Influence Of Birth Weight Research Articles

Componentes Reprodutivos e Produtivos no Rebanho de Corte da Embrapa Cerrados

O objetivo deste trabalho foi analisar os diversos fatores que influenciam o intervalo de partos (IEP), a fertilidade real (FR), razão do peso do bezerro ao nascer (RPN) ou desmame (RPD) em relação ao peso da vaca ao parto, no rebanho de gado mestiço da Embrapa Cerrados. Foram analisados dados de 4469 parições, coletados no período entre 1976 e 1999, usando os procedimentos GLM, CORR e PRINCOMP do SAS. As características incluíram as relações peso ao nascimento do bezerro/peso da vaca no parto (RPN), peso ao desmame do bezerro/ peso da vaca no parto (RPD) e a fertilidade real (FR), bem como a condição corporal (CC) e os pesos dos animais. A CC da vaca no parto (CCVP) não afetou a mortalidade, o peso ao nascer dos bezerros, ou o IEP. A FR elevou-se com o aumento da CCVP, seguindo a tendência oposta que o IEP. Verificaram-se menor IEP e maior FR com maiores valores de CC da vaca ao desmame (CCVD). O grupo genético do pai não influenciou nenhuma das características analisadas, enquanto o grupo da mãe foi significativo para todas as características estudadas. Somente o ano do nascimento influenciou a mortalidade dos bezerros. O ambiente (mês, ano e número do parto da mãe) e a genética (sexo) influenciaram significativamente os pesos ao nascer e ao desmame. As correlações entre as características estudadas foram, em geral, baixas e, às vezes, negativas para RPN e RPD, enquanto com FR foram mais altas. Os dois primeiros componentes explicam 56% da variação total entre as características examinadas.

Maternal leptin receptor gene variant Gln223Arg is not associated with variation in birth weight or maternal body mass index in UK and South Asian populations

Leptin is an adipocyte secreted hormone involved in regulation of body weight and metabolism in man. Placenta leptin levels correlate positively with birth weight. It is therefore possible that variation in the leptin receptor gene (LEPR) may contribute to obesity and influence birth weight. This study investigates the influence of the leptin receptor gene variant Gln223Arg (A-->G, 668), on maternal body mass index (BMI), foetal gestational length and birth weight in a cohort of 455 healthy pregnant women of Asian Indian (India, Bangladesh, Pakistan) and UK/Irish origin. Maternal genotype distributions did not differ from those expected under Hardy-Weinberg equilibrium conditions in either population of origin. Maternal genotype for the Gln223Arg leptin receptor gene polymorphism showed no significant association with foetal birth weight (adjusted for gestational length) or with maternal BMI during first trimester (adjusted for age) in either population group. These results suggest that the Gln223Arg variant in the maternal leptin receptor gene does not explain the association between placental leptin levels and birth weight, and is not associated with variation in maternal BMI in early pregnancy in our sample.

Fetal leptin influences birth weight in twins with discordant growth.

