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Introduction Efforts to improve maternal and fetal nutrition during pregnancy have focused on achieving appropriate energy intake and ensuring that the intake of specific nutrients is adequate to meet maternal and fetal requirements. Although the need for appropriate weight gain during pregnancy has long been recognized, clinical and public health recommendations for weight gain have changed over the years as new data have become available. In the 1940s and l950s it was standard practice in the United States to restrict weight gain during pregnancy to less than 9 kg (20 lb), with the intent of reducing the risk of toxemia and of birth complications that were believed to occur more often with larger babies. In 1967, the Food and Nutrition Board's (FNB's) Committee on Maternal Nutrition referred to a 10.9-kg (24-lb) average weight gain for pregnant women in the United States in Nutrition in Pregnancy and Lactation (NRC, 1967), a report trans- mitted to the Children's Bureau of the Department of Health, Education, and Welfare. Following publication of results from the Collaborative Peri- natal Project (Eastman and Jackson, 1968), there was increased awareness that mothers who gained less than 9 kg had smaller babies who had poorer chances for survival. Shortly thereafter, the FNB's Committee on Mater- nal Nutrition completed a more comprehensive report entitled Maternal Nutrition During the Course of Pregnancy (NRC, 1970a), which reviewed problems, practices, and research bearing on the relation between nutrition and the course and outcome of pregnancy and provided recommendations for weight gain and intake of certain nutrients. That volume, along with 27

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28 NUTRITIONAL STATUS AND WEIGHT GAIN its companion Summary Report (NRC, 1970b), had a major impact on the medical and nutrition community. Since publication of the 1970 report, a number of studies have shown that desirable weight gain during pregnancy varies as a function of prepreg- nancy weight for height (Abrams and Laros, 1986; Miller and Merritt, 1979; Naeye, 1979, 1981; Peckham and Christianson, 1971; Winikoff and Debrovner, 1981~. In particular, the evidence suggests that in order to achieve optimal fetal growth, women with inadequate prepregnancy weight for height may need to gain more weight during pregnancy and that women who are overweight prior to pregnancy may not need to gain as much (Borberg et al., 198~, Brown, 1988; Brown et al., 1981; Campbell, 1983; Edwards et al., 1978; Gormican et al., 1980; Harrison et al., 1980~. In light of these new data, it has been suggested that recommendations for nutri- tional guidelines during pregnancy should be revised to take prepregnangy nutritional status into account (Koops et al., 1982; Rosso, 1985~. In considering the relationship between gestational weight gain and pregnancy outcome, attention has centered on birth weight. One reason for this is that birth weight is the pregnancy outcome most frequently examined in epidemiologic studies. But a more fundamental justification for the emphasis on birth weight is its widely recognized association with infant mortality and morbidity. The United States has lagged behind a number of other developed countries in reducing infant mortality, despite recent advances in perinatal intensive care and marked improvements in birth weight-specific mortality rates (McCormick, 1985; Wegman, 1988~. The lag appears to be related to an unfavorable birth weight distribution and, in particular, a high proportion of infants with low (<2,500 g) and very low (<1,500 g) birth weights, particularly among blacks (Kessel et al., 1984; Kleinman and Kessel, 1987~. Although in the United States most neonatal deaths (which account for most deaths in the first year of life) are related to preterm birth (i.e., <37 weeks of gestation), and although the effects of gestational weight gain on fetal growth are better documented than those on length of gestation (see Chapter 8), a shift in the distribution of birth weight for gestational age would nonetheless lead to some reduction in perinatal deaths (Prentice et al., 1988; Sappenfield et al., 1987~. The specific task assigned to the Subcommittee on Nutritional Status and Weight Gain During Pregnancy was to "evaluate and document the current scientific evidence and formulate recommendations for desirable weight gain during pregnancy." The subcommittee was asked to consider several issues in its deliberations and report, including the effect of prepreg- nancy nutritional status on overall weight gain and the patterns of weight gain, the effect of dietary intake during pregnancy on overall weight gain and patterns of weight gain, and the relative advantages and disadvantages

