6
Consequences of Gestational Weight Gain for the Child

The emphasis of the report Nutrition During Pregnancy (IOM, 1990) was on the short-term consequences of gestational weight gain (GWG). Not only was there a lack of data on long-term outcomes, but also the research community was only just beginning to understand the importance of the intrauterine environment for long-term child health. Since then, the literature on the topic has expanded, and more information is now available on neonatal as well as long-term consequences of both inadequate and excessive GWG during pregnancy. The discussions in this chapter review the current evidence and strive to quantify, wherever possible, potential causal relationships between GWG and childhood outcomes.

Only by knowing the magnitude of causal relationships can one say with certainty that recommending a certain amount of GWG will result in altered frequency of adverse child health outcomes. Observational studies are often susceptible to mixing effects of confounding factors with the predictor of real interest, in this case GWG. Although reverse causality is less of a problem in cohort than in cross-sectional studies, confounding remains a concern in any observational study. It is possible that associations of GWG with outcomes do not result from GWG itself, but rather to underlying factors that influence both weight gain and the outcomes (e.g., maternal diet composition or physical activity level). In particular, it is important to determine whether these relationships are independent of prepregnancy body mass index (BMI) or if they differ by prepregnancy BMI. Only with large, well-designed, and carefully controlled randomized studies can causal relationships be inferred with a high degree of confidence. Limited experi-



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6 Consequences of Gestational Weight Gain for the Child The emphasis of the report Nutrition During Pregnancy (IOM, 1990) was on the short-term consequences of gestational weight gain (GWG). Not only was there a lack of data on long-term outcomes, but also the research community was only just beginning to understand the importance of the intrauterine environment for long-term child health. Since then, the literature on the topic has expanded, and more information is now available on neonatal as well as long-term consequences of both inadequate and ex- cessive GWG during pregnancy. The discussions in this chapter review the current evidence and strive to quantify, wherever possible, potential causal relationships between GWG and childhood outcomes. Only by knowing the magnitude of causal relationships can one say with certainty that recommending a certain amount of GWG will result in altered frequency of adverse child health outcomes. Observational studies are often susceptible to mixing effects of confounding factors with the pre- dictor of real interest, in this case GWG. Although reverse causality is less of a problem in cohort than in cross-sectional studies, confounding remains a concern in any observational study. It is possible that associations of GWG with outcomes do not result from GWG itself, but rather to underly- ing factors that influence both weight gain and the outcomes (e.g., maternal diet composition or physical activity level). In particular, it is important to determine whether these relationships are independent of prepregnancy body mass index (BMI) or if they differ by prepregnancy BMI. Only with large, well-designed, and carefully controlled randomized studies can causal relationships be inferred with a high degree of confidence. Limited experi- 

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 WEIGHT GAIN DURING PREGNANCY mental data from randomized controlled trials in humans, however, im- pedes efforts to determine how much of any observed association is causal. In the following discussions, inferences regarding causality were made using the best data available in consideration of plausible biologic mechanisms, susceptibility to confounding and other aspects of the study methodology, and patterns of results. GENERAL CONCEPTS Causal Concepts When considering potential causal relationships between GWG and the various child outcomes reviewed, the committee relied on the same conceptual model that it utilized when evaluating the determinants of GWG (see Figure 6-1). This model fits well with two paradigms that offer useful conceptual frameworks for considering long-term effects on the offspring. The first—the “life course approach to chronic disease”—invokes two axes (Kuh and Ben-Shlomo, 2004): time, with temporal factors acting in the pre- conceptional through the prenatal period, into infancy, childhood, and be- yond to determine risk of chronic disease; and hierarchy, with hierarchical GESTATIONAL WEIGHT GAIN (OVERALL AND PATTERN) Mother Fetus Fat-free mass Fetal growth Fat mass -Fat-free mass Placenta -Fat mass Amniotic fluid NEONATAL OUTCOME Stillbirth Birth defects Infant mortality Fetal growth Preterm birth LONG-TERM CONSEQUENCES Neonatal body composition Infant weight gain Breastfeeding Obesity Neurodevelopment Allergy/Asthma Cancer indicates possible causal influences FIGURE 6-1 Schematic summary of neonatal, infant, and child consequences of GWG. Figure 6-1.eps

