3
Composition and Components of Gestational Weight Gain: Physiology and Metabolism

Gestational weight gain (GWG) is a unique and complex biological phenomenon that supports the functions of growth and development of the fetus. Gestational weight gain is influenced not only by changes in maternal physiology and metabolism, but also by placental metabolism (Figure 3-1). The placenta functions as an endocrine organ, a barrier, and a transporter of substances between maternal and fetal circulation. Changes in maternal homeostasis can modify placental structure and function and thus impact fetal growth rate. Conversely, placental function may influence maternal metabolism through alterations in insulin sensitivity and systemic inflammation and thus influence GWG.

This chapter provides relevant background material on normal physiologic and metabolic changes that occur during pregnancy and are related to GWG. The discussion begins with a review of total and pattern of GWG in singleton, twin, and triplet pregnancies. Next, the unique chemi-

FIGURE 3-1 Schematic summary of components of gestational weight gain.

FIGURE 3-1 Schematic summary of components of gestational weight gain.



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 71
3 Composition and Components of Gestational Weight Gain: Physiology and Metabolism Gestational weight gain (GWG) is a unique and complex biological phenomenon that supports the functions of growth and development of the fetus. Gestational weight gain is influenced not only by changes in maternal physiology and metabolism, but also by placental metabolism (Figure 3-1). The placenta functions as an endocrine organ, a barrier, and a transporter of substances between maternal and fetal circulation. Changes in maternal homeostasis can modify placental structure and function and thus impact fetal growth rate. Conversely, placental function may influence maternal metabolism through alterations in insulin sensitivity and systemic inflam- mation and thus influence GWG. This chapter provides relevant background material on normal physi- ologic and metabolic changes that occur during pregnancy and are related to GWG. The discussion begins with a review of total and pattern of GWG in singleton, twin, and triplet pregnancies. Next, the unique chemi- TOTAL AND OVERALL PATTERN OF GESTATIONAL WEIGHT GAIN Mother Fetus Fat-free mass Fetal growth Fat mass -Fat-free mass Placenta -Fat mass Amniotic fluid indicates possible causal influences FIGURE 3-1 Schematic summary of components of gestational weight gain.  Figure 3-1.eps

OCR for page 71
 WEIGHT GAIN DURING PREGNANCY cal composition and accretion rates of maternal, placental, and fetal com- ponents of GWG are presented, followed by discussions of the maternal and fetal-placental physiology underlying weight gain in pregnancy. Lastly, pathophysiologic conditions that may adversely affect GWG are reviewed to provide a foundation for understanding changes in body weight and composition during pregnancy. TOTAL AND PATTERN OF GESTATIONAL WEIGHT GAIN Total Gestational Weight Gain The total amount of weight gained in normal-term pregnancies varies considerably among women. Nevertheless, some generalizations can be made regarding tendencies and patterns of GWG in singleton and multiple pregnancies. Singleton Pregnancies An examination of studies published in the United States from 1985 to the present indicate that the mean total GWG of normal weight adult women giving birth to term infants ranged from a low of 10.0 to a high of 16.7 kg (Appendix C [Tables C-1A and C-1B] contains a tabular summary of the studies examined by the committee). Among adolescents, in general, GWG tended to be higher compared with adult women (means ranged from 14.6 to 18.0 kg in the studies examined). A consistent finding across studies was an inverse relationship between GWG and pregravid body mass index (BMI). Figure 3-2 illustrates a similar relationship with data derived from Abrams et al. (1986). Since the release of the report Nutrition During Pregnancy (IOM, 1990) and its guidelines for GWG, a number of studies have examined GWG among overweight and obese women. Bianco et al. (1998) found that the mean GWG for 613 obese (BMI > 35) women averaged 9.1 ± 7.4 kg. Thirteen percent of the women, however, gained more than 16 kg, and 9 percent either lost or failed to gain weight. In a cohort study using birth certificate data from 120,251 obese women in Missouri, 18, 30, and 40 percent of the women gained < 6.8 kg in obese classes I, II, and III, respectively. The amount of total gain associated with minimal risk for preeclampsia, caesarean delivery, large-for-gestational age (LGA), and small-for-gestational age (SGA) outcomes was 4.6-11.4 and 0-4.1 for class I and II obesity, respectively; and weight loss of 0-4.1 kg for class III obesity (Kiel et al., 2007) (see Chapter 2 for definition of obesity classes). A prospective study of a cohort of 245,526 Swedish women confirmed that GWG among obese women (BMI = 30-34.9) and very obese women

OCR for page 71
 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN 3,600 Very Overweight 3,500 Estimated Birth Weight (Kg) Moderately Overweight 3,400 3,300 3,200 Ideal Weight 3,100 3,000 Underweight 2,900 0 2 4 6 8 10 12 14 16 18 20 Maternal Weight Gain (Kg) FIGURE 3-2 Birth weight as a function of maternal weight gain and prepregnancy weight for height. Figure 3-2.eps SOURCE: Modified from Abrams and Laros (1986). This article was published in the American Journal of Obstetrics and Gynecology 154(3), Prepregnancy weight, redrawn weight gain, and birth weight, pp. 503-509. Copyright Elsevier (1986). (BMI ≥ 35) was lower (11.1 and 8.7 kg, respectively) than among non- obese women (Cedergren, 2006). Low GWG (< 8 kg) occurred in 30.2 and 44.6 percent of the obese and very obese women, respectively. Among the 62,167 women in the Danish National Birth Cohort with data on GWG, about 36 percent of the obese women exhibited low rates of gain (0.28 kg per week). Fifty percent gained between 0.28 and 0.68 kg per week, and 14 percent gained > 0.68 kg per week (Nohr et al., 2007). Obese women (BMI = 30-40) participating in a prenatal intervention gained less weight (adjusted GWG = 7.52 kg) than controls (adjusted GWG = 9.78 kg) and experienced no difference in pregnancy outcome (Claesson et al., 2008). In summary, from a population perspective, obese women as a group gain less weight than non-obese women, nevertheless GWG can vary widely. Twin Pregnancies Total GWG in twin pregnancies is generally higher than in singleton pregnancies with means ranging from 15 to 22 kg (Appendix C, Table C-2).

OCR for page 71
 WEIGHT GAIN DURING PREGNANCY The cumulative weight gain stratified by pregravid BMI for mothers of twins born at 37-42 weeks of gestation and with an average twin birth weight ≥ 2,500 g is shown in Table 3-1. Cumulative and rates of weight gain by trimester are presented in Appendix C, Tables C-3A and C-3B. Outcomes associated with GWG in twin pregnancies, as with single- ton pregnancies, are a function of pregravid BMI. Several studies have shown that, when stratified by pregravid BMI, increased GWG is associ- ated with increased twin birth weight among underweight, normal weight, and overweight, but not obese, women (Brown and Schloesser, 1990; Luke et al., 1992; Lantz et al., 1996). Yeh and Shelton (2007) found that mean twin birth weights in the population studied increased incrementally from 2,237 g to 2,753 g for total GWG 55 pounds, respectively. The odds of having a twin delivery at ≥ 36 weeks gestation and birth weight ≥ 2,500 g were significantly lower among women who gained < 35 pounds (adjusted odds ratio [AOR] 0.49, 95% confidence interval TABLE 3-1 Summary of Adjusted and Unadjusted* Cumulative Weight Gain, by Pregravid BMI Status for Mothers of Twins at Gestational Ages 37-42 Weeks, and with Average Twin Birth Weight > 2,500 g Interquartile 25th-75th Percentile Ranges of Cumulative Weight Gain Cumulative Weight Gain (To 37-42 weeks) (To 37-42 weeks) Pregravid BMI kg lbs kg lbs 20.9 ± 0.3 45.9 ± 0.7 Weighta Normal (n = 409) 16.8-24.5 37-54 (21.0 ± 6.1)* (46.2 ± 13.4)* 18.9 ± 0.5 41.6 ± 1.1 Overweightb (n = 154) 14.1-22.7 31-50 (18.7 ± 7.0)* (41.1 ± 15.5)* 15.7 ± 0.5 34.6 ± 1.2 Obesec (n = 143) 11.4-19.1 25-42 (15.4 ± 7.2)* (34.0 ± 15.9)* NOTES: Results are presented as least square means ± standard error of mean (SEM) from models controlling for diabetes and gestational diabetes, preeclampsia, smoking during preg- nancy, primiparity, and placental membranes (monochorionicity and missing chorionicity). Total cumulative gain is also adjusted for length of gestation. Results in parentheses are the un- adjusted means ± standard deviation (SD) (also see Appendix C, Tables C-3A through C-3D). aBMI = 18.5-24.9 kg/m2. bBMI = 25.0-29.9 kg/m2. cBMI = ≥ 30 kg/m2. SOURCE: Historical cohort of twin births delivered at Johns Hopkins Hospital, Baltimore, Jackson Memorial Hospital, Miami, Medical University of South Carolina, Charleston, and University of Michigan, Ann Arbor, provided by Barbara Luke, Sc.D., M.P.H., R.D., and Mary L. Hediger, Ph.D. For more details on this historical cohort, see Luke et al. (2003).