The objective of this study was to determine the plasma leptin concentrations in twin pregnancies in relation to chorionicity and discordant fetal growth. We studied 53 twin pregnancies of which 26 had growth discordance of > or =20% and 27 were concordant for growth (discordance of < or =10%). Paired maternal and fetal blood samples were obtained at birth. Plasma leptin concentrations were measured by RIA. In discordant monochorionic pregnancies, fetal plasma leptin concentrations in the intrauterine growth-restricted twins were lower than the co-twins with normal growth (mean difference, 3 ng/mL; 95% CI, 2.2 to 3.3 ng/mL; p < 0.001), whereas no such differences were present between concordant monochorionic twin pairs (mean difference, 0.1 ng/mL; 95% CI, -0.2 to 0.5 ng/mL; NS). Similarly, fetal plasma leptin concentrations in appropriate-for-gestational-age twins were higher than in the intrauterine growth-restricted twins of the discordant dichorionic pregnancies (mean difference, 2.4 ng/mL; 95% CI, 1.8 to 3.1 ng/mL; p < 0.001). No such differences were present between the concordant dichorionic twin pairs (mean difference, 0.2 ng/mL; 95% CI, -0.1 to 0.5 ng/mL; NS). Maternal plasma leptin concentrations were comparable among all four groups and were higher than the fetal levels. Fetal plasma leptin concentrations of the intrauterine growth-restricted twins of discordant monochorionic and dichorionic pregnancies were comparable. There was a positive association between cord plasma leptin concentrations and the birth weight of twin pairs (y = 0.002x - 0.32; r = 0.63; p < 0.001; n = 106). A significant positive association was also found between percent differences in birth weight and fetal delta plasma leptin concentrations of the discordant monochorionic and dichorionic twin pairs (y = 0.057x + 0.93; r = 0.60; p < 0.001, n = 26). In conclusion, irrespective of chorionicity, plasma leptin concentrations in intrauterine growth-restricted twins were 2-fold lower than their co-twins with normal growth. These differences may be attributed to placental factors.

Analysis of 44 279 blood glucose estimations in relation to outcomes in 80 pregnant diabetic women

A retrospective study was conducted to assess glycaemic control in relation to pregnancy outcomes in pre-existing and gestational diabetics. Computerised blood glucose records from 47 pre-existing diabetic patients and 33 gestational diabetics were collected prospectively and then analysed retrospectively in relation to pregnancy outcomes. There were two spontaneous miscarriages from the pre-existing diabetic cohort. A total of 44 279 individual blood glucose estimations were made. The mean fasting glucose for pre-existing diabetic patients fell significantly throughout pregnancy, being 7·7 - 2·1, 7·2 - 3·1 and 6·5 - 2·4 mmol/l, respectively, for trimesters 1,2 and 3 ( P <0·01). The mean post-prandial glucose for each trimester were 8·9 - 2·0, 8·6 - 1·6 and 8·2 - 1·2 mmol/l ( P <0·01). The HbAlc for pre-existing diabetic patients for each trimester was 7·5 - 1·4%, 6·1 - 1·0% and 5·9 - 0·7%, respectively. Gestational diabetic patients had a mean fasting glucose of 5·6 - 1·5 mmol/l and a mean post-prandial glucose of 8·0 - 2·1 mmol/l during trimester 3. Home glucose monitoring correlated reasonably well with first trimester HbA1c ( r 2 =0·43, P <0·001), but this relationship became less valid as pregnancy progressed. The mean gestation at delivery was 37 weeks, although 30% of women were delivered between 34 and 37 weeks and 8% delivered before 34 weeks. Labour was induced in 49% of patients and the overall caesarean section rate was 58%. The mean birth weight for pre-existing diabetic patients was 3479 g (1410-5000 g) and for women with gestational diabetes was 3605 g (1890-5920 g). For pre-existing diabetic patients HbA1c did not correlate with birth weight; however, home blood glucose data from trimester 2 did correlate ( r 2 =0·15, P <0·005) and there appeared to be stronger relationship with trimester 3 data ( r 2 =0·24, P <0·005). There was no association between trimester 3 glucose data and birth weight in the gestational cohort. The babies born to pre-existing diabetic mothers had a high incidence of admission to a neonatal unit and over 50% of the babies had proven hypoglycaemia. Our present computerised system for home blood glucose monitoring has shown that for pre-existing diabetes patients but not gestational diabetic patients, glycaemic control in the second and third trimester influences birth weight. The current degree of glycaemic control in the mothers did not prevent a high rate of neonatal hypoglycaemia.

Putative quantitative trait locus affecting birth weight on bovine chromosome 2.

