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. 2026 Jul 3;68(4):e70180. doi: 10.1002/dev.70180

Low Pregnancy Cortisol and Infant Socioemotional Problems: The Mediating Role of Postpartum Depressive Symptoms

Jennifer E Khoury 1,✉, Lauren Giles 2, Mackenna Pattison 2, Tanya Tulipan 3, Victoria Allen 4, Marsha Campbell‐Yeo 5, Tara Perrot 2
PMCID: PMC13329804  PMID: 42396820

ABSTRACT

Infant socioemotional development has important implications for later functioning, reflecting capacities for emotional regulation, stress responsivity, and social engagement. Stress and mental health during pregnancy and the postpartum can adversely influence infant socioemotional functioning. This study examined whether postpartum depressive and anxiety symptoms mediate associations between prenatal maternal hair cortisol concentration (HCC) and infant socioemotional development. A sample of 128 participants was followed from the third trimester of pregnancy to 6 months postpartum. Maternal HCC was collected during the third trimester to reflect cortisol during the second half of pregnancy. Symptoms of depression and anxiety were measured at 2 weeks postpartum, and infant socioemotional problems were assessed at 6 months of age. Structural equation modeling tested postpartum depression and anxiety as parallel mediators. Results indicated that lower HCC in pregnancy predicted greater postpartum depression (B = −3.676, p = 0.003) and anxiety (B = −3.41, p = 0.009); depression was associated with greater infant socioemotional problems at 6 months (B = 1.900, p < 0.001). HCC was not directly associated with infant socioemotional outcomes (B = 1.071, p = 0.792); however, the indirect effect, through depressive symptoms, was significant (B = −6.99, p = 0.01). These findings suggest that prenatal physiological stress may influence infant socioemotional development indirectly through early postpartum depressive symptoms, highlighting the importance of integrated perinatal processes.

1. Introduction

Infant socioemotional development in the first year of life is critical for later socioemotional functioning, reflecting early capacities for emotional regulation, stress responsivity, and social engagement (Bailes and Leerkes 2023; Ilyka et al. 2021 ). Early socioemotional difficulties—such as affect dysregulation, heightened negative affect, and difficulty soothing—have been linked to increased risk for later behavioral and emotional problems (Toffol et al. 2019; Troxel et al. 2013). Guided by the Developmental Origins of Health and Disease (DOHaD; Barker 1990) framework, growing evidence suggests that these infant socioemotional outcomes are influenced by the maternal perinatal environment (Briggs‐Gowan et al. 2006; Madigan et al. 2015). Prenatal neuroendocrine stress processes, such as maternal hypothalamic–pituitary–adrenal (HPA) axis activity, and postnatal psychological functioning, including symptoms of depression and anxiety, may both play important roles in shaping infant socioemotional development (Glover et al. 2018; Madigan et al. 2018; O'Donnell and Meaney 2017). Together, this highlights the importance of considering both prenatal and postnatal influences when examining early infant socioemotional outcomes.

1.1. Socioemotional Development in Infancy

At 6 months of age, infants are undergoing substantial changes in socioemotional development, characterized by increasingly organized patterns of emotional expression, regulation, and social engagement (Ilyka et al. 2021). During this period, infants show more differentiated affect, greater responsiveness to social cues, and more coordinated interactions with caregivers, including the emergence of contingent, reciprocal exchanges that support the development of early relationships (Ilyka et al. 2021; Provenzi et al. 2016). These early capacities are embedded within the caregiving environment and are supported through both infant‐initiated and caregiver‐assisted regulation. In particular, infants begin to integrate rudimentary self‐regulatory strategies (e.g., gaze aversion, self‐soothing behaviors) with ongoing reliance on caregivers for external regulation (Gennis et al. 2022; Manian et al. 2025; Planalp and Braungart‐Rieker 2015). As such, these developing processes remain highly sensitive to variations in caregiver responsiveness and emotional availability, both of which are directly related to maternal mental health problems (Manian et al. 2025; Radoš et al. 2018; Rusanen et al. 2025).

Socioemotional functioning in early infancy is considered a meaningful indicator of later socioemotional development. For example, difficulties such as heightened negative affect, poor affect regulation, or reduced social engagement in infancy have been associated with later child internalizing and externalizing symptoms, as well as challenges in social competence and attachment relationships (Bilgin et al. 2025; Edwards et al. 2017; Karakaş et al. 2021; Koegel et al. 2014). Importantly, the first 6 months of infancy represent a sensitive window during which early patterns of emotional and relational functioning are becoming more stable, yet remain malleable to environmental influences (Bozicevic et al. 2025; Gee 2020). As such, examining socioemotional development at this stage provides a valuable opportunity to identify early markers of risk and better understand the processes that shape longer‐term mental health outcomes.

