Although the causes of high birthweight include both genetic and environmental factors, the rapid increase in the prevalence of large newborns has environmental causes. The evidence is extensive that maternal overweight and associated metabolic changes, including type 2 and gestational diabetes, play a central role. There is a paucity of studies of the effect of intervention before and/or during pregnancy on the risk of having an 'overweight newborn'. It appears rational, however, that preventive measures should primarily be implemented before pregnancy and should include guidance about nutrition and physical activity in order to reduce the prevalence of overweight. In pregnancy, limited weight gain, especially in obese women, seems to reduce the risk of macrosomia, as do good control of plasma glucose among those with diabetes. Prediction of fetal macrosomia remains an inaccurate task even with modern ultrasound equipment. There is little evidence that routine elective delivery (induction or caesarean section) for the mere reason of suspected macrosomia should be employed in a general population. Vaginal delivery of a macrosomic fetus requires considered attention by an experienced obstetrician and preparedness for operative delivery, shoulder dystocia and newborn asphyxia.

Human low density lipoprotein (LDL) was incubated with an established line of rabbit aortic endothelial cells. Density gradient fractionation showed a time-, concentration-, and temperature-dependent increase in the average density ofthe LDL (from about 1.036 to as high as 1.070 g/ml). Incubation without cells or with other types of cultured cells (fibroblasts, henatocytes, 3T3-L1 cells) caused no significant change in density. '2I-Labeled LDL ('25I-LDL) recovered after incubation with endothelial cells (EC-modified LDL) was taken up and degraded 3 to 4 times more rapidly than control LDL by resident mouse peritoneal macrophages and by an established tumor line of mouse macro hages (J774 cells). Macrophage degradation of EC-modified 5I-LDL exhibited saturation kinetics (>85% inhibited by excess unlabeled EC-modified LDL). Degradation was also inhibited by unlabeled acetylated LDL and, conversely, unlabeled ECmodified LDL inhibited degradation of acetylated '2'I-LDL. Incubation of LDL with conditioned medium removed from endothelial cell cultures modified neither its density nor its rate of degradation by macrophages. These studies show that endothelial cells have the potential to metabolically modify the LDL molecule, generating a form that is more rapidly degraded by macrophages and that is recognized by the macrophage receptor for acetylated LDL. This process may play a significant role in the pathogenesis of atherosclerosis.

No abstract

Even modest increases in maternal BMI were associated with increased risk of fetal death, stillbirth, and neonatal, perinatal, and infant death. Weight management guidelines for women who plan pregnancies should take these findings into consideration to reduce the burden of fetal death, stillbirth, and infant death.

No abstract