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 222
10
Causality and Opportunities
for Intervention
One of the major issues under consideration by this subcommittee is
the relationship between gestational weight gain and a variety of maternal
and child health outcomes. In particular, its interest focuses on gestational
weight gain as an etiologic determinant, i.e., a cause, of these maternal
and child outcomes. An understanding of cause is often a prerequisite
for effecting change (improving maternal and child health). As mentioned
in Chapters 2 and 4, however, low gestational weight gain might also be
of potential value as a noncausal marker of risk for adverse pregnancy
outcome.
A change in pregnancy outcome therefore depends on the ability to
alter causal determinants. Since clinicians and public health practitioners
cannot directly affect gestational weight gain (without surgically removing
or adding tissue to the pregnant woman), factors that can be modified
must be considered. The two major modifiable factors are energy intake
and expenditure (as they have an impact on energy balance). But these
can be modified only indirectly, such as by offering nutritional advice or
supplementation, either in the context of regular prenatal care or as part
of a special program. It may also be possible to change maternal attitudes
that have an impact on energy intake, either by apprising the community
of recent research findings and expert opinion or through more formal
avenues of health education.
In identifying modifiable factors and the likely impact of such modi-
fications on maternal and child health, the entire causal pathway depicted
in Figure 2-3 must be considered, beginning with attitudes, counseling, and
222
OCR for page 223
CAUSALITY AND OPPORI~UNIlIES FOR INTERVENTION
223
supplementation and working through actual increases or decreases in en-
ergy intake; subsequent changes in gestational weight gain; the short-term
maternal and fetal/child outcomes of pregnancy; and finally, longer-term
maternal and child health. In the following section, these causal links are
discussed in greater detail.
THE CAUSAL PATHS
Most of the evidence examined by the subcommittee concerns the
possible causal relationship between gestational weight gain and a variety
of short-term health outcomes for the mother (mortality, complications of
pregnancy, lactation performance, and postpartum obesity) and the fetus
and infant (mortality, fetal growth, gestational duration, spontaneous abor-
tion, and congenital anomalies). As discussed in Chapter 2 and as shown in
Figure 2-3, however, these limited causal paths require both proximal and
distal extensions. They need to be extended proximally because neither
clinical and public health interventions nor changes in maternal attitudes
have a direct impact on gestational weight gain. Consideration must be
given, at least briefly, to causal paths from maternal attitudes, nutritional
counseling, and energy supplementation to energy intake, and from energy
intake to gestational weight gain. The paths must be extended distally
to examine the relationship between the short-term outcomes enumerated
above and the longer-term maternal and child health outcomes that may
be of greater importance. For the mother, the main long-term outcome
of interest is obesity. For the child, such outcomes include all aspects
of survival, morbidity, growth, and performance that could be affected by
changes in fetal growth or gestational duration.
Very few reports directly link the proximal factors to the important
long-term health outcomes at the end of the causal pathway. Exceptions
include publications by Naeye and Chez (1981), Singer et al. (1968), and
l~vris and Read (1982), which link childhood cognitive development to
maternal weight gain. Moreover, there is no strong evidence that long-
term outcomes are affected directly, i.e., independently of shorter-term
outcomes. In the remainder of this chapter, therefore, discussion is limited
to examination of the evidence involving each of the individual causal links.
Although most of the evidence and most of the deliberations of the sub-
committee focus on links between gestational weight gain and maternal and
child outcomes, the entire causal pathway summarized in Figure 2-3 needs
to be kept in mind when formulating recommendations and contemplating
possible clinical or public health interventions.
In examining the evidence for causality in these individual links,
the subcommittee based its inferences on standard epidemiologic crite-
ria. These criteria include the strength, biologic gradient (dose-response
OCR for page 224
224
NUTRITIONAL STATUS AND WEIGHT GAIN
effect), lack of bias, statistical significance, specificity, consistency, and bi-
ologic plausibility and coherence of the association between exposure (the
putative cause) and outcome (DHEW, 1964; Hill 1965; Susser 1973, 1988~.
THE EVIDENCE
Do Nutritional Counseling, Energy Supplementation, and Maternal
Attitudes Affect Energy Intake?
