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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: J Clin Child Adolesc Psychol. 2019 Jun 20;50(1):105–117. doi: 10.1080/15374416.2019.1622122

Infant vagal tone and maternal depressive symptoms: A bottom-up perspective

Jennifer A Somers 1, Sarah G Curci 1, Linda J Luecken 1
PMCID: PMC6923632  NIHMSID: NIHMS1530323  PMID: 31219700

Abstract

Objective:

Children vary in their susceptibility to environmental exposures such as maternal depression (Blandon et al., 2008; Somers et al., 2018b; Yan, Benner, Tucker-Drob, & Harden, 2017), but little is known about how children shape those same environments. When raising an infant with low arousal, mothers at risk of depression may experience decreased parenting self-efficacy and increased depressive symptoms. We evaluated a longitudinal mediated moderation model that hypothesized interactive effects of infant vagal tone (indexed by respiratory sinus arrhythmia, RSA) and maternal postpartum depressive (PPD) symptoms on maternal depressive symptoms in early childhood, via parenting self-efficacy.

Method:

Among a sample of 322 very low-income Mexican-American mother-infant dyads (46% male infants), infant RSA was assessed at six weeks of age; mothers (Mage = 27.8, SD = 6.5) reported PPD symptoms every three weeks from six weeks to six months, parenting self-efficacy at 18 and 24 months, and depressive symptoms at 18 and 36 months.

Results:

Higher PPD symptoms predicted higher maternal depressive symptoms at 36 months especially among mothers whose infants had lower resting RSA. The interactive effect of PPD symptoms and infant RSA on 36 month depressive symptoms was partially mediated by lower parenting self-efficacy.

Conclusions:

Lower infant RSA may exacerbate the detrimental effects of PPD symptoms on subsequent maternal well-being, via damage to mothers’ beliefs in their ability to parent effectively.

Keywords: maternal depression, vagal tone, parenting self-efficacy

The early childhood years are demanding, and as many as one in three women caring for young children experience depression (McLennan, Kotelchuck, & Cho, 2001). The sequelae of maternal depression can be detrimental to both mother and the developing child. Mothers with high levels of depressive symptoms are typically less able to foster an environment that nurtures children’s developing emotion regulation abilities (Ashman & Dawson, 2002; Goodman & Tully, 2006; Harnish et al., 1995; Moehler et al., 2006; Weinberg et al., 2001). Both clinical and subclinical levels of depressive symptoms are associated with impaired maternal functioning, including lower maternal sensitivity (Cummings, Keller, & Davies, 2005; Goodman & Gotlib, 2002; Musser, Ablow, & Measelle, 2012; Weinberg et al., 2011). A recent meta-analysis concluded that maternal depressive symptoms (assessed as either clinical diagnosis or self-report depressive symptom rating) adversely impact children’s positive and negative affective functioning, and increases the risk of internalizing and externalizing behavior problems and general psychopathology (Goodman et al., 2011).

Though maternal and child mental health are intimately related, research on this potentially reciprocal relationship typically focuses on the effects of maternal mental health on child development (Gross, Shaw, Burwell, & Nagin, 2009). For example, differential susceptibility theories suggest that some children are more likely to flourish in supportive caregiving environments, but display the poorest psychological adjustment in adverse environments. The literature has documented evidence of susceptibility to myriad environmental exposures, including maternal depression (Blandon et al., 2008; Somers et al., 2018b; Yan et al., 2017), but little attention has been paid to whether (and if so, how) susceptible children shape their environments. In contrast to the “top-down” view of how mothers influence their children, the current study takes a “bottom-up” view by considering the fundamental role of the newborn baby in maternal psychological adaptation.

One well-known risk factor for mothers’ depressive symptoms during early childhood is the experience of postpartum depressive (PPD) symptoms, which have significant potential to negatively impact women for years following childbirth (Philipps & O’Hara, 1991). For approximately one-third to one-half of women, PPD can lead to a chronic or recurring depressive disorder throughout a woman’s life (e.g., Cooper & Murray, 1995; Goodman, 2004; Vliegen et al., 2014). Even women with elevated, but subclinical, levels of depressive symptoms in the postpartum period are at risk for developing a depressive disorder later in life (Kessler et al., 2003). On the other hand, there is considerable variability in the course of depression (Goodman & Gotlib, 1999) and for some women depressive symptoms will remit after the postpartum period (Vliegen et al., 2014), warranting examination of factors that modify and explain the course of depressive symptoms from the postpartum period to later childhood years. In addition to tending to their own well-being, postpartum women are influenced by, and need to adapt to, the unique characteristics of their infants. For women experiencing PPD symptoms, a difficult parenting experience may challenge their capacity to adapt. For example, women with infants high in negative affectivity are at risk of increased PPD symptoms (Britton, 2011; Luecken et al., 2015). However, these studies are limited by maternal report of both their infant’s temperament and their own affective well-being.

Infant vagal tone, which refers to the state of parasympathetically-mediated influence of the vagus nerve on cardiac output (Porges, 2007), is thought to promote flexibility and adaptability in the social environment (Beauchaine, 2001; Porges, 2007). Infants with lower resting respiratory sinus arrhythmia (RSA), an index of vagal tone, have been shown to demonstrate more negativity and behavioral reactivity (Huffman et al., 1998; Porter, Porges, & Marshall, 1988). We recently reported that lower infant RSA confers infant susceptibility to maternal social support and PPD symptoms, for better and for worse (Somers et al., 2018a; Somers et al., 2018b). For example, lower RSA infants whose mothers endorsed higher maternal PPD symptoms exhibited the most behavior problems, but lower RSA infants whose mothers endorsed fewer PPD symptoms exhibited the fewest behavior problems at 36 months child age (Somers et al., 2018b). The current paper proposes that infant RSA may also represent an objective measure of an infant characteristic that can challenge maternal adaptation, especially among mothers who experienced elevated PPD symptoms.

