Hum. Reprod. Advance Access published online on October 23, 2008
Human Reproduction, doi:10.1093/humrep/den342
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Presence of depressive symptoms during early pregnancy and the risk of preterm delivery: a prospective cohort study
Division of Research, Kaiser Foundation Research Institute, Kaiser Permanente, 2000 Broadway, Oakland, CA 94612, USA
* Correspondence address. Tel: +1-510-891-3755; Fax: +1-510-891-3761; E-mail: dkl{at}dor.kaiser.org
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Abstract |
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BACKGROUND: The impact of prenatal depression on pregnancy outcomes is largely unknown.
METHODS: We conducted a population-based prospective cohort study among pregnant women of the Kaiser Permanente Medical Care Program to examine the impact of prenatal depression on the risk of preterm delivery. We interviewed pregnant women in their early pregnancy. Women's depressive symptoms were ascertained using the standard Center for Epidemiological Studies Depression Scale (CESD). The presence of significant prenatal depressive symptoms and severe depressive symptoms was determined by CESD scores 
16 and 22, respectively.
RESULTS: Among the 791 participants who answered CESD questions and delivered a live birth, after controlling for potential confounders using the Cox proportional hazard regression, women with CESD scores 16 had almost twice the risk of preterm delivery compared with women without depressive symptoms: adjusted hazard ratio (aHR) = 1.9, 95% confidence interval (CI) 1.0–3.7. The risk of preterm delivery increased with increasing severity of depression: aHR = 1.6 (CI 0.7–3.6) for CESD 16–21 and aHR = 2.2 (CI 1.1–4.7) for CESD 22. The risk of preterm delivery associated with prenatal depression appears to be exacerbated by low educational level, a history of fertility problems and the presence of obesity and stressful events. The observed associations were not confounded by the use of antidepressants, although some of the associations did not reach statistical significance.
CONCLUSIONS: Our findings show that pregnant women with depressive symptoms are at increased risk of preterm delivery and, in addition, provide preliminary evidence that social and reproductive risk factors as well as obesity and stressful events may exacerbate the effect.
Key words: preterm delivery/premature birth/depression/Center for Epidemiological Studies Depression Scale/epidemiology
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Introduction |
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Preterm delivery, defined as delivery at less than 37 completed weeks of gestation, is the leading cause of infant mortality and morbidity as well as medical expenditure for infants. The annual economic costs due to preterm delivery and its resulting conditions were estimated at a staggering $26.2 billion in 2005 in the USA including medical expenditures estimated at minimum $16.9 billion (Cuevas et al., 2005
; Armstrong, 2007; Board of Health Sciences Policy, 2007). Despite decades of research effort, the incidence of preterm delivery has not declined (Branum and Schoendorf, 2002) and the etiology of preterm delivery remains largely unknown. Other than host factors (e.g. a history of preterm delivery and other adverse pregnancy outcomes), very few other risk factors for preterm delivery have been identified. Psychopathological factors have emerged as potentially important risk factors for preterm delivery (Neggers et al., 2006; Alder et al., 2007). It is well recognized that the placental and neuroendocrine functions play a central role in maintaining the health of a pregnancy and determining the onset of labor. Emerging research has also demonstrated that mood disorders, especially depression during pregnancy, may influence the levels of placental hormones and placental functions (Wadhwa et al., 1996; Austin and Leader, 2000; Pike, 2005; Diego et al., 2006; Neggers et al., 2006). Therefore, psychopathologies could be important risk factors for preterm delivery that have been overlooked in the previous research on the etiology of preterm delivery. There is certainly a solid biological foundation to examine the potential effect of psychosomatic factors such as depression during pregnancy on the risk of preterm delivery.
