Abstract
OBJECTIVE:
To estimate the association between antenatal depression with spontaneous preterm birth (SPTB) relative to medically-indicated preterm birth (MPTB).
STUDY DESIGN:
A secondary analysis of a nested case-control study of PTB. The exposure was a clinical diagnosis of antenatal depression. The outcome was PTB<37 weeks classified as SPTB (spontaneous labor, PPROM, placental abruption, and cervical shortening); and MPTB (preeclampsia and IUGR). Multinomial logistic regression models compared women without PTB versus MPTB and SPTB, adjusting for age, race, parity, tobacco use, insurance status, and pre-pregnancy body mass index; and history of PTB for SPTB.
RESULTS:
Among 443 pregnant women, 15.6% had a SPTB and 8.6% MPTB; and 16% were diagnosed with antenatal depression. Women with a SPTB were three times more likely to have antenatal depression compared to women without a SPTB (AOR 2.81 [95%CI: 1.40 – 5.63]). No significant association was identified between antenatal depression and MPTB (AOR: 1.77 [95%CI: 0.67 – 4.62]). The association between antenatal depression and SPTB did not change after adjusting the above model for a history of PTB and antidepressant use.
CONCLUSIONS:
Antenatal depression may differentially affect the risk of PTB via an increase in the odds of SPTB. These results have implications for future studies aimed at prevention and treatment options for depression and PTB.
Keywords: pregnancy, depression, preterm birth
INTRODUCTION
Preterm birth (PTB) is a leading cause of infant morbidity and mortality. In the United States 12% of deliveries are preterm, and roughly half are spontaneous as opposed to medically indicated1–3. Antenatal depression may affect more than 15% of pregnant women and increasing efforts have been underway to screen and treat women for depression in pregnancy4–6. A growing evidence base suggests antenatal depression, as well as antidepressant use and untreated depression, is associated with PTB <37 weeks of gestation due to any indication7–10; however, the question remains to what extent does antenatal depression alter the risk of different phenotypes of PTB, namely spontaneous PTB (SPTB) relative to medically-indicated PTB (MPTB)8,11,12.
PTB is the common end result of multiple pathways. SPTB, often characterized by intrauterine or decidual inflammation, includes preterm labor, preterm premature rupture of membranes (PPROM), placental abruption, and cervical shortening; and MPTB, though of diverse etiologies, can be associated with aberrant placentation, including preeclampsia and intrauterine growth restriction (IUGR)13. It is biologically plausible that antenatal depression could affect SPTB directly through several of these pathways, such as inflammation and oxidative stress14–17, or indirectly through health behaviors and poor self-care18. However, some epidemiological data have suggested an association between antenatal depression and subtypes of MPTB, including preeclampsia19,20 and having a small for gestational age infant at birth8,21. Data concurrently comparing the impact of antenatal depression with SPTB versus MPTB are lacking.
Given the biological plausibility for an association between depression and SPTB compared to MPTB, we hypothesized that antenatal depression would primarily be associated with SPTB as opposed to MPTB, and that these associations would be impacted by antidepressant medication use in pregnancy. We sought to determine the association between antenatal depression and clinical subtypes of PTB, namely SPTB relative to MPTB, in a cohort of pregnant women at high-risk for PTB.
MATERIALS AND METHODS:
The current study is a secondary analysis of a nested case-control study of PTB within a prospective cohort (LIFECODES birth cohort) at Brigham and Women’s Hospital (Boston, MA) from 2006–200822,23. Briefly, in that original analysis, all singleton cases of PTB <37 weeks gestation due to any etiology (N=130) were randomly matched 1:3 to singleton term controls born at or after 37 weeks gestation (N=352), without further matching on additional variables (previously described)22. This dataset was selected for the current analysis given the detailed and rigorous characterization of clinical subtypes of PTB. The study was approved by the Institutional Review Board at Brigham and Women’s Hospital.
During the first trimester (median of 10 weeks gestation), enrolled women completed a demographic questionnaire. The following variables were assessed at enrollment, including: age, race/ethnicity, parity, and pre-pregnancy body mass index (BMI) (calculated by dividing a subject’s weight by the square of her height, kg/m2); and at delivery: gestational age, diagnosis of chronic hypertension, gestational hypertension, and preeclampsia, and clinical indications for delivery. A history of prior PTB included any past delivery, regardless of clinical indication, between 21weeks 0 days, and 36 weeks 6 days gestation.