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 GESTATIONAL WEIGHT GAIN FOR THE CHILD factors ranging from the social/built/natural environment (macro) through behavior, physiology, and genetics (micro) (see Chapter 4) and interacting with each other over the life course, with different determinants being more or less important at different life stages. The other paradigm—the “devel- opmental origins of health and disease” paradigm—focuses primarily on the prenatal and early postnatal periods, because they are the periods of most rapid somatic growth and organ development (Gillman, 2005; Sinclair et al., 2007; Hanson and Gluckman, 2008). Both of these frameworks in- voke the concept of programming, which refers to perturbations or events that occur at early, plastic, and perhaps critical phases of development and can have long-lasting, sometimes irreversible, health consequences. The pe- riod of plasticity may vary for different organs and systems (Gluckman and Hanson, 2006a, 2006b). The model used by the committee predicts that adult risk factors can only partially modify the trajectories of health and disease patterns established in earlier life (Barker et al., 2002; Ben-Shlomo and Kuh, 2002; McMillen and Robinson, 2005; Sullivan et al., 2008). Potential Mechanisms Linking Gestational Weight Gain to Long-Term Offspring Health The existence of plausible biological mechanisms is one criterion for establishing causal relationships between GWG and child health outcomes based on observational data. The following discussion focuses primarily on potential mechanisms linking GWG to offspring obesity and its conse- quences. Gestational weight gain is clearly about weight, so it is appropriate to address weight-related outcomes. Also most of the emerging evidence on long-term outcomes is based on these endpoints. The epidemiologic evidence for effects of GWG on other important child health outcomes are addressed later this chapter. Deelopmental Programming Developmental programming, including the possible role of epigenetics, as a potential determinant of GWG, is discussed in Chapter 4. In this chap- ter, the role of developmental programming as a mechanism for some of the effects of GWG on postnatal outcomes is discussed. Many animal models have demonstrated that altering the environment in utero can have lifelong consequences. Perturbations of the maternal diet during pregnancy (typi- cally by severe energy or protein restriction; administration of hormones such as glucocorticoids; mechanical means, such as ligation of the uterine artery; or induction of anemia or hypoxia) have postnatal consequences on a number of metabolic and behavioral traits. Effects are inducible in rodents and other mammals, including non-human primates. Inasmuch as humans

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 WEIGHT GAIN DURING PREGNANCY differ from other animal species in duration of pregnancy, placentation, and other important factors, the importance of the findings from animal studies lies not in the specific interventions but rather in the general principle that altering the supply of nutrients, hormones, and oxygen to the growing em- bryo and fetus or exposing them to stressors and toxicants can have long- term effects. Much of this animal research has focused on obesity-related outcomes such as adiposity, fat distribution, sarcopenia, insulin sensitivity, glucose intolerance, and blood pressure. These are related to the leading causes of morbidity—and ultimately, mortality—in the United States. The ways in which GWG could influence obesity-related child health outcomes through developmental programming is discussed below (in Childhood Obesity and Its Consequences). Until recently, most of the research in animal models concentrated on the long-term effects of interventions that cause offspring to be born small, typically small-for-gestational age (SGA), rather than early. Such work has been a good companion to a series of epidemiologic observations made within the past two decades that lower birth weight, apparently resulting from both reduced fetal growth and reduced length of gestation, is associ- ated with higher risks of central obesity, insulin resistance, the metabolic syndrome, type 2 diabetes, hypertension, and coronary heart disease later in life. These associations are potentiated by rapid weight gain in childhood (Bhargava et al., 2004; Barker et al., 2005). It is important to note, however, that in recent years researchers have recognized that higher birth weight is also associated with later obesity and its consequences. Greater GWG is associated with increased weight at birth (reviewed in the Fetal Growth section of this chapter) based on either the absolute amount of GWG and indicators of excessive gain (based on total GWG relative to the recommendations for gain within a given prepreg- nancy BMI category). Excessive GWG appears to be rising over time (see Chapter 2), highlighting questions about the long-term adverse effects of higher weight gains in pregnancy. Animal experiments that involve “over- nutrition” of the mother during pregnancy are discussed briefly below. In addition, it is critical to recognize that effects of GWG, or indeed any factor that alters the in utero environment, may have long-term effects on the offspring without any alterations of fetal growth or length of gestation. Thus the most important epidemiologic evidence for long-term effects of GWG does not depend on birth weight, gestational age, or birth weight for gestational age as exposures or outcomes, but rather provides data on the direct associations of GWG with various health outcomes in the offspring. With this in mind, the committee considered “fetal growth” outcomes, including SGA and large-for-gestational age (LGA), and preterm birth as short-term outcomes. These measures have demonstrable and substantial associations with neonatal morbidity and mortality. Other short-term out-

