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Editorials |
1 From the Department of Paediatrics, University of British Columbia, Vancouver, Canada.
See corresponding article on page 292.
2 Reprints not available. Address correspondence to SM Innis, British Columbia Research Institute for Children's & Women's Health, 950 West 28th Avenue, Vancouver, British Columbia V5Z 4H4 Canada. E-mail: sinnis{at}unixg.ubc.ca.
Large amounts of the long-chain polyunsaturated fatty acid arachidonic acid (20:4n-6) are found in phospholipids throughout the body, whereas docosahexaenoic acid (22:6n-3) is found in high amounts in specific cells and membranes, such as the nonmyelin membranes of the brain, retina, and spermatozoa. Arachidonic acid (20:4n-6) as well as di-homo-
-linolenic acid (20:3n-6) and eicosapentaenoic acid (20:5n-3) are precursors of eicosanoids, which have a variety of important regulatory functions. Not unexpectedly, large amounts of 20:4n-6 and 22:6n-3 are needed for synthesis of structural lipids for the central nervous system, muscle, and other organs during fetal and postnatal development.
The n-6 and n-3 fatty acids are essential dietary nutrients and are transported across the placenta to the fetus. After birth, breast-fed infants are provided with the essential fatty acids linoleic acid (18:2n-6) and 
-linolenic acid (18:3n-3) as well as 20:4n-6 and 22:6n-3 and other n-6 and n-3 fatty acids. Formula-fed infants receive 18:2n-6 and 18:3n-3 from the fat in the formula, which currently in the United States and Canada does not contain 20:4n-6 and 22:6n-3. Many studies have shown that term and preterm infants fed conventional infant formulas with no 20:4n-6 or 22:6n-3 have lower plasma and red blood cell 20:4n-6 and 22:6n-3 concentrations than do infants fed human milk. Addition of 20:4n-6 and 22:6n-3 to infant formulas increases the blood concentrations of these fatty acids (1).
Recently, considerable effort has focused on clinical trials aimed at assessing whether various aspects of visual function and psychomotor development and growth are better in infants fed formulas supplemented with 20:4n-6, 22:6n-3, or both, than in infants fed formulas that do not contain these fatty acids. Studies in premature infants fed formulas with 22:6n-3 reported higher visual acuity (2) and higher visual evoked potential acuity (3) and decreased growth in association with lower blood 20:4n-6 concentrations compared with infants fed formulas without 22:6n-3 (4). Results from studies of the role of dietary 22:6n-3 in visual and psychomotor development of term infants have been inconsistent (1, 5–7). Many factors may contribute to inconsistencies in the findings among studies of the n-6 and n-3 fatty acid requirements of infants. These factors include possible lower or different requirements for fatty acids in term than in preterm infants at birth; differences in the types of oils used to provide 20:4n-6 and 22:6n-3 in these studies; differences in the 18:2n-6 and 18:3n-3 contents of the formulas fed; confounding effects of the home environment, particularly in term infants as opposed to preterm infants, who in the early and possibly critical phase of the study are in intensive care units; and an inadequate number of infants or inappropriate methodology to detect treatment effects (1–9).
The infant's 20:4n-6 and 22:6n-3 status at birth is another important variable that could influence infant growth and development and subsequent vulnerability to inadequacies in the postnatal diet. The paper by Guesnet et al (9) in this issue of the Journal provides provocative data showing that postnatal changes in the blood lipid n-6 and n-3 fatty acid concentrations of term infants are dependent on both the 20:4n-6 and 22:6n-3 status at birth and on the fat composition of the milk or formula fed.
Several studies showed that the maternal dietary intake of n-3 fatty acids has an important effect on the 22:6n-3 status of infants (10), reflecting placental transfer of maternal dietary 22:6n-3 to the fetus. Furthermore, fetal blood 22:6n-3 concentrations increase with advancing gestation (11, 12), and an association between high maternal intakes of marine foods and length of gestation was also shown (13, 14). Thus, the length of gestation can be expected to influence infant 22:6n-3 status at birth. Information with respect to 20:4n-6 seems less consistent; both an increase (12) and no change (11) in 20:4n-6 concentrations with advancing gestation have been reported.
Guesnet et al (9) report in this issue of the Journal that postnatal changes in plasma and erythrocyte 20:4n-6 and 22:6n-3 concentrations in a group of 83 term infants were negatively correlated with their respective fatty acid concentrations at birth. Thus, the higher the 20:4n-6 and 22:6n-3 concentrations at birth, the greater the postnatal decline in 20:4n-6 and 22:6n-3 concentrations. After birth, the infants were fed for 6 wk with breast milk, formula not supplemented with 22:6n-3, or formula supplemented with 22:6n-3 from fish oil with either a high or low 20:5n-3 content; none of the formulas contained 20:4n-6. As expected from previous studies (1), blood lipid 22:6n-3 concentrations after 6 wk of feeding were significantly lower in the infants fed formula without 22:6n-3 than in infants fed 22:6n-3-supplemented formula. Analysis of covariance, however, showed that 34–54% of the variability in postnatal changes in infant blood lipid 22:6n-3 concentrations could be explained by the 22:6n-3 status at birth, with 13–32% of the variance explained by the postnatal diet.
Foreman-van Drongelen et al (11) similarly showed that the 20:4n-6 and 22:6n-3 status of preterm infants (mean gestational age: 32 wk) at term (
8 wk later) is determined both by postnatal diet and by the 20:4n-6 and 22:6n-3 status at birth. Higher 22:6n-3 concentrations at birth resulted in higher postnatal concentrations of 22:6n-3.
From these studies it is clear that an appropriate prenatal supply of 22:6n-3, as determined by the maternal diet and the length of gestation over which to acquire it, is important. Whether the variability in 20:4n-6 and 22:6n-3 status at birth among infants is of functional significance is not yet clear. However, the potential effect of maternal dietary n-6 and n-3 fatty acid intakes and the infant's n-6 and n-3 fatty acid status at birth will clearly need to be considered in future studies of the role of these fatty acids in infant growth and development.
REFERENCES
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  J. C McCann and B. N Ames Is docosahexaenoic acid, an n-3 long-chain polyunsaturated fatty acid, required for development of normal brain function? An overview of evidence from cognitive and behavioral tests in humans and animals Am. J. Clinical Nutrition, August 1, 2005; 82(2): 281 - 295. [Abstract] [Full Text] [PDF]
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