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*
School of Dietetics and Human Nutrition, McGill University, Montreal, Canada H9X 3V9,
Public Health Module-Cree Region, Montreal General Hospital, Montreal, Canada H3C 2M2 and
**
Departments of Pediatrics and of Epidemiology and Biostatistics, McGill University, Montreal, Canada H3A 1A2
2To whom correspondence should be addressed.
 |
ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • macrosomia • diabetes • ethnicity • humans • birth weight
|
INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, Hod et al. 1991
, Stevenson et al. 1982
). The
long-term consequences of infant macrosomia are not clear, with
some authors reporting subsequent obesity (Berkey et al. 1998
, Binkin et al. 1988
, Braddon et al. 1986
, Kramer et al. 1985
) but others refuting
this finding (Hulman et al. 1998
).
Infant macrosomia has been variably defined as birth weight >4000 g,
>4500 g or >90th percentile for gestational age
and sex (Berard et al. 1998
, Sacks 1993
).
High macrosomia rates (birth weight >4000 g) of 16–31% have been
reported among several North American Native groups (Armstrong et al. 1998
, Caulfield et al. 1998
, Dyck and Tan 1995
, Murphy et al. 1993
, Pettitt et al. 1985
, Thomson 1990
) compared with ~10%
in the general North American population (Boyd et al. 1983
). Predictors of infant macrosomia in the general
population include advanced maternal age, multiparity, pregravid
overweight, tall stature, high gestational weight gain, diabetes, male
sex of the infant and postmaturity (ACOG 1992
). It is
unclear whether the high prevalence of macrosomia seen among North
American Native groups is attributable to differences in the
distribution of risk factors for infant macrosomia, including maternal
weight and gestational diabetes mellitus
(GDM).3
Recently, elevated rates of GDM have been
reported among several Native groups in North America (Benjamin et al. 1993
, Harris et al. 1997
,
Rodrigues et al. 1999
). Alternatively, the high mean
birth weight of Native infants may be genetic.
The Cree of Eastern James Bay have a high prevalence of GDM at 12.8%
(Rodrigues et al. 1999
), and ~36% of their infants
weighed 
4000 g at birth (Armstrong et al. 1998
). The present study was thus designed to examine
predictors of infant macrosomia among Cree women, compare these to
predictors in the general Canadian population and determine whether
differences in macrosomia prevalence between the two populations could
be explained by differences in maternal age, pregravid weight, height,
gestational weight gain, glycemic status and smoking status.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The Cree of James Bay belong to the Algonquian language family and
subarctic culture area (Brassard et al. 1993
). About
11,000 Cree now occupy nine communities in James Bay (northern Quebec).
Most communities are accessible by year-round roads. All women have
good access to prenatal care, which is provided by physicians and
nurses at the local community clinics in each village. Most deliveries
are done at the northern Quebec hospitals, namely Val-d’Or,
Chibougamou and Chisasibi, all of which have facilities for cesarean
delivery.
Information on all infants born to Cree women in the nine communities
of eastern James Bay between January 1995 and December 1996 was
compiled from two sources: the Government of Quebec’s official
declaration of births and the birth registry maintained by the Cree
Board of Health and Social Services of James Bay. There were 615 births
to Cree women in 1995–1996, and data for an additional 66 pregnancies
in 1997 were available for participants in a nutrition intervention
study ending in June 1997 (Gray-Donald et al. 2000
).
Information on 681 births was thus available. Data for this study were
abstracted from clinic charts by two trained dietitians and one of the
authors (SR) and also obtained prospectively for participants in the
nutrition intervention study (Gray-Donald et al. 1999).
Data for non-Native Canadian pregnancies from January 1, 1990, to
March 31, 1996, (n = 20,982) were extracted from the
McGill Obstetrics and Neonatal Database (MOND), which is a computerized
database of all deliveries at the Royal Victoria Hospital
(RVH)(Montreal, Canada) since 1978 (Boyd et al. 1983
). Ethical approval for the study was obtained from the
Human Ethics Review Board of McGill University, and informed consent
was obtained from participants in the nutrition intervention study.
Definitions of variables.
The main outcome of interest was infant macrosomia, defined as birth
weight >90th percentile for gestational age and
sex based on the California reference of Williams et al. (1982)
.
Definitions of macrosomia used in separate analyses were absolute birth
weight >4000 g or >4500 g. Predictors of fetal growth were also
explored to determine which factors influence birth weight. Information
on the following variables of interest was abstracted for both
populations: maternal age, parity, pregravid weight, height, weight
gain during pregnancy, gestational age at delivery, smoking status and
gestational diabetes.