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INTRODUCTION Factor A 29 1 1 Factor D ~ Causal influence Factor B Factor E _ Modification of effect indicated by arrow on which it abuts Statistical association (not necessarily causal or directional) between two variables Factor C FIGURE 2-1 Schematic diagram of causal paths: determinants, consequences, confounders, and effect modifiers. Factor A is a detennu~ant (cause) of Factor B. which, therefore, is a consequence (effect) of Factor ~ Factor B is a determinant of Factor C Therefore Factor A is also a determinant of Factor C. Factor B can be called a mediating variable by which Factor A causes Factor C. Alternatively, Factor A is sometimes referred to as an indirect determinant of Factor C, whereas Factor B is a direct determinant. Factor D is a confounding variable (confounder) in the relationship between Factors B and C, i.e., it biases (increases or decreases) the apparent effect of Factor B on Factor C. Because of this bias, the true effect of Factor B on Factor C is actually different from (less or more than) the apparent effect. Note that Factor B does not confound the relationship between Factors A and C, since it lies on the causal path between the two (see text). Factor E is an effect modifier in the relationship between Factors B and C, i.e., it modifies (increases or decreases) the true effect of Factor B on Factor C. Of various anthropometric methods for assessing nutritional status during pregnancy. In addition to the specific request to consider special recom- mendations for women with different prepregnancy nutritional statuses, the subcommittee was also asked to consider differential recommendations according to age and ethnic background, in particular the needs of preg- nant adolescents; women over age 35; and women of black, Hispanic, and Southeast Asian origin. The section that follows concerns the relationships among maternal factors, nutritional intervention, gestational weight gain, and maternal and child health in healthy women in a developed country (especially the United States). Standard epidemiologic terms and concepts are used to charac- terize these relationships (particularly as they relate to cause and effect) by making frequent reference to determinants, consequences, confounders, and effect modifiers. These concepts are illustrated in Figure 2-1. Determinants are causal (etiologic) factors; consequences are the health outcomes caused by those determinants. The health outcomes considered

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30 NUTRITIONAL STATUS AND WEIGHT GAIN in this report all have multifactorial etiologies; thus, no single factor is a sufficient cause of any of these outcomes. (The use of the word determinant, therefore, does not imply that a given factor automatically determines the outcome.) A given factor can be both a consequence of a factor that precedes it and a determinant of a factor that succeeds it (e.g., Factor B in Figure 2-1~. Thus, gestational weight gain can be a consequence of energy intake during pregnancy and a determinant of fetal growth. The term mediating variable is sometimes used to indicate a factor that, like gestational weight gain, lies on the causal path between a preceding determinant (energy intake) and a subsequent consequence (fetal growth). Another way of expressing the same idea is to refer to a determinant (weight gain) immediately preceding a given consequence (fetal growth) as a direct determinant, and to an earlier factor on the causal path (energy intake) as an indirect determinant. A confounding variable (confounder) distorts (biases up or down) the apparent relationship between an exposure (putative determinant) and outcome (putative consequence) under study; i.e., it makes the relationship appear stronger or weaker than it really is. This factor must fulfill three criteria: . It must itself be a determinant of the outcome. It must be associated (without implying causality or directionality) with the exposure. . It must not lie on the causal path between exposure and outcome. As an example, energy intake is likely to confound the apparent relationship between maternal anemia and fetal growth. Women with low energy intake are also likely to have low iron intake. Energy intake is a likely determinant of fetal growth, but does not lie on the causal path between maternal anemia or iron status and fetal growth. Gestational weight gain does not confound the relationship between energy intake and fetal growth, even though it is associated with energy intake and is a determinant of fetal growth, because it lies on the causal path between the two. An elect modifier is a factor that modifies (i.e., increases or decreases) the magnitude of the effect of a determinant on a particular consequence. Factor E in Figure 2-1 alters the degree to which Factor B affects Factor C. Thus, despite the apparent simplicity suggested by the causal arrow from Factor B to Factor C, the magnitude and perhaps even the existence of the causal effect depend on Factor E. Effect modifiers do not cause bias per se, but failure to consider effect modification by reporting only an overall effect can be extremely misleading. For example, if large weight gains were beneficial for thin women but deleterious for overweight women, there might not be a net effect in women examined overall. But this

