In 1990, the Institute of Medicine (IOM) evaluated the available scientific evidence and set guidelines for total gestational weight gain ranges1 that vary according to prepregnancy body mass index (BMI). The IOM recommended that their guidelines for pregnancy weight gain be examined for associations with perinatal complications. Since then, several studies have observed that the infants of women with pregnancy weight gains within the IOM recommendations are relatively less likely to be at the extremes of birth weight for a given gestational age.2–5 Although excessive pregnancy weight gain has been associated with an increased risk of delivering an infant who is large for gestational age, there is limited data on whether it is positively or negatively associated with other serious neonatal complications such as hypoglycemia and hyperbilirubinemia. Maternal obesity has been associated with serious neonatal hypoglycemia6,7 and hyperbilirubinemia,8 suggesting maternal weight and possibly weight gain may play a role in the development of these outcomes.
Total pregnancy weight gain is affected by the length of gestation, and also by the weight of the term infant, which usually comprises at least 25% of the total gestational weight gain.9,10 Therefore, the use of rate of maternal pregnancy weight gain (total pregnancy weight gain minus infant birth weight divided by gestational weeks) has been suggested as a better measure against which to assess the risk of neonatal outcomes.9 It is also plausible that there are specific periods during pregnancy that are critical for fetal growth and development. Pregnancy weight gain consists of enlarging maternal fluid and soft tissue compartments and the growing fetus. 11 After the first trimester maternal weight gain remains fairly constant, whereas fetal weight increases exponentially, with the greatest gain during the third trimester.1,12 Therefore, weight gain before the third trimester may provide a useful measure of maternal weight gain.
To address the issues related to pregnancy weight gain described above we examined within the Kaiser Permanente Medical Care Program Northern California the occurrence of macrosomia, neonatal hypoglycemia, and neonatal hyperbilirubinemia in relation to 1) total pregnancy weight gain according to the IOM recommendations, 2) rate of maternal pregnancy weight gain (total pregnancy weight gain minus infant birth weight divided by weeks of gestation), and 3) rate of pregnancy weight gain before the third trimester.
MATERIALS AND METHODS
This analysis was conducted as an ancillary study of a nested case–control study examining pregnancy plasma glucose levels below the National Diabetes Data Group thresholds for gestational diabetes mellitus (GDM) and the risk of neonatal macrosomia, hypoglycemia, and hyperbilirubinemia (Ferrara A, Weiss NS, Hedderson MM, Quesenberry CP, Selby JV, Ergas IJ, et al. Pregnancy plasma glucose levels exceeding the American Diabetes Association thresholds but below the National Diabetes Data Group Thresholds for Gestational Diabetes Mellitus are related to the risk of neonatal macrosomia, hypoglycemia, and hyperbilirubinemia [in press]. Diabetologia). During the original study we collected information on pregnancy weight gain to examine the effects of weight gain, independent of plasma glucose, on these outcomes. For each of the three outcomes of interest, we calculated minimum detectable relative odds across IOM recommended weight gain categories (below [referent category], within, above), given the sample size and observed distribution in controls, and sample sizes for each of the three case groups. Calculations were based on the likelihood ratio test and a logistic regression model, as presented by Self et al13 and as implemented in software package EGRET (EGRET SIZ Reference Manual [revision 10]. Seattle (WA): Statistics and Epidemiology Research Corporation. 1992). For the purposes of power calculations we assumed a linear trend in log odds across categories, but power calculations were conservatively based on treating the risk factor as a categorical variable in the regression model (ie, 2 degree of freedom test of general association rather than a 1 degree of freedom test for linear trend). The minimum detectable pattern of odds ratios across IOM weight gain categories were: 1.0 (reference), 1.32, 1.73; 1.0 (reference), 1.34, 1.79; 1.0 (reference), 1.30, 1.70; for macrosomia, hypoglycemia, and hyperbilirubinemia, respectively.