One mechanism by which the joint contributions of maternal PPD symptoms and infant RSA may affect later maternal depression is through maternal parenting self-efficacy. Maternal parenting self-efficacy is broadly defined as mothers’ beliefs about their ability to effectively parent their children in ways that promote healthy development. In general, higher maternal stress and depressive symptoms are linked with lower maternal parenting self-efficacy (Fox & Gelfand, 1994; Gross, Conrad, Fogg, & Wothke, 1994; Porter & Hsu, 2003). Higher maternal distress in the postpartum period, specifically, predicts lower parenting self-efficacy (Leahy-Warren, McCarthy, & Corcoran, 2011). Feeling ineffective as a parent may correspondingly increase a mother’s feelings of depression (Gross et al., 1994; Hudson, Elek, & Fleck, 2001; Weaver, Shaw, Dishion, & Wilson, 2008). In general, higher maternal parenting self-efficacy is consistently associated with higher quality parenting behaviors (e.g., warmth, consistent discipline, positive parenting) and more adaptive child outcomes in infancy through adolescence (Coleman & Karraker, 2003; Jones & Prinz, 2005). In a study of mothers of infants, maternal parenting self-efficacy explained the impact of maternal depression on competent parenting behaviors (Teti & Gelfand, 1991), implicating the importance of further understanding the complex interplay between maternal parenting self-efficacy and maternal and child well-being.

Maternal parenting self-efficacy is not only affected by maternal characteristics, but also by child characteristics. Several studies have generated support for the hypothesis that mothers of temperamentally difficult children feel less efficacious relative to those with “easier” children (Cutrona & Troutman, 1986; Gross et al., 1994; Porter & Hsu, 2003). In a cross-sectional study of predominantly middle-class, Caucasian, primiparous mothers and their 5-month-old infants, infant soothability positively predicted maternal self-efficacy, even after accounting for maternal parenting history and global self-esteem, highlighting the influence of infant temperamental characteristics on maternal self-efficacy (Leerkes & Crockenberg, 2002). Similarly, a recent study demonstrated that mothers of infants with high negative emotionality reported less efficacy at eight weeks postpartum than mothers of non-irritable infants (Troutman, Moran, Arndt, Johnson, & Chmielewski, 2012). Existing studies primarily focus on parenting self-efficacy in the postpartum period, and there are few longitudinal studies of parenting self-efficacy in the preschool years (Sevigny & Loutzenhiser, 2010). Further, previous work often relies on maternal report of infant temperament. Although temperamental traits are thought to be biologically-based, little is known about the effects of objective, biological measures of infant characteristics on maternal self-efficacy.

The extent to which child characteristics influence maternal self-efficacy may depend on maternal characteristics, including maternal mental health. Mothers with elevated PPD symptoms may find it difficult to cope with an infant who is less reactive, and may be more likely to negatively attribute these infant characteristics to their own parenting capability. Women with elevated depressive symptoms are more likely to view their child as difficult or challenging (Luecken et al., 2015), which may further threaten parenting self-efficacy (Jones & Prinz, 2005; Leahy-Warren et al., 2011), and in turn, increase risk for future depressive symptoms (Gross et al., 1994). On the other hand, mothers who are not struggling with PPD symptoms may be able to reap the benefits of having a less reactive baby, which may promote feelings of self-efficacy and buffer against future depressive symptoms.

Despite assertions that self-efficacy theories are broadly applicable across cultures (Bandura, 2002), cultural values may influence women’s parenting self-efficacy beliefs or exacerbate the affective consequences of low self-efficacy. Women from low-income and ethnic minority backgrounds, including Mexican-American mothers, are disproportionately affected by PPD symptoms and are at elevated risk for depression or dysthymia across the lifespan (Chaudron et al., 2005; Kuo et al., 2004; Riolo, Nguyen, Greden, & King, 2005). Most research on maternal parenting self-efficacy is based on predominantly Caucasian, well-educated samples (Leahy-Warren et al., 2011), raising questions about factors that impact parenting self-efficacy and its consequences among low-income, ethnic minority mothers. Within Latino culture, the value of familismo emphasizes the importance of placing children and family members above one’s own needs (Castillo & Cano, 2007). Embedded in familismo and specific to Latina women, marianismo encompasses female gender role expectations that place a primary focus on motherhood and caring for her family. Implicit in these values is the expectation that women will be good mothers, placing the needs of their children above their own. Thus, feelings of low parenting self-efficacy may be especially detrimental to Latina women’s mental health.

Current Study

In a sample of very low-income Mexican-American women, we evaluated joint maternal and child contributions to maternal depressive symptoms during early childhood. The study builds on existing research by employing a longitudinal design with an objective biological measure of a child-level factor (infant RSA) that may influence the relation between PPD symptoms and subsequent maternal depressive symptoms. We evaluated a mediational pathway via parenting self-efficacy to explain how maternal PPD symptoms and infant RSA interactively influence maternal depressive symptoms three years later. Relative to mothers of infants with higher resting RSA, we predicted that mothers of infants with lower resting RSA would exhibit more depressive symptoms at 36 months if they also experienced elevated PPD symptoms. We further expected that mothers with elevated PPD symptoms and infants with low resting RSA would report lower parenting self-efficacy, and in turn, that parenting self-efficacy would mediate the effects of infant RSA and maternal PPD symptoms on maternal depressive symptoms when their children were three years old.