A genome scan for chromosomal regions influencing birth weight was performed using 151 progeny of a single Hereford x composite bull and 170 microsatellite markers spanning 2.497 morgans on 29 bovine autosomes. A QTL was identified at the telomeric end of bovine chromosome 2 (maximum effect at 114 cM) accounting for approximately 2.8 kg of birth weight or 0.64 residual standard deviations (after adjustment for sex of calf, age of dam, and breed of dam). No significant effect on growth from birth to weaning was detected in this region. The presence of this QTL within a resource herd composed of breeds common to the Northern Great Plains provides an opportunity to initiate marker-assisted selection to reduce birth weight with minimal effect on postnatal growth. Thus, potentially the amount and degree of dystocia can be reduced and the economic loss associated with calving difficulty lessened without compromise of subsequent growth performance. In addition, this finding indicates that significant genetic variation for birth weight (and presumably other production-related traits) exists within herds composed of commercially adapted Bos taurus germplasm.

Maternal diabetes alters birth weight in glucokinase-deficient (MODY2) kindred but has no influence on adult weight, height, insulin secretion or insulin sensitivity

Altered fetal insulin secretion caused by fetal or maternal glucokinase mutations influence birth weight. Here, we attempt to answer two additional questions: firstly, whether this variation in birth weight (from low birth weight to macrosomia) has an effect on adult height or weight. Secondly, whether maternal hyperglycaemia during fetal life has an effect on metabolic phenotypes of the adult offspring. We studied 447 family members from 37 MODY2 kindred, divided into four groups according to the presence or absence of a glucokinase mutation in the subject (S+ or S-, respectively) and his/her mother (M+ or M-). Birth weight data were obtained from a questionnaire sent to the mothers. Birth weight was reduced in the presence of a fetal mutation (M-S+) and increased in the presence of a maternal mutation (M+ S-). These effects are additive as similar birth weights were observed in M+ S+ and M-S- offspring. Adult height, weight or body mass index (weight/height2) were, however, similar in the four groups of subjects. Non-diabetic adult offspring, regardless of the glycaemic status of the mothers (M+ S- or M-S-), had similar insulin secretion, insulin sensitivity, blood pressures and lipid profiles. These variables as well as the severity of hyperglycaemia were similar in adult M+ S+ and M-S+ MODY2 subjects. Maternal environment and fetal genotypes could alter growth in utero by changing fetal insulin secretion but these effects do not result in a persistent programming in latter life.

Hyperemesis gravidarum in a contemporary population in Oslo

Sociodemographic studies of hyperemesis gravidarum are conflicting. During the last few years, there has been a clinical impression in Norway that immigrants are more afflicted than ethnic Norwegians. Of 175 patients hospitalized with the diagnosis hyperemesis gravidarum 1993-1997, 120 had complete records and were compared to a control group of 115 patients without hyperemesis gravidarum, drawn at random from the labor ward protocol. Ethnicity, age, height, weight at the beginning and at the end of pregnancy, body mass index, gravidity, parity, smoking, gestational age at labor, birth weight, placental weight. The patient's first name was used as an indication of ethnicity. Having a non-Norwegian name means, in the majority of cases, being a first generation immigrant from a developing country. SPSS statistical package for regression analyses, the chi-square test with Yates correction and the Mann-Whitney U-test. Risk factors for hyperemesis: non-Norwegian name (OR 3.4, 95% CI 1.5-7.6), female sex of the infant (OR 2.6, 95% CI 1.3-5.3), gravidity number (OR 1.4, 95% CI 1.1-1.9). These two last variables were of significance only in patients with a Norwegian name. The hyperemesis group had a lower weight gain and birth weight. In a stepwise multiple regression birth weight (g) was dependent on weight increase (kg) (B=19.0, p=0.001), weight in early pregnancy (kg) (B=8.0, p =0.02) and parity (B= 107.1, p=0.02). Hyperemesis, when corrected for weight increase, did not influence birth weight. Risk factors vary between different populations. Hyperemesis patients are at risk of having infants with reduced growth.

Combined analyses of data from quantitative trait loci mapping studies. Chromosome 4 effects on porcine growth and fatness.

