Skip to main content
American Journal of Public Health logoLink to American Journal of Public Health
. 2014 Feb;104(Suppl 1):S90–S95. doi: 10.2105/AJPH.2013.301425

Gestational Weight Gain and Risk of Infant Death in the United States

Regina R Davis 1,, Sandra L Hofferth 1, Edmond D Shenassa 1
PMCID: PMC4011101  PMID: 24354832

Abstract

Objectives. We examined the association of prepregnancy body mass index (BMI) and gestational weight gain (GWG) with risk of death during infancy using the Institute of Medicine’s (IOM’s) Pregnancy Weight Gain Guidelines.

Methods. We obtained maternal and infant data for 2004–2008 from 159 244 women with a singleton, full-term, live birth in the 41 states that participated in phase 5 of the Pregnancy Risk Assessment Monitoring System. We fit logistic regression models to estimate the association between prepregnancy BMI, GWG, and risk of death during infancy, controlling for confounders.

Results. Only 34% of women gained the IOM-recommended amount of weight during pregnancy. Infants born to underweight, normal-weight, and overweight women with inadequate GWG had odds of mortality during infancy that were 6.18, 1.47, and 2.11 times higher, respectively, than those of infants born to women with adequate GWG. Infants born to obese women with excessive weight gain had a 49% decreased likelihood of mortality.

Conclusions. A significant association exists between inadequate GWG and infant death that weakens with increasing prepregnancy BMI; weight gain beyond the recommended amount appears to be protective against infant mortality.


For more than a century, researchers have attempted to determine the ideal gestational weight gain (GWG) for maximizing the likelihood of positive birth outcomes.1 Extant evidence has suggested inadequate GWG is a risk factor for intrauterine growth restriction, preterm birth, low birth weight, and perinatal mortality.2–4 However, an excessive amount of weight gain also presents risks. As GWG increases, poor pregnancy outcomes for the mother, such as preeclampsia, cesarean birth, and fetal macrosomia, also rise.2–4 Although GWG has been linked to leading causes of infant mortality, such as preterm birth and low birth weight, its association with infant mortality independent of these factors is less well understood.2,4,5 There is a dearth of research examining the link between GWG and infant mortality.2,5–7 Moreover, few studies have taken into account prepregnancy body mass index (BMI; defined as weight in kilograms divided by height in meters squared) in recognition of its modifying effect on GWG–adverse outcome associations.5,6

Only 2 studies have examined the link between GWG and infant mortality.2,5 Chen et al.5 found that among underweight, normal-weight, and most overweight women, low GWG is linked to an elevated risk of infant mortality relative to women of normal weight with average GWG (0.30–0.44 kg/wk). Among overweight women who gained 0.45 kilograms per week and for all obese women, the odds of infant death were higher than those of normal-weight women with average GWG. In a study conducted among a relatively small state birth certificate sample of overweight women, Langford et al.,2 by contrast, found that compared with women with lower GWG, the risk of infant mortality for women with higher GWG did not increase and the proportion of low birth-weight infants declined. The former study used data that were more than 20 years old, and the latter study did not account for the full range of prepregnancy BMI. Given that the US prevalence of obesity has changed across all age groups, with 34% of women obese from 2007 to 2009 compared with 21% in 1990,8 there is a need to analyze more recent data than the existing body of evidence reflects.6

As a measure of healthy GWG, the Institute of Medicine (IOM) published guidelines specific to a woman’s prepregnancy BMI that recommend the amount of weight a woman should gain to optimize the health of a fetus and, by extension, an infant. To replicate the IOM guidelines and investigate the link between GWG and risk of death during infancy, we analyzed data from phase 5 of the Pregnancy Risk Assessment Monitoring System (PRAMS). The analysis fills an important gap in the literature by using data from an ongoing, population-based surveillance system that is both reflective of current rates of infant mortality and includes prepregnancy height and weight, allowing BMI calculation. We estimated the risk of infant death associated with inadequate and excessive GWG compared with normal weight gain.