OCR for page 71
 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN [CI]: 0.37-0.65) and significantly higher among women who gained > 55 pounds (AOR 2.24, 95% CI: 1.51-3.33) compared to those who gained 35-45 pounds. Interestingly, GWG > 55 pounds was associated with an approximate 1.5 times greater likelihood of having a maternal complication (cumulative of gestational diabetes mellitus [GDM], pregnancy-induced hypertension, preeclampsia, and anemia [AOR 1.63, 95% CI: 1.02-2.60] or cesarean delivery [AOR 1.85, 95% CI: 1.20-2.87]). In summary, GWG in twin gestations mirrors that in singleton preg- nancies, i.e., there is an inverse relationship between maternal GWG and maternal prepregnancy BMI. These results suggest that a balance is needed between optimal GWG for maternal and twin outcomes. Triplet and Quadruplet Pregnancies Fewer studies are available on triplet and quadruplet pregnancies (Ap- pendix C, Table C-2). Reported GWG among mothers carrying triplets ranged from 20.5 to 23.0 kg at 32-34 weeks and for quadruplets from 20.8 to 31.0 kg at 31-32 weeks (Luke, 1998). Total GWG in 38 triplet pregnan- cies was 20.2 kg at 33.4 weeks (Luke et al., 1995). The rate of gain was 0.48 kg per week before 24 weeks’ gestation and 0.96 kg per week after 24 weeks (Luke et al., 1995). Again, as with singleton and twin pregnan- cies, GWG is a function of BMI category; median gains were 15.5, 21.8, and 15 kg for low-, normal-, and high-BMI categories, respectively (Eddib et al., 2007). Pattern of Gestational Weight Gain The pattern of GWG is most commonly described as sigmoidal (Hytten and Chamberlain, 1991), but linear, concave, and convex patterns of weight gain have been observed as well (Villamor et al., 1998). The following dis- cussion summarizes the committee’s review of the evidence on rate of GWG in singleton and twin pregnancies; observed relationships between GWG pattern and prepregnancy BMI; and birth weight outcomes associated with varying patterns of GWG in twin pregnancies. Singleton Pregnancies In the report Nutrition During Pregnancy (IOM, 1990) mean rates of GWG for well-nourished women with uncomplicated singleton pregnan- cies were reported as approximately 0.45 kg per week during the second trimester and 0.40 kg per week during the third trimester. Several studies, published since then indicate higher rates of weight gain in the second and third trimesters among American women with BMI values in the normal

OCR for page 71
 WEIGHT GAIN DURING PREGNANCY range (Appendix C, Tables C-1A and C-1B). For example, the pattern of GWG by maternal BMI category was examined in a large cohort of women visiting the University of California, San Francisco clinics (Abrams and Selvin, 1995; Carmichael et al., 1997). Mean rate of gain was 0.169 kg per week in the first trimester. Mean weight gains were higher in the second (0.563 kg per week) than the third trimester (0.518 kg per week) in all groups except for obese women; and mean gains in the second and third trimester were higher in underweight and normal weight women than in overweight and obese women. Birth weight was correlated most strongly with gain in the second trimester (32.8 g/kg GWG versus 18 and 17 g/kg in the first and third trimesters, respectively). In another study, mean rates of GWG in non-obese, low-income black and white women were 2.48 kg in the first trimester and 0.49 and 0.45 kg per week in the second and third trimesters, respectively (Hickey et al., 1995). In contrast, GWG rates among predominantly Hispanic women (n = 7,589) participating in the Prematurity Prevention Project were similar in the second (0.52 kg per week) and third trimesters (0.53 kg per week) (Siega-Riz et al., 1996); although the third-trimester gain was slightly lower in women who delivered preterm (0.50 vs. 0.53 kg per week). A similar GWG pattern has been observed in adolescents, although the median gain and rate of gain were higher throughout gestation; from mid-pregnancy to term, the rate of gain was 0.51 kg per week (Hediger et al., 1990). In summary, the pattern of GWG is generally higher in the second trimester and is related to maternal pregravid BMI. However, pattern of GWG can vary depending on maternal ethnicity and age. Twin Pregnancies Luke and colleagues (1992) conducted a series of observational studies on outcomes associated with the rate of GWG in women with twin preg- nancies who delivered infants at 37-42 weeks’ gestation and with mean birth weights exceeding 2,500 g. They (1992) found that low rate of GWG, defined as < 1.0 pound/week, was associated with a significant decrease in mean birth weight for twins compared to singletons (β, -0.137; p = 0.001). Significantly higher rates of GWG in the third trimester were observed among women whose mean birth weights for twins were ≥ 2,500 g com- pared to women with birth weights for twins that were < 2,500 g, regard- less of BMI category; and no significant differences were seen for first and second trimester GWG rates. Among a large multiethnic population of 646 twin pregnancies at ≥ 28 weeks’ gestation, birth weight increased by 14, 20, and 17 g for each pound of weight gained between 0 and 20 weeks’ gestation, 20 and 28 weeks’ gesta- tion, and 28 weeks to birth, respectively (Luke et al., 1997). Mean total GWG

OCR for page 71
 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN was 17.4 kg in a larger cohort of 1,564 twin births of > 28 weeks’ gestation from the same population (Luke et al., 1998). In a similar study, Luke et al. (2003) found that rates of GWG associated with optimal outcomes were greater for underweight and normal weight women than for overweight and obese women. These results are similar to those of singleton pregnancies. COMPONENTS OF GESTATIONAL WEIGHT GAIN As pregnancy progresses, protein, fat, water, and minerals are deposited in the fetus, placenta, amniotic fluid, uterus, mammary gland, blood, and adipose tissue (Figure 3-3). The products of conception (placenta, fetus, amniotic fluid) comprise approximately 35 percent of the total GWG (Pitkin, 1976). The extent to which these changes in body composition are critical for normal fetal development or are incidental to pregnancy is not completely understood. Maternal Components of Gestational Weight Gain The committee reviewed evidence on maternal total body water (TBW) accretion, fat-free mass (FFM) accretion (i.e., protein accretion), and fat mass (FM) accretion. Each of these maternal components of GWG exhibit FIGURE 3-3 Components of gestational weight gain. NOTE: LMP = last menstrual period. Figure 3-3.eps SOURCE: Pitkin, 1976. Nutritional support in obstetrics and gynecology. Clinical Obstetrics and Gynecology 19(3):bitmap image with permission. 489-513. Reprinted

