The DHA in newborn infants must come from the mother. During the first year, an infant then gains additional DHA from food. Successive pregnancies may deplete maternal supplies and provide less DHA to later newborns. Woods J; Ward G; Salem N. Is docosahexaenoic acid necessary in infant formula? Evaluation of high linolenate diets in the neonatal rat. Pediatric Research 1996; 40: 687-694.

In rhesus monkey and human infants, diets low in omega-3 fatty acids result in lowered DHA levels in cerebral cortex and retina that is associated with abnormalities in retinal function and slower development of visual acuity. Consistent differences in cognitive development have been more difficult to demonstrate. One specific domain of infant development, visual attention, has shown consistent positive effects of omega-3 fatty acid status in several studies in both monkey and human infants. Omega-3 fatty acid deficiency may slow the development of visual information processing or impair the ability to shift attention. Fixation duration was not correlated with visual acuity in either species, so that the effect on visual attention appears to be independent of the effect on acuity development. Juvenile and young adult monkeys with a long-term history of omega-3 fatty acid deficiency showed increased locomotor activity and stereotyped behaviors compared with those fed high levels of linolenic acid. Deficient monkeys also showed increased reactivity to a variety of social and nonsocial stimuli, including increased approach and interaction.

In an artificial rearing procedure, infant rats were removed from their mothers, gastrostomized, and fed synthetic formula, to produce rapid changes in CNS levels of DHA. At eight weeks of age, the n 3 deficient group exhibited less than 50% of control total DHA content in brain, accompanied by more arachidonic acid (AA) (20:4n 6) and docosapentaenoic acid (22:5n 6) and total PUFA levels in the brain were not lower. At both ten days of age and again at eight weeks, offspring of the n 3 deficient mothers exhibited less than 10% total DHA content. These differences are greater than those commonly reported after 2 3 generations of normal dietary deprivation in rodents. Ward G; Woods J; Reyzer M; Salem N. Artificial rearing of infant rats on milk formula deficient in n 3 essential fatty acids: A rapid method for the production of experimental n 3 deficiency. LIPIDS 1996; 31: 71 77.

Fetal accretion of LC PUFA occurs during the last trimester of gestation, and premature infants are born with minimal LC PUFA reserves. Postnatally, human milk provides LC PUFA to the newborn. Maternal LC PUFA reserves depend upon diet and can be improved by supplementation of docosahexaenoic acid and arachidonic acid during pregnancy and lactation. Hamosh M; Salem N. Long chain polyunsaturated fatty acids. BIOLOGY OF THE NEONATE 1998; 74: 106 120.

Periconceptional alcohol use was associated with a 30% higher proportion of docosahexaenoic acid (22:6n 3) in cord blood (3.0% of total lipid in control infants compared with 3.9% in alcohol exposed infants; P < 0.01). The higher 22:6n 3 gave a higher ratio of n 3 to n 6 fatty acids and long chain n 3 to n 6 fatty acids (P < 0.055), fitting the hypothesis that 22:6n 3 may be conserved selectively. Denkins YM; Woods J; Whitty JE; Hannigan JH; Martier SS; Sokol RJ; Salem N. Effects of gestational alcohol exposure on the fatty acid composition of umbilical cord serum in humans. AMERICAN JOURNAL OF CLINICAL NUTRITION 2000; 71: 300S 306S.