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close this bookCauses and Mechanisms of Linear Growth Retardation (International Dietary Energy Consultative Group - IDECG, 1993, 216 pages)
close this folderPrenatal influences on postnatal growth: Overview and pointers for needed research
View the document(introductory text...)
View the document1. Introduction and background
View the document2. Fetal growth
View the document3. Intrauterine growth retardation
View the document4. Small-for-gestational-age infants
View the document5. Genetic and environmental factors
View the document6. Reference values for fetal growth
View the documentReferences
View the documentDiscussion
View the documentReferences

3. Intrauterine growth retardation

It is not intended to discuss causation of IUGR, but only to consider its possible relationships with postnatal growth.

Utero-placental and umbilical blood flow can be important factors, as can the transfer of glucose through the placenta or the production of fetal insulin. The roles of fetal pituitary growth hormone and fetal thyroid hormone need continuing study; anencephalic and athyroid fetuses, for example, seem not to exhibit fetal growth retardation (Vorherr, 1982). Placental lactogen and somatomedin and a somatostatin-like substance of the placenta and fetus may well influence fetal growth, and animal experiments certainly suggest the assistance of placental-fetal growth-promoting and - controlling factors. Their identification in the human would contribute much to our knowledge of fetal growth, health and adaptation.

Regarding the placenta, Lechtig et al. (1975; 1977) indicated that nutritional supplementation of the mother during pregnancy is associated with improved placental weight and higher levels of alkaline ribonuclease activity. Leaf et al. (1992), in a very recent study of essential fatty acids at birth, showed that placental function is important in the transfer of some fatty acids from mother to fetus, and that these fatty acid levels were correlated with fetal growth and maturation in the premature infants they studied. Clearly, the placenta has very complex metabolic and endocrine functions. IUGR associated with placental dysfunction tends to occur later in pregnancy and head growth appears spared, whereas early onset IUGR tends not to spare head growth (see later discussion on SGA infants).

It is well established that malnutrition and infection can cause IUGR. During the past decade it has been documented that prenatal intrauterine infection increases fetal IgM. Mekki et al. (1988) and Lechtig et al. (1974) sampled cord blood and showed that IgM levels were higher in newly born infants from very poor environmental backgrounds.

There is certainly a pressing need for detailed studies on the role of infection in IUGR, particularly in tropical and underdeveloped countries. Pardi et al. (1993) showed that techniques for sampling cord blood in utero (cordocentesis) offer the opportunity to assess a fetus's metabolic environment before parturition. In fetuses with IUGR, the detection of, for example, hypoxia, acidemia, low amino-acidemia, and endocrine abnormalities, creates a greater opportunity to study many aspects of not only IUGR but also fetal growth. Kempley, Gamso & Nicolaides (1993), using Doppler ultrasound, measured left renal artery blood flow in the first postnatal week of very low birth weight SGA infants. Compared with weight-and gestation-matched controls, SGA infants had significantly lower blood flow velocity. Thus, abnormalities of blood flow velocity appear to persist after delivery in those SGA infants.

Doyle et al. (1990) found positive correlations between maternal nutrient intake, assessed during one week towards the end of the first trimester of pregnancy on the one hand, and weight, length and head circumference of the newborns on the other, especially in infants with birth weights below 2500 g. Vitamin/mineral supplementation of mothers during the last two trimesters of pregnancy, however, had no significant effects on birth dimensions.