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INTRODUCTION 31 would hide the fact that there are important (and opposite) effects in the two subgroups. Unlike confounders, effect modifiers may have no association with either exposure (determinant) or outcome (consequence). The principal effect modifiers under consideration by the subcommittee are those that may alter the impact of gestational weight gain on pregnancy outcome: prepregnancy weight for height, age, and ethnic origin. Figure 2-2 summarizes the potential determinants, consequences, and effect modifiers of gestational weight gain. Figure 2-3 presents the factors explicitly addressed in this report. It is essential to consider the deter- minants of gestational weight gain, because clinicians and public health policymakers cannot intervene directly to influence maternal weight gain during pregnancy. Nor do changing maternal attitudes have a direct impact on gestational weight gain, whether they arise from alterations in public awareness that filter into the community through media reports of research findings and expert opinions or from more formal health education efforts. Instead, interventions and attitude changes should be aimed at energy in- take and expenditure. The resultant changes in energy balance would affect gestational weight gain. The consequences of physical activity and energy expenditure during pregnancy were reviewed by another FNB committee (IOM, 1989~. The present report focuses on the intake component. The recommendations in Part I are intended to be used by clinicians in advis- ing their patients on energy intake and gestational weight gain; by those involved in planning and implementing health education, counseling, and supplementation programs for pregnant women; and by those who deliver health messages to the general public, thereby increasing awareness and reshaping attitudes. To gain an understanding of the consequences of different gestational weight gains for both mother and fetus, it is important to separate nutri- tional and nonnutritional contributions. As discussed in greater detail in subsequent chapters, many of the studies in this area have not distinguished changes in fat stores or lean body mass from weight increases as a result of increases in the size of the fetus, placenta, and amniotic fluid, on the one hand, or from increases in the size of the maternal breast and uterus and in plasma volume and extravascular body water, on the other. Ideally, in examining the maternal and child health consequences of different ges- tational weight gains, distinctions in components of weight gain should be considered. As indicated above, the term consequence implies causality. Any as- sociation between gestational weight gain and subsequent maternal and child health outcomes will be most important to the extent that gestational weight gain is a cause of those outcomes. Any clinical or public health interventions to affect gestational weight gain will be ineffective in improv- ing maternal and child health outcomes if the associations between weight

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32 NUTRITIONAL STATUS AND WEIGHT GAIN MATERNAL FACTORS Sociodemographic (age, parity, ethnic background, socioeconomic status) Nutritional (body mass index or relative weight, height, lean body mass body fat) Genetic (other than height and ethnic background) Health/illness (diabetes, hypertension, chronic disease, systemic or genital tract infection) Environmental (geography, climate) Behavioral (attitudes; stress/anxiety; cigarette, alcohol, and illicit drug use) Prenatal care NUTRITIONAL INTERVENTIONS ~:ner ;~~nel 9Y I . Intake _ Balance Expenditure Nutritional counseling, supplementation _ Health education _ , GESTATIONAL WEIGHT GAIN (OVERALL AND PATTERN) Mother Lean body mass Fat Plasma volume Extravascular body water Breasts Uterus Products of Conception Fetus Placenta Amniotic fluid -11 1 ~. SHORT-TERM HEALTH OUTCOMES F Mother Mortality Complications of pregnancy, labor, and delivery Postpartum nutritional status Lactation performance Fetus, Child Fetal growth (birth weight, length, head circumference) Gestational duration Spontaneous abortion Congenital anomalies Condition at birth Mortality and morbidity _ 1 ~ , l l LONGER-TERM HEALTH OUTCOMES POSTNATAL (CHILD) FACTORS Mother Child Nutritional intake Nutritional status Mortality Living conditions Fecundity Morbidity _ Environmental stimulation, Chronic disease Growth education Performance l indicates possible causal influences, I denotes possible modification of effect indicated by arrow on which it abuts FIGURE 2-2 Schematic summary of potential determinants, consequences, and effect modifiers for gestational weight gain.