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 GESTATIONAL WEIGHT GAIN FOR THE CHILD comes include stillbirth and birth defects. In contrast, neonatal body com- position is included in the discussion of long-term outcomes because of the hypothesis (still unproven, however) that relative amounts of adiposity and lean mass—and their physiologic consequences—in fetal and neonatal life are important in setting long-term cardio-metabolic trajectories. It also bears noting that this report focuses primarily on GWG, rather than prepregnancy BMI. Nevertheless, because the two factors are closely linked, one must account for confounding and effect modification by BMI in addressing offspring effects of GWG. Also it is possible that factors in infancy or childhood (e.g., growth in stature, adiposity, and infant feeding) could mediate effects of GWG on long-term child health. Childhood Obesity and Its Consequences The following discussion focuses primarily on mechanisms linking GWG to childhood obesity and its consequences, although similar mecha- nisms likely underlie associations of GWG with fetal growth. One issue that hampers inferences regarding fetal growth is that fetal growth is usually characterized by (gestational-age-specific) weight at birth, with less consid- eration of trajectory from the time of conception to delivery of weight, body length, or body composition (see Chapters 3 and 4 for a review of existing studies that address these issues). In contrast to the prenatal period, serial measurements of length/height and weight are common during childhood but data on body composition are relatively scarce. Insulin resistance and glucose intolerance during pregnancy may medi- ate effects of GWG on long-term child outcomes. Weight gain in pregnancy is partly a gain in adiposity, which is accompanied by a state of relative insulin resistance starting in mid-pregnancy, among other metabolic altera- tions (Reece et al., 1994; Williams, 2003; Catalano et al., 2006; King, 2006; Hwang et al., 2007) (also see Chapter 3). This is an adaptive response, as it allows more efficient transfer of fuels across the placenta to the grow- ing fetus (King, 2006). In overweight and obese pregnant women, these changes are magnified; insulin resistance is more severe than in normal weight women, substantially raising the risk of impaired glucose tolerance and frank gestational diabetes mellitus. This increased risk of impaired glucose tolerance has consequences for the fetus since glucose freely crosses the placenta; specifically, in pregnant women who have hyperglycemia, the fetus also experiences hyperglyce- mia. In a hypothesized sequence that Freinkel et al. (1986) termed “fuel- mediated teratogenesis,” fetal hyperglycemia causes fetal hyperinsulinemia, which in turn causes increased adiposity in the fetus. This increase is manifest as larger size at birth, which translates into higher rates of LGA and lower rates of SGA newborns (see discussion below and in Chapter 3).

