Association of a Womans Own Birth Weight with Her Subsequent Risk for Pregnancy-induced Hypertension
Kim E. Innes1,2 ,
Tim E. Byers1,
Julie A. Marshall1,
Anna Barón1,
Miriam Orleans1 and
Richard F. Hamman1
1 Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, CO.
2 Southeastern Rural Mental Health Research Center, University of Virginia, Charlottesville, VA.
Received for publication March 10, 2003; accepted for publication April 22, 2003.
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ABSTRACT
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Studies have linked low birth weight to elevated risk for adult hypertension and insulin resistance. However, the relation between birth weight and later risk for pregnancy-induced hypertension (PIH), a disorder associated with insulin resistance and predictive of chronic hypertension, has not been well studied. This case-control study used linked hospital discharge and vital record data from New York State. Subjects were healthy women born in New York State who completed a first pregnancy there between 1994 and 1998. Records from each womans own birth (19701985) were linked to those from her first pregnancy. Cases were 2,180 women diagnosed with PIH. Controls were the 22,955 remaining women with no record of PIH. Birth weight showed a U-shaped relation to risk for PIH, with the highest risks associated with very low and very high birth weights. Relative to women born at 3.54.0 kg, odds ratios adjusted for gestational age were 2.1 (95% confidence interval (CI): 1.1, 3.9) and 1.6 (95% CI: 1.1, 2.4), respectively, for women with birth weights less than 1.5 kg and greater than 4.5 kg. Adjustment for other perinatal factors reduced the association with high birth weight to 1.1 (95% CI: 0.7, 1.7) but strengthened that with lower birth weights, leaving a strong, inverse relation between birth weight and PIH risk (p for trend < 0.0001). These findings support a possible role for early life factors, particularly fetal growth, in the etiology of PIH.
birth weight; hypertension; insulin resistance; pre-eclampsia; pregnancy
Abbreviations:
Abbreviations: CI, confidence interval; OR, odds ratio; PIH, pregnancy-induced hypertension.
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INTRODUCTION
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Studies of older adults have repeatedly demonstrated inverse associations between markers of fetal growth and blood pressure (1) and hypertension (2), lending support to the "fetal origins" hypothesisthat susceptibility to hypertension and related chronic adult conditions may be programmed in utero. However, studies of younger populations continue to yield more conflicting findings (1, 311), and observed effects have been small and of unclear clinical significance (12). Several investigators have also argued that the observed relation between hypertension and impaired fetal growth could be confounded by later environmental influences and/or by relative postnatal growth (1214). In addition, few studies in any age group have adjusted for the potentially important confounding influence of maternal hypertension (10, 1518), which could lead to both impaired fetal growth and chronic hypertension in the offspring (12, 16).
Pregnancy-induced hypertension (PIH) is a common disorder of gestation that predicts future hypertension, cardiovascular disease, and diabetes (19, 20). PIH shares many features of the metabolic syndrome (19, 20) and is an easily measurable condition that occurs relatively early in life. PIH is therefore well suited for testing the fetal origins hypothesis in young adult populations. To date, only two published studies have examined the associations between markers of a womans growth as a fetus and her subsequent risk for hypertension as a pregnant adult (15, 21). Although results from these studies suggest that impaired fetal growth may increase risk for PIH, interpretation of findings is limited by small sample sizes, which precluded detailed evaluation of dose-response associations, of the relative influence of high birth weight, and of potentially important modifiers such as body mass index and race/ethnicity. In this paper, we describe findings from a large, population-based study designed to address these limitations.
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MATERIALS AND METHODS
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Data for this case-control study were drawn from two large, computerized state databases maintained by the New York State Department of Health: the livebirth registry and the New York State hospital discharge records. Eligible subjects included all women who completed a first pregnancy (and delivered a liveborn infant) in Upstate New York between 1994 and 1998, and who were also born in New York State in 1970 or later. The Bureau of Biometrics of the New York State Department of Health performed all subject selection and record linkages and produced the final anonymous data set of linked pregnancy and birth records. Matching procedures are described elsewhere (22). The study was approved by the Colorado Multiple Institutional Review Board and the New York State Department of Health Institutional Review Board.
