OBJECTIVE: To estimate how maternal weight gain and maternal glucose relate to fetal macrosomia risk (greater than 4,000 g) among a population universally screened for gestational diabetes mellitus (GDM).
METHODS: Between 1995 and 2003, 41,540 pregnant women in two regions (Northwest/Hawaii) of a large U.S. health plan had GDM screening using the 50-g glucose challenge test; 6,397 also underwent a 3-hour, 100-g oral glucose tolerance test. We assessed the relationship between level of maternal glucose with glucose screening and fetal macrosomia risk after adjustment for potential confounders, including maternal age, parity, and ethnicity and sex of the newborn. We stratified by maternal weight gain (40 lb or fewer compared with more than 40 lb) because excessive maternal weight gain modified results.
RESULTS: Among women with both normal and abnormal GDM screenings, increasing level of maternal glucose was linearly related to macrosomia risk (P<.001 for trend in all groups). Women with excessive weight gain (more than 40 lb) had nearly double the risk of fetal macrosomia for each level of maternal glucose compared with those with gestational weight gain of 40 lb or fewer. For example, among women with normal post–glucose challenge test glucose levels (less than 95 mg/dL) and excessive weight gain, 16.5% had macrosomic newborns compared with 9.3% of women who gained 40 lb or fewer. Moreover, nearly one third of women (29.3%) with GDM who gained more than 40 lb had a macrosomic newborn compared with only 13.5% of women with GDM who gained 40 lb or fewer during pregnancy (P=.018).
CONCLUSION: Excessive pregnancy weight gain nearly doubles the risk of fetal macrosomia with each increasing level of maternal glucose, even among women with GDM.
LEVEL OF EVIDENCE: II
Excessive weight gain in pregnancy nearly doubles the risk of macrosomia associated with each maternal glucose screening level, including women treated for gestational diabetes.
From the 1Center for Health Research, Kaiser Permanente Northwest, Portland, Oregon; the 2Center for Health Research, Kaiser Permanente Hawaii, Honolulu, Hawaii; 3Kaiser Permanente Hawaii, Honolulu, Hawaii; 4Oregon Health & Science University, Portland, Oregon; and the 5Sansum Diabetes Research Institute, Santa Barbara, California.
Supported by a Research Award from the American Diabetes Association.
Presented in part at the European Diabetes Epidemiology Group (EDEG) meetings in Cambridge, UK, March 31 to April 3, 2007.
Corresponding author: Teresa Hillier, MD, MS, Center for Health Research, Kaiser Permanente Northwest, 3800 North Interstate Avenue, Portland, OR 97227; e-mail: firstname.lastname@example.org.
Financial Disclosure The authors have no potential conflicts of interest to disclose.
Although treatment of gestational diabetes mellitus (GDM) reduces fetal macrosomia risk by more than 50%,1,2 and, conversely, not treating GDM has a twofold to fourfold increase in macrosomia risk,3,4 the relationship between maternal glucose and macrosomia is less clear among women who do not have GDM. Additionally, although maternal weight and weight gain during pregnancy are risk factors for macrosomia in all women,5–10 how maternal weight gain may modify the relationship between maternal glucose and macrosomia risk is little studied.
Our study aims were to estimate the relationship between maternal glucose during GDM screening—ranging from normal to GDM—and macrosomia risk in a diverse population. We hypothesized that macrosomia risk would be evident even among glucose levels considered normal by current GDM criteria and that maternal weight gain might modify the relationship between maternal glucose and fetal macrosomia. We tested our hypotheses among 41,540 women in a large, multi-ethnic U.S. population universally screened for GDM and their newborns, who had weight measured at birth (N=83,080).
MATERIALS AND METHODS
The study population was drawn from a combined membership of more than 650,000 at two Kaiser Permanente regions: Hawaii and Northwest. Both regions’ memberships are 20% of the areas’ general populations and reflect their demographic/sociographic characteristics. In Hawaii, low-income individuals enroll under the State Health Insurance Plan for Medicaid, about 10% of the state and Kaiser Permanente Hawaii population. During the study period, Kaiser Permanente Northwest served 8% of Medicaid members through the Oregon Health Plan, a population demographically similar to the area population.11 All members in both regions have access to medically necessary services from Kaiser Permanente or by referral from their primary care physician.