OCR for page 71
 WEIGHT GAIN DURING PREGNANCY unique patterns of accretion during pregnancy, with varying effects on outcome. Total Body Water Accretion Total body water accretion is largely under hormonal control and is highly variable during pregnancy. Across several studies, TBW accretion measured by deuterium or antipyrine tracers averaged about 7-8 liters (L) in healthy pregnancies (Hytten and Chamberlain, 1991). Expansion of the extracellular fluid (ECF) measured using the tracer sodium thiocyanate is estimated to be about 6-7 L. For a reference 12.5-kg GWG, total water gain at term is distributed in the fetus (2,414 g), placenta (540 g), amniotic fluid (792 g), blood-free uterus (800 g), mammary gland (304 g), blood (1,267 g), and ECF (1,496 g) with no edema or leg edema and ECF (4,697 g) with generalized edema (Hytten and Chamberlain, 1991). Maternal age, parity, and height did not affect the incidence of edema, but overweight women had greater generalized edema than underweight women. As pregnancy ad- vances, plasma volume expansion measured using Evans blue dye increases up to 45 percent (Rosso, 1990); maternal plasma volume expansion cor- relates positively with birth weight. Monthly bioimpedance analysis (BIA) measurements in 170 healthy pregnant women confirmed the progressive expansion of TBW, intracellular water (ICW), and ECF during pregnancy (Larciprete et al., 2003). Larciprete et al. (2003) also found that total body water accretion was positively correlated with birth weight, in agreement with other investigations (Langhoof-Roos et al., 1987; Lederman et al., 1997; Mardones-Santander et al., 1998; Butte et al., 2003). Fat-Free Mass: Protein Accretion Protein is accrued predominantly in the fetus (42 percent), but also in the uterus (17 percent), blood (14 percent), placenta (10 percent), and breasts (8 percent) (Hytten and Chamberlain, 1991). Protein accrual occurs predominantly in late pregnancy. Protein deposition has been estimated from measurements of total body potassium (TBK) accretion derived by whole-body counting in a number of studies of pregnant women (King et al., 1973; Emerson et al., 1975; Pipe et al., 1979; Forsum et al., 1988; Butte et al., 2003). King et al. (1973) observed a rate of TBK accretion of 24 milliequivalents (meq) per week between 26 and 40 weeks’ gestation. Pipe et al. (1979) found a 312 meq potassium (K) increase. Lower incre- ments of 110 and 187 meq at 36 weeks were found over pregravid values in two other studies (Forsum et al., 1988; Butte et al., 2003). Based on a potassium-nitrogen ratio in fetal tissues of 2.15 meq potassium/g nitro- gen, the total protein deposition estimated from the longitudinal studies

OCR for page 71
 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN of King et al. (1973), Pipe et al. (1979), Forsum et al. (1988), and Butte et al. (2003) is 686 g. A study of 108 black adolescents showed a mean rate of TBK accretion of 21 meq per week between 16 and 35 weeks’ gestation, consistent with adult studies (Stevens-Simon et al., 1997). In summary, these recent studies suggest that protein accretion may be less than the approximate (~1 kg) estimates of the earlier findings of Hytten and Chamberlin (1991). Fat Mass: Fat Accretion Based on serial measurements of skinfold thickness at seven sites made in 84 healthy, pregnant women, fat appears to be deposited preferentially over the hips, back, and upper thighs up to about 30 weeks’ gestation (Figure 3-4; Taggart et al., 1967). This pattern of fat deposition is unique to pregnancy. Sohlstrom and Forsum (1995) used magnetic resonance imaging to show that the majority of fat deposited during pregnancy is subcutaneous. Based on estimates of fat deposition and distribution both before and after Thigh 5 Change in Skinfold Thickness (mm) 4 Suprailiac 3 2 Scapula 1 Costal Biceps 0 Knee Triceps –1 10 20 30 40 Weeks of Pregnancy FIGURE 3-4 Longitudinal changes in skinfold thickness throughout pregnancy. SOURCE: Taggart et al., 1967. Changes in skinfolds during pregnancy. British Figure 3-4.eps Journal of Nutrition 21(2): 439-451. Reprinted with the permission of Cambridge redrawn University Press.

OCR for page 71
0 WEIGHT GAIN DURING PREGNANCY pregnancy, they found that of the adipose tissue gained during pregnancy, 76 percent was deposited subcutaneously, similar to the fat distribution before pregnancy. Of the total fat deposition, 46 percent was in the lower trunk, 32 percent in the upper trunk, 16 percent in the thighs, 1 percent in the calves, 4 percent in the upper arms, and 1 percent in the forearms. Postpartum, fat was mobilized more completely from the thighs than the trunk, and non-subcutaneous fat in the upper trunk actually increased post- partum. Evidence obtained with computer tomography from 14 women suggests that childbearing may be associated with acquisition of visceral fat (Gunderson et al., 2008). Measurement of fat mass during pregnancy is technically challenging because the usual methodology is imprecise, invalid, or not applicable to pregnancy. Skinfold measurements lack the precision necessary to estimate changes in fat mass accurately. Two-component body composition methods based on TBW, body density, and TBK are invalid during pregnancy be- cause of the increased hydration of FFM that occurs during pregnancy; the constants for hydration, density, and K content of FFM used in two-com- partment models are not applicable to pregnant women and would lead to erroneous estimations of FFM and FM. However, two-component models that use corrected constants for the hydration, density, and K content of FFM in pregnancy, as determined by van Raaij et al. (1988) and Hopkinson et al. (1997) are satisfactory for use with pregnant women, as are three- or four-component models (Fuller et al., 1992) in which the hydration or density of FFM is measured. Fat accretion models estimated in pregnant women using corrected two-component models or three- and four-compo- nent body composition are summarized in Appendix C, Table C-4. Figure 3-5 shows a four-compartment body composition model of FM, TBW, protein, bone mineral, and non-osseous mineral measured by hy- drodensitometry, deuterium dilution, and densitometry (dual energy X-ray absorptometry, DXA) (Lederman et al., 1997). When applied (after preg- nancy) to 200 healthy women at 14 and 37 weeks of gestation, the model showed that obese women gained significantly less fat than underweight and normal weight women (8.7 vs. 12.6 and 12.2 kg, respectively). There were no differences in the amount of TBW gained among the under- weight, normal weight or obese women. The majority of women studied did not conform to the recommendations of the Institute of Medicine (IOM) (1990). Sixty-seven percent of underweight, 61 percent of normal weight, 69 percent of overweight, and 78 percent of obese women gained outside the recommended ranges. Fat accretion paralleled GWG; FM gain was posi- tively correlated with GWG (r = 0.81) and inversely correlated (r = -0.25) with pregravid weight. For those that gained within the IOM (1990) rec- ommended ranges, FM gain was highest among the underweight (6.0 kg), followed by the normal weight (3.8 kg), overweight (2.8 kg), and obese