Women with pregestational diabetes were excluded from the present
study. GDM among the Cree and non-Natives was defined in accordance
with the National Diabetes Data Group (NDDG) criteria (National Diabetes Data Group 1979
). In brief, all pregnant women are
asked to undergo a 50-g oral glucose screen between 24 and 30 wk
gestation. A positive screen (plasma glucose 7.8 mmol/L) is
used as indication for a 3-h 100-g oral glucose tolerance test (OGTT)
after an overnight fast. GDM is diagnosed if any two of the four
threshold values on the OGTT are met or exceeded. Among the Cree, women
with a history of GDM are generally screened during the first trimester
and are screened again between 24 and 30 wk gestation if the early
screen is negative. Details about GDM screening and diagnosis among the
Cree have been published elsewhere (Rodrigues et al. 1999
). As an association between birth weight and maternal
glycemic status has been reported at lower levels of glucose
intolerance (Lindsay et al. 1989
), the relationship
between birth weight/macrosomia and impaired glucose tolerance (IGT)
was also explored in this study. IGT was defined as one abnormal value
on the 3-h 100 g OGTT (Lindsay et al. 1989
).
The standard of GDM management was very different between Cree and
non-Native women. GDM treatment at the RVH (for non-Native
women) is very intensive and involves a multidisciplinary team
including an endocrinologist and a dietitian, home blood glucose
monitoring, dietary and weight gain restrictions, careful dietary
monitoring through the maintenance of daily food records by patients
and initiation of insulin therapy if hyperglycemia persists despite
dietary modification (Snyder et al. 1994
). In contrast,
treatment for GDM among the Cree is less stringent. Women diagnosed
with GDM or IGT are generally advised by nurses at the community clinic
to restrict "sugar" intake and are given a blood glucose meter.
Before July 1995, services of only one dietitian were available to the
nine Cree communities. Following the initiation of a nutrition
intervention study in July 1995, services of two additional dietitians
were available in two inland and two coastal Cree communities until
June 1997. Nutrition counseling by dietitians involved suggestions for
improving diet and encouraging more physical activity during pregnancy
rather than enforcing any strict dietary or weight gain restrictions.
Results of the intervention study have been published elsewhere
(Gray-Donald et al. 2000
). In brief, the intervention
study was not successful in reducing either weight gain during
pregnancy or the incidence of GDM (Gray-Donald et al. 1999).
The estimation of gestational age at delivery was based on the reported
last normal menstrual period if it agreed within 1 wk of ultrasound
dating done between 16 and 20 wk (Kramer et al. 1989
);
in cases of disagreement >1 wk, the latter estimate was used. Weekly
rate of net weight gain during pregnancy was calculated as [last
recorded weight before delivery (kg)- pregravid weight (kg)-infant
birth weight (kg)]/gestational duration (wk). Body mass index (BMI)
was calculated as pregravid weight (kg)/height
(m2). Obesity in this study was defined as
pregravid weight >77 kg because of the large number of missing
heights. This cut-off corresponds with a BMI of 29
kg/m2 for a woman of average stature (1.6 m for
both Cree and non-Native women), recommended as the obesity
cut-off by the Institute of Medicine (Institute of Medicine 1990
).
Pregravid weight information for Cree women was based on maternal recall (35.6%) (if within 5 kg of measured weight up to 10 wk gestation or within 7 kg of measured weight between 10 and 20 wk gestation) or the first available weight prior to 20 wk gestation (64.4%). Height was either measured (64.3%) or based on maternal report at booking (35.7%). Information on parity and smoking status was based on maternal report. Smoking was defined as any cigarette smoking during pregnancy. For the non-Native sample (MOND), information on pregravid weight, height, parity and smoking status was based on maternal reports at hospital booking.
Inclusion criteria.
Only singleton live births were used in the analyses. In addition, the
following exclusion criteria were applied to both populations: preterm
births (<37 wk), pregestational diabetes and glucocorticoid therapy.
Further, high-risk referrals from other hospitals and women born
outside North America and Europe were excluded from MOND to ensure a
sample with a large Caucasian majority. Extreme outliers for weight
gain during pregnancy were identified and eliminated using a method
described by Tukey (1977)
. As there were only three Cree women with a
low BMI (<19.8 kg/m2), women with a BMI <19.8
kg/m2 were excluded from both samples to make
them more comparable.
