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American Journal of Clinical Nutrition, Vol. 87, No. 6, 1818-1824, June 2008
© 2008 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Gestational weight gain and risk of overweight in the offspring at age 7 y in a multicenter, multiethnic cohort study1,2,3

Brian H Wrotniak, Justine Shults, Samantha Butts and Nicolas Stettler

1 From the Division of Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia, Philadelphia, PA (BHW and NS), and the Center for Clinical Epidemiology and Biostatistics (BHW, JS, SB, and NS) and the Division of Infertility and Reproductive Endocrinology (SB), University of Pennsylvania School of Medicine, Philadelphia, PA

2 The National Collaborative Perinatal Project was supported by the National Institute of Neurologic Disease and Stroke. The present study was supported by the Nutrition Center of The Children's Hospital of Philadelphia.

3 Address reprint requests and correspondence to BH Wrotniak, Division of Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia, 3535 Market Street, Philadelphia, PA 19104-4399. E-mail: wrotniak{at}email.chop.edu.

See corresponding editorial on page 1587.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: The earliest determinants of obesity may operate during intrauterine life, and gestational weight gain may influence the intrauterine environment in a way that may affect the risk of overweight in the offspring.

Objective: The purpose of this study was to examine the association of gestational weight gain with offspring overweight.

Design: This was a retrospective cohort study of 10 226 participants from the Collaborative Perinatal Project (1959–1972). Anthropometric and sociodemographic variables were assessed during gestation, at birth, and at age 7 y. The association between gestational weight gain and offspring overweight at 7 y was examined after adjustment for important confounding factors.

Results: The odds of overweight in offspring at age 7 y increased by 3% for every 1 kg of gestational weight gain (adjusted odds ratio: 1.03; 95% CI: 1.02, 1.05). When gestational weight gain was examined using Institute of Medicine guidelines, the odds of overweight was 48% greater for children of mothers who gained more than the weight gain recommendations than for children of mothers who met the weight gain guidelines (adjusted OR: 1.48; 95% CI: 1.06, 2.06). The association remained significant after additional adjustment for birth weight. The association between gestational weight gain and overweight in the offspring was strongest for women who were underweight before pregnancy (P for interaction < 0.01).

Conclusion: Helping pregnant women to meet the recommended weight gain during pregnancy may be an important and novel strategy for preventing pediatric obesity.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Childhood obesity continues to be a serious public health problem. Children who are overweight are at risk of health conditions that include dyslipidemia, hypertension, and type 2 diabetes (1). Childhood obesity is also a risk factor for obesity in adulthood (2) and associated diseases such as cardiovascular disease and cancer (3). A life course approach to chronic disease epidemiology and prevention suggests that the development of excessive weight may be the result of complex interactions between environmental, genetic, and psychological variables that occur throughout the life span (4). By understanding the early determinants of obesity, it may be possible to influence the course of excessive weight gain and help curtail the obesity epidemic.

The earliest influences on human development may occur within the intrauterine environment (5–7). The concept that chronic health conditions may be programmed in early life has been demonstrated in research examining intrauterine exposures that influence fetal growth, such as maternal smoking (8) and gestational diabetes (9). Similarly, the amount of weight a woman gains during pregnancy may be a potentially important modifiable risk factor that influences the growth and health of the fetus as well as outcomes later during childhood and adulthood. Excessive gestational weight gain may be complicated by insulin resistance or even gestational diabetes, which is associated with fetal macrosomia and health risks in the offspring (9, 10). The Institute of Medicine (IOM) provides recommendations that weight gain for pregnant women be based on prepregnancy body mass index (BMI; in kg/m2) (11) (Table 1Go).


