Which healthy lifestyle factors are associated with a lower risk of suicidal ideation among adolescents faced with cyberbullying?

Cyberbullying is associated with negative mental health outcomes including adolescent suicidal ideation. This requires effective and accessible preventive efforts. Healthy lifestyles are factors adolescents themselves can modify that may lower their risk of suicidal ideation. The aim of this study was to examine associations between physical activity, (outdoor) sport participation, a healthy diet, higher sleep duration and low levels of smoking and alcohol use, and suicidal ideation when faced with cyberbullying. A cross-sectional survey was administered in 2014-2015 to 1037 adolescents (12-18 years, M age = 15; 50% girls) in Flanders, Belgium. Logistic regression analyses were conducted to assess direct effects of cyberbullying involvement (victim, perpetrator, bystander) on suicidal ideation, and interaction effects between cyberbullying involvement, healthy lifestyles and suicidal ideation. Results showed that cyberbullying victimization, perpetration and bystanding were associated with higher suicidal ideation, but that the association with cyberbullying perpetration disappeared when corrected for other cyberbullying involvement forms. More physical activity, sleeping longer, more often taking a healthy diet and lower levels of smoking were associated with lower suicidal ideation. Some associations of healthy lifestyles with suicidal ideation disappeared at higher levels of cyberbullying involvement. Low alcohol consumption and (outdoor) sport participation were not associated with suicidal ideation, and sport participation was even associated with higher suicidal ideation at low levels of cyberbullying involvement. These findings suggest a novel approach to suicide prevention may be warranted, by strengthening healthy lifestyles as factors that adolescents themselves can modify to increase their resilience and reduce suicidal ideation.

Mitochondrial energetic and AKT status mediate metabolic effects and apoptosis of metformin in human leukemic cells.

Previous reports demonstrate that metformin, an anti-diabetic drug, can decrease the risk of cancer and inhibit cancer cell growth. However, its mechanism in cancer cells is still unknown. Metformin significantly blocks cell cycle and inhibits cell proliferation and colony formation of leukemic cells. However, the apoptotic response to metformin varies. Furthermore, daily treatment with metformin induces apoptosis and reduces tumor growth in vivo. While metformin induces early and transient activation of AMPK, inhibition of AMPKα1/2 does not abrogate anti-proliferative or pro-apoptotic effects of metformin. Metformin decreases electron transport chain complex I activity, oxygen consumption and mitochondrial ATP synthesis, while stimulating glycolysis for ATP and lactate production, pentose phosphate pathway for purine biosynthesis, fatty acid metabolism, as well as anaplerotic and mitochondrial gene expression. Importantly, leukemic cells with high basal AKT phosphorylation, glucose consumption or glycolysis exhibit a markedly reduced induction of the Pasteur effect in response to metformin and are resistant to metformin-induced apoptosis. Accordingly, glucose starvation or treatment with deoxyglucose or an AKT inhibitor induces sensitivity to metformin. Overall, metformin elicits reprogramming of intermediary metabolism leading to inhibition of cell proliferation in all leukemic cells and apoptosis only in leukemic cells responding to metformin with AKT phosphorylation and a strong Pasteur effect.