Sample size.
Of the 681 births among the Cree, 599 met the inclusion criteria. Missing data for the following variables decreased the sample size in a hierarchical manner: GDM status (n = 124), pregravid weight (n = 79), smoking status (n = 10), parity (n = 1) and height (n = 133). This resulted in a final sample of 385 Cree pregnancies with complete information except height or 252 pregnancies with all information including height.
Of the 20,982 births in the MOND, 12,353 met the inclusion criteria. Of these, information was missing for pregravid weight on 5,833, weight gain on 769, smoking status on 107 and height on 1,306. This resulted in a final sample of 5,644 MOND pregnancies without missing data for all variables except height and 4,338 pregnancies with information on all variables including height.
Statistical analyses.
Predictors of both birth weight and macrosomia were assessed in this study. Because height is often not recorded in prenatal files, we initially ran the analyses without height and BMI. All analyses were also rerun substituting height and BMI for pregravid weight (n = 4338 non-Natives, n = 252 Cree). Analyses were also repeated after restricting the data to the most recent pregnancy for each woman with more than one pregnancy during the study period. Of the 5,644 pregnancies to non-Native women, 502 women had two pregnancies, 22 women had three pregnancies and 2 women had four pregnancies between January 1990 to March 1996. Of the 385 pregnancies among the Cree, 15 women had two pregnancies between January 1995-December 1996. The sample size in the analysis excluding repeat pregnancies was thus 5,092 non-Native and 370 Cree pregnancies.
Student’s independent t test and chi-square tests were
used to test group differences between continuous and categorical
variables, respectively. Multiple logistic regression analysis was used
to examine predictors of infant macrosomia and estimate adjusted odds
ratios and 95% confidence intervals. Multiple linear regression
analysis was used to identify predictors of birth weight. The level of
significance was set at P 
0.05 to test for
significance of predictors and at P 0.1 to detect
interactions between predictors. All analyses were conducted using the
Statistical Analysis System (SAS, version 6.12, Cary, NC). The
population attributable fraction (PAF) for GDM and pregravid obesity
was estimated using the formula: PAF = Ip-Iu/Ip,
where Ip is the incidence rate of
macrosomia in the total population and Iu
is the incidence rate among the unexposed (Last 1988
).
The PAF reflects what proportion of macrosomia cases in each population
can be attributed to GDM or pregravid obesity.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. The distribution was shifted to the right for Cree infants; they were
heavier than non-Native infants by 338 g on average (3859
± 519 g vs. 3521 ± 450 g, P < 0.001). The groups had comparable gender distribution and length of
gestation (39.7 ± 1.2 vs. 39.7 ± 1.2 wk, P
= 0.78).
|
indicates the prevalence of infant macrosomia by maternal and infant
characteristics, stratified by ethnicity. In univariate analysis,
infant macrosomia among the Cree was more common among women who were
taller, heavier, had GDM, had a longer gestation and did not smoke
during pregnancy. Among non-Natives, infant macrosomia was more
common among women who were older, multiparous, heavier, taller, had
high weight gains, longer gestation and did not smoke. However, in
almost all strata of predictors, macrosomia was at least twice as high
among Cree infants as among non-Native infants. The frequency of
cesarean delivery among the Cree was not higher among macrosomic vs.
nonmacrosomic infants, whereas among the non-Natives, cesarean
delivery rates were significantly associated with infant macrosomia
(Table 1)
. The overall cesarean delivery rate for the Cree was
significantly lower than non-Natives (15.7% vs. 20.8%,
P = 0.02).
|
. Significant predictors of macrosomia among the Cree were pregravid
weight and GDM, whereas among non-Natives, age, multiparity,
pregravid weight and net rate of weight gain were positive predictors;
smoking during pregnancy was a negative predictor. The odds ratios for
most predictors were not different between the Cree and non-Natives
with the exception of GDM.
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Multiparity did not increase the risk for macrosomia among Cree infants
but had a significant effect among non-Native infants. Similarly,
net rate of weight gain during pregnancy did not increase the risk for
macrosomia among the Cree but was an important predictor among the
non-Natives (Table 2)
. When pregravid BMI and height were
substituted for pregravid weight, a 5-unit or kg/m2
increase in BMI increased the odds for macrosomia by a factor of 1.29
(95% CI: 1.03–1.65), while a 5-cm increase in height increased the
odds for macrosomia by a factor of 1.48 (95% CI: 1.13–1.96) among the
Cree. Among non-Natives, for an equivalent increase in BMI and
height, the odds ratios for macrosomia were 1.66 (95% CI: 1.48–1.86)
and 1.35 (95% CI: 1.26–1.46), respectively. In all analyses
performed, the results were very similar when macrosomia was defined as
birth weight >4,000 g or >4,500 g. When analyses were restricted to
the most recent pregnancy among Cree (n = 370) and
non-Native women (n = 5092), the results were
similar (data not presented).
