Background At any given gestational age, infants with low birth weight have relatively high morbidity and mortality. It is not known, however, whether there is a threshold weight below which morbidity and mortality are significantly greater, or whether that threshold varies with gestational age. Methods We analyzed the neonatal outcomes of death, five-minute Apgar score, umbilical-artery blood pH, and morbidity due to prematurity for all singleton infants delivered at Parkland Hospital, Dallas, between January 1, 1988, and August 31, 1996. A distribution of birth weights according to week of gestation at birth was created. Infants in the 26th through 75th percentiles for weight served as the reference group. Data on preterm infants (those born at 24 to 36 weeks of gestation) were analyzed separately from data on infants delivered at term (37 or more weeks of gestation). Results A total of 122,754 women and adolescents delivered singleton live infants without malformations between 24 and 43 weeks of gestat...

Birth weight in relation to morbidity and mortality among newborn infants.

Objective: To establish whether fetal growth rate (as distinct from size at birth) is associated with mortality from ischaemic heart disease. Design: Cohort study based on uniquely detailed obstetric records with 97% follow up over the entire life course and linkage to census data in adult life. Subjects: All 14 611 babies delivered at the Uppsala Academic Hospital, Sweden, during 1915-29 followed up to end of 1995. Main outcome measures: Mortality from ischaemic heart disease and other causes. Results: Cardiovascular disease showed an inverse association with birth weight for both men and women, although this was significant only for men. In men a 1000 g increase in birth weight was associated with a proportional reduction in the rate of ischaemic heart disease of 0.77 (95% confidence interval 0.67 to 0.90). Adjustment for socioeconomic circumstances at birth and in adult life led to slight attenuation of this effect. Relative to the lowest fourth of birth weight for gestational age, mortality from ischaemic heart disease in men in the second, third, and fourth fourths was 0.81 (0.66 to 0.98), 0.63 (0.50 to 0.78), and 0.67 (0.54 to 0.82), respectively. The inclusion of birth weight per se and birth weight for gestational age in the same model strengthened the association with birth weight for gestational age but removed the association with birth weight. Conclusions: This study provides by far the most persuasive evidence of a real association between size at birth and mortality from ischaemic heart disease in men, which cannot be explained by methodological artefact or socioeconomic confounding. It strongly suggests that it is variation in fetal growth rate rather than size at birth that is aetiologically important.

https://www.bmj.com/content/bmj/317/7153/241.full.pdf

Reduced fetal growth rate and increased risk of death from ischaemic heart disease: cohort study of 15 000 Swedish men and women born 1915-29

In this paper, we review the evidence bearing on socio-economic disparities in pregnancy outcome, focusing on aetiological factors mediating the disparities in intrauterine growth restriction (IUGR) and preterm birth. We first summarise what is known about the attributable determinants of IUGR and preterm birth, emphasising their quantitative contributions (aetiological fractions) from a public health perspective. We then review studies relating these determinants to socio-economic status and, combined with the evidence about their aetiological fractions, reach some tentative conclusions about their roles as mediators of the socio-economic disparities. Cigarette smoking during pregnancy appears to be the most important mediating factor for IUGR, with low gestational weight gain and short stature also playing substantial roles. For preterm birth, socio-economic gradients in bacterial vaginosis and cigarette smoking appear to explain some of the socio-economic disparities; psychosocial factors may prove even more important, but their aetiological links with preterm birth require further clarification. Research that identifies and quantifies the causal pathways and mechanisms whereby social disadvantage leads to higher risks of IUGR and preterm birth may eventually help to reduce current disparities and improve pregnancy outcome across the entire socio-economic spectrum.

Socio-economic disparities in pregnancy outcome: why do the poor fare so poorly?

http://wealthandhealth.ltd.uk/articles/Barker%20hyphothesis.pdf

Maternal Nutrition, Fetal Nutrition, and Disease in Later Life

Children's exposure to tobacco constituents during fetal development and via environmental tobacco smoke (ETS) exposure is perhaps the most ubiquitous and hazardous of children's environmental exposures. A large literature links both prenatal maternal smoking and children's ETS exposure to decreased lung growth and increased rates of respiratory tract infections, otitis media, and childhood asthma, with the severity of these problems increasing with increased exposure. Sudden infant death syndrome, behavioral problems, neurocognitive decrements, and increased rates of adolescent smoking also are associated with such exposures. Studies of each of these problems suggest independent effects of both pre- and postnatal exposure for each, with the respiratory risk associated with parental smoking seeming to be greatest during fetal development and the first several years of life.

https://pediatrics.aappublications.org/content/pediatrics/113/Supplement_3/1007.full.pdf

Prenatal and Postnatal Environmental Tobacco Smoke Exposure and Children’s Health

