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Introduction: Long-chain polyunsaturated (LCP) fatty acids (FA) are important during infant development. Mother-to-infant FA-transport occurs at the expense of the maternal status. Maternal and infant FA-status change rapidly after delivery., Methods: Comparison of maternal (mRBC) and infant erythrocyte (iRBC)-FA-profiles at delivery and after 3 months exclusive breastfeeding in relation to freshwater-fish intakes. Approximation of de-novo-lipogenesis (DNL), stearoyl-CoA-desaturase (SCD), elongation-of-very-long-chain-FA-family-member-6 (Elovl-6), delta-5-desaturase (D5D) and delta-6-desaturase (D6D)-enzymatic activities from their product/essential-FA and product/substrate-ratios., Results and Discussion: Increasing iRBC-14:0 derived from mammary-gland DNL. Decreasing mRBC-ω9, but increasing iRBC-ω9, suggest high ω9-FA-transfer via breastmilk. Decreasing (m+i)RBC-16:0, DNL- and SCD-activities, but increasing (m+i)RBC-18:0 and Elovl-6-activity suggest more pronounced postpartum decreases in DNL- and SCD-activities, compared to Elovl-6-activity. Increasing (m+i)RBC-18:3ω3, 20:5ω3, 22:5ω3, 18:2ω6, mRBC-20:4ω6 and (m+i)D5D-activity, but decreasing mRBC-22:6ω3 and (m+i)D6D-activity and dose-dependent changes in iRBC-22:6ω3 confirm that D6D-activity is rate-limiting and 22:6ω3 is important during lactation. Fish-intake related magnitudes of postpartum FA-changes suggest that LCPω3 influence DNL-, SCD- and desaturase-activities., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Homo sapiens has evolved on a diet rich in alpha-linolenic acid and long chain polyunsaturated fatty acids (LCP). We have, however, gradually changed our diet from about 10,000 years ago and accelerated this change from about 100 to 200 years ago. The many dietary changes, including lower intake of omega3-fatty acids, are related to 'typically Western' diseases. After a brief introduction in essential fatty acids (EFA), LCP and their functions, this contribution discusses our present low status of notably LCPomega3 in the context of our rapidly changing diet within an evolutionary short time frame. It then focuses on the consequences in pregnancy, lactation and neonatal nutrition, as illustrated by some recent data from our group. We discuss the concept of a 'relative' EFA/LCP deficiency in the fetus as the outcome of high transplacental glucose flux. This flux may in the fetus augment de novo synthesis of fatty acids, which not only dilutes transplacentally transported EFA/LCP, but also causes competition of de novo synthesized oleic acid with linoleic acid for delta-6 desaturation. Such conditions were encountered by us in mothers with high body mass indices, diabetes mellitus and preeclampsia. The unifying factor might be compromised glucose homeostasis. In search of the milk arachidonic acid (AA) and docosahexaenoic acid (DHA) contents of our African ancestors, we investigated women in Tanzania with high intakes of freshwater fish as only animal lipid source. These women had milk AA and DHA contents that were well above present recommendations for infant formulae. Both studies stimulate rethinking of 'optimal homeostasis'. Subtle signs of dysbalanced maternal glucose homeostasis may be important and observations from current Western societies may not provide us with an adequate basis for dietary recommendations.

Low status of long-chain polyunsaturated fatty acids (LCP) and essential fatty acids (EFA) in the fetus is associated with less favorable neonatal neurological condition. A 'relative', rather than 'absolute' EFA deficiency might explain this finding. A relative EFA deficiency may derive from impaired maternal glucose homeostasis. We measured fatty acids in umbilical vessels of infants born to 7 mothers with (gestational) diabetes mellitus and of 258 infants born to healthy mothers. Umbilical veins of infants of diabetic mothers had higher omega7 and omega9 fatty acids and DHA deficiency index and lower 20:4omega6 and EFA index. Their umbilical arteries had higher omega7 and omega9 fatty acids, and lower 20:4omega6, LCP and EFA index. We conclude that children born to mothers with poor glucose homeostasis have lower EFA and LCP status, which is consistent with a 'relative deficiency' deriving from augmented de novo fatty acid synthesis from the abundant glucose.

Aim: Previously, we found a beneficial effect of 2 mo supplementation of infant formula with long-chain polyunsaturated fatty acids (LC-PUFA) on neurological condition at 3 mo in healthy term infants. The aim of the present follow-up study was to evaluate whether the effect on neurological condition persists until 18 mo., Methods: A prospective, double-blind, randomized control study was conducted. Three groups were formed: a control (CF; n = 169), an LC-PUFA-supplemented (LF; n = 146) and a breastfed (BF; n = 159) group. Information on potential confounders was collected at enrolment. At the age of 18 mo, neurodevelopmental condition was assessed by the age-specific neurological examination of Hempel and the Bayley scales. The Hempel assessment resulted in a clinical neurological diagnosis, a total optimality score and a score on the fluency of motility. The Bayley scales resulted in mental and psychomotor developmental indices. Attrition at 18 mo was 5.5% and non-selective. Multivariate regression analyses were carried out to evaluate the effect of type of feeding while adjusting for confounders., Results: None of the children had developed cerebral palsy and 23 (CF: n = 8; LF: n = 10; BF: n = 5) showed minor neurological dysfunction. The groups did not show statistically significant differences in clinical neurological condition, neurological optimality score, fluency score, and the psychomotor and mental development indices. Multivariate analysis confirmed that there was no effect of type of feeding on neurological condition., Conclusion: This study indicates that the beneficial neurodevelopmental effect of 2 mo LC-PUFA supplementation in healthy term infants can not be detected at the age of 18 mo.

Background: Whether long-chain polyunsaturated fatty acids (LCPs) play a role in the development of the young nervous system in term infants is debated., Objective: We investigated whether supplementation of formula with LCPs for 2 mo improves the quality of general movements (GMs) in healthy term infants at 3 mo of age., Design: A prospective, double-blind, randomized controlled study was conducted with 2 groups of healthy term infants: a control-formula (CF) group (n = 131) and an LCP-supplemented-formula (LF) group (n = 119). A breastfed (BF) group (n = 147) served as a reference. Information on potential confounders was collected at enrollment. Videotapes were made of the infants' spontaneous motor behavior at 3 mo of age to assess the quality of their GMs. On the basis of quality, normal GMs were classified as normal-optimal or normal-suboptimal, and abnormal GMs were classified as mildly or definitely abnormal. Attrition at 3 mo of age was 15% and nonselective. Multivariate regression analyses with adjustment for confounders were carried out to evaluate the effect of the type of feeding., Results: None of the infants had definitely abnormal GMs. Infants in the CF group had mildly abnormal GMs significantly more often than did infants in the LF and BF groups (31% compared with 19% and 20%, respectively). Infants in the BF group had normal-optimal GMs more frequently than did infants in the LF and CF groups (34% compared with 18% and 21%, respectively). Logistic regression analyses confirmed these findings., Conclusion: Supplementation of healthy term infants with LCPs during the first 2 mo of life reduces the occurrence of mildly abnormal GMs.