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  		TABLE 1. Recommended maternal gestational weight gain based on prepregnancy BMI, as defined by the Institute of Medicine (12)

 
Previously, there has been an emphasis to promote sufficient weight gain during pregnancy in an effort to reduce low-birth-weight deliveries and adverse perinatal outcomes (12). However, despite the increase in the obesity epidemic and the increase in the percentage of women gaining more than the IOM weight gain recommendations (from 37% to 46% between 1993 and 2003; 11), the role of gestational weight gain in obesity in the offspring has received relatively limited attention. Most studies examining the potential role of intrauterine factors on future obesity have examined factors other than gestational weight gain, such as birth weight, maternal parity, maternal smoking, and gestational age (13, 14). The few studies that have examined gestational weight gain as a determinant of future obesity in the offspring have reported mixed results (15–19).

The purpose of this study was to examine the association of gestational weight gain with the risk of overweight in offspring at 7 y of age in a multicenter, multiethnic cohort study design. It was hypothesized that gestational weight gain would be positively associated with overweight in offspring at age 7 y after the control for other factors that may influence weight gain. Secondary aims were to explore possible effect modification by child sex, race, and maternal prepregnancy BMI and to assess the role of birth weight as a potential mediator in the association between gestational weight gain and overweight in the offspring.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects
The National Collaborative Perinatal Project was a multicenter cohort study initiated in 1959 to investigate risk factors for cerebral palsy at 12 US sites (20). Between 1959 and 1965, 58 760 women with singleton pregnancies presenting for prenatal care in these centers were enrolled in the study after informed consent was obtained. Among them, 6454 were lost to follow-up before delivery or experienced fetal death, resulting in a cohort of 52 306 live births. Follow-up data were collected for the children on multiple occasions up to age 7 y.

For the present study, the baseline sample was restricted to the 27 889 children with birth documented to be at term gestation to eliminate the potential for confounding by differences in the duration of pregnancy on gestational weight gain. For participants that were excluded, gestational age was <37 wk for 2973 participants, >42 wk for 1494 participants, and unavailable for 19 950 births, primarily from children born before 1962, when this information began to be widely recorded as part of the research protocol. An additional 2 participants with mothers diagnosed with gestational diabetes were also excluded. At the 7-y time point, 8121 participants were lost to follow-up, and gestational weight gain data were missing for 9540 subjects, which resulted in an overall sample for these analyses of 10 226 (37% of the eligible sample). The study was approved by the Institutional Review Board of The Children's Hospital of Philadelphia.

Measurements
Maternal data were collected at enrollment by using a questionnaire and included maternal prepregnancy weight, age, race, number of cigarettes smoked per day, number of siblings in the household, and number of previous pregnancies. Maternal weight and height were measured at the time of delivery and used to calculate gestational weight gain. Gestational weight gain was determined as the difference between measured weight at delivery and reported prepregnancy weight. Prepregnancy BMI was computed by dividing reported prepregnancy weight (in kg) by height (in m2), measured at the time of delivery. All obstetric examinations and procedures in study participants were conducted by trained study staff. Recommended, excess, and insufficient gestational weight gain was determined on the basis of the IOM recommendations for healthy weight gain for pregnant women, by prepregnancy BMI category (12) (Table 1Go). Because the IOM does not identify an upper healthy gestational weight gain boundary for women with a BMI > 29 before pregnancy, we conservatively set it at 11.5 kg, the upper limit recommended for women with a prepregnancy BMI between 26 and 29 (21).

Variables collected by trained research staff for the children included sex, gestational age at birth, weight at birth, and weight and height at the 7-y visit. Gestational age was determined by the senior physician who assumed responsibility for the delivery using all clinical and historical information. Study labor and delivery records were completed by the delivering obstetrician immediately after delivery. Children were considered as first born if the mother reported no previous delivery or no other children living in the household at the time of delivery, depending on which question was asked at that time. Children ≥95th BMI percentile of a reference population for age and sex at the 7-y pediatric examination visit were considered to be overweight (22).