Of the 95,309 pregnancy records from 1994 to 1998 indicating birth of the mother in Upstate New York in 1970 or later, 57,588 (60 percent) were successfully linked to the womens own birth records. From these linked records, all but those pertaining to first pregnancies were then excluded, leaving a total of 29,924 linked birth and first pregnancy records. We then further excluded from the study any woman whose pregnancy was complicated by multifetal gestation (n = 270), by the use of illegal drugs (n = 678), or by heart disease, essential hypertension, renal disease, diabetes mellitus, acute or chronic lung disorders, or other serious acute or preexisting chronic conditions requiring medication or monitoring (n = 3,482) as indicated on her hospital discharge or infants birth record. Women with gestational diabetes (n = 608) were also excluded, leaving a final sample of 25,135 eligible primigravida subjects. Among eligible subjects, age at delivery ranged from 12 to 28 years and averaged 21.1 years (standard deviation, 3.5).
Cases were defined as eligible subjects with a record of pregnancy-related hypertension, preeclampsia, or eclampsia on their infants birth records and/or a diagnosis, according to the International Classification of Diseases, Ninth Revision, of transient hypertension (codes 642.0642.3), hypertension complicating pregnancy (code 642.9), mild preeclampsia (code 642.4), severe preeclampsia (code 642.5), or eclampsia (code 642.6) on their hospital discharge records. A total of 2,180 cases of PIH (8.7 percent of all eligible first pregnancies) were identified on linked birth registry and hospital discharge records. Cases included 1,044 pregnancies complicated by gestational hypertension, 1,095 by preeclampsia, and 41 by eclampsia. Because the association of PIH with markers of fetal growth and other perinatal factors did not differ appreciably by PIH category (gestational hypertension vs. preeclampsia/eclampsia), diagnostic severity (mild vs. severe preeclampsia), or diagnostic source (vital record vs. hospital discharge data), and the risk profiles for these case groups were similar, all PIH cases were combined for the analyses presented here. Controls were defined as all remaining eligible subjects whose first pregnancies were not complicated by PIH (n = 22,955).
Growth in utero was measured as the womans own birth weight and gestational age (clinical estimate in weeks) as indicated on her birth certificate. Birth weight was evaluated both alone (as a measure of absolute birth size) and adjusted for gestational age in weeks (as an indicator of relative fetal growth). Implausibly extreme values (e.g., birth weights less than 450 g and gestational ages less than 22 weeks or greater than 46 weeks) were set to missing. Using New York State vital record information, we assessed the relation of PIH risk to other factors characterizing the subjects own birth and experience in utero, including multifetal gestation, subject birth order (firstborn vs. later born), maternal age and parental educational levels at the time of the subjects birth, and preeclampsia, chronic hypertension, diabetes, or other serious conditions complicating the pregnancy of the womans mother. In addition, we assessed the effects of potential risk factors for PIH that characterized the womans first pregnancy, including her race/ethnicity, age, marital status, educational level, employment and insurance status, participation in welfare, onset of prenatal care, tobacco use during pregnancy, height, prepregnancy body mass index (calculated as weight (kg)/height (m)2), and pregnancy weight gain.
We used multiple logistic regression analysis to determine the independent effects of a womans own birth size, relative fetal growth gestational age, and other factors on the development of PIH, to evaluate the influence of potential confounders and to assess linear trends. To assess the influence of birth weight adjusted for gestational age (a measure of relative fetal growth) on PIH risk, we included gestational age (in weeks) as a covariate in the multiple logistic regression model. We conducted additional analyses stratified by factors known or suspected to modify the association between fetal growth and PIH or chronic disease risk, including prepregnancy body mass index, height, race/ethnicity, and smoking status. Multiplicative interactions were also assessed using logistic regression.
Primigravida women whose pregnancy records could not be linked to those from their own birth were more likely than matched women to be Black (20 percent vs. 12 percent) and receiving Medicaid (46 percent vs. 38 percent), and they averaged slightly younger ages at the time of delivery (20.7 vs. 21.1 years). However, unmatched women did not differ from matched women in other demographic or anthropometric characteristics in the onset of prenatal care or in tobacco use during pregnancy. Most importantly, linkage to a birth record was not associated with the prevalence of PIH either overall or within different categories of age and race/ethnicity.
