Pregnancy Weight Gain Before Diagnosis and Risk of PreeclampsiaNovelty and Significance
A Population-Based Cohort Study in Nulliparous Women
Weight gain in early pregnancy may influence a woman’s risk of developing preeclampsia. However, the consequences of weight gain throughout pregnancy up to the diagnosis of preeclampsia are unknown. The aim of this study was to determine whether pregnancy weight gain before the diagnosis of preeclampsia is associated with increased risks of preeclampsia (overall and by preeclampsia subtype). The study population included nulliparous pregnant women in the Swedish counties of Gotland and Stockholm, 2008 to 2013, stratified by early pregnancy body mass index category. Electronic medical records were linked with population inpatient and outpatient records to establish date of preeclampsia diagnosis (classified as any, early preterm <34 weeks, late preterm 34–36 weeks, or term ≥37 weeks). Antenatal weight gain measurements were standardized into gestational age-specific z scores. Among 62 705 nulliparous women, 2770 (4.4%) developed preeclampsia. Odds of preeclampsia increased by ≈60% with every 1 z score increase in pregnancy weight gain among normal weight and overweight women and by 20% among obese women. High pregnancy weight gain was more strongly associated with term preeclampsia than early preterm preeclampsia (eg, 64% versus 43% increased odds per 1 z score difference in weight gain in normal weight women, and 30% versus 0% in obese women, respectively). By 25 weeks, the weight gain of women who subsequently developed preeclampsia was significantly higher than women who did not (eg, 0.43 kg in normal weight women). In conclusion, high pregnancy weight gain before diagnosis increases the risk of preeclampsia in nulliparous women and is more strongly associated with later-onset preeclampsia than early-onset preeclampsia.
Preeclampsia is a predictor of cardiovascular disease and other metabolic disorders in later life.1 Identifying modifiable risk factors for preeclampsia is an important priority for preventing disease onset during pregnancy and potentially reducing longer-term health risks. Although prepregnancy obesity is a well-established modifiable risk factor for preeclampsia,2–4 the role of high weight gain during pregnancy is less clear.
Several studies have found that women with high pregnancy weight gain are more likely to develop pregnancy hypertensive disorders, including preeclampsia.5–14 However, many of these studies only measured total pregnancy weight gain (ie, weight gain up to the time of delivery). This introduces a serious methodological flaw15 because one of the symptoms of preeclampsia is edema, leading to higher weight gain because of water retention.16 Past findings, therefore, likely suffer from reverse causality (ie, higher weight gain is the result of, rather than a cause of, preeclampsia).
A major challenge in overcoming bias because of reverse causation is that information on timing of preeclampsia onset is rarely available in population perinatal databases. Typically, only the woman’s final preeclampsia status at delivery is available. As a result, identifying weight gain patterns before disease diagnosis has been difficult. Several studies have examined weight gain in early or mid-pregnancy,11–14 as by definition, preeclampsia cannot be diagnosed until after 20 weeks. However, this analytic approach does not consider the role of weight gain during the second half of pregnancy when the majority of weight gain occurs.17 Furthermore, these studies did not investigate the role of weight gain according to preeclampsia subtypes, which may be etiologically distinct.18
The aims of this study were to:
Determine whether pregnancy weight gain before diagnosis is associated with increased risks of preeclampsia, overall and according to disease subtype (early preterm diagnosis <34 weeks, late preterm diagnosis 34–36 weeks, term diagnosis ≥37 weeks).
Establish the gestational age at which the pregnancy weight gain trajectories of women who go on to develop preeclampsia diverge from those of women without preeclampsia.