Methods

Participants

The sample included 322 mother-child dyads who participated in a broader examination of postpartum adjustment among very low-income, Mexican-origin women, Las Madres Nuevas. Maternal eligibility criteria was assessed at a prenatal visit and included: 1) self-identification as Mexican or Mexican American, 2) fluency in English or Spanish, 3) 18 years of age or older, 4) low-income status (family income below $25,000 or eligibility for Medicaid or Federal Emergency Services coverage for childbirth), and 5) anticipated delivery of a singleton baby with no significant health or developmental problems. The Arizona State University Institutional Review Board (IRB) and the Maricopa Integrated Health System IRB approved all study procedures prior to recruitment or data collection. All measures were refined for local cultural adaptation, translated to Spanish, back-translated to English and recentered, and locally tested to ensure cultural sensitivity and fit for the sample (Behling & Law, 2000).

Women were between 18 and 42 years of age when they entered the study (mean 27.8 years, SD = 6.5). Most women (86.3%) who participated in the study were born in Mexico. On average, women had moved to the United States 17 years prior to study entry (ranging from less than a year to 35 years ago). At study entry, women were asked to select from a range of household income categories to describe their household income; the modal family income was $10,001 - $15,000. The average household size of four. Approximately 77.3% of women were married or living with a partner. Women varied in the number of biological children they had at study entry (i.e., prior to the birth of the target child for the study); 22% of the sample had no other biological children (i.e., were first-time mothers), 23 percent had one other child, 19 percent had two other children, 18 percent had three other children, 8 percent had four other children, 7 percent had five other children, and less than 3 percent had six or more other children The women who participated gave birth to 149 (46.3%) boys and 173 (53.7%) girls.

Recruitment

During a prenatal care visit, women were recruited from hospital-based prenatal clinics that serve low-income women. A bilingual female interviewer initially approached women and obtained permission to make a prenatal home visit (26–39 weeks gestation), during which informed consent was obtained. Data for the present analyses come from a survey administered during the prenatal home visit, depressive symptom inventories completed with women every three weeks, from six weeks to six months postpartum, and university-based laboratory visits completed when children were 18, 24, and 36 months of age.

To reduce participant burden, a “planned missing” design (Enders, 2010) was employed during the postpartum home visits. Participants were randomly assigned to miss either the 12-, 18-, or 24-week postpartum visit, which produces data missing completely at random (MCAR) and does not introduce bias into parameter estimates (Enders, 2010). Data were corrected for planned missingness using Full Information Maximum Likelihood (FIML; Allison, 2003).

Participant attrition.

Of the 322 women who met inclusion criteria and consented to participate in the study during the initial prenatal home visit, 312 (97%) completed the 6-week assessment, 307 (95%) completed the 9-week assessment, 203 (99% of expected completers based on planned missingness design) completed the 12-week assessment, 302 (94%) completed the 15-week assessment, 209 (96% of expected completers) completed the 18-week assessment, 299 (94%) completed the 21-week assessment, and 209 (93% of expected completers) completed the 24-week assessment. 237 dyads (73.6%) completed the 18-month lab visit, 243 dyads (75.5%) completed the 24-month lab visit, and 215 dyads (61.7%) completed the 36-month laboratory visit.

Analyses of missing data.

Missingness on infant 6-week RSA data was not related to maternal age, maternal country of origin, parity, birth outcomes, child sex, postpartum depressive symptoms, 18- or 24-month self-efficacy, or 36-month maternal depressive symptoms (all p’s > .05). Attrition at 18-, 24-, and 36-months was not related to parity, birth outcomes, child sex, PPD symptoms, or infant RSA (all p’s > .05). Mothers born in the United States were more likely to have missing data at 18-, 24-month, and 36-month lab visits, p’s ≤ .001. Younger mothers were more likely to have missing data at these visits, p’s < .05. Therefore, maternal age and country of birth were included as covariates in statistical models.

Procedures

Interviews at the prenatal visit and at 6-, 12-, 18-, and 24-weeks postpartum were conducted in participants’ homes. The 9-week, 15-week, and 21-week assessments were conducted over the telephone. Approximately eighty percent of interviews were conducted in Spanish. Given the varying degrees of literacy in the sample, a bilingual interviewer read survey questions aloud to all participants, and participants were given visual aids with written and graphic depictions of item response formats. Women were compensated $75 for the prenatal interview and $50 and small gifts for the child (e.g., bibs, rattles) were provided for the 6-, 12-, 18-, and 24-week home-based interviews. Women were compensated $10 for each telephone assessment they completed. The 18-, 24-, and 36-month visits were conducted in the laboratory. Women were compensated $100 for their time during each of the laboratory visits. Transportation to the laboratory was provided or women were reimbursed $50 for their travel costs.

Measures

Resting RSA.