1.2. Prenatal Maternal Neuroendocrine Functioning and Infant Socioemotional Development

Because socioemotional development in early infancy is highly sensitive to environmental influences, it is important to identify specific prenatal biological pathways that may influence these outcomes. Maternal HPA axis functioning during pregnancy has been identified as a biological pathway through which prenatal stress may shape offspring development (Barker 1990; Wadhwa et al. 2009). Across gestation, the maternal HPA axis undergoes normative adaptations, including increases in circulating cortisol, particularly in the third trimester (Buss et al. 2012; Jung et al. 2011; Vrijkotte et al. 2023). Maternal cortisol can cross the placenta and contributes to the development of the fetal HPA axis. This transfer is partially regulated by the placental enzyme 11β‐hydroxysteroid dehydrogenase type 2 (11β‐HSD2), which converts cortisol into its inactive form (Jahnke et al. 2021; Togher et al. 2014). Under conditions of heightened stress, the efficiency of this protective mechanism may be reduced, particularly later in pregnancy, potentially increasing fetal exposure to maternal cortisol (Jahnke et al. 2021; Seth et al. 2015). As such, dysregulation of maternal HPA axis activity—reflected in both elevated and attenuated cortisol levels—has been proposed as a mechanism influencing early neurodevelopment and socioemotional functioning (Tadanki et al. 2025; Van Den Bergh et al. 2020). Associations between maternal cortisol during pregnancy and early markers of infant socioemotional development have been documented, although findings remain mixed. Studies using salivary cortisol have shown that higher average third‐trimester cortisol is associated with greater infant irritability and negative reactivity in early infancy (Braithwaite et al. 2017; Davis et al. 2007). In contrast, lower average cortisol across pregnancy has been linked to later externalizing behaviors in childhood (Fleck et al. 2023). These findings suggest that both higher and lower‐than‐average HPA activity may confer risk, and that the type and timing of cortisol measurement during pregnancy may be important in understanding these complex associations.

Hair cortisol concentration (HCC) has been examined less frequently but offers a promising approach for capturing cumulative cortisol production over several months, providing an index of long‐term maternal HPA activity during pregnancy. Higher than average late‐pregnancy HCC has been associated with greater negative emotional reactivity in infants (Bosquet Enlow et al. 2017). However, other studies have reported null associations between HCC and infant socioemotional outcomes (Bruinhof et al. 2022; Conradt et al. 2020). Furthermore, recent evidence suggests that lower‐than‐average HCC during the third trimester is associated with elevated socioemotional problems at 2 and 5 years of age (Mustonen et al. 2024). In addition to these main effects, Mustonen et al. (2024) found that the combination of lower late‐pregnancy HCC and elevated prenatal depressive symptoms predicted greater internalizing and dysregulation difficulties in children at 2 years of age. Taken together, these findings suggest that maternal HPA axis functioning during pregnancy may play an important, yet complex, role in influencing offspring socioemotional development, highlighting the need for further longitudinal research. While maternal HPA axis functioning during pregnancy represents an important biological pathway, psychological processes in the early postpartum period are also evidenced to play a key role in influencing infant socioemotional development.

1.3. Postpartum Maternal Mental Health and Infant Socioemotional Development

The postpartum period is marked by substantial psychological adjustment, during which approximately one in five individuals experience symptoms of depression and/or anxiety, underscoring the prevalence and public health importance of these conditions (Feldman et al. 2025; Gheorghe et al. 2021; Micha et al. 2022; Ogallar et al. 2025; Shorey et al. 2018; Wang et al. 2021). Beyond their impact on maternal well‐being, postpartum mental health difficulties have important implications for the caregiving environment. Symptoms of depression and anxiety have been associated with reduced maternal sensitivity, lower responsiveness, and disruptions in affective attunement, which are critical for supporting early regulatory development and dyadic interaction (Field et al. 2010; Hakanen et al. 2019; Madigan et al. 2018; Saharoy et al. 2023).

Consistent with this, a substantial body of research indicates that postpartum depression and anxiety are associated with greater infant socioemotional difficulties, including increased infant negative affect, poorer regulation, and reduced social engagement (Korja et al. 2024; Madigan et al. 2018; Subbiah et al. 2024). Although findings in terms of postpartum anxiety are mixed, some studies report associations with infant socioemotional outcomes (Davis et al. 2007), while others suggest smaller or less consistent effects relative to depression (Madigan et al. 2018). For example, recent longitudinal work has reported a small negative association between postpartum anxiety and infant socioemotional development after accounting for depressive symptoms (Subbiah et al. 2024), and a previous systematic review noted limited and methodologically variable evidence for postnatal anxiety, while still indicating preliminary support for a small effect on child emotional outcomes (Rees et al. 2019). As such, maternal experiences of both depressive and anxiety symptoms during the postpartum period may have implications for infant socioemotional outcomes.

1.4. Linking Prenatal Neuroendocrine Stress to Postpartum Mental Health

Given that maternal mental health problems can adversely impact infant socioemotional development, and that mitigating this risk is important, it is essential to identify factors that may contribute to the development of mental health difficulties in the postpartum period. The Stress Diathesis Hypothesis suggests that mental health problems develop from a combination of individual biopsychosocial vulnerability and exposure to stress (Monroe and Simons 1991). Importantly, evidence suggests that dysregulation of the maternal HPA axis, including altered cortisol levels during pregnancy, is associated with increased risk for postpartum depression and anxiety symptoms (Caparros‐Gonzalez et al. 2022; Maguet et al. 2024). Research indicates that a blunted cortisol awakening response (Seth et al. 2016) and greater salivary cortisol reactivity to psychosocial stress are associated with postpartum depressive symptoms (e.g., Nierop et al. 2006). Other research has not found significant associations between urinary or serum cortisol levels and postpartum depression or anxiety symptoms (Figueiredo and Costa 2009; Yim et al. 2009).