The primary exposure was antenatal depression, defined as a clinical diagnosis of depression at any time in pregnancy documented by the obstetric or the primary care provider in the electronic medical record (EMR). We also secondarily assessed the impact of antidepressant use on the primary association between antenatal depression and subtype of PTB by adjusting for treatment. The following depression-related variables were also collected: exposure to an antidepressant medication during pregnancy (yes/no), including selective serotonin reuptake inhibitor (SSRI), benzodiazepine, antipsychotic, mood stabilizer, or other psychotropic medication, and a history of depression before pregnancy. All psychiatric diagnoses and medications in the EMR, including a diagnosis of antenatal depression, use of an antidepressant medication during pregnancy, and a prior history of depression before pregnancy, were reviewed and confirmed by a study obstetrician (KKV). Exposure ascertainment (i.e. depression) was completed while blinded to study outcome (i.e. PTB). A documented clinical diagnosis was confirmed by thorough review of the entire EMR, including outside medical records prior to pregnancy; as well as by whether the patient received a psychotropic medication and had a history of psychiatric illness prior to pregnancy. Only 3 women who were prescribed an antidepressant medication in pregnancy did not also have a documented clinical diagnosis of antenatal depression. It is important to note that this study was conducted prior to routine universal screening for depression during pregnancy in Massachusetts24, and hence, a diagnosis of depression was assigned during the provision of routine prenatal care or primary care before pregnancy. Antenatal depression may include a wide range of clinical symptomatology and morbidity and our definition based on clinical diagnosis does not capture information on illness severity, including duration of exposure, prior hospitalization, or further psychometric assessment.
With regards to study outcomes, SPTB and MPTB were compared to no PTB (reference). PTB was defined as any birth <37 weeks of gestation and was then separated into SPTB and MPTB. SPTB, often characterized by intrauterine or decidual inflammation, was defined as a birth <37 weeks of gestation due to a primary diagnosis of 1) preterm premature rupture of membranes (PPROM), 2) spontaneous labor, 3) placental abruption, and 4) cervical shortening. MPTB, associated with aberrant placentation, was defined as a birth<37 weeks of gestation due to either preeclampsia or IUGR13. A third group of PTB <37 weeks of gestation for a non-placentally mediated maternal or fetal indication, such as non-reassuring fetal testing or delivery of an otherwise stable mother for cholestasis, placenta previa, prior intrauterine fetal demise, abdominal cerclage, or prior classical delivery, was excluded from the current analysis due to a lack of a unifying biological mechanism for the association with antenatal depression. Assignment of PTB outcomes by clinical chart review was independently performed and validated by two maternal-fetal medicine specialists based on criteria of the American College of Obstetricians and Gynecologists and standard clinical practice25. When disagreement in pregnancy outcome or characteristic arose, the case was re-reviewed and a consensus conference was held to determine the final characterization.
Statistical analysis:
Given the comparison between SPTB and MPTB relative to no PTB (i.e., three level outcome), we first utilized multinomial (polytomous) logistic regression models to allow for a non-binary outcome. This allowed for comparing the two outcomes of SPTB and MPTB to the baseline comparator of no PTB. Based on a priori confounding between depression and PTB as well as univariate statistical significance (p<0.20), all models were adjusted for the following covariates: maternal age at delivery, race, parity, tobacco use, insurance status, and pre-pregnancy BMI; and history of prior PTB for the outcome of SPTB. In secondary analyses, once we identified a significant association between antenatal depression and SPTB, but not MPTB, we then utilized logistic regression to further examine the association between antenatal depression and SPTB: 1) adjusting for a history of prior PTB, and 2) adjusting for antidepressant use during pregnancy. When the outcome was SPTB versus no PTB (i.e., binary outcome), we excluded women with MPTB from this analysis. With regards to antidepressant use in pregnancy, we compared women with antenatal depression exposed to an antidepressant and women with antenatal depression not exposed to an antidepressant to women without antenatal depression (i.e. three-level variable). All analyses were performed using STATA (STATACORP, version 10.0, College Station, TX).
RESULTS:
Among the 482 women included in the original case-control study of PTB, 460 (95%) women had an available EMR for abstraction of information on antenatal depression and PTB in the current pregnancy. Given the focus of this analysis was on SPTB versus MPTB, we excluded 17/460 (3.7%) women who had a scheduled PTB<37 weeks gestation for a non-placentally mediated maternal (11/17) or fetal indication (6/7), which were not associated with antenatal depression (p=0.18). There were no statistically significant differences between women in the current analysis (n=443) compared to the original cohort (n=482) by age, race, parity, or gestational age at delivery (p>0.05 for all 4 variables).