Both regions maintain administrative and clinical electronic databases on inpatient admissions and deliveries, outpatient visits, laboratory tests, pharmacy dispenses, chronic-disease registries, and outside claims/referrals. All regional databases are linked through each member’s unique health record number. Both regions also have ongoing validated diabetes registries,12,13 so women with preexisting diabetes can be excluded from analyses. The institutional review boards of both Kaiser Permanente regions and the State of Hawaii Department of Health approved this study.
Both Kaiser Permanente Hawaii and Kaiser Permanente Northwest universally screen for GDM, initially using a 50-g, 1-hour glucose challenge test. Those who fail the glucose challenge test (more than 140 mg/dL) then receive the 100-g, 3-hour oral glucose tolerance test (OGTT). For women screened more than once during pregnancy, we used the latest test. All plasma venous glucose concentrations collected for GDM screening were measured in the regional Kaiser Permanente centralized laboratories, both of which are nationally (Clinical Laboratory Improvement Amendments) certified.
Both the National Diabetes Data Group and Carpenter Coustan criteria for GDM diagnosis require that two or more of the four possible glucose concentrations measured with the 100-g OGTT be met or exceeded, although they have different threshold cut-offs. The National Diabetes Data Group’s thresholds (any two of these four) are (in mmol/L): fasting 105 mg/dL or more, 1 hour 190 mg/dL or more, 2 hours 165 mg/dL or more, 3 hours 145 mg/dL or more. The more recent Carpenter Coustan criteria have lower thresholds (any two of these four): fasting 95 mg/dL or more, 1 hour 180 mg/dL or more, 2 hours 155 mg/dL or more, 3 hours 140 mg/dL or more.14–16 We have calculated GDM using both criteria sets.
We identified 43,491 singleton, term, live births at Kaiser Permanente Hawaii and Kaiser Permanente Northwest during the period from 1995–2003 in which the mothers had continuous membership from the estimated date of conception through delivery. Mothers with preexisting diabetes (n=486) were excluded from analysis (elevated HbA1c, provider-diagnosed diabetes, or in regional diabetes registry), leaving a pool of 43,005 without preexisting diabetes. Because both regions universally screen for GDM, we had available laboratory measurements for 41,540 women (97% screening rate), which was the final study sample of 41,540 mother–newborn pairs (N=83,080 individuals).
We used electronic medical records as our primary data source and supplemented them with state birth certificate records when data were not available electronically. Birth weight was available in both the electronic inpatient record and birth certificate data; rare discrepancies were manually reviewed and adjudicated. We defined macrosomia as birth weight of 4,000 g or more.17 Ethnicity classification was based on the mother’s reported race on the states’ official birth certificates. As per state algorithms for classifying race, if the mother reported being any part Native Hawaiian, ethnicity was classified as Native Hawaiian. If she did not list Native Hawaiian but a non-white race, we classified the child into that group. Race was classified as white only if no other race/ethnicity was reported. State birth certificates also provided the mother’s reported parity and pregnancy weight gain. We did several procedures to validate the use of self-reported weight gain from the birth certificate. To evaluate the effect of excluding women with missing maternal weight gain, we performed analyses that included these women and dummy variables for 1) weight gain less than 40 lb, 2) weight gain more than 40 lb, and 3) missing weight gain. Our findings were consistent with those that are reported; odds ratios (ORs) and confidence intervals (CIs) relating maternal glucose to macrosomia were similar. Furthermore, on a subset of 13,721 women with measured pregnancy weight gain available, we compared electronically measured weight gain (prepregnancy to delivery) with self-report. On average, measured weight gain was only 1.8 lb greater (standard deviation 16.7) than self-reported weight gain. Maternal age, sex of the newborn, and prepregnancy weight were obtained from the electronic medical records.