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RESULTS
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Relative to non-Hispanic White women, African-American women had a higher PIH risk (odds ratio (OR) = 1.2, 95 percent confidence interval (CI): 1.0, 1.3), and women of Hispanic origin had a lower risk (OR = 0.75, 95 percent CI: 0.6, 1.0). PIH was weakly associated with marital status, age, education, employment during pregnancy, and Medicaid coverage (table 1).
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TABLE 1. Association of demographic factors characterizing a womans first pregnancy (19941998) and early life with her risk for pregnancy-induced hypertension, among previously healthy, New York-born women
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The risk for PIH rose strongly with increasing prepregnancy body mass index and pregnancy weight gain (table 2). Relative to women in the lowest body mass index quartile, those in the highest quartile were over three times as likely to develop PIH (unadjusted OR = 3.3, 95 percent CI: 2.9, 3.7). Likewise, the risk for PIH was over twofold higher among women who gained 45 pounds (20.412 kg) or more during pregnancy than among those who gained less than 25 pounds (11.340 kg) (OR = 2.3, 95 percent CI: 2.1, 2.7). Women who smoked during pregnancy were less likely to develop PIH (OR = 0.7, 95 percent CI: 0.6, 0.8) (table 2). Adjustment for other perinatal factors did not alter the protective effect of smoking on risk for PIH and slightly strengthened the relation of prepregnancy body mass index and pregnancy weight gain to PIH risk.
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TABLE 2. Relation of factors characterizing a womans first pregnancy to her risk for pregnancy-induced hypertension, New York State, 19941998
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Birth weight, both alone and adjusted for gestational age, showed a U-shaped relation to risk for PIH, with very low and very high birth weights demonstrating the most pronounced increase in risk (adjusted ORs for <1.5 kg and
4.5 kg = 2.10 (95 percent CI: 1.1, 3.9) and 1.6 (95 percent CI: 1.1, 2.4), respectively) (table 3). With birth weight up to 4,000 g, the risk for PIH decreased progressively with rising birth weight (p for trend = 0.007). Adjustment for other perinatal factors strengthened this inverse, dose-response relation. In contrast, controlling for other risk factors and, specifically, prepregnancy body mass index and pregnancy weight gain largely eliminated the relation between high birth weight and risk for PIH (OR for birth weight of
4.5 kg after adjustment for these two factors alone = 1.1, 95 percent CI: 0.7, 1.7) (p for trend < 0.0001). These associations did not differ appreciably by PIH category (adjusted ORs for birth weight of <2,000 g = 1.7 (95 percent CI: 1.0, 2.9) (p for trend = 0.02) for gestational hypertension vs. 2.0 (95 percent CI: 1.2, 3.3) (p for trend = 0.002) for preeclampsia) (table 4). Likewise, these associations were similar by source of diagnosis (adjusted ORs for birth weight of <2,000 g = 1.7 (95 percent CI: 0.9, 3.5) (p for trend = 0.009) for cases identified on vital records vs. 1.9 (95 percent CI: 1.1, 3.4) (p for trend = 0.025) for cases identified on hospital discharge records). Including women with a record of both gestational diabetes mellitus and PIH (n = 98) in the analysis slightly strengthened the inverse relation between birth weight and PIH (adjusted OR for <1.5 kg = 2.3 (95 percent CI: 1.1, 4.5) (p for trend < 0.0001)).
