A total of 171 infants (91% of the sample) were included in the final data analysis (95 males and 76 females; mean age of 180 ± 17 days). The remaining 18 infants were tested but excluded from the analyses secondary to the following reasons: 1) Saliva volume for three or more samples was insufficient for assay (n = 8); 2) The infant became too fussy to complete the protocol (n = 6); 3) Cortisol concentrations for three or more samples represented statistical outlier values (i.e., >3 SDs above the mean; n = 4). Infants excluded from the sample did not differ significantly from those included in terms of rates of either maternal depression (χ2(1,189) = 1.13, p = .29) or maternal anxiety (χ2(1,189) = 0.01, p = 1.0).
Preliminary analyses examined the relationship between potential confounds and each of the dependent variables of interest (see ). Three of the potential confounds were positively related to one or more of the cortisol measures, and were therefore statistically controlled in analyses of those variables (i.e., number of siblings, r = .16, p = .04 with baseline; mother’s use of psychotropic drugs during pregnancy t = −3.08, p < .01 for baseline, t = −2.04, p = .04 for mean; and delivery complications, r = .18, p = .02 for baseline, r = .23, p < .01 for mean). As noted above, we also included the baseline cortisol measure (pre-stressor tasks) as a statistical control in our analyses of reactivity.
Relationship between potential confounds and infant cortisol measures
Cortisol values were log-transformed prior to analyses (NB: non-transformed values are presented in the figures for ease of interpretation). Regression analyses or analyses of covariance were completed to test each hypothesis as specified below, and an alpha of .05 was used throughout.
Maternal depression and infant cortisol
presents the results from separate regression analyses predicting infant baseline, mean, and reactivity cortisol from maternal lifetime history of depression (with statistical controls as outlined above). Lifetime maternal depression significantly predicted both baseline (ΔF(1,165) = 4.64, p = .03) and mean infant cortisol (ΔF(1,167) = 7.45, p < .01), but not cortisol reactivity (ΔF(1,151) = 2.52, p = .12).
Maternal depression and infant cortisol concentrations
A second set of regression analyses examining the contribution of maternal peripartum depression, above and beyond the effect of maternal lifetime depression (see ), revealed that maternal depression occurring in the peripartum phase predicted to infant cortisol reactivity (ΔF(1,150) = 4.91, p = .03).
We further broke down the peripartum exposure group to examine whether infant cortisol levels would differ according to pregnancy exposure only (n = 32), postpartum exposure only (n = 36), or both (n = 36). ANCOVAs revealed no significant differences in infant cortisol in these three groups (baseline: F(2, 103) = .14, p = .87, eta-squared = .00; mean: F(2, 104) = 1.07, p = .35, eta-squared = .02; reactivity: F(2, 94) = 2.57, p = .08, eta-squared = .06).
We also examined the contribution of current maternal depressive state to infant cortisol responses. Multiple regression analyses revealed that current maternal BDI scores were not significant predictors of infant cortisol measures (baseline: ΔF(1,159) = .36, p = .55, beta = −.05; mean: ΔF(1,161) = .01, p = .94, beta = −.01; reactivity: ΔF(1,146) = 3.77, p = .06, beta = .14). It should be noted that the addition of the variable representing exposure to maternal depression in the postpartum period (as assessed by the SCID) into the regression analysis substantially reduced the BDI-reactivity association (reactivity: ΔF(1,145) = .26, p = .61, beta = .04).
Maternal depression, maternal anxiety and infant cortisol
In order to examine the relationship between maternal depression, comorbid anxiety and infant cortisol, we completed a series of linear regression analyses where statistical controls were entered in Block 1, comorbid anxiety disorder was added in Block 2, and maternal depression was added in Block 3. Results from these analyses are reported in . As can be seen, depression comorbid with anxiety predicted infant cortisol reactivity (ΔF(1,151) = 5.25, p = .02)., but depression separate from comorbid anxiety did not (ΔF(1,150) = .57, p = .45). The opposite pattern was observed for infant baseline and mean cortisol levels with comorbid anxiety having no significant effect on these outcomes (baseline ΔF(1,165) = .03, p = .86; mean ΔF(1,167) = 2.27, p = .13), and maternal depression predicting each of them even when comorbid anxiety was controlled (baseline ΔF(1,164) = 5.51, p = .03; mean ΔF(1,166) = 5.46, p = .02).
Maternal depression and anxiety and infant cortisol concentrations
Disorder versus medication exposure in pregnancy
Finally, we examined whether exposure to psychotropic medication during pregnancy might have independent effects on infant cortisol concentrations, above and beyond the effects of exposure to maternal anxiety or depression. We also explored whether maternal psychotropic medication use during pregnancy moderated the effects of prenatal exposure to anxiety or depression on infant cortisol outcomes. Specifically, we completed a series of linear regressions predicting to infant cortisol outcomes with statistical controls and lifetime and prenatal exposure to anxious / depressive disorders entered in Block 1, use of psychotropic medications in pregnancy entered into Block 2, and the maternal disorder during pregnancy X maternal medication during pregnancy interaction term entered into Block 3. As can be seen in , psychotropic medication use during pregnancy interacted with maternal disorder during pregnancy to predict infant mean cortisol (ΔF(1,164) = 6.88, p = .01) and infant cortisol reactivity (ΔF(1,148) = 4.23, p = .04).
Maternal depression and anxiety, psychotropic medications during pregnancy, and infant cortisol concentrations
In order to interpret these interaction effects, we examined infant mean cortisol and cortisol reactivity in groups with or without exposure to maternal disorder and maternal psychotropic medication during pregnancy. These results are presented in . As can be seen, maternal medication treatment during pregnancy appeared to offset the effects of maternal disorder on infant cortisol outcomes. Notably, infants who were exposed to maternal depression or anxiety, and whose mothers were not medicated during pregnancy, display the highest cortisol levels.
Mother prenatal disorder and medication use and infant cortisol