Infant birth weight is related to maternal arterial oxygenation at high altitude

1982 ◽  
Vol 52 (3) ◽  
pp. 695-699 ◽  
Author(s):  
L. G. Moore ◽  
S. S. Rounds ◽  
D. Jahnigen ◽  
R. F. Grover ◽  
J. T. Reeves

Infant birth weight is reported to decrease at high altitude as a reulst of fetal growth retardation (McCullough, Reeves, and Liljegren. Arch. Environ, Health. 32: 36--39, 1977) but not all babies born at high altitude are small. We hypothesized that maternal characteristics acting to lower arterial O2 content would contribute to smaller infant birth weight. To test this hypothesis, we measured arterial oxygenation serially during pregnancy and again postpartum in 44 residents of Leadville, CO (elevation 3,100 m). We identified three maternal characteristics--ventilation, hemoglobin concentration, and smoking habits--that were related to the birth weight of the offspring. Mothers of smaller babies (less than 2,900 g) compared to mothers of larger babies (greater than 3,500 g) were characterized by hypoventilation, no change or a decrease in ventilation and arterial O2 saturation from early to late gestation, and a falling hemoglobin concentration that combined to lower arterial O2 content in the 3rd trimester. Maternal smoking at 3,100 m was associated with a two to threefold greater reduction in infant birth weight (-546 g) than reported from sea level. Thus, maternal arterial oxygenation during pregnancy may be important for predicting fetal growth retardation and the process of adaptation to high altitude.

PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 446-453
Author(s):  
Alistair G.S. Philip

Sixty-three term newborn infants with fetal growth retardation were evaluated within three days of birth. They were classified by length and head circumference. In group 1, both length and head circumference were less than the tenth percentile; in group 2, either length or head circumference was less than the tenth percentile; and in group 3, both length and head circumference were greater than the tenth percentile. Ponderal index (weight/length ratio), anterior fontanel size, and amount of epiphyseal ossification were also determined. Significantly lower birth weights and decreased ossification were found when groups 1 or 2 were compared separately with group 3. These differences were most marked when the weight/length ratio was less than 2.25. When the ponderal index was less than 2.0, epiphyseal ossification was usually absent (suggesting a chronic process). Epiphyseal ossification was positively correlated with birth weight and length but was unrelated to anterior fontanel size. Ossification was more often absent in males than in females. There was a negative (inverse) correlation between birth weight and anterior fontanel size. Follow-up of 32 of these infants at age 1 year showed marked individual variations, but there were significant differences in incremental linear growth between groups 1 and 3, a finding which supports results of animal studies showing that catch-up growth may be related to skeletal immaturity. Physical measurements at birth in the individual baby with fetal growth retardation do not reliably predict subsequent growth.


PEDIATRICS ◽  
1972 ◽  
Vol 50 (4) ◽  
pp. 547-558
Author(s):  
J. Urrusti ◽  
P. Yoshida ◽  
L. Velasco ◽  
S. Frenk ◽  
A. Rosado ◽  
...  

Intrauterine growth was assessed in a series of 128 cases. Thirty-six infants were small for gestational age, and showed the usual signs of intrauterine growth retardation (IUM). The head circumference of these infants was small, with reference to normal term babies (FT) and comparable to premature infants, appropriately sized for a gestational age (ACA) five weeks less than that of the IUM's. There were 12 neonatal deaths, three among IUM infants within 24 hours and nine in the low birth weight AGA group within 72 hours. The mothers of these three groups of infants were similar with respect to age, weight, height, nutritional patterns, and prior pregnancy histories.


1995 ◽  
Vol 7 (3) ◽  
pp. 639 ◽  
Author(s):  
BM Johnston

Epidemiological studies have linked low birth weight and increased placental weight with increased risk of hypertension in adult life. It has been proposed that the cardiovascular changes which lead to hypertension are initiated in utero by processes associated with intrauterine growth retardation. The alternative possibility, that hypertension may result from genetic influences which also determine fetal and placental size, has had less support because birth weight is not determined genetically in humans. However, in the spontaneously hypertensive rat (SHR) essential hypertension is known to be transmitted genetically. Fetal and placental weights were, therefore, measured at Day 20 gestation in SHRs and compared with those in the normotensive Wistar Kyoto (WKY) control strain. Fetal weight (1.93 +/- 0.04 g) was significantly (P < 0.001) reduced in SHRs compared with WKY fetuses (2.23 +/- 0.01 g) but placental weight was heavier (P < 0.001) in SHRs (0.347 +/- 0.005 g) than in WKY rats (0.300 +/- 0.006 g) although litter size was not different. As expected, maternal blood pressure recorded under 1% halothane anaesthesia was higher (126 +/- 2.7 mm Hg) in SHR than WKY rats (100 +/- 2.1 mm Hg; 1 mm Hg = 133 Pa). In addition the concentration of maternal blood glucose in SHR was significantly (P < 0.001) higher (4.8 +/- 0.32 mM v. 3.7 +/- 0.11 mM) and the concentration of plasma insulin was significantly (P < 0.05) lower in SHRs (18.8 +/- 3.0 ng mL-1) than in WKY dams (29.4 +/- 3.1 ng mL-1). Thus, the data support human population studies which show an association between adult hypertension and a reduced fetal:placental weight ratio at birth. However, because hypertension in the SHR is genetically determined, these data suggest that fetal growth retardation and increased placental weight may also be determined genetically.


2014 ◽  
Vol 46 (18) ◽  
pp. 687-697 ◽  
Author(s):  
Abigail W. Bigham ◽  
Colleen G. Julian ◽  
Megan J. Wilson ◽  
Enrique Vargas ◽  
Vaughn A. Browne ◽  
...  

