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SUMMARY
DHA and AA,wich are commponents of breast milk but not infant
formulas marketed in the United State and some other countries, are
important components of the brain, and DHA is a major component of
the retina. Also many studies have demonstrated advantages of
breastfeeding versus formula-feeding on subsequent cognitive and
visual function; however, available data are insufficient to justify
the conclusion that the persence of DHA and AA in breast milk is
paritally or solely responsible for the apparent advantages of
breastfeeding. On the other hand, many studies of DHA (and
AA)-supplemented versus unsupplemented formulas have shown clear
advantages of the supplemented formulas on visual acuity at 2 and 4
months of age or neurodevelopmental status at 12 to 18 months of
age. Although one logically may assume that these early effects may
have long-term effects, this assumption is not warranted by the
available data. One of the major problems is the difficulty of
assessing visual and cognitive function of infants. Scores on
standard neurodevelopmental tests at 1 year of age, for example, are
only weakly correlated with performance at school age (when more
definitive assessments are possible), and little is known about the
predictability of later visual function from behavioral or
electrophysiologic assessments of visual function early in life.
Even
prematurely born infants can synthesize DHA and AA and other
w-3
and
w-6 LC-PUFAs from the
dietary EFAs, LA and ALA.Nonetheless, plasma, erythrocyte and brain
lipid levels of DHA are lower in infants whose diets do not contain
DHA. Whether more optimal intakes of ALA result in higher plasma and
tissue levels of this FA is unclear.
The breast-milk content of LC-PUFAs is not regulated by the mammary
gland but, rather, reflects the concentrations of LC-PUFAs in
maternal plasma lipids that, in turn, are dependent on maternal diet
and, probably, maternal activities of the desaturases and elongases
involved in converting dietary LA and ALA to LC-PUFAs. This
occurrence suggests that some infants receive sufficient LC-PUFAs
to support normal rates of deposition, whereas others may not. Also,
some infants probably can synthesize additional LC-PUFAs from the LA
and ALA contents of human milk. Thus, depending on maternal diet and
maternal and infant desaturase and elongase activities, some
breastfed infants may receive less than adequate LC-PUFAs to support
normal rates of deposition.
Clearly , the role of LC-PUFAs in infant development is not a
simple issue. Also , no foolproof method exists to ensure an
adequate but not excessive intake . Thus, because some evidence
shows that dietary LC-PUFAs (DHA,AA,or both) as components of
breast milk or formula confers at least transient developmental
benefits, supplementation of infant formulas with LC-PUFAs is
supportable provided that the supplements used are safe. The safety
of all available supplements is unknown; however, some trials reveal
few reasons for major concerns about the safety of single-cell oils,
low-EPA fish oil, or egg-yolk phospholipid or triglyceride
fractions.
(The Pediatric Clinic of North America)
BREASTFEEDING 2001, PART I:
THE EVIDENCE FOR BREASTFEEDING
Volume 48.Number1.February 2001
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