Schizophrenia (SZ), bipolar disorder (BD), and depressive disorder (DEP) are disabling diseases influenced by genetic and environmental factors. Several risk factors have been identified for these disorders in various systematic reviews, meta-analyses, and umbrella reviews. Identifying risk factors for these disorders is essential to be able to target disorder-specific or transdiagnostic interventions. We aimed to systematically review existing meta-analyses on selected risk factors for SZ, BD, and DEP. We systematically searched for meta-analyses of risk factors relating to pregnancy and birth, childhood and adolescence, lifestyle, somatic conditions, infectious agents, and environmental exposures published since 2000. The transdiagnostic comparison included 70 meta-analyses, encompassing results for 55 risk factors that were studied across at least two of the three disorders. In our extensive transdiagnostic umbrella, 74% of reported effect sizes for the risk factors from meta-analyses were statistically significant. Childhood maltreatment was a robust transdiagnostic risk factor for all three disorders. We also found differences in risk factors, for example, pregnancy and birth complications associated strongly with SZ risk, and several somatic conditions were associated with DEP. It should be noted that many meta-analyses were low quality and based on a small number of original studies. More high-quality longitudinal research is needed on many risk factors to be able to evaluate their validity in single outcomes and their potential specificity or non-specificity.

Starvation is a fundamental physiological stressor that triggers conserved adaptive responses across species, however, its effects are shaped by both developmental stage and prior nutritional history. This study aimed to investigate the effects of acute nutrient deprivation in Artemia franciscana, comparing newly hatched nauplii and adult individuals previously exposed to reduced caloric intake during development. Organisms were subjected to starvation for 24, 48, and 72 h, and mortality, morphometric parameters, and locomotor activity were assessed, complemented by in silico analysis of starvation-related pathways. Starvation induced distinct responses between groups, with markedly higher mortality in adults compared to nauplii. While these differences reflect developmental stage-associated responses, they are also influenced by prior nutritional history. Body length was significantly reduced under starvation in both developmental stages, while antennal length remained largely unchanged. Locomotor activity, including distance travelled and swimming velocity, was consistently decreased, indicating energy-conserving behavioral adaptation. Partial recovery of locomotor performance and antennal length was observed following restoration of feeding. Bioinformatic analysis suggested the presence of conserved autophagy-related genes and enrichment of pathways associated with autophagy and TOR signaling. However, these findings should be interpreted as hypothesis-generating, given the reliance on a proxy species for pathway inference. These findings indicate that starvation responses in A. franciscana are shaped by an interaction between developmental stage and prior nutritional history, supported by conserved stress–response pathways, highlighting the potential of this model for studying metabolic stress responses.