Does early nutrition in infants born before term programme later blood pressure?

OBJECTIVES--To test whether nutrition early in infants'' development programmes later blood pressure and whether the reported relation between low birth weight and later high blood pressure is due to poor nutrition or growth before full term. DESIGN--Prospective randomisation of preterm infants to early diets differing greatly in nutrient content in four parallel multicentre trials, with blinded follow up 7.5-8 years later. SETTING--Neonatal units at Cambridge, Ipswich, King''s Lynn, Norwich, and Sheffield. SUBJECTS--758 children weighing under 1850 g at birth. MAIN OUTCOME MEASURE--Blood pressure at age of 7.5-8 years. RESULTS--There were major differences in nutrient intake from randomised diets (preterm formula v standard formula and preterm formula v donor breast milk; in each case with or without mother''s milk), but follow up showed no differences in later blood pressure. Individual subjects showed large variation in protein and energy intakes and in growth performance, including degrees of growth failure seldom seen in utero, but these factors were also unrelated to later blood pressure. CONCLUSION--Extremes of nutritional intake and growth performance in preterm infants do not programme later blood pressure at 7.5-8 years of age. These findings do not support the hypothesis that high blood pressure has early nutritional origins. We suggest that the long term rise in blood pressure reported in individuals who had low birthweight (at full term) is not, as previously speculated, due to poor fetal nutrition or growth as such.     

Arginine deficiency in preterm infants: biochemical mechanisms and nutritional implications

Arginine, an amino acid that is nutritionally essential for the fetus and neonate, is crucial for ammonia detoxification and the synthesis of molecules with enormous importance (including creatine, nitric oxide, and polyamines). A significant nutritional problem in preterm infants is a severe deficiency of arginine (hypoargininemia), which results in hyperammonemia, as well as cardiovascular, pulmonary, neurological, and intestinal dysfunction. Arginine deficiency may contribute to the high rate of infant morbidity and mortality associated with premature births. Although hypoargininemia in preterm infants has been recognized for more than 30 years, it continues to occur in neonatal intensive care units in the United States and worldwide. On the basis of recent findings, we propose that intestinal citrulline and arginine synthesis (the major endogenous source of arginine) is limited in preterm neonates owing to the limited expression of the genes for key enzymes (e.g., pyrroline-5-carboxylate synthase, argininosuccinate synthase and lyase), thereby contributing to hypoargininemia. Because premature births in humans occur before the normal perinatal surge of cortisol (an inducer of the expression of key arginine-synthetic enzymes), its administration may be a useful tool to advance the maturation of intestinal arginine synthesis in preterm neonates. Additional benefits of cortisol treatment may include the following: 1) allowing early introduction of enteral feeding to preterm infants, which is critical for intestinal synthesis of citrulline, arginine, and polyamines as well as for intestinal motility, integrity, and growth; and 2) shortening the expensive stay of preterm infants in hospitals as a result of accelerated organ maturation and the restoration of full enteral feeding. Further studies of fetal and neonatal arginine metabolism will continue to advance our understanding of the mechanisms responsible for the survival and growth of preterm infants. This new knowledge will be beneficial for designing the next generation of enteral and parenteral amino acid solutions to optimize nutrition and health in this compromised population.     

Gastrointestinal peptides and the adaptation to extrauterine nutrition

The adaptation to extrauterine nutrition involves complex physiological changes at birth which may be regulated by genetic endowment; enteral nutrients, secretions, and bacteria; and endogenous hormones and exogenous hormones in breast milk. The hypothesis is explored that enteral feeding after birth may trigger key adaptations in the gut and in metabolism partly through the mediation of gastrointestinal hormone secretion. Gut peptides are found in the early human fetal gut and by the second trimester some are found in high concentrations in the fetal circulation and amniotic fluid. Major plasma hormonal surges occur during the neonatal period in term and preterm infants: notably in enteroglucagon, gastrin, motilin, neurotensin, gastrointestinal peptide, and pancreatic polypeptide. These events do not occur in neonates deprived of enteral feeding. A progressive development of dynamic gut hormonal responses to feeding is observed. The pattern of gut endocrine changes after birth is influenced by the type and route of feeding. Potential pathophysiological effects of depriving high risk neonates of enteral feeding are considered. It is speculated that infants committed to prolonged total parenteral nutrition from birth may benefit from the biological effects of intraluminal nutrients used in subnutritional quantities.     

