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OCR for page 176
8
Effects of Gestational Weight Gain on
Outcome in Singleton Pregnancies
The subcommittee reviewed the evidence concerning the effects of
gestational weight gain on short-term fetal, infant, and maternal health
outcomes, as well as maternal factors that could modify those effects. The
following outcomes were considered: fetal and neonatal mortality, fetal
growth, gestational duration, spontaneous abortion (miscarriage), congen-
ital anomalies, maternal mortality, complications of pregnancy, lactation
performance, and postpartum obesity. The concepts and terms illustrated
in Figure 2-1 were used to analyze and review published studies of human
populations bearing on these potential consequences of maternal weight
gain. Particular attention was given to controlling for other maternal
factors that could confound the relationship between weight gain and preg-
nancy outcome. Animal studies were considered only when the clinical
and epidemiologic literature was too sparse or contradictory to permit rea-
sonable inferences (e.g., for lactation performance). The discussion here
is restricted to singleton pregnancies; twin pregnancies are considered in
Chapter 9.
The subcommittee focused on the links between gestational weight
gain and short-term pregnancy outcomes because data relating weight gain
to long-term outcomes are relatively scanty, and there is no strong evidence
indicating that weight gain affects long-term outcomes directly, i.e., without
first affecting shorter-term outcomes. For example, several reports (Naeye
and Chez, 1981; Singer et al., 1968; Tavris and Read, 1982) have linked
maternal weight gain to subsequent cognitive development in the offspring,
but none has shown that such effects occur independently of the effects on
176
OCR for page 177
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
25
20
CO
a)
a:
.^ 15
o
10
a)
CL
5
o
-
\
\
>135%
(Overweight) _
_ _
_ ~ 90-13
Curves Are % of Mean Prepregnancy
Weight-for-Height Values (Metropolitan)
. -
< 90%
(Underweight)
10
177
15
Pregnancy Weight Gain, kg
FIGURE ~1 Pennatal mortality as a function of maternal weight gain. From Naeye (1979)
with permission.
fetal (including brain) growth. The long-term child health consequences
of preterm birth and intrauterine growth retardation (IUGR) are reviewed
briefly later in this chapter. Links between other short-term and longer-
term outcomes for both mothers and children (see Figure 2-3) are discussed
in Chapter 10, along with other general issues regarding the entire causal
pathway.
FETAL AND INFANT OUTCOMES
Mortality
Fetal and infant mortality rates have been used extensively to track
progress in improving infant health and, indeed, to reflect the overall health
status of the nation. Because these rates are quite low (approximately 1%),
however, very large numbers of births are required to study the relationship
between weight gain and fetal and infant deaths. Thus, few such studies
have been conducted. No exceptions are the Collaborative Perinatal
Project (Naeye, 1979) and a National Center for Health Statistics (NCHS)
study linking data from the 1980 National Fetal Mortality Survey and the
1980 National Natality SuIvey (duffel, 1986).
Data from the Collaborative Perinatal Project (Figure 8-1) indicate that
the relationship between gestational weight gain and perinatal mortality is
strongly influenced by maternal prepregnancy nutritional status; i.e., there
is evidence for important effect modification (see Chapter 2). For women
OCR for page 178
178
NUTRITIONAL STATUS AND WEIGHT GAIN
who were underweight prior to pregnancy, the greater the gestational
weight gain, the lower the perinatal mortality. However, for women with
desirable prepregnancy weight for height (based on the 1959 Metropolitan
Life Insurance Company's tables), perinatal mortality began to rise with
gestational weight gains in excess of 11.4 kg (25 lb), which might be partially
explained by a rise in the rate of high birth weight and a corresponding
increased risk for shoulder dystocia and other complications of labor and
delivery (see below). For weight gains above 6.8 to 7.3 kg, (15 to 16 lb) the
highest perinatal mortality rates occurred among overweight women (i.e.,
those with prepregnancy weights greater than 135% of standard weight for
height). Data shown in Figure 8-1 may be biased (because women who
deliver preterm infants will have had less time to gain weight, and preterm
infants are at increased risk for perinatal death). Nevertheless, other data
in the same report indicate similar trends even when gestational weight gain
was considered as a percentage of a gestational age-adjusted "optimum"
gain. According to Naeye, the effects shown were not confounded by
maternal age, parity, race, family income, number of prenatal care visits,
cigarette smoking, or prior pregnancy history.