For many species several similar QTL mapping populations have been produced and analyzed independently. Joint analysis of such data could be used to increase power to detect QTL and evaluate population differences. In this study, data were collated on almost 3000 pigs from seven different F(2) crosses between Western commercial breeds and either the European wild boar or the Chinese Meishan breed. Genotypes were available for 31 markers on chromosome 4 (on average 8.3 markers per population). Data from three traits common to all populations (birth weight, mean backfat depth at slaughter or end of test, and growth rate from birth to slaughter or end of test) were analyzed for individual populations and jointly. A QTL influencing birth weight was detected in one individual population and in the combined data, with no significant interaction of the QTL effect with population. A QTL affecting backfat that had a significantly greater effect in wild boar than in Meishan crosses was detected. Some evidence for a QTL affecting growth rate was detected in all populations, with no significant differences between populations. This study is the largest F(2) QTL analysis achieved in a livestock species and demonstrates the potential of joint analysis.

Relation of birth weight to lean and fat thigh tissue in young men.

Birth weight is positively associated with body mass index (BMI, kg/m2) in later life, but is inversely associated with cardiovascular risk. To understand this paradox, we examined the relationships between birth weight, adult BMI, and estimations of lean and fat tissue in young men. From 192 applicants for military service (ages 17-22 y, mean BMI 23.2 kg/m2) with known birth weights we measured the circumference and anterior skinfold thickness at midthigh to estimate thigh muscle+bone area and subcutaneous fat area. Linear regression models including birth weight as the independent variable were adjusted for race and adult height. BMI was linearly associated with birth weight (standardized regression coefficient, [SRC]=+0.27; P=0.0004), as was the thigh muscle+bone area (SRC=+0.22; P=0.0029), but not the thigh subcutaneous fat area (SRC=+0.13; P=0.086). The BMI-birth weight association was reduced by 68% when the regression model was further adjusted for thigh muscle+bone area. Separate adjustment for thigh subcutaneous fat, however, reduced the BMI-birth weight association by only 30%. Waist circumference was also associated with birth weight (SRC=+0.24; P=0.0014), sagittal abdominal diameter was weakly associated (SRC=+0.17; P=0.028), but waist/thigh ratio and abdominal diameter index were not associated with birth weight. The larger BMI associated with higher birth weight may reflect increments in lean tissue more than increments in fat. Birth weight's influence on lean tissue is observed in the thigh and, among fit young men, perhaps at the waist. Increased muscularity in young men may partly explain the cardiovascular benefit in middle age ascribed to higher birth weight.

Birth weight influences long-term catch-up growth and height prognosis of GH-deficient children treated before the age of 2 years

To investigate which pretreatment variables most significantly affect long-term growth response to GH therapy in children with apparently idiopathic GH deficiency (GHD) treated from a similar and very young age (less than 2 years), for the same period (7 years) and with the same therapeutic protocol. Twelve children with either isolated GHD or multiple pituitary hormone deficiency were treated with biosynthetic human GH (0.7IU/kg per week) and were examined every 6 months. Height measurements were performed by Harpenden stadiometers. Bone age was evaluated every 12 months. The onset of therapy was followed in all patients by an important height gain, which attained its zenith during the first year of treatment and became progressively less evident during the next 4 years. Cumulative height gain was 3.0+/-1.7SDS. Thanks to the therapy, at the end of the 7-year treatment period, average height in the entire series was not significantly far from mean target height (TH) (-0.7+/-1.3 vs -0. 3+/-0.4SDS) and average predicted height (PH) (-0.2+/-1.4SDS) was very close to TH. A stepwise regression analysis showed that both catch-up growth under therapy and PH at the end of the 7-year treatment period were positively influenced by birth weight (BW). a) Our 7-year prospective study on GHD infants treated with GH from less than 2 years of age confirmed the importance of early diagnosis and treatment of GHD in childhood. b) The influence of BW on growth response to GH therapy in GHD children persists over time, at least when treatment is begun from less than 2 years of age.