While post-partum depression has long been recognized as a serious public health problem that can lead to maternal functional disability and chronic depression, and adversely impact infant psychological and physiological development (Philipps and O'Hara, 1991; Beck, 1996; Civic and Holt, 2000; Miller, 2002), depression during pregnancy has not been well studied. Although there has been an increase in the number of reports on the use of antidepressants during pregnancy (Wisner et al., 1999; Simon et al., 2002; Oberlander et al., 2004), the number of studies on depression itself during pregnancy remains limited. The prevalence of depression during pregnancy and its impact on pregnancy outcomes are still largely unknown. The controversy about the risk and risk-benefit of using antidepressants during pregnancy is largely due to a lack of knowledge of whether depression during pregnancy itself leads to adverse pregnancy outcomes. Given the emerging literature providing a strong biological foundation, understanding the potential effect of prenatal depression on the risk of preterm delivery and likely subsequent early diagnosis and prevention of prenatal depression would have significant clinical and public health significance. Therefore, in a population-based prospective cohort study of pregnant women in the Kaiser Permanente Medical Care Program (KPMCP), we examined the risk of preterm delivery associated with the presence of depressive symptoms during pregnancy.
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Materials and Methods |
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This was a population-based prospective cohort study conducted among pregnant KPMCP members, an integrated healthcare delivery system, in Northern California. KPMCP members are representative of the underlying racially/ethnically and socio-economically diverse population in the San Francisco Bay Area. The cohort was originally assembled to examine risk factors for miscarriage (Li et al., 2002
; Li et al., 2003a,b; Weng et al., 2008). We recruited pregnant women at early gestational ages if they met the following eligibility criteria: (i) resided in the San Francisco and South San Francisco area, (ii) had a positive pregnancy test, (iii) spoke English and (iv) intended to carry the pregnancy to term at the time of recruitment. Every woman who submitted a urine or blood sample for a pregnancy test at those two facilities was given a flyer explaining the purpose of the study and the possibility of being contacted for participation in the study. Regardless of whether a home pregnancy test has already been done, KPMCP requires that a pregnancy test be confirmed by the KPMCP laboratories. Our trained female interviewers contacted those who did not return the refusal card to answer their questions about the study and to schedule an interview if they agreed to participate. We recruited 1063 women who completed the interview from 2729 eligible pregnant women for the original study of miscarriage (Li et al., 2002). The main reasons for non-participation were ‘too busy’, ‘not interested’ or ‘too stressful’.
Information on depressive symptoms during pregnancy was ascertained during an in-person interview conducted around 10 weeks of gestation on average (6–18 weeks). The severity of depressive symptoms during pregnancy was assessed using the Center for Epidemiological Study Depression Scale (CESD), a 20 question inventory used to measure depressive symptoms (Radloff 1977, 1991). While it is not a clinical diagnosis, CESD has been demonstrated to have high internal consistency (coefficient 
0.85 in the general population and 0.90 in patient population) and has been widely used in epidemiological studies of depression and its consequences (Roberts, 1980; Hann et al., 1999; Dole et al., 2004). Depressive symptoms ascertained through CESD have also been demonstrated to be a good indicator for clinical diagnosis of depression (Myers and Weissman, 1980; Roberts, 1980; Roberts and Vernon, 1983). CESD has a sensitivity of 0.95 and specificity of 0.70 for clinical depression, compared with the Diagnostic Interview Schedule for the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV, Thomas et al., 2001). CESD has a total score of 60. We used widely accepted cutoff scores of 16 to represent ‘significant depressive symptoms’ and score 22 to represent ‘severe depressive symptoms’ (Orr and Miller, 1995; Hoffman and Hatch, 2000; Orr et al., 2002b; Alder et al., 2007). During the interview, we also ascertained detailed information on known or potential risk factors for adverse pregnancy outcomes including preterm delivery, socio-demographic characteristics and a complete history of reproduction and illness.