Remarkably few studies have been conducted to assess the efficacy
of nutritional counseling (without supplementation) on energy intake by
pregnant women either within or outside the context of regular prenatal
care. In early studies carried out at the Montreal Diet Dispensary, for
example, counseling was combined with some degree of energy supplemen-
tation, and inappropriate comparisons were made between women who
either were referred for or requested those nutrition services and those
who did not (Higgins, 1976; Primrose and Higgins, 1971~. Thus, the rather
large increases in net energy intake (and birth weight) attributed to use of
the nutrition services are likely to be overestimates. Rush (1981) attempted
to pair-match Montreal Diet Dispensary participants and nonparticipants
according to potential confounding factors. The increases in energy intake
and birth weight were more modest than those reported by Higgins (1976)
and Primrose and Higgins (1971), but they were still in the expected direc-
tion. Higgins et al. (1989) found an increase in infant birth weight among
mothers who participated in the program in the second but not the first of
two pregnancies, but they provided no data on differences in energy intake.
The Special Supplemental Food Program for Women, Infants, and
Children (WIC) in the United States also includes a mixture of nutritional
counseling and supplementation. Pregnant women are given vouchers that
can be used to obtain highly nutritious foods; however, there is no guarantee
that the women will consume these foods and not share them with others.
Several evaluations of WIC, including the largest and most recent one by
Rush et al. (1988), indicate that WIC participants increase their energy
intake and have higher gestational weight gains as a result of participation
in the program (Edozien et al., 1979; Endres et al., 1981; Metcoff et al.,
1985; Rush et al., 1988~. The net increase in energy intake is modest,
however, probably on the order of 100 to 150 kcaVday.
Supplementation trials indicate that women who are given energy
supplements during pregnancy increase their total energy intakes (Lechtig
et al., 1975; Mora et al., 1979; Prentice et al., 1983; Rush et al., 1980), but in
most studies, the magnitude of the increased intake ranged from 100 to 250
kcal/day-less than the energy content of the supplement provided. Larger
OCR for page 225
CAUSALITY AND OPPORTUNITIES FOR INTERVENTION
225
increments have been achieved in certain undernourished populations in
developing countries, e.g., in The Gambia (Prentice et al., 1983~.
The subcommittee found no formal research to determine the effect
of maternal attitudes on energy intake. These attitudes change slowly in
response to many factors, including the reporting (and mass media dis-
semination) of new research findings, recommendations by national and
international bodies or individual experts, health education (including that
provided at schools and public prenatal classes), practices of health care
providers, and word of mouth. Such factors are difficult to measure ob-
jectively. Moreover, concurrent controls are often impossible to obtain,
since entire countries tend to be exposed to the messages simultaneously.
Before-and-after comparisons may therefore be the only feasible way to
assess the influence of these factors on energy intake. Unfortunately, small
changes in energy intake are also difficult to measure (see Chapter 7~.
Thus, any attempt to assess changes in energy intake as a consequence of
(i.e., caused by) changes in maternal attitudes would be difficult, to say the
least.
Nonetheless, as discussed in Chapter 3, authorities have increased their
recommended energy intakes and target weight gains for pregnant women
over the past 30 to 40 years, and these changes have been accompanied by
corresponding increases in gestational weight gain. It is difficult to ascribe
recent weight gain changes to anything other than increased energy-intake
during pregnancy (see discussion below). Although increased energy intake
may be attributable, in part, to individual nutritional counseling by obste-
tricians, nurse-midwives, dietitians, and other health care professionals, it
seems reasonable to infer that gradual changes in public awareness and
maternal attitudes have also played a role.
Does Energy Intake Affect Gestational Weight Gain?
Everyday experience and carefully controlled experimental studies
(Sims et al., 1968) have demonstrated that people who consume excess
energy gain weight. There is no reason to believe that pregnant women are
an exception to this general rule. Many of the clinical and epidemiologic
studies linking energy intake to gestational weight gain have found rather
modest, and often nonsignificant, correlations between the two, in part
because most women with high energy intakes also have high energy ex-
penditures and, in part, because of the difficulty of accurately measuring the
change in energy intake. Problems in measurement of energy intake have
probably led to underestimates of the true correlation between maternal
energy intake and gestational weight gain.
The clearest evidence favoring the link between energy intake and
gestational weight gain comes from studies of human famine and from
OCR for page 226
226
NUTRITIONAL STATUS AND WEIGHT GAIN
supplementation trials. It is clear from the Dutch famine study that reduced
energy intake leads to reduced gestational weight gain (Stein et al., 1975;
Susser and Stein, 1982~. It is equally clear from supplementation trials
in both developed (Rush et al., 1980) and developing (More et al., 1979)
countries that increased energy intake leads to larger maternal weight gains.