METHODS

Infants were identified through phase 5 of the PRAMS, administered between 2004 and 2008.9 PRAMS was first conducted in 1988 among 5 states (Indiana, Maine, Michigan, Oklahoma, and West Virginia) and the District of Columbia and has been administered annually ever since. Today, 41 states participate in PRAMS, representing approximately 78% of all live births in the United States.9 Using a stratified probability sampling scheme from a frame of eligible state birth certificates, PRAMS samples women (n = 1300–3400 in each state) 2 to 3 months after birth and collects survey data on maternal reproductive history and neonatal health. Women with poor key birth outcomes (e.g., low birth weight) and women from populations historically at higher risk for adverse pregnancy outcomes are oversampled. Women are recruited through a series of contacts that culminate in 3 attempts to collect information by mail, and questionnaires are accepted up to 9 months after birth. Telephone follow-up is initiated for all nonrespondents within 2 weeks after mailing the third questionnaire.10 PRAMS uses standardized data collection instruments to allow comparative analyses across all participating states. Mothers’ responses are linked to select birth certificate data items, and appropriate population weights are calculated.11

Only data from women with a singleton live birth were analyzed, as GWG guidelines vary for women with multiple fetuses. GWG was estimated as the difference between maternal weight at delivery and prepregnancy weight. We calculated prepregnancy BMI from maternal height and weight before pregnancy and then categorized women according to the IOM guidelines as underweight (< 18.5), normal weight (18.5–24.9), overweight (25.0–29.9), and obese (≥ 30). The adequacy of weight gain was classified according to the IOM definitions as inadequate, adequate, and excessive. Recommended weight gains varied by prepregnancy BMI such that underweight women were expected to gain 28 to 40 pounds; normal-weight women, 25 to 35 pounds; overweight women, 15 to 25 pounds; and obese women, 11 to 20 pounds. Initial analyses documented statistically significant interactions between GWG and prepregnancy weight (not shown). We examined the influence on infant mortality of inadequate or excessive GWG compared with normal GWG among women in each of the 4 categories of prepregnancy BMI, adjusting for potential confounders. Stratifying permitted the assessment of the potential moderating effects of prepregnancy weight on the relationship between GWG and infant death.

We parameterized infant mortality, our dependent variable, as whether the infant was alive or deceased at the time of the survey, which was administered, on average, 119 days after the child’s birth (range = 61–450 days; SD = 35.91). Low birth weight was defined as less than 2500 grams, and gestation at time of delivery was classified into 3 groups: 33 weeks or less, 34 to 36 weeks, and 37 weeks or more. We included potential confounders as controls: maternal age, race/ethnicity, education, marital status, cigarette smoking, alcohol use, diabetes, hypertension, and parity. Normal GWG served as the reference category because it has been associated with minimum risk of mortality for infants in other populations.6 We fit logistic regression models to estimate odds ratios (ORs) and associated 95% confidence intervals (CIs) for GWG and infant death and included low birth weight and gestational age along with other covariates in the regression models. Statistical analysis was conducted using SAS software version 9.2 (SAS Institute, Cary, NC). The Surveylogistic procedure with the weight option was used to apply the Centers for Disease Control and Prevention–provided population sample weights and to adjust the standard errors for the complex sampling design, noncoverage, and nonresponse.

A total of 159 244 mothers with singleton births were included in the study. We excluded 30 866 women from the analysis as a result of missing or implausible information for gestational weight change, birth weight, gestational age, substance use, and medical and demographic characteristics. Two-sample t-test analyses comparing women included in the analytic sample with those excluded showed a number of statistical differences, but only a few differences of practical significance (not shown). Excluded women were more likely to have had a previous live birth. Included women were more likely to be married and to have more than 12 years of education.

RESULTS

The analytic sample is described in Table 1. Mothers in the study sample had a mean GWG of 29.13 pounds. Nearly 25% experienced inadequate weight gain, 34.3% gained the recommended amount of weight, and 40.8% gained more than recommended. The risk of infant mortality in the study sample was 1.7%. Mortality risks in the study sample were 3.9% among infants of mothers who gained an inadequate amount of weight during pregnancy, 1.2% among infants of mothers who gained an adequate amount of weight, and 0.7% among mothers who gained more than the recommended amount (not shown). Approximately 27% and 21% of the infants in the sample were born low birth weight and preterm, respectively.