早产儿喂养不耐受与肠道菌群关系的研究进展

喂养不耐受是指无法实现肠内营养的目标摄入量的同时出现了胃肠道功能障碍的症状,如大量胃潴留、腹胀、腹泻及呕吐等。菌群与宿主之间的动态平衡是维持机体健康的重要保证,对消化道营养吸收、内脏感知及运动、黏膜免疫以及量代谢调节等起关键作用。随着新一代测序技术的发展,关于早产儿喂养不耐受与肠道菌群的关系有了更深刻的认识,最新研究发现喂养不耐受早产儿的肠道菌群具有致病菌的相对丰度增加而有益菌的相对丰度减少的特点,本文就喂养不耐受与肠道菌群的关系相关的研究进展作一综述。     

Qualitative and quantitative comparison of gut bacterial colonization in enterally and parenterally fed neonatal pigs

Total parenteral nutrition (TPN) has been associated with mucosal atrophy, impaired gut barrier function, and translocation of luminal bacteria with resultant sepsis in preterm human infants. Currently, we examined the effects of enteral (ENT) or TPN treatments on translocation events in neonatal pigs and on colonization and composition of microbiota in the neonatal gut. Newborn, colostrum-deprived pigs (<24 hours old) were fitted with intravenous catheters and were fed either ENT (n = 13) or TPN (n = 13) for 7 days. After 7 days of treatment, pigs were euthanized and samples were collected for bacterial culture from the blood, intestinal tract and organs. ENT pigs had increased numbers of bacterial genera isolated, higher concentrations of bacteria (CFU/g), and increased colonization of all segments of the intestinal tract compared to the TPN pigs. Translocation of bacteria from the intestinal tract to tissues or blood was similar (8 of 13) for both groups. The ENT group had 1/13 positive for Clostridium difficile toxin A whereas the TPN group had 5/13. We concluded that ENT favored increased bacterial concentrations comprised of more speciation in the gastrointestinal tract compared to TPN, and that TPN-treated piglets were at higher risk of colonization by toxin-expressing strains of C. difficile.     

益生菌制剂治疗极低出生体重儿喂养不耐受的临床研究

目的探讨益生菌制剂对极低出生体重儿（very low birth weight infant,VLBW）喂养不耐受的影响。方法将56例极低出生体重儿随机分成治疗组和对照组,每组28例。2组均予静脉营养及早产儿配方奶喂哺,治疗组在早产儿配方奶喂哺时添加益生菌制剂,每次0．5g,3次／d,2组同时记录恢复出生体重时间、达全胃肠喂养时间及黄疽消退时间。结果治疗组恢复出生体重时间、达全胃肠喂养时间均显著短于对照组（P〈0．01）,治疗组黄疸消退时间也明显缩短（P〈0．05）。微生态制剂治疗过程中无不良反应发生。结论益生菌制剂可改善极低出生体重儿喂养不耐受,促进患儿体重增长,缩短达到全胃肠喂养时间,值得推广应用。     

INTRAVENOUS ADMINISTRATION OF FAT EMULSIONS—Metabolic and Clinical Studies

Fat emulsions alone or in alternation with amino acid mixtures were administered by continuous intravenous infusion to human subjects. Adequate nutrition was maintained thereby, without untoward effects. Upon too rapid administration of such emulsions, toxic manifestations occurred, apparently referable to an “overload” of the enzyme systems concerned with fat catabolism and storage.     

Gut responses to enteral nutrition in preterm infants and animals

Preterm birth is associated with immature digestive function that may require the use of total parenteral nutrition and special oral feeding regimens. Little is known about the responses to oral food in the preterm neonate and how enteral nutrients affect the immature gastrointestinal tract (GIT). In vivo studies are difficult to perform in laboratory rodents because of their small body size and that of immature organs at birth, and this makes the large farm animals (e.g., pigs, cattle, sheep) more attractive models in this field. In these species, preterm delivery at 88%-95% gestation is associated clinical complications and degrees of GIT immaturity similar to those in infants born at 70%-90% gestation. Studies in both animals and infants indicate that the immature GIT responds to the first enteral food with rapid increases in gut mass and surface area, blood flow, motility, digestive capacity, and nutrient absorption. To a large extent, the enteral food responses are birth independent, and can be elicited also in utero, at least during late gestation. Nevertheless, preterm neonates show compromised GIT structure, function, and immunology, particularly when delivered by caesarean section and fed diets other than mother's milk. Formula-fed preterm infants are thus at increased risk of developing diseases such as necrotizing enterocolitis, unless special care is taken to avoid excessive nutrient fermentation and bacterial overgrowth. The extent to which results obtained in preterm animals (most notably the pig) can be used to reflect similar conditions in preterm infants is discussed.     