OCR for page 71
 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN 18 18 All (n=196) Gain < IOM Rec. (n=51) 15 15 Unmeasured TBW gain (L) 12 12 FM gain (kg) GWG (kg) 9 9 6 6 3 3 0 0 -3 -3 -6 -6 Low Normal High Very high Low Normal High Very high 18 18 Gain within IOM Rec. (n=68) Gain > IOM Rec. (n=78) 15 15 12 12 9 9 6 6 3 3 0 0 -3 -3 -6 -6 Low Normal High Very high Low Normal High Very high BMI Category BMI Category FIGURE 3-5 Body weight and composition changes in 196 women are presented by pregravid BMI category (low n = 21, normal n = 118, high n = 29, and very Figure 3-5.eps high n = 28). Gains in total body water and fat mass and gestational weight gain also are presented by compliance with the IOM 1990 recommendations for weight gain: women gaining less than (n = 51), within (n = 68), and more than (n = 78) the recommendations from IOM (1990). SOURCE: Lederman et al., 1997. (-0.6 kg). For those who gained less than the recommendations, FM gain was 0.6 kg in the underweight, 1.3 kg in the normal weight, 0.3 kg in the overweight, and -5.2 kg in the obese. For those that gained more than the recommendations, FM was highest in the underweight (6.9 kg), followed by the normal weight (6.0 kg), overweight (4.2 kg), and obese (3.1 kg). Butte et al. (2003) used a four-compartment body composition model based on TBK, TBW, body volume, and bone mineral content measured by whole-body counting, deuterium dilution, hydrodensitometry, bone, and DXA (pre- and postgravid only) before pregnancy; at 9, 22, and 36 weeks

OCR for page 71
00 WEIGHT GAIN DURING PREGNANCY differences between groups, but by 16 and 18 hours, the pregnant women had substantial increases in free fatty acid (FFA) and β-hydroxybutyrate (βHA), both of which were inversely correlated with glucose levels. There was a significant difference in FFA concentrations between obese and lean pregnant women only at 16 hours of fasting. In contrast, there were no significant differences in βHA levels at any time point between lean and obese women. Ketonuria and Ketonemia in Pregnancy As first described by Freinkel (1980), pregnancy can be considered a condition of “accelerated starvation” because of the changes in maternal metabolism that occur because of the increase in insulin resistance. As dis- cussed previously, the accelerated starvation occurs as a result of increased insulin resistance, particularly related to lipid metabolism. There is an increased risk of developing ketonuria and ketonemia in pregnancy even among women with normal glucose tolerance. Chez and Curcio (1987) reported that eight of nine women with clinically normal pregnancies de- veloped ketonuria at various times during their pregnancy. Using a portable capillary meter, Gin et al. (2006) measured capillary blood ketones and βHA in women with normal glucose tolerance (controls) and those with GDM three times a day from 25 to 37 weeks’ gestation. Fasting ketonuria was strongly correlated with ketonemia in controls but not in women with GDM. There was a chronic increase in ketonemia levels in 12 percent of the controls and 47 percent of the women with GDM. Pregnant women develop ketonemia much earlier than nonpregnant women during prolonged fasting because of the accelerated starvation. Felig (1973) studied women between 16 and 22 weeks’ gestation who elected termination of pregnancy and were willing to undergo prolonged fasting and compared them with a nonpregnant control group. After an overnight fast of at least 12 hours and for the first 36 to 60 hours of starvation, blood βHA and acetoacetate concentrations were two- to threefold higher in the pregnant group than in the nonpregnant group. The increase in lipolysis among the pregnant women was attributed to increases in hPL. The ketone concentrations in maternal blood were equivalent to those in amniotic fluid and were fortyfold above levels in fed subjects. The assumption is that amniotic fluid levels represent maternal-to-fetal transport. Felig (1973) also hypothesized that ketones become an important metabolic fuel for the fetal brain once glucose concentrations decrease, because the human fetal brain has the enzymes necessary for ketone oxidation. Coetzee et al. (1980) reported that 19 percent of obese, insulin-dependent diabetic women on 1,000-kilocalorie (kcal) diets developed ketonuria. In contrast, in diabetic women eating higher-energy diets, only 14 percent had

OCR for page 71
0 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN ketonuria, and in pregnant nondiabetic women, only 7 percent developed ketonuria. Measurement of blood ketones was never positive if the urine measure was ≤ 2 plus and acetoacetate levels were always less than 1 mmol/L. There was no difference in neonatal outcomes among the three groups. In summary, pregnant women are more likely to develop elevated mea- sures of blood βHA and acetoacetate during prolonged fasting (after 12-18 hours) as a result of the metabolic and hormonal changes that occur dur- ing pregnancy. Although pregnant women with diabetes are more likely to develop elevated blood ketones than women with normal glucose tolerance, a substantial proportion of pregnant women with normal glucose tolerance have elevated blood ketone levels at some time during gestation. Although the evidence is based on associations and does not demonstrate causality, caution should be exercised regarding weight loss during pregnancy or no GWG, given the propensity to develop ketonemia, increased urinary nitro- gen excretion, and decreased gluconeogenic amino acids. As discussed in Chapter 6, there are significant consequences of caloric insufficiency, low GWG, and poorly controlled diabetes for the child, and these are discussed in Chapter 6. FINDINGS AND RECOMMENDATIONS Findings 1. Total GWG in normal-term pregnancies displays considerable vari- ability; nevertheless, some generalizations can be made regarding mean tendencies and patterns of GWG: a. A consistent inverse relationship is observed between GWG and pregravid BMI category. b. Mean GWG ranges from 10.0 to 16.7 kg in normal weight adults and 14.6 to 18.0 kg in adolescents giving birth to term infants. c. The pattern of GWG is most commonly described as sigmoidal, with mean weight gains higher in the second than the third trimester across BMI categories, except for obese women. d. Lower GWGs, on the order of 11 kg and 9 kg, have been con- firmed in large cohorts of obese women and very obese women, respectively. 2. In its evaluation of GWG in multiple pregnancies, the committee relied on observational GWG data of women giving birth to twins born at 37-42 weeks of gestation and with an average twin birth weight ≥ 2,500 g:

OCR for page 71
0 WEIGHT GAIN DURING PREGNANCY a. Mean GWG of normal weight women with twin births ranges from 15.5 to 21.8 kg. b. GWG for triplets ranges from 20.5 to 23.0 kg at 32-34 weeks and for quadruplets from 20.8 to 31.0 kg at 31-32 weeks. 3. When stratified by the World Health Organization (WHO) pre- pregnancy BMI categories, sample sizes from data on twins are insufficient to designate a range for underweight women with pre- gravid BMI < 18.5 kg/m2. 4. The extent to which fat mass accretion is critical rather than inci- dental to pregnancy is not clear, but unrestrained weight gain leads to postpartum weight retention. 5. Placental size is strongly correlated with fetal growth, averaging approximately 500 g in singleton pregnancies. 6. Amniotic fluid weight may affect maternal gestational weight gain by as much as 1 kg at term. 7. Gestational gains in weight, total body water, total body potas- sium, protein, and FFM, but not FM, are positively correlated with birth weight across all BMI categories. 8. Poor plasma volume expansion is associated with a poorly growing fetus and poor reproductive performance. 9. Pregnancy is a condition of systemic inflammation that also influ- ences maternal and fetal nutrient utilization. 10. During prolonged fasting, i.e., 16-18 hours, pregnant women are more likely to develop elevated measures of blood βHA and ace- toacetate. In women with diabetes, plasma FFA and βHA are in- versely associated with intellectual development of the offspring at 3-5 years of age. Therefore, caution is warranted regarding periods of prolonged fasting and weight loss during pregnancy and the development of ketonuria. Research Recommendations Research Recommendation 3-1: The committee recommends that the Na- tional Institutes of Health and other relevant agencies should provide support to researchers to conduct studies in all classes of obese women, stratified by the severity of obesity, on the determinants and impact of GWG, pattern of weight gain, and its composition on maternal and child outcomes. Research Recommendation 3-2: The committee recommends that the Na- tional Institutes of Health and other relevant agencies should provide support to researchers to conduct studies on the eating behaviors, pat- terns of dietary intake and physical activity, and metabolic profiles of