Analyses
Most variables were skewed, as has been shown in other populations for biological variables (23, 24) and are, therefore, described using medians, 2.5th, and 97.5th percentiles. Categorical variables are reported as proportions in percentage. Baseline characteristics for participants who were followed up and for those with incomplete data were compared by using the chi-square or Wilcoxon's rank-sum test, as appropriate. For the main analysis, the primary dichotomous outcome variable was childhood overweight status. Childhood overweight was considered to be a BMI ≥ 95th percentile for age and sex, and the reference category of nonoverweight was a BMI < 95th percentile for age and sex. A categorical measure of childhood overweight was selected rather than a continuous outcome because there is no strong evidence that variations within the normal range affect long-term health. Additionally, because only 5.7% of offspring at 7 y of age were overweight in our sample, most of the variability would be in the healthy range if a continuous measure of BMI was used, which we were not interested in predicting. Of 10 226 women, 530 (5.2%) were included more than once (519 twice and 11 three times) because they had more than one child enrolled in the study. Because the percentage of women who were included more than once was relatively small, we used logistic regression for our primary analyses. However, we also assessed the sensitivity of our findings to the fact that we have duplicate measurements on some women by adjusting the SEs in our analyses using the cluster option in STATA (Stata Corp, College Station, TX). The findings were not changed when we adjusted for clustering of observations by mother, so the results reported in this article are based on the primary analyses. Our analytic plan involved a 3-tier approach. First, a single univariate logistic regression model was used to examine the unadjusted association between the continuous measure of gestational weight gain and childhood overweight. Next, overweight status was regressed on gestational weight gain after adjustment for potential confounding variables chosen a priori: maternal race, age, prepregnancy BMI, number of cigarettes smoked per day, gestational age, child sex, age, first-born status, and study site. Finally, birth weight was added to the adjusted model to assess its influence as a potential mediator of the association between gestational weight gain and overweight status. Unadjusted and adjusted ORs and 95% CIs for overweight status were calculated, and statistical significance was assessed by using a Wald's test.

All analyses were then repeated by using a model that included indicator variables for "excessive weight gain" and "insufficient weight gain," with "healthy weight gain" as the referent group, as defined by the IOM, instead of the continuous measure of gestational weight gain.

Additional analyses were performed to test possible interactions between excessive or insufficient weight gain and offspring overweight by offspring's sex and race in the logistic regression models. To test whether the association between gestational weight gain and overweight in the offspring was modified by maternal prepregnancy BMI, we used stepwise regression on IOM prepregnancy weight categories and pregnancy weight gain categories and their interaction terms. The logistic model included indicator variables for maternal prepregnancy underweight (BMI < 19.8), overweight (BMI = 26–29.0), and obese IOM categories (BMI > 29.0), with normal weight (BMI = 19.8–26.0) as the reference category. In addition, the model included indicator variables for insufficient and excessive maternal weight gain, with healthy weight gain as the reference category. The model also included BMI categories by maternal weight gain interaction terms that were constructed as the product of the indicator variables for IOM prepregnancy and maternal weight gain categories. Backwards stepwise logistic regression and a manual backwards stepwise logistic regression procedure were used to select the final model, and terms with a significance level of <0.10 were retained as potential predictor variables; both procedures resulted in the same model. After a final model was obtained that showed one significant interaction, the model was modified to include additional covariates, including child sex, gestational age, first-born status, child age, mother's race, maternal age, smoking, and study site. The Hosmer Lemeshow test (25) was used to test the hypothesis of reasonable fit for all logistic regression models. Analyses stratified by prepregnancy BMI categories were then conducted, as prepregnancy BMI coding modified the association between excessive weight gain and overweight in the offspring. All statistical tests were 2-tailed and a P value < 0.05 considered statistically significant. Analyses were conducted using STATA version 8.2 (Stata Corp) (26).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Maternal baseline characteristics for the participants in the original cohort who were not analyzed because of loss to follow-up or missing gestational weight gain data (n = 17 661) were not significantly different from the sample studied (n = 10 226) in maternal smoking, first-born status, or child sex. However, mothers with complete data were more likely to have a slightly higher prepregnancy BMI (22.9 compared with 22.8; P = 0.01), to be slightly younger (aged 24.0 versus 24.1 y, P = 0.03), have a different racial distribution (black: 48% compared with 45%; white: 50% compared with 44%; Hispanic: 1% compared with 10%; other: 1% compared with 1%; P < 0.001), and have a child with a slightly higher birth weight (3.25 kg compared with 3.22 kg; P < 0.001) and with a slightly higher gestational age (39.8 wk compared with 39.7 wk; P < 0.001).