We assessed the relationship between glucose screening tests and macrosomia and then stratified maternal glucose screening results into five categories: 1) normal glucose challenge test (referent group), 2) positive glucose challenge test, normal OGTT, 3) one abnormality on the OGTT by either National Diabetes Data Group or Carpenter Coustan criteria (two or more abnormalities are required to diagnose GDM by either criteria set), 4) GDM by the lower Carpenter Coustan criteria but not by National Diabetes Data Group, 5) GDM by National Diabetes Data Group criteria (during the study period, this is the GDM-treated group).
We conducted all initial analyses for Kaiser Permanente Hawaii and Kaiser Permanente Northwest separately, both overall by region and for the white subgroups, to confirm that results were similar between the two regions. We also assessed relationships among varying ethnic subgroups to confirm that results were similar before combining into one nonwhite category.
Of the 41,540 women screened, 7,633 failed the glucose challenge test with a 1-hour glucose more than 140 mg/dL (18%) and 6,397 had additional OGTT testing (a 3-hour 100-g test). We evaluated the 1,266 women who had a positive glucose challenge test but did not go on to have full OGTT testing to rule out potential biases. Some of the women (248 or 20%) had a glucose challenge test more than 200 mg/dL and were assumed to have GDM18–20 and not tested further; they are included in the GDM treatment group for analyses. The remainder (n=1,018) had a lower prevalence of excessive weight gain (16.7%) than the entire included sample (21.4%). Ethnicity, parity, and maternal age were also similar. Finally, because those without follow-up OGTT testing had a macrosomia prevalence of 12.5%, most similar to those with a normal OGTT, these missing OGTT values would be unlikely to bias results.
We conducted all statistical analyses using the SAS Statistical Analysis System 6.12 (SAS Institute, Cary, NC). We used t tests, Pearson χ2 test, and Mantel-Haenszel χ2 tests to evaluate univariable relationships with potential confounders and macrosomia. Cochrane-Armitage methods were used to test for trends. We used multiple logistic regression to calculate ORs and CIs adjusted for other covariates. All the statistical tests that we report are two-sided; the term statistically significant implies P<.05.
Excessive pregnancy weight gain is a strong independent predictor of macrosomia,7 and weight change ranged markedly in our cohort (−4 to +98 lb, median 31 lb). Therefore, we assessed the relationship between maternal weight gain and macrosomia initially by quartiles. The risk of macrosomia increased most significantly with the highest quartile of maternal weight gain (more than 40 lb), and thus we dichotomized maternal weight gain (more than 40 lb) for the multivariable analyses. Moreover, because we found that a maternal weight gain of more than 40 lb had a significant interaction with level of maternal glucose and macrosomia outcomes, we stratified results by maternal weight gain (40 lb or fewer compared with more than 40 lb). Of note, currently recommended pregnancy weight gain ranges from 15–40 lb, depending on prepregnancy weight, and thus 40 lb of pregnancy weight gain would be excessive regardless of prepregnancy weight.21
Table 1 presents characteristics of the 41,540 multi-ethnic mother–newborn pairs (83,080 individuals). Overall, macrosomia occurred in 5,182 (12.5%) births.
Increasing level of maternal glucose was linearly related to fetal macrosomia risk in women with both normal and abnormal GDM screenings (Tables 2 and 3, P<.001 for trend in all groups). Additionally, women with excessive weight gain (more than 40 lb) also had approximately double the risk of fetal macrosomia for each level of increasing maternal glucose (Tables 2 and 3).
Among women with a normal glucose challenge test, we stratified into categories based on potentially clinically useful thresholds (Table 2). Among women with normal weight gain, each increasing level of glycemia significantly differed from women within the referent group (1-hour glucose less than 95 mg/dL; Table 2). In women with excessive weight gain, the underlying prevalence of macrosomia was much higher in all levels of maternal glucose, and only women with a 1-hour glucose of 120 or more were significantly worse than the reference group (glucose less than 95 mg/dL) (Table 2).