Kaiser Permanente Medical Care Program is a group practice prepaid health plan, which serves approximately 3.0 million members in 16 hospitals. The Kaiser Permanente Medical Care Program Northern California membership represents approximately 30% of the surrounding population and it is representative of the population living in the same geographic area demographically, ethnically, and socioeconomically, except for the extremes of the income distribution.14,15
Using electronic databases we identified a cohort of 45,245 pregnancies resulting in a singleton livebirth between January 1, 1996, and June 31, 1998, from among women not known to have pregestational or a history of gestational diabetes and who were screened at 24–28 weeks of gestation by a 50-g, 1-hour oral glucose challenge test.16 Subjects meeting the National Diabetes Data Group criteria17 for GDM by these tests were excluded from the cohort. Among this cohort we conducted a nested case–control study, with three case groups (macrosomia, neonatal hypoglycemia, and hyperbilirubinemia) and one control group (652 controls).
We searched the hospital databases and the database of the regional laboratory (where all tests are performed) to identify newborns who had the following complications: 1) macrosomia, (birth weight more than 4,500 g, n=1,073); 2) hypoglycemia (at least one plasma glucose less than 40 mg/dL, n=666); and 3) hyperbilirubinemia (at least one total serum bilirubin of 20 mg/dL or more, n=909). We then randomly ordered and selected 600 of each case type and medical chart review was completed on 505 macrosomia cases, 498 hypoglycemia cases, and 588 hyperbilirubinemia cases. Trained abstractors reviewed the medical records of the mother–infant pairs and confirmed eligibility criteria and case definitions. Macrosomia was confirmed if the infant had a birth weight more than 4,500 g and did not have fetal hydrops (n=488). All of the 488 macrosomia cases were also large for gestational age (defined as a birth weight exceeding the 90th percentile of the gestational age-specific weight distribution). Hypoglycemia was confirmed if a laboratory test showed a plasma glucose value less then 40 mg/dL during the first 3 days of life (n=486). Hyperbilirubinemia was confirmed if at least one total serum concentration of 20 mg/dL or more (n=578) was identified during the first 30 days of life and the following conditions were not present: positive direct antiglobulin test, glucose-6-phosphate dehydrogenase deficiency, ABO incompatibility, or RH alloimmunization.
From the remaining women in this cohort, we reviewed the medical records of 960 mother–infant pairs who were randomly selected as controls and confirmed eligibility for 879 of them. If a potential control infant met the criteria for one of the three conditions it was excluded from that particular analysis, but it was allowed to serve as a control in the other case–control analyses. In addition, if a control infant had a capillary glucose test strip test performed in the hospital and the value was less than 40 mg/dL, he or she was excluded from the analysis of hypoglycemia.
Medical chart abstracters recorded weights noted in the woman’s prenatal form, including self-reported prepregnancy weight, measured weights at the first prenatal visit, weight measured at or before the patient had her 50-g, 1-hour glucose screening test (between 24 and 28 weeks of gestation), and the last weight measured before delivery.
Prepregnancy weight was based on mother’s self-reported prepregnancy weight recorded on the prenatal form at her first prenatal visit. For the 30% of women for whom these data were not available, the measured weight recorded in the chart closest to the woman’s last menstrual period (but no more than 12 months before her last menstrual period) was used. To examine agreement between the two methods of estimating prepregnancy weight, we compared self-reported prepregnancy weight and a weight measured within 12 months of last menstrual period of the 695 women for whom both data were available. The Pearson correlation coefficient between the two weights was 0.97 and the mean self-reported weight was 1.6 kg less than the measured weight. This is similar to findings in previous studies.18–21
Other information abstracted from the mother’s medical charts included height, last menstrual period, parity, smoking, screening glucose values, and gestational age estimated by the earliest ultrasound performed before 24 weeks of gestation. Gestational age at each visit when maternal weight was measured was calculated from the earliest ultrasound performed before 24 weeks of gestation.