OCR for page 71
0 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN pregnant women, especially obese women, who experience low gain or weight loss during pregnancy. In addition, the committee recommends that researchers should conduct studies on the effects of weight loss or low GWG, including periods of prolonged fasting and the development of ketonuria/ketonemia during gestation, on growth and on develop- ment and long-term neurocognitive function in the offspring. Areas for Additional Investigation The committee identified the following areas for further investigation to support its research recommendation. The research community should conduct studies on: • Potential effects of maternal weight loss on components of mater- nal body composition for both the mother and the fetus, particu- larly in obese women; and • Mechanisms by which placental hormonal factors and systemic inflammation impact the regulation of maternal metabolism during pregnancy. REFERENCES Abramovich D. R. 1969. The weight of placenta and membranes in early pregnancy. Journal of Obstetrics and Gynaecology of the British Commonwealth 76(6): 523-526. Abrams B. F. and R. K. Laros, Jr. 1986. Prepregnancy weight, weight gain, and birth weight. American Journal of Obstetrics and Gynecology 154(3): 503-509. Abrams B. and S. Selvin. 1995. Maternal weight gain pattern and birth weight. Obstetrics and Gynecology 86(2): 163-169. Ananth C. V. and S. W. Wen. 2002. Trends in fetal growth among singleton gestations in the United States and Canada, 1985 through 1998. Seminars in Perinatology 26(4): 260-267. Ananth C. V., A. M. Vintzileos, S. Shen-Schwarz, J. C. Smulian and Y. L. Lai. 1998. Standards of birth weight in twin gestations stratified by placental chorionicity. Obstetrics and Gynecology 91(6): 917-924. Archie J. G., J. S. Collins and R. R. Lebel. 2006. Quantitative standards for fetal and neonatal autopsy. American Journal of Clinical Pathology 126(2): 256-265. Ballew C. and J. D. Haas. 1986. Altitude differences in body composition among Bolivian newborns. Human Biology 58(6): 871-882. Baumann M. U., S. Deborde and N. P. Illsley. 2002. Placental glucose transfer and fetal growth. Endocrine 19(1): 13-22. Bernstein I. M., M. I. Goran, S. B. Amini and P. M. Catalano. 1997. Differential growth of fetal tissues during the second half of pregnancy. American Journal of Obstetrics and Gynecology 176(1 Pt 1): 28-32. Bianco A. T., S. W. Smilen, Y. Davis, S. Lopez, R. Lapinski and C. J. Lockwood. 1998. Pregnancy outcome and weight gain recommendations for the morbidly obese woman. Obstetrics and Gynecology 91(1): 97-102.

OCR for page 71
0 WEIGHT GAIN DURING PREGNANCY Bleker O. P. and H. J. Hoogland. 1981. Short review: ultrasound in the estimation of human intrauterine placental growth. Placenta 2(3): 275-278. Blickstein I. 2002. Normal and abnormal growth of multiples. Seminars in Neonatology 7(3): 177-185. Brace R. A. and E. J. Wolf. 1989. Normal amniotic fluid volume changes throughout preg- nancy. American Journal of Obstetrics and Gynecology 161(2): 382-388. Brown J. E. and P. T. Schloesser. 1990. Prepregnancy weight status, prenatal weight gain, and the outcome of term twin gestations. American Journal of Obstetrics and Gynecology 162(1): 182-186. Buchanan T. A., B. E. Metzger, N. Freinkel and R. N. Bergman. 1990. Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes. American Journal of Obstetrics and Gynecology 162(4): 1008-1014. Butte N. F. 2000. Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus. American Journal of Clinical Nutrition 71(5 Suppl): 1256S- 1261S. Butte N. F., K. J. Ellis, W. W. Wong, J. M. Hopkinson and E. O. Smith. 2003. Composition of gestational weight gain impacts maternal fat retention and infant birth weight. American Journal of Obstetrics and Gynecology 189(5): 1423-1432. Carmichael S., B. Abrams and S. Selvin. 1997. The association of pattern of maternal weight gain with length of gestation and risk of spontaneous preterm delivery. Paediatric and Perinatal Epidemiology 11(4): 392-406. Catalano P. M. and H. M. Ehrenberg. 2006. The short- and long-term implications of maternal obesity on the mother and her offspring. British Journal of Obstetrics and Gynaecology 113(10): 1126-1133. Catalano P. M., E. D. Tyzbir, N. M. Roman, S. B. Amini and E. A. Sims. 1991. Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women. American Journal of Obstetrics and Gynecology 165(6 Pt 1): 1667-1672. Catalano P. M., E. D. Tyzbir, R. R. Wolfe, N. M. Roman, S. B. Amini and E. A. Sims. 1992. Longitudinal changes in basal hepatic glucose production and suppression during insulin infusion in normal pregnant women. American Journal of Obstetrics and Gynecology 167(4 Pt 1): 913-919. Catalano P. M., E. D. Tyzbir, R. R. Wolfe, J. Calles, N. M. Roman, S. B. Amini and E. A. Sims. 1993. Carbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes. American Journal of Physiology 264(1 Pt 1): E60-E67. Catalano P. M., N. M. Drago and S. B. Amini. 1995. Factors affecting fetal growth and body composition. American Journal of Obstetrics and Gynecology 172(5): 1459-1463. Catalano P. M., N. M. Roman-Drago, S. B. Amini and E. A. Sims. 1998. Longitudinal changes in body composition and energy balance in lean women with normal and abnormal glucose tolerance during pregnancy. American Journal of Obstetrics and Gynecology 179(1): 156-165. Catalano P. M., S. E. Nizielski, J. Shao, L. Preston, L. Qiao and J. E. Friedman. 2002. Down- regulated IRS-1 and PPARgamma in obese women with gestational diabetes: relationship to FFA during pregnancy. American Journal of Physiology Endocrinology and Metabo- lism 282(3): E522-E533. Catalano P. M., A. Thomas, L. Huston-Presley and S. B. Amini. 2003. Increased fetal adi- posity: a very sensitive marker of abnormal in utero development. American Journal of Obstetrics and Gynecology 189(6): 1698-1704. Catalano P. M., M. Hoegh, J. Minium, L. Huston-Presley, S. Bernard, S. Kalhan and S. Hauguel-De Mouzon. 2006. Adiponectin in human pregnancy: implications for regula- tion of glucose and lipid metabolism. Diabetologia 49(7): 1677-1685.