Diferencia en peso de nacimiento promedio según tres variables biológicas en recién nacidos normales

The most important determinant of birth weight is gestational age. However, other biological variables may influence this parameter. To study the influence of maternal parity, height and neonatal gender on the birth weight of normal newborns in a public Hospital of Southern Chile. A computer registry of all deliveries attended in Temuco Hospital between 1993 and 1998 was analyzed. Normal deliveries giving birth to newborns of more than 2,500 g and from women who did not suffer from conditions that could influence birth weight, such as hypertension, undernutrition or smoking, were selected. From 27,736 deliveries, 12,580 were selected for the study. Male newborns with gestational ages from 37 to 42 weeks, had a higher weight than their female counterparts. Multiparous women and those with a height over 154 cm gave birth to newborns with a higher weight than nulliparous women or than those with a height of less than 154 cm. According to these results, birth weight must be corrected by gender and maternal features, to define those newborns that have a low birth weight for their gestational age.

Second-trimester measurements of placental volume by three-dimensional ultrasound to predict small-for-gestational-age infants.

The objective of this study was to investigate the value of second-trimester three-dimensional sonographic placental volume measurements to predict infants who are below the 10th centile for birth weight. Placental volume measurements were performed using three-dimensional ultrasound in 382 women with normal singleton pregnancies at 16-23 weeks' gestation. Logistic multivariate regression consisting of variables considered to influence birth weight was used to predict infants with a birth weight below the 10th centile from the placental volume measurements. Prognostic influence could be shown for placental volume (p < or = 0.0001), gestational week at the time of measurement (p = 0.0002) and maternal weight at the time of registration (p = 0.0025). Values for specificity and sensitivity achieved by choosing an 'optimal' cut-off point of 0.16 for the estimation probability for a small-for-gestational-age (SGA) infant were low at 82.5% and 52.5%, respectively. Three-dimensional sonographic measurement of the placental volume alone is not a satisfactory technique for predicting SGA infants.

Maternal Body Composition Near Term and Birth Weight

Objective: To assess the relative influence of maternal body composition at late gestation on birth weight. Methods: Maternal body composition was estimated in 224 women near term using a deuterium dilution technique. Using a stepwise multiple linear regression analysis, we studied the association with birth weight of eight factors, including maternal fat-free mass and fat mass. Results: Maternal fat-free-mass was the most important variable influencing birth weight ( R 2 = .144, P < .001), followed by maternal fat mass ( R 2 = .051, P < .001). Gestational age at delivery was the third strongest influence on birth weight ( R 2 = .047, P < .001). Conclusion: In late pregnancy, fat-free mass was the most important maternal body component associated with birth weight. The implementation of longitudinal studies could shed more light on the influence of maternal body composition on birth weight.

Maintenance of maternal diet-induced hypertension in the rat is dependent on glucocorticoids.

Recent epidemiological evidence suggests that adult cardiovascular risk is determined by birth weight and factors that influence birth weight, such as maternal nutrition. Data from animal models suggest that an interaction between nutrition and glucocorticoid hormones "programs" increased risk of adult hypertension. Increased fetal exposure to maternal glucocorticoids that is proposed to occur from a reduction in the placental barrier to maternal glucocorticoid, 11beta-hydroxysteroid dehydrogenase, is suggested to program hypertension in the resultant offspring from both glucocorticoid-treated and maternally protein-restricted rats. The extent to which postnatal glucocorticoid stimulation may influence the progression of hypertension in the offspring from protein-restricted rat dams was assessed in 6-week-old male Wistar rats, prenatally exposed to either an 18% casein (control) or 9% casein (low protein) diet. Rats from each dietary group were sham operated, adrenalectomized or adrenalectomized, and treated with 20 mg corticosterone/kg body weight per day. Before surgery, systolic blood pressure was significantly higher in the low protein-exposed rats compared with controls (165+/-3.8 versus 142+/-3.3 mm Hg, P<.0001). Adrenalectomy of the low protein-exposed animals significantly reduced the blood pressure to control levels, while corticosterone replacement restored the hypertensive state. No effect of adrenalectomy on blood pressure was observed in 18% casein controls. In both dietary groups adrenalectomy decreased brain, but not hepatic, glucocorticoid-sensitive enzyme activities and corticosterone treatment elevated activities of all enzymes. The data suggest that maternal diet-induced hypertension is dependent on an intact adrenal gland postnatally and that glucocorticoids are key trophic agents in maintaining the high blood pressure.