TABLE 1—

Select Descriptive Statistics of Mothers and Infants: Pregnancy Risk Assessment Monitoring System, Phase 5; United States; 2004–2008

Variable % (No.)
Mortality
 Surviving (Ref) 98.32 (156 572)
 Died 1.68 (2672)
Prepregnancy BMIa
 Underweight (< 18.5) 5.72 (9112)
 Normal weight (18.5–24.9; Ref) 51.78 (82 469)
 Overweight (25.0–29.9) 23.04 (36 691)
 Obese (≥ 30) 19.45 (30 972)
Gestational weight gainb
 Inadequate 24.96 (39 741)
 Normal (Ref) 34.27 (54 565)
 Excessive 40.78 (64 438)
Birth weight, g
 > 2500 (Ref) 73.22 (116 603)
 ≤ 2500 26.78 (42 641)
Gestational age, wks
 Term birth (≥ 37; Ref) 78.66 (125 267)
 34–36 11.81 (18 807)
 ≤ 33 9.53 (15 170)
Prenatal Care Utilization Index, Kotelchuck
 Inadequate (< 50% of expected visits; Ref) 11.46 (18 254)
 Intermediate (50%–79% of expected visits) 12.84 (20 448)
 Adequate (> 80% of visits) 75.70 (120 542)
Maternal age, y
 ≤ 34 (Ref) 84.73 (134 922)
 ≥ 35 15.27 (24 322)
Maternal education, y
 < high school (< 12; Ref) 16.36 (26 045)
 Completed high school (= 12) 30.73 (48 933)
 Some college (13-15) 24.40 (38 860)
 Completed college (≥ 16) 28.51 (45 406)
Race/ethnicity
 White (Ref) 56.62 (90 156)
 African American 16.73 (26 645)
 Hispanic 12.68 (20 193)
 Asian or Pacific Islander 8.39 (13 367)
 American Indian/Alaska Native 3.94 (6278)
 Other 1.64 (2605)
Marital status
 Married 62.23 (99 257)
 Other (Ref) 37.67 (59 987)
Diabetes
 Yes 4.05 (6455)
 No 95.95 (152 789)
Hypertension
 Yes 7.98 (12 701)
 No 92.02 (146 543)
No. of previous live births, grouped
 None (Ref) 44.21 (70 400)
 1 30.47 (48 527)
 ≥ 2 25.32 (40 317)
No. of cigarettes/d during past 3 mo of pregnancy
 None (Ref) 84.95 (135 276)
 1–5 7.80 (12 422)
 ≥ 6 7.25 (11 546)
No. of alcoholic drinks/wk during past 3 mo of pregnancy
 None (Ref) 93.51 (148 909)
 1–3 6.10 (9716)
 4–6 0.21 (332)
 ≥ 7 0.18 (287)

Note. BMI = body mass index, defined as weight in kilograms divided by height in meters squared. The sample size and percentages are unweighted. Percentages may not total 100 because of rounding. The sample size was n = 159 244.

a

Mean = 25.51 kg/m2.

b

Mean = 29.31 lbs. Recommended weight gains varied by prepregnancy BMI such that underweight women were expected to gain 28–40 lbs; normal-weight women, 25–35 lbs; overweight women, 15–25 lbs; and obese women, 11–20 lbs.

Table 2 shows the results from a series of nested logistic regression models predicting infant death. In all models, inadequate GWG was associated with infant mortality. Model 1 displays the ORs for infant death associated with the 2 weight gain categories. Inadequate maternal weight gain was associated with elevated odds of infant death (OR = 2.57; 95% CI = 2.08, 3.16; P < .01). GWG beyond the recommended range was associated with a reduced risk of infant mortality (OR = 0.69; 95% CI = 0.53, 0.88; P < .01).

TABLE 2—

Association Between Gestational Weight Gain and Risk of Infant Mortality: Pregnancy Risk Assessment Monitoring System, Phase 5; United States; 2004–2008

Variable Model 1, OR (95% CI) Model 2, OR (95% CI) M1 to M2 Risk Reduction, % Model 3, OR (95% CI) M2 to M3 Risk Reduction, %
Gestational weight gaina
 Inadequate 2.57*** (2.08, 3.16) 1.68*** (1.35, 2.08) 57 1.48*** (1.18, 1.85) 29
 Normal (Ref) 1.00 1.00 1.00
 Excessive 0.69** (0.53, 0.88) 0.79 (0.61, 1.02) 32 0.82 (0.63, 1.06) 14
Gestational age, wks
 ≤ 33 12.2*** (9.00, 16.55)
 34–36 1.67* (1.09, 2.57)
 ≥ 37 (Ref) 1.00
Birth weight, g
 ≤ 2500 3.31*** (2.37, 4.63)
 > 2500 (Ref) 1.00