The NCHS study (duffel, 1986) focused on late fetal deaths (>28 weeks
of gestational age). The results, stratified by gestational age (Figure 8-2),
are consistent with those from the Collaborative Perinatal Project. The
trend toward higher fetal deaths per 1,000 live births for women with lower
weight gains (below 11.8 kg, or 26 lb) was most marked among women with
low prepregnancy weights and persisted after stratification (one variable at
a time) for maternal age, education, and cigarette smoking.
Beyond this direct evidence, there is a fairly strong link between fetal
growth and mortality (see discussion below). Because of this strong rela-
tionship, it is also reasonable to assume, even in the absence of abundant
direct evidence, that any effects of gestational weight gain on intrauter-
ine growth will be reflected by corresponding, albeit smaller, effects on
mortality.
Fetal Growth
Importance of Birth Weight as a Pregnancy Outcome
Infant size at birth is a key determinant of child health, especially in
early infancy, but even beyond (see the review by McCormick, 1985~. As
shown in Figure 8-3A, for example, neonatal mortality decreases sharply
with increasing birth weight up to 2,700 or 2,800 g, declines more slowly up
to 3,500 g, is relatively flat from 3,500 to 4,250 g, and then begins to rise
slightly (Hogue et al., 1987~. A similar but less pronounced trend is seen
for postneonatal mortality (Figure 8-3B).
OCR for page 179
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
60
50
40
30
a)
CO
o 20
In
._
m
a)
._
J
lo
lo
lo
-
a)
Q
In
-
Ct
a)
CO
a)
a)
-
_
10
9
8
7
6
4
3
2
1
.
.,
i,
Under 32 weeks
32-35 weeks
36 weeks
AJI gestational periods
37-39 weeks
40 weeks and over
. 1 1 1 1
413 ~9.3
1 ~9A' ss6
Maternal Weight Gain, kg
`~5 sib\ ~67
7
179
FIGURE S-2 Fetal death ratios by maternal weight gain and period of gestation in the
United States, based on data from the 1980 National Natality and National Fetal Mortality
Surveys. From duffel (1986~.
In an attempt to identify those infants at highest risk, many researchers
and policymakers have compared infants with low birth weights (LBWs),
i.e., <2,500 g, with infants who weigh more. This dichotomy is crude but
provides striking contrasts in outcomes: compared with infants who weigh
>2,500 g, LBW babies are nearly 40 times as likely to die during the
neonatal period, and those that survive are five times as likely to die during
the postneonatal period. Of those who survive infancy, LBW babies are
OCR for page 180
18()
NUTRITIONAL STATUS AND WEIGHT GAIN
1 ,000
cn
._
m
~ 100
to
to
to
a)
Q 10
in
-
ct
o
In 1,000
o
2
in
~ 100
o
it
g
~10
a,
Q
in
Cat
~O
-a A
_ \`
I'm
V-N
All Races
Blacks
Whites
V'N
N.x
-;~
500 1,500
~ B
1 1
500 1,500
2,500 3,500 4,500
Birth Weight, 9
HI Races
- Blacks
VVhites
2,500 3,500 4,500
Birth Weight, 9
FIGURE 8-3 (A) Neonatal mortality risks By race and birth weight, United States, 1980
live birth cohort. (B) Postneonatal mortality risks by race and birth weight, United States,
neonatal survivors of 1980 live-birth cohorts. From Hogue et al. (1987).
about 50% more likely to have serious developmental problems or other
illnesses (Shapiro et al., 1980).
Further subdivisions based on birth weight have been used to refine
risk categories. For example, the LBW group is often subdivided into very
low birth weight (VLBW), i.e., <1,500 g, and moderately LBW, i.e., 1,500
to 2,499 g. The VLBW infants are at much greater risk of death and
OCR for page 181
GESTATIONAL WEIGH GAIN IN SINGLETON PREGNANCIES
181
disability than are infants in the moderately LBW group (Kleinman and
Kessel, 1987~. At the other end of the scale, high-birth-weight (>4,000 g)
infants, especially those weighing >4,500 g, are also at higher risk than
normal-weight infants (2,500 to 4,000 g) for adverse outcomes, including
mortality (but less so than for the moderately LBW group; see Figure
8-3A), meconium aspiration, clavicular fracture, brachial plexus injury, and
birth asphyxia (Boyd et al., 1983; Koff and Potter, 1939; Modanlou et al.,
1980~.