Does Gestational Weight Gain Affect Short-Term MaternaVChild Health?
Virtually all epidemiologic studies with adequate sample sizes have
demonstrated an association between gestational weight gain and fetal
growth. Many supplementation trials and observational studies have been
based on rigorous epidemiologic methods to minimize most sources of bias;
however, reverse causality (temporal precedence) has not received adequate
attention. For example, the amount of weight that a woman gains during
a pregnancy is influenced not only by the deposition of fat, protein, and
glycogen stores potentially available for provision of nutrients to the fetus
but also by large increases in body water. It is well known that expanded
plasma volume and modest degrees of dependent edema are associated with
favorable pregnancy outcomes (Campbell and MacGillivray, 1975; Duffus
et al., 1971; Hytten and Thomson, 1976; Naeye, 1981a,b; Thomson et al.,
1967~; but in the absence of data establishing that increases in body water
precede increases in fetal growth rate, they may just as likely be an effect,
rather than a cause, of a well-functioning fetoplacental unit. A specific
example of reverse causality is provided by the evidence that twin births
are associated with higher net maternal weight gains. Thus, it seems clear
that the fetus and placenta can affect maternal weight gain apart from the
weight they contribute.
Furthermore, the amount of weight gained during pregnancy is inDu-
enced by the weights of the fetus, placenta, and amniotic fluid. Nonetheless,
studies that examined net (i.e., maternal) weight gain have shown smaller,
but consistent, effects on fetal growth (see Chapter 8~.
The strongest evidence that gestational weight gain can affect fetal
growth is provided by supplementation trials (Lechtig et al., 1975; Mora
et al., 1979, Prentice et al., 1983; Rush et al., 1980) and studies of human
famine (Stein et al., 1975; Susser and Stein, 1982~. In both of these
settings, changes in energy intake result in changes in both gestational
weight gain and gestational age-adjusted birth weight. Both nutritional and
nonnutritional (i.e., expansion of body water) factors may be involved in
producing the effect of gestational weight gain on fetal growth, as suggested
by the trial of Campbell and MacGillivray (1975) that included use of
energy restriction and diuretics. The causal link is further strengthened
by coincidental temporal trends over the last 20 to 30 years: increasing
gestational weight gains and mean birth weights and decreasing rates of
intrauterine growth retardation.
OCR for page 227
CAUSALITY AND OPPORTUNITIES FOR INlERVENTION
227
However, the magnitude of the causal effect size (e.g., increase in birth
weight) is modest. The data indicate, for example, that in women with a
normal prepregnancy weight for height, birth weight increases 20 g, on
average, for a change of 1 kg in gestational weight gain (Kramer, 1987~.
Thus, a 5-kg (11-lb) difference in gestational weight gain is associated with
an average difference in birth weight of only 100 g. The actual change
in birth weight for an individual woman who increases or decreases her
gestational weight gain by this amount is likely to vary considerably around
this average. Moreover, the 20-g/kg effect is probably an overestimate,
since the analyses in most studies are based on total rather than on net
weight gain (see Chapter 4~. When based on net weight gain, the effect
appears to be reduced by one-third to about 13 g of birth weight per 1 kg
(2.2 lb) of gestational weight gain (Kramer et al., 1989~.
Given this modest effect size and the large variability in weight gains as-
sociated with optimal fetal growth, even within groups with similar prepreg-
nancy weights for height, knowledge of an individual mother's weight gain
does not substantially enhance her (or her physician's) ability to predict
the growth of her fetus. Nor is the evidence bearing on this causal link
particularly useful in the diagnostic setting. The low birth weight of an
infant born to a mother who gained only 5 kg (11 lb) cannot, therefore, be
confidently attributed to her low gestational weight gain, nor can the high
birth weight of a baby whose mother gained 25 kg (55 lb) be attributed
to the high gestational weight gain. Thus, despite the strong evidence that
gestational weight gain can affect fetal growth, the chance that it will (or
did) in an individual case may be far from clear (Kramer, 1988; Lane,
1984~.