Note. CI = confidence interval; M1 = model 1; M2 = model 2; M3 = model 3; OR = odds ratio. Model 1 includes no controls; model 2 includes all controls except gestational age and birth weight; and model 3 includes all controls plus gestational age and birth weight. Controls are prenatal care, maternal age, maternal education, race/ethnicity, marital status, diabetes, hypertension, parity, smoking, and drinking. The sample size was n = 159 244.

a

Recommended weight gains varied by prepregnancy BMI such that underweight women were expected to gain 28–40 lbs; normal-weight women, 25–35 lbs; overweight women, 15–25 lbs; and obese women, 11–20 lbs.

*P < .05; **P < .01; ***P < .001.

In model 2, inadequate GWG remained significant after controlling for maternal and infant characteristics. The risk of infant mortality caused by inadequate GWG was reduced 57% after adding controls to the model.

Birth weight and gestational age were added to model 3. Infants born to women with inadequate GWG had odds of infant death that were 48% higher than the odds for the reference group of infants. The risk of infant mortality caused by inadequate GWG was reduced 29% after adding gestational age and birth weight. Inadequate GWG remained statistically significant in all models.

As presented in Table 3, the association between both inadequate and excessive GWG and risk of infant mortality differed depending on prepregnancy BMI. Infants born to women with inadequate GWG had a higher risk of mortality across all prepregnancy weight categories except obese women. Among underweight women, inadequate GWG was associated with a 6-fold increase in risk of infant death (OR = 6.18; 95% CI = 2.45, 15.56). The association was less pronounced among infants born to normal-weight women (OR = 1.47; 95% CI = 1.08, 2.01). Among infants born to overweight women, inadequate GWG was associated with a 2-fold elevation in the risk of mortality (OR = 2.11; 95% CI = 1.30, 3.42). Among infants born to obese women, inadequate GWG was independent of risk of mortality (OR = 1.01; 95% CI = 0.63, 1.64).

TABLE 3—

Association Between Gestational Weight Gain and Infant Death by Prepregnancy BMI: Pregnancy Risk Assessment Monitoring System, Phase 5; United States; 2004–2008

Variable Model 1, OR (95% CI) Model 2, OR (95% CI)
Underweight (BMI < 18.5)
 Inadequate 6.56*** (2.61, 16.48) 6.18*** (2.45, 15.56)
 Normal (Ref) 1.00 1.00
 Excessive 1.19 (0.48, 2.98 1.34 (0.51, 3.54)
Normal weight (BMI = 18.5–24.9)
 Inadequate 1.75* (1.30, 2.37) 1.47* (1.08, 2.01)
 Normal (Ref) 1.00 1.00
 Excessive 0.62 (0.39, 0.98) 0.64 (0.40, 1.02)
Overweight (BMI = 25–30)
 Inadequate 2.32*** (1.45, 3.69) 2.11*** (1.30, 3.42)
 Normal (Ref) 1.00 1.00
 Excessive 1.06 (0.71, 1.60) 1.21 (0.80, 1.85)
Obese (BMI ≥ 30.0)
 Inadequate 1.12 (0.71, 1.78) 1.01 (0.63, 1.64)
 Normal (Ref) 1.00 1.00
 Excessive 0.48** (0.30, 0.77) 0.51** (0.31, 0.84)

Note. BMI = body mass index; CI = confidence interval; OR = odds ratio. BMI is defined as weight in kilograms divided by height in meters squared. Recommended weight gains varied by prepregnancy BMI such that underweight women were expected to gain 28–40 lbs; normal-weight women, 25–35 lbs; overweight women, 15–25 lbs; and obese women, 11–20 lbs. Model 1 includes all controls except gestational age and birth weight; model 2 includes all controls, gestational age and birth weight. Controls are prenatal care, maternal age, maternal education, race/ethnicity, marital status, diabetes, hypertension, parity, smoking, and drinking. The sample size was n = 159 244.