The PAF for GDM and pregravid obesity was estimated to determine what proportion of macrosomia cases in each population could be explained by these risk factors. Among Cree women, GDM accounted for 13% of all macrosomia cases, whereas pregravid obesity accounted for 24%. Among non-Native women, GDM was not a significant risk factor whereas pregravid obesity accounted for 12% of the macrosomia cases.
In order to determine the risk for infant macrosomia imparted by
ethnicity (Cree vs. non-Native), multiple logistic regression analysis
was performed, combining data for the two ethnic groups and adjusting
simultaneously for the effects of maternal age, parity, pregravid
weight, net rate of weight gain, GDM status, gestational age and
smoking status. After controlling for the effects of these risk
factors, Cree infants were 3.6 times more likely to be macrosomic than
non-Native infants (Table 3
). To check whether the relationship between ethnicity and macrosomia
was affected by the interaction of ethnicity with GDM, we added the
interaction term to the aforementioned multivariate model. The adjusted
odds ratio for ethnicity was very similar even after adjusting for the
interaction between GDM and ethnicity (odds ratio: 3.09, 95% CI:
2.24–4.25).
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|
DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, Dyck and Tan 1995
, Murphy et al. 1993
, Pettitt et al. 1985
, Thomson 1990
) or any other ethnic group worldwide.
Pregravid weight, height and GDM were independent predictors of
macrosomia among the Cree. This is congruent with other reports in the
Native literature (Caulfield et al. 1998
, Dyck and Tan 1995
, Murphy et al. 1993
, Pettitt et al. 1985
, Thomson 1990
). Several studies
among North American Native groups report an increased mean birth
weight or macrosomia prevalence among women with GDM. Among the Pima
Indians of Arizona (Pettitt et al. 1985
), the prevalence
of infant macrosomia (birth weight >90th percentile for gestational
age) was much higher among women with GDM compared with women with
normal glucose tolerance (44.4% vs. 17.4%). Similarly, among the
Yup’ik Eskimos of Alaska, infants born to women with GDM weighed
149 g more, on average, than infants of negative screenees
(Murphy et al. 1993
). In a study among the Natives of
Sioux-Lookout Zone, Ontario, Canada, the risk for infant macrosomia
(birth weight >4,000 g) was higher among women with GDM only if they
had fasting hyperglycemia (Caulfield et al. 1998
).
Ethnic differences in the magnitude of effect of maternal diabetes on
infant birth weight have been reported between African-Americans
and Whites in the United States (Goldenberg et al. 1996
,
Kieffer et al. 1998
). In a recent study (Kieffer et al. 1998
), maternal diabetes increased mean birth weight by
212 g among African-American infants vs. 116 g among
White infants after adjusting for the effects of maternal place of
birth, age, education, parity, prenatal care, hypertension and
gestational age. The odds ratio for infant macrosomia (birth weight
>4,000 g) was 2.98 (2.89–3.12) for African-American infants vs.
1.83 (1.78–1.89) for White infants. However, this finding may be due
to ethnic differences in pregravid weight, which were not controlled in
this study. This is plausible because the prevalence of obesity among
African-American women is higher compared with U.S.-Caucasian women
(Kumanyika 1987
), and obesity is a strong determinant of
both diabetes (Lipton et al. 1993
) and infant macrosomia
(Okun et al. 1997
). The type of diabetes or treatment
was not specified in the study by Kieffer et al. (1998)
.
Despite the significant impact of GDM on infant macrosomia among the
Cree, GDM accounted for only 13% of all macrosomia cases, whereas
pregravid obesity accounted for 24% of all cases as determined by the
population attributable fraction. This is because pregravid obesity is
more common than among the Cree GDM (52 and 11.7%, respectively, in
this study). Our observations are supported by a study on macrosomia
among the Cree and Ojibwa of the Sioux Lookout Zone which reported the
PAF to be 25% for pregravid obesity and 10% for maternal diabetes
(Caulfield et al. 1998
). In our non-Native
population, pregravid obesity accounted for 12% of the macrosomia
cases, whereas GDM was not a significant risk factor.