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TABLE 3. Relation of factors characterizing a womans own birth (19701986) to her later risk for pregnancy-induced hypertension in her first pregnancy (19941998), New York State
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TABLE 4. Association of a womans own weight at birth (19701986) with her later risk for pregnancy-induced hypertension in her first pregnancy (19941998), stratified by diagnostic category, New York State*
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The inverse association of birth weight with risk for PIH was more pronounced among thinner than among heavier women (table 5: p for interaction < 0.0001;
21 df = 45.59). Although risk for PIH decreased progressively with increasing birth weight among women with low and average prepregancy body mass index (p for trend = 0.0006 and 0.001, respectively), no directional trend was apparent among heavier women (p for trend = 0.53). The association of birth weight with PIH risk was also weaker among Black women than among other racial/ethnic groups (table 6: p for interaction = 0.006;
21 df = 7.72). Although Black women in this study weighed significantly less at birth than did non-Black subjects (3,022 g (standard deviation, 545) vs. 3,226 g (standard deviation, 514) and were more than twice as likely to have been low birth weight as newborns (OR = 2.2, 95 percent CI: 2.0, 2.5), reduced birth weight was not related to PIH risk in this group and did not explain the increased risk for PIH observed among Black women. Stratifying Black women by body mass index or gestational age at birth did not alter these results.
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TABLE 5. Association between a womans own weight at birth (19701986) and her later risk for pregnancy-induced hypertension in her first pregnancy (19941998), stratified by the subjects prepregnancy body mass index, New York State*,
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TABLE 6. Association between a womans own weight at birth (19701986) and her later risk for pregnancy-induced hypertension in her first pregnancy (19941998), stratified by the subjects race/ethnicity, New York State*,
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Women born to mothers whose pregnancies were complicated by hypertension were themselves at approximately 50 percent increased risk of developing PIH in their first pregnancies (ORs = 1.6 (95 percent CI: 1.1, 2.1) for maternal preeclampsia and 1.5 (95 percent CI: 1.1, 1.9) for any form of maternal hypertension). Although adjustment for a womans own birth weight and gestational age did not appreciably alter these risk estimates, further adjustment for body mass index, smoking, and other factors attenuated the strength of these associations (table 3). Excluding women born to mothers whose pregnancies were complicated by hypertension did not appreciably change either the strength or the magnitude of the relation between birth weight and risk for PIH (OR adjusted for body mass index and other factors = 2.1, 95 percent CI: 1.0, 4.6) (p for trend = 0.007).
We found little evidence for an association between risk for PIH and other factors characterizing the subjects own birth, including maternal age, parental educational level, birth order, prematurity, and multifetal gestation. Similarly, a womans height, timing of first prenatal care visit, or participation in low income programs was not related to her risk of developing PIH.
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DISCUSSION
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In this population-based study of young, primigravida New York women, we found a marked U-shaped association between a womans risk for PIH in her first pregnancy and her own birth weight as a newborn, both alone and adjusted for gestational age. Adjustment for other perinatal factors, in particular prepregnancy body mass index and pregnancy weight gain, considerably attenuated the association with high birth weight but strengthened that with low birth weights, leaving a strong, inverse dose-response relation between birth weight and risk for PIH. This inverse association was less apparent among Black women and among women with a prepregnancy body mass index of 25 or greater.
Our finding of increased risk for PIH among women born at lower birth weights is consistent with those of two recent investigations (15, 21). In our previous study of young Colorado-born women, we observed an elevated risk for PIH with low birth weight but no significant directional trend (21). However, the power of this study was limited by its small size (345 cases). Similarly, in a recent prospective study of Danish women, Klebanoff et al. (15) found that women born small for gestational age were at elevated risk for hypertension in pregnancy (adjusted OR = 1.8, 95 percent CI: 1.1, 2.8). However, again case numbers were small (157 hypertensive pregnancies), and the dose-response relation was not evaluated in detail.
The inverse association between birth weight and PIH risk observed in the present study also parallels recently published findings regarding fetal growth and subsequent risk for gestational diabetes mellitus (2225), suggesting a possible etiologic link between these disorders. In particular, our recent study in the same population of primiparous New York-born women demonstrated a similar U-shaped relation between a womans own birth weight and gestational diabetes mellitus (22). Consistent with findings of the current study, adjustment for prepregnancy body mass index largely eliminated the effect of high birth weight but strengthened the inverse association between birth weight and subsequent risk for gestational diabetes mellitus (22).