Our study population was drawn from singleton deliveries in the Stockholm-Gotland Obstetrical database between 2008 and 2013.17 The database contains electronic medical records from all antenatal and delivery visits for births in the counties of Stockholm and Gotland, Sweden, and has been linked with the national Prescribed Drug Register and the National Patient Register, which contains summaries of all diagnoses and procedures during inpatient and outpatient visits. We excluded women with prepregnancy hypertension and restricted our cohort to nulliparous women because preeclampsia status in a woman’s first pregnancy strongly predicts her risks of preeclampsia in subsequent pregnancies.19 We excluded pregnancies of women without early-pregnancy body mass index (BMI; kg/m2) or no gestational weight gain measurement and cases of preeclampsia where the date of diagnosis was unknown. Our study was approved by The Regional Ethics Committee in Stockholm, and all clinics in the database consented to medical record access. Sharing of these data is not permissible because according to Swedish law and The Stockholm Regional Ethical Review Board, it is prohibited to publicly share data with personal information. Statistical code is available on request from the corresponding author.
Weight and Weight Gain
Early-pregnancy BMI was calculated as the first measured weight in kilograms <14 completed gestational weeks divided by height in m2 (median age at first measurement at 9 weeks gestation, interquartile range [IQR], 8–10). We defined normal weight as an early-pregnancy BMI of 18.5 to 24.9 kg/m2, overweight as 25 to 29.9 kg/m2, and obese as ≥30 kg/m2.20 Gestational weight gain was calculated as the measured weight at the time of antenatal care or delivery minus early-pregnancy weight. In Sweden, the typical schedule of routine antenatal visits is at weeks 8 to 12, week 24, week 28, weeks 31 to 32 and, thereafter, every second week until birth. Women are weighed at most, but not all, visits as part of routine antenatal care. For women with preeclampsia, we calculated weight gain using only measurements before the date of diagnosis. Gestational weight gain measurements were standardized for gestational duration into zscores using previously published, BMI-specific weight-gain-for-gestational-age charts derived for our population.17 The use of z scores ensures that the weight gain before preeclampsia diagnosis is compared with the weight gain of women without preeclampsia at the same point in pregnancy (instead of to the weight gain at delivery, which is usually at a later gestational age). That is, they account for the fact that women who remain pregnant longer have a greater opportunity to gain weight than women who deliver earlier because of preeclampsia. Z scores are the World Health Organization–recommended approach to assess change in anthropometry (eg, weight gain).21 They have conventionally been used to assess pediatric growth, but charts have recently been produced for pregnancy weight gain.17
Preeclampsia was defined using International Classification of Diseases, Tenth Revision codes O14 or O15 in the National Patient Register at either (1) an inpatient admission, or (2) an outpatient visit followed by either (a) ≥1 outpatient visits or (b) ≥1 inpatient admissions with a preeclampsia code or (c) a preeclampsia diagnosis at delivery. That is, diagnosis could not be based only on a single outpatient visit, reflecting that in clinical practice patients with preeclampsia would be followed-up either at delivery or in clinic. The clinical definition of preeclampsia during the study period was a new onset of hypertension (blood pressure of ≥140/90) combined with proteinuria (≥0.3 g per 24 hours or ≥1 on a urine dipstick on at least 2 subsequent occasions) at 20 weeks gestation or later.
The date of preeclampsia diagnosis was defined as the first outpatient visit or inpatient admission with a diagnosis of O14 or O15. In accordance with International Society for the Study of Hypertension in Pregnancy guidelines, we defined early preterm onset preeclampsia as cases diagnosed (although not necessarily delivered) before 34 weeks gestation, late preterm onset preeclampsia as cases diagnosed between 34 and 36 weeks gestation, and term onset preeclampsia as cases diagnosed at or beyond 37 weeks.22
We described the characteristics of women with versus without preeclampsia, overall and according to preeclampsia subtype, using means with SD or counts with percentages. We examined the association between the last measured weight before delivery (or diagnosis, for preeclampsia cases), expressed as a weight gain z score, and preeclampsia using multivariable logistic regression. Results were estimated for each prepregnancy BMI category. We did not build models for underweight women because of the small number of cases (n=56). We assessed linearity by regressing preeclampsia against quintiles of weight gain and visually examining the pattern of the resulting coefficients with 95% confidence intervals.