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INTRODUCTION ~IFIENTIONS _1 Nutritional counseling, supplementation ~ L Health education 33 MATERNAL FACTORS Nutritional (body mass index or relative weight, height, lean body mass body fat) Sociodemographic ( age, parity, ethnic background, socioeconomic status) Behavioral (attitudes, cigarettes, alcohol) 1 Intake _~;= _ ~ L~! ~ GESTATIONAL WEIGHT GAIN (OVERALL AND PATTERN) . Mother Products of Conception Lean body mass Fetus Fat Total body water SHORT-TERM HEALTH OUTCOMES Mother Mortality Complications of pregnancy, labor, and delivery Lactation performance Obesity . 1~ Fetus, Child Mortality Fetal growth (birth weight, length, head circumference) Gestational duration Spontaneous abortion Congenital anomalies LONGER-TERM HEALTH OUTCOMES Mother Obesity Child Somatic growth Neurocognitive development denotes possible modification of effect indicates possible causal influences, I indicated by arrow on which it abuts FIGURE 2-3 Determinants, consequences, and effect modifiers discussed in this report. gain and those outcomes are noncausal (or if the direction of causality is reversed). The elements used by the subcommittee to assess the epi- demiologic evidence for causality are based on the report of the Surgeon General's Advisory Committee on Smoking and Health (D HEW, 1964), and on the work of Hill (1965) and Susser (1973, 1988~. These elements include the strength, biologic gradient (dose-response effect), lack of bias,

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34 NUTRITIONAL STATUS AND WEIGHT GAIN statistical significance, specificity, consistency, and biologic plausibility and coherence of the association. In emphasizing gestational weight gain as a potential cause of maternal and fetal outcomes, the subcommittee in no way wishes to impugn its potential value as a marker of risk for adverse pregnancy outcome. For example, women with low gestational weight gain could be targeted for an intervention aimed at a modifiable causal determinant, e.g., cigarette smoking. Unfortunately, there are no data demonstrating the efficacy of this type of approach. Moreover, detailed consideration of interventions that do not have either a direct or indirect impact on gestational weight gain lies outside the mandate of the subcommittee. The subcommittee has given considerable thought to the problem of reverse causality (discussed in greater detail in Chapter 10~. A larger fetus and placenta and a greater volume of amniotic fluid will obviously lead to a larger maternal weight gain. It may even be that faster-growing fetuses provide a greater physiologic stimulus to increase maternal plasma and extracellular fluid volume. Another obvious, but surprisingly unappreci- ated, source of reverse causality is the effect of gestational age. Shorter pregnancies are, of course, associated with smaller total gestational weight gains. This does not necessarily indicate, however, that decreased total weight gain is a cause of shortened gestation. As discussed in Chapters 4 and 8, basing analyses on the rate of weight gain (e.g., grams of weight gained per week) is one way of adjusting for length of gestation. It is important to distinguish short-term maternal and child outcomes from longer-term outcomes. Both may be worthy of consideration, but such short-term outcomes as early postpartum maternal nutritional status and birth weight are potentially less serious than longer-term maternal nutritional status and child morbidity, growth, and performance. Despite the importance the subcommittee attaches to these longer-term outcomes, however, the majority of the epidemiologic evidence concerning the erects of gestational weight gain bears on birth weight and fetal growth. The following nine chapters are based on the concepts summarized above. Chapter 3 provides a historical