Characteristics of the women and their offspring included in this analysis are listed in Table 2Go. Twenty-two percent of the women had a prepregnancy BMI < 19.8, 60% had a prepregnancy BMI of 19.8–26.0, 9% had a prepregnancy BMI of 26.0–29.0, and 9% had a prepregnancy BMI > 29. According to the current IOM recommendations and on the basis of these prepregnancy BMI categories, 11% of women gained excessive weight, 24% gained adequate weight, and 65% gained insufficient weight. The percentage of women who gained excessive, recommended, and insufficient weight during gestation by prepregnancy BMI category differed between categories ({chi}2 = 670.0, P < 0.001) and are displayed in Table 3Go. The prevalence of overweight in the offspring at 7 y by prepregnancy BMI category was as follows: BMI < 19.8, 2.2%; BMI of 19.8–26.0, 5.4%; BMI of 26.0–29.0, 7.6%; BMI > 29.0, 13.2% ({chi}2 = 153.0, P < 0.001). Of the gestational weight gain categories, the prevalence of offspring overweight differed for women with a prepregnancy BMI < 19.8 ({chi}2 = 15.7, P < 0.001) and with a prepregnancy BMI of 19.8 to 26.0 ({chi}2 = 8.0, P = 0.02) (Figure 1Go). The risk of overweight in the offspring was lowest for mothers with a BMI < 19.8 who gained an insufficient amount of weight during pregnancy (prevalence of childhood overweight = 1.7%) and greatest for mothers with a BMI > 29 who had gained an excessive amount of weight during pregnancy (prevalence of childhood overweight = 14.5%) (Figure 1Go).


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  		TABLE 2. Characteristics of mothers and of their offspring at birth and at 7 y of age1

 

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  		TABLE 3. Percentage of women who gained insufficient, recommended, and excessive weight during gestation by prepregnancy BMI1

 

Figure 1
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  		FIGURE 1.. Prevalence of childhood overweight at 7 y by maternal prepregnancy BMI categories and gestational weight gain categories. In chi-square analyses, the prevalence of offspring overweight differed (P < 0.02) between gestational weight gain categories for women with a prepregnancy BMI < 19.8 and with a prepregnancy BMI of 19.8 to 26.0. The risk of overweight in the offspring was lowest for mothers with a BMI < 19.8 who gained an insufficient amount of weight during pregnancy (prevalence of childhood overweight = 1.7%) and greatest for mothers with a BMI > 29 who had gained an excessive amount of weight during pregnancy (prevalence of childhood overweight = 14.5%). Excessive, recommended, and insufficient gestational weight gain are defined based on criteria from the Institute of Medicine (12).

