Parenting, Peers and Psychosocial Adjustment: Are the Same-or Different-Children Affected by Each?

The prospective research presented herein extends work on parent and peer effects on adolescent psychosocial adjustment by looking beyond average effects. Instead, it considers variation in susceptibility to each source of influence in order to assess the extent to which those individuals most and least susceptible to parent effects are similarly-or differentially-susceptible to peer effects. Data from the NICHD Study of Early Child Care and Youth Development (n = 1364, 48.3% female, age range: 10-15 yrs., race/ethnicity: 80.4% white, 12.9% black and 6.7% other) was analyzed to assess the degree to which each child was susceptible to parent and peer effects. Toward this end, an influence statistic, DFBETAS, was used. A significant and moderate positive association between the two susceptibility effects indicated that children most or least susceptible to the effects of quality of parenting proved to be similarly affected by their peers, although this was not the case for a substantial minority of youth. The fact that at least some children vary dramatically in the effects to which they are most susceptible is discussed with respect to potential targets of intervention, namely, parents or peers.

Infant temperament, early-childhood parenting, and early-adolescent development: Testing alternative models of Parenting × Temperament interaction.

Here we evaluate whether infant difficult temperament (6 months) functions as a vulnerability or more general plasticity factor when investigating effects of early-childhood parenting (8-42 months) on both positive and negative early-adolescent socioemotional development (age 8-11 years). Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 14,541) and a re-parameterized model-testing approach to distinguish alternative person × environment conceptual models, results indicated that temperament × parenting interacted in predicting externalizing (i.e., hyperactivity, conduct problems), but not other behavior (i.e., emotional symptoms, peer problems), in a (weak) differential susceptibility manner. While more and less supportive parenting predicted, respectively, fewer and more behavior problems, it did so more strongly for children who were more difficult as infants.

Differential susceptibility 2.0: Are the same children affected by different experiences and exposures?

Differential susceptibility theory stipulates that some children are more susceptible than others to both supportive and adverse developmental experiences/exposures. What remains unclear is whether the same individuals are most affected by different exposures (i.e., domain general vs. specific). We address this issue empirically for the first time using, for illustrative and proof-of-principle purposes, a novel influence-statistics' method with data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care. Results indicated that previously documented effects of greater quality of care on enhanced pre-academic skills and greater quantity of care on more behavior problems apply mostly to different children. Analyses validating the new method indicated, as predicted, that (a) the quantity-of-care effect applied principally to children from more socioeconomically advantaged families and that (b) being highly susceptible to both, one or neither childcare effect varied as a function of a three-gene, polygenic-plasticity score (serotonin transporter linked polymorphic region [5-HTTLPR], dopamine receptor D4 [DRD4], brain-derived neurotrophic factor [BDNF]) in a dose-response manner (i.e., 2>1>0). While domain-specific findings involving child-care effects cannot be generalized to other environmental influences, the influence-statistics' approach appears well suited for investigating the generality-specificity of environment effects, that is, of "differential, differential susceptibility."

What is a pair bond?

Pair bonding is a psychological construct that we attempt to operationalize via behavioral and physiological measurements. Yet, pair bonding has been both defined differently in various taxonomic groups as well as used loosely to describe not just a psychological and affective phenomenon, but also a social structure or mating system (either social monogamy or just pair living). In this review, we ask the questions: What has been the historical definition of a pair bond? Has this definition differed across taxonomic groups? What behavioral evidence do we see of pair bonding in these groups? Does this observed evidence alter the definition of pair bonding? Does the observed neurobiology underlying these behaviors affect this definition as well? And finally, what are the upcoming directions in which the study of pair bonding needs to head?

Maternal distress across the postnatal period is associated with infant secretory immunoglobulin A.

Employing a longitudinal design, relationships between maternal distress (i.e., perceived stress, negative affect, depressive symptomology), and infant secretory immunoglobulin A (sIgA) across the peripartum period were examined in 51 mother-infant dyads. Indices of maternal distress were assessed at four time periods: third trimester of pregnancy and 1, 3, and 6 months postpartum. Infant saliva samples were collected at each of the three time points in the postpartum period to assess sIgA levels. No relationships were found between prenatal maternal distress and infant sIgA. Results indicated that during the postnatal period, higher concurrent maternal distress was associated with reduced infant sIgA. Maternal distress did not prospectively predict infant sIgA. These findings advance our understanding of the social-context of infant development, highlighting the significance of maternal regulation of infant immunity.

Experiences with Prenatal and Postpartum Contraceptive Services among Women with a Preterm Birth.

BACKGROUND: Providing postpartum contraception can help to achieve recommended interpregnancy intervals (≥18 months from birth to next pregnancy), decrease the risk of preterm birth, and thus improve maternal and infant health outcomes of future pregnancies. However, the experiences of women with preterm birth regarding contraceptive services have not been documented. We sought to better understand contraceptive counseling experiences and postpartum contraception of women with a preterm birth. METHODS: We interviewed 35 women, ages 18-42 years, with a recent preterm birth in California. The transcribed interviews were analyzed using ATLAS.ti v.8. RESULTS: Women had public (n = 15), private (n = 16), or no insurance (n = 4) at the time of the interview. Women were mainly Latina (n = 14), Caucasian (n = 9), or African American (n = 6); 15 women were foreign born. Women's experiences ranged from spontaneous preterm births to births with severe medical complications. We identified five themes that were associated with women's engagement in the contraceptive method choice and understanding of birth spacing: 1) timing and frequency of contraceptive counseling; 2) quality of patient-provider interaction and ability to follow up on questions; 3) women's personal experiences with contraceptive use and experiences of other women; 4) context in which contraceptive counseling was framed; and 5) system barriers to contraceptive use. CONCLUSIONS: Postpartum contraceptive counseling should address women's preterm birth experience, medical conditions, age, contraceptive preference, and childbearing plans. Having a preterm birth intensifies gaps in hospital and outpatient clinic coordination and provider-patient communication that can lead to use of less effective or no contraceptive methods and risk of early subsequent unplanned pregnancies.

Prenatal stress enhances postnatal plasticity: The role of microbiota.

Separate fields of inquiry indicate (a) that prenatal stress is associated with heightened behavioral and physiological reactivity and (b) that these postnatal phenotypes are themselves associated with increased susceptibility to both positive and negative environmental influences. Collectively, this work supports Pluess and Belsky's (Psychopathology, 2011, 23, 29) claim that prenatal stress fosters, promotes or "programs" postnatal developmental plasticity. Herein, we review animal and human evidence consistent with this hypothesis before advancing the novel idea that infant intestinal microbiota may be one candidate mechanism for instantiating developmental plasticity as a result of prenatal stress. We then review research indicating that prenatal stress predicts differences in infant intestinal microbiota; that infant intestinal microbiota is associated with behavioral and physiological reactivity phenotypes; and, thus, that prenatal stress may influence infant intestinal microbiota in a way that results in heightened physiological and behavioral reactivity and, thereby, postnatal developmental plasticity. Finally, we offer ideas for testing this claim and consider implications for intervention and use of probiotics during early infancy.