Using the following three methods, we were able to ascertain pregnancy outcomes for all but two women (99.8%): (i) searching the KPMCP automated databases, (ii) reviewing medical records and (iii) contacting women whose outcomes could not be determined through the previous two methods. The gestational age of >97% of deliveries was determined by medical professionals. By definition, women who ended their pregnancy before 20 weeks of gestation (e.g. miscarriage) were excluded from the study. Therefore, we restricted our study population to 847 women who carried their pregnancy beyond 20 weeks of gestation. Women who did not have complete answers to the CESD questions (n = 23) and women with missing or unreliable information on gestational age (n = 23) were excluded from the analyses. We also excluded extremely preterm cases (<33 weeks) because extremely early preterm delivery (<33 weeks) frequently has other known medical causes. Preterm delivery was defined as gestational age less than 37 completed weeks (<259 days). Ultimately, 791 subjects who had information on both gestational age and CESD were included in the final analyses.
We used the Cox proportional hazard regression to take into account the possible differing gestational ages at entry and delivery between women who did and did not have depressive symptoms. The entry time in our study was the gestational age at the positive pregnancy test because a woman's pregnancy was followed beginning at her positive pregnancy test. The median gestational age at entry for our study population was 40 days. The variables included in the model for adjustment were potential confounders and known risk factors for preterm delivery as well as common socioeconomic and demographic variables. Hazard ratio (HR) together with its 95% confidence interval (CI) was used to estimate the risk of preterm delivery associated with depressive symptoms during early pregnancy after adjustment for potential confounders.
To examine whether stress factors modify the association between depressive symptoms during pregnancy and the risk of preterm delivery, we classified women into low- and high-stress categories based on their answers to 17 questions about stressful life events modified from the Holmes and Rahe Stress Scale Inventory to be suitable for pregnancy. The cutoff for low- and high-stress categories was equivalent to the score of 100 on the Holmes and Rahe stress scale (about 7th percentile of the total scores). A value of P < 0.05 was considered significant.
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Results |
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In our study population, 41.2% of the pregnant women reported significant depressive symptoms (CESD
16) and 21.7% reported severe depressive symptoms (CESD 22) during early pregnancy, around 10 weeks of gestation. Table I presents the characteristics between women who did and did not have significant depressive symptoms (CESD 16) early in their pregnancy. Women who had significant depressive symptoms during early pregnancy tended to be younger (<25 years old), unmarried and African American, had less education and lower family income, were slightly more likely to have had prior pregnancies, and a history of subfertility and preterm delivery. They were also more likely to have smoked, used illicit drugs, or vomited, and less likely to have planned the index pregnancy and used vitamin supplements during pregnancy. There was little difference in the history of spontaneous miscarriage, and urinary tract infection during pregnancy, and gestational age at entry to the study.
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After adjustment for maternal age, education, race/ethnicity, gravidity, a history of miscarriage, preterm delivery or low birthweight, vitamin use, vomiting and smoking during pregnancy, there was a dose–response relationship of increased risk of preterm delivery associated with increased severity of depressive symptoms (CESD
16) during early pregnancy (P < 0.01 for trend test). Compared with women without the depressive symptoms (CESD <16), women with a CESD score 22 had a greater than two-fold increased risk of preterm delivery [adjusted hazard ratio (aHR) = 2.2, 95% CI 1.1–4.7], whereas women with a CESD score of 16–21 had about 60% increased risk (aHR = 1.6, 95% CI 0.7–3.6) (Table II). Further adjustment for other variables in Table I did not change the results. In addition, removal of the CESD questions that might be influenced by pregnancy-related symptoms such as fatigue and eating disturbance did not change the HR of preterm delivery associated with the depressive symptoms.