We adjusted for maternal age at delivery (years), maternal height (cm), smoking status (nonsmoker, 1–9 cigarettes per day, ≥10 cigarettes per day), cohabitation status (living with partner, not living with partner), and prepregnancy diabetes mellitus. We further adjusted for early-pregnancy BMI to account for potential residual confounding within each BMI category. We did not control for gestational diabetes mellitus because we hypothesized that is was a downstream consequence of pregnancy weight gain.
The analyses were repeated using the outcomes of early preterm, late preterm, and term onset preeclampsia. For early preterm (<34 weeks) models, the entire cohort was included in the denominator while for late preterm and term onset preeclampsia, only women remaining pregnant at or beyond 34 and 37 weeks were retained in the denominator, respectively.
We used a multilevel random effects model with a random intercept and random slope to express the serial pregnancy weight gain measurements as a function of gestational age. The random intercept allowed each woman’s weight gain measurements to vary above or below the population average weight gain while the random slope allowed each woman’s rate of weight gain to vary above or below the population average. We used all available weight measurements for women without preeclampsia and weight gain measurements before diagnosis for women with preeclampsia. Gestational age was modeled as a restricted cubic spline with 5 knots to allow a smoothed, curvilinear weight gain curve. The same confounders were adjusted for as in the logistic regression models.
We first examined weight gain patterns for women with versus without preeclampsia separately and visually compared the estimated curves in each group. We then built a combined model that included an interaction term between preeclampsia status and gestational age to allow the shapes of the weight gain curves to vary according to preeclampsia status. We used this model to estimate the adjusted difference in pregnancy weight gain between women with and without preeclampsia at select periods in gestation with 95% confidence intervals using the margins command in Stata.23
As a sensitivity analysis, we repeated our primary analyses replacing the last measured weight before diagnosis with the weight gain at the time of the last normal blood pressure documented in the antenatal or delivery admission records. This excluded weight gain measurements in which the woman was being prescribed antihypertensive medication (defined as Anatomical Therapeutic Chemical Classification System–codes: C02, C03, C07, C08, and C09). This conservative approach ensured that weight gain measurements taken shortly before diagnosis (eg, when a woman had a high blood pressure but did not meet the diagnostic criteria for preeclampsia because of lack of proteinuria) were not included.
There were 151 710 singleton pregnancies in Stockholm-Gotland from 2008 to 2013. Excluding 15 916 pregnancies because of missing early-pregnancy BMI, missing weight gain, prepregnancy hypertension, and without a known date of preeclampsia data left 135 794 pregnancies. Further restricting to nulliparous women left 62 705 women with 2770 cases of preeclampsia (4.4%) for analysis. Exclusions are detailed in Figure 1. Among women with preeclampsia, 1920 (69%) had term onset preeclampsia (≥37 weeks).
Table 1 compares the characteristics of women with versus without preeclampsia. Women who developed preeclampsia had systematically higher BMI in early pregnancy than women who did not develop preeclampsia (15.0% versus 6.3% obese, respectively) and were more likely to have prepregnancy diabetes mellitus (2.0% versus 0.4%). Women with preeclampsia delivered a median of 6 days earlier than women without preeclampsia (275 and 281 days, respectively). The median gestational age at diagnosis was 269 days, and the median diagnosis-to-delivery interval was 3 days (IQR, 1–10).
Total pregnancy weight gain was 1.5 kg higher in women with versus without preeclampsia, but given that women with preeclampsia delivered nearly a week earlier, this corresponded to a meaningful difference in gestational age–standardized weight gain zscores: 0.60 versus 0.14, respectively. When weights measured after a woman’s preeclampsia diagnosis were excluded, the z score for the last measured weight gain in women with preeclampsia decreased to 0.54, suggesting that the rate of weight gain in women with preeclampsia increased after diagnosis (potentially because of edema).
