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 27
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
OCR for page 28
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
OCR for page 29
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
OCR for page 30
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
OCR for page 31
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
OCR for page 32
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.
OCR for page 33
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,
OCR for page 34
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
OCR for page 35
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.
OCR for page 36
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.
Representative terms from entire chapter:
gestational weight