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To determine whether the association of depressive symptoms during pregnancy with the risk of preterm delivery was affected by other characteristics, we further examined the association according to several social, demographic, reproductive and behavioral factors that are likely related to both depressive symptoms and/or preterm delivery (Table III). While none of the interaction terms reached statistical significance, the association appeared to be influenced by women's educational level, race/ethnicity, reproductive history and the presence of stressful life events. The effect of depressive symptoms during early pregnancy on the risk of preterm delivery was exacerbated when women had less than a college education (aHR = 5.0, 95% CI 1.1–23.3), two or more prior pregnancies (aHR = 4.5, 95% CI 1.0–21.3), a history of subfertility (aHR = 3.8, 95% CI 1.0–15.0) and the presence of stressful life events (aHR = 2.1, 95% CI 1.0–4.6). The association was stronger among Whites (aHR = 2.7, 95% CI 0.9–7.9), whereas, in contrast, having prenatal depressive symptoms did not increase the risk of preterm delivery among African Americans. The association also appeared to be stronger among both underweight women and women who were overweight, although the stronger association among underweight women was largely due to the very low risk of preterm delivery among those without depressive symptoms in this group (Table III). Whether the index pregnancy was planned or not did not have an effect on the association.
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Discussion |
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In this representative population-based prospective cohort study, we observed that a large proportion of pregnant women had significant (CESD
16) or severe (CESD >22) depressive symptoms in early pregnancy, around 10 weeks of gestation. The percentage of women with depressive symptoms observed in our study was quite comparable to the prevalence reported in a different study using CESD (Dole et al., 2004), supporting the argument for both the representativeness of our study population and the validity of our measurement of prenatal depressive symptoms. More importantly, women with severe depressive symptoms during early pregnancy had more than twice the risk of preterm delivery compared with women who did not have depressive symptoms during early pregnancy. The risk of preterm delivery increased with increasing severity of depressive symptoms, demonstrating a dose–response relationship between depressive symptoms and the risk of preterm delivery. The relationship between depressive symptoms in early pregnancy and the risk of preterm delivery in a racially/ethnically diverse population has not been well examined. A few studies reported examination of the relationship (Steer et al., 1992; Copper et al., 1996; Dayan et al., 2002; Orr et al., 2002a; Dole et al., 2004). However, some were limited to inner-city minority or underprivileged populations (Steer et al., 1992; Orr et al., 2002a) and others were using a slightly different outcome (Dayan et al., 2002; Macones, 2002). Nevertheless, three of four of these studies also reported an increased risk of preterm delivery/labor associated with depression during pregnancy, consistent with our findings despite the fact that many of these studies measured depressive symptoms at various gestational ages, usually in the second or third trimester, later than the present study. A significant strength of our study was the prospective design. We ascertained depressive symptoms early in gestation (10 weeks on average), long before the occurrence of preterm delivery. Therefore, women's reports of their depressive symptoms were not influenced by the presence of preterm delivery. In addition, unlike retrospective studies, the reported depressive symptoms in our prospective study were not the result of preterm delivery.
Another strength of this study is the lack of widespread use of antidepressants in our study population. Examination of our pharmacy records revealed that only 1.5% of our study population was prescribed any antidepressants during the study period (1996–1998), and excluding those subjects from our analysis did not change the results. Without the confounding by antidepressants, our results provided more direct evidence that prenatal depressive symptoms themselves increase the risk of preterm delivery. Considering the increased use of antidepressants among pregnant women, the findings from this study may provide a rare opportunity to evaluate the effect of depression on the risk of preterm delivery without the entanglement of antidepressants.
One limitation of the study is a lack of repeated measures of depressive symptoms throughout the pregnancy. Although we only measured depressive symptoms once during early pregnancy, any changes in the status of depressive symptoms by women throughout pregnancy were likely to attenuate the strength of our observed association between depressive symptoms and the risk of preterm delivery. In other words, without such a limitation, we would have likely observed an even greater risk of preterm delivery associated with prenatal depressive symptoms. If a woman who had depressive symptoms during our measurement time, but later recovered from depression; or a woman who did not have depressive symptoms at the measurement, but later developed depressive symptoms, this change would have led to misclassification of the true exposure status. Such non-differential misclassification (equally among women with or without preterm delivery) would have resulted in attenuation of the true association because of the prospective nature of the study. Without such misclassification, the observed association would have been even stronger. Another limitation is potential participation bias due to relatively low participation rates in the study, although the prospective nature of the study design (not likely related to preterm delivery) reduced the impact of low participation rates.