As expected, the interval between diagnosis and delivery was longer among women diagnosed with preeclampsia at preterm ages compared with term diagnoses (median interval between diagnosis and delivery of 10 days [IQR, 3–23] in early preterm, 11 days [IQR, 5–20] in late preterm, and 2 days [IQR, 1–5] at term; Table 1). After restricting to weight gain before diagnosis, women with late preterm and term preeclampsia gained relatively more weight than women with early term preeclampsia (z scores of 0.54 and 0.57 versus 0.36, respectively). Table S1 in the online-only Data Supplement details the differences in weight gain in women with versus without preeclampsia by early pregnancy BMI status.
Association Between Gestational Weight Gain Z Scores and Preeclampsia
The associations between pregnancy weight gain z score before diagnosis and risk of preeclampsia by early pregnancy BMI status are shown in Table 2. After adjusting for confounders, higher pregnancy weight gain was associated with increased odds of preeclampsia in normal weight, overweight, and obese women although the magnitude of risk was higher in normal weight and overweight women (both ≈60% for every 1 z score increase in weight gain than in obese women; 19% for every 1 z score increase in weight gain). These z score differences correspond to 4.6 kg for normal weight, 5.9 kg for overweight, and 6.9 kg for obese at 37 weeks’ gestation. A spreadsheet calculator for conversion of zscores into kilograms is provided in the online-only Data Supplement.
The odds ratios for the association between weight gain and preeclampsia were generally stronger for preeclampsia cases with a later pregnancy onset than for early-onset preeclampsia (Table 2). In normal weight women, every 1 z score increase in weight gain was associated with 64% to 70% increased odds for late preterm and term preeclampsia, but only 43% increased odds for early preterm preeclampsia. Similar patterns were observed in overweight women. In obese women, associations were close to the null for early preterm and late preterm preeclampsia, but 30% higher odds for term preeclampsia.
Gestational Weight Gain Trajectories and Preeclampsia Risk
The estimated weight gain trajectories of women with versus without preeclampsia are shown in Figure 2, and the adjusted differences in weight gain between these 2 groups of women at select gestational ages are shown in Table 3. Weight gain patterns were similar in the first half of pregnancy for women with versus without preeclampsia across all early pregnancy BMI groups. For normal weight and overweight women, significant differences in weight gain were apparent by 25 weeks’ gestation, with differences of 0.43 and 0.52 kg, respectively. By 40 weeks, these differences had increased to 2.62 and 2.54 kg, respectively. In obese women, the weight gain trajectories of women with and without preeclampsia diverged at a later gestational age, with no significant differences at 25 weeks’ gestation (0.20 kg [−0.18, 0.59]), but a difference of 0.81 kg emerging by 30 weeks, and a difference of 2.02 kg at 40 weeks.
Results were essentially unchanged in our sensitivity analysis replacing the last measured weight before diagnosis with the weight gain at the time of the last normal blood pressure documented in the antenatal or delivery admission records (Table S2).
This is the first study to examine how pregnancy weight gain before diagnosis is linked with risk of preeclampsia subtypes. In this large population-based cohort of women with serial weight gain measurements and known date of preeclampsia diagnosis, we found that high weight gain was more strongly associated with later-onset preeclampsia. Furthermore, risks associated with high weight gain were more pronounced in leaner women. The weight gain trajectories of women with preeclampsia began to diverge at ≈25 weeks and continued to diverge until delivery, highlighting the importance of weight gain in mid- and late pregnancy in disease pathogenesis and in antenatal care.