*P < .05; **P < .01; ***P < .001.

Weight gain beyond the recommended range was not associated with risk of mortality among infants born to women who were underweight (OR = 1.34; 95% CI = 0.51, 3.54), normal weight (OR = 0.64; 95% CI = 0.40, 1.02), or overweight (OR = 1.21; 95% CI = 0.80, 1.85) before pregnancy. By contrast, excessive GWG was associated with a 49% reduced risk of mortality among infants born to women with obese prepregnancy BMI (OR = 0.51; 95% CI = 0.31, 0.84). This association was independent of birth weight, gestational age, prenatal care, maternal age, maternal education, race/ethnicity, marital status, diabetes, hypertension, parity, smoking, and drinking.

DISCUSSION

We examined the association of prepregnancy BMI and GWG with risk of death during infancy using the IOM guidelines for weight gain during pregnancy and a current, national data set. In our sample, inadequate GWG was a significant predictor of infant mortality independent of gestational age and birth weight. When considered as a whole, our findings support the premise that GWG may have effects on the infant without any alterations of fetal growth that are indicated by birth weight and gestational age.

A nutritional mechanism is implicated by our finding that prepregnancy underweight coupled with inadequate GWG conferred the highest risk of infant mortality and that the risk of infant death associated with inadequate GWG, though still statistically significant, was lower among women with normal prepregnancy BMI. Additionally, we found no evidence that excessive GWG increased mortality risk in any of the prepregnancy BMI groups. In fact, excessive GWG was protective of risk of infant death among women who were obese before pregnancy, even with the full set of controls included.

Previous research has documented the effects of intrauterine nutrition deprivation on subsequent adult health and has provided insight into how maternal diet can modify the fetus’s epigenome, affecting its health and well-being.12,13 Diets insufficient in caloric and micronutrient value can change the programming and development of body function and structure and permanently alter an organ’s function, leading to the development of a number of diseases throughout life.14–16 Nutritional programming has been successfully demonstrated in a range of mammals.17 These animal experiments have shown that poor nutrition in utero leads to persisting changes in blood pressure, cholesterol metabolism, insulin response to glucose, and a range of other life-sustaining functions.18

Although the potential mechanism cannot be directly tested, the analysis conducted by Chen et al.5 found that the causes of death they observed were consistent with a nutritional explanation. Our ongoing research has confirmed these conclusions.19 Using data from 9268 death certificates included in the 2005 Cohort Linked Birth-Infant Death File and the 10th revision of the International Classification of Diseases,20 we regressed causes of infant deaths, grouped into 6 broad nutrition-related causes compared with non–nutrition-related and rare causes (n = 3923; 42.33%), on inadequate GWG and calculated odds of death for each cause. Nutrition-related causes of death were more likely to be linked to inadequate GWG than deaths from rare or implausible causes. Infants of mothers with inadequate GWG had odds of infant death from disorders related to length of gestation and fetal malnutrition that were 2.06 times the odds of infant deaths from rare or implausible causes. Inadequate GWG was also associated with deaths from respiratory conditions and birth defects. Mothers with inadequate GWG had approximately 40% lower risk for infant deaths from diseases of the genitourinary system and sudden infant death syndrome.

An elevated risk of infant death among underweight women with inadequate GWG was expected and in accordance with the previous study analyzing 1988 US National Maternal and Infant Health Survey data.5 What we did not anticipate, however, was that obese women with inadequate weight gain would not have elevated risks of infant death. The accessibility of fat stores among obese women to support fetal development when weight gain is less than optimal is suspected as a cause, though direct evidence is lacking. These research findings reinforce the need to further investigate the mechanisms whereby inadequate GWG influences infant mortality as data improve.

We also found an association of excessive GWG with reduced risk of mortality among infants of obese women. Further exploration is necessary to determine why weight gain beyond the recommended range for this group had a protective effect, because research has found that obese prepregnancy BMI is one of the strongest modifiable risk factors for poor birth outcomes (e.g., birth defects, still birth).16 Evidence has consistently shown more negative consequences of excessive GWG for the mother (e.g., cesarean birth, hemorrhages, and hypertensive syndromes in pregnancy) than for the infant (e.g., fetal macrosomia).2–4,21,22 Factors that are protective for the infant, such as a continuous supply of nutrients to the fetus, may not be so for the mother. Should our finding of a protective effect of weight gain beyond the IOM guidelines be replicated in future studies, research into how such weight gain may influence outcomes for women with different prepregnancy weight statuses is warranted.