With regard to the effects of gestational weight gain on gestational
duration, the evidence for causality is considerably weaker than that for
fetal growth. Once again, reverse causality is a key issue and one that has
not been adequately considered in most epidemiologic studies, especially
those in which gestational weight gain has been based on total weight
gain, rather than on early weight gain or rate of weight gain. Obviously,
a pregnancy that ends prematurely will be associated with a smaller total
weight gain, because the mother will have had less total time in which to
gain weight.
Birth weight can be measured without appreciable random or system-
atic error. By contrast, as mentioned above, gestational age is difficult to
estimate and errors in such estimates, particularly at the extremes of ma-
turity (Kramer et al., 1988), are likely to lead to misclassification of some
growth-retarded babies as preterm and preterm babies as growth retarded.
Nonetheless, evidence from many of the better epidemiologic studies
does suggest that a low rate of gestational weight gain can increase the risk
of preterm delivery (Abrams et al., 1989; Berkowitz, 1981; Hediger et al.,
1989; Miller and Merritt, 1979; Scholl et al., 1989; van den Berg and Oechsli,
OCR for page 228
228
NUTRITIONAL STATUS AND WEIGHT GAIN
1984~. The evidence is not unanimous, however (Kleinman, 1990), and
there is no clear biologic mechanism whereby changes in gestational weight
gain would lead to earlier or later labor and delivery. Furthermore, there
has been no clear trend toward increasing gestational duration paralleling
the increase in gestational weight gain in the United States during the
past two or three decades. For all these reasons, the subcommittee finds
that the evidence for an important causal impact on gestational duration is
. .
Inconclusive.
There are fewer data concerning the links between gestational weight
gain and the other short-term maternal and child outcomes shown in Figure
2-3. Data from the Collaborative Perinatal Project (Naeye, 1979) and the
1980 National Fetal Mortality Survey Duffel, 1986) indicate an increased
perinatal mortality rate among infants born to women with low gestational
weight gains, especially those with low prepregnangy weights for height. The
evidence does not suggest that gestational weight gain affects congenital
anomalies, spontaneous abortion, maternal mortality, or the volume or
composition of human milk during lactation.
Evidence from the large body of literature concerning the effects of
gestational weight gain on fetal growth indicates that large gestational
weight gains do increase the risk of high-birth-weight infants (Ounsted and
Scott, 1981; Scholl et al., 1988; Udall et al., 1978), which can lead to
fetopelvic disproportion and, secondarily, to increased risks of midforceps
delivery, cesarean delivery, shoulder dystocia, meconium aspiration, clavic
ular fracture, brachial plexus injury, and neonatal asphyxia (Acker et al.,
1985; Boyd et al., 1983; Koff and Potter, 1939; Modanlou et al., 1980;
Sandmire and O'Halloin, 1988~. But the magnitude of the erect of gesta
tional weight gain on these outcomes appears to be small. In particular,
very little of the recent marked increase in the rate at which cesarean
deliveries are performed can be attributed to larger maternal weight gains.
Finally, published evidence indicates that women who have large weight
gains during pregnancy tend to remain somewhat heavier in the immediate
postpartum period (Billewicz and Thomson, 1970; Greene et al., 1988~.
Do Short-Term Maternal and Child Health Effects Lead
to Longer-Term Effects?
Most of the questions about the long-term effects of gestational weight
gain on maternal or child health concern postpartum maternal obesity and
the survival, morbidity, growth, and performance of the offspring. Some
maternal weight added during pregnancy may be retained permanently,
particularly if weight is retained following each of several pregnancies (see
Chapter 8~. Further research in this area is clearly required. Obesity
has well-documented adverse health consequences, including hypertension,
OCR for page 229
CAUSALITY AND OPPORTUNITIES FOR INTERVENTION
229
non-insulin-dependent diabetes mellitus, gallbladder disease, osteoarthritis,
and increased overall mortality (Hoffmans et al., 1988; Mann, 1974a,b;
NIH, 1985; Van Itallie, 1979~. Therefore, any tendency toward excessive
fat retention must be regarded as undesirable. Fortunately, most women
retain only an average of approximately 1 kg (2.2 lb) per pregnancy,
although this figure might underestimate weight retentions associated with
the large weight gains observed in recent years.