Similarly, among women with normal weight gain during pregnancy, any abnormality on the OGTT was significantly worse than in women with a normal glucose challenge test. Among women with excessive weight gain, the adjusted odds of macrosomia were 1.97 (95% CI 1.31–2.95) for women with GDM compared with women with a normal glucose challenge test. In fact, the combination of GDM and excessive weight gain resulted in the highest prevalence of macrosomia. Nearly one third (29.3%) of women with GDM and excessive weight gain had a macrosomic newborn compared with only 13.5% of women with GDM who gained 40 lb or fewer (P=.018).
The increasing macrosomia risk associated with both increasing maternal glucose and excessive weight gain was consistent across ethnic groups and study sites. During the entire study period, GDM by National Diabetes Data Group criteria was treated in both regions. Beginning in January 2001, all women in Kaiser Permanente Hawaii with GDM by Carpenter Coustan also were treated; for Kaiser Permanente Northwest, incorporating Carpenter Coustan treatment is recent and not universal. Therefore, we did a subanalysis of births from 1995–2000, when only GDM by National Diabetes Data Group criteria was clearly treated to better differentiate treatment effect. The highest adjusted risk of macrosomia among women who gained 40 lb or fewer was also with GDM by Carpenter Coustan criteria (which was untreated) (OR 1.54, 95% CI 1.10–2.17). Among the highest maternal glucose group, which was treated (GDM by National Diabetes Data Group criteria), fetal macrosomia risk was attenuated and was not statistically different from women with a normal glucose screening (OR 1.21, CI 0.97–1.53). Moreover, among women with a weight gain of more than 40 lb, those with GDM by National Diabetes Data Group criteria remained the highest-risk group despite treatment (OR 2.29, CI 1.41–3.71). These results are consistent with the entire cohort (Table 3) and more clearly underscore the potential reversibility of macrosomia with treatment among women who gain 40 lb or fewer.
We did a separate analysis comparing fasting with other abnormalities on the OGTT with macrosomia risk. Again, there was a linear relationship between increased maternal glucose level on screening and fetal macrosomia risk regardless of weight-gain group (P<.001). Fasting maternal hyperglycemia on the OGTT had a higher risk of macrosomia than did other OGTT abnormalities in both weight-gain risk groups. Of note, the risk of fetal macrosomia was still higher among women with normal glycemia who gained more than 40 lb (glucose challenge test) than among women with abnormal fasting glucose levels on the OGTT who gained 40 lb or fewer during pregnancy (18.3% compared with 17.0%, P=.039) (Fig. 1).
Among our population of more than 80,000 mothers and newborns, we found that fetal macrosomia risk increased linearly with increasing maternal glucose level among women with normal glucose challenge test screenings and among those who went on to the OGTT. Excessive maternal weight gain (more than 40 lb) modified this relationship. For each maternal glucose stratum—including women with GDM that was treated—fetal macrosomia risk was about double with excessive maternal weight gain (more than 40 lb) compared with weight gain of 40 lb or fewer. Excessive maternal weight gain also significantly increased the risk of fetal macrosomia across all glucose concentrations, even among women with a normal glucose challenge test. In fact, women with the lowest glucose on screening (post–glucose challenge test glucose less than 95 mg/dL) and excessive weight gain had a higher prevalence of fetal macrosomia than did treated women with GDM who gained 40 lb or fewer (16.5% compared with 13.5%, respectively) (Tables 2 and 3).
Cedergren found that gestational weight gain—independent of maternal prepregnancy weight—was a significant predictor of large-for-gestational age newborns among 245,526 women in the Swedish registry, but this study did not evaluate maternal glucose.5 Others have also found gestational weight gain to be a significant predictor of birth weight and macrosomia independent of prepregnancy weight,6–10 but the relationship of weight gain to GDM or levels of maternal glucose is less clear and little studied.22,23 In a case-control study of 390 women, Catalano and colleagues did not find a relationship between gestational weight gain and neonatal birth weight among any women with GDM, regardless of prepregnancy weight.23 They also found that women with GDM gained 2.5 kg less average weight than did those without GDM (P=.0006), but they did not stratify by excessive weight gain. In our cohort study of more than 40,000 births, we observed that excessive weight gain had an increased risk of macrosomia across increasing levels of maternal glucose, including GDM.