To our knowledge, this is the first study to demonstrate a clear dose-response association between birth weight and risk for PIH. Our results meet the criteria recently outlined by Lucas et al. (14), who have argued that, in order for data to support the fetal origins hypothesis, birth weight should have a significant inverse effect in models unadjusted for current weight or body mass index. Some previous investigations have reported an inverse relation between birth weight and blood pressure that is apparent only after adjustment for current body size (14) or that is stronger among heavy (9, 26) individuals, suggesting that greater postnatal change in size may explain or amplify the influence of birth weight. In contrast, our finding of a stronger relation between low birth weight and subsequent PIH risk among leaner than among heavier women suggests that the influence of reduced fetal growth on risk for PIH is neither explained by relative postnatal weight gain nor amplified by adult obesity. These results also suggest that the effects of low birth size and obesity are independent and may influence PIH risk in part via different pathways.
Black women have a higher prevalence of both low birth weight and hypertension (5). However, reduced birth size was not strongly related to risk for PIH among Black women in our study and did not explain their elevated incidence of PIH. In contrast, we observed a strong inverse relation between birth size and PIH risk among non-Black subjects. Although the reasons for this racial difference are unclear, our findings are consistent with recent studies of Black Americans showing no relation between birth weight and adult blood pressure (5, 27).
PIH is characterized by relative insulin resistance, glucose intolerance, and hyperlipidemia and by endothelial dysfunction and elevated levels of specific coagulation and fibrinolytic factors known to predict cardiovascular disease (19, 20). Biologic mechanisms underlying the link between birth size and the later development of PIH may include early alterations in lipid metabolism, endothelial function, and carbohydrate metabolism. Low birth weight has been linked to impaired endothelial function (28), dyslipidemia (29, 30), insulin resistance (3032), and reduced glucose tolerance (31, 32) later in life, and a growing body of experimental work in animals suggests that these changes can be programmed in utero (31, 33, 34). The hyperlipidemia and insulin resistance that normally accompany pregnancy are exacerbated in women who develop PIH (20). Such metabolic alterations may compromise a womans ability to meet the diabetogenic and lipogenic challenges of pregnancy and thus render her more likely to develop PIH.
Exposure to maternal hypertension, which has been associated with both impaired fetal growth (12) and PIH in the female offspring (35), could also help explain the association between low birth weight and the subsequent development of high blood pressure in pregnancy. However, although our results indicated that maternal hypertension was indeed a risk factor for PIH in the daughter, neither adjustment for maternal hypertension nor exclusion of subjects exposed to this or other maternal pregnancy complications altered the observed inverse relation between birth size and PIH. Consistent with our findings, adjustment for maternal hypertension did not alter the association of a womans own impaired fetal growth with her subsequent risk for PIH in a prospective study of Danish women (15). Likewise, in studies of European children and adolescents, investigators did not find maternal blood pressure during pregnancy to alter the observed association between birth weight and blood pressure in the offspring (17, 26).
In the present study, the risk for PIH rose with increasing prepregnancy body mass index and pregnancy weight gain. In agreement with our findings, several previous studies have demonstrated an elevated risk for both preeclampsia and gestational hypertension among heavier women (36, 37). Increased pregnancy weight gain has been prospectively linked to elevated risk for PIH in several previous investigations (38, 39). Obesity and weight gain are associated with insulin resistance and dyslipidemia (4042), and weight loss improves both insulin sensitivity and lipid profiles (40). Because sudden weight gain is considered a symptom of severe preeclampsia, it could be argued that pregnancy weight gain should not be considered as a covariate in the model. However, removing pregnancy weight gain from the model did not appreciably alter the inverse association between birth weight and risk for PIH (adjusted for body mass index only, OR = 1.9 (95 percent CI: 1.0, 3.8) for birth weight of <1,500 g (p for trend = 0.025)), and milder forms of PIH, which are not generally characterized by precipitous weight gain, were as strongly related to pregnancy weight gain as was preeclampsia. In addition, prior studies suggest that excessive weight gain may itself predispose to the development of PIH (38, 39).