OCR for page 71
0 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN Catalano P. M., A. Thomas, L. Huston-Presley and S. B. Amini. 2007. Phenotype of infants of mothers with gestational diabetes. Diabetes Care 30(Suppl 2): S156-S160. Cedergren M. 2006. Effects of gestational weight gain and body mass index on obstetric out- come in Sweden. International Journal of Gynaecology and Obstetrics 93(3): 269-274. Challier J. C., S. Basu, T. Bintein, J. Minium, K. Hotmire, P. M. Catalano and S. Hauguel- de Mouzon. 2008. Obesity in pregnancy stimulates macrophage accumulation and in- flammation in the placenta. Placenta 29(3): 274-281. Chez R. A. and F. D. Curcio, 3rd. 1987. Ketonuria in normal pregnancy. Obstetrics and Gynecology 69(2): 272-274. Claesson I. M., G. Sydsjo, J. Brynhildsen, M. Cedergren, A. Jeppsson, F. Nystrom, A. Sydsjo and A. Josefsson. 2008. Weight gain restriction for obese pregnant women: a case-control intervention study. British Journal of Obstetrics and Gynaecology 115(1): 44-50. Coetzee E. J., W. P. Jackson and P. A. Berman. 1980. Ketonuria in pregnancy—with special reference to calorie-restricted food intake in obese diabetics. Diabetes 29(3): 177-181. Desoye G. and S. Hauguel-de Mouzon. 2007. The human placenta in gestational diabetes mel- litus. The insulin and cytokine network. Diabetes Care 30(Suppl 2): S120-S126. Desoye G. and P. Kaufman. 2005. The human placenta in diabetes. In Diabetology of Preg- nancy (Frontiers in Diabetes), Vol . J. Djelmis, G. Desoye and M. Ivasinevic. Basel, Switzerland: Karger; pp. 94-109. Diamant Y. Z., B. E. Metzger, N. Freinkel and E. Shafrir. 1982. Placental lipid and glycogen content in human and experimental diabetes mellitus. American Journal of Obstetrics and Gynecology 144(1): 5-11. Durnwald C., L. Huston-Presley, S. Amini and P. Catalano. 2004. Evaluation of body com- position of large-for-gestational-age infants of women with gestational diabetes mellitus compared with women with normal glucose tolerance levels. American Journal of Ob- stetrics and Gynecology 191(3): 804-808. Eddib A., J. Penvose-Yi, J. A. Shelton and J. Yeh. 2007. Triplet gestation outcomes in relation to maternal prepregnancy body mass index and weight gain. Journal of Maternal-Fetal & Neonatal Medicine 20(7): 515-519. Emerson K., Jr., E. L. Poindexter and M. Kothari. 1975. Changes in total body composition during normal and diabetic pregnancy. Relation to oxygen consumption. Obstetrics and Gynecology 45(5): 505-511. Felig P. 1973. Maternal and fetal fuel homeostasis in human pregnancy. American Journal of Clinical Nutrition 26(9): 998-1005. Felig P. and V. Lynch. 1970. Starvation in human pregnancy: hypoglycemia, hypoinsulinemia, and hyperketonemia. Science 170(961): 990-992. Florini J. R., G. Tonelli, C. B. Breuer, J. Coppola, I. Ringler and P. H. Bell. 1966. Charac- terization and biological effects of purified placental protein (human). Endocrinology 79(4): 692-708. Fomon S. J., F. Haschke, E. E. Ziegler and S. E. Nelson. 1982. Body composition of reference children from birth to age 10 years. American Journal of Clinical Nutrition 35(5 Suppl): 1169-1175. Forsum E., A. Sadurskis and J. Wager. 1988. Resting metabolic rate and body composition of healthy Swedish women during pregnancy. American Journal of Clinical Nutrition 47(6): 942-947. Freinkel N. 1980. Banting Lecture 1980. Of pregnancy and progeny. Diabetes 29(12): 1023- 1035. Friedman J. E., T. Ishizuka, J. Shao, L. Huston, T. Highman and P. Catalano. 1999. Impaired glucose transport and insulin receptor tyrosine phosphorylation in skeletal muscle from obese women with gestational diabetes. Diabetes 48(9): 1807-1814.

OCR for page 71
0 WEIGHT GAIN DURING PREGNANCY Friedman J. E., J. P. Kirwan, M. Jing, L. Presley and P. M. Catalano. 2008. Increased skeletal muscle tumor necrosis factor-alpha and impaired insulin signaling persist in obese women with gestational diabetes mellitus 1 year postpartum. Diabetes 57(3): 606-613. Fuller N. J., S. A. Jebb, M. A. Laskey, W. A. Coward and M. Elia. 1992. Four-component model for the assessment of body composition in humans: comparison with alternative methods, and evaluation of the density and hydration of fat-free mass. Clinical Science (London) 82(6): 687-693. Gabbe S., J. Niebyl and J. Simpson, Eds. (1991). Obstetrics Normal & Problem Pregnancies. New York: Churchill Livingstone. Garrow J. S. and S. F. Hawes. 1971. The relationship of the size and composition of the human placenta to its functional capacity. Journal of Obstetrics and Gynaecology of the British Commonwealth 78(1): 22-28. Germain S. J., G. P. Sacks, S. R. Sooranna, I. L. Sargent and C. W. Redman. 2007. Systemic inflammatory priming in normal pregnancy and preeclampsia: the role of circulating syncytiotrophoblast microparticles. Journal of Immunology 178(9): 5949-5956. Gielen M., P. J. Lindsey, C. Derom, R. J. Loos, R. Derom, J. G. Nijhuis and R. Vlietinck. 2007. Twin birth weight standards. Neonatology 92(3): 164-173. Gin H., A. Vambergue, C. Vasseur, V. Rigalleau, P. Dufour, A. Roques, M. Romon, D. Millet, P. Hincker and P. Fontaine. 2006. Blood ketone monitoring: a comparison between gestational diabetes and non-diabetic pregnant women. Diabetes and Metabolism 32(6): 592-597. Girard J. and P. Ferre. 1982. Metabolic and hormonal changes around birth. In Biochemical Deelopment of the Fetus and Neonate. C. T. Jones. New York: Elsevier Biomedical Press; p. 517. Glinianaia S. V., R. Skjaerven and P. Magnus. 2000. Birthweight percentiles by gestational age in multiple births. A population-based study of Norwegian twins and triplets. Acta Obstetricia et Gynecologica Scandinaica 79(6): 450-458. Glinoer D. 2004. Increased TBG during pregnancy and increased hormonal requirements. Thyroid 14(6): 479-480; author reply 479-480. Gonzalez C., A. Alonso, N. Alvarez, F. Diaz, M. Martinez, S. Fernandez and A. M. Patterson. 2000. Role of 17beta-estradiol and/or progesterone on insulin sensitivity in the rat: im- plications during pregnancy. Journal of Endocrinology 166(2): 283-291. Grattan D. R., S. R. Ladyman and R. A. Augustine. 2007. Hormonal induction of leptin resistance during pregnancy. Physiology & Behaior 91(4): 366-374. Grumbach M. M., S. L. Kaplan, J. J. Sciarra and I. M. Burr. 1968. Chorionic growth hormone- prolactin (CGP): secretion, disposition, biologic activity in man, and postulated function as the “growth hormone” of the 2d half of pregnancy. Annals of the New York Academy of Sciences 148(2): 501-531. Gunderson E. P., B. Sternfeld, M. F. Wellons, R. A. Whitmer, V. Chiang, C. P. Quesenberry, Jr., C. E. Lewis and S. Sidney. 2008. Childbearing may increase visceral adipose tissue independent of overall increase in body fat. Obesity (Siler Spring) 16(5): 1078-1084. Haggarty P. 2002. Placental regulation of fatty acid delivery and its effect on fetal growth—a review. Placenta 23(Suppl A): S28-S38. Harvey N. C., J. R. Poole, M. K. Javaid, E. M. Dennison, S. Robinson, H. M. Inskip, K. M. Godfrey, C. Cooper and A. A. Sayer. 2007. Parental determinants of neonatal body com- position. Journal of Clinical Endocrinology and Metabolism 92(2): 523-526. Hauguel-de Mouzon S. and M. Guerre-Millo. 2006. The placenta cytokine network and inflammatory signals. Placenta 27(8): 794-798. Hauguel-de Mouzon S. and E. Shafrir. 2001. Carbohydrate and fat metabolism and related hormonal regulation in normal and diabetic placenta. Placenta 22(7): 619-627.