 
The unadjusted and adjusted associations between gestational weight gain and childhood overweight at 7 y are reported in Table 4Go. The unadjusted frequency of offspring overweight represents 10 cases per 100 women with excessive weight gain compared with 6 cases per 100 women who meet the weight gain recommendations. A strong predictor of childhood overweight was maternal prepregnancy BMI (unadjusted OR: 1.10; 95% CI: 1.09, 1.12; adjusted OR: 1.14; 95% CI: 1.11, 1.16). The relation between gestational weight gain and overweight in the offspring was not modified by sex or race. However, this association was modified by maternal prepregnancy BMI categories. After the use of backward stepwise regression to test a model that included indicator variables for maternal weight gain and prepregnancy BMI categories, the significant terms remaining in the final model included maternal underweight (OR: 0.35; 95% CI: 0.25, 0.50), maternal overweight (OR: 1.38; 95% CI: 1.03, 1.83), maternal obesity (OR: 2.56; 95% CI: 2.04, 3.23), excessive gestational weight gain (OR: 1.33; 95% CI: 1.04, 1.70), and a maternal underweight x excessive versus healthy gestational weight gain interaction (OR: 3.18; 95% CI: 1.34, 7.59), which indicated that the association between gestational weight gain and overweight in the offspring is strongest for children of underweight mothers. These associations and interaction remained significant after the model was further adjusted for child sex, gestational age, first-born status, child age, mother's race, maternal age, smoking, and study site. To assess the importance of catch-up-growth in the development of childhood obesity, additional analyses were conducted to examine the association between gestational weight gain and birth weight, and then the interaction of this association with prepregnancy BMI. A positive association between birth weight and gestational weight gain was found (adjusted β = 18.26 g of birth weight per every 1 kg gain in gestational weight; 95% CI: 16.5, 20.0; P < 0.001), but there was no significant interaction by prepregnancy BMI. The Hosmer Lemeshow test indicated good fit for all logistic regression models ({chi}2 > 0.05). Because of the significant interaction by prepregnancy BMI, the main analyses were repeated after stratifying by underweight status (Table 4Go).


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  		TABLE 4. Association between maternal gestational weight gain and overweight in the offspring at 7 y of age1

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The results of this study indicate that gestational weight gain is associated with overweight in the offspring at 7 y of age even after adjustment for maternal race, age, prepregnancy BMI, cigarette smoking, gestational age, child sex, age, first-born status, and study city. Compared with children of mothers who met the gestational weight gain recommendations, children of mothers who gained excessive weight during pregnancy had a 48% greater odds of overweight at 7 y of age. The magnitude of the association between excessive gestational weight gain and childhood overweight decreased after infant birth weight was added to the logistic regression model, suggesting that birth weight is likely on the pathway between gestational weight gain and child adiposity, but is unlikely to entirely explain this association.

Our findings are consistent with other research that support a positive association between gestational weight gain and overweight in the offspring (15–17, 27). Oken et al (15), using the same IOM gestational weight gain recommendations, but where the outcome was measured at 3 y of age, found a stronger association between gestational weight gain and offspring overweight compared with our findings. This suggests that the association between gestational weight gain and offspring overweight may decrease as children grow older. In contrast with Oken et al's findings we did not find an association between overweight in the offspring of mothers who had recommended compared with insufficient gestational weight gain. This may be because in Oken et al's study the reference group was children with a BMI < 50th percentile. An additional explanation could be influences of different environmental exposures on cohorts from 2 different time periods. Mothers who experience undernutrition and insufficient weight gain during pregnancy may conserve energy by suppressing metabolic rate and gaining little fat as a means of protecting fetal growth and theoretically preventing potential future morbidity in the offspring (28).

The association between gestational weight gain and overweight in the offspring was strongest for women who were underweight before pregnancy, and may reflect the fact that pregnancy weight gain has a greater impact in underweight women. Birth weight has been shown to be more strongly related to gestational weight gain in women of lower BMI compared with higher BMI (29). A greater likelihood of childhood overweight among underweight mothers who gain more weight during pregnancy is consistent with a published preliminary report (30). A possible explanation for why the odds of offspring overweight is strongest in underweight women who gain excessive weight during pregnancy is that there are different cutoffs for excessive weight gain by prepregnancy BMI category. To explore this possibility, we investigated the interaction between prepregnancy BMI and gestational weight gain as a continuous variable in relation to childhood overweight. The results revealed a statistically significant interaction and support the finding that women who are underweight and gain more gestational weight have the greatest odds of offspring overweight (data not shown).