The timing of the measurement of depressive symptoms was largely determined by the design of the original study (i.e. for miscarriage). The observed association between depressive symptoms in early gestational age and the risk of preterm delivery could reflect the underlying biological mechanism that starts in early pregnancy. Emerging evidence has provided strong support for the link between depression during early pregnancy and the risk of preterm delivery through its interference with neuroendocrine pathways and placental function. On the other hand, depressive symptoms in early pregnancy could simply be a correlate for depressive symptoms in late gestational age that may be more biologically relevant for preterm delivery. If this was the case, such non-differential misclassification due to ‘imperfect’ timing would have attenuated the strength of the observed association as described above in the context of single measurement. In other words, if the timing of measurement was perfect, the observed association would have been even stronger. Furthermore, the previous reports of a similar association (Steer et al., 1992; Copper et al., 1996; Dayan et al., 2002; Orr et al., 2002a; Dole et al., 2004), while measuring depressive symptoms at later gestational ages than the present study, provide further support for the validity of our findings.
While the actual mechanisms for the increased risk of preterm delivery associated with prenatal depression are not known at this point, hormonal and immunological factors have been reported to be related to the risk of preterm delivery (Wadhwa et al., 1998; Austin and Leader, 2000; Lee et al., 2001; Li et al., 2004; Wadhwa et al., 2004; Rich-Edwards and Grizzard, 2005). The placenta and neuroendocrine functions play a central role in maintaining the health of a pregnancy and determining the onset of labor. Emerging research has demonstrated that mood disorders, especially depression during pregnancy, influence the levels of placental hormones and functions (Wadhwa et al., 1996; Austin and Leader, 2000; Pike, 2005; Diego et al., 2006; Neggers et al., 2006). Thus, it is biologically plausible that depression during pregnancy could influence the risk of preterm delivery by interfering with placental and hormonal functions as well as immune capacity (Anisman et al., 1993; Young et al., 2000; Soares et al., 2001; Anisman and Merali, 2002; Anisman et al., 2002; Harlow et al., 2003; Freeman et al., 2004; Simmons and Broderick, 2005). Psychopathological factors have emerged as potentially important and biologically plausible risk factors for preterm delivery (Steer et al., 1992; Wadhwa et al., 1996; Dayan et al., 2002; Orr et al., 2002a; Mancuso et al., 2004; Neggers et al., 2006; Alder et al., 2007).
Our study has also provided tentative new suggestions that the effect of depressive symptoms on the risk of preterm delivery may be impacted by other factors including socio-demographic characteristics, reproductive history and presence of other stressors. While the interactions presented in Table III did not reach statistical significance, the consistency in the directions of the interactions among those factors, which are all biologically plausible, deserves further evaluation. For example, it is conceivable that low educational level and the presence of other stressful events could exacerbate the effect of depressive symptoms on the risk of preterm delivery through social and environmental mechanisms. The results in Table III also reveal that the presence of other causes of preterm delivery may obscure the association between depressive symptoms during pregnancy and the risk of preterm delivery such as is the case among African Americans. Similarly, an absence of other causes of preterm delivery in some subgroups may partially explain the apparently stronger association among underweight women, because the risk of preterm delivery among women without depressive symptoms in this group was noticeably low (1.1%). These new findings of the interaction between prenatal depression and other characteristics may have important public health and clinical implications. They provide insight into intervention strategies and foundations for prioritization. For example, interventions to reduce prenatal depression and preterm delivery could be focused on women with low educational levels, high parity, a history of fertility problems, presence of other stressful events and a diagnosis of obesity. However, these new findings would need further confirmation.
