Depression, stress, and anxiety versus internet addiction in early and middle adolescent groups: the mediating roles of family and school environments.

BACKGROUND: Family and school environment play a crucial role across the different developmental stages of adolescence. This paper investigates the potential mediating role of family and school environments in the relationship between the three psychosocial predictors of depression, anxiety, stress, and Internet addiction (IA). Specifically, it focuses on the two stages of early and middle adolescence. METHODS: The study involved a survey of 407 adolescents from Qatar, comprising 250 early adolescents and 157 middle adolescents. Inclusion criteria for the study included adolescents between the ages of 10 to 17 years old, residents of Qatar and studying in a Qatar-based school. To assess the constructs of the three psychosocial predictors, IA, family environment, the study utilized the Depression, Stress, and Anxiety Scale (DASS), the Internet Addiction Diagnostic Questionnaire (IADQ), and the Brief Family Relationship Scale, respectively. School environment was measured using questions from the "Health Behavior in School-aged Children: WHO Collaborative Cross-National survey/study (HBSC) 2013-2014. The study applied standard mediation analysis between the DASS components and IA with family and school environment as the mediators. RESULTS: Results from the mediation analysis reveal insights into the relationships between psychosocial predictors and IA. The findings indicate that family and school environments partially mediated the relationship with regards to depression, stress, and anxiety in early adolescents. In middle adolescents, family environment partially mediated the relationship with depression and stress and fully mediating the relationship with anxiety. Meanwhile, school environment only exhibited partial mediation in the relationship with anxiety in middle adolescence. CONCLUSIONS: These results highlight the crucial role parents and schools play in addressing problematic technology usage that develops as a response to depression, anxiety, and stress among adolescents. Moreover, the study reveals nuances in the mediating role of family and school environment in early and middle adolescence. This highlights the evolving nature of these influences across the different stages of development. Notably, this study contributes to the literature by moving beyond the conventional focus on the so-called WEIRD population, and offering valuable insights from a region that is underrepresented in current research.

Loss of the auxiliary α2δ1 voltage-sensitive calcium channel subunit impairs bone formation and anabolic responses to mechanical loading.

Voltage-sensitive calcium channels (VSCCs) influence bone structure and function, including anabolic responses to mechanical loading. While the pore-forming (α1) subunit of VSCCs allows Ca2+ influx, auxiliary subunits regulate the biophysical properties of the pore. The α2δ1 subunit influences gating kinetics of the α1 pore and enables mechanically induced signaling in osteocytes; however, the skeletal function of α2δ1 in vivo remains unknown. In this work, we examined the skeletal consequences of deleting Cacna2d1, the gene encoding α2δ1. Dual-energy X-ray absorptiometry and microcomputed tomography imaging demonstrated that deletion of α2δ1 diminished bone mineral content and density in both male and female C57BL/6 mice. Structural differences manifested in both trabecular and cortical bone for males, while the absence of α2δ1 affected only cortical bone in female mice. Deletion of α2δ1 impaired skeletal mechanical properties in both sexes, as measured by three-point bending to failure. While no changes in osteoblast number or activity were found for either sex, male mice displayed a significant increase in osteoclast number, accompanied by increased eroded bone surface and upregulation of genes that regulate osteoclast differentiation. Deletion of α2δ1 also rendered the skeleton insensitive to exogenous mechanical loading in males. While previous work demonstrates that VSCCs are essential for anabolic responses to mechanical loading, the mechanism by which these channels sense and respond to force remained unclear. Our data demonstrate that the α2δ1 auxiliary VSCC subunit functions to maintain baseline bone mass and strength through regulation of osteoclast activity and also provides skeletal mechanotransduction in male mice. These data reveal a molecular player in our understanding of the mechanisms by which VSCCs influence skeletal adaptation.