At the 6-week home visit, infants were seated upright in a car seat at rest and a research assistant placed electrodes on the infants’ left shoulder and right and left waist in a standard lead configuration. Heart rate data were recorded at 256 Hz with electrocardiography (ECG) equipment from Forest Medical, LLC (Trillium 5000; East Syracuse, NY, USA) during a seven-minute resting period. QRSTool software 1.2.2 (Allen, Chambers, & Towers, 2007) was used to process the data and automatically obtain R-spikes from the ECG data. Coders then used the QRSTool software to manually correct misidentified or unidentified R-spikes, and obtain R-R interval data. Using CardioBatch software (Brain-Body Center, 2007), a moving polynomial filter was applied to the R-R interval data to extract heart rate variability in the frequency band of RSA (for infants, 0.3–1.3 Hz; Brain-Body Center, 2007). The RSA estimates were log-transformed, and a mean resting RSA value averaged from 30-second epochs during the first five minutes of the resting period was obtained. RSA data was unusable for 16.5% of the infants. Although measures of resting RSA are stable markers of individual differences in vagal functioning from infancy to childhood (Alkon et al., 2011; Bornstein & Suess, 2000; Weiner & McGrath, 2017), we assessed infant RSA at 6 weeks given the possibility that maternal depressive symptoms may influence infant vagal tone (Hinnant, Erath, & El-Sheikh, 2015). Maternal resting RSA was also obtained at the 6-week visit with the same procedures as described above.

Maternal postpartum depressive symptoms.

The 10-item Edinburgh Postnatal Depression Scale (EPDS; Cox, Holden, & Sagovsky, 1987) was administered every three weeks from six weeks to six months. Women responded using a scale from 0 to 3; item scores are summed and higher scores correspond to more severe depressive symptoms. The EPDS has been validated in English and Spanish (Garcia-Esteve, Ascaso, Ojuel, & Navarro, 2003); Cronbach’s α ranged from .82 to .85. Clinically significant symptoms are indicated by total scores of 13 or more (Cox, Holden, & Sagovsky, 1987). Eighty percent of the sample did not endorse clinically significant symptoms at any measurement time point, 10 percent endorsed clinically significant symptoms at one postpartum visit, and 10 percent endorsed clinically significant symptoms at more than one postpartum visit.

An error in the response set rendered two of the ten items on the EPDS unusable for 82 participants at the 6-week time point, 50 participants at 12-weeks, 42 participants at 18-weeks and 43 participants at 24-weeks. For these participants, item-level multiple imputation (Mplus 7; Muthén & Muthén, 2012) was used to impute the missing values which were then used to calculate a full scale score. The imputation variables included parity, survey administration language, the two depression items, and parcels created by averaging the remaining eight EPDS items. Using data on depressive symptoms from six weeks to six months, total depressive symptoms across the postpartum period were calculated as area under the curve with respect to ground (AUCg). AUCg offers advantages over other summary measures (e.g., average or sum) in that it reflects the overall magnitude of depressive symptoms over multiple time points during a specified period (Pruessner, Kirschbaum, Meinlschmid, & Hellhammer, 2003). One potential outlier (+3 SD from the mean) on maternal postpartum depressive symptoms was identified; the pattern of results was not changed when this case was excluded, therefore the final analyses include all participants.

Maternal parenting self-efficacy at 18 and 24 months.

Maternal parenting self-efficacy was assessed using the 17-item Parenting Sense of Competence Scale, which yields measures of parenting satisfaction, efficacy, and interest (PSOC; Johnston & Mash, 1989). One item (“Being a good mother/father is a reward in itself”) was not asked due to prior work demonstrating that this item did not load on any factor (Gilmore & Cuskelly, 2009). Example parenting self-efficacy items include: “I would make a fine model for a new mother/father to follow in order to learn what she/he would need to know in order to be a good parent,” “I meet my own personal expectations for expertise in caring for my child,” and “If anyone can find the answer to what is troubling my child, I am the one.” Mothers indicate their agreement with each item on a scale of 1 to 6, with higher scores indicating higher self-efficacy. Internal consistency of the efficacy subscale was good (Cronbach’s α =.71 at 18 months; α =.78 at 24 months).

Maternal depressive symptoms at 18 and 36 months.

The Center for Epidemiologic Studies Depression scale (CES-D; Radloff, 1977) was administered to assess mothers’ depressive symptoms when their children were 18 and 36 months of age (18-month Cronbach’s α = .90; 36-month Cronbach’s α = .89). Items are rated on a scale from 0–4, with higher scores indicating greater frequency of depressive symptoms. The CES-D has been validated in Spanish among Mexican Americans (Roberts, Vernon, & Rhoades, 1989). Clinically significant symptoms are indicated by total scores of 16 or more (Radloff, 1977). Twenty-three percent of the sample endorsed clinically significant depressive symptoms at 18 months and 13 percent of the sample endorsed clinically significant depressive symptoms at 36 months.

Maternal prenatal parenting self-efficacy.

At the prenatal visit, maternal expectations of parenting self-efficacy were assessed based on two items. One item was taken from the Prenatal Expectations Scale for Mexican Americans (PES-MA; Gress-Smith et al, 2013), which asked, “You will know how to comfort your baby quickly when he or she cries.” Women rated this item on a scale of 1 (“not at all”) to 5 (“completely”). The second item, developed for this study, asked women to rate how “prepared they felt to take care for baby” on a scale of 1 (“not prepared”) to 5 (“a lot/very much”). Responses to the two items were positively correlated, r = .309, p < .001. The two items were standardized and aggregated; higher scores indicate higher expected parenting self-efficacy.

Potential covariates.

Child gender and birth outcomes (gestational age; birthweight; 1-minute APGAR [Appearance, Pulse, Grimace, Activity, and Respiration] score, an index of overall newborn health (Apgar, 1953); birth complications) were obtained through medical record review. Number of biological children, mother’s country of origin, maternal age, and maternal relationship status were obtained from mother’s report at the prenatal visit.

