Omega-3 Fatty Acid Deficiency and Behavior

Abstract

Much of the impetus for studies of omega-3 fatty acid (FA) deficiency originates from the need to determine whether these FA should be added to human infant formulas, and if so in what form: as the precursor omega-3 FA, linolenic acid (18:3 omega-3, or as the derived form, docosahexaenoic acid ([DHA], 22:6 omega-3), which is present at high levels in retina and brain. After early studies showed effects of omega-3 FA deficiency on visual development in monkeys (Neuringer et al., 1984, 1986), levels of linolenic acid were increased in many infant formulas, especially those in the United States, beginning in 1987. However, DHA levels in erythrocytes of human infants fed formulas with either low or high levels of linolenic acid were lower than the DHA levels of infants who received DHA directly either in breast milk or in fish oil supplemented formulas (Pita et al., 1988; Carlson et al., 1986; Makrides et al., 1993; Uauy et al., 1994). This finding suggested that human infants do not elongate and desp.turate an adequate amount of linolenic acid into DHA. This hypothesis was supported by more recent postmortem studies that reported lower DHA levels in the cerebral cortex of infants fed formulas with linolenic acid than in breast-fed infants (Farquharson et al., 1992; Makrides et al., 1994).