Most of the issues regarding the effects on the child focus on the
prognostic Implications of intrauterine growth retardation (IUGR) or high
birth weight. There is fairly convincing evidence that IUGR infants have
increased morbidity in the newborn period, including increased risks of
polycythemia, hypoglycemia, hypocalcemia, and birth asphyxia (Arora et
al., 1987; Kramer et al., 1989; Ounsted et al., 1988; Usher, 1970~. The
evidence also indicates that IUGR leads to small but persistent effects
in stature, brain growth, and neurocognitive performance (as reviewed by
Teberg et al., 1988), although control for confounding postnatal influences
has not always been adequate in previous studies. In addition, a small but
definite risk of fetal and infant mortality seems to be attributable to IUGR
(Arora et al., 1987; Haas et al., 1987; Koops et al., 1982; Kramer et al.,
1989; Usher, 1970~. High-birth-weight infants, on the other hand, tend to
be taller and heavier throughout childhood and have an increased risk of
obesity (Binkin et al., 1988; Fisch et al., 1975; Kramer et al., 1985; Ounsted
et al., 1982~.
If there is confirmation of several recent studies suggesting that in-
creased maternal weight gain can increase gestational duration and that
women with low weight gain are at increased risk for preterm delivery, the
promotion of gestational weight gain might have important long-term bene-
fits for child health. Preterm infants, especially those born before 34 weeks
of gestation, are at greatly increased risk for perinatal and infant mortal-
ity, as well as rather severe and persistent pulmonary and neurocognitive
sequelae. The causal impact of preterm birth on these adverse outcomes
is extremely well established and of large magnitude. Thus, even if insuf-
ficient gestational weight gain increases the risk of preterm birth only to
a small degree, the negative effects on child health may be large. These
considerations once again underline the need for further research on the
link between maternal weight gain and gestational duration.
IMPLICATIONS
The evidence suggests that an across-the-board increase in gestational
weight gain among U.S. women would have both beneficial and adverse
effects on maternal and child health. Fetal and infant mortality would be
reduced, as would the incidence of IUGR (and its short-term and longer
OCR for page 230
230
NUTRITIONAL STATUS AND WEIGHT GAIN
term sequelae). Such an increase in weight gain would also result in an
increased risk of maternal obesity (and its secondary health sequelae) for
women with very large weight gains and an increased incidence of high-
birth-weight infants, which has some undeniable consequences both for
mothers and infants.
A formal decision analysis, in which probabilities and utilities (values)
are assigned to each potential outcome, might assist in balancing these
risks and benefits. Essential components of such an analysis include the
probability of each beneficial and adverse outcome occurring with and with-
out nutritional counseling, energy supplementation, or changes in maternal
attitudes and the value that mothers, children, and society place on each
of those outcomes. Even then, it is important to consider who would be
helped and who would be harmed, as well as whose values should be con-
sidered. For example, if increased energy intakes lead to an elevated risk
of maternal obesity but better overall outcomes in the infants, how should
risks to the mother be balanced against benefits to the child? And who will
make the decision?
The analysis could be refined by taking into account the fact that the
risks and benefits are likely to differ according to the mother's prepregnancy
weight for height, existing energy intake, and other factors that affect the
outcomes under consideration. It may well be possible to maximize benefits
and minimize risks by focusing educational efforts, individual nutritional
counseling, and energy supplementation on women who are undernourished
or who have other risk factors. Increased energy intakes by such women
can be expected to have a substantial impact on intrauterine growth and its
longer-term child health sequelae without incurring the appreciable risks
of maternal obesity and high birth weight.
Finally, even if the overall benefits of increased energy intake exceed
the risks, and even if the above technical and philosophical objections can
be overcome, society will need to consider the costs of these interventions.
Cost-benefit and cost-effectiveness analytic techniques could be used to de-
cide whether the net benefit is worth the expense, or whether the required
resources can be more productively channeled in other directions. Public
media campaigns, individual nutritional counseling, and energy supplemen-
tation all require financial resources. Even if those resources were kept
within the maternal and child health sector, the benefit:cost ratio for the
various interventions should be compared with that for public health and
clinical interventions to convince mothers to stop smoking during pregnancy
and with that for family planning and contraceptive services (particularly
for adolescents). Although such a balancing of benefits, risks, and costs
should play an important role in public health policy in this domain, these
considerations extend considerably beyond the subcommittee's mandate.
OCR for page 231
CAUSALITY AND OPPORTUNITIES FOR INTERVENTION
REFERENCES
231
Abrams, B., V. Newman, T. Key, and J. Parker. 1989. Maternal weight gain and preterm
delivery. Obstet. Gynecol. 74:577-583.