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00 WEIGHT GAIN DURING PREGNANCY Presumably through developmental programming mechanisms, increased fetal adiposity also results in increased adiposity in the growing child. Other fuels besides glucose may also be involved. For example, increased fetal production of anabolic hormones and growth factors, in combination with the increased levels of glucose, lipids, and amino acids that are typical of GDM, can cause fetal macrosomia (birth weight > 4,500 g) and increase the risk for neonatal complications (Catalano et al., 2003). Crowther et al. (2005) and Pirc et al. (2007) showed that diet and insulin therapy along with blood glucose monitoring in pregnant women with mild GDM could lower plasma insulin and leptin (but not glucose) concentrations in cord blood, decreasing the risk of macrosomia by more than 50 percent (Crowther et al., 2005). This same impaired physiologic milieu may also increase the risk for long-term complications, particularly obesity and its metabolic sequelae. Observational studies suggest that this may be the case. For example, among 5- to 7-year-old children in two American health plans, Hillier et al. (2007) showed that risk of high weight for age was lower among those whose mothers had been treated for GDM than those who had not been treated; the weight status of the “treated” offspring was similar to those whose mothers had normal glucose tolerance. However, long-term child follow-up studies and relevant randomized trials are necessary to conclu- sively determine if treatment of GDM or impaired glucose intolerance dur- ing pregnancy can reduce adiposity and related physiology. Most of the evidence in support of the Freinkel hypothesis comes from animal experiments, such as those of van Assche and colleagues (1979), and more recently Plagemann and colleagues (1998). By pharmacologi- cally induced GDM in rats, both groups of researchers observed fetal hy- perglycemia and hyperinsulinemia, as hypothesized, as well as changes in the hypothalamus that give rise to hyperphagia, overweight, and impaired glucose tolerance in maturing offspring. Another way to induce offspring metabolic derangement in rats is through overfeeding the pregnant dam. For example, Samuelsson et al. (2008) reported that maternal diet-induced obesity resulted in increased adult adiposity and evidence of cardiovascular and metabolic dysfunction in the offspring (which was not present in the offspring of lean dams). Earlier work by Dorner et al. (1988) and Diaz and Taylor (1998) showed that a period of overfeeding or GDM in the pregnant dam during a developmentally sensitive period in gestation not only could change the metabolic phenotype of the immediate offspring, but also that the induced metabolic phenotype persisted for two succeeding generations. In their review of animal studies, Aerts and Van Assche (2003) demonstrate that these intergenerational physiologic effects are maternally transmitted, most likely through epigenetic processes. Seemingly paradoxically, in ani-

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0 GESTATIONAL WEIGHT GAIN FOR THE CHILD mal experiments it is also possible to produce offspring that have insulin resistance, features of the metabolic syndrome, and diabetes, including GDM, by reducing energy or macronutrient intake of the mother during pregnancy. This situation can also result in intergenerational amplification of obesity and its consequences. For example, in rats, Benyshek et al. (2006) were able to alter glucose metabolism in the grand-offspring by restricting protein during pregnancy and lactation. In summary, animal experiments show that offspring obesity and re- lated metabolic sequelae can be induced experimentally, either through pharmacological induction of GDM or through either over- or underfeed- ing pregnant dams as well as through mechanical means like uterine artery ligation. Epigenetic modifications likely explain many of these phenomena (Simmons, 2007). A human counterpart to the animal experimental work is epidemiologic studies showing that higher birth weight is related to later obesity and type 2 diabetes while lower birth weight is associated with central obesity, the metabolic syndrome, and indeed, type 2 diabetes as well (Gillman, 2005). In other words, a U-shape relationship exists between birth weight and obesity-related health outcomes. The extent to which these observations on metabolic dysfunction and offspring obesity have relevance for GWG guidelines is still unclear. Few animal studies directly assess the influence of GWG on short- or long- term offspring outcomes. Animal experimentalists typically do not measure weight gain during pregnancy, and it is not clear whether appropriate ani- mal models exist to study GWG and offspring obesity-related outcomes. Neither is it clear that models of either diet-induced obesity or GDM are instructive for assessing effects of GWG. Likewise, human population studies that rely on birth weight or its components, duration of gestation, and size at birth as predictors of later outcomes (e.g., Hofman et al., 2004; Hovi et al., 2007) also do not di- rectly assess GWG. Further, intervention studies to treat GDM do not in themselves provide evidence for making recommendations for appropriate GWG. Only randomized trials that alter weight gain during pregnancy can address that goal directly. In a randomized controlled trial of reduced weight gain among obese pregnant women, Wolff and colleagues (2008) reported that reduced weight gain led to reduced insulin and leptin concen- trations but that glucose values were hardly altered. Mean weight gain in the intervention group was 6.6 kg (± 5.5 kg) vs. 13.3 kg (± 7.5 kg) in the control group a mean difference of 6.7 kg (95% CI: 2.6-10.8, p = 0.002). Although the study was small, with only 50 participants, the results none- theless raise the possibility that moderating GWG may reduce the risk of GDM and, in turn, childhood obesity, but larger and longer-term studies are needed to address this question directly.