Among the 443 assessed pregnant women, 11.3% were <25 years of age, 40.6% were of non-white race, and 45.1% were multiparous, and these covariates did not differ between preterm and term births (Table 1). Women with antenatal depression were more likely to be obese (35.8% vs. 16.0; p<0.001), be enrolled in a public insurance program (33.3% vs. 17.2%; p=0.002), be diagnosed with preeclampsia during the current pregnancy (19.1% vs. 9.9%; p=0.02), and report a history of a prior PTB (20.0% vs. 9.8%; p=0.02).
Table 1.
Maternal characteristics overall and by antenatal depression status
| Maternal characteristic | Overall N=443 n (%) |
Antenatal depression N=68 n (%) |
No antenatal depression N=375 n (%) |
p-value |
|---|---|---|---|---|
| Maternal age <25 years | 50/443 (11.3) | 9/68 (13.2) | 41/375 (10.9) | 0.58 |
| Other | 49 (11.1) | 5 (7.4) | 44 (11.7) | |
| Non-white race | 180/443 (40.6) | 22/68 (32.4) | 158/375 (42.1) | 0.13 |
| Multiparous | 200/443 (45.1) | 28/68 (41.2) | 172/375 (45.9) | 0.47 |
| Tobacco use during pregnancy | 26/443 (5.9) | 7/68 (10.3) | 19/375 (5.1) | 0.09 |
| Enrolled in public insurance | 85/433 (19.2) | 22/66 (33.3) | 63/367 (17.2) | 0.002 |
| Obese, BMI>30 | 83/435 (19.1) | 24/67 (35.8) | 59/368 (16.0) | <0.001 |
| Preeclampsia | 50/443 (11.3) | 13/68 (19.1) | 37/375 (9.9) | 0.02 |
| History of prior PTB | 50/431 (11.6) | 13/65 (20.0) | 36/366 (9.8) | 0.02 |
| Antidepressant medication exposure in pregnancy | 45/443 (10.2) | 45/68 (66.2) | -- | -- |
| History of depression before pregnancy | 59/443 (13.3) | 34/68 (50.0) | 25/375 (6.6) | <0.001 |
| PTB <37 weeks | 107/443 (24.2) | 26/68 (38.2) | 81/375 (21.6) | 0.003 |
| MPTB | 38/443 (8.6) | 10/68 (14.7) | 28/375 (7.5) | |
| Short cervix | 3/69 (4.4) | 0 | 3/55 (5.5) | |
| IUGR | 12/38 (31.6) | 1/10 (10.0) | 11/28 (39.3) |
A total of 107/443 (24.2%) women had a PTB <37 weeks gestation, and 34/443 (7.7%) had a PTB 34 weeks gestation. The median gestational age at birth was 38.0 weeks (IQR: 37.0 – 39.9), which did not differ between cases of SPTB vs. MPTB (35.4 vs. 35.8 weeks, respectively). By clinical type of PTB, 15.6% (69/443) of women had a SPTB, and 8.6% (38/443) had a MPTB. The primary clinical diagnoses for SPTB were preterm labor (50.7%; 35/69) and PPROM (36.2%; 25/69), and for MPTB, preeclampsia (68.4%; 29/38) and IUGR (31.6%; 12/38). Fifteen percent (68/443) of women were diagnosed with antenatal depression. With regards to treatment of depression, 66.2% (45/68) of women with antenatal depression were treated with an antidepressant medication during pregnancy.
Women with antenatal depression were more likely to have a PTB <37 weeks compared to women without antenatal depression (38.2% vs. 21.6%; odds ratio, OR: 2.24, 95% CI: 1.29 – 3.88). By clinical type of PTB, women with antenatal depression were similarly more likely to have a SPTB (23.5% vs. 14.1%: OR: 2.11, 95% CI: 1.10 – 4.03), as well as MPTB (14.7% vs. 7.5%; OR: 2.50, 95% CI: 1.13 – 5.51), compared to women without depression.
In multivariable multinomial regression analyses, comparing women with a SPTB or a MPTB versus women without a PTB, women with a SPTB were three times more likely to have antenatal depression compared to women without a SPTB (adjusted odds ratio, AOR: 2.81 [95% CI: 1.40 – 5.63]) (Table 2). However, women with a MPTB were not significantly more likely to have a diagnosis of antenatal depression (AOR: 1.77 [95% CI: 0.67 – 4.62]). Women who were obese, parous, and used tobacco during pregnancy were more likely to have a MPTB. Women enrolled in a public insurance program were less likely to have a SPTB compared to those with private insurance.