There are a number of possible mechanisms responsible for the association between gestational weight gain and overweight in the offspring. From a life course perspective, intrauterine development may be a critical time period during which maternal weight gain may contribute to the programming of future risk of childhood overweight, perhaps through insulin resistance (15). Excessive gestational weight gain and hyperglycemia may overstimulate fetal pancreatic β cells and consequently bring about fetal hyperinsulinism. Insulin itself is a growth hormone for the fetus, resulting in higher birth weight (9, 31) and in impaired glucose tolerance and obesity in adolescence (31). In animal studies, fetal hyperinsulinism can elevate the expression of neuropeptide Y neurons in the arcuate hypothalamic nucleus (32), which results in hyperphagia and weight gain in postnatal life (33). An alternative explanation for the association of gestational weight gain with offspring overweight is that mothers with greater gestational weight gain may have children who gain more weight through shared mechanisms that may include genetics, dietary preferences, and physical activity patterns. It is not possible to distinguish between those possibilities based on this study. However, the strength of the association between gestational weight gain and offspring overweight was only slightly reduced after adjustment for variables that included prepregnancy BMI, which suggests that shared genes and extrauterine exposures may not primarily mediate the relation. This finding, in addition to the experiential data from animal models reported above, tends to support a causal association between gestational weight gain and overweight in the offspring.

There are several limitations of this study. Prepregnancy weight was self-reported and therefore may have been underreported. However, if some women who were overweight were incorrectly misclassified as normal weight, this would have biased estimates toward the null. Thus, our estimates of risk are conservative. A second limitation was that the analyses were based on a cohort of individuals born in US cities during the 1960s whose behavioral practices and environmental exposures may be different from those experienced by individuals today. However, if these associations are based on physiologic mechanisms, it is unlikely that the associations observed in the present study would be different now. The historical nature of this cohort may however explain the fact that only 11% of mothers in the sample gained an excessive amount of weight and that such a large proportion of women (65%) gained insufficient weight during pregnancy. Because of the percentage of women gaining excessive weight during pregnancy is significantly higher today, if the association described in the current study is confirmed in a contemporary cohort, the public health importance of excessive gestational weight gain for childhood obesity may be larger than can be estimated here. Additional limitations of this study include the amount of missing data due to changes in the data collected over the study, and that the individuals lost to follow-up had a higher prepregnancy BMI and birth weight. These potential limitations would only create a biased estimate of the results if the association of gestational weight gain with offspring overweight was different among those with complete and missing data. Additionally, there were no differences between the groups in maternal smoking, first-born status, or child sex, and the differences in characteristics reported between the samples were statistically significant because of the large sample size, but were small in magnitude. Another limitation of this study was that, because all cases of preeclampsia could not be definitively identified at the time the data were collected (20), there may have been some cases in the data set that could have influenced the findings. Likewise, the reason for the apparently low prevalence of gestational diabetes in the data set was unclear, but was likely related to the fact that our study was restricted to full-term infants that lived to 7 y of age. During the time period of the study cohort, there was a higher incidence of perinatal deaths, stillbirths, neonatal deaths, and prematurity among mothers with gestational diabetes. Thus, the effects of medical complications of gestational diabetes on the offspring may have resulted in the exclusion of many offspring of women with gestational diabetes. However, there may have been some cases of gestational diabetes mellitus that were not identified at the time the data were collected, and this limitation could also have influenced the findings. Finally, because BMI is not a measure of adiposity, having a more direct estimate of adiposity, such as skinfold thickness, would have been more clinically relevant.

There are unique strengths of this research. The sample studied was a multiethnic cohort from 12 sites throughout the United States that was followed for 7 y. It is the largest study to have examined the relation between gestational weight gain and overweight in the offspring using criteria defined by the IOM. Because the research was retrospective and part of a research protocol investigating other health outcomes, the potential for reporting bias was reduced. The number and quality of the measures also allowed for meaningful adjustment for a large number of potential confounders. Other than another preliminary report (30), this is the only study to suggest that the relation between gestational weight gain and childhood overweight is strongest among underweight mothers. This finding requires further research before being translated into recommendations, because it is possible that a large pregnancy weight gain among underweight mothers may confer some benefits to the offspring and the mother.

