Dr. Stewart Forsyth, Tayside Institute for Child Health, University of Dundee, Scotland, United Kingdom
“A recurring feature of randomized controlled studies investigating the effects of docosahexaenoic acid (DHA) supplementation on cognitive function in infancy is that the variation in the DHA status of infants within each of the randomized groups is either not characterized or is not separately considered in the analysis of the study. This means that most publications reporting on the effect of DHA supplementation on cognitive function are including in their analysis infants who are not DHA-deficient. Moreover, it also means that there is very little data specifically on the effects of DHA supplementation on DHA-deficient infants. The study by Meldrum et al. (1), for example, continues this pattern of investigating the effects of DHA supplementation in infants with above-average DHA status at the start of the study. The cohort was recruited from an affluent and educated community; maternal nutrition included oily fish and mothers were also allowed to take fish oil supplements. More than 98 % of infants were breast fed and if infant formula was used, a formula fortified with long-chain PUFA was most commonly chosen.
This abundance of DHA in maternal and infant nutritional intake was reflected in the high erythrocyte DHA levels in infants at birth and at 6 months of age. These DHA-enriched infants were randomized to a high-dose fish oil supplement. The outcome was that supplementation with DHA was not associated with significant differences between the infant intervention and control groups in infant and toddler development or child behavior. The authors of this study concluded that increased postnatal omega-3 fatty acid intake in the first 6 months of life using high-dose infant fish oil supplementation was not beneficial to global infant neurodeve-lopment. Considering that this may ultimately be the only evaluation that researchers, policymakers and the media take from the study, it would have been preferable if they had qualified their conclusion by underlining that the mothers and infants in their study were already unusually well endowed with DHA through their DHA-enriched dietary intakes, and in those relatively unusual circumstances it may be that additional high-dose DHA supplementation will not lead to measurable improvements in cognition during infancy.
The Meldrum study (1) raises a more general question: why are we continuing to undertake DHA supplemen-tation studies on infants who are DHA rich – and is this a research priority? Despite nearly 20 years of intensive investigation into the role of DHA in the development and function of the human brain, there remain fundamental gaps in our knowledge concerning the impact that DHA may have on the health and well-being of children. In particular, three closely related questions remain unanswered: what are the optimum DHA requirements for normal development in term and premature infants, what is classed as a normal level of DHA, and what is the optimum dose and duration of DHA supplementation for at-risk mothers, infants and children?
Would it not be more informative to study the effects of DHA supplementation in cohorts that are known to be relatively deficient in DHA? Priority could be given to groups that are at a high risk of both DHA deficiency and the impairment of cognitive function. This would include premature infants and those small for gestatio-nal age, low-income families in both the developed and developing world and infants and children with a family history of development and behavioral conditions such as developmental coordination disorder, dyslexia, and attention deficit hyperactivity disorder, which are becoming increasingly prevalent and dealing considerable blows to public health and society. Research in these areas is currently very limited.”
Based on: Forsyth S. Why are we undertaking DHA supplementation studies in infants who are not DHA-deficient? British Journal of Nutrition. Published online June 2012.