Data Analysis

Primary analyses tested mediated moderation models of the interaction effect of mother’s PPD symptoms and infant RSA on mother’s depressive symptoms at 36 months, mediated by mother’s parenting self-efficacy at 18 and 24 months. First, we evaluated a model predicting maternal depressive symptoms at 36 months from the primary predictors (Model 1), followed by a more complex model that includes mediators and covariates (Model 2). Maternal age and country of origin were included as covariates in this model. Given the possibility that poor parenting self-efficacy could reflect a continuation of low prenatal self-efficacy, which would not be influenced by child contributions, our analyses also adjusted for maternal prenatal expected parenting self-efficacy. In addition, to adjust for possible shared genetic contributions between mother and child resting RSA, statistical models adjusted for maternal resting RSA. Finally, considering the conceptual overlap between low self-efficacy and cognitive vulnerability for depression (e.g., negative attributions about the self, hopelessness), we adjusted for depressive symptoms at 18 months to account for the overlap between concurrent parenting self-efficacy and depressive symptoms as well as to control for the stability of maternal depressive symptoms. By including 18-month depressive symptoms in the prediction of 36-month depressive symptoms, the outcome in this model can be interpreted as change in depressive symptoms from 18 to 36 months.

We evaluated the proposed mediation model with the joint significance test (MacKinnon, Lockwood, Hoffman, West, & Sheets, 2002). Several different tests have been developed to evaluate single-mediator models, yet less attention has been paid to multiple-mediator models, such as the model proposed in the present study (Taylor, MacKinnon, & Tein, 2008). The joint significance test is a recommended causal steps approach for evaluating multiple-mediator or long-chain mediation models as it has the best balance of statistical power and control for type I error (Taylor et al., 2008; MacKinnon et al., 2002). According to the joint significance test, there is evidence in support of mediation if each of the individual paths in the mediated effect is statistically significant (MacKinnon et al., 2002).

Results

Preliminary Analysis

Descriptive statistics.

Table 1 presents descriptive statistics and zero-order correlations for the primary study variables. Maternal depressive symptoms at 36 months were correlated with infant RSA at 6 weeks, r = −.177, p = .022, maternal depressive symptoms from 6 weeks to 6 months postpartum (AUCg), r = .349, p ≤ .001, maternal depressive symptoms at 18 months, r = .418, p ≤ .001, and maternal parenting self-efficacy at 18 months, r = −.171, p = .017.

Table 1.

Descriptive statistics and zero-order correlations among primary study variables

Mean SD 1 2 3 4 5 6 7
1. Maternal prenatal parenting self-efficacy −.00 1.62 ---
2. Infant RSA at 6 weeks 2.52 0.96 .023 ---
3. Maternal RSA at 6 weeks 6.31 1.32 .052 .121 ---
4. Maternal depressive symptoms from 6 weeks to 6 months (AUCg) 21.95 20.98 −.159 .041 −.045 ---
5. Maternal depressive symptoms at 18 months 9.91 9.16 −.083 −.008 −.011 .494 ---
6. Maternal parenting self-efficacy at 18 months 35.21 4.46 .381 .001 −.029 −.261 −.256 ---
7. Maternal parenting self-efficacy at 24 months 34.33 5.04 .345 .007 −.003 −.237 −.185 .454 ---
8. Maternal depressive symptoms at 36 months 7.79 8.11 −.152 −.177 .106 .349 .418 −.171 −.102
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Note. All ages refer to child age. Correlation coefficients presented in bold are statistically significant, p < .05.

Correlations between potential covariates (maternal country of origin, age, number of biological children, relationship status, and child gender) and primary study variables were evaluated. Of these potential covariates, only maternal age and country of origin were significantly correlated with primary study variables. Maternal age at prenatal visit was positively correlated with maternal postpartum depressive symptoms, r = .121, p = .030, and positively correlated with maternal parenting self-efficacy at 24 months, r = .148, p = .021. Infants whose mothers were born in the United States had higher RSA (M = 2.99, SD = 1.37) than those whose mothers were born in Mexico (M = 2.47, SD = 0.88; t(253) = 2.748, p = .006). Maternal age and country of origin were retained as covariates in the final statistical model.

Maternal RSA was included in the final statistical model to adjust for mother’s genetic influence on child RSA. Following recommendations for controlling for confounders in interaction studies (Keller, 2014), we evaluated models that also adjusted for the interaction effects between maternal RSA and maternal postpartum depressive symptoms, and interaction effects between maternal RSA and infant RSA. The direction and statistical significance of the parameter estimates were unchanged when these interaction terms were included in the model; therefore, in the interest of parsimony, we retained only maternal RSA in the model.

Primary Analyses.

Model 1: Base model predicting 36-month maternal depressive symptoms from primary predictors.

We ran an initial regression model predicting maternal depressive symptoms at 36 months from mother’s PPD symptoms, infant RSA, and their interaction. The interaction term was a significant predictor of 36-month maternal depressive symptoms, Est = −0.073, SE Est = 0.030, p = .015, ΔR2= .037. The overall model accounted for 20.1% of the variance in maternal depressive symptoms at 36 months (95% CI for R2: .124, .278).

Significant interaction effects were probed by testing the significance of the simple slopes of the regression of maternal depressive symptoms at 36 months on maternal postpartum depressive symptoms at average, low (−1 SD) and high (+1 SD) levels of infant RSA (Aiken & West, 2001). The simple slopes of maternal depressive symptoms at 36 months on maternal postpartum depressive symptoms were statistically significant for children with below average, Est = 0.215, SE Est = 0.044, p ≤ 0.001, average, Est = 0.145, SE Est = 0.026, p ≤ 0.001, and above average levels of RSA, Est = 0.075, SE Est = 0.033, p = .022; See Figure 2). Among mothers with higher PPD symptoms, mothers who had children with low RSA exhibited the most depressive symptoms at 36 months.