Findings linking prenatal HCC to postpartum mental health outcomes have also been mixed, likely reflecting differences in the timing of cortisol assessment across pregnancy, methodological approaches to measuring HCC, and variability in how postpartum mental health is operationalized. For example, women with higher HCC in the first and third trimesters were at greater risk for postpartum depression at 2 weeks postpartum, and hair cortisol levels predicted 21.7% of the variance of postpartum depression symptoms (Caparros‐Gonzalez et al. 2017). Similarly, higher HCC in the first trimester has been associated with greater depressive symptoms at 40 weeks’ gestational age (Hoffman et al. 2016). Interestingly, Maguet et al. (2024) found that women with third‐trimester HCC levels in the second quartile (i.e., moderate levels) exhibited an increased risk for depressive symptoms at 2 months postpartum. In contrast, Jahangard et al. (2019) reported that lower mid‐pregnancy HCC was associated with heightened postpartum depressive symptoms at 12 weeks postpartum. Similarly, lower‐than‐average HCC in the first trimester predicted higher postpartum depressive symptoms at 3 months postpartum (Sobol et al. 2025).

Relatively few studies have examined the association between prenatal maternal HCC and postpartum anxiety, specifically. One study demonstrated that higher HCC, collected during the third trimester, was positively associated with higher composite stress, anxiety, and depression scores at 2 weeks postpartum, but not at 6 months postpartum (Madigan et al. 2024). Notably, this study relied on a composite of depressive and anxiety symptoms, which, despite their high comorbidity, may obscure disorder‐specific associations and limit the ability to identify potentially distinct patterns of risk. Examining these processes within an integrated framework that treats postpartum depressive and anxiety symptoms as separate mediating pathways may help clarify how prenatal neuroendocrine risk is transmitted across the perinatal period to influence infant socioemotional outcomes.

Taken together, existing research suggests that maternal HPA axis functioning during pregnancy is associated with both postpartum mental health problems and early infant socioemotional outcomes, while postpartum mental health is itself a well‐established predictor of infant development. This points to a potential pathway through which prenatal neuroendocrine stress may influence infant development indirectly via maternal postpartum mental health. However, these literatures have largely developed in parallel, with prenatal neuroendocrine stress and postnatal mental health examined as independent predictors rather than as components of a mediational pathway, which limits the ability to understand how biological stress processes during pregnancy may translate into variations in the postnatal caregiving environment that subsequently shape infant socioemotional development.

In addition, findings linking maternal HPA axis activity—particularly HCC—to both mental health and child outcomes have been inconsistent, suggesting that direct associations may not fully capture the complexity of these associations. One possibility is that postpartum mental health problems represent an intermediary mechanism through which prenatal neuroendocrine stress exerts downstream effects on infant outcomes. Examining this potential mediating pathway may therefore help reconcile mixed findings in the literature and provide a more coherent framework for understanding how early biological and psychological processes jointly contribute to infant socioemotional development.

1.5. Study Aims and Hypotheses

The present study aimed to (1) examine associations between maternal hair cortisol during the second half of pregnancy and early postpartum depressive and anxiety symptoms; (2) evaluate associations between maternal pregnancy hair cortisol and infant socioemotional outcomes at 6 months postpartum; (3) assess the relationship between postpartum maternal mental health and infant socioemotional problems; and (4) test whether postpartum depressive and anxiety symptoms mediate the association between pregnancy hair cortisol and infant socioemotional outcomes.

It is hypothesized that maternal pregnancy hair cortisol levels will be associated with postpartum depressive and anxiety symptoms (H1) and with infant socioemotional problems at 6 months (H2). It is further hypothesized that higher levels of postpartum depressive and anxiety symptoms will be associated with greater infant socioemotional problems (H3). Finally, it is expected that postpartum depressive and anxiety symptoms will mediate the association between maternal pregnancy hair cortisol and infant socioemotional outcomes (H4).

2. Materials and Methods

2.1. Participants and Study Design

Participants included 128 individuals from Nova Scotia, Canada, who were recruited during pregnancy through social media and community postings. Inclusion criteria were that individuals (1) live in Nova Scotia, (2) were pregnant with a singleton pregnancy ≤36 weeks’ gestational age, (3) were 19 years of age or older, and (4) read and write English. This longitudinal cohort study included three study time points—one during the third trimester of pregnancy (T1), another at 2 weeks postpartum (T2), and the last at 6 months postpartum (T3). T1 and T3 sessions were conducted at Mount Saint Vincent University (MSVU) in Halifax, Nova Scotia, and T2 sessions were conducted either at MSVU or as home visits, based on participant preference. Informed consent was given by all participants.

2.2. Measures

2.2.1. HCCs

Hair samples (approximately 50 strands) were cut from the posterior vertex region of participants’ heads during the third trimester of pregnancy (T1). At the time of collection, detailed information on potential confounding factors was obtained, including oral, inhaled, and topical corticosteroid use, smoking status, and the use of chemical hair treatments (e.g., relaxing or perming). Samples were placed in tin foil inside an envelope and stored in a filing cabinet at room temperature until processing. For processing, a 3‐cm hair segment1 was cut from the proximal end of the sample (i.e., the segment closest to the scalp) and used for analysis. This segment reflects cumulative cortisol production over the approximately 3 months preceding sample collection, corresponding to late second to third trimester HPA axis activity (Preinbergs et al. 2023). The hair segments were washed twice with isopropanol, ground into powder form, and extracted by adding ethanol to the samples. Prior to assay, samples were centrifuged at 2800 rpm for 10 min. Cortisol was assayed in duplicate using Salimetrics Cortisol Enzyme‐Linked ImmunoSorbent Assay (ELISA) kits. Sample cortisol concentrations were calculated based on sample weight (pg/mg). The interassay and intraassay coefficients of variation were 5.63% and 8.69%, respectively.