Aeker, D.B., B.P. Saehs, and E.A. Friedman. 1985. Risk factors for shoulder dystocia.
Obstet. Gyneeol. 66:762-768.
Arora, N.K., V.K. Paul, and M. Singh. 1987. Morbidity and mortality in term infants with
intrauterine growth retardation. J. Crop. Pediatr. 33:186-189.
Berkowitz, G.S. 1981. An epidemiologic study of preterm delivery. Am. J. Epidemiol.
113:81-92.
Billewiez, W.Z., and A M. Thomson. 1970. Body weight in parous women. Br. J. Prev. Soc.
Med. 24:97-104.
Binkin, N.J., R. Yip, L. Fleshood, and FL. Drawbridge. 1988. Birth weight and childhood
growth. Pediatrics 82:828-834.
Boyd, M.E., R.H. Usher, and F.H. McLean. 1983. Fetal maerosomia: prediction, risks,
proposed management. Obstet. Gynecol. 61:715-72Z
Campbell, D.M., and I. MaeGillivray. 1975. The effect of a low calorie diet or a
thiazide diuretic on the incidence of pre-eelampsia and on birth-weight. Br. J. Obstet.
Gynaecol. 82:572-577.
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.
Duffus, G.M., I. MaeGillivray, and K.J. Dennis. 1971. Ibe relationship between baby
weight and changes in maternal weight, total body water, plasma volume, electrolytes
and proteins, and urinary oestriol excretion. J. Obstet. Gynaecol. Br. Commonw.
78:97-104.
Edozien, J.C., B.R. Switzer, and R.B. Bryan. 1979. Medical evaluation of the Special
Supplemental Food Program for Women, Infants, and Children. Am. J. Clin. Nutr.
32:677-692.
Endres, J.M., M. Sawieki, and J.A. Casper. 1981. Dietary assessment of pregnant women
in a supplemental food program. J. Am. Diet. Assoe. 79 121-126.
Fiseh, R.O., M.K. Bilek, and R. Ulstrom. 1975. Obesity and leanness at birth and their
relationship to body habitue in later childhood. Pediatrics 56:521-528.
Greene, G.W. , H. Smieiklas-Wright, T. O. Scholl, and RJ. Karp. 1988. Postpartum weight
change: how much of the weight gained in pregnancy will be lost after delivery.
Obstet. Gyneeol. 71:701-707.
Haas, J.D., H. Baleazar, and L. Caulfield. 1987. Variation in early neonatal mortality for
different types of fetal growth retardation. Am. J. Phys. Anthropol. 73:467473.
Hediger, M.L., TO. Scholl, D.H. Belsly, I.G. Anees, and R.W. Salmon. 1989. Patterns of
weight gain in adolescent pregnancy: effects on birth weight and preterm delivery.
Obstet. Gyneeol. 74:6-12.
Higgins, A.C. 1976. Nutritional status and the outcome of pregnancy. J. Can. Diet. Assoe.
37:17-35.
Higgins, A. C., J.E. Moxley, P. B. Pencharz, D. Mikolainis, and S. . Dubois. 1989. Impact of
the Higgins Nutrition InteIvention Program on birth weight a within-mother analysis.
J. Am. Diet. Assoc. 89:1097-1103.
Hill, A.B. 1965. We environment and disease: association or causation? Proe. R. Soe.
Med. 58:295-300.
Hoffmans, M.D., D. Kromhout, and C. de Lezenne Coulander. 1988. The impact of body
mass index of 78,612 18-year old Dutch men on 32-year mortality from all causes. J.
Clin. Epidemiol. 41:749-756.
Hytten, F.E., and A.M. Thomson. 1976. Weight gain in pregnant. Pp. 179-187 in M.D.
Lindheimer, NI. Katz, and F.P. Zuspan, eds. Hypertension in Pregnancy. John Wiley
& Sons, New York.
OCR for page 232
232
NUTRITIONAL STATUS AND WEIGHT GAIN
Kleinman, J.C. 1990. Maternal Weight Gain During Pregnancy Determinants and Conse-
quences. NCHS Working Paper Series No. 33. National Center for Health Statistics,
Public Health Service, U.S. Department of Health and Human Services, Hyattsville,
Md. 24 pp.
Koff, ~K, and E.L Potter. 1939. The complications associated with excessive development
of the human fetus. Am. J. Obstet. Gynecol. 38:412-423.
