Consistent with previous studies [13
], we found that infant physiology and behavior was significantly influenced by caregiving behavior. Higher levels of HRV have been associated with more adaptive emotion regulation in children [40
] and adults [41
]. We found that infants of highly sensitive mothers had higher resting HRV than did infants of less sensitive mothers. These results are consistent with developmental [42
] and transactional models [43
] of emotional health, which assert that biobehavioral adaptation is shaped, in part, by interactions with the social environment. The perception of control and social support during mild stress has been shown to predict decreased heart rate reactivity [44
], and increased HRV [46
] in both adults and children. Thus, differences in HRV among infants of HS and LS mothers may reflect the larger amount of stress experienced in the unfamiliar laboratory environment by infants whose mothers do not consistently attend to the child’s needs.
Surprisingly, we did not find reduced HRV in infants of antenatally depressed/anxious mothers, as we had hypothesized. However, this inconsistency with previous research [3
] could be explained by another unexpected finding. Although other studies report depressed and anxious mothers tend to be less sensitive in their parenting [15
], we observed no difference in sensitivity ratings for depressed and anxious women in our sample2
. As a result, our sample allowed for the dissociation between prenatal influences (e.g. antenatal depression/anxiety) and postnatal influences (e.g. sensitivity) on infant autonomic regulation.
Neither antenatal diagnosis nor maternal sensitivity alone predicted infant baseline cortisol level, but the interaction between the two factors was significant. Infants of women without an antenatal diagnosis had comparatively low baseline cortisol levels regardless of their mother’s sensitivity. However, infants of women with an antenatal diagnosis had significantly higher cortisol levels if their mothers were less sensitive, but were indistinguishable from infants of control women if they received more sensitive parenting. Consistent with the fetal programming hypothesis [8
], these findings suggest that antenatal diagnostic status influences infant stress–related physiology, potentially mediated by genetic transmission and/or mood–based alterations in women’s HPA–axis that affect fetal physiological development. However, this infant HPA–axis programming appears to be modulated by maternal sensitivity, indicating that a developmental programming model can be complemented by other theories of development [9
], such as those focusing on the social context of biopsychological adaptation.
Maternal sensitivity, but not antenatal psychiatric status, was associated with EA assessment of child responsiveness during the free-play session. Infants whose mothers were rated as more sensitive showed greater positive affect and engagement in the free–play session compared to infants whose mothers were rated as less sensitive. These results are consistent with previous work showing the significant influence of caregiving characteristics in child socialization and self–regulation [47
]. Our findings highlight the role of maternal caregiving behavior in shaping infant biobehavioral development. However, we also investigated the alternative hypothesis that infant temperament constrains the quality of mothers’ caregiving so that temperament qualities in the infant “lead” the dyadic interaction and the associated effects on infant development. Specifically, we examined the hypothesis that compared to sensitive caregivers, women who are less sensitive with their infants describe them as more difficult. This hypothesis was not supported. Mothers’ subjective reports of infant temperament did not differ as a function of sensitivity group. Our results are consistent with those from Hane & Fox [13
], who found that the quality of maternal care did not differ with objective classifications of temperament.
Although the interaction between antenatal stress and postnatal caregiving behavior has been studied extensively in the animal literature [49
], until recently, no studies had addressed the interaction between similar prenatal and postnatal influences on physiology and behavior in human infants. In 2006, Diego et al.
] found that right frontal EEG asymmetry was most pronounced for infants of depressed women who were also characterized as withdrawn or intrusive, suggesting that insensitive caregiving may exacerbate the adverse effects of prenatal depression. In the current study, we present evidence that maternal sensitivity modulates the effect of antenatal depression and anxiety on infant cortisol, suggesting that the epigenetic processes leading to associations between antenatal mood and stress-related physiology in the perinate can be over–ridden by postnatal environmental factors such as the quality of parenting.
There are some limitations to this study. Our measures of HRV and cortisol were not taken in response to a stressor or stimulus, and thus cannot inform how parental sensitivity interacts with antenatal psychiatric status to influence infant stress reactivity. HRV data was based on a brief assessment period and may be more susceptible to minor variations in the RR intervals than if it were based on a longer EKG sample. Because we did not find a main effect of antenatal psychiatric status on HRV or on cortisol, these data contrast somewhat with previous work showing that antenatal depression and anxiety is associated with decreased HRV in newborns and infants [3
] and with elevated levels of awakening cortisol in 10-year-olds [6
]. This discrepancy may be due, in part, to differences between the metrics used to assess HRV in the present study and in previous studies. Furthermore, the size of our patient group may have limited our statistical power to detect an effect of antenatal diagnostic status on these infant outcome variables. The patient group included in the present study may represent pregnant women with only mild to moderate depression/anxiety, and thus the current findings may not be generalizeable to populations with more severe depression and anxiety.
Collectively, the results of this study illustrate the significant influence of maternal sensitivity on infant physiology and emotional responsiveness. Sensitive parenting may provide the infant with repeated instances of appropriate support and successful coping, which may ultimately contribute to the shaping of physiologic regulation to future stressors. In addition, maternal sensitivity may promote appropriate behavioral responses from the child, which may subsequently influence others’ responses to the child throughout development. Interestingly, it appears that the in utero programming of autonomic and HPA–axis regulation may be open to postnatal shaping of brain–behavior development, a finding that supports the compatibility of fetal programming and social–context models of infant biobehavioral development. As such, these findings, and those from similar studies, have promising implications for pre and postnatal clinical intervention.