Factors associated with birth weight in Sweden: the study of men born in 1913.

STUDY OBJECTIVE: To analyse factors associated with birth weight and to evaluate the validity of obstetrical data. DESIGN: Obstetrical data were retrieved for singleton men born in 1913 and living...

Analyzing sibship correlations in birth weight using large sibships from Norway.

Data from the Medical Birth Registry of Norway were used to estimate sibship correlations in large sibships (each with > or = 5 infants among singleton live births surviving the first year of life), while adjusting for covariates such as infant gender, gestational age, maternal age, parity, and time since last pregnancy. This sample of 12,356 full sibs in 2,462 sibships born in Norway between 1968 and 1989 was selected to maximize the information on parity, and a robust approach to estimating both regression coefficients and the sibship correlation using generalized estimating equations (GEE) was employed. In concordance with previous studies, these data showed a high overall correlation in birth weight among full sibs (0.48 +/- 0.01), but this sibship correlation was influenced by parity. In particular, the correlation between the firstborn infant and a subsequent infant was slightly lower than between two subsequent sibs (0.44 +/- 0.01 vs. 0.50 +/- 0.01, respectively). The effect of time between pregnancies was statistically significant, but its predicted impact was modest over the period in which most of these large families were completed. While these data cannot discriminate whether factors influencing birth weight are maternal or fetal in nature, this analysis does illustrate how robust statistical models can be used to estimate sibship correlations while adjusting for covariates in family studies.

Lowering the threshold for the diagnosis of gestational diabetes

OBJECTIVE: Our purpose was to determine whether lowering the diagnostic threshold for gestational diabetes mellitus on 3-hour 100 gm oral glucose tolerance testing will select a population at risk for adverse perinatal outcome. STUDY DESIGN: In this retrospective study 434 patients with an abnormal 50 gm glucose screen result (≥140 mg/dl) underwent a standardized 3-hour oral glucose tolerance test. The results were stratified according to maternal weight and the criteria recommended by Sacks or Carpenter. Birth weight and rate of macrosomia were the primary perinatal outcome variables analyzed. RESULTS: Analysis of the data set stratified according to the Sacks criteria revealed results very similar to the Carpenter criteria data set. Patients who would have been newly diagnosed with gestational diabetes mellitus only if the lowered criteria were used (group 2) were older and heavier. No other variable comparisons achieved statistical significance. When the same patients were stratified according to prepregnancy weight, overweight patients were older, gained less weight during the third trimester, underwent cesarean section more often, and had higher cumulative maternal morbidity. Regression analysis showed that the degree of hyperglycemia did not predict macrosomia or influence birth weight, but prepregnant maternal body mass index was associated with macrosomia. CONCLUSIONS: Fetal macrosomia is influenced by maternal prepregnant body mass index. Lowering the glucose tolerance test threshold would result in overdiagnosis of gestational diabetes mellitus without improving perinatal outcome. (Am J Obstet Gynecol 1996;175:961-5.)