Women’s self reported race or ethnicity and education were abstracted from the infant’s birth certificate found in the medical chart. From the infants’ medical records we abstracted information on weight at birth and blood tests and results (glucose and bilirubin).
We defined total pregnancy weight gain as the difference between the final recorded weight at the last prenatal visit (within 2 weeks of the delivery date) and prepregnancy weight. On average, the last predelivery weight measured was 4 days before delivery. Rate of maternal pregnancy weight gain was calculated as total pregnancy weight gain minus infant birth weight divided by weeks of gestation when the last weight was measured. Rate of pregnancy weight gain before the third trimester was calculated using the weight measured at or before the screening test for GDM (performed between 24 and 28 weeks of gestation) minus prepregnancy weight divided by weeks of gestation.
We used total pregnancy weight gain for the analysis of pregnancy weight gain by IOM recommendation. Prepregnancy BMI was calculated as prepregnancy weight (kg) divided by height squared (m2). Pregravid BMI categories were constructed according to the IOM recommendations1: less than 19.8 kg/m2 (underweight), 19.8–26.0 kg/m2 (normal weight), 26.1–29.0 kg/m2 (overweight), greater than 29.0 kg/m2 (obese). Based on the IOM guidelines, “underweight” women are advised to gain 12.5 to 18.0 kg, “normal” women 11.5 to 16.0 kg, “overweight” women 7.0 to 11.5 kg, and “obese” women at least 6.8 kg. We categorized women as below, within, or above the IOM recommendations based on their total weight gain and the recommended weight gain range for their specific BMI. However, because the IOM1 did not recommend an upper limit of weight gain for obese women, we classified obese women as meeting the IOM recommendations if their weight gain was at least 6.8 kg but did not exceed the upper limit (11.5 kg) for overweight women.
Of the eligible mothers of the 488 macrosomic infants, 486 infants with hypoglycemia and 578 infants with hyperbilirubinemia, and 879 control infants for whom chart review was completed, the following mother–infant pairs were excluded during all analyses due to missing information: pregravid weight (17.5% of cases and 15.7% of controls); height (1.4% of cases and 1.7% of controls); and no weight measured at prenatal visit within 2 weeks of delivery (9.7% of cases and 12.1% of controls). This left 391 cases of macrosomia, 328 cases of hypoglycemia, 432 cases of hyperbilirubinemia, and 652 controls for analysis. Of the 391 macrosomia cases, 24 had hypoglycemia and 3 had hyperbilirubinemia. Of the 328 hypoglycemia cases, 7 had hyperbilirubinemia. Of the 652 controls included in the final analysis, there were 5 with macrosomia, 1 with hyperbilirubinemia, and 17 with hypoglycemia according to plasma glucose or capillary glucose test strip Dextrostik measurements.
We used χ2 tests to compare differences in the distributions of pregnancy weight gain by case and control status. Unconditional logistic regression was used to obtain odds ratios (ORs) as estimates of the relative risk of each infant complication (macrosomia, hyperbilirubinemia, and hypoglycemia) associated with pregnancy weight gain. For rate of maternal weight gain and rate of weight gain before 24–28 weeks of gestation, we categorized the distribution into quartiles based on levels in the controls. We included weeks between last weight measured and delivery in the models examining IOM recommendations and infant complications. We adjusted all models for maternal age (years), parity (0, 1, 2 or more), race–ethnicity (non-Hispanic, white, Hispanic, Asian, African-American, other) and prepregnancy BMI (except the models with the IOM recommendations, which already account for BMI). The models examining the IOM recommendations and rate of maternal weight gain were also adjusted for screening glucose values measured 1 hour after the 50-g oral glucose challenge test (“normal” less than 140 mg/dL compared with “abnormal” 140 mg/dL or more). The other potentially confounding variables entered into the model individually as covariates were maternal years of education (12 or fewer, 13–15, 16, more than 16), smoking during pregnancy (yes or no). However, none of these variables changed the odds ratio by as much as 10% and were therefore not included in the final models.