Implementation of Nutritional Strategies Decreases Postnatal Growth Restriction in Preterm Infants

Background

Prevention of postnatal growth restriction of very preterm infants still represents a challenge for neonatologists. As standard feeding regimens have proven to be inadequate. Improved feeding strategies are needed to promote growth. Aim of the present study was to evaluate whether a set of nutritional strategies could limit the postnatal growth restriction of a cohort of preterm infants.

Methodology/Principal Findings

We performed a prospective non randomized interventional cohort study. Growth and body composition were assessed in 102 very low birth weight infants after the introduction of a set of nutritional practice changes. 69 very low birth weight infants who had received nutrition according to the standard nutritional feeding strategy served as a historical control group. Weight was assessed daily, length and head circumference weekly. Body composition at term corrected age was assessed using an air displacement plethysmography system. The cumulative parenteral energy and protein intakes during the first 7 days of life were higher in the intervention group than in the historical group (530±81 vs 300±93 kcal/kg, p<0.001 and 21±2.9 vs 15±3.2 g/kg, p<0.01). During weaning from parenteral nutrition, the intervention group received higher parental/enteral energy and protein intakes than the historical control group (1380±58 vs 1090±70 kcal/kg; 52.6±7 vs 42.3±10 g/kg, p<0.01). Enteral energy (kcal/kg/d) and protein (g/kg/d) intakes in the intervention group were higher than in the historical group (130±11 vs 100±13; 3.5±0.5 vs 2.2±0.6, p<0.01). The negative changes in z score from birth to discharge for weight and head circumference were significantly lower in the intervention group as compared to the historical group. No difference in fat mass percentage between the intervention and the historical groups was found.

Conclusions

The optimization and the individualization of nutritional intervention promote postnatal growth of preterm infants without any effect on percentage of fat mass.     

Prematurity and insulin sensitivity

Premature infants of low and extremely low birth weight represent a challenge for neonatal intensive care units and paediatricians. These neonates may be at increased risk of insulin resistance and diabetes perinatally and during childhood. During the first week of postnatal life, infants born prematurely are at risk of abnormalities in glucose homeostasis. Additionally, there are major differences in their glucose/insulin homeostasis compared with infants born at term. Preterm infants are at risk of hypoglycaemia, due to decreases in deposits of glycogen and fat that occur during the third trimester, and also to transient hyperinsulinaemia. Hyperglycaemia may also be observed in preterm infants during the perinatal period. These infants are unable to suppress glucose production within a large range of glucose and insulin concentrations, insulin secretory response is inappropriate, insulin processing is immature and there is an increased ratio of the glucose transporters Glut-1/Glut-2 in fetal tissues, which limits sensitivity and hepatocyte reaction to increments in glucose/insulin concentration during hyperglycaemia. In addition, increased concentrations of tumour necrosis factor alpha present in intrauterine growth retardation (IUGR) and induce insulin resistance. It has been proposed that the reduced insulin sensitivity may result from adaptation to an adverse in utero environment during a critical period of development. We have investigated postnatal insulin resistance in 60 children born with very low birth weight and either small for gestational age or at an appropriate size for gestational age. This study showed that IUGR, rather than low birth weight itself, was associated with increased fasting insulin levels. As poor fetal growth may be associated with the development of obesity, type 2 diabetes and the metabolic syndrome in later life, it is important that we continue to increase our understanding of the effects of IUGR on postnatal growth and metabolism.     

Altered Glutamatergic Metabolism Associated with Punctate White Matter Lesions in Preterm Infants