This study has several strengths, including the population-based design, the racial and ethnic diversity of the study population, and the large sample sizes, which allowed us to evaluate in detail the relation between birth weight and PIH risk and to assess potentially important modifying or confounding factors. Because the data on birth characteristics were derived from vital records, and thus gathered well in advance of the pregnancy outcomes, biases in measurement or diagnosis are unlikely. Using linked vital record and hospital discharge data also enabled us to increase the sensitivity in detecting PIH and other conditions complicating pregnancy. Studies in New York (M. Zdeb, New York State Department of Health, unpublished data) and other states (43) have shown that linking birth registry to hospital discharge data considerably increases the sensitivity in detecting obstetric and birth outcomes. Moreover, although sensitivities for conditions complicating pregnancy are often low for vital records, accuracy, as indicated by positive and negative predictive values, can be high. For example, a large Tennessee validation study of birth certificate information demonstrated low-to-moderate sensitivities but good-to-excellent predictive values for reporting of diabetes, chronic hypertension, and pregnancy-induced hypertension (44).
The use of vital record and hospital discharge data also presents limitations. We were unable to adjust for certain known and potential risk factors for PIH, including family history of hypertension or diabetes, dietary intake, exercise habits, and maternal smoking. However, it is improbable that confounding by unmeasured variables could explain our findings. In several previous investigations, adjustment for maternal smoking (10, 45), socioeconomic status (6, 15, 4547), and other potential confounders (6, 48, 49) did not appreciably alter observed associations between blood pressure or hypertension and birth weight. Another limitation is the probable underreporting of certain pregnancy complications in the New York State vital records during the period between 1970 and 1985. In particular, our ascertainment of maternal hypertension (hypertension complicating the pregnancy of the subjects mother) is likely incomplete, based on prevalence reported in previous studies (15, 36). Nonetheless, in a recent study (15) in which the authors obtained comprehensive information on hypertension complicating the mothers pregnancy, the risk estimates for PIH associated with maternal hypertension (ORs = 1.31.8) were similar to those observed in our investigation. Because gestational age estimates were based on the last menstrual period, a method that tends to overestimate true gestational age (50), preterm birth is also likely to have been underreported. Certain lifestyle factors characterizing a womans first pregnancy are also likely to be underreported, including smoking. However, the observed negative association between tobacco use and PIH risk is consistent with that of previous studies (51).
PIH in the womans own pregnancy is also likely to have been underascertained, leading to misclassification of controls. Preeclampsia is estimated to complicate 710 percent of all first pregnancies (36, 52), in contrast to our observed incidence of 4.5 percent. Similarly, recent studies have reported gestational hypertension to complicate 517 percent of first pregnancies without chronic hypertension or diabetes (36, 53), whereas we observed a rate of 4.2 percent. However, since any resulting misclassification of controls is unlikely to be differentially related to a womans birth weight, incomplete ascertainment of PIH would likely lead to an underestimation of the association between PIH and birth weight.
This study did not include any women over the age of 28 years, precluding generalization of our results to older primiparas. We were also unable to link approximately 40 percent of the pregnancy and birth records, raising the possibility of selection bias. However, primigravida women whose records could not be linked were similar to matched women in most demographic factors, in anthropometric characteristics, in lifestyle choices during pregnancy, and in the timing of prenatal care initiation. Most importantly, the prevalence rates of PIH, both overall and within specific age and racial/ethnic groups, were similar in the matched and unmatched samples, as were the associations of demographic and anthropometric factors with PIH risk.
In summary, this large study of young, primiparous, New York-born women showed a significant, inverse relation between a womans own birth weight and her later risk for PIH, an important complication of pregnancy and marker for chronic disease risk. These findings are consistent with the hypothesis that susceptibility to hypertension and related insulin resistance conditions may be programmed in utero, and they suggest that early life factors and, in particular, fetal growth may be important in the etiology of PIH.
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ACKNOWLEDGMENTS
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This study was supported by grant 1RO3HL59467-d from the National Institute of Diabetes and Digestive and Kidney Diseases.
The authors thank Gene Therriault, Director, and Robert Draiss, Senior Computer Analyst, of the New York State Health Department Bureau of Biometrics for their assistance in creating the anonymous linked data set for us and for offering numerous helpful suggestions and comments during various stages of this project.
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NOTES
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Correspondence to Dr. Kim E. Innes, Southeastern Rural Mental Health Research Center, McLeod Hall, University of Virginia, 202 15th Street SW, Charlottesville, VA 22903-3306 (e-mail: kei6n{at}virginia.edu). 
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