The 2009 Committee to Reexamine Institute of Medicine Pregnancy Weight Gain Guidelines reviewed the literature on the consequences of pregnancy weight gain for maternal and child health.15 Six of 10 studies linking total pregnancy weight gain with preeclampsia found increased risks among women with higher weight gain, but the studies were deemed “inconclusive and problematic due to methodological flaws” (page 187) and excluded from consideration in the guidelines.15 Our finding that weight gain z scores at delivery for women with preeclampsia were systematically higher than their zscores for weight gain before diagnosis confirms that use of total pregnancy weight gain likely introduces some degree of bias because of reverse causation. More recent studies based on total pregnancy weight gain are, therefore, likely equally inconclusive.8–10
Four studies have examined the association between weight gain in the first or second trimester and risk of preeclampsia.11–14 A large population-based study from China (n=84 656) found that weight gain ≥600 g/wk between 8 and 18 weeks was associated with a 69% higher risk of preeclampsia compared with women gaining <200 g week in a cohort of predominantly normal weight women.11 No increased risks were observed among women gaining 200 to 399 or 400 to 599 g per week. In the ALSPAC cohort (Avon Longitudinal Study of Parents and Children) from the United Kingdom, there was a 31% increase in risk for every 200 g per week increase in weight gained before 18 weeks, with no differences according to prepregnancy BMI.13
In contrast, the Generation R cohort from the Netherlands (n=6956) found no significant association between first or second trimester pregnancy weight gain and preeclampsia.12 A smaller cohort study of 1441 women from the United States examined rate of pregnancy weight gain up to 28 weeks in relation to mild and severe preeclampsia.14 The study found no association between a rate of weight gain above the Institute of Medicine recommendations (versus within recommendations) and mild or severe preeclampsia. However, with only 17 cases of mild preeclampsia and 58 cases of severe preeclampsia, the study was likely underpowered to detect small-moderate effect sizes. The study did find a 70% increased risk for any hypertensive disorder of pregnancy with weight gain above recommendations.
Our study agrees with the studies from China and the United Kingdom demonstrating that higher pregnancy weight gain increases risk of preeclampsia. However, 1 major difference between these studies and ours is that we did not find a difference in weight gain between those with versus without preeclampsia until week 25. Hence, our results suggest that later pregnancy weight gain is more important, potentially explaining the null findings of the Dutch12 and US studies.14
Our finding of a stronger association between excessive pregnancy weight gain and late preeclampsia may be explained by differences in the pathophysiology of the disease phenotypes. Early preeclampsia has a strong association with poor placentation,24,25 which occurs early in pregnancy and is regulated, in part, by immunologic factors.26 Late preeclampsia is usually accompanied by normal placental function24,25 but is linked to maternal factors. One important predisposing factor for late preeclampsia is high BMI.4 Preeclampsia is characterized by a generalized maternal inflammatory systemic response incorporating a substantive component of endothelial cell dysfunction.26 Adipose tissue is a hormonally active tissue and produces, for example, several inflammatory mediators that can act to alter endothelial function,27 making the mother more vulnerable to develop preeclampsia. Consequently, not only obesity but also excessive weight gain during pregnancy has been associated with increased concentrations of inflammatory factors,28 which might predispose the woman to preeclampsia.
Excessive pregnancy weight gain seemed to be a stronger risk factor of preeclampsia in lean than in obese women in our study. The mechanism underlying this finding is unknown, but the relative increase in levels of inflammatory factors might act differently depending on state of inflammation in early pregnancy. Furthermore, it is unknown whether distribution of fat mass accrual differs in lean and obese women. Because fat distribution is important concerning cardiovascular risk, we could expect that fat distribution may also important for preeclampsia.27
Strengths and Limitations
Strengths of this study included our linkage of multiple population registries, including electronic medical records and inpatient/outpatient visit records, to produce a novel population-based cohort with information on date of preeclampsia diagnosis. Our large sample size allowed us to examine preeclampsia subtypes while retaining good statistical precision.
Several limitations should be noted. First, the date of preeclampsia diagnosis is not the same as the date of disease onset. As a result, use of the last measured weight before diagnosis could have included weight measurements influenced by early stages of disease. Nevertheless, our sensitivity analysis restricting weight measurements to the time of last normal blood pressure measurement reduces the likelihood that this bias influenced our findings. Second, early pregnancy BMI is an insufficient proxy for prepregnancy BMI. However, it reduces the measurement error associated with self-reported prepregnancy BMI29,30 and is a pragmatic measure because it reflects the information available to the clinician at the time of the first antenatal visit. Third, our diagnosis of preeclampsia was based on International Classification of Diseases coding in hospital and outpatient administrative databases. Previous validation studies from Swedish and other Scandinavian data registries have found that preeclampsia is coded with reasonable accuracy in population databases.31–33 Our outcome definition required confirmation of an initial outpatient diagnosis with subsequent visit or diagnosis at the delivery admission. Nevertheless, we cannot rule out outcome misclassification because of other factors, such as variability in physician diagnostic practices or error in blood pressure measurement.34 Finally, our population consisted of predominantly white women attending publicly funded antenatal care with an uptake of ≈100%. For this reason, the generalizability to other races or medical insurance systems is uncertain. This relative homogeneity is also strength, however, because it reduces the likelihood of confounding by differences in patient characteristics and access to care.