In the present study, HCC is treated as a continuous index of relative differences in cumulative HPA axis activity within the sample, rather than as a clinical indicator of dysregulation relative to established normative thresholds.

2.2.2. Depressive Symptoms

Depressive symptoms experienced over the previous 7 days were assessed at T2 using the 10‐item Edinburgh Postnatal Depression Scale (EPDS) (Cox et al. 1987). The EPDS is widely used to evaluate the severity of depression during the perinatal period (Levis et al. 2020). The EPDS has a range of 0–30. An established cutoff score of 13 signifies clinically elevated depressive symptoms. The EPDS demonstrated good internal consistency in the current sample (Cronbach's α = 0.83 at T2).

2.2.3. Anxiety Symptoms

Anxiety symptoms experienced over the previous 2 weeks were assessed using the 7‐item Generalized Anxiety Disorder scale (GAD‐7; Spitzer et al. 2006). The GAD is a reliable and validated measure in perinatal populations (Vogazianos et al. 2022; Zhong et al. 2015). The established cutoff for clinically elevated anxiety symptoms on the GAD is 10. The GAD showed strong internal consistency in the current sample (Cronbach's α = 0.90 at T2).

2.2.4. Infant Socioemotional Problems

The Ages and Stages Questionnaires: Social‐Emotional, Second Edition (ASQ:SE‐2; Bernt 2017) was used to assess infant socioemotional development, valid for infants 1–72 months of age. Mothers completed the ASQ:SE‐2 when their infants were 6 months of age. The ASQ:SE‐2 assesses different domains of socioemotional functioning, including self‐regulation, compliance, communication, affect, autonomy, social interaction, and adaptive functioning, and higher total scores indicate greater socioemotional challenges.

2.2.5. Sociodemographic Characteristics and Potential Covariates

At T1, sociodemographic characteristics and potential covariates that were collected included education, income, race, age, relationship status, number of children, and time spent doing housework.

2.3. Statistical Analyses

Preliminary analyses, including descriptive statistics and bivariate correlations, were conducted in IBM SPSS Statistics 29. Bivariate correlations were conducted between sociodemographic variables (e.g., household income, number of children, etc.) and postpartum depressive symptoms, anxiety symptoms, and infant socioemotional problems. Variables that were significantly correlated with outcomes of interest were tested as covariates in subsequent path analyses.

Next, a parallel mediation model was conducted using the lavaan package in R. The model applied full information maximum likelihood (FIML) to handle missing data (Collins et al. 2001) and bootstrapped 95% confidence intervals (5000 iterations). Model fit was assessed using chi‐square values, CFI, RMSEA, and standardized root mean square residual (SRMR). Values ≥0.90 for CFI and ≤0.08 for RMSEA and SRMR indicate acceptable model fit (Rioux and Little 2021). This parallel mediation model examined the relations between the maternal HCC during pregnancy and infant socioemotional problems at 6 months postpartum, with postpartum depression symptoms and postpartum anxiety symptoms as mediators. Postpartum depression and anxiety symptoms were allowed to covary in the model. The model included a direct path from pregnancy HCC to infant socioemotional problems and two indirect paths, via postpartum depression and anxiety symptoms. Sociodemographic variables were considered as covariates in the SEM to control for potential confounding effects. Stepwise model simplification, based on statistical significance and theoretical rationale, was used to obtain the most parsimonious model (i.e., nonsignificant covariates and paths were removed). To address the possibility that concurrent maternal mental health symptoms may influence maternal ratings of infant socioemotional functioning, maternal depressive and anxiety symptoms assessed at the 6‐month postpartum session were included as covariates on infant socioemotional functioning in the mediation model.

A sensitivity analysis assessing the effect of cutting errors in 6 samples demonstrated that none of these samples were outliers in HCC. In addition, results of mediation analyses remain consistent regardless of whether these samples are included or excluded. Results reported in this manuscript include these six samples. Similarly, of the 12 participants who reported current steroid use (oral or topical), none had extreme HCC values, and excluding these participants did not change the results of mediation analyses. Accordingly, these participants were retained to maximize sample size and statistical power.

3. Results

3.1. Sample Characteristics

At the time of the pregnancy assessment (T1), participants were in the third trimester of pregnancy and were between 27 and 37 weeks’ gestational age (M = 30.96 weeks’ gestational age, SD = 2.49); T2 occurred at 2 weeks postpartum (M = 16.29 days postpartum, SD = 6.16); and T3 occurred at 6 months postpartum (M = 6.29 months postpartum, SD = 0.81). The average maternal age during pregnancy was 32.28 years (SD = 3.82, range = 24–43 years). Most participants identified as White (92.2%), were in a relationship (98.4%), reported an annual household income of $90,000 or more (71.9%), and had earned at least a bachelor's (undergraduate) degree (85.1%). Approximately half of the participants (55.5%) were nulliparous. Approximately half of the infants were male (51 .6 %). Additional demographic details are presented in Table 1.