We also sought to estimate whether the size of the association between weight gain and each outcome differed according to race–ethnicity (non-Hispanic white compared with nonwhite) prepregnancy BMI (less than 19.8, 19.8–26.0, more than 26.0) and age (35 or more years compared with less than 35 years). The SAS 6.1122 (SAS Institute Inc., Cary, NC) software was used for all analyses. This study was approved by the human subjects committee of the Kaiser Foundation Research Institute.
Modest variation in a number of demographic and clinical characteristics was observed between controls and one or more case groups (Table 1). Women giving birth to infants with one of the neonatal complications were more likely to have gained more than the IOM recommended amount of weight and to be in the highest weight gain quartile for maternal rate of weight gain and pregnancy rate of weight gain before the third trimester than were women in the control group (Table 2). Table 3 presents the ORs and 95% confidence intervals (CIs) for pregnancy complications associated with pregnancy weight gain. Compared with women who gained the IOM recommended amount of weight, women who gained more than recommended were three times more likely to have a macrosomic infant, and about 50% more likely to have an infant with hypoglycemia or hyperbilirubinemia, after adjusting for maternal age, race or ethnicity, parity, 1-hour screening glucose value, and the difference between gestational age at delivery and at the time the last weight was measured (Table 3). However, women who gained less than recommended were 62% less likely to have macrosomia infants as women with a weight gain in the recommended range.
Among non-Hispanic white women, a pregnancy weight gain below the IOM recommendations was associated with a decreased risk of hypoglycemia (0R 0.39, 95% CI 0.18–0.84), whereas among women from U.S. race–ethnicity minority groups, a pregnancy weight gain below the IOM recommendations was associated an increased risk of hypoglycemia (OR 1.69, 95% CI 1.08–2.64). No differences by race–ethnicity were observed in the associations between pregnancy weight gain above the recommendations and any of the infant complications.
In analyses stratified by prepregnancy BMI, women who were underweight before pregnancy (BMI less than 19.8) and gained more than the IOM recommendations were not at an increased risk of hyperbilirubinemia (OR 1.03, 95% CI 0.46–2.31) or hypoglycemia (OR 0.66, 95% CI 0.24–1.80), but there was some suggestion they may be at increased risk of macrosomia (OR 2.70, 95% CI 0.83–8.61); however, this finding did not reach statistical significance. Women who were normal weight (BMI 19.8–26.0) were at increased risk of hyperbilirubinemia (OR 1.56, 95% CI 1.03–2.32), hypoglycemia (OR 1.54, 95% CI 0.99–2.39), and macrosomia (OR 3.6, 95% CI 2.27–5.83). Women who were overweight or obese (BMI more than 26.0) and gained more than the IOM recommendations were also at increased risk of macrosomia (OR 2.00, 95% CI 1.14–3.47), but they were not at significantly increased risk of hyperbilirubinemia (OR 1.34, 95% CI 0.74–2.42) or hypoglycemia (OR 1.15, 95% CI 0.66–2.02). However, these results should be interpreted cautiously given the small sample size in the stratified analysis.
Compared with women in the second fourth of the distribution of rate of maternal pregnancy weight gain (0.22–0.31 kg/wk), those in the upper fourth (more than 0.40 kg/wk), had an increased risk of having an infant with macrosomia, hypoglycemia, or hyperbilirubinemia (Table 3). Infants of women with an intermediate rate of weight gain (0.32–0.39 kg/wk) were not at increased risk of these conditions. Women in the lowest fourth of rate of pregnancy weight gain (−0.26 to 0.21 kg/wk) had a decreased risk of bearing a macrosomic infant (OR 0.52, 95% CI 0.34–0.79), but their infants were not at an appreciably reduced risk of hypoglycemia and hyperbilirubinemia. Results were similar when rate of weight gain reached by the end of the second trimester was examined (Table 3).