Table 2.
Unadjusted and adjusted analyses of the association between antenatal depression with SPTB and MBTB compared to no PTB (N=429)1
| Outcome | Unadjusted odds ratio, OR (95% CI) | Adjusted odds ratio, AOR (95% CI)2 |
|---|---|---|
| SPONTANEOUS PRETERM BIRTH (SPTB) | ||
| Antenatal depression | 2.11 (1.10 – 4.03)* | 2.81 (1.40 – 5.63)* |
| Maternal age <25 years | 0.91 (0.41 – 2.05) | 1.16 (0.45 – 2.96) |
| Non-white race | 1.14 (0.67 – 1.93) | 1.72 (0.94 – 3.16) |
| Multiparous | 0.74 (0.43 – 1.26) | 0.69 (0.39 – 1.23) |
| Tobacco use during pregnancy | 1.23 (0.39 – 3.80) | 1.18 (0.36 – 3.84) |
| Enrolled in public insurance | 0.63 (0.30 – 1.30) | 0.41 (0.17 – 0.97)* |
| Obese, BMI>30 | 0.84 (0.40 – 1.75) | 0.63 (0.29 – 1.39) |
| MEDICALLY INDICATED PRETERM BIRTH (MPTB) | ||
| Antenatal depression | 2.50 (1.13 – 5.51)* | 1.77 (0.67 – 4.62) |
| Maternal age <25 years | -- | -- |
| Non-white race | 0.97 (0.48 – 1.92) | 1.43 (0.62 – 3.30) |
| Multiparous | 1.87 (0.94 – 3.72) | 3.68 (1.63 – 8.29)* |
| Tobacco use during pregnancy | 3.75 (1.36 – 10.26)* | 3.60 (1.08 – 11.94)* |
| Enrolled in public insurance | 0.75 (0.30 – 1.87) | 0.67 (0.21 – 2.15) |
| Obese, BMI>30 | 3.66 (1.79 – 7.45)* | 4.26 (1.86 – 9.72)* |
| SECONDARY ANALYSES | ||
| Association between depression and SPTB after adjusting for a history of prior PTB | -- | 2.47 (1.26 – 4.86)* |
| No depression | 1.00 | 1.00 |
This analysis consists of 429/443 (96.8%) of the cohort with complete data on all covariates.
All multivariable models were adjusted for the following variables: age, race, parity, tobacco use, insurance status, and body mass index.
Reflects a statistically significant association (p<0.05)
Next, in multivariable logistic regression analyses adjusting for the same covariates as above, comparing women with a SPTB versus women without a PTB (i.e., excluding those with a MPTB), the above association between antenatal depression and SPTB persisted after adjusting for a history of a prior PTB <37 weeks (AOR: 2.47 [95% CI: 1.26 – 4.86]).
When assessing the impact of antidepressant treatment on the association between antenatal depression and SPTB adjusting for the same covariates as above, women with antenatal depression exposed to an antidepressant medication during pregnancy were at an over 2-fold increased odds of SPTB compared to women without depression (AOR: 2.79 [95% CI: 1.22 – 6.37]); however, women with antenatal depression not exposed to an antidepressant medication during pregnancy were not at an increased odds of SPTB compared to women without depression (AOR: 0.95 [95% CI: 0.23 – 3.82]).
DISCUSSION
Women diagnosed with antenatal depression were at an over 2-fold increased odds of SPTB compared to those women without antenatal depression. However, women diagnosed with antenatal depression were at an increased but not statistically significant odds of MPTB. Though repeated observational studies have demonstrated a significant association between antenatal depression and any PTB <37 weeks of gestation12, this study suggests that the impact of antenatal depression on PTB may be more important for SPTB rather than MPTB. If further studies find that the primary association between antenatal depression and PTB is via SPTB, this epidemiologic association has implications for future research aimed at understanding a possible underlying mechanism, as well as interventions aimed at preventing and treating depression in pregnancy and PTB.