Birth weight is a composite of two outcomes: the rate of fetal growth
and gestational duration. Thus, the use of birth weight often hides more
than it reveals. For example, survival among VLBW infants with the
same birth weights is considerably higher among those who are small for
gestational age (SGA) than it is among those who have a lower gestational
age but are larger for their age (Arnold et al., 1988~.
A combined classification based on both birth weight and gestational
age provides a more discriminating basis for etiologic and prognostic distinc-
tions. It is possible to distinguish those LBW infants who are small because
they are born preterm (gestational age <37 weeks) from those with IUGR
(also referred to as SGA), which is usually defined as a birth weight below
the 10th percentile for gestational age. This definition obviously depends
on the choice of reference population.
Birth weight and gestational age have independent effects on fetal and
neonatal mortality (Erhardt et al., 1964; Hoffman et al., 1977; Koops et al.,
1982; Lubchenco et al., 1972; Yerushalmy et al., 1965~. Both IUGR and,
to a greater extent, preterm infants have an increased risk of developing
cerebral palsy (Ellenberg and Nelson, 1979~. Preterm infants (especially
those born extremely early) have a far greater risk of developing respira-
tory distress syndrome, apnea, ~ntracranial hemorrhage, seps~s, retrolental
fibroplasia, and other conditions related to physiologic immaturity.
IUGR infants appear to have increased risks of hypoglycemia, hypocal-
cemia, polycythemia, and birth asphyxia (Arora et al., 1987; Kramer et al.,
1989; Ounsted et al., 1988; Usher, 1970~. The extent to which these
neonatal complications are responsible for the increased risk of mortality
or later neurocognitive deficits (see below) is not clear. Some degree of
deficit in both stature and head circumference may persist (Babson, 1970;
Babson and Phillips, 1973; Fancourt et al., 1976; Fitzhardinge and Inwood,
1989; Fitzhardinge and Steven, 1972; Hill et al., 1984; Low et al., 1982;
Neligan et al., 1976; Ounsted and lkylor, 1971; Villa r et al., 1984; Walther,
1988; Walther and Ramaekers, 1982; Westwood et al., 1983~. Long-term
deficits in neurocognitive performance have been observed in IUGR infants
(Fitzhardinge and Steven, 1972; Neligan et al., 1976; Ounsted et al., 1984;
Rubin et al., 1973; Westwood et al., 1983; Ylitalo et al., 1988~. However,
since asphyxia is a frequent concomitant of growth retardation and studies
OCR for page 182
182
NUTRITIONAL STATUS AND WEIGHT GAIN
have not been limited to nonasphyxiated infants (Westwood et al., 1983),
the magnitude of neurocognitive deficits due to growth retardation may be
somewhat less than is generally reported.
Heterogeneity of IUGR
Several methodologic issues should be kept in mind before considering
the relationship between gestational weight gain and fetal growth. Problems
include measurement of gestational age, as discussed in Chapter 4, and
the definition of retarded fetal growth (IUGR). Growth-retarded infants
represent a highly heterogeneous group in terms of etiology, severity, and
body proportionality. A number of chromosomal and other congenital
anomalies associated with growth retardation may lead to prognoses much
worse than those for infants without those anomalies. Major congenital
anomalies affect only a small percentage of IUGR infants but account for
a disproportionate number of deaths. For example, Ounsted et al. (1981)
reported that 6.9% of the IUGR infants in their study had such anomalies
but represented 62% of the total deaths.
It would be quite surprising if two full-term infants, one weighing 2,000
g and the other weighing 2,800 g, had the same prognosis for subsequent
morbidity and mortality. Yet, follow-up studies have not subdivided their
IUGR cohorts by severity of growth retardation. Thus, little is known about
the magnitude of such prognostic distinctions.