Preterm infants (∼10% of all births) are at high-risk for long-term neurodevelopmental disabilities, most often resulting from white matter injury sustained during the neonatal period. Glutamate excitotoxicity is hypothesized to be a key mechanism in the pathogenesis of white matter injury; however, there has been no in vivo demonstration of glutamate excitotoxicity in preterm infants. Using magnetic resonance spectroscopy (MRS), we tested the hypothesis that glutamate and glutamine, i.e., markers of glutamatergic metabolism, are altered in association with punctate white matter lesions and “diffuse excessive high signal intensity” (DEHSI), the predominant patterns of preterm white matter injury. We reviewed all clinically-indicated MRS studies conducted on preterm infants at a single institution during a six-year period and determined the absolute concentration of glutamate, glutamine, and four other key metabolites in the parietal white matter in 108 of those infants after two investigators independently evaluated the studies for punctate white matter lesions and DEHSI. Punctate white matter lesions were associated with a 29% increase in glutamine concentration (p = 0.002). In contrast, there were no differences in glutamatergic metabolism in association with DEHSI. Severe DEHSI, however, was associated with increased lactate concentration (p = 0.001), a marker of tissue acidosis. Findings from this study support glutamate excitotoxicity in the pathogenesis of punctate white matter lesions, but not necessarily in DEHSI, and suggest that MRS provides a useful biomarker for determining the pathogenesis of white matter injury in preterm infants during a period when neuroprotective agents may be especially effective.     

Size at birth, postnatal growth and risk of obesity

Epidemiological studies over the last 15 years have shown that size at birth, early postnatal catch-up growth and excess childhood weight gain are associated with an increased risk of adult cardiovascular disease and type 2 diabetes. At the same time, rising rates of obesity and overweight in children, even at pre-school ages, have shifted efforts towards the identification of very early factors that predict risk of subsequent obesity, which may allow early targeted interventions. Overall, higher birth weight is positively associated with subsequent greater body mass index in childhood and later life; however, the relationship is complex. Higher birth weight is associated with greater subsequent lean mass, rather than fat mass. In contrast, lower birth weight is associated with a subsequent higher ratio of fat mass to lean mass, and greater central fat and insulin resistance. This paradoxical effect of lower birth weight is at least partly explained by the observation that infants who have been growth restrained in utero tend to gain weight more rapidly, or 'catch up', during the early postnatal period, which leads to increased central fat deposition. There is still debate as to whether there are critical early periods for obesity: does excess weight gain during infancy, childhood or even very early neonatal life have a greater impact on long-term fat deposition and insulin resistance? Early identification of childhood obesity risk will be aided by identification of maternal and fetal genes that regulate fetal nutrition and growth, and postnatal genes that regulate appetite, energy expenditure and the partitioning of energy intake into fat or lean tissue growth.     

A review of ratite nutrition

This paper reviews the literature available on ostrich, emu and rhea nutrition. Information on the unique characteristics of the gastrointestinal tract and general biological information about these flightless birds is presented. The following information is discussed: nutrient digestibility in ostriches and emus, nutrient requirements of ratites, lysine requirements of growing emus, and ostrich and emu performance. To the author's knowledge, there are no scientific studies published on rhea performance or nutrition.     

Chronic undernutrition and traditional weaning foods are associated with fat stores in ariaal infants of Northern Kenya

The high proportion of human infant fat is hypothesized to protect infant brains by mobilizing against growth disturbances caused by acute nutritional and pathogen stress during weaning. However, individuals who experience chronic nutritional stress have been shown to store fat rather than mobilize fat stores, although this has not been demonstrated during infancy. This study investigated the relationship between fat development, diet, and nutritional status among 239 breastfeeding Ariaal infants, a group of settled pastoralists who experience both acute and chronic nutritional stress residing in Marsabit District, Kenya. This study had three goals: 1) To investigate the pattern of fat accumulation among Ariaal infants compared with a reference population; 2) to explore the relationship between chronic nutritional stress and fat deposits; and 3) to determine the relationship between traditional weaning foods, particularly cow's milk, and infant's fat. Infants, particularly infants experiencing chronic nutritional stress, were found to accumulate fat deposits in a manner that suggests reduced oxidation of fat stores. Infant upper arm fat area significantly increases with age over the weaning period compared with reference populations, who show a decline in body fat. Chronically undernourished infants were particularly likely to have increased levels of upper arm fat compared with normal infants or acutely undernourished infants. In addition, infants who consume cow's milk are significantly fatter than those that do not. These results suggest that Ariaal infants have both physiological and cultural mechanisms for fat storage in the face of their nutritionally stressed environment. Am J Phys Anthropol 153:286–296, 2014. © 2013 Wiley Periodicals, Inc.     