Koops, B.L~, LO. Morgan, and F.C. Battaglia. 1982. Neonatal mortality risk in relation to
birth weight and gestational age: update. J. Pediatr. 101:969-977.
Kramer, M.S. 198~7. Determinants of low birth weight: methodological assessment and
meta-analysis. Bull. W.H.O. 65:663-737.
Kramer, M.S. 1988. Causality. Pp. 255-269 in Clinical Epidemiology and Biostatistics: A
Primer for Clinical Investigators and Decision-Makem. Springer-Verlag, Berlin.
Kramer, M.S ., R.G. Barr, D. G. Leduc, C. BoisJoly, and I.B. Pless. 1985. Infant determinants
of childhood weight and adiposity. J. Pediatr. 107:104-107.
Kramer, M.S., F.H. McLean, M.E. Boyd, and R.H. Usher. 1988. The validity of gestational
age estimation by menstrual dating in term, preterm, and postterm gestations. J. Am.
Med. Assoc. 260:330~3308.
Kramer, M.S., F.H. McLean, M. Olivier, D.M. W'llis, and R.H. Usher. 1989. Body
proportionality and head and length 'sparing' in growth-retarded neonates: a critical
reappraisal. Pediatrics 84:717-723.
Lane, D.A. 1984. A probabilist's view of causality assessment. Drug Inf. J. 18:323-330.
Lechtig, ^, J.P. Habicht, H. Delgado, R.E. Klein, C. Yarbrough, and R. Martorell. 1975.
Effect of food supplementation during pregnancy on birthweight. Pediatrics 56:508-520.
Mann, G.V. 1974a. The influence of obesity on health (first of two parts). N. Engl. J. Med.
291:178-185.
Mann, G.V. 1974b. The influence of obesity on health (second of two parts). N. Engl. J.
Med. 291:226-232.
Metcoff, J., P. Costiloe, W.M. Crosby, S. Dutta, H.H. Sandstead, D. Milne, C.E. Bodwell,
and S.H. Majors. 1985. Effect of food supplementation (WIC) during pregnancy on
birth weight. Am. J. Clin. Nutr. 41:933-947.
Miller, H.C., and T.A. Merritt. 1979. Fetal Growth in Humans. Year Book Medical
Publishers, Chicago. 180 pp.
Modanlou, H.D., W.L Dorchester, A. Thorosian, and R.K Freeman. 1980. Macrosomia
maternal, fetal, and neonatal implications. Obstet. Gynecol. 55:420~24.
Mora, J.O., B. de Paredes, M. Wagner, L~ de Navarro, J. Suescum, N. Christiansen, and
M.G. Herrera. 1979. Nutritional supplementation and the outcome of pregnancy. I.
Birth weight. Am. J. Clin. Nutr. 32:455-462.
Naeye, R.L~ 1979. Weight gain and the outcome of pregnan~y. Am. J. Obstet. Gynecol.
135:3-9.
Naeye' R.L~ 1981a. Maternal blood pressure and fetal growth. Am. J. Obstet. Gynecol.
141:780-787.
Naeye, R.L. 1981b. Nutritional/nonnutritional interactions that affect the outcome of
pregnanc~r. Am. J. Clin. Nutr. 34:727-731.
Naeye, R.L, and R.A. Chez. 1981. Effects of maternal acetonuria and low pregnancy weight
gain on children's psychomotor development. Am. J. Obstet. Gynecol. 139:189-193.
NIH (National Institutes of Health). 1985. Health implications of obesity: National
Institutes of Health Consensus Development Conference Statement. Ann. Intern.
Med. 103:1073-1077.
Ounsted, M., and A. Scott. 1981. Associations between maternal weight, height, weight-
for-height, weight-gain and birth weight. Pp. 113-129 in J. Dobbing, ed. Maternal
Nutrition in Pregnancy: Eating for Two? Academic Press, London.
Ounsted, M., V. Moar, and ~ Scott. 1982. Growth in the first four years. II. Diversity
within groups of small-for-date and large-for-date babies. Early Hum. Dev. 7:29-39.
Ounsted, M., V.A. Moar, and A. Scott. 1988. Neurological development of small-for-
gestational age babies during the first year of life. Early Hum. Dev. 16:163-172.
Prentice, A.M., R.G. Whitehead, M. Watkinson, W.H. Lamb, and TJ. Cole. 1983. Prenatal
dietary supplementation of African women and birth-weight. Lancet 1:489~92.