High pregnancy weight gain before diagnosis is an important risk factor for preeclampsia in nulliparous women, particularly in leaner women. Our finding that the association between pregnancy weight gain and preeclampsia was more pronounced in preeclampsia developing later in gestation supports the hypothesis that early preterm and term onset preeclampsia may have different pathogenic pathways. Randomized trials assessing if interventions to reduce pregnancy weight gain lower the risk of preeclampsia would be an appropriate next step in our efforts to reduce the burden of this disease.
Research designed by J.A. Hutcheon, K. Johansson, O. Stephansson, and A.-K. Wikström. Research conducted by L.M. Bodnar, S. Cnattingius, J.A. Hutcheon, K. Johansson, O. Stephansson, and A.-K. Wikström. J.A. Hutcheon, K. Johansson analyzed data and performed statistical analysis. The drafting of the article was also done by J.A. Hutcheon and K. Johansson. Critical revision of the article for important intellectual content was done by L.M. Bodnar, S. Cnattingius, O. Stephansson, and A.-K. Wikström. J.A. Hutcheon and K. Johansson have the primary responsibility for final content. All authors read and approved the final article. Ethics approved by the regional ethics committee at Karolinska Institutet Stockholm, Sweden (DNR: 2009/275-31 with amendment 2013/792-32).
Sources of Funding
The study was supported by grants from Swedish Research Council for Health, Working Life and Welfare (grant no. 2014-0073 to S. Cnattingius and 2015-00251 to O. Stephansson, K. Johansson), Stockholm County Council (grant no. 20140105 to S. Cnattingius and 20150179 to O. Stephansson). J.A. Hutcheon is the recipient of New Investigator awards from the Canadian Institutes of Health Research and the Michael Smith Foundation for Health Research. O. Stephansson was supported by the Swedish Research Council (grant no. 2013–2429) and the Strategic Research Program in Epidemiology at Karolinska Institutet. K. Johansson was the recipient of a grant from Karolinska Institutet Research Foundations. A.-K. Wikström was supported by the Swedish Research Council (grant no. 2014–3561). S. Cnattingius was supported from an unrestricted grant from Karolinska Institutet (Distinguished Professor Award). L.M. Bodnar is supported by the National Institute of Child Health & Human Development (R01 HD072008).
All authors have completed the International Committee of Medical Journal Editors uniform disclosure form at http://www.icmje.org/coi_disclosure.pdf and declare: no support from any organization for the submitted work.
The online-only Data Supplement is available with this article at http://hyper.ahajournals.org/lookup/suppl/doi:10.1161/HYPERTENSIONAHA.118.10999/-/DC1.
- Received February 6, 2018.
- Revision received March 4, 2018.
- Accepted May 7, 2018.
- © 2018 American Heart Association, Inc.
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Novelty and Significance
What Is New?
High weight gain during pregnancy may increase a woman’s risk of developing preeclampsia. However, previous studies have only investigated the effect of total pregnancy weight gain or early pregnancy weight gain and risk of preeclampsia. Furthermore, studies have not had information on the timing of diagnosis to examine whether the risks associated with high weight gain differ according to preeclampsia subtypes (early preterm, late preterm, or term diagnosis).
What Is Relevant?
This is the first study to examine how pregnancy weight gain before diagnosis is linked with risk of preeclampsia and its subtypes.
We found that high pregnancy weight gain increases the risk of preeclampsia and that risks were more strongly associated with later-onset preeclampsia and among leaner women.