NUTRITIONAL ASPECTS OF ANASTOMOTIC OPERATIONS—With Special Reference to the Sprue Syndrome

Necessary but radical operation which results in short-circuits between various levels of the digestive tract, with or without resections of portions of the esophagus, stomach or intestine, frequently cures the condition for which the operation was done, but leaves the patient with difficult nutritional problems. These nutritional disturbances are usually associated with inability to maintain or gain weight as a result of badly regulated movement of food material through the altered digestive tract, and by the removal or diversion of important digestive secretions, such as those elaborated by the stomach, pancreas, duodenum and small bowel.Increased intestinal rate and diminished specific gastrointestinal secretions reduce the ability of the small bowel to properly absorb food, with resulting malnutrition, deficiency disease, and at times specific avitaminosis. Inability to absorb fat and fat-soluble substances is a constant feature of these conditions. Successful treatment of the nutritional problems involves constant, prolonged overfeeding of nonbulky foods, usually given in regular, frequently administered meals of small volume. Vitamin concentrates may occasionally be of some temporary assistance but are not needed if a balanced diet is given and may cause undesirable and sometimes dangerous symptoms. The use of supplemental substances, such as liver extract and a wetting agent, such as “Tween 80,” to improve fat absorption have been demonstrated to be of value.The postoperative conditions described are fairly similar to the condition known as sprue, and it is possible that the general principles underlying the treatment of this disease apply to the entire group of post-operative nutritional disturbances alluded to.     

Investigation of the intestinal microbiota in preterm infants using different methods

Modifications in microbial colonization of the human gut are believed to affect intestinal homeostasis and increase the risk of gastrointestinal diseases. The present study examined different methods for investigating the dynamic characterization of the intestinal microbiota in preterm infants. Fecal samples were collected weekly from ten preterm infants during their stay in a neonatal intensive care unit. The infants had a mean gestational age of 29 weeks (range: 28–32 weeks) and a mean birth weight of 1233 g (range: 935–1450 g). Bacterial colonization was assessed using conventional culture techniques and molecular biological methods. More specifically, the recently developed denaturing high performance liquid chromatography (dHPLC) technique was compared to established methods such as temporal temperature gradient gel electrophoresis (TTGE) and rRNA gene library sequencing. Our results indicate that the gastrointestinal tract of preterm infants, born at a gestational age of less than 33 weeks, has a low biodiversity of mainly, culturable bacteria. Finally, dHPLC was evaluated in terms of speed, labor and sensitivity for its use as a tool to analyze microbial colonization in preterm infants. We found that this technique provided major improvements over gel-based fingerprinting methods, such as TTGE, that are commonly used for studying microbial ecology. As such, it may become a common analytical tool for this purpose.     

Impact of periconceptional nutrition on maternal and fetal leptin and fetal adiposity in singleton and twin pregnancies

It has been proposed that maternal nutrient restriction may alter the functional development of the adipocyte and the synthesis and secretion of the adipocyte-derived hormone, leptin, before birth. We have investigated the effects of restricted periconceptional undernutrition and/or restricted gestational nutrition on fetal plasma leptin concentrations and fetal adiposity in late gestation. There was no effect of either restricted periconceptional or gestational nutrition on maternal or fetal plasma leptin concentrations in singleton or twin pregnancies during late gestation. In ewes carrying twins, but not singletons, maternal plasma leptin concentrations in late gestation were directly related to the change in ewe weight that occurred during the 60 days before mating [maternal leptin = 0.9 (change in ewe weight) + 7.8; r = 0.6, P < 0.05]. In twin, but not singleton, pregnancies, there was also a significant relationship between maternal and fetal leptin concentrations (maternal leptin = 0.5 fetal leptin + 4.2, r = 0.63, P < 0.005). The relative mass of perirenal fat was also significantly increased in twin fetal sheep in the control-restricted group (6.0 +/- 0.5) compared with the other nutritional groups (control-control: 4.1 +/- 0.4; restricted-restricted: 4.4 +/- 0.4; restricted-control: 4.3 +/- 0.3). In conclusion, the impact of maternal undernutrition on maternal plasma leptin concentrations during late gestation is dependent on fetal number. Furthermore, we have found that there is an increased fetal adiposity in the twins of ewes that experienced restricted nutrition throughout gestation, and this may be important in the programming of postnatal adiposity.     