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Author's role |
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D.-K.L. conceived the concept, designed the study, obtained funding, oversaw the data collection and analyses and was responsible for the interpretation of results and preparation of the manuscript. L.L. was responsible for data analysis and was involved in interpretation of the data and preparation of the manuscript. R.O. was involved in the data collection and preparation of the manuscript. D.-K.L. is the guarantor of this paper who took full responsibility for the conduct of the study, had access to the data and controlled the decision to publish.
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Funding |
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The study was supported in part by funds from the California Public Health Foundation.
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Footnotes |
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Some of the findings of the study were presented at the 2005 Annual Meeting of the Society for Pediatric and Perinatal Epidemiology. 
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References |
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Alder J, Fink N, Bitzer J, Hosli I, Holzgreve W. Depression and anxiety during pregnancy: a risk factor for obstetric, fetal and neonatal outcome? A critical review of the literature. J Matern Fetal Neonatal Med (2007) 20:189–209.[CrossRef][Web of Science][Medline]
Anisman H, Merali Z. Cytokines, stress, and depressive illness. Brain Behav Immun (2002) 16:513–524.[CrossRef][Web of Science][Medline]
Anisman H, Zalcman S, Zacharko RM. The impact of stressors on immune and central neurotransmitter activity: bidirectional communication. Rev Neurosci (1993) 4:147–180.[CrossRef][Medline]
Anisman H, Hayley S, Turrin N, Merali Z. Cytokines as a stressor: implications for depressive illness. Int J Neuropsychopharmacol (2002) 5:357–373.[CrossRef][Web of Science][Medline]
Armstrong J. 17 Progesterone for preterm birth prevention: a potential 2 billion dollar opportunity. Am J Obstet Gynecol (2007) 196:194–195.[CrossRef][Web of Science][Medline]
Austin MP, Leader L. Maternal stress and obstetric and infant outcomes: epidemiological findings and neuroendocrine mechanisms. Aust N Z J Obstet Gynaecol (2000) 40:331–337.[Web of Science][Medline]
Beck CT. A meta-analysis of the relationship between postpartum depression and infant temperament. Nurs Res (1996) 45:225–230.[CrossRef][Web of Science][Medline]
Board of Health Sciences Policy. Societal Costs of Preterm Birth. (2007) 398.
Branum AM, Schoendorf KC. Changing patterns of low birthweight and preterm birth in the United States, 1981-98. Paediatr Perinat Epidemiol (2002) 16:8–15.[CrossRef][Web of Science][Medline]
Civic D, Holt VL. Maternal depressive symptoms and child behavior problems in a nationally representative normal birthweight sample. Matern Child Health J (2000) 4:215–221.[CrossRef][Medline]
Copper RL, Goldenberg RL, Das A, Elder N, Swain M, Norman G, Ramsey R, Cotroneo P, Collins BA, Johnson F, et al. The preterm prediction study: maternal stress is associated with spontaneous preterm birth at less than thirty-five weeks' gestation. National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Am J Obstet Gynecol (1996) 175:1286–1292.[CrossRef][Web of Science][Medline]
Cuevas KD, Silver DR, Brooten D, Youngblut JM, Bobo CM. The cost of prematurity: hospital charges at birth and frequency of rehospitalizations and acute care visits over the first year of life: a comparison by gestational age and birth weight. Am J Nurs (2005) 105:56–64.[Medline]
Dayan J, Creveuil C, Herlicoviez M, Herbel C, Baranger E, Savoye C, Thouin A. Role of anxiety and depression in the onset of spontaneous preterm labor. Am J Epidemiol (2002) 155:293–301.
Diego MA, Jones NA, Field T, Hernandez-Reif M, Schanberg S, Kuhn C, Gonzalez-Garcia A. Maternal psychological distress, prenatal cortisol, and fetal weight. Psychosom Med (2006) 68:747–753.
Dole N, Savitz DA, Siega-Riz AM, Hertz-Picciotto I, McMahon MJ, Buekens P. Psychosocial factors and preterm birth among African American and White women in central North Carolina. Am J Public Health (2004) 94:1358–1365.