To rule out the possibility that the associations with hypoglycemia and hyperbilirubinemia were confounded due to the presence of macrosomia we re-ran all analyses with pregnancy weight gain and risk of hypoglycemia and hyperbilirubinemia after excluding the cases with macrosomia (n=24 hypoglycemia and n=3 hyperbilirubinemia) and results were not appreciably changed (results not shown).
Our findings suggest that whether measured against IOM recommendations or as weight gain per week, increased pregnancy weight gain is associated with increased risk of macrosomia, hypoglycemia, and hyperbilirubinemia. Several limitations should be considered when interpreting the results of this study. First, we used prepregnancy weights that were (in most mothers) self-reported. Although earlier studies have observed that self reported prepregnancy weight approximates the true value,19,22 it has been found that the degree of underreporting weight varies directly with BMI.24 Second, although we attempted to isolate pregnancy weight gain of the mother by subtracting infant birth weight, we were unable to distinguish accurately the components of gestational weight gain (placenta, fat, fluid, and fetus), which can also be altered in a pregnancy resulting in neonatal complications.11,25,26 We also did not have information on immediate postpartum weight, which could have helped us to isolate maternal weight gain. Third, the data came from a study that excluded women who met the National Diabetes Data Group criteria for GDM as of 24–28 weeks of gestation. A large amount of weight gain before the third trimester could have led to the development of GDM, which is associated with increased risk of neonatal macrosomia, hypoglycemia, and hyperbilirubinemia.27,28 Therefore, in attempting to isolate the effects of pregnancy weight gain from those of GDM, we have almost certainly underestimated the total adverse effects of a large amount of pregnancy weight gain. Finally, we did not investigate whether weight gain influences other important outcomes, such as low birth weight and neonatal mortality.29
Pregnancy weight gain above the IOM recommendations was associated with a three-fold increased risk of macrosomia. Our data are consistent with previous findings that pregnancy weight gain above the IOM recommendations is associated with an increased risk of macrosomia.2–5 In addition, our findings of an association between maternal pregnancy weight gain (total pregnancy weight gain minus infant birth weight) and weight gain before 24–28 weeks and increased risk of macrosomia suggest that this association may be attributable to maternal weight gain independent of fetal size; however, we were unable to account for other products of pregnancy, such as placental weight and amniotic fluid. Gaining less weight than recommended by the IOM and being in the lowest fourth of the weight gain distribution was related to a reduced risk of macrosomia. During the later part of pregnancy, increased insulin resistance favors the transfer of nutrients to the fetus.30 A large amount of weight gain during pregnancy may increase the flux of maternal amino acids, glucose, free fatty acids, and triglycerides from maternal to fetal compartments and may affect fetal growth and development.31–33 The association between excess pregnancy weight gain and macrosomia persisted after adjusting for maternal glycemia, suggesting the effects of weight gain may be mediated by substrates other than maternal glucose. However, given that the screening glucose test only measures a woman’s glucose at one point during her pregnancy, it is possible that we may not have adequately controlled for maternal glycemia.
Weight gain above the IOM recommendations, being in the highest fourth of the distribution of weight gain per week, and in the highest fourth of maternal pregnancy weight gain through the second trimester were all associated with an increased risk of hypoglycemia. However, among women from U.S. minority race or ethnicity groups gaining less than recommended was also associated with an increased risk of hypoglycemia. The IOM suggested that the effects of gestational weight gain on pregnancy outcomes may vary by ethnic group.1 There is limited data available with adequate sample sizes to examining the association between pregnancy weight gain and the occurrence of neonatal hypoglycemia. However, maternal obesity has been associated with an increased risk of infant hypoglycemia.6,7 Animal studies have shown that pups of prepregnancy obese rats have persistent neonatal hypoglycemia compared with pups of nonobese controls, which appears to be due to reduced hepatic glycogen mobilization in the former.7 It is possible that large amounts of pregnancy weight gain may induce similar reduced hepatic glycogen mobilization in newborn.