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0 WEIGHT GAIN DURING PREGNANCY EFFECTS ON NEONATAL MORBIDITY AND MORTALITY There is a substantial literature on prepregnancy BMI and neonatal morbidity and mortality; maternal prepregnancy BMI is strongly associated with infant mortality and a number of other clinically important outcomes, including stillbirth and preterm birth (Figure 6-2). The literature on GWG in relation to these outcomes remains more limited, with the exception of its influence on fetal growth (Cedergren, 2006; Kiel et al., 2007). The following discussion summarizes the committee’s evaluation of evidence on associations between GWG and a range of neonatal morbid- ity and mortality outcomes. Given that GWG, which is lower on aver- age for heavier women, differs in relation to prepregnancy BMI, studies that examine GWG without stratifying by prepregnancy BMI are subject 8 7.5 7.0 7 Non-obese Class I 6.0 Class II 5.9 6 Morbid obesity 5.6 5.3 4.9 5 Rate per 1,000 4.3 4 3 2 1.4 1.5 1.0 1.0 1 0 Total Neonatal Deaths Early Neonatal Deaths Late Neonatal Deaths FIGURE 6-2 Rate of neonatal, early, and late neonatal death by obesity subclass. SOURCE: Salihu et al., 2008. Obesity and extreme obesity: new insights into the black-white disparity in neonatal mortality. Obstetrics and Gynecology 111(6): Figure 6-2.eps 1410-1416. Reprinted with permission. redrawn

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0 GESTATIONAL WEIGHT GAIN FOR THE CHILD to confounding. These component relationships (prepregnancy BMI and GWG; and prepregnancy BMI and health outcome) are sufficiently strong that studies of GWG and neonatal outcomes that fail to account for pre- pregnancy BMI are of limited value in addressing the independent effects of GWG. Stillbirth Inadequate and excessive GWG have the potential to affect fetal vi- ability in later pregnancy, specifically risk of stillbirth (defined as pregnancy loss after 20 weeks’ gestation). Naeye (1979) and NCHS (1986) showed that women with both low prepregnancy BMI and low GWG tended to have elevated risk of fetal or perinatal mortality (a combination of stillbirth and neonatal mortality) and that women with both elevated prepregnancy BMI and excessive GWG experienced increased risk of the same adverse outcomes. Many studies on the potential association between GWG and stillbirths have been limited by confounding factors. For example, an analysis from the California Child Health and Development Studies of the School of Pub- lic Health, University of California, Berkeley (Tavris and Read, 1982) found a strong inverse association between total GWG and fetal death, but the association was found to be an artifact of using cumulative weight gain as the predictor; so it reflected the fact that duration of gestation for stillbirths was notably shorter than gestational duration of live births, not that lower GWG predicted fetal death. When the analysis was restricted to births of greater then 35 weeks’ gestation, there was no association. A case-control study of stillbirths in Sweden reported a strong positive association between prepregnancy BMI and stillbirth, with odds ratios ap- proaching 3.0 for obese women, but the authors reported no effect of GWG measured in either early or late pregnancy among term births (Stephansson et al., 2001). Although the large size of the study (649 cases and 690 con- trols) and the authors’ consideration of an array of covariates are notable, the results for total GWG were not presented in the publication. In summary, the research on GWG and stillbirth remains quite limited in quantity and quality. In addition to considering prepregnancy BMI, there is a need to avoid the error of comparing total GWG in pregnancies resulting in stillbirths with those resulting in live births because of the time in pregnancy when stillbirth is likely to occur. Although early studies sug- gested adverse effects of low GWG among women with low prepregnancy BMI and also of high GWG among women with elevated prepregnancy BMI, more detailed studies have not been done to corroborate or refute this pattern. Recent, better studies largely do not support an association between GWG and stillbirth.