Figure 2.

Figure 2

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Effect of Postpartum Depressive Symptoms on Maternal Depressive Symptoms at 36 Months, by Infant RSA

Model 2: Full mediation model predicting 36-month maternal depressive symptoms, adjusted for covariates.

Next, a mediated moderation model was evaluated that predicted maternal depressive symptoms at 36 months from 6-week infant RSA, maternal PPD symptoms and their interaction; maternal parenting self-efficacy at 18 and 24 months; maternal depressive symptoms at 18 months; maternal RSA; and maternal prenatal parenting self-efficacy (see Figure 1). Complete results are shown in Table 2 and Figure 1.

Figure 1.

Figure 1

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Structural Equation Model Predicting Maternal Depressive Symptoms in Early Childhood

Note. RSA = Respiratory sinus arrhythmia. PPD - Postpartum depressive symptoms (AUCg). Mo = Months. Yrs = Years. Dashed lines mdicate non-significant paths; solid thin lines indicate significant direct paths; solid thick lines indicate significant indirect paths.

Table 2.

Model Predicting Parenting Self-Efficacy and Maternal Depressive Symptoms

DV IV Est SE Est p-value 95% CI
Maternal Depressive Symptoms at 36 Months .249, .413
Maternal parenting self-efficacy at 24 months −.173 .087 .046 −.345, −.003
Maternal parenting self-efficacy at 18 months −.055 .085 .518 −.220, .110
Infant RSA at 6 weeks −1.556 .608 .010 −2.772, −.399
Maternal postpartum depressive symptoms .064 .030 .030 .009, .124
Infant RSA x Maternal Postpartum Depressive Symptoms −.054 .026 .034 −.107, −.006
Maternal depressive symptoms at 18 months .237 .079 .003 .081, .387
Maternal prenatal parenting self-efficacy −.341 .307 .266 −.969, .226
Maternal RSA .666 .301 .027 .108, 1.280
Maternal parenting self-efficacy at 24 months .132, .286
Maternal parenting self-efficacy at 18 months .528 .077 .000 .362, .673
Infant RSA at 6 weeks .387 .597 .517 −.753, 1.560
Maternal postpartum depressive symptoms −.019 .028 .496 −.073, .035
Infant RSA x Maternal Postpartum Depressive Symptoms −.013 .028 .626 −.072, .039
Maternal depressive symptoms at 18 months −.019 .057 .741 −.137, .088
Maternal prenatal parenting self-efficacy .158 .263 .548 −.351, .702
Maternal RSA −.547 .380 .150 −1.214, .264
Maternal parenting self-efficacy at 18 months .238, .402
Infant RSA at 6 weeks .983 .764 .198 −0.530, 2.444
Maternal postpartum depressive symptoms −.049 .032 .130 −0.112, .014
Infant RSA x Maternal Postpartum Depressive Symptoms .071 .031 .023 .013, .140
Maternal depressive symptoms at 18 months −.310 .065 .000 −.444, −.191
Maternal prenatal parenting self-efficacy .071 .308 .818 −.560, .655
Maternal RSA .240 .441 .587 −.739, 1.066
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Note. *** p ≤ .001. 95% bootstrap confidence interval (CI), based on 5,000 bootstrap samples, presented in bold do not contain zero and are statistically significant.

R2 = .331, p < .001.

In support of the hypothesized mediational model, the interaction of infant RSA and maternal PPD symptoms was a statistically significant predictor of maternal parenting self-efficacy at 18 months, maternal parenting self-efficacy at 18 months predicted parenting self-efficacy at 24 months, and maternal parenting self-efficacy at 24 months predicted maternal depressive symptoms at 36 months. Because each of the three paths in the mediated effect (i.e., from the interaction effect to 18-month parenting self-efficacy to 24-month parenting self-efficacy to 36-month depressive symptoms) is significantly nonzero (i.e., p-value < .05 and 95% bootstrap confidence interval did not include zero), there is evidence for mediation (see Figure 1). Maternal depressive symptoms at 18 months, maternal PPD symptoms, infant RSA, and maternal RSA were also statistically significant predictors of maternal depressive symptoms at 36 months.

We probed significant interaction effects of maternal PPD symptoms and infant RSA on parenting self-efficacy at 18 months by testing the significance of the simple slopes at average, low (−1 SD) and high (+1 SD) levels of infant RSA (Aiken & West, 2001). The simple slope of maternal parenting self-efficacy at 18 months on maternal PPD symptoms was only statistically significant for children with low RSA, Est = −0.117, SE Est = 0.046, p = .011. The simple slope of maternal parenting self-efficacy at 18 months on maternal PPD symptoms was not statistically significant for children with average, Est = −0.048, SE Est = 0.032, p = .131, or above average RSA, Est = 0.020, SE Est = 0.042, p = .624. As shown in Figure 3, among mothers with higher PPD symptoms, those mothers who had children with low RSA exhibited the least parenting self-efficacy at 18 months whereas mothers whose children had high RSA exhibited the most parenting self-efficacy at 18 months, after accounting for prenatal parenting self-efficacy.

Figure 3.