OCR for page 71
0 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN Hauguel-de Mouzon S., J. Lepercq and P. Catalano. 2006. The known and unknown of leptin in pregnancy. American Journal of Obstetrics and Gynecology 194(6): 1537-1545. Hediger M. L., T. O. Scholl, I. G. Ances, D. H. Belsky and R. W. Salmon. 1990. Rate and amount of weight gain during adolescent pregnancy: associations with maternal weight- for-height and birth weight. American Journal of Clinical Nutrition 52(5): 793-799. Hickey C. A., S. P. Cliver, S. F. McNeal, H. J. Hoffman and R. L. Goldenberg. 1995. Prenatal weight gain patterns and spontaneous preterm birth among nonobese black and white women. Obstetrics and Gynecology 85(6): 909-914. Hopkinson J. M., N. F. Butte, K. J. Ellis, W. W. Wong, M. R. Puyau and E. O. Smith. 1997. Body fat estimation in late pregnancy and early postpartum: comparison of two-, three-, and four-component models. American Journal of Clinical Nutrition 65(2): 432-438. Hull H. R., M. K. Dinger, A. W. Knehans, D. M. Thompson and D. A. Fields. 2008. Impact of maternal body mass index on neonate birthweight and body composition. American Journal of Obstetrics and Gynecology 198(4): 416 e411-e416. Hytten F. and G. Chamberlain. 1991. Clinical Physiology in Obstetrics. Oxford: Blackwell Scientific Publications. Ibanez L., G. Sebastiani, A. Lopez-Bermejo, M. Diaz, M. D. Gomez-Roig and F. de Zegher. 2008. Gender specificity of body adiposity and circulating adiponectin, visfatin, insulin, and insulin growth factor-I at term birth: relation to prenatal growth. Journal of Clinical Endocrinology and Metabolism 93(7): 2774-2778. IOM (Institute of Medicine). 1990. Nutrition During Pregnancy. Washington, DC: National Academy Press. Kalhan S. C. 2000. Protein metabolism in pregnancy. American Journal of Clinical Nutrition 71(5 Suppl): 1249S-1255S. Kalkhoff R. K. 1982. Metabolic effects of progesterone. American Journal of Obstetrics and Gynecology 142(6 Pt 2): 735-738. Kalkhoff R., A. Kissebah and H. Kim. 1979. Carbohydrate and lipid metabolism during nor- mal pregnancy: relationship to gestational hormone action. In The Diabetic Pregnancy: A Perinatal Perspectie. I. Merkatz and P. Adam. New York: Grune & Straton; pp. 3-21. Kiel D. W., E. A. Dodson, R. Artal, T. K. Boehmer and T. L. Leet. 2007. Gestational weight gain and pregnancy outcomes in obese women: how much is enough? Obstetrics and Gynecology 110(4): 752-758. Kierans W. J., K. S. Joseph, Z. C. Luo, R. Platt, R. Wilkins and M. S. Kramer. 2008. Does one size fit all? The case for ethnic-specific standards of fetal growth. BMC Pregnancy and Childbirth 8(1): 1. King J. C., D. H. Calloway and S. Margen. 1973. Nitrogen retention, total body 40 K and weight gain in teenage pregnant girls. Journal of Nutrition 103(5): 772-785. Kirwan J. P., S. Hauguel-De Mouzon, J. Lepercq, J. C. Challier, L. Huston-Presley, J. E. Friedman, S. C. Kalhan and P. M. Catalano. 2002. TNF-alpha is a predictor of insulin resistance in human pregnancy. Diabetes 51(7): 2207-2213. Klebanoff M. A., B. R. Mednick, C. Schulsinger, N. J. Secher and P. H. Shiono. 1998. Father’s effect on infant birth weight. American Journal of Obstetrics and Gynecology 178(5): 1022-1026. Koo W. W., J. C. Walters and E. M. Hockman. 2000. Body composition in human infants at birth and postnatally. Journal of Nutrition 130(9): 2188-2194. Kühl C. 1991. Aetiology of gestational diabetes. Baillieres Clinical Obstetrics and Gynaecol- ogy 5(2): 279-292. Langhoff-Roos J., G. Lindmark and M. Gebre-Medhin. 1987. Maternal fat stores and fat ac- cretion during pregnancy in relation to infant birthweight. British Journal of Obstetrics and Gynaecology 94(12): 1170-1177.

OCR for page 71
0 WEIGHT GAIN DURING PREGNANCY Lantz M. E., R. A. Chez, A. Rodriguez and K. B. Porter. 1996. Maternal weight gain pat- terns and birth weight outcome in twin gestation. Obstetrics and Gynecology 87(4): 551-556. Larciprete G., H. Valensise, B. Vasapollo, F. Altomare, R. Sorge, B. Casalino, A. De Lorenzo and D. Arduini. 2003. Body composition during normal pregnancy: reference ranges. Acta Diabetologica 40(Suppl 1): S225-S232. Lederman S. A., A. Paxton, S. B. Heymsfield, J. Wang, J. Thornton and R. N. Pierson, Jr. 1997. Body fat and water changes during pregnancy in women with different body weight and weight gain. Obstetrics and Gynecology 90(4 Pt 1): 483-488. Lesser K. B. and M. W. Carpenter. 1994. Metabolic changes associated with normal preg- nancy and pregnancy complicated by diabetes mellitus. Seminars in Perinatology 18(5): 399-406. Leturque A., S. Hauguel, M. T. Sutter Dub, P. Maulard and J. Girard. 1989. Effects of placen- tal lactogen and progesterone on insulin stimulated glucose metabolism in rat muscles in vitro. Diabetes & Metabolism 15(4): 176-181. Lindsay C. A., A. J. Thomas and P. M. Catalano. 1997. The effect of smoking tobacco on neonatal body composition. American Journal of Obstetrics and Gynecology 177(5): 1124-1128. Luke B. 1998. What is the influence of maternal weight gain on the fetal growth of twins? Clinical Obstetrics and Gynecology 41(1): 56-64. Luke B., J. Minogue and H. Abbey. 1992. The association between maternal weight gain and the birth weight of twins. The Journal of Maternal-Fetal Medicine 1: 267-276. Luke B., E. Bryan, C. Sweetland, S. Leurgans and L. Keith. 1995. Prenatal weight gain and the birthweight of triplets. Acta Geneticae Medicae et Gemellologiae 44(2): 93-101. Luke B., B. Gillespie, S. J. Min, M. Avni, F. R. Witter and M. J. O’Sullivan. 1997. Critical periods of maternal weight gain: effect on twin birth weight. American Journal of Ob- stetrics and Gynecology 177(5): 1055-1062. Luke B., S. J. Min, B. Gillespie, M. Avni, F. R. Witter, R. B. Newman, J. G. Mauldin, F. A. Salman and M. J. O’Sullivan. 1998. The importance of early weight gain in the intrauter- ine growth and birth weight of twins. American Journal of Obstetrics and Gynecology 179(5): 1155-1161. Luke B., M. L. Hediger, C. Nugent, R. B. Newman, J. G. Mauldin, F. R. Witter and M. J. O’Sullivan. 2003. Body mass index—specific weight gains associated with optimal birth weights in twin pregnancies. Journal of Reproductie Medicine 48(4): 217-224. MacLaughlin S. M., S. K. Walker, C. T. Roberts, D. O. Kleemann and I. C. McMillen. 2005. Periconceptional nutrition and the relationship between maternal body weight changes in the periconceptional period and feto-placental growth in the sheep. The Journal of Physiology 565(Pt 1): 111-124. Mardones-Santander F., G. Salazar, P. Rosso and L. Villarroel. 1998. Maternal body composi- tion near term and birth weight. Obstetrics and Gynecology 91(6): 873-877. Marseille-Tremblay C., M. Ethier-Chiasson, J. C. Forest, Y. Giguere, A. Masse, C. Mounier and J. Lafond. 2008. Impact of maternal circulating cholesterol and gestational diabetes mellitus on lipid metabolism in human term placenta. Molecular Reproduction and Deelopment 75(6): 1054-1062. Metzger B. E., V. Ravnikar, R. A. Vileisis and N. Freinkel. 1982. “Accelerated starvation” and the skipped breakfast in late normal pregnancy. Lancet 1(8272): 588-592. Min S. J., B. Luke, B. Gillespie, L. Min, R. B. Newman, J. G. Mauldin, F. R. Witter, F. A. Salman and M. J. O’Sullivan. 2000. Birth weight references for twins. American Journal of Obstetrics and Gynecology 182(5): 1250-1257. Mitchell M., D. T. Armstrong, R. L. Robker and R. J. Norman. 2005. Adipokines: implica- tions for female fertility and obesity. Reproduction 130(5): 583-597.