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0 WEIGHT GAIN DURING PREGNANCY Birth Defects The authoring committee of the IOM (1990) report did not identify any studies on the association between GWG and birth defects. Since the etiologic period for congenital defects is so early in pregnancy, GWG is not likely to be causally relevant. Although the literature on prepregnancy BMI and congenital defects now suggests an increased risk of birth defects with increasing BMI (Watkins et al., 2003; Anderson et al., 2005; Villamor et al., 2008), only one study has directly addressed GWG in relation to birth de- fects. Shaw (2001) reported that infants born to mothers who gained less than either 5 or 10 kg during pregnancy were at increased risk of neural tube defects. An additional report indicated that dieting to lose weight dur- ing pregnancy was associated with an increased risk of neural tube defects (Carmichael et al., 2003). It seems more likely that an association of GWG and birth defects would result from reverse causality (abnormal fetal de- velopment affecting weight gain) rather than a direct causal effect of GWG on risk of birth defects. Infant Mortality Infant mortality is obviously of great clinical and public health impor- tance and is often used as a summary indicator of a population’s reproduc- tive health status. In fact, concern with fetal growth and preterm birth as health outcomes stems largely from the known relationships between those outcomes and infant mortality (as well as morbidity); studies that directly address mortality can be helpful in interpreting the patterns seen with those other, intermediate outcomes such as preterm birth or growth restriction. However, very limited research assessing GWG and infant mortality exists. In the IOM (1990) report, only one study on perinatal mortality was exam- ined (NCHS, 1986). Since then, there has been only one additional study. As part of the National Maternal and Infant Health Survey (NMIHS), Chen et al. (2009) examined maternal prepregnancy BMI and GWG among 4,265 infant deaths and 7,293 controls. Among underweight and normal- weight women, low GWG was associated with a marked increase in infant mortality, with relative risks on the order of 3-4 compared to those with the highest GWG; the effects were more modest among overweight and obese women, with both lower and higher GWG associated with about two-fold increases in the risk of infant mortality. In all cases, the patterns were stronger for neonatal deaths (in the first 30 days of life) than for post- neonatal deaths (those occurring after 1 month but before the completion of 1 year). In the lowest weight gain group, the relative risks for neonatal death were 3.6 among underweight women, 3.1 among normal weight women, 2.0 among overweight women, and 1.2 among obese women,

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0 GESTATIONAL WEIGHT GAIN FOR THE CHILD showing a diminishing effect of low GWG with increasing BMI. In the high- est GWG group, the relative risks for neonatal mortality for underweight, normal weight, overweight, and obese women were 1.0, 1.2, 1.4, and 1.8, respectively, showing the exact opposite tendency—excessive GWG was more strongly associated with neonatal death with increasing prepregnancy BMI. Maternal age at delivery did not affect neonatal mortality. After ad- justing for gestational age at delivery, no association was found between teenage pregnancy and neonatal mortality. The same general pattern was seen for postneonatal deaths but was less pronounced (see Table 6-1). More studies of infant mortality are needed, but the evidence from Chen et al. (2009) warrants serious consideration not only because of the TABLE 6-1 Maternal Prepregnancy BMI and Gestational Weight Gain of Infant Deaths and Controls (1988 National Maternal and Infant Health Survey [NMIHS]) Total Weight Maternal Gain During Postneonatal Pregnancya Prepregnancy Neonatal Death Death Infant Death BMI (kg/m2) ORb (95% CI) ORb (95% CI) ORb (95% CI) (kg) < 18.5 < 6.0 3.55 (1.92-6.54) 2.96 (1.42-6.15) 3.26 (1.86-5.72) 6.0-11.6 1.35 (0.88-2.06) 1.34 (0.83-2.14) 1.34 (0.93-1.92) 12.0-17.6c 1.00 1.00 1.00 ≥ 18.0 0.99 (0.63-1.54) 0.55 (0.32-0.95) 0.79 (0.53-1.17) < 6.0 18.5-24.9 3.07 (2.45-3.85) 1.96 (1.51-2.55) 2.58 (2.12-3.14) 6.0-11.6 1.41 (1.19-1.68) 1.12 (0.92-1.36) 1.29 (1.11-1.49) 12.0-17.6c 1.00 1.00 1.00 ≥ 18.0 1.15 (0.96-1.37) 0.94 (0.77-1.15) 1.06 (0.91-1.23) < 6.0 25-29.9 1.98 (1.34-2.92) 0.81 (0.51-1.29) 1.42 (1.02-1.99) 6.0-11.6 1.20 (0.85-1.68) 0.64 (0.43-0.95) 0.94 (0.71-1.25) 12.0-17.6c 1.00 1.00 1.00 ≥ 18.0 1.41 (1.00-2.00) 0.87 (0.58-1.31) 1.16 (0.87-1.56) ≥ 30 < 6.0 1.19 (0.69-2.06) 0.81 (0.40-1.62) 1.04 (0.64-1.70) 6.0-11.6 0.67 (0.39-1.17) 0.91 (0.47-1.78) 0.78 (0.48-1.26) 12.0-17.6c 1.00 1.00 1.00 ≥ 18.0 1.78 (0.96-3.33) 1.29 (0.58-2.84) 1.61 (0.92-2.81) NOTE: Midpoint and range values for outcomes (neonatal death, postnatal death, infant death) are derived using a separate reference group for each BMI category. aWeight gain during pregnancy projected to 40 weeks’ gestation. bAdjusted for race, maternal age at pregnancy, maternal education, maternal smoking during pregnancy, child’s sex, live birth order, and plurality. cReferent group for comparisons within BMI stratum. SOURCE: Modified from Chen et al., 2009.