In conclusion, additional research is needed to clarify whether the association between greater gestational weight gain and increased odds of overweight in the offspring is causal and exists in today's obesogenic environment. If our findings are confirmed, improving compliance with pregnancy weight gain recommendations may be an important and novel strategy in preventing childhood obesity, because almost half of US women exceed these recommendations.


   ACKNOWLEDGMENTS
 
The authors' responsibilities were as follows—BHW and NS: participated in the design of the present retrospective study, in the analysis and interpretation of the data, and in the writing of the manuscript; JS: participated in the analysis and interpretation of the data and contributed to the writing of the manuscript; and SB: participated in the interpretation of the data and contributed to the writing of the manuscript. None of the authors had a conflict of interest.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Must A, Strauss R. Risks and consequences of childhood and adolescent obesity. Int J Obes Relat Metab Disord 1999;23(suppl):S2–11.
  2. Serdula M, Ivery D, Coates R, Freedman D, Williamson D, Byers T. Do obese children become obese adults? A review of the literature. Prev Med 1993;22:167–77.[Medline]
  3. Dietz W. Health consequences of obesity in youth: childhood predictors of adult disease. Pediatrics 1998;101:518–25.[Abstract/Free Full Text]
  4. Ben-Shlomo Y, Kuh D. A life course approach to chronic disease epidemiology: conceptual models, empirical challenges and interdisciplinary perspectives. Int J Epidemiol 2002;31:285–93.[Free Full Text]
  5. Reik W, Dean W, Walter J. Epigenetic reprogramming in mammalian development. Science 2001;293:1089–93.[Abstract/Free Full Text]
  6. Lucas A. Programming by early nutrition: an experimental approach. J Nutr 2004;128(suppl):401S–6S.
  7. Gluckman PD, Lillycrop KA, Vickers MH, et al. Metabolic plasticity during mammalian development is directionally dependent on early nutritional status. Proc Natl Acad Sci USA 2007; 104:12796–800.[Abstract/Free Full Text]
  8. Oken E, Huh SY, Taveras EM, Rich-Edwards JW, Gillman MW. Associations of maternal prenatal smoking with child adiposity and blood pressure. Obes Res 2005;13:2021–8.[Medline]
  9. Gillman MW, Rifas-Shiman S, Berkey CS, Field AE, Colditz GA. Maternal gestational diabetes, birth weight, and adolescent obesity. Pediatrics 2003;111:e221–6.[Abstract/Free Full Text]
  10. Oken E, Gillman MW. Fetal origins of obesity. Obes Res 2003;11:496–506.[Medline]
  11. National Research Council and Institute of Medicine. Influence of pregnancy weight on maternal and child health. Workshop Report. Committee on the Impact of Pregnancy Weight on Maternal and Child Health. Board on Children, Youth, and Families, Division of Behavioral and Social Sciences and Education and Food and Nutrition Board, Institute of Medicine. Washington, DC: The National Academies Press, 2007.
  12. Institute of Medicine. Nutrition during pregnancy. Washington, DC: National Academy Press, 1990.
  13. Reilly JJ, Armstrong J, Dorosty AR, et al. Early life risk factors for obesity in childhood: cohort study. BMJ 2005;330:1357.[Abstract/Free Full Text]
  14. Ong KK, Dunger DB. Birth weight, infant growth and insulin resistance. Eur J Endocrinol 2004;151:U131–9.[Abstract]
  15. Oken E, Taveras EM, Kleinman KP, Rich-Edwards JW. Gestational weight gain and child adiposity at age 3 years. Am J Obstet Gynecol 2007;196:322–8.[Medline]