In recent studies, IUGR infants have been subdivided according to
their body proportions, especially as defined by Rohrer's ponderal index
(birth weight divided by the length cubed). Those with low ponderal indices
are said to be d~sproporaonal (also referred to as asymmetric or wasted).
Several investigators have reported higher neonatal mortality rates among
disproportional IUGR infants (Guaschino et al., 1986; Haas et al., 1987;
Hoffman and Bakketeig, 1984), but better early catch-up growth and better
prognoses for long-term growth and development than for those among
proportional IUGR infants (Fancourt et al., 1976; Harvey et al., 1982; Hill
et al., 1984; Villar et al., 1984~. Unfortunately, most studies in this area
have not controlled for the severity of IUGR, with which disproportionality
appears to be associated (Kramer et al., 1989), nor have they ensured
accurate measurements of gestational age or controlled for confounding by
short maternal stature or the postnatal nutritional and other environmental
influences listed in Figure 2-2.
Other Methodologic Caveats
Interpretation of the literature relating gestational weight gain to fetal
growth requires adequate consideration of several other factors: problems
in measurement of length of gestation and gestational weight gain (Chapter
OCR for page 183
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
183
4), differences in components of the gain (Chapter 6), and maternal factors
that might either confound or modify the relationship (Chapter 5~.
The subcommittee emphasizes that use of total weight gain leads to
overstatements of the association between gestational weight gain and fetal
growth. That is, if the baby's weight is not subtracted from the mother's
weight gain, the association is biased by a part-whole correlation problem
(i.e., y is being correlated with x + y). Net gain avoids this problem by
subtracting the baby's weight.
Overstatements of the association of gestational weight gain and fetal
growth are also expected unless birth weight is adjusted for gestational age,
either by dividing net weight gain by the number of weeks of gestation or
by using analytic methods to adjust for the expected gain at each week of
gestation. The most appropriate measure of weight gain would be based on
serial measurements of weight gain (i.e., the pattern of weight gain) during
the course of normal pregnancies.
Effects on Birth Weight (for Gestational Age)
Despite the methodologic caveats discussed in the preceding section,
the published data concerning the effect of gestational weight gain on fetal
growth are quite convincing. Methodologically acceptable studies have
been virtually unanimous in reporting a positive relationship of gestational
weight gain with gestational age-adjusted birth weight and with the risk
for IUGR. Based on a meta-analysis (Kramer, 1987) of 61 English- and
French-language studies published between 1970 and 1984, the average
magnitude of the effect on mean birth weight in women with adequate
prepregnancy weight for height is approximately 20 g/kg of total weight
gain. The relative risk for IUGR in women with low (<7 kg, or 15 lb)
total gestational weight gain is approximately 2.0. Given the prevalence
of low weight gain, the etiologic fraction (population attributable risk) in
women with average prepregnancy weight for height in developed countries
is approximately 14%. In other words, low weight gain can account for
about one in seven cases of IUGR. All these quantitative estimates are
likely to be inflated, because they are based on total weight gain and thus
reflect some degree of part-whole correlation. The effect on mean birth
weight, for example, appears to be reduced by about one-third (from 20
to 13 g/kg) when based on net gain rather than total gain (Kramer et al.,
1989~.
Investigators who have examined the effect of a given gestational
weight gain in women with different prepregnancy weight-for-height status
have been virtually unanimous in concluding that the two factors strongly
interact (i.e., that prepregnancy weight for height is an effect modipery
(see Chapter 2~. Miller and Merritt (1979), for example, showed a clear
trend for increasing rates of IUGR with decreasing prepregnant weight
OCR for page 184
184
NUTRITIONAL STATUS AND WEIGHT GAIN
3,600
3,500
, 3 400
~,
._
a)
s
m
a)
._
an
3,300
3,200
3,100
3,000
2,900
Very Overweight
- Moderately Overweight
~~
Ideal weight/'
~ Underweight
I 1 1 1 1 1 1 1 1
0 2 4 6 8 10 12 14 16 18 20
Maternal Weight Gain, kg
FIGURE 8-4 Birth weight as a [unction of maternal weight and prepregnangy weight for
height. Adapted from Abrams and Laros (1986) with permission.
for height among women with low gestational weight gain. Similar results
were reported in several studies investigating mean birth weight (Abrams
and Laros, 1986; Frentzen et al., 1988; Mitchell and Lerner, 1989; Naeye,
1981b,d; Seidman et al., 1989; Winikoff and Debrovner, 1981~. Illustrative
data from Abrams and Laros (1986), as adapted by B. Abrams (University
of California at Berkeley, personal communication, 1989), are shown in
Figure 8-4. Thus, underweight women appear to derive a greater benefit
from a given gestational weight gain than do those with adequate or
excessive weights.