OCR for page 233
CAUSALITY AND OPPORTUNITIES FOR INTERVENTION
233
Primrose, T., and A. Higgins. 1971. A study in human antepartum nutrition. J. Reprod.
Med. 7:257-264.
Rush, D. 1981. Nutritional services during pregnancy and birthweight: a retrospective
matched pair analysis. Can. Med. Assoc. J. 125:567-576.
Rush, D., Z. Stein, and M. Susser. 1980. A randomized controlled trial of prenatal
nutritional supplementation in New York City. Pediatrics 65:683~97.
Rush, D., N.L~ Sloan, J. Leighton, J.M. Alvir, D.G. Hontitz, W.B. Seaver, G.C Garbowski,
S.S. Johnson, R.A Kulka, M. Holt, J.W. Devore, J.T. Lynch, M.B. Woodside, and
D.S. Shanklin. 1988. The National WIC Evaluation: evaluation of the Special
Supplemental Food Program for Women, Infants, and Children. V. Longitudinal study
of pregnant women. Am. J. Clin. Nutr. 48:439~83.
Sandmire, H.F., and T.J. O'Halloin. 1988. Shoulder dystocia: its incidence and associated
risk factors. Int. J. Gynaecol. Obstet. 26:65-73.
Scholl, T.O., M.L~ Hediger, I.G. Ances, and C.E. Cronk. 1988. Growth during early teenage
pregnancies. Lancet 1:701-702.
Scholl, T.O., M.L. Hedi~er, R.W. Salmon, D.H. Belsky, and I.G. Ances. 1989. Influence of
prepregnant body mass and weight gain for gestation on spontaneous preterm delivery
and duration of gestation during adolescent pregnancy. Am. J. Hum. Biol. 1:657-664.
Sims, E.A.H., R.~. Goldman, CM. Gluck, E.S. Horton, P.C. Kelleher, and D.W. Rowe.
1968. Experimental obesity in man. Trans. Assoc. Am. Physicians 81:153-170.
Singer, J.E., M. Westphal, and K. Niswander. 1968. Relationship of weight gain during
pregnancy to birth weight and infant growth and development in the fimt year of life:
a report from the Collaborative Study of Cerebral Palsy. Obstet. Gynecol. 31:417-423.
Stein, ~, M. Susser, G. Saenger, and F. Marolla. 1975. Famine and Human Development:
The Dutch Hunger W~nter of 1944-1945. Oxford University Press, New York. 284 pp.
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.
Susser, M., and Z. Stein. 1982. Third variable analysis: application to causal sequences
among nutrient intake, maternal weight, birthweight, placental weight, and gestation.
Stat. Med. 1:105-120.
Taffel, S.M. 1986. Maternal Weight Gain and the Outcome of Pregnancy: United States,
1980. Vital and Health Statistics, Series 21, No. 44. DHHS Publ. No. (PHS) 86-1922.
National Center for Health Statistics, Public Health Se~vice, U.S. Department of
Health and Human Services, Hyattsville, Md. 25 pp.
Tavris, D.R., and J.A. Read. 1982. Effect of maternal weight gain on fetal, infant, and
childhood death and on cognitive development. Obstet. G:rnecol. 60:689~94.
Teberg, A.J., FJ. Walther, and I.C. Penal 1988. Mortality, morbidity, and outcome of the
small-for-gestational age infant. Semin. Perinatol. 12:84-94.
Thomson, A.M., F.E. Hytten, and W.Z. Billewicz. 1967. The epidemiology of oedema
during pregnangy. J. Obstet. Gynaecol. Br. Commonw. 74:1-10.
Udall, J.N., G.G. Harrison, Y. Vaucher, P.D. Walson, and G. Morrow III. 1978. Interaction
of maternal and neonatal obesity. Pediatrics 62:17-21.
Usher, R.H. 1970. Clinical and therapeutic aspects of fetal malnutrition. Pediatr. Clin.
North Am. 17:169-183.
van den Berg, BJ., and F.W. Oechsli. 1984. Prematurity. Pp. 69-85 in M.B. Bracken, ed.
Perinatal Epidemiology. Oxford Univemity Press, New York.
Van Itallie, T.B. 1979. Obesity: adverse effects on health and longevity. Am. J. Clin. Nutr.
32:2723-2733.
OCR for page 234
Representative terms from entire chapter:
gestational weight
