Maternal depression alters stress and immune biomarkers in mother and child

maternal depression, immune system, Hashimoto

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Maternal depression has been repeatedly linked with negative child outcomes as increased psychopathology: poor socioemotional adaptation, externalizing (conduct) and internalizing symptom (anxiety/depression, somatic complaints, social withdrawal), and emotion dysregulation. In addition, maternal depression is related to poor physical health throughout life.

Studies show that prenatal maternal depressive symptoms are associated with poor physical health across early childhood, which in turn predicted health-related stress and diminished social functioning at age 20.

Early life stress increases the risk for disease in adulthood and one mechanism proposed to account for the long-term effects of ELS on health is the disruption to the developing stress response caused by chronic early stress, including both the hypothalamic pituitary axis (HPA) and the immune system, which maintain ongoing crosstalk among them. Prenatal maternal stress alters the development of adaptive immune response in the infant and new-borns of prenatally stressed mothers showed deficient cytokine levels. These early effects of stress on immunity are long lasting and prenatal maternal depression has been shown to predict offspring inflammation at 25 years.

HPA-axis dysfunction has been linked with disruptions to the immune system, which in turn may exacerbate psychopathology in children of depressed mothers. Depression is related to immune system abnormalities partly mediated by HPA hyperactivity, which may lead to production of proinflammatory cytokines, including interleukin 6(IL-6) and C-reactive protein. Patients with major depression show chronic activation of inflammatory responses and studies describe links between stress, maternal depression, and immunosuppression during pregnancy.

These studies suggest that the mutual influences between the two systems in the mother may transfer to the child via mechanisms of endocrine synchrony, potentially impacting the child’s immunity and risk for psychopathology.

Secretory immunoglobulin A (s-IgA) is the most prevalent antibody in mucosal tissues and serves as an immunological barrier for pathogenic penetration. S-IgA serves many immunomodulatory and anti-inflammatory roles and studies have utilized s-IgA as a biomarker of the immune system.

Such findings suggest that maternal depression functions as a distinct early life stress that shapes children’s stress response and physical health in ways that require further investigation. Recent study examined the effects of maternal depression on mother and child’s stress and immune system biomarkers and social behaviour and how these mediate the effects of maternal depression on child psychopathology. This is the first study to show that HPA-axis and immune system biomarkers integrate with maternal and child’s social behaviour to chart three mediating pathways linking maternal depression with child externalizing and internalizing symptoms.

Stress and immune biomarkers jointly mediated the effects of maternal depression on child symptoms via four independent paths: 1) by augmenting maternal and child’s cortisol production, 2) by increasing s-IgA levels, 3) by impairing maternal and child relational behaviour, and 4) via a mixed hormonal-immune pathway by which maternal s-IgA impacts child’s cortisol.

Overall, the results provide evidence for the pervasive effects of maternal depression on child stress and immune systems intactness and social repertoire, increasing child vulnerability, reducing resilience, and rendering children more susceptible to psychopathology. It is important to note, however, that the findings describe a pattern of associations and in no way imply causality and such intercorrelations may be impacted by other unmeasured variables, such as genetic and epigenetic influences.

In addition to HPA-axis dysregulation, higher s-IgA evening levels were found in both depressed mothers and their children.

The second path from maternal depression to child outcomes charts an immune system pathway. Depression was associated with higher maternal s-IgA, which correlated with higher child s-IgA and linked with higher  symptoms. Such pathway describes the disruptions to the immune system in depressed mothers and their children and shows its relation to psychopathology in children. However, higher maternals-IgA was also associated with reduction in child’scortisol, which in turn was related to lower externalizing and internalizing symptoms.

An important limitation of the study is that it did not measure other immune biomarkers. Generally, s-IgA is relevant to inflammation in the sense that the endocrine and sympathetic nervous systems are connected to the immune system, but it is not a direct biomarker of inflammation as it is associated with both pro-inflammatory and anti-inflammatory processes. Another limitation is that we did not measure fathers’ cortisol and s-IgA, as fathering can exert a mitigating effect on child psychopathology in the context of maternal depression.

Though, exposure to maternal depression at any time-point in childhood bears negative consequences for children’s immunity and emotional well-being.

 

Reference:

Ulmer‐Yaniv, A., Djalovski, A., Priel, A., Zagoory‐Sharon, O., & Feldman, R. (2018). Maternal depression alters stress and immune biomarkers in mother and child. Depression and Anxiety. doi:10.1002/da.22818

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