Low birth weight and intrauterine growth restriction (IUGR) increase the risk of mortality and morbidity during the perinatal period as well as in adulthood. Environmental and genetic factors contribute to IUGR, but the influence of maternal genetic variation on birth weight is largely unknown. We implemented a gene-by-environment study wherein we utilized the growth restrictive effects of high altitude. Multigenerational high-altitude residents (Andeans) are protected from altitude-associated IUGR compared with recent migrants (Europeans). Using a combined cohort of low- and high-altitude European and Andean women, we tested 63 single nucleotide polymorphisms (SNPs) from 16 natural selection-nominated candidate gene regions for associations with infant birth weight. We identified significant SNP associations with birth weight near coding regions for two genes involved in oxygen sensing and vascular control, PRKAA1 and EDNRA, respectively. Next, we identified a significant association for the PRKAA1 SNP with an intermediate phenotype, uterine artery diameter, which has been shown to be related to Andean protection from altitude-associated reductions in fetal growth. To explore potential functional relationships for the effect of maternal SNP genotype on birth weight, we evaluated the relationship between maternal PRKAA1 SNP genotype and gene expression patterns in general and, in particular, of key pathways involved in metabolic homeostasis that have been proposed to play a role in the pathophysiology of IUGR. Our observations suggest that maternal genetic variation within genes that regulate oxygen sensing, metabolic homeostasis, and vascular control influence fetal growth and birth weight outcomes and hence Andean adaptation to high altitude.


1986 ◽  
Vol 60 (4) ◽  
pp. 1401-1406 ◽  
Author(s):  
L. G. Moore ◽  
P. Brodeur ◽  
O. Chumbe ◽  
J. D'Brot ◽  
S. Hofmeister ◽  
...  

To test the hypothesis that increased hypoxic ventilatory responsiveness (HVR) raised maternal ventilation and arterial oxygenation during high-altitude pregnancy and related to the birth weight of the offspring, we studied 21 residents of Cerro de Pasco, Peru (4,300 m), while eight of them were 36 +/- 0 wk pregnant and 15 of them 13 +/- 0 wk postpartum. HVR was low in the nonpregnant women (mean +/- SE shape parameter A = 23 +/- 8) but increased nearly fourfold with pregnancy (A = 87 +/- 17). The increase in HVR appeared to account for the 25% rise in resting ventilation with pregnancy (delta VE observed = 2.4 +/- 0.7 l/min BTPS vs. delta VE predicted from delta HVR = 2.6 +/- 1.7 l/min BTPS, P = NS). Hyperoxia decreased ventilation in the pregnant women (P less than 0.01) to levels similar to those measured when nonpregnant. The increased ventilation of pregnancy raised arterial O2 saturation (SaO2) from 83 +/- 1 to 87 +/- 0%, and SaO2 was correlated positively with HVR in the pregnant women. The rise in SaO2 compensated for a 0.9 g/100 ml decrease in hemoglobin concentration to preserve arterial O2 content at levels present when nonpregnant. Cardiac output in the 36th wk of pregnancy did not differ significantly from values measured postpartum. The increase in HVR correlated positively with infant birth weight. An increase in HVR may be an important contributor to increased maternal ventilation with pregnancy and infant birth weight at high altitude.


2008 ◽  
Vol 42 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Vera Maria Freitas da Silveira ◽  
Bernardo Lessa Horta

OBJETIVO: Analisar as evidências na literatura do efeito do peso ao nascer sobre a ocorrência de síndrome metabólica em adultos. MÉTODOS: Foram pesquisados nas bases PubMed and LILACS, no período de 1966 a maio de 2006, artigos publicados usando os seguintes descritores: "birth weight" , "birthweight" , "intra-uterine growth restriction (IUGR)", "fetal growth retardation", "metabolic syndrome", "syndrome X", "Reaven's X syndrome". Foram selecionados 224 estudos considerados elegíveis que relatavam estimativas de associação entre peso ao nascer e síndrome metabólica ou seus componentes. Desses, 11 apresentavam razões de odds e foram usados na meta-análise. RESULTADOS: Com exceção de dois estudos, os demais relataram associação inversa entre peso ao nascer e síndrome metabólica. Comparadas com pessoas de peso normal, a razão de odds do efeito combinado naquelas que nasceram com baixo peso foi de 2,53 (IC 95%: 1,57;4,08). O gráfico de funil sugere viés de publicação e o resultado permanece estatisticamente significativo mesmo em estudos com mais de 400 pessoas (efeito combinado 2,37; IC 95%: 1,15;4,90). CONCLUSÕES: Baixo peso ao nascer aumenta o risco de síndrome metabólica na idade adulta.


PEDIATRICS ◽  
1982 ◽  
Vol 69 (6) ◽  
pp. 724-727
Author(s):  
Richard L. Naeye ◽  
Ellen C. Peters

In order to determine whether pregnancy outcome was altered when women were employed outside their homes, 7,722 pregnancies were analyzed. Gestations were not shortened but newborns of women who worked in the third trimester weighed 150 to 400 gm less than newborns of mothers who remained at home. The growth retardation was greatest when women were underweight pregravid and had a low pregnancy weight gain, when they were hypertensive, or when the work required standing. The growth retardation remained after the data were stratified by race, socioeconomic status, and other maternal factors that commonly influence fetal growth. The frequency of large placental infarcts progressively increased when women continued stand-up work into late gestation. Such infarcts reached a peak of 250/1,000 births after the 37th week of gestation in stand-up workers. Low uteroplacental blood flow is a likely explanation for both the fetal growth retardation and the large placental infarcts.


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