Nonetheless, prepregnancy weight for height is itself a determinant
of fetal growth above and beyond the effect of gestational weight gain
(Kramer, 1987~. Women who are thinner before pregnancy tend to have
smaller babies than do heavier women with the same weight gain. Thus,
desirable weight gains in thin women are higher than those in normal-
weight women, despite the effect modification, and desirable weight gains
for overweight and obese women are lower.
The effect of gestational weight gain on fetal growth is weak, or perhaps
OCR for page 185
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
185
even absent, in obese women (~35% of standard prepregnancy weight for
height) (Abrams and Laros, 1986; Brown et al., 1986; Frentzen et al., 1988;
Harrison et al., 1980; Luke et al., 1981; Mitchell and Lerner, 1987; Naeye,
1981b; Rosso, 1985; Winikoff and Debrovner, 1981~. Nonetheless, obese
women clearly have infants that are larger than those of nonobese women
for the same weight gain (Kramer, 1987~. It seems prudent to recommend
that obese women gain a minimum equivalent to the weight of the products
of conception (6.8 kg, or 15 lb), although lower weight gains in such women
are often compatible with optimal birth weights. The subcommittee has
not identified an upper limit for this group.
The evidence for other effect modifiers is not nearly as strong as that for
prepregnancy weight for height. Recent data indicate that the relationship
of gestational weight gain to fetal growth is similar in adolescents and older
women after controlling for prepregnancy weight for height and other
potentially confounding differences (Scholl et al., 1988), although one
recent Israeli study reported a substantially (but nonsignificantly) reduced
relationship in women under age 20 (Seidman et al., 1989~. These data are
concordant with the results of several earlier studies indicating no significant
differences in fetal growth in adolescents (even those within 1 or 2 years
of menarche), once differences in gestational weight gain, prepregnancy
weight, and other confounders have been controlled (Duenhoelter et al.,
1975; Horon et al., 1983; Scholl et al., 1984), thus undermining the notion
of a competition between the adolescent's own requirements for growth
and those of the fetus.
Research findings have not been unanimous on this point, however,
especially for younger adolescents (<16 years). In an analysis of young,
black adolescent mothers in the Collaborative Perinatal Project, Naeye
(1981d) found significantly lower mean birth weights among infants born
at 38 to 44 weeks of gestation to nonsmokers who were not obese prior
to pregnancy. This was particularly true in those aged 10 to 14, in whom
deficits averaged approximately 150 to 200 g. However, potential differences
in alcohol or drug use were not controlled. In a study of poor, young, urban
Peruvian mothers, Frisancho et al. (1985) reported a birth weight deficit of
approximately 200 g in young adolescents (<15 years) compared with that in
older women (17 to 25 years), even after controlling for gestational weight
gain. But these results were not controlled for potentially confounding
differences in parity or socioeconomic status. A recent study from New
York City (Haiek and Lederman, 1989) showed large (200 to 400 g)
deficits in birth weight among full-term infants born to young adolescents
(<15 years) compared with those born to 19- to 30-year-old women, even
after stratification by weight for height at full-term, unless the adolescents
had achieved 140~o of their standard (nonpregnant) weight for height.
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186
NUTRITIONAL STATUS AND WEIGHT GAIN
Potentially confounding differences in cigarette, alcohol, and drug use were
not controlled.