background, including secular trends in gestational weight gain, prepregnancy nutritional status, age at menarche, parity, cigarette smoking, birth weight, gestational age, and utilization of prenatal care and supplementation programs. Chapter 3 also contains a history of recommendations regarding weight gain and energy intake. Chapter 4 focuses on definitions and methodologic issues in the assessment of maternal weight gain and body composition in the clinical, research, and surveillance settings. In Chapter 5, the subcommittee describes total weight gain and the pattern of weight gain over the course of pregnancy. It also examines

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INTRODUCTION 35 physiologic and maternal determinants of gestational weight gain, includ- ing prepregnancy nutritional status, age, ethnic origin, cigarette smoking, parity, alcohol consumption, marital status, and work and physical activ- ity. Chapter 6 summarizes knowledge about changes in body composition during pregnancy, including alterations in body fat, lean tissue, and body water. Energy requirements during pregnancy and the relationship between energy intake and gestational weight gain are considered in Chapter 7. In Chapter 8, the subcommittee reviews the evidence concerning the mater- nal and child health consequences of variations in gestational weight gain, including fetal/infant mortality, fetal growth, gestational duration, spon- taneous abortion, congenital anomalies, maternal mortality, complications of pregnancy, lactation performance, and maternal obesity. Chapter 9 is a summary of the literature bearing on weight gain in twin gestations, including its description, determinants, and consequences. Chapter 10 relates the material covered in Chapters 3 through 9 to the causal links in the overall conceptualization shown in Figure 2-3, with an emphasis on feasible interventions and their likely impact on short- and long-term maternal and child health. Chapter 1 presents the conclusions and recommendations reached by the subcommittee as a result of its research and deliberation. REFERENCES Abrams, B.F., and R.K Laros, Jr. 1986. Prepregnan~y weight, weight gain, and birth weight. Am. J. Obstet. Gynecol. 154:503-509. Borberg, C., M.D.G. Gillmer, EJ. Brunner, PJ. Gunn, N.W. Oakley, and R.W. Beard. 1980. Obesity in pregnancy: the effect of dietary advice. Diabetes Care 3:476481. Brown, J.E. 1988. Weight gain during pregnancy: what is "optimal"? Clin. Nutr. 7:181-190. Brown, J.E.. H.N. Jacobson, L-H. Askue, and M.G. Peick. 1981. Influence of pregnancy ~ 7 _ . _ weight gain on the size of infants born to underweight women. obstet. tiynecol. 57:13-17. Campbell, D.M. 1983. Dietary restriction in obesity and its effect on neonatal outcome. Pp. 243-250 in Nutrition in Pregnancy: Proceedings of the Tenth Study Group in the Royal College of Obstetricians and Gynaecologists, September, 1982. The Royal College of Obstetricians and Gynaecologists, London. DHEW (Department of Health, Education, and Welfare). 1964. Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public Health Service. PHS Publ. No. 1103. Public Health Service, U.S. Department of Health Education, and Welfare. U.S. Government Printing Office, Washington, D.C 387 pp. Eastman, NJ., and E. Jackson. 1968. Weight relationships in pregnancy: I. The bearing of maternal weight gain and pre-pregnangy weight on birth weight in full term pregnancies. Obstet. Gynecol. Surv. 23:1003-1025. Edwards, L.E., W.F. Dickes, I.R. Alton, and E.Y. Hakanson. 1978. Pregnancy in the massively obese: course, outcome, and obesity prognosis of the infant. Am. J. Obstet. Gynecol. 131:479-483. Gormican, A, J. Valentine, and E. Satter. 1980. Relationships of maternal weight gain, prepregnangy weight, and infant birthweight. Interaction of weight factors in pregnancy. J. Am. Diet. Assoc. 77:662-667.