OCR for page 71
0 COMPOSITION AND COMPONENTS OF GESTATIONAL WEIGHT GAIN Molteni R. A., S. J. Stys and F. C. Battaglia. 1978. Relationship of fetal and placental weight in human beings: fetal/placental weight ratios at various gestational ages and birth weight distributions. Journal of Reproductie Medicine 21(5): 327-334. Nohr E. A., B. H. Bech, M. Vaeth, K. M. Rasmussen, T. B. Henriksen and J. Olsen. 2007. Obesity, gestational weight gain and preterm birth: a study within the Danish National Birth Cohort. Paediatric and Perinatal Epidemiology 21(1): 5-14. Oken E., K. P. Kleinman, J. Rich-Edwards and M. W. Gillman. 2003. A nearly continuous measure of birth weight for gestational age using a United States national reference. BMC Pediatrics 3: 6. Okereke N. C., L. Huston-Presley, S. B. Amini, S. Kalhan and P. M. Catalano. 2004. Lon- gitudinal changes in energy expenditure and body composition in obese women with normal and impaired glucose tolerance. American Journal of Physiology Endocrinology and Metabolism 287(3): E472-E479. Orskou J., U. Kesmodel, T. B. Henriksen and N. J. Secher. 2001. An increasing proportion of infants weigh more than 4000 grams at birth. Acta Obstetricia et Gynecologica Scandi- naica 80(10): 931-936. Pasqualini J. R. 2005. Enzymes involved in the formation and transformation of steroid hormones in the fetal and placental compartments. Journal of Steroid Biochemistry and Molecular Biology 97(5): 401-415. Pinar H., M. Stephens, D. B. Singer, T. K. Boyd, S. M. Pflueger, D. L. Gang, D. J. Roberts and C. J. Sung. 2002. Triplet placentas: reference values for weights. Pediatric and Deelop- mental Pathology 5(5): 495-498. Pipe N. G., T. Smith, D. Halliday, C. J. Edmonds, C. Williams and T. M. Coltart. 1979. Changes in fat, fat-free mass and body water in human normal pregnancy. British Journal of Obstetrics and Gynaecology 86(12): 929-940. Pitkin R. M. 1976. Nutritional support in obstetrics and gynecology. Clinical Obstetrics and Gynecology 19(3): 489-513. Ross M. G. and R. A. Brace. 2001. National Institute of Child Health and Development Conference summary: amniotic fluid biology—basic and clinical aspects. Journal of Maternal-Fetal Medicine 10(1): 2-19. Rosso P. 1990. Nutrition and Metabolism in Pregnancy: Mother and Fetus. New York: Oxford University Press. Rovere-Querini P., M. T. Castiglioni, M. G. Sabbadini and A. A. Manfredi. 2007. Signals of cell death and tissue turnover during physiological pregnancy, pre-eclampsia, and autoim- munity. Autoimmunity 40(4): 290-294. Ryan E. A. and L. Enns. 1988. Role of gestational hormones in the induction of insulin resis- tance. Journal of Clinical Endocrinology and Metabolism 67(2): 341-347. Ryan E. A., M. J. O’Sullivan and J. S. Skyler. 1985. Insulin action during pregnancy. Studies with the euglycemic clamp technique. Diabetes 34(4): 380-389. Sewell M. F., L. Huston-Presley, D. M. Super and P. Catalano. 2006. Increased neonatal fat mass, not lean body mass, is associated with maternal obesity. American Journal of Obstetrics and Gynecology 195(4): 1100-1103. Siega-Riz A. M., L. S. Adair and C. J. Hobel. 1996. Maternal underweight status and inad- equate rate of weight gain during the third trimester of pregnancy increases the risk of preterm delivery. Journal of Nutrition 126(1): 146-153. Sohlstrom A. and E. Forsum. 1995. Changes in adipose tissue volume and distribution during reproduction in Swedish women as assessed by magnetic resonance imaging. American Journal of Clinical Nutrition 61(2): 287-295. Spady D. W. 1989. Normal body composition of infants and children. In Report of the th Ross Conference on Pediatric Research. Body composition measurements in infants and children, Ross Laboratories; p. 67.

OCR for page 71
0 WEIGHT GAIN DURING PREGNANCY Sparks J. W. 1984. Human intrauterine growth and nutrient accretion. Seminars in Perinatol- ogy 8(2): 74-93. Stevens-Simon C., E. R. McAnarney, K. J. Roghmann and G. B. Forbes. 1997. Composition of gestational weight gain in adolescent pregnancy. Journal of Maternal-Fetal Medicine 6(2): 79-86. Stewart M. O., P. G. Whittaker, B. Persson, U. Hanson and T. Lind. 1989. A longitudinal study of circulating progesterone, oestradiol, hCG and hPL during pregnancy in type 1 diabetic mothers. British Journal of Obstetrics and Gynaecology 96(4): 415-423. Surkan P. J., C. C. Hsieh, A. L. Johansson, P. W. Dickman and S. Cnattingius. 2004. Reasons for increasing trends in large for gestational age births. Obstetrics and Gynecology 104(4): 720-726. Swanson L. D. and C. Bewtra. 2008. Increase in normal placental weights related to increase in maternal body mass index. Journal of Maternal-Fetal & Neonatal Medicine 21(2): 111-113. Taggart N. R., R. M. Holliday, W. Z. Billewicz, F. E. Hytten and A. M. Thomson. 1967. Changes in skinfolds during pregnancy. British Journal of Nutrition 21(2): 439-451. Teasdale F. 1980. Gestational changes in the functional structure of the human placenta in relation to fetal growth: a morphometric study. American Journal of Obstetrics and Gynecology 137(5): 560-568. Thame M., C. Osmond, F. Bennett, R. Wilks and T. Forrester. 2004. Fetal growth is directly related to maternal anthropometry and placental volume. European Journal of Clinical Nutrition 58(6): 894-900. Thomas P., J. Peabody, V. Turnier and R. H. Clark. 2000. A new look at intrauterine growth and the impact of race, altitude, and gender. Pediatrics 106(2): E21. van Raaij J. M., M. E. Peek, S. H. Vermaat-Miedema, C. M. Schonk and J. G. Hautvast. 1988. New equations for estimating body fat mass in pregnancy from body density or total body water. American Journal of Clinical Nutrition 48(1): 24-29. Villamor E., R. Gofin and B. Adler. 1998. Maternal anthropometry and pregnancy outcome among Jerusalem women. Annals of Human Biology 25(4): 331-343. Weiner C. P., R. E. Sabbagha, N. Vaisrub and R. Depp. 1985. A hypothetical model suggesting suboptimal intrauterine growth in infants delivered preterm. Obstetrics and Gynecology 65(3): 323-326. Widdowson E. M. 1950. Chemical composition of newly born mammals. Nature 166(4224): 626-628. Widdowson E. M. and C. M. Spray. 1951. Chemical development in utero. Archies of Disease in Childhood 26(127): 205-214. Xiang A. H., M. Kawakubo, T. A. Buchanan and S. L. Kjos. 2007. A longitudinal study of lipids and blood pressure in relation to method of contraception in Latino women with prior gestational diabetes mellitus. Diabetes Care 30(8): 1952-1958. Xu H., G. T. Barnes, Q. Yang, G. Tan, D. Yang, C. J. Chou, J. Sole, A. Nichols, J. S. Ross, L. A. Tartaglia and H. Chen. 2003. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. Journal of Clinical Inestigation 112(12): 1821-1830. Yeh J. and J. A. Shelton. 2007. Association of pre-pregnancy maternal body mass and maternal weight gain to newborn outcomes in twin pregnancies. Acta Obstetricia et Gynecologica Scandinaica 86(9): 1051-1057.