A large amount of pregnancy weight gain was also associated with an increased risk of neonatal hyperbilirubinemia. No appreciable alterations in risk of neonatal hyperbilirubinemia were observed in infants of mothers with a relatively small amount of pregnancy weight gain. The effects of pregnancy weight gain on neonatal jaundice have not been well studied. However, a high maternal prepregnancy BMI has been associated with increased neonatal hyperbilirubinemia.8 Although the mechanism behind this association is not clear, it is possible that excess maternal substrates induce fetal hyperinsulinemia, which in turn increases fetal oxygen uptake during glycolysis and which leads to increased erythropoiesis. The later may have adverse consequences for the newborn, such as hyperbilirubinia.34,35
The effects of weight gain on the three outcomes studied may not be independent of prepregnancy BMI; data from our stratified analyses suggest that underweight women who gain more than the IOM recommendations may not be at increased risk of hypoglycemia and hyperbilirubinemia. However, more data are needed to clarify how the associations between weight gain and these outcomes vary by BMI, given our limited power. Appropriate pregnancy weight gain guidelines need to balance the benefits of improving fetal nutrition with the risk of harm to the mother and infant, while identifying those at increased risk of adverse outcomes. The full range of risks and benefits associated with varying degrees of maternal weight gain are not known. Results of this study suggest that for neonatal macrosomia, hypoglycemia, and hyperbilirubinemia, a large degree of maternal weight gain increases the risk.
1. Institute of Medicine, Subcommittee on Nutritional Status and Weight Gain During Pregnancy. Nutrition during Pregnancy. Washington, DC: National Academy of Sciences; 1990.
2. Caulfield LE, Witter FR, Stoltzfus RJ. Determinants of gestational weight gain outside the recommended ranges among black and white women. Obstet Gynecol 1996 May;87:760–6.
3. Parker JD, Abrams B. Prenatal weight gain advice: an examination of the recent prenatal weight gain recommendations of the Institute of Medicine. Obstet Gynecol 1992 May;79: 664–9.
4. Schieve LA, Cogswell ME, Scanlon KS. An empiric evaluation of the Institute of Medicine’s pregnancy weight gain guidelines by race. Obstet Gynecol 1998 Jun;91:878–84.
5. Cogswell ME, Serdula MK, Hungerford DW, Yip R. Gestational weight gain among average-weight and overweight women—what is excessive? Am J Obstet Gynecol 1995 Feb;172:705–12.
6. Kliegman RM, Gross T. Perinatal problems of the obese mother and her infant. Obstet Gynecol 1985;66:299–306.
7. Heng J, Kliegman RM. Effects of maternal obesity on fasting metabolism in newborn rats. Int J Obes 1990;14:505–13.
8. Callaway LK, Prins JB, Chang AM, McIntyre HD. The prevalence and impact of overweight and obesity in an Australian obstetric population. Med J Aust 2006;184:56–9.
9. Selvin S, Abrams B. Analysing the relationship between maternal weight gain and birthweight: exploration of four statistical issues. Paediatr Perinat Epidemiol 1996;10:220–34.
10. Kramer MS, McLean FH, Eason EL, Usher RH. Maternal nutrition and spontaneous preterm birth. Am J Epidemiol 1992;136:574–83.
11. Lederman SA, Paxton A, Heymsfield SB, Wang J, Thornton J, Pierson RN Jr. Body fat and water changes during pregnancy in women with different body weight and weight gain. Obstet Gynecol 1997;90:483–8.
12. Abrams B, Selvin S. Maternal weight gain pattern and birth weight. Obstet Gynecol 1995;86:163–9.
13. Self SG, Mauritsen RJ, O’Hara J. Power calculations for likelihood ratio tests in generalized linear models. Biometrics 1982;48:31–3.
