Impacts of Parental Technoference on Parent-Child Relationships and Child Health and Developmental Outcomes: A Scoping Review.

Parental technological immersion during parenting activities has been shown to alter parent-child interactions. This concept, referred to as parental technoference, has the potential to affect parent-child relationships and children's health and development. This scoping review utilized the Joanna Briggs Institute (JBI) methodology to identify, describe, and summarize: (a) evidence of parental technoference on parent-child relationships, and children's health and development; (b) definitions and measurements of parental technoference; (c) research designs and methodologies used to investigate parental technoference; and (d) literature gaps. We searched MEDLINE, APA PsycInfo, Cochrane Central Register of Controlled Trials, Cochrane Database for Systematic Reviews, JBI EBP Database, Embase, CINAHL, and Scopus, as well as the reference lists of included studies for literature on parental technology use during parenting and parent-child interactions and its effects on parent-child relationships, and children's health and development. Sixty-four studies, found in 61 publications, met the review criteria. The effect of parental technoference on parent-child relationships was most studied, and findings demonstrated that parents recognized, and researchers observed, changes in parents' and children's behaviors. Adolescent self-reported mental health concerns and maladaptive technological behaviors (e.g., cyberbullying) were associated with more parental technoference, and findings highlighted safety concerns for children. Other aspects of children's development, although less studied, were also negatively impacted by parental technoference. No significant associations were found between parental technoference and children's medical and physiological health, yet these associations were the least studied. Additional research is needed to understand these associations and evaluate interventions designed to mitigate technoference harms.

Cross-Generational Impact of Innate Immune Memory Following Pregnancy Complications.

Pregnancy complications can have long-term negative effects on the health of the affected mothers and their children. In this review, we highlight the underlying inflammatory etiologies of common pregnancy complications and discuss how aberrant inflammation may lead to the acquisition of innate immune memory. The latter can be described as a functional epigenetic reprogramming of innate immune cells following an initial exposure to an inflammatory stimulus, ultimately resulting in an altered response following re-exposure to a similar inflammatory stimulus. We propose that aberrant maternal inflammation associated with complications of pregnancy increases the cross-generational risk of developing noncommunicable diseases (i.e., pregnancy complications, cardiovascular disease, and metabolic disease) through a process mediated by innate immune memory. Elucidating a role for innate immune memory in the cross-generational health consequences of pregnancy complications may lead to the development of novel strategies aimed at reducing the long-term risk of disease.

Aberrant inflammation in rat pregnancy leads to cardiometabolic alterations in the offspring and intrauterine growth restriction in the F2 generation.

Children of women with pre-eclampsia have increased risk of cardiovascular (CV) and metabolic disease in adult life. Furthermore, the risk of pregnancy complications is higher in daughters born to women affected by pre-eclampsia than in daughters born after uncomplicated pregnancies. While aberrant inflammation contributes to the pathophysiology of pregnancy complications, including pre-eclampsia, the contribution of maternal inflammation to subsequent risk of CV and metabolic disease as well as pregnancy complications in the offspring remains unclear. Here, we demonstrate that 24-week-old female rats (F1) born to dams (F0) exposed to lipopolysaccharide (LPS) during pregnancy (to induce inflammation) exhibited mild systolic dysfunction, increased cardiac growth-related gene expression, altered glucose tolerance, and coagulopathy; whereas male F1 offspring exhibited altered glucose tolerance and increased visceral fat accumulation compared with F1 sex-matched offspring born to saline-treated dams. Both male and female F1 offspring born to LPS-treated dams had evidence of anemia. Fetuses (F2) from F1 females born to LPS-treated dams were growth restricted, and this reduction in fetal growth was associated with increased CD68 positivity (indicative of macrophage presence) and decreased expression of glucose transporter-1 in their utero-placental units. These results indicate that abnormal maternal inflammation can contribute to increased risk of CV and metabolic disease in the offspring, and that the effects of inflammation may cross generations. Our findings provide evidence in support of early screening for CV and metabolic disease, as well as pregnancy complications in offspring affected by pre-eclampsia or other pregnancy complications associated with aberrant inflammation.