Fetal leptin is a signal of fat mass independent of maternal nutrition in ewes fed at or above maintenance energy requirements

In adults, circulating leptin concentrations are dependent on body fat content and on current nutritional status. However, the relationships among maternal nutrient intake, fetal adiposity, and circulating leptin concentrations before birth are unknown. We investigated the effects of an increase in nutrient intake in the pregnant ewe on fetal adiposity and plasma leptin concentrations during late gestation. Between 115 and 139-141 days gestation (term = 147 +/- 3 days gestation), ewes were fed a diet calculated to provide either maintenance (control, n = 6) or approximately 155% of maintenance requirements (well-fed, n = 8). The fetal fat depots (perirenal and interscapular) were dissected, and the relative proportion of unilocular and multilocular adipocytes in each depot was determined. Maternal plasma glucose and leptin concentrations were significantly increased in well-fed ewes. Fetal plasma glucose concentrations were also higher in the well-fed group (115-139 days gestation: control, 1.65 +/- 0.14 mmol/L; well-fed, 2.00 +/- 0.14 mmol/L; F = 5.76, P < 0.04). There was no effect of increasing maternal feed intake on total fat mass, the relative mass of unilocular fat, or fetal plasma leptin concentrations (115-139 days gestation: control, 5.2 +/- 0.8 ng/ml; well-fed, 4.7 +/- 0.7 ng/ml). However, in both the control and well-fed groups fetal plasma leptin concentrations (y) were positively correlated with the relative mass of unilocular fat (x): y = 1.51x + 1.70; (R = 0.76, P < 0.01). Thus, fetal leptin may play a role as a signal of unilocular fat mass in the fetus when maternal nutrient intake is at or above maintenance requirements.     

Nutritional modulation of the gut microbiota and immune system in preterm neonates susceptible to necrotizing enterocolitis

The gastrointestinal inflammatory disorder, necrotizing enterocolitis (NEC), is among the most serious diseases for preterm neonates. Nutritional, microbiological and immunological dysfunctions all play a role in disease progression but the relationship among these determinants is not understood. The preterm gut is very sensitive to enteral feeding which may either promote gut adaptation and health, or induce gut dysfunction, bacterial overgrowth and inflammation. Uncontrolled inflammatory reactions may be initiated by maldigestion and impaired mucosal protection, leading to bacterial overgrowth and excessive nutrient fermentation. Tumor necrosis factor alpha, toll-like receptors and heat-shock proteins are identified among the immunological components of the early mucosal dysfunction. It remains difficult, however, to distinguish the early initiators of NEC from the later consequences of the disease pathology. To elucidate the mechanisms and identify clinical interventions, animal models showing spontaneous NEC development after preterm birth coupled with different forms of feeding may help. In this review, we summarize the literature and some recent results from studies on preterm pigs on the nutritional, microbial and immunological interactions during the early feeding-induced mucosal dysfunction and later NEC development. We show that introduction of suboptimal enteral formula diets, coupled with parenteral nutrition, predispose to disease, while advancing amounts of mother's milk from birth (particularly colostrum) protects against disease. Hence, the transition from parenteral to enteral nutrition shortly after birth plays a pivotal role to secure gut growth, digestive maturation and an appropriate response to bacterial colonization in the sensitive gut of preterm neonates.     

n-6 and n-3 Long-chain polyunsaturated fatty acids in the erythrocyte membrane of Brazilian preterm and term neonates and their mothers at delivery

Placental transfer of the long-chain polyunsaturated fatty acids (LCPUFA) arachidonic (AA) and docosahexaenoic (DHA) acids is selectively high to maintain accretion to fetal tissues, especially the brain. The objectives of the present study were to investigate the essential fatty acid (EFA) and LCPUFA status at birth of preterm and term Brazilian infants and their mothers, from a population of characteristically low intake of n-3 LCPUFA, and to evaluate the association between fetal and maternal status, by the determination of the fatty acid composition of the erythrocyte membrane. Blood samples from umbilical cord of preterm (26-36 weeks of gestation; n = 30) and term (37-42 weeks of gestation; n = 30) infants and the corresponding maternal venous blood were collected at delivery. The LCPUFA composition of the erythrocyte membrane and DHA status were similar for mothers of preterm and term infants. Neonatal AA was higher (P < 0.01) whereas its precursor 18:2n-6 was lower (P < 0.01) than maternal levels, as expected. There was no difference in LCPUFA erythrocyte composition between preterm and term infants, except for DHA. Term infants presented a worse DHA status than preterm infants (P < 0.01) and than their mothers (P < 0.01) at delivery. There was a negative correlation of neonatal DHA with maternal AA and a positive correlation between neonatal AA and maternal AA and 18:2n-6 only at term. These results suggest that the persistent low DHA maternal status, together with the comparatively better AA and 18:2n-6 status, might have affected maternal-fetal transfer of DHA when gestation was completed up to term, and possibly contributed to the worse DHA status of term neonates compared with the preterm neonates.