TABLE 1.

Sample characteristics and descriptive statistics.

N (%) M (SD) Range
Number of children
0 71 (55.5%) — —
1 42 (32.8%) — —
2 13 (10.2%) — —
≥3 2 (1.6%) — —
Relationship status
In a relationship 126 (98.4%) — —
Not in a relationship 2 (1.6%) — —
Race
White 118 (92.2%) — —
Asian 5 (3.9%) — —
Other race 5 (3.9%) — —
Education
High school diploma or equivalent 4 (3.1%) — —
Nonuniversity postsecondary 11 (8.6%) — —
University below bachelor's 4 (3.1%) — —
Bachelor's degree 54 (42.2%) — —
Master's degree 47 (36.7%) — —
PhD 4 (3.1%) — —
MD 4 (3.1%) — —
Annual household income
<$20,000 1 (0.8%) — —
$20,000–$34,999 2 (1.6%) — —
$35,000–$69,999 17 (13.3%) — —
$70,000–$89,999 16 (12.5%) — —
$90,000–$109,999 20 (15.6%) — —
$110,000–$149,999 35 (27.3%) — —
$150,000–$199,999 29 (22.7%) — —
≥200,000 8 (6.3%) — —
Maternal BMI (T1, kg) — 29.95(5.42) 20.90‐42.93
Maternal anxiety (GAD, T2) — 4.96(4.07) 0‐20
Maternal depressive symptoms (EPDS, T2) — 6.77 (4.05) 0‐19
Maternal hair cortisol (T1)
Raw — 4.39 (4.92) 0.96–48.50
Log‐10 — 0.55 (0.26) −0.02 to 1.69
Infant socioemotional outcome (ASQ, T3) — 22.95 (14.02) 0–60
Infant sex (male) 6 6 (51 .6 %) — —
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Note: Number of children not including current pregnancy; income reported in Canadian dollars. T1 = pregnancy; T2 = postpartum.

Abbreviations: ASQ SE, Ages and Stages Questionnaires: Social‐Emotional; BMI, body mass index (kg/m2); EPDS, Edinburgh Postnatal Depression Scale; GAD, Generalized Anxiety Disorder scale.

3.2. Missing Data

In total, 128 individuals participated in the study in the third trimester of pregnancy (T1), 116 participated at 2 weeks postpartum (T2), and 106 participated at 6 months postpartum (T3). At T1, hair cortisol samples were missing due to opting out of providing a hair sample (n = 8) or providing a hair sample with insufficient weight for processing (n = 7). At T2, 10.2% (n = 13) of EPDS and 9.4% (n = 12) GAD questionnaires were missing due to incomplete questionnaires or attrition, and at T3, 17.2% (n = 22) of the ASQ questionnaires were missing due to attrition. Overall, 75.0% of participants (n = 96) provided complete data across all three time points.

Participants who completed the follow‐up sessions at T2 or T3 did not differ from those who did not complete follow‐up on key sociodemographic characteristics (maternal age, income, education, ethnicity, number of children, relationship status, ps range = 0.06–0.99) or pregnancy hair cortisol levels (ps range = 0.21–0.44). FIML was used to estimate missing data, under the assumption that data were missing at random, and the full sample size (N = 128) was used in the mediation analysis.

3.3. Descriptive Statistics

Descriptive statistics for measures are presented in Table 1. In terms of postpartum depressive and anxiety symptoms, 8.62% reported depressive symptoms within the clinical range (EPDS total score ≥13), and 14.66% reported anxiety symptoms within the clinical range (GAD total score ≥10). In total, 4.7% of the infants scored above the cutoff for ASQ socioemotional problems, and 23.4% scored in the monitoring zone. Maternal HCC during pregnancy was skewed due to two extreme outliers (>3 SD below the mean) and was log‐transformed to minimize skew. Both raw and log‐10‐transformed values are reported in Table 1. Log‐10 HCC values were used in subsequent analyses. No participants reported smoking or chemically treated hair. Twelve participants reported current steroid use (oral or topical). There were no extreme outliers in the variables of interest.

3.4. Preliminary Bivariate Correlations

As shown in Table 2, household income was significantly negatively associated with infant socioemotional problems at 6 months. In addition, the number of hours spent doing housework was significantly positively correlated with depressive symptoms and/or anxiety symptoms at 2 weeks postpartum.

TABLE 2.

Preliminary correlations.