Freeman EW, Sammel MD, Liu L, Gracia CR, Nelson DB, Hollander L. Hormones and menopausal status as predictors of depression in women in transition to menopause. Arch Gen Psychiatry (2004) 61:62–70.
Hann D, Winter K, Jacobsen P. Measurement of depressive symptoms in cancer patients: evaluation of the Center for Epidemiological Studies Depression Scale (CES-D). J Psychosom Res (1999) 46:437–443.[CrossRef][Web of Science][Medline]
Harlow BL, Wise LA, Otto MW, Soares CN, Cohen LS. Depression and its influence on reproductive endocrine and menstrual cycle markers associated with perimenopause: the Harvard Study of Moods and Cycles. Arch Gen Psychiatry (2003) 60:29–36.
Hoffman S, Hatch MC. Depressive symptomatology during pregnancy: evidence for an association with decreased fetal growth in pregnancies of lower social class women. Health Psychol (2000) 19:535–543.[CrossRef][Web of Science][Medline]
Lee D, Yip A, Chiu H, Leung T, Chung T. A psychiatric epidemiological study of postpartum Chinese women. Am J Psychiatry (2001) 158:220–226.
Li DK, Odouli R, Wi S, Janevic T, Golditch I, Bracken TD, Senior R, Rankin R, Iriye R. A population-based prospective cohort study of personal exposure to magnetic fields during pregnancy and the risk of miscarriage. Epidemiology (2002) 13:9–20.[CrossRef][Web of Science][Medline]
Li DK, Janevic T, Odouli R, Liu L. Hot tub use during pregnancy and the risk of miscarriage. Am J Epidemiol (2003) a 158:931–937.
Li DK, Liu L, Odouli R. Exposure to non-steroidal anti-inflammatory drugs during pregnancy and risk of miscarriage: population based cohort study. BMJ (2003) b 327:368.
Li DK, Odouli R, Liu L, Vinson M, Trachtenberg E. Transmission of parentally shared human leukocyte antigen alleles and the risk of preterm delivery. Obstet Gynecol (2004) 104:594–600.[Web of Science][Medline]
Macones GA. Is preterm labor a valid endpoint in perinatal research? Am J Epidemiol (2002) 155:302–304.
Mancuso RA, Schetter CD, Rini CM, Roesch SC, Hobel CJ. Maternal prenatal anxiety and corticotropin-releasing hormone associated with timing of delivery. Psychosom Med (2004) 66:762–769.
Miller LJ. Postpartum depression. JAMA (2002) 287:762–765.
Myers JK, Weissman MM. Use of a self-report symptom scale to detect depression in a community sample. Am J Psychiatry (1980) 137:1081–1084.
Neggers Y, Goldenberg R, Cliver S, Hauth J. The relationship between psychosocial profile, health practices, and pregnancy outcomes. Acta Obstet Gynecol Scand (2006) 85:277–285.[Web of Science][Medline]
Oberlander TF, Misri S, Fitzgerald CE, Kostaras X, Rurak D, Riggs W. Pharmacologic factors associated with transient neonatal symptoms following prenatal psychotropic medication exposure. J Clin Psychiatry (2004) 65:230–237.[Web of Science][Medline]
Orr ST, Miller CA. Maternal depressive symptoms and the risk of poor pregnancy outcome. Review of the literature and preliminary findings. Epidemiol Rev (1995) 17:165–171.
Orr ST, James SA, Blackmore PC. Maternal prenatal depressive symptoms and spontaneous preterm births among African-American women in Baltimore, Maryland. Am J Epidemiol (2002) a 156:797–802.
Orr ST, James SA, Blackmore PC. Maternal prenatal depressive symptoms and spontaneous preterm births among African-American women in Baltimore, Maryland. Am J Epidemiol (2002) b 156:797–802.
