. Brain FA composition, learning and memory, and hippocampal synaptic protein expression were evaluated at 6 mo by gas chromatography, the Morris water maze test, and western blot analysis, respectively. Maternal dietary ω-3 FA deprivation decreased DHA by >50% in the brain of their offspring at 3 wk of age. The Def group showed significantly worse learning and memory at 6 mo than those groups fed the adequate diet. These pups also had decreased hippocampal expression of postsynaptic density protein 95 (43% of Adeq group), Homer protein homolog 1 (21% of Adeq group), and synaptosome-associated protein of 25 kDa (64% of Adeq group). Changing mice to the adequate diet at 3 wk, 2 mo, or 4 mo of age restored brain DHA to the age-matched adequate concentration. However, deficits in hippocampal synaptic protein expression and spatial learning and memory were normalized only when the diet was changed at 3 wk. Developmental deprivation of brain DHA by dietary ω-3 FA depletion in mice may have a lasting impact on cognitive function if not corrected at an early age.

Autism spectrum disorders (ASD) are a common neurodevelopmental disorder of unknown etiology. Studies suggest a link between autism and neonatal jaundice. A 1:3 matched case–control study was conducted with children enrolled in the Military Health System born between October 2002 and September 2009. Diagnostic and procedure codes were used for identifying ASD and hyperbilirubinemia. Two definitions for hyperbilirubinemia were evaluated: an inpatient admission with a diagnosis of jaundice and treatment with phototherapy. A total of 2917 children with ASD and 8751 matched controls were included in the study. After adjustment, there remained an association between ASD in children and an admission with a diagnosis of jaundice (odds ratio = 1.18; 95% confidence interval = 1.06-1.31; P = .001) and phototherapy treatment (odds ratio = 1.33; 95% confidence interval = 1.04-1.69; P = .008). Children who develop ASD are more likely to have an admission with a diagnosis of jaundice in the neonatal period and more likely to require treatment for this jaundice.

Early exposure to oral erythromycin in young infants, particularly in the first 2 weeks of life, has previously been associated with the development of hypertrophic pyloric stenosis. We report a case of an infant who received an abbreviated 4-day course of oral erythromycin for suspected Chlamydia conjunctivitis at 5 days of life then underwent pyloromyotomy for pyloric stenosis less than 2 weeks later. Health care providers should use erythromycin judiciously in neonates because only a few days of exposure to this medication may lead to the development of a surgical condition of gastric outlet obstruction.

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