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0 WEIGHT GAIN DURING PREGNANCY LGA. Despite a limited number of randomized controlled trials, biological plausibility from animal models is strong. Relative risks for GWG and SGA appear to be higher among women with lower prepregnancy BMI. 4. The evidence for a relationship between GWG and preterm birth, or between GWG and gestational age at birth is weaker than evidence for an association between GWG and fetal growth, and biological plausibility is weak. Most studies show associations be- tween lower GWG and preterm birth among underweight, and to a lesser extent, normal weight women. Higher GWG among all BMI categories may also be associated with preterm birth. Evidence is insufficient on associations with spontaneous vs. induced preterm birth. 5. A small number of studies show that GWG is directly associated with fat mass in the newborn period. Insufficient evidence is avail- able on associations between GWG and adiposity in infancy. 6. A small number of relatively large and recent epidemiologic stud- ies show that higher GWG is associated with childhood obesity as measured by BMI. Although biological plausibility is strong, evidence is insufficient to address effect modification by maternal BMI. Only one study has examined blood pressure as an outcome (finding associations in the same direction as BMI), and none has evaluated fat mass or other cardio-metabolic consequences of adiposity. 7. Lower GWG may be associated with risk of childhood asthma, chiefly through complications of preterm birth, although evidence is limited. 8. Higher GWG may be associated with ALL, breast cancer, and ADHD, but the evidence is largely indirect and limited in quantity. 9. Concern exists that metabolic consequences of weight loss during pregnancy may be associated with poorer childhood neurodevel- opmental outcomes. Data are limited but raise the possibility that ketonemia among diabetic women could lead to suboptimal neu- rologic development. Recommendation for Research Research Recommendation 6-1: The committee recommends that the Na- tional Institutes of Health and other relevant agencies should pro- vide support to researchers to conduct observational and experimental studies to assess the impact of variation in GWG on a range of child outcomes, including duration of gestation and weight and body com-

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 GESTATIONAL WEIGHT GAIN FOR THE CHILD position at birth, and neurodevelopment, obesity and related outcomes, and asthma later in childhood. Areas for Additional Investigation The committee identified the following areas for further investigation to support its research recommendations. The research community should conduct studies on the following topics: • Child outcomes related to GWG to provide support for causal inference. Randomized trials and a combination of observational epidemiology and animal models may be more attainable bench- marks to enhance certainty regarding causal links between GWG and infant outcomes. • Statistical models that follow sound theoretical frameworks and clearly distinguish among confounding, mediating, and moderating (effect modifying) variables. Statistical models based on path analy- sis such as structural equation modeling may be able to improve interpretation of complex data. • Preventing excessive weight gain with all of the attributes listed above for observational studies. Even relatively small studies that can evaluate intermediate endpoints, if not the clinically important outcomes, would make a significant contribution. Furthermore, future research on GWG and child outcomes should: • not assume linear relationships between GWG and offspring obe- sity, but should look for U- or J-shaped associations as well; • determine whether the pattern of maternal weight gain affects short- or long-term child outcomes, e.g., whether weight gain ear- lier in pregnancy is more harmful than later gain; and • determine whether critical or sensitive periods of adiposity accre- tion exist in pregnant women and, if so, when weight gain is an adequate measure to capture those periods. REFERENCES ACOG (American College of Obstetricians and Gynecologists). 2006. ACOG Committee Opinion. Number 333, May 2006 (replaces Number 174, July 1996): The Apgar score. Obstetrics and Gynecology 107(5): 1209-1212. Aerts L. and F. A. Van Assche. 2003. Intra-uterine transmission of disease. Placenta 24(10): 905-911. Ahlgren M., J. Wohlfahrt, L. W. Olsen, T. I. Sorensen and M. Melbye. 2007. Birth weight and risk of cancer. Cancer 110(2): 412-419.

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