Philipps LH, O'Hara MW. Prospective study of postpartum depression: 4 1/2-year follow-up of women and children. J Abnorm Psychol (1991) 100:151–155.[CrossRef][Web of Science][Medline]
Pike IL. Maternal stress and fetal responses: evolutionary perspectives on preterm delivery. Am J Hum Biol (2005) 17:55–65.[CrossRef][Web of Science][Medline]
Radloff LS. The CES-D scale: a self-report depression scale for research in the general population. Appl Psychol Meas (1977) 1:385–401.[CrossRef]
Radloff LS. The Use of the Center for Epidemiologic Studies Depression Scale in Adolescents and Young Adults. J Youth Adolesc (1991) 20:149–166.[CrossRef][Web of Science]
Rich-Edwards JW, Grizzard TA. Psychosocial stress and neuroendocrine mechanisms in preterm delivery. Am J Obstet Gynecol (2005) 192:S30–S35.[CrossRef][Web of Science][Medline]
Roberts RE. Reliability of the CES-D Scale in different ethnic contexts. Psychiatry Res (1980) 2:125–134.[CrossRef][Web of Science][Medline]
Roberts RE, Vernon SW. The Center for Epidemiologic Studies Depression Scale: its use in a community sample. Am J Psychiatry (1983) 140:41–46.
Simmons DA, Broderick PA. Cytokines, stressors, and clinical depression: augmented adaptation responses underlie depression pathogenesis. Prog Neuropsychopharmacol Biol Psychiatry (2005) 29:793–807.[CrossRef][Medline]
Simon GE, Cunningham ML, Davis RL. Outcomes of prenatal antidepressant exposure. Am J Psychiatry (2002) 159:2055–2061.
Soares CN, Almeida OP, Joffe H, Cohen LS. Efficacy of estradiol for the treatment of depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. Arch Gen Psychiatry (2001) 58:529–534.
Steer RA, Scholl TO, Hediger ML, Fischer RL. Self-reported depression and negative pregnancy outcomes. J Clin Epidemiol (1992) 45:1093–1099.[CrossRef][Web of Science][Medline]
Thomas JL, Jones GN, Scarinci IC, Mehan DJ, Brantley PJ. The utility of the CES-D as a depression screening measure among low-income women attending primary care clinics. The Center for Epidemiologic Studies-Depression. Int J Psychiatry Med. (2001) 31:25–40.[CrossRef][Web of Science][Medline]
Wadhwa PD, Dunkel-Schetter C, Chicz-DeMet A, Porto M, Sandman CA. Prenatal psychosocial factors and the neuroendocrine axis in human pregnancy. Psychosom Med (1996) 58:432–446.
Wadhwa PD, Porto M, Garite TJ, Chicz-DeMet A, Sandman CA. Maternal corticotropin-releasing hormone levels in the early third trimester predict length of gestation in human pregnancy. Am J Obstet Gynecol (1998) 179:1079–1085.[CrossRef][Web of Science][Medline]
Wadhwa PD, Garite TJ, Porto M, Glynn L, Chicz-DeMet A, Dunkel-Schetter C, Sandman CA. Placental corticotropin-releasing hormone (CRH), spontaneous preterm birth, and fetal growth restriction: a prospective investigation. Am J Obstet Gynecol (2004) 191:1063–1069.[CrossRef][Web of Science][Medline]
Weng X, Odouli R, Li DK. Maternal caffeine consumption during pregnancy and the risk of miscarriage: a prospective cohort study. Am J Obstet Gynecol (2008) 198:279e1–279e8.
Wisner KL, Gelenberg AJ, Leonard H, Zarin D, Frank E. Pharmacologic treatment of depression during pregnancy. JAMA (1999) 282:1264–1269.
Young EA, Midgley AR, Carlson NE, Brown MB. Alteration in the hypothalamic-pituitary-ovarian axis in depressed women. Arch Gen Psychiatry (2000) 57:1157–1162.
Submitted on March 4, 2008; resubmitted on August 11, 2008; accepted on August 18, 2008.
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