14. Krieger N. Overcoming the absence of socioeconomic data in medical records: validation and application of a census-based methodology. Am J Public Health 1992;82:703–10.
15. Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 2001;285:2370–5.
16. Ferrara A, Kahn HS, Quesenberry C, Riley C, Hedderson MM. An increase in the incidence of gestational diabetes mellitus: Northern California, 1991–2000 [published erratum appears in Obstet Gynecol. 2004;103:799]. Obstet Gynecol 2004;103:526–33.
17. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group. Diabetes 1979;28:1039–57.
18. Rowland ML. Self-reported weight and height. Am J Clin Nutr 1990;52:1125–33.
19. Yu SM, Nagey DA. Validity of self-reported pregravid weight. Ann Epidemiol 1992;2:715–21.
20. Stevens-Simon C, Roghmann KJ, McAnarney ER. Relationship of self-reported prepregnant weight and weight gain during pregnancy to maternal body habitus and age. J Am Diet Assoc 1992;92:85–7.
21. Gunderson EP, Abrams B, Selvin S. Does the pattern of postpartum weight change differ according to pregravid body size? Int J Obes Relat Metab Disord 2001;25:853–62.
22. SAS Institute, Inc. SAS/STAT software: changes and enhancements through release 6.11. Cary (NC): SAS Institute, Inc.; 1998.
23. Harris HE, Ellison GT. Practical approaches for estimating prepregnant body weight. J Nurse Midwifery 1998;43:97–101.
24. Schieve LA, Perry GS, Cogswell ME, Scanion KS, Rosenberg D, Carmichael S, et al. Validity of self-reported pregnancy delivery weight: an analysis of the 1988 National Maternal and Infant Health Survey. NMIHS Collaborative Working Group. Am J Epidemiol 1999;150:947–56.
25. Witter FR, Caulfield LE, Stoltzfus RJ. Influence of maternal anthropometric status and birth weight on the risk of cesarean delivery. Obstet Gynecol 1995;85:947–51.
26. Abrams B, Carmichael S, Selvin S. Factors associated with the pattern of maternal weight gain during pregnancy. Obstet Gynecol 1995;86:170–6.
27. Persson B, Hanson U, Marcus C. Gestational diabetes mellitus and paradoxical fetal macrosomia– a case report. Early Hum Dev 1995;41:203–13.
28. Szabo AJ, Szabo O. Placental free-fatty-acid transfer and fetal adipose-tissue development: an explantation of fetal adiposity in infants of diabetic mothers. Lancet 1974;2:498–9.
29. Scholl TO, Hediger ML, Schall JI, Ances IG, Smith WK. Gestational weight gain, pregnancy outcome, and postpartum weight retention. Obstet Gynecol 1995;86:423–7.
30. Knopp RH, Bergelin RO, Wahl PW, Walden CE, Chapman M, Irvine S. Population-based lipoprotein lipid reference values for pregnant women compared to nonpregnant women classified by sex hormone usage. Am J Obstet Gynecol 1982;143:626–37.
31. Kitajima M, Oka S, Yasuhi I, Fukuda M, Rii Y, Ishimaru T. Maternal serum triglyceride at 24–32 weeks’ gestation and newborn weight in nondiabetic women with positive diabetic screens. Obstet Gynecol 2001;97:776–80.
32. Knopp RH, Magee MS, Walden CE, Bonet B, Benedetti TJ. Prediction of infant birth weight by GDM screening tests. Importance of plasma triglyceride. Diabetes Care 1992;15: 1605–13.
33. Kalkhoff RK. Impact of maternal fuels and nutritional state on fetal growth. Diabetes 1991;40 suppl:61–5.
34. Persson B, Hanson U. Neonatal morbidities in gestational diabetes mellitus. Diabetes Care 1998;21 suppl:B79–84.
35. Hoegsberg B, Gruppuso PA, Coustan DR. Hyperinsulinemia in macrosomic infants of nondiabetic mothers. Diabetes Care 1993;16:32–6.