In the current study, the above association between antenatal depression and SPTB held after accounting for multiple confounding variables, including a history of prior PTB. The exact mechanism by which antenatal depression may increase the risk of SPTB remains to be elucidated, and plausible biologic mechanisms include neuroendocrine18,26 and inflammatory alterations14–17. It is possible that antenatal depression may be a surrogate measure for other social determinants of health that are associated with SPTB. While multiple observational studies have identified antenatal depression as a risk factor for PTB more generally7–10,27, few studies have examined clinical subtypes of PTB. These studies have solely limited their analyses to antenatal depression with SPTB, limiting comparisons to other clinical types of PTB, including MPTB. A prior European study conducted among 681 pregnant women found that those women with depressive symptoms had a 3-fold increased odds of SPTB28. Another study conducted among 1,399 African-American women found close to a 2-fold increased odds of SPTB for women with depressive symptoms29. With regards to other psychiatric diagnoses, a study of >16,000 deliveries from the Veterans Health Administration found that pregnant women with active PTSD (i.e. within a year of delivery) had a 35% higher chance of SPTB compared to women with historical or no PTSD30. The observations of the current study are consistent and of the same order of magnitude as these earlier studies limited to the outcome of SPTB.
The current study allows for a head-to-head comparison of the impact of antenatal depression on not only SPTB, but also MPTB. It should be noted that prior studies have shown an association between antenatal depression and clinical subtypes of MPTB31, including preeclampsia19,20 and having a small for gestational age infant at birth8,21, which we did not find in the current study. This could be due to lack of an adequate sample of preterm deliveries in these earlier studies or a lack of an adequate sample size to detect an effect between antenatal depression and MPTB in the current study.
In secondary analyses, we noted that the association between antenatal depression and SPTB persisted after adjustment for antidepressant use during pregnancy. Recent data suggest that antidepressant use may alter the inflammatory milieu among pregnant depressed women32, which could be associated with SPTB. It should be noted that depressed women on an antidepressant may have had more severe depression, or may have also been at a higher risk for SPTB due to other risk factors, despite controlling for multiple confounding variables (i.e. confounding by indication)33. Differential misclassification is possible so that women with documented antenatal depression not on medications were not depressed during pregnancy. A recent meta-analysis found that women who received SSRIs during pregnancy had a significantly higher risk of PTB, which remained when comparing depressed women on SSRIs with women not on SSRIs34. A major limitation was that none of the included studies stratified data for type of PTB, limiting the ability to determine the biologic plausibility of a drug-PTB association. Future studies with more information about antidepressant use, including medication adherence, dosing, duration of use by trimester, and timing of initiation, are needed to better understand the role of antidepressants on the association between antenatal depression and SPTB.
This study must be interpreted within the context of its design. A major limitation of this analysis was that the exposure of antenatal depression was based on a clinical diagnosis by the obstetrician, which does not capture information on disease severity. We did not have information on the duration of diagnosis, prior hospitalization, or other measures of depression severity. This rather simplified clinical diagnosis of depression will need to be investigated in further depth, including by disease severity (i.e. type and duration of psychotropic medication, duration of exposure, prior hospitalization, or further psychometric assessment) in future studies assessing the relationship between depression and PTB. The frequency of antenatal depression is likely a conservative estimate because we relied on a clinical diagnosis rather than universal screening, which was not performed at the time of this study. Women with overt depressive symptoms would be more likely to be identified by their clinical providers. However, misclassification of depression was likely not impacted by PTB status, and hence would be non-differential, which would bias our results towards the null. Though it is possible that providers screened for depression and documented a diagnosis more frequently among women at higher risk for PTB leading to differential misclassification, which may have overestimated the association between depression and PTB. Of note, only 50% of women with antenatal depression had a documented diagnosis prior to pregnancy. Prior data has suggested that there is considerable overlap in symptoms between depression and anxiety in pregnancy24. We did not document whether women with antenatal depression also had a concurrent anxiety diagnosis during pregnancy. This is a secondary analysis of nested case-control study of PTB, and these results may not be generalizable to all women. The prevalence of antenatal depression in the current study was consistent with recent data from large observational cohorts, and given the original study design of over-sampling women with PTB, the sample size may not have been adequate to examine the association between antenatal depression and subtypes of PTB, as well as the impact of antidepressant treatment on PTB.
In conclusion, antenatal depression may differentially impact the risk of PTB via primarily an increase in the risk of SPTB. These results have implications for future studies aimed at understanding mechanisms, prevention, and treatment of antenatal depression and PTB.
Footnotes
CONFLICT OF INTEREST: All of the study authors declare they have no conflicts of interest to disclose.
PRESENTATION: Society for Maternal-Fetal Medicine 38th Annual Meeting (Dallas, TX), Poster #707.
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