Even those studies showing reduced fetal growth in young adolescents
do not necessarily demonstrate a true effect modification of weight gain by
age. Even if the infants of young teenage mothers have lower birth weights
for gestational age after controlling for gestational weight gain (and a
variety of potential confounders), this may not indicate a smaller effect of
a given weight gain on fetal growth. The lower birth weights might reflect
true biologic differences in potential for fetal growth (perhaps related to
the young adolescents' own nutritional requirements for growth (Scholl et
al., 1989) or to other, unknown mechanisms) in fetal growth or unmeasured
or inadequately controlled confounding factors. Of the three studies cited
above (Frisancho et al., 1985; Haiek and Lederman, 1989; Naeye, 1981d),
only Frisancho et al. present data that directly bear on effect modification.
Although the regression coefficients (adjusted slopes) for gestational weight
gain in that study decrease with lower maternal age (13 to 15 years), the
absolute magnitude of the slopes for 16 year aids (44.4-g birth weight per
kilogram of total gestational weight gain) and 17 to 25 year olds (52.2 g/kg)
is far higher than the usual effect size of approximately 20 g/kg cited above
and, therefore, is difficult to accept at face value, even considering the
poor, potentially undernourished population under study. These extremely
large effect sizes strongly suggest the existence of residual confounding by
socioeconomic or other differences. But lower birth weights seen in infants
of young adolescents compared with those seen in infants of older women
with the same weight gain, even in the absence of effect modification,
argue for promotion of weight gains toward the upper end of the range
recommended for older women with a similar weight for height.
The subcommittee was able to locate only a single study (Seidman et
al., 1989) bearing on possible effect modification by older age (i.e., >35
years). That study reported a slightly but significantly increased effect of
gestational weight gain in Israeli women over age 30 as compared with those
between the ages of 20 and 30, after controlling for prepregnancy weight
for height and other potential confounding variables. (The reported effect
was 16.6- compared with 14.0-g birth weight per kilogram of gestational
weight gain, respectively.) In addition, since weight does increase with age,
older women might be protected to some degree against the adverse effects
of low weight gains.
Few data are available concerning differences in the effect of weight
gain on fetal growth among women of different racial or ethnic back-
grounds. Analysis of the 1980 National Natality Survey Duffel, 1986),
however, indicates similar effects of gestational weight gain on mean birth
weight among white as well as black women. But as with the case of young
OCR for page 201
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
201
of subsequent gestational hypertensive disorders, but firmer inferences must
await the results of future research.
As previously discussed, large gestational weight gains are associated
with an increased risk of high birth weight and a corresponding increase
in risk for dysfunctional labor, midforceps delivery, and cesarean delivery
(Boyd et al., 1983; Koff and Potter, 1939; Modanlou et al., 1980~. Moreover,
there is some evidence that these consequences of fetopelvic disproportion
are exacerbated in women with short stature or small pelvic size (Frame et
al., 1985; Hughes et al., 1987~. Cesarean delivery rates have skyrocketed
over the last 15 to 20 years (Placek and Taffel, 1980; Placek et al., 1983), but
the remarkable increase has been accompanied by rather modest increases
in the rates of high birth weight (see Chapter 3~. Thus, even if larger
gestational weight gains are partly responsible for the trend toward slightly
larger infants, their contribution to complications of labor and delivery
must be quite small.
Varma (1984) examined the direct relationship between gestational
weight gain and pregnancy complications. Although he reports a signifi-
cantly higher rate of forceps and cesarean deliveries among women with
fetal weight gains >16 kg (35.2 lb), and especially >21 kg (46.2 lb), these re-
sults are unadjusted for potentially confounding differences among women
with different weight gains. Using a more sophisticated multivariate ap-
proach, however, Shepard et al. (1986) confirmed that women with large
weight gains (~35% of their prepregnancy weight) had higher rates of
cesarean deliveries and other operative deliveries (forceps and vacuum
extraction), as well as a prolonged second stage of labor.
Lactation Performance
There is a general perception that fat deposition during pregnancy is
required for optimal lactation performance. Although several studies have
examined the relationship between milk production and maternal nutrition
during lactation, few have related lactation performance to gestational
weight gain.
In one longitudinal study of well-nourished women in the United
States, gestational weight gain was not related to milk quantity or quality
(Butte et al., 1984~. Fat mobilization was not a prerequisite to adequate milk
production, as indicated by the inverse relationship between the amount of
energy mobilized from maternal stores and dietary energy intake.