The Role of Social Change in Preventing Low Birth Weight

The authors of this article examine the relationship between social factors and low birth weight and the ways in which disparities in socioeconomic status have been addressed over time. The evidence regarding the effectiveness of various efforts to influence birth weight by mitigating the consequences of disadvantage are also assessed. Low socioeconomic status has been shown to influence low birth weight through its various correlates. Historically and today, most programs and policies directed at low birth weight prevention attempt to address the individual health consequences of economic and social disadvantage. By and large, these efforts have produced mixed results. Efforts to affect low birth weight by addressing the underlying causes of social and economic disadvantage have been similarly inconclusive, reflecting the paucity of research on the subject, as well as the historical and ongoing failure to make the research link between health and social policy. The authors argue that reducing persistent disparities in low birth weight requires several steps, including embracing a broader definition of health which incorporates social dimensions, recasting the focus of research and interventions from pregnancy outcomes and infant health exclusively to include the notion of women's health more globally, expanding the research agenda to unravel the paradox of socioeconomic factors and health, and pursuing a dedicated, national commitment to assuring adequate support to individuals and families, including both adequate income and health care.

Smoking in pregnancy

Given that 1 in 3 women smoke during pregnancy, smoking is a significant source of morbidity and mortality in fetuses, infants and women themselves. It has been estimated that 4300 miscarriages each year in the UK are smoking-related and low birth weight, placenta praevia, placenta abruptia and sudden infant death syndrome add considerably to this toll. In addition, babies born to mothers who smoke during pregnancy suffer from poor intellectual and physical growth and are more likely to have respiratory ailments, asthma and glue ear. In women in Britain, lung cancer has overtaken breast cancer as a cause of death, reflecting the increasing prevalence of smoking in women over the last 4 decades. Women feel that smoking confers certain positive benefits, such as the ability to control mood and it is a relatively inexpensive form of enjoyment. Those who smoke during pregnancy tend to be younger, unmarried, of poor educational attainment, lower occupational status, socially disadvantaged, feel addicted to smoking and, importantly, have a partner who smokes. Interventions to help women to stop smoking during pregnancy and beyond have been successful in ante-natal clinic settings, particularly when personalised. Such interventions, by encouraging smoking cessation or reinforcing cessation in women who give up early in pregnancy, also appear to influence birth weight and are therefore of major public health significance.

Relationship between placental development and calf birth weight in beef cattle

Relationships between circulating concentrations of estrone sulfate and progesterone in the dam prepartum and weight of the calf and placenta at birth were evaluated at first parity in Hereford × Angus heifers ( n=27) bred to a purebred Angus bull. Blood samples were collected from the tail vein of all heifers at 14 day intervals throughout the last trimester of gestation, and a complete placenta was obtained from 22 heifers at parturition. Estrone sulfate was measured as free estrone after incubation with sulfatase enzyme, and both estrone and progesterone levels were quantitated by radioimmunoassay. Maternal plasma estrone sulfate concentrations increased ( P<0.01) quadratically from Day 100 to Day 10 prepartum (Day 100, 6.4 ng ml −1; Day 10, 19.0 ng ml −1), and were correlated negatively ( r=−0.84, P<0.01) with changes in plasma progesterone for the same period (Day 100, 11.4 ng ml −1; Day 10, 6.2 ng ml −1). Birth weight was greater for male than female calves (38.3 vs. 32.9 kg, P<0.01), but maternal plasma estrone sulfate and progesterone concentrations and placental weights were not affected ( P > 0.1) by the sex of the fetus. Calf birth weight was correlated positively with maternal plasma estrone sulfate concentrations between Days 10 and 1 prepartum ( r=0.65, P<0.01) and with the dry weight of the cotyledons ( r=0.76, P<0.01), intercotyledonary membranes ( r=0.48, P<0.05) and total placenta ( r=0.71, P<0.01). Three neonatal calf deaths occurred; dams for two of the calves had a 50% reduction in plasma estrone sulfate concentrations for the last 20 days of gestation and a reduction in cotyledonary surface area. Collectively, these results suggest that variation among dams (i.e. either of inherent or pathological origin) for total mass and (or) function of the placentomes within the placenta may influence birth weight, and possibly neonatal viability, of calves born to first parity beef heifers. Furthermore, estrone sulfate concentrations in the maternal circulation provide an index of fetal-placental-maternal well-being and placental insufficiency in cattle.