Others have similarly found that elevated glucose levels not diagnostic for GDM are associated with macrosomia, but they did not evaluate the potential modifying effect of weight gain.24–31 Ferrara and colleagues evaluated 45,245 women and found that both maternal fasting and 1-hour, but not 2- or 3-hour, post-OGTT glucose levels were independent predictors of macrosomia risk.32 We previously found that maternal fasting hyperglycemia on the OGTT is a significant predictor of childhood overweight and obesity at age 5–7.13 Our current findings further suggest that maternal fasting hyperglycemia is an important risk factor for offspring overweight beginning at birth.
Our study has important strengths. The population is a large, multi-ethnic U.S. sample of more than 40,000 mother–newborn pairs with universal maternal GDM screening and follow-up through birth to collect newborn birth weight. Our universal, two-step GDM screening program (50-g glucose challenge test; if positive, a diagnostic OGTT) allows us to evaluate the effects of a large range of maternal glucose levels, from normal glucose challenge test to GDM, including women treated for GDM. Evaluation of potential confounders such as ethnicity and maternal age and weight gain are also strengths. Additionally, we could determine that the relationships observed between maternal glucose and macrosomia risk were consistent among differing ethnic groups in our diverse population.
Our study also has limitations. Because the outpatient electronic medical record was just beginning for Kaiser Permanente Northwest during the study period and was not in place at Kaiser Permanente Hawaii, prepregnancy weights are available only for a subset of 4,395 women at Kaiser Permanente Northwest. However, in these 4,395 mother–newborn pairs, excessive pregnancy weight gain (more than 40 lb) remained a similarly significant independent risk factor for macrosomia among normal-weight (body mass index [BMI] less than 25), overweight (BMI 25–29), and even obese (BMI 30 or more) women (BMI is calculated as weight (kg)/[height (m)]2). Also of note is that our classification of maternal glucose is based on GDM screening results at one time point in pregnancy; multiple measures of glycemia are not electronically available for the population. Similarly, we do not have home glucose monitoring records electronically available among those with GDM to assess glucose control. However, the proportion of women requiring insulin (in addition to diet treatment) did not differ by weight-gain group (18.2% of the women with GDM who gained fewer than 40 lb required insulin compared with 18.7% of women with GDM who gained 40 lb or more, P=.437) Because providers in our health plan use the same GDM treatment guidelines for insulin initiation based on glucose control, it is unlikely that the weight-gain groups differed markedly in glucose control.
The marked effect of maternal weight gain on macrosomia and the relationship between increasing glucose and macrosomia in women who gained in excess of 40 lb is notable because this is excessive pregnancy weight gain for any U.S. woman by current guidelines.21 Our results are particularly important given both recent trends of increased weight gain during pregnancy33 and the clinical provider’s advice being an independent predictor of pregnancy weight gain.34 Moreover, because a recent study found that one third of women reported receiving no provider advice on gestational weight gain,34 our findings emphasize the need for both advising and monitoring women to avoid excessive weight gain. Our results should be interpreted with the perspective that the goal is ideal weight gain because low gestational weight gain also is associated with adverse pregnancy outcomes.5
In summary, we found that macrosomia risk is increased across the spectrum of maternal glucose measured with GDM screening and that this relationship is further modified by excessive maternal weight gain. Irrespective of maternal glucose screening results, maternal weight gain of more than 40 lb was associated with nearly twice the prevalence of macrosomia. Awaiting further evidence, clinicians should consider the importance of both maternal glucose and excessive pregnancy weight gain as potentially modifiable risk factors for fetal macrosomia.
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