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.
1. Maternal age
2. Education 0.280**
3. Income 0.277** 0.520**
4. Race −0.084 −0.162 −0.266**
5. Rel. status −0.057 0.291** 0.156 0.029
6. Num. children 0.229** 0.029 −0.074 0.170 0.014
7. Housework 0.075 0.087 −0.039 0.155 0.037 0.250**
8. Infant sex 0.023 0.0593 −0.050 −0.059 −0.011 0.095 0.092
9. Infant weight −0.047 −0.025 −0.017 −0.170 0.042 0.174 0.239* −0.029
10. Infant age −0.114 0.095 −0.037 −0.139 0.079 −0.035 −0.020 0.061 0.349**
11. Maternal BMI 0.018 −0.133 −0.009 0.001 −0.121 0.073 0.111 −0.154 0.200* −0.159
12. ASQ SE −0.061 −0.134 −0.212* 0.024 −0.095 0.040 0.019 −0.020 0.049 0.068 −0.065
13. Log HCC 0.232* 0.046 0.089 −0.081 −0.039 −0.001 −0.008 0.023 −0.077 −0.200* 0.127 −0.134
14. GAD T2 −0.150 −0.092 −0.041 0.095 −0.067 0.027 0.279** 0.035 0.094 0.190* −0.103 0.363** −0.232*
15. GAD T3 −0.122 −0.211* −0.166 0.095 −0.233* 0.121 0.102 0.001 0.027 0.048 0.146 0.231* −0.171 0.602**
16. EPDS T2 −0.104 −0.021 −0.078 −0.003 −0.123 −0.057 0.233* 0.087 0.006 0.157 −0.105 0.473** −0.248* 0.742** 0.581**
17. EPDS T3 −0.153 −0.159 −0.234* 0.090 −0.186 0.059 0.117 0.097 −0.036 0.034 0.099 0.383** −0.180 0.524** 0.805** 0.653**
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Note: Maternal age at T1; Rel. status, relationship status (0 = not in a relationship, 1 = in a relationship); Num children, number of children not including current pregnancy; Housework, average hours per week during pregnancy; Infant weight at birth (kg); Infant age, gestational age at birth (weeks); T1, pregnancy; T2, 2 weeks postpartum.

Abbreviations: ASQ SE, Ages and Stages Questionnaires: Social‐Emotional; BMI, body mass index (kg/m2); EPDS, Edinburgh Postnatal Depression Scale; GAD, Generalized Anxiety Disorder scale; Log HCC, log‐transformed hair cortisol concentration.

**Correlation is significant at the 0.01 level; *correlation is significant at the 0.05 level.

3.5. Path Mediation Model

A path model was utilized to examine the direct and indirect associations among maternal HCC during pregnancy, postpartum depression and anxiety symptoms, and infant socioemotional outcomes at 6 months postpartum, as shown in Figure 1. The final model fit well, χ 2(2) = 0.619, p = 0.734 and CFI = 1.000, RMSEA = 0.00, and SRMR = 0.011. Among covariates, lower household income at T1 was significantly associated with higher infant socioemotional difficulties and thus was retained in the model. However, housework was not significantly associated with postpartum depression or anxiety symptoms; as such, this covariate was removed from the final model. Concurrent depressive and anxiety symptoms were included as covariates on infant socioemotional outcomes; however, they were not significant, and their inclusion resulted in poor model fit. Thus, these covariates were removed from the final model (Table 3; Figure 1). The model with concurrent mental health covariates is reported in the Supporting Information (Table S1; Figure S1).

FIGURE 1.

FIGURE 1

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Parallel mediation model with standardized effects for the association between maternal hair cortisol during pregnancy and infant socioemotional outcomes, mediated by postpartum depressive and anxiety symptoms, controlled by household income. * p < 0.05; ** p < 0.001.

TABLE 3.

Direct, indirect, and total effects for mediation models examining the impact of the maternal hair cortisol concentration during pregnancy on infant socioemotional outcomes mediated through postpartum depression and anxiety.

Model pathways Path label Unstd. Estimate Std. estimate Std. Error p‐value 95% CI
lgHCC‐T1 → ASQ‐SE‐T3 c’ 1.07 0.02 4.06 0.79 [−7.30, 8.79]
EPDS‐T2 → ASQ‐SE‐T3 b1 1.90 0.53 0.51 <0.001 [0.88, 2.89]
GAD‐T2 → ASQ‐SE‐T3 b2 −0.09 −0.02 0.55 0.87 [−1.10, 1.06]
lgHCC‐T1 → EPDS‐T2 a1 −3.68 −0.24 1.22 0.003 [−5.90, −1.07]
lgHCC‐T1 → GAD‐T2 a2 −3.41 −0.23 1.30 0.009 [−5.93, −0 .85]
Indirect effect via EPDS‐T2 ab1 −6.99 −0.13 2.84 0.01 [−12.78, −1.79]
Indirect effect via GAD‐T2 ab2 0.31 0.01 2.02 0.88 [−3.72, 4.63]
Total effect (direct + indirect) c = c’ + ab1 + ab2 −5.61 −0.10 4.36 0.20 [−13.81, 3.31]
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As shown in Table 3, lower maternal HCC during pregnancy was significantly associated with higher depressive (B = −3.68, 95% CI [−5.90, −1.07]) and higher anxiety symptoms (B = −3.41, 95% CI [−5.93, −0.85]) at 2 weeks postpartum. Additionally, higher depressive symptoms were significantly associated with higher infant socioemotional problems at 6 months (B = 1.90, 95% CI [0.88, 2.89]). However, postpartum anxiety symptoms were not significantly associated with infant socioemotional problems (B = −0.09, 95% CI [−1.10, 1.06]).