Other studies on humans do not support the hypothesis that fat de-
posited during pregnancy is necessarily mobilized later during lactation. In
one study of Swedish women, the mean gestational weight gain (13.8 kg, or
~30 lb) included substantial quantities of fat (5.8 kg, or ~13 lb) (Sadurskis
et al., 1988~. During the first 2 months of lactation, total body fat did not
OCR for page 202
202
NUTRITIONAL STATUS AND WEIGHT GAIN
change; milk production and composition were normal. Energy costs of
lactation were met by increased energy intake, not by body fat mobilization.
By contrast, investigators from The Gambia have inferred that fat
deposition during pregnancy is of crucial importance for lactation perfor-
mance. In one Gambian study, milk output at 3 months post partum was
negatively correlated with the change in skinfold thicknesses from 6 to 12
weeks post partum (Paul et al., 1979~. In women who were replenish-
ing their fat stores during the dry (harvest) season, milk output was low.
Although the investigators interpreted this observation to indicate compe-
tition between replenishment of maternal body fat and milk production,
the data are also consistent with mobilization of maternal fat for milk pro-
duction. Subsequent, conflicting results indicated higher milk production
rates during the dry season compared with those during the wet (farming)
season (Prentice and Whitehead, 1987~. One study conducted in East Java,
Indonesia, demonstrated that energy supplementation in the last trimester
of pregnancy did not increase milk output among women with habitually
low energy intakes (van Steenbergen et al., 1989~.
The limited evidence from studies on the relationship between ges-
tational weight gain and lactation performance in humans can be supple-
mented with findings from animal studies. Extrapolation of data on re-
production from nonprimate animal models to humans can be hazardous,
since marked differences in the energy costs of gestation and lactation exist
between primates and other mammals. Nonetheless, the evidence from
animal studies indicates that gestaizonal nutrition is less important than
postpartum nutrition for lactation (Jenness, 1986; Kliewer and Rasmussen,
1987; Lodge, 1969; O'Grady et al., 1973; Sadurskis, 1988~. This evidence
thus supports the notion that gestational weight gain in humans has little
impact on subsequent milk quantity or quality.
Postpartum Obesity
It is often alleged that women in developing countries become pro-
gressively malnourished (experience maternal depleiion) and have corre-
spondingly worse outcomes with successive pregnancies (Jelliffe, 1966~. In
contrast, many investigators report a net increase in body weight among
women in industrialized countries during the interconceptional period that
may persist and even increase with successive pregnancies.
Studies by Stander and Pastore (1940), Beazley and Swinhoe (1979),
and Samra et al. (1988) did not control for the expected weight increase
that normally occurs with age. In several population-based cross-sectional
studies (Forster et al., 1986; Heliovaara and Aromaa, 1981; McKeown and
Record, 1957; Newcombe, 1982; Noppa and Bengtsson, 1980), stratification
or multivariate statistical approaches have been used to adjust for the
OCR for page 203
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
203
confounding effect of age and, in some cases, for interpregnancy interval,
socioeconomic status, and other potential confounders. But cross-sectional
studies are prone to cohort effects; i.e., there has been a trend over time
toward higher total body weights at any given age and parity. A recent
longitudinal study in The Netherlands (Rookus et al., 1987) reported a
slightly (but nonsignificantly) higher increase in BMI at 9 months post
partum in 49 pregnant women compared with that in 400 nonpregnant
controls followed for the same period. Similarly, in a cross-sectional study
(Cederlof and Kaij, 1970) comparing parous monoygotic twins with their
childless co-twins, and in longitudinal studies of repeated pregnancies in
Scotland (Billewicz and Thomson, 1970) and the United States (Greene et
al., 1988), an independent effect of parity on body weight was confirmed.
Overall, the evidence suggests an average weight retention of approximately
1 kg (2.2 lb) per birth.
The studies in Scotland and the United States are the only ones
found by the subcommittee that attempt to relate the magnitude of the
parity effect to the amount of weight gained in the preceding pregnancies.
Billewicz and Thomson (1970) reported that weight increases (adjusted for
age and cohort effects) above 2.5 kg (5.5 lb) between the first and second
pregnancies were associated with high weight gains (average 10 to 12 kg, or
22 to 26 lb) after 20 weeks of gestation during the first pregnancy. Greene
et al. (1988) reported an analysis of 7,116 women who had at least two
singleton births in the 1959-1965 Collaborative Perinatal Project. There was
a monotonic trend toward increasing (adjusted) interpregnancy retention
of weight with increasing gestational weight gains in the earlier pregnancy.