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36 NUTR1IIONAL STATUS AND WEIGHT GAIN Harrison, G.G., J.N. Udall, and G. Morrow III. 1980. Maternal obesity, weight gain in pregnancy, and infant birth weight. Am. J. Obstet. Gynecol. 136:411412. Hill, A.B. 1965. The environment and disease: association or causation? Proc. R. Soc. Med. 58:295-300. IOM (Institute of Medicine). 1989. The Impact of Diet and Physical Activity on Pregnancy and Lactation: Women's Work in the Developing World. Report of the Subcommittee on Diet, Physical Activity, and Pregnancy Outcome, Committee on International Nutrition Programs, Food and Nutrition Board. Report transmitted to the Office of Nutrition, Bureau for Science and Technology, U.S. Agency for International Development, Washington, D.C. 129 pp. Kessel, S.S., J. Villar, H.W Berendes, and R.P. Nugent. 1984. The changing pattern of low birth weight in the United States: 1970 to 1980. J. Am. Med. Assoc. 251:1978-1982. Kleinman, J.C., and S.S. Kessel. 1987. Racial differences in low birth weight: trends and risk factors. N. Engl. J. Med. 317:749-753. Koops, B.L^, IN. Morgan, and F.C. Battaglia. 1982. Neonatal mortality risk in relation to birth weight and gestational age: update. J. Pediatr. 101:969-977. McCormick, M.C. 1985. The contribution of low birth weight to infant mortality and childhood morbidity. N. Engl. J. Med. 312:82-90. Miller, H.C., and T.A. Merritt. 1979. Fetal Growth in Humans. Year Book Medical Publishers, Chicago. 180 pp. Naeye, R.L" 1979. Weight gain and the outcome of pregnancy. Am. J. Obstet. Gynecol. 135:3-9. Naeye, R.L. 1981. Maternal nutrition and pregnancy outcome. Pp. 89-111 in J. Dobbing, ed. Maternal Nutrition in Pregnancy: Eating for l~o? Academic Press, London. NRC (National Research Council). 1967. Nutrition in Pregnancy and Lactation. Report of the Committee on Maternal Nutrition, Food and Nutrition Board. National Academy of Sciences, Washington, D.C. 67 pp. NRC (National Research Council). 1970a. Maternal Nutrition and the Course of Pregnancy. Report of the Committee on Maternal Nutntion, Food and Nutrition Board. National Academy of Sciences, Washington, D.C. 241 pp. NRC (National Research Council). 1970b. Maternal Nutrition and the Course of Pregnancr: Summa~y Report. Report of the Committee on Maternal Nutrition, Food and Nutrition Board. National Academy of Sciences, Washington, D.C. 23 pp. Peckham, C H., and R.E. Christianson. 1971. The relationship between prepregnangy weight and certain obstetric factors. Am. J. Obstet. Gynecol. 111:1-7. Prentice, AM., T.J. Cole, and R.G. Whitehead. 1988. Food supplementation in pregnant women. Eur. J. Clin. Nutr. 42:87-91. Rosso, P. 1985. A new chart to monitor weight gain during pregnancy. Am. J. Clin. Nutr. 41:64~652. Sappenfield, W.M., J.Vi Buehler, N.J. Binkin, CJ.R. Hogue, L^T. Strauss, and J.C Smith. 1987. Di~erencies in neonatal and postneonatal mortality by race, birth weight, and gestational age. Public Health Rep. 102:182-192. Susser, M. 1973. Causal Thinking in the Health Sciences: Concepts and Strategies of Epidemiology. Oxford University Press, New York. 181 pp. Susser, M. 1988. Falsification, verification and causal inference in epidemiology: reconsid- erations in the light of Sir Karl Popper's philosophy. Pp. 33-57 in KJ. Rothman, ed. Causal Inference. Epidemiology Resources, Chestnut Hill, Mass. Wegman, M.E. 1988. Annual summary of vital statistics 1987. Pediatrics 82:817-827. W~niko~, B., and CH. Debrovner. 1981. Anthropometric determinants of birth weight. Obstet. Gynecol. 58:678-684.