The direct effect of pregnancy HCC on infant socioemotional problems was not significant (B = 1.07, 95% CI [−7.30, 8.79]), suggesting that HCC was not directly associated with infant socioemotional problems when mediators were included in the model. However, significant indirect effects were observed for the path of pregnancy HCC to infant socioemotional problems via depressive symptoms (B = −6.99, 95% CI [−12.78, −1.79]). The indirect effect of pregnancy HCC on infant socioemotional problems via anxiety symptoms (B = 0.31, 95% CI [−3.72, 4.63]) and the total effect of pregnancy HCC on infant socioemotional outcomes (B = −5.61, 95% CI [−13.81, 3.31]) were not statistically significant. These results suggest that lower prenatal HCC is associated with elevated maternal postpartum depression symptoms, which in turn relate to poorer socioemotional outcomes in infants. Although there were significant associations between pregnancy HCC and anxiety symptoms, the mediation pathway through anxiety was not significant.

In addition, associations remained statistically significant after adjusting for concurrent maternal depressive and anxiety symptoms at 6 months postpartum (see Table S1 and Figure S1), indicating that the observed findings were robust to adjustment for maternal mental health at the time infant ASQ ratings were completed.

4. Discussion

This study examined whether prenatal physiological stress, indexed by maternal hair cortisol during the second half of pregnancy, contributes to infant socioemotional development, and whether this association operates indirectly through early postpartum maternal mental health. Findings indicate that lower levels of maternal HCC were associated with greater anxiety and depressive symptoms at 2 weeks postpartum, but that only higher depressive symptoms predicted infant socioemotional problems at 6 months of age. Although HCC was not directly associated with infant socioemotional development, lower HCC was indirectly linked to more infant socioemotional problems through higher maternal postpartum depressive symptoms. This study provides novel insights into longitudinal patterns of association between prenatal physiological stress, postpartum mental health, and early infant socioemotional development.

Lower levels of hair cortisol were associated with greater depressive and anxiety symptoms at 2 weeks postpartum. This finding aligns with prior findings that lower‐than‐average HPA activity during pregnancy is a risk factor for postpartum depression (Jahangard et al. 2019; Sobol et al. 2025). Our results are also in line with other research showing that lower cortisol levels are associated with mental health problems in nonpregnant samples (Staufenbiel et al. 2013). However, these findings are in contrast to studies showing that higher pregnancy HCC is associated with greater postpartum mental health problems (Caparros‐Gonzalez et al. 2017) and studies demonstrating no significant associations between pregnancy HCC and postpartum mental health (Braig et al. 2016; Galbally et al. 2022; Stickel et al. 2021). These discrepancies may be explained, in part, by methodological differences, including the timing of cortisol collection and measurement of postpartum mental health. Lower/blunted cortisol levels may be indicative of hypocortisolism, a marker of dysregulated HPA activity, which has been associated with reduced physiological capacity to adapt to stress (Fries et al. 2005; Heim et al. 2008). Chronically low/blunted HPA activity has also been associated with chronic experiences of stress, trauma, and early adversity (Khoury et al. 2019). Given the role of cortisol in regulating arousal and cognition, lower cortisol during pregnancy may increase vulnerability to postpartum stressors, thereby increasing an individual's risk for experiencing postpartum mental health problems (Juster et al. 2010). Alternatively, lower cortisol levels observed in the current study may reflect a deviation from the typical pregnancy‐related increase in cortisol, rather than chronically low basal HPA activity. Cortisol levels are expected to rise substantially across gestation, particularly in the third trimester, and failure to exhibit this adaptive increase may represent a distinct form of HPA axis dysregulation during pregnancy. This deviation from expected late‐pregnancy cortisol levels may reflect reduced HPA axis adaptation, potentially increasing vulnerability to postpartum mental health difficulties. Future longitudinal research beginning prior to pregnancy and spanning each trimester of pregnancy is needed to assess pregnancy‐related elevations in cortisol.

We also found that higher depressive symptoms, but not anxiety symptoms, in the early postpartum period (2 weeks postpartum) were associated with greater socioemotional problems in infants at 6 months of age, as reported by mothers. These results align with prior work highlighting postpartum depression, compared to anxiety, as a more consistent predictor of infant socioemotional outcomes, and may reflect more variable effects of postpartum anxiety on childhood socioemotional development (Madigan et al. 2018). By distinguishing between depressive and anxiety symptomatology and testing separate indirect pathways for both, rather than relying solely on direct associations, the current study aimed to clarify whether previously observed mixed findings may, in part, reflect untested mediation processes or differences in how postpartum mental health has been operationalized in prior research. The effect of depression, but not anxiety, on socioemotional outcomes may be due to the particular impact of depression on disrupting parent–child bonding and caregiving quality (Bödeker et al. 2019; Hakanen et al. 2019; Schmitt et al. 2025).

Although pregnancy cortisol levels play an important role in prenatal developmental processes, we did not find evidence of a direct association between pregnancy HCC and infant socioemotional outcomes in this sample. One potential explanation is placental regulation of fetal glucocorticoid exposure via 11β‐HSD2, which may buffer the fetus from variations in maternal cortisol. However, this interpretation is less straightforward in the context of the observed indirect effect, which involved lower, rather than elevated, maternal hair cortisol. An alternative explanation for the nonsignificant direct effect is that a single measurement of maternal hair cortisol may not adequately capture the dynamic nature of HPA axis activity across pregnancy. It is possible that cortisol levels at other gestational periods may show stronger or more direct associations with infant socioemotional outcomes. Repeated assessments of maternal cortisol across pregnancy will be important in future work to more precisely characterize the timing and nature of these associations.