For the minority of women who had very high gestational weight gains,
the increases were substantial: 5 kg (10.9 lb) for women gaining 16.4 to
18.2 kg (36 to 40 lb) and 8.0 kg (17.7 lb) for those gaining more than
18.2 kg. (The mean weight gain among the study women was 9.5 kg, or
20.8 lb.) These data should be interpreted with caution, however, since
the pregnancies studied occurred nearly four decades ago, when gestational
weight gains were considerably lower than those observed more recently
(see Chapter 3~. Women gaining >16.4 kg (36 lb) represented only 8% of
those studied; that percentage would be far higher today. The fact that the
study population was skewed toward black, urban, and poor women and
was restricted to the 7,116 women with at least two singleton births during
the study period (out of the 58,760 total study population) also limits the
generalizabili~ of the findings.
In summary, the evidence suggests that women with average gestational
weight gains retain about 1 kg (2.2 lb) above and beyond their expected
weight increase with age. The 1-kg figure is based largely on data from
older studies, however, and may underestimate weight retention associated
with the higher gestational weight gains seen in recent years. Women
OCR for page 204
204
NUTRITIONAL STATUS AND WEIGHT GAIN
with very large weight gains appear to be at risk for considerably larger
postpartum weight increases. For women who are well- or over-nourished
prior to pregnancy, these large increases may contribute to the development
of obesity and its adverse health sequelae. Since a given weight increase
will have a greater impact on relative weight and, hence, obesity in short
women, large weight gains may be particularly undesirable in such women.
Further studies are required to document the effects of high gestational
weight gain on subsequent maternal obesity.
SUMMARY
A large body of evidence indicates that gestational weight gain is a
determinant of fetal growth, although the magnitude of the causal impact
is somewhat less than that usually reported because of the failure of
previous studies to adjust total weight gain for fetal weight. Even after
such adjustment, however, lower net weight gains are associated with
an increased risk of IUGR and increased perinatal mortality (probably
mediated by effects on IUGR), whereas higher weight gains are associated
with high birth weight and, secondarily, prolonged labor, shoulder dystocia,
cesarean delivery, and birth trauma and asphyxia. There is convincing
evidence that the effect of maternal weight gain on fetal growth is modified
by pregnancy weight for height. Published data do not suggest an effect
modification by age or ethnic background.
Data concerning the effects of maternal weight gain on gestational
duration are suggestive but less conclusive, particularly in light of the
difficulties in determining gestational age with accuracy. Further research
is clearly indicated in this area, because even small reductions in risk for
preterm deliveries, especially those that occur very early in gestation, would
have a favorable impact on perinatal and later mortality and on infant and
child morbidity and performance.
There is little evidence to suggest an important association between
gestational weight gain and spontaneous abortion (miscarriage), congeni-
tal anomalies, maternal mortality, or lactation performance. There does
appear to be a statistical association with PIH and preeclampsia, but it
is difficult to interpret this association because of directionality (increased
body water leads to increased weight gain) and the absence of data relating
PIH to early gestational changes in maternal fat or lean body mass.
Pregnancy, in general, and gestational weight gain, in particular, are
associated with retained maternal weight post partum. Women with ex-
tremely high weight gains during pregnancy may be at increased risk of
subsequent obesity.
OCR for page 205
GESTATIONAL WEIGHT GAIN IN SINGLETON PREGNANCIES
CLINICAL IMPLICATIONS
205
· Recommendations for gestational weight gain must be based on
an adequate appreciation of potential benefits and risks for fetal growth,
perinatal mortality, complications of labor and delivery, and birth trauma
and asphyxia.
Desirable weight gains are highest in thin women and lowest In
obese, overweight, and short women (see Bible 1-1 in Chapter 1~.
· Young adolescent and black mothers should be encouraged to strive
for weight gains toward the upper range desirable for adult white mothers
with similar prepregnancy weights for height and heights.
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Representative terms from entire chapter:
birth weight