A key strength of these analyses is the use of a high-quality, population-based data set. The data were collected recently, from a geographically diverse sample, and allowed for the calculation of prepregnancy BMI and the evaluation of weight gain adequacy at delivery. The study data, however, are not without limitations. First, they may be subject to a degree of recall bias because they were collected retrospectively. Second, dietary information was not available, so the nutrition mechanism posited could not be directly tested. Third, although we controlled for a full set of standard behavioral, medical, and sociodemographic factors, confounding by unknown variables cannot be ruled out. Currently, however, no other population-based surveys exist with more detailed data on the experiences of pregnant women and their infants than PRAMS.

Overall, our findings support the conclusion that inadequate GWG is an independent risk factor for infant mortality. However, GWG alone should not be used as a screening or diagnostic tool because the amount of total weight gain is widely variable among women.7 Altogether the results support the IOM position that GWG and prepregnancy BMI together have important influences on birth outcomes.6 Given study confirmation of previous research that only 30% to 40% of US women actually gain within the IOM recommended ranges,6,23 effective interventions could facilitate providing childbearing women with BMI-specific GWG information. Integrating nutrition counseling into pre- and interconceptional care may be an important approach to achieving optimal pregnancy outcomes for both infant and mother. Health care providers could provide individualized counseling, including recording prepregnancy height and weight, setting a GWG goal, monitoring weight gain, and providing advice about diet and physical activity.24 Underweight women as well as others who are at risk for consuming diets of lower nutritional value are likely to benefit. Such preventive measures have the potential to improve birth outcomes and the health and well-being of infants.

Acknowledgments

We thank the Pregnancy Risk Assessment Monitoring System (PRAMS) working group of the Centers for Disease Control and Prevention Division of Reproductive Health for making the data available for analysis.

Human Participant Protection

The PRAMS data set was approved by the Centers for Disease Control and Prevention institutional review board, and respondents provided informed consent. The study was also determined exempt from oversight by the University of Maryland, College Park institutional review board.

