Age and DietaryRelated Distributions of Hepatic Arachidonic and Docosahexaenoic Acid in Early Infancy

A dietary-related deficiency of docosahexaenoic acid [C22:6(n-3)] in infant cerebral cortex has been identified. Absence or very low rates of hepatic synthesis from the essential fatty acid precursor, α-linolenic acid [C18:3(n-3)], in early life may have been a contributory factor. We have analyzed liver total lipid fatty acid compositions in 27 term (37–42 wk gestation) and 4 preterm (30–33 wk gestation) infants who died within the first 6 mo of life from sudden infant death syndrome. The infants were fed exclusively either human or formula milks. Formula-fed infants were subdivided into two groups, one receiving SMA milk with an α-linolenic acid content at 1.5 of total fatty acids and the other a composite group fed milks with low α-linolenic acid concentrations (<0.1 to 0.4). The hepatic content of arachidonic acid [C20:4(n-6)] and docosahexaenoic acid was generally lower in both formula-fed groups than in the human milk-fed group. The age-related distributions of docosahexaenoic acid showed that coincident minimum levels were present in both formula groups in the third month of life. This may indicate that the hepatic enzymes involved in the final stage (A4-desaturation) conversion of α-linolenic acid to docosahexaenoic acid could be inactive in the first months of life. Emphasis must be on provision of preformed dietary docosahexaenoic acid and possibly arachidonic acid as well as their essential fatty acid precursors, to both term and preterm infants for at least the first 16 wk of life.