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Maternal psychopathology during pregnancy is associated with negative outcomes in offspring. Increased placental transfer of maternal cortisol may contribute to mediate this association. Hair cortisol concentrations (HCCs) appear to be a good biomarker of long-term prenatal stress exposure. Little is known about the associations between severe maternal psychopathology and perinatal infant HCCs.
We assessed HCCs in the perinatal period in mother–infant dyads with and without severe psychiatric disorders.
We examined group differences in HCCs of mother–infant dyads (n = 18) subjected to severe maternal psychiatric disorders versus healthy control dyads (n = 27). We assessed the correlation of HCCs between mother and infant within both groups, and the association between current maternal symptoms and HCCs in patient dyads.
Median (interquartile range) and distribution of HCC differed in patients compared with control mothers (U = 468.5, P = 0.03). HCCs in infants of patients did not differ from control infants (U = 250.0, P = 0.67). Subsequently, we found that HCCs within healthy control dyads were correlated (n = 27, r 0.55 (0.14), P = 0.003), but were not within patient dyads (n = 18, r 0.082 (0.13), P = 0.746). HCCs in infants of patients showed a positive correlation with maternal symptoms (n = 16, r = 0.63 (0.06), P = 0.008).
These preliminary findings suggest that infant HCC reflect perinatal stress exposure. In infants, these early differences could influence lifetime hypothalamic–pituitary–adrenal axis functioning, which might be associated with increased susceptibility to later disease.
Early childhood aggressive behaviour is a predictor of future violence. Therefore, identifying risk factors for children’s aggressive behaviour is important in understanding underlying mechanisms. Maternal postpartum depression is a known risk factor. However, little research has focused on the influence of paternal behaviour on early childhood aggression and its interaction with maternal postpartum depression.
This study was performed in two cohorts: the Fathers Project, in the United Kingdom (n = 143) and the Generation R Study, in The Netherlands (n = 549). In both cohorts, we related paternal antisocial personality (ASP) traits and maternal postpartum depressive (PPD) symptoms to childhood aggressive behaviour at age two (Fathers Project) and age three (Generation R Study). We additionally tested whether the presence of paternal ASP traits increased the association between maternal PPD–symptoms and early childhood aggression.
The association between paternal ASP traits and early childhood aggressive behaviour, corrected for maternal PPD-symptoms, was similar in magnitude between the cohorts (Fathers Project: standardized β = 0.12, p = 0.146; Generation R: β = 0.14, p = 0.001), although the association was not statistically significant in the Fathers Project. Strikingly, and in contrast to our expectations, there was evidence of a negative interaction between paternal ASP traits and maternal PPD-symptoms on childhood aggressive behaviour (Fathers Project: β = −0.20, p = 0.020; Generation R: β = −0.09, p = 0.043) in both studies. This meant that with higher levels of paternal ASP traits the association between maternal PPD-symptoms and childhood aggressive behaviour was less and vice versa.
Our findings stress the importance of including both maternal and paternal psychopathology in future studies and interventions focusing on early childhood aggressive behaviour.
Postpartum psychosis is a life-threatening psychiatric emergency, which often occurs without significant premorbid symptoms. Although many studies have postulated an involvement of the immune and endocrine systems in the onset of postpartum psychosis, the specific aetiological factors have remained unknown.
To examine the hypothesis that autoimmune thyroid dysfunction may be associated with the onset of postpartum psychosis.
Thirty-one consecutive primiparous women with no prior psychiatric history were referred to our in-patient unit for postpartum psychosis. The control group (n = 117) comprised primiparous women with consecutive deliveries at a community practice. Blood samples were obtained from all participants at 4 weeks and 9 months postpartum. Thyroperoxidase antibody levels were quantified as immunological measures of autoimmune thyroid disease (AITD). Thyroid-stimulating hormone and free thyroxine levels were measured to assess clinical thyroid dysfunction.
At 4 weeks postpartum and prior to the initiation of mood stabiliser therapy, 19% of women with postpartum psychosis had AITD compared with only 5% in the control group. Women with both postpartum psychosis and AITD had a dramatically higher risk of progression to clinical thyroid dysfunction (67%) than control participants with AITD (20%).
Women with postpartum psychosis are at higher risk not only of AITD but also of clinical thyroid failure. These data implicate thyroid function as an important clinical outcome in patients with postpartum psychosis. Further, AITD represents a potentially strong aetiological factor for the development of postpartum psychosis. Therefore, screening for thyroperoxidase antibodies is warranted in patients with postpartum psychosis.
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