References

  • 1.National Research Council and Institute of Medicine. Influence of Pregnancy Weight on Maternal and Child Health. Workshop report. Washington, DC: National Academies Press; 2007. [Google Scholar]
  • 2.Langford A, Joshu C, Chang J, Myles T, Leet T. Does gestational weight gain affect the risk of adverse maternal and infant outcomes in overweight women? Matern Child Health J. 2011;15(7):860–865. doi: 10.1007/s10995-008-0318-4. [DOI] [PubMed] [Google Scholar]
  • 3.DeVader S, Neeley H, Myles T, Leet T. Evaluation of gestational weight gain guidelines for women with normal prepregnancy body mass index. Obstet Gynecol. 2007;110(4):745–751. doi: 10.1097/01.AOG.0000284451.37882.85. [DOI] [PubMed] [Google Scholar]
  • 4.Frederick IO, Williams MA, Sales AE, Martin DP, Killien M. Pre-pregnancy body mass index, gestational weight gain, and other maternal characteristics in relation to infant birth weight. Matern Child Health J. 2008;12(5):557–567. doi: 10.1007/s10995-007-0276-2. [DOI] [PubMed] [Google Scholar]
  • 5.Chen A, Feresu S, Fernandez C, Rogan W. Maternal obesity and the risk of infant death in the United States. Epidemiology. 2009;20(1):74–81. doi: 10.1097/EDE.0b013e3181878645. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Institute of Medicine and National Research Council. Weight Gain During Pregnancy: Reexamining the Guidelines. Washington, DC: National Academies Press; 2009. [PubMed] [Google Scholar]
  • 7. National Center for Health Statistics. Maternal Weight Gain and the Outcome of Pregnancy, United States, 1980. Vital and health statistics, Series 21, No. 44. DHHS Pub. No. (PHS) 86–1922. Washington, DC: Government Printing Office; 1986. [PubMed]
  • 8.Shields M, Carroll M, Ogden C. Adult Obesity Prevalence in Canada and the United States. NCHS Data Brief No. 56. Hyattsville, MD: National Center for Health Statistics; 2011. [Google Scholar]
  • 9.Centers for Disease Control and Prevention, Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion. Pregnancy Risk Assessment Monitoring System (PRAMS): How are PRAMS data used? 2010. Available at: http://www.cdc.gov/prams/AboutPRAMS.htm. Accessed October 18, 2012. [Google Scholar]
  • 10.Dillman D. Mail and Internet Surveys: The Tailored Design Method. New York, NY: Wiley; 2000. [Google Scholar]
  • 11.Centers for Disease Control and Prevention. Pregnancy Risk Assessment Monitoring System (PRAMS): Model Surveillance Protocol. Atlanta, GA: Centers for Disease Control and Prevention; 2009. [Google Scholar]
  • 12.Schulz L. The Dutch Hunger Winter and the developmental origins of health and disease. Proc Natl Acad Sci U S A. 2010;107(39):16757–16881. doi: 10.1073/pnas.1012911107. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Paul A. Origins: How the Nine Months Before Birth Shape the Rest of Our Lives. New York, NY: Simon and Schuster; 2010. [Google Scholar]
  • 14.Barker DJ. The developmental origins of adult disease. J Am Coll Nutr. 2004;23(6):588S–595S. doi: 10.1080/07315724.2004.10719428. [DOI] [PubMed] [Google Scholar]
  • 15.Butte NF. Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus. Am J Clin Nutr. 2000;71(5 suppl):1256S–1261S. doi: 10.1093/ajcn/71.5.1256s. [DOI] [PubMed] [Google Scholar]
  • 16.Lu M, Lu J. Maternal Nutrition and Infant Mortality in the Context of Relationality: The Courage to Love: Infant Mortality Commission Implications for Care, Research, and Public Policy to Reduce Infant Mortality Rates. Washington, DC: Joint Center for Political and Economic Studies Health Policy Institute; 2007. [Google Scholar]
  • 17.Desai M, Hales C. Role of fetal and infant growth in programming metabolism in later life. Biol Rev Camb Philos Soc. 1997;72(2):329–348. doi: 10.1017/s0006323196005026. [DOI] [PubMed] [Google Scholar]
  • 18.Barker D. Maternal nutrition, fetal nutrition, and disease in later life. Nutrition. 1997;13(9):807–813. doi: 10.1016/s0899-9007(97)00193-7. [DOI] [PubMed] [Google Scholar]
  • 19.Davis R, Hofferth S, Shenassa E. Inadequate gestational weight gain and cause-specific infant death. Poster presented at: the 18th Annual Maternal and Child Health Epidemiology Conference; December 12–14, 2012; San Antonio, TX. [Google Scholar]
  • 20.International Classification of Diseases, 10th Revision. Geneva, Switzerland: World Health Organization; 1991. [Google Scholar]
  • 21.Siega-Riz A, King J. American Dietetic Association, American Society of Nutrition. Position of the American Dietetic Association and American Society for Nutrition: obesity, reproduction, and pregnancy outcomes. J Am Diet Assoc. 2009;109(5):918–927. doi: 10.1016/j.jada.2009.03.020. [DOI] [PubMed] [Google Scholar]
  • 22.Kiel DW, Dodson EA, Artal R, Boehmer TK, Leet TL. Gestational weight gain and pregnancy outcomes in obese women. Obstet Gynecol. 2007;110(4):752–758. doi: 10.1097/01.AOG.0000278819.17190.87. [DOI] [PubMed] [Google Scholar]
  • 23.Abrams B, Altman S, Pickett K. Pregnancy weight gain: still controversial. Am J Clin Nutr. 2000;71(5 suppl):1233S–1241S. doi: 10.1093/ajcn/71.5.1233s. [DOI] [PubMed] [Google Scholar]
  • 24.Committee on Genetics. ACOG Committee opinion no. 383: evaluation of stillbirths and neonatal deaths. Obstet Gynecol. 2009;110(4):963–966. doi: 10.1097/01.AOG.0000263934.51252.e0. [DOI] [PubMed] [Google Scholar]

Articles from American Journal of Public Health are provided here courtesy of American Public Health Association

RESOURCES