Figure 3

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Effect of Postpartum Depressive Symptoms on Maternal Parenting Self-Efficacy at 18 Months, by Infant RSA

Discussion

Mothers often experience elevated depressive symptoms during their children’s early years (e.g., McLennan, Kotelchuck, & Cho, 2001). Mothers living in poverty and Mexican-American mothers are at particularly elevated risk for depression or dysthymia (Kahn et al., 2000; Riolo et al., 2005), which bear risk for both maternal and child functioning. Mothers with high levels of depressive symptoms are typically less sensitive in their interactions with their children (Cummings, Keller, & Davies, 2005; Goodman & Gotlib, 2002; Musser, Ablow, & Measelle, 2012; Weinberg et al., 2011).and less able to foster an environment that nurtures children’s developing emotion regulation abilities (Ashman & Dawson, 2002; Goodman & Tully, 2006; Harnish et al., 1995; Moehler et al., 2006; Weinberg et al., 2001).. Among children from low-SES families, those who receive little parental support and warmth may be at even greater risk for problems later in life (e.g., Miller & Chen, 2013). Although it is commonly accepted that bidirectional influences exist between caregivers and their children, theoretical and empirical work typically focus on the impact of maternal depressive symptoms on infants’ development, with little attention to infant characteristics that can substantially influence caregiver affective adjustment. We tested the novel prediction that infant biological characteristics may contribute to variability in maternal well-being in early childhood, especially among mothers who experienced elevated PPD symptoms. We hypothesized that mothers with higher PPD symptoms whose children had low vagal tone in infancy would exhibit the most depressive symptoms when their children were three years old, and that this effect would be partially accounted for by mothers’ lower parenting self-efficacy over time. Results from our analyses provided strong support for the hypothesized mediational path, even after adjusting for potential covariates and confounds including prenatal expected parenting self-efficacy and maternal RSA.

Consistent with our hypotheses, mothers with higher PPD symptoms whose infants had lower RSA reported the lowest parenting self-efficacy and the highest subsequent depressive symptoms. Although the literature is mixed, evidence supports theoretical claims that higher RSA supports the capacity to actively engage in the environment (Beauchaine, 2001). Infants with lower RSA may have a reduced capacity for arousal and regulation, and thus may require relatively more attention, stimulation, and support from their mothers (Mateus et al., 2018), which may be especially difficult for women suffering from PPD symptoms. In our study, mothers with lower PPD symptoms whose infants had lower RSA reported the highest parenting self-efficacy. For mothers who have more psychological resources at their disposal to support infant regulatory needs, lower infant RSA may boost parenting self-efficacy and promote maternal well-being. However, mothers in our study with lower PPD symptoms whose infants had higher RSA reported the fewest subsequent depressive symptoms, which may reflect an affective boost from interacting with an active and engaged baby.

Our results also support the hypothesized mediational role of parenting self-efficacy at 18 and 24 months in accounting for the joint effects of maternal PPD symptoms and infant RSA on maternal depressive symptoms when children are three years old. Our investigation builds on existing knowledge of parenting self-efficacy predictors, and to our knowledge, is the first to evaluate joint maternal and child contributions to parenting self-efficacy. Parenting self-efficacy may be an especially salient mechanism in the prediction of maternal depression among low acculturated, Mexican-American women. Traditional Mexican values, such as marianismo and familismo, emphasize the importance of motherhood, specifically the self-sacrificial role of mothers within the family unit (Castillo & Cano, 2007; Connelly, Hazen, Baker-Ericzén, Landsverk, & Horwitz, 2013). Latina women may experience significant damage to parenting self-efficacy when unable to stimulate or regulate a child with low RSA, which in turn leads to psychological distress. More than half of depressed Latina mothers do not receive mental health services (Ertel, Rich-Edwards, & Koenen, 2011), and maternal parenting self-efficacy may be an especially important, modifiable target for prevention and intervention in a variety of health care settings.

Maternal parenting self-efficacy may be similarly pertinent to prevention and intervention of children’s mental health problems. Fostering parental competence is the foundation of many parenting-based child interventions, but a strengthened skillset may not predict more effective parent-child interactions without additional beliefs of parenting self-efficacy (Conrad, Gross, Fogg, & Ruchala, 1992; Reyno & McGrath, 2006). The importance of parenting self-efficacy in promoting healthy child development may be especially relevant among low-income populations, in which parents must navigate limited resources (Coleman & Karraker, 2003). Increased maternal parenting self-efficacy may simultaneously impact maternal and child well-being.

Maternal RSA at six weeks postpartum was also associated with maternal depressive symptoms when offspring were in early childhood. Whereas lower infant RSA was associated with higher maternal depressive symptoms at 36 months, an effect that was qualified by maternal postpartum depressive symptoms, lower maternal RSA at six weeks was directly associated with fewer maternal depressive symptoms. This finding is surprising given that lower resting RSA has been associated with a wide range of adult psychopathology, including depression (Beauchaine, 2001; Beauchaine & Thayer, 2015). Future research is necessary to replicate this finding, and to better understand the relation of RSA to depressive symptoms during the transition to parenthood and in this unique population.