Previous prognostic studies of infants with intrauterine growth retardation (IUGR) have not adequately considered the heterogeneity of IUGR in terms of cause, severity, and body proportionality and have been prone to misclassification of IUGR because of errors in estimation of gestational age. Based on a cohort of 8719 infants with early-ultrasound-validated gestational ages and indexes of body proportionality standardized for birth weight, the consequences of severity and cause-specific IUGR and proportionality for fetal and neonatal morbidity and mortality were assessed. With progressive severity of IUGR, there were significant (all P less than .001) linear trends for increasing risks of stillbirth, fetal distress (abnormal electronic fetal heart tracings)O during parturition, neonatal hypoglycemia (minimum plasma glucose less than 40 mg/dL), hypocalcemia (minimum Ca less than 7 mg/dL), polycythemia (maximum capillary hemoglobin greater than or equal to 21 g/dL), severe depression at birth (manual ventilation greater than 3 minutes), 1-minute and 5-minute Apgar scores less than or equal to 6, 1-minute Apgar score less than or equal to 3, and in-hospital death. These trends persisted for the more common outcomes even after restriction to term (37 to 42 weeks) births. There was no convincing evidence that outcome among infants with a given degree of growth retardation varied as a function of cause of that growth retardation. Among infants with IUGR, increased length-for-weight had significant crude associations with hypoglycemia and polycythemia, but these associations disappeared after adjustment for severity of growth retardation and gestational age.(ABSTRACT TRUNCATED AT 250 WORDS)

Impact of intrauterine growth retardation and body proportionality on fetal and neonatal outcome.

Despite the popular current distinction between "proportional" and "disproportional" intrauterine growth retardation, it has never been shown that variation in body proportions is greater among growth-retarded than nongrowth-retarded infants of the same birth weight, nor that proportionality is distributed bimodally among growth-retarded infants. Based on a cohort of 8719 neonates born between 1980 and 1986 of mothers with concordant (+/- 7 days) menstrual dating and early ultrasound estimates of gestational age, we used a continuous measure of birth weight for gestational age to define four study groups: nongrowth retarded (n = 5163) and mild (n = 411), moderate (n = 226), and severe (n = 147) intrauterine growth retardation. Compared with non-growth-retarded infants of the same gestational age, growth-retarded infants had substantially lower lengths, head circumferences, and proportionality ratios, and the magnitude of the deficits increased significantly with increasing degrees of growth retardation. When the comparison was based on birth weight rather than gestational age, however, growth-retarded infants had slightly but significantly greater lengths and head circumferences, with increased variability in body proportions, but no evidence of the bimodality that would characterize two distinct subtypes. The analysis suggests that proportionality among intrauterine growth-retarded infants represents a continuum, with progressive disproportionality as severity of growth retardation increases. Moreover, despite evidence of some "sparing," the absolute magnitudes of the deficits in length and head growth remain substantial.

Body proportionality and head and length 'sparing' in growth-retarded neonates: a critical reappraisal.

Previous studies of fetal growth and body proportionality have been based on error-prone gestational age estimates and on inappropriate comparisons of infants with dissimilar birth weights. Based on a cohort of 8719 infants with validated (by early ultrasonography) gestational ages and indexes of body proportionality standardized for birth weight, potential maternal and fetal determinants of fetal growth and proportionality were assessed. Maternal history of previous low birth weight infants, pregnancy-related hypertension (particularly if severe), diabetes, prepregnancy weight, net gestational weight gain, cigarette smoking, height, parity, and fetal sex were all significantly associated with fetal growth in the expected directions. Consistent with previous reports, maternal age, marital status, and onset or total amount of prenatal care had no significant independent effects. Fetal growth ratio (relative weight for gestational age), pregnancy-related hypertension, fetal sex, and maternal height were the only significant determinants of proportionality. Infants who were growth-retarded, those with taller mothers, those whose mothers had severe pregnancy-related hypertension, and males tended to be longer and thinner and had larger heads for their weight, although these variables explained only a small fraction of the variance in the proportionality measures. Among infants with intrauterine growth retardation, gestational age was not independently associated with proportionality (in particular, late term and post-term infants did not tend to be more disproportional), a finding that does not support the hypothesis that earlier onset of growth retardation leads to more proportional growth retardation. The results raise serious questions about previous studies of proportionality, particularly those suggesting a nutritional etiology for proportional intrauterine growth retardation.(ABSTRACT TRUNCATED AT 250 WORDS)

Marielle Olivier

Papers

Impact of intrauterine growth retardation and body proportionality on fetal and neonatal outcome.

Body proportionality and head and length 'sparing' in growth-retarded neonates: a critical reappraisal.

Determinants of fetal growth and body proportionality