  16. Moreira P, Padez C, Mourao-Carvalhal I, Rosado V. Maternal weight gain during pregnancy and overweight in Portuguese children. Int J Obes Relat Metab Disord 2007;31:608–14.[Medline]
  17. Fisch RO, Bilek MK, Ulstrom R. Obesity and leanness at birth and their relationship to body habits in later childhood. Pediatrics 1975;56:521–8.[Abstract/Free Full Text]
  18. Whitaker RC. Predicting preschooler obesity at birth: The role of maternal obesity in early pregnancy. Pediatrics 2004;114:e29–36.[Abstract/Free Full Text]
  19. Ong KK, Ahmed ML, Emmett PM, Preece MA, Dunger DB. Association between postnatal catch-up growth and obesity in childhood. BMJ 2000;320:967–71.[Abstract/Free Full Text]
  20. The Collaborative Perinatal Study, The National Institute of Neurologic Disease and Stroke. The women and their pregnancies. Washington, DC: US Government Printing Office, 1972. [DHEW publication no. (NIH) 73-379.]
  21. Schieve LA, Cogswell ME, Scanlon KS. Trends in pregnancy weight gain within and outside ranges recommended by the Institute of Medicine in a WIC population. Matern Child Nutr 1998;2:111–6.
  22. Himes J, Dietz W. Guidelines for overweight in adolescent preventive services: recommendations from an expert committee. The Expert Committee on Clinical Guidelines for Overweight in Adolescent Preventive Services. Am J Clin Nutr 1994;59:307–16.[Abstract/Free Full Text]
  23. Flegal KM. Epidemiologic aspects of overweight and obesity in the United States. Physiol Behav 2005;86:599–602.[Medline]
  24. Cole TJ, Green PJ. Smoothing reference centile curves: the LMS method and penalized likelihood. Stat Med 1992;11:1305–19.[Medline]
  25. Hosmer DW, Lemeshow S. Applied logistic regression. New York, NY: Wiley & Sons Inc, 2000.
  26. StataCorp. Stata statistical software: release 8.2. College Station, TX: StataCorp LP, 2004.
  27. Schack-Nielson L, Mortensen EL, Michaelsen KF, Sorensen TIA. High maternal prepregnancy weight gain is associated with an increased risk of obesity in childhood and adulthood independent of maternal BMI. Pediatr Res 2005;58:1020(abstr).
  28. Poppitt SD, Prentice AM, Goldberg GR, Whitehead RG. Energy-sparing strategies to protect human fetal growth. Am J Obstet Gynecol 1994;171:118–25.[Medline]
  29. Zhou W, Olsen J. Gestational weight gain as a predictor of birth and placenta weight according to pre-pregnancy body mass index. Acta Obstet Gynecol Scand 1997;76:300–7.[Medline]
  30. Sharma AJ, Cogswell ME, Grummer-Strawn LM. The association between pregnancy weight gain and childhood overweight is modified by mother's pre-pregnancy BMI. Pediatr Res 2005;58:1038 (abstr).
  31. Silverman BL, Rizzo TA, Cho NH, Metzger BE. Long-term effects of the intrauterine environment. The Northwestern University Diabetes in Pregnancy Center. Diabetes Care 1998;21:B142–9.[Medline]
  32. Plagemann A, Harder T, Melchior K, Rake A, Rohde W, Dorner G. Elevation of hypothalamic neuropeptide Y-neurons in adult offspring of diabetic mother rats. Neuroreport 1999;10:3211–6.[Medline]
  33. Kalra SP, Dube MG, Pu S, Xu B, Horvath TL, Kalra PS. Interacting appetite-regulating pathways in the hypothalamic regulation of body weight. Endocr Rev 1999;20:68–100.[Abstract/Free Full Text]
  34. Kuczmarski RJ, Ogden CL, Grummer-Strawn LM, et al. CDC growth charts: United States. Adv Data 2000;8:1–27.[Medline]
Received for publication September 7, 2007. Accepted for publication January 6, 2008.


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