The current study has a number of strengths. Among an underrepresented sample of low-income Mexican-American women with children, we evaluated a mechanistic model of the development of maternal depressive symptoms. Our model integrated two distinct research traditions by taking into account joint contributions of maternal and child factors to maternal well-being. As opposed to commonly used maternal-reports of infant characteristics, we evaluated infant RSA, an objective, biological marker. Infant RSA was measured at six weeks, prior to significant environmental influence. Our statistical model is strengthened by the inclusion of several a priori covariates. We adjusted for maternal RSA in the statistical model to account for shared genetic contributions to RSA (Sneider et al., 1997) and bolster our argument that child-level biological influences alter the effect of maternal PPD symptoms on subsequent parenting self-efficacy and, in turn, depressive symptoms. This claim is further strengthened by statistical adjustment for prenatal expected parenting self-efficacy to account for “trait” self-efficacy and aspects of parenting self-efficacy that could not be attributed to the child. The study benefited from longitudinal data collection that included repeated assessments of PPD symptoms, parenting self-efficacy, and subsequent depressive maternal symptoms, which allowed us to establish temporal precedence in our mediational model. Lastly, we adjusted for maternal depressive symptoms concurrent with 18-month parenting self-efficacy to account for the conceptual overlap between low self-efficacy and cognitive vulnerability for depression and to control for the stability of maternal depressive symptoms.

The results should be viewed in light of several limitations. Compared to rates of clinically significant PPD symptoms reported among low-income Hispanic women in prior research (e.g., Gress-Smith, Luecken, Lemery-Chalfant, & Howe, 2012), most women in this study endorsed relatively low levels of depressive symptoms: 20 percent of the sample endorsed clinically significant PPD symptoms during at least one of the seven points in the postpartum period. At any specific point in the postpartum period, less than 10 percent of the sample endorsed clinically significant PPD symptoms. Twenty-three percent of the sample at 18 months and 13 percent at 36 months endorsed clinically significant symptoms. Although these rates are comparable to observed rates of depression among parents living in poverty (Child Trends Databank, 2014), our results may not generalize to population samples pre-selected for high depression risk. Nevertheless, subclinical depressive symptoms pose substantial risk for impaired maternal functioning and child adjustment (Cummings, Keller, & Davies, 2005; Goodman & Gotlib, 2002; Musser, Ablow, & Measelle, 2012; Weinberg et al., 2011), warranting examination of factors that contribute to elevated depressive symptoms in broad community samples. Although multiple sources of data (biological and questionnaire) from multiple assessments were modeled, mothers reported on their depressive symptoms and parenting self-efficacy, which could overinflate associations between depressive symptoms and parenting self-efficacy. However, the interaction effect of mother-reported depressive symptoms and an infant biological measure on maternal parenting self-efficacy and depressive symptoms would be less affected by within-reporter biases, and the elapsed time between longitudinal measures further reduces concern. Finally, we evaluated the proposed model among low-income Mexican-American families, and our results may not generalize to women and children from different ethnic and socioeconomic backgrounds.

Future research could expand on the proposed model in several important ways. First, an important question concerns how low infant RSA influences the affective and behavioral experience of parenting. Understanding behavioral correlates of infant RSA may be one avenue for understanding the effects of infant RSA on attitudes and expectations about parenting as well as on specific parenting behaviors. Lower RSA may indicate child behavior problems, which may exacerbate parenting daily hassles and generate stressful life events, which in turn could weaken maternal parenting self-efficacy and exacerbate depressive symptoms, although behavioral correlates of infant RSA may show heterotypic continuity (Fox, 1989). Parents may also consciously or unconsciously sense their children’s physiological arousal and responsiveness to the environment, before those cues are manifested in children’s behavior. Second, although infant RSA is moderately stable (Alkon et al., 2011; Bornstein & Suess, 2000; Jewell, Suk, & Luecken, 2018; Weiner & McGrath, 2017), and was unrelated to maternal postpartum depressive symptoms among this sample, environmental exposures, including maternal depressive symptoms, may influence the development of children’s vagal functioning (Dierckx et al., 2009; El-Sheikh & Hinnant, 2011; Hinnant et al., 2015). Taken together, the literature points to the possibility of dynamic processes between maternal depressive symptoms and vagal tone that unfold over time. Elucidating dynamic and transactional processes between infant biological factors and maternal parenting experiences may enhance our understanding of maternal, child, and dyadic well-being. Finally, future research may want to consider heterogeneity within Mexican-American families, and build on existing research documenting the influence of cultural values, such as marianismo and familismo, as well as acculturative stress, on maternal depression (e.g., D’Anna-Hernandez, Aleman, & Flores, 2015). Maternal characteristics as well as aspects of her broader environment, such as social support, may contribute directly to maternal depression and may also buffer against or enhance risk for developing depressive symptoms associated with low infant vagal tone.

In sum, the present study provides support for a model of the interactive effects of maternal PPD symptoms and infant vagal tone on maternal depressive symptoms during early childhood, via parenting self-efficacy. This study advances the literature by addressing our limited understanding of how infant and maternal characteristics mutually influence maternal mental health. Our results suggest that low infant RSA can exacerbate the detrimental effects of higher maternal PPD symptoms on parenting self-efficacy and, in turn, increase the risk of subsequent depressive symptoms. Overall, the consideration of infant characteristics may help identify which mothers may be most resilient and which may be at greatest risk for elevated depressive symptoms during critical childrearing years.

Acknowledgments:

We thank the mothers and infants for their participation; Kirsten Letham, Monica Gutierrez, Elizabeth Nelson, and Jody Southworth-Brown for their assistance with data collection and management; Dr. Dean Coonrod and the Maricopa Integrated Health System for their assistance with recruitment; and the interviewers for their commitment and dedication to this project.

Funding information: The study was funded by the National Institute of Mental Health (R01 MH083173–01 and R01 MH083173–01A1S). The first author is also supported by a Graduate Research Fellowship from the National Science Foundation (Fellow ID: 2016228976).

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