GDF15 and Anxiety: Mechanistically, these pathway interactions occur through several means: (1) metabolic burden amplification, stress-related GDF15 signaling can overload already weakened mitochondrial systems impacted by ceramide accumulation; (2) shared vulnerability nodes, brain regions with high metabolic demands (such as the prefrontal cortex and hippocampus) work as convergence points where multiple pathways intersect; and (3) compensatory mechanisms, individuals with strong mitochondrial function might resist both GDF15-related anxiety signals and ceramide-driven dysfunction [20,21].