Abstract

Having demonstrated a deficiency in infant cerebral cortex docosahexaenoic acid of formula fed compared with breast milk fed infants, we sought to identify why the extensive subcutaneous tissue triglyceride fatty acid reserves in term new-born infants appeared to be ineffectual in its prevention. In addition to 24 term and six preterm infants who died from 'cot death', tissue was analysed from four perinatal surgical patients and in the former the results were correlated with dietary milk intake. The higher amounts (about 15% by weight) of unsaturated linoleic acid supplied in the formula milks were quantitatively incorporated into the subcutaneous tissue largely at the expense of the saturated palmitic acid possibly compromising adipocyte fluidity. The six preterm infants were in two formula fed groups and there was only one significant difference, namely a higher subcutaneous tissue concentration of alpha-linolenic acid in one of the preterm groups, distinguishing them from their term counterparts. This may imply that the enzymes involved in absorption and digestion of fatty acids are mature in the preterm infant. From birth the mean weight percentage of docosahexaenoic acid (0.4%) fell rapidly to undetectable levels (< 0.05%) in the formula fed group after about two months. It is therefore concluded that if breast feeding is not possible then a minimum daily requirement of 30 mg docosahexaenoic acid (approximately 0.2 g/100 g fatty acids) should be supplied in formulas designed for term infants to prevent the cerebral cortical deficiency of docosahexaenoic acid.