Our study is the first to report a significant interaction between
ethnicity and GDM as a determinant of macrosomia in well-controlled
analyses. We do not know the reason(s) for this ethnic difference in
the impact of GDM on risk for macrosomia. One potential explanation may
be difference in treatment strategies for GDM between the two ethnic
groups. The literature on the effectiveness of GDM treatment in
decreasing the incidence of macrosomia is equivocal, and very few
randomized trials have addressed this issue (Adams et al. 1998
, Coustan and Imarah 1984
, Coustan and Lewis 1978
, Garner et al. 1997
, Li et al. 1987
, Persson et al. 1985
). However, there
is some evidence from observational studies that intensive management
of GDM can decrease the risk for infant macrosomia (Langer et al. 1994
, Thompson et al. 1994
). An earlier
study at the hospital (RVH) from which our non-Native controls were
derived demonstrated that an intensive treatment regimen for GDM was
effective in normalizing birth weight through a reduction in
gestational weight gain, and fasting and postprandial glycemic levels
(Snyder et al. 1994
). The average birth weight of
infants born to women with GDM in the latter study was 3,542 g similar
to that seen among our non-Native women with GDM (3,522 g). Another
explanation may be differences in the severity of hyperglycemia between
Cree and non-Native women with GDM. However, there is no perception
of this by health practitioners in the Cree communities, and in fact
few Cree women with GDM were treated with insulin compared with
non-Native women.
Unlike non-Native women, multiparity, gestational weight gain and
cigarette smoking did not affect infant birth weight among the Cree.
The smaller sample size for the Cree may partly account for these
differences. The lack of importance of gestational weight gain as an
independent predictor of birth weight among the Cree may be related to
the high average pregravid weight among Cree women. Overweight women
generally gain less weight during pregnancy, and gestational weight
gain among these women does not affect birth weight to the same extent
as among normal weight women (Abrams and Laros 1986
).
Smoking during pregnancy is reported to decrease birth weight by
150–200 g, the impact depending on the number of cigarettes smoked
(Kramer 1987
, Zaren et al. 1996
).
Although a higher percentage of Cree women smoked cigarettes during
pregnancy compared with non-Native women, the average number of
cigarettes smoked per day was lower (5 vs. 13 cigarettes) and may
explain why maternal smoking status did not influence birth weight
among the Cree.
The high mean birth weight of Cree infants compared with non-Native
infants after controlling for differences in important maternal and
fetal indicators may in part reflect genetic differences in fetal
growth. Despite their low socio-economic status, the Cree have a
low birth weight (<2,500 g) rate of only 2.6% (Armstrong et al. 1998
) compared with 5.9% for the general Canadian
population (Joseph and Kramer 1997
). The large size of
Cree infants may reflect selective survival of large healthy infants
through a process of natural selection.
A limitation of this study was the large reduction in sample size for Cree and non-Native women due to missing information on pregravid weight. However, most indicators were similar between non-Native women with missing information for pregravid weight (n = 5833) and non-Native women with complete data (n = 5644) with the exception that GDM prevalence was lower by 3.3% (P < 0.001) in the former group. This difference is likely due to better follow-up and more complete medical records for women with GDM. All characteristics of Cree women with missing pregravid weight (n = 79) were very similar to Cree women with complete data (n = 385), with the exception of a minor difference in mean birth weight (3743 ± 454 vs. 3859 ± 519 g, P = 0.05).
In conclusion, Cree infants are at higher risk for infant macrosomia
than non-Native infants even after adjusting for the effects of
potential confounders. The risk is exacerbated by the high prevalence
of GDM and its impact on macrosomia among Cree women. The consequences
of macrosomia in the short- or long-term among the Cree remains to
be determined although a study among the Swampy Cree women of James Bay
noted that high birth weights were associated with high rates of
shoulder dystocia (Godwin et al. 1999
). The high average
birth weight and risk for macrosomia among Cree women particularly in
those with GDM point to the importance of modifying body weight and
glycemic control.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: BMI, body mass index; GDM, gestational diabetes mellitus; IGT, impaired glucose tolerance; MOND, McGill Obstetrics and Neonatal Database; NDDG, National Diabetes Data Group; OGTT, oral glucose tolerance test; RVH, Royal Victoria Hospital; PAF, population attributable fraction.
Manuscript received July 19, 1999. Initial review completed September 16, 1999. Revision accepted December 15, 1999.
|
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