Despite this nonsignificant direct effect, we found that lower pregnancy hair cortisol levels were indirectly associated with greater socioemotional problems through a higher frequency of postpartum depressive symptoms. This highlights lower cortisol in pregnancy as a potential prenatal biomarker for both maternal postpartum depressive symptoms and infant socioemotional challenges. With a paucity of evidence in this area, our study demonstrated that postpartum mental health problems can act as a mechanism explaining the association between gestational cortisol levels and infant socioemotional development.

4.1. Clinical Implications

These findings align with recent North American clinical practice guidelines that emphasize the importance of early screening for perinatal mental health issues (Avalos et al. 2019; Vigod et al. 2025). Our findings underscore the need to monitor physiological stress during pregnancy, as well as mental health problems, in the very early postpartum period, as both of these factors have implications for early infant development. Providing tailored support for postpartum mental health is critical for promoting parental well‐being and childhood development. Importantly, the perinatal period is a key time when maternal depression can be addressed, presenting a valuable opportunity to reduce the risk of socioemotional difficulties in children.

Although measuring socioemotional development at 6 months with the ASQ is limited to detecting relatively pronounced difficulties in early development, our results suggest that maternal cortisol during late pregnancy and depressive symptoms during the early postpartum period may already be associated with early socioemotional difficulties in infants. Such early patterns can influence later cognitive, emotional, and social development (Briggs‐Gowan et al. 2006; Golm and Brandt 2024; Troxel et al. 2013), potentially through their effects on parent–infant interactions and co‐regulation (Bailes et al. 2024; Bailes and Leerkes 2023). Ongoing monitoring of infant socioemotional development can help detect emerging difficulties early, allowing timely support and intervention. Timely support for maternal mental health may therefore promote both maternal well‐being and optimal early infant development, highlighting the perinatal period as a critical window for intervention.

4.2. Strengths, Limitations, and Future Directions

This study has several strengths, including the longitudinal design spanning pregnancy, 2 weeks postpartum, and 6 months postpartum. In addition, the multimethod design enabled the assessment of HPA functioning through hair cortisol as well as questionnaires to measure depressive and anxiety symptoms and infant socioemotional development. Although the hypotheses were guided by theory and prior research, the correlational design  limitour ability to draw conclusions about causal associations between variables. Hair cortisol was assessed at a single time point during pregnancy; however, given that the 3‐cm hair segment reflects approximately 3 months of cortisol accumulation, this measure captured HPA activity spanning both the late second and early third trimester. As such, we were unable to isolate trimester‐specific effects, which may contribute to inconsistencies between the present findings and prior research specific to the third trimester. Future work would benefit from repeated sampling across pregnancy. Pregnant individuals reported both mental health problems and infant socioemotional problems, potentially introducing shared method variance. Although analyses adjusted for concurrent maternal depressive and anxiety symptoms at 6 months postpartum, residual bias associated with maternal reports cannot be ruled out. Future research would benefit from incorporating multiple informants (e.g., another caregiver) and/or observational assessments of infant socioemotional functioning. Further, the sample was relatively low risk in terms of sociodemographic characteristics (e.g., education, income), and therefore, the results may not generalize to more diverse populations. In addition, the sample size is relatively small. Additional multimethod longitudinal studies with larger, more diverse samples are needed to further our understanding of the relationship between maternal cortisol during pregnancy and perinatal mental health problems and early childhood socioemotional development. Such research may further explain the role of cortisol in the different trimesters of pregnancy and into the extended postpartum period. Future research should also explore protective factors (e.g., social support, resilience) that may mediate the effects of pregnancy cortisol and postpartum mental health problems on early childhood socioemotional functioning.

5. Conclusion

This study provides novel findings that lower hair cortisol during the second half of pregnancy may elevate the risk for postpartum depressive symptoms, which in turn are associated with more infant socioemotional problems. Although pregnancy cortisol was not directly associated with infant outcomes, its indirect effect via maternal depressive symptoms highlights the importance of both perinatal biological stress and mental health as risk factors for infant development. These findings underscore the need for early identification and support for maternal stress and mental health to promote optimal childhood socioemotional development.

Funding

This work was funded by a Research Nova Scotia New Health Investigator Grant (RNS‐NHIG‐2022‐2024​, Khoury PI). This work was supported by a Tier II Canadian Research Chair (CRC) in Interdisciplinary Studies in Neurosciences awarded to Dr. Jennifer Khoury. This work was also supported by a Canadian Institutes of Health Research (CIHR) Canada Graduate Scholarship—Doctoral (CGS‐D) awarded to Lauren Giles and a Nova Scotia Graduate Scholarship awarded to Lauren Giles and Mackenna Pattison.

Ethics Statement

This study was approved by the Mount Saint Vincent University Research Ethics Board (2021‐244).

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Supplementary materials: dev70180‐supp‐0001‐SuppMat.docx

DEV-68-e70180-s001.docx (37.3KB, docx)

Acknowledgments

We would like to thank the pregnant and postpartum individuals who contributed their time to this research. We would also like to thank the research assistants and staff who contributed to this research.

Footnotes

1

There was an error in cutting 6 hair samples, such that these samples ranged in length from 3.9 to 4.5cm. See results for sensitivity analysis.

Data Availability Statement

The data presented in this manuscript are available upon reasonable request to the corresponding author.

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