## 4 Discussion
The findings further suggest that \"c\" factor scores may be a psychometrically efficient way to capture overall cerebral function, but alternative theoretical frameworks may ultimately prove more useful for understanding the complex relationships between cognition and psychopathology. The relationships we observed between the \"c\" factor and our validation criteria provide preliminary support for both the mitochondrial and fitness indicator theories of its underlying mechanism. The strong association between \"c\" and intracranial volume (r = 0.39) aligns with the mitochondrial hypothesis, as brain size and energy consumption are closely linked; the brain consumes approximately 20% of the body's energy despite comprising only 2% of its mass [58], suggesting that larger brains may require more efficient mitochondrial functioning. The robust correlations between \"c\" and both socioeconomic indicators (parent education r = 0.43; neighborhood SES r = 0.47) could support either theoretical framework; from a mitochondrial perspective, higher SES environments may promote better mitochondrial function through improved nutrition, reduced environmental stressors, and better access to healthcare; from a fitness indicator perspective, these correlations suggest the kind of positive manifold across different domains that would be expected if \"c\" represents overall genetic quality. Note it is difficult to say what the higher end of genetic \"quality\" means here. Strictly speaking, \"high-quality\" genes are simply genes that built humans who were especially good at reproducing in our ancestral environment. And as discussed above, sexual selection likely played a role, in which case \"high-quality\" simply means desirable to the opposite sex. Regardless, it is easier to imagine what \"low-quality\" genes might be, including systematic phenomena like deletions and duplications, as well as de novo mutations with deleterious effects. Perhaps most telling is the predictive relationship between \"c\" and longitudinal psychosis outcomes (d = 0.30-0.57), as both theoretical frameworks would predict such prognostic utility. Mitochondrial dysfunction has been implicated in psychosis progression (as evidenced by our findings in 22q11.2 deletion syndrome), while the fitness indicator framework would expect more severe psychopathology to emerge in individuals with lower overall genetic quality. The association between \"c\" and global functioning (r = 0.27) similarly supports both perspectives, as both frameworks would predict that higher \"c\" scores indicate better overall system integrity, whether measured through mitochondrial efficiency or genetic quality. While our data cannot definitively adjudicate between these theoretical explanations, the consistent pattern across multiple domains suggests these mechanisms may operate in parallel rather than being mutually exclusive. Future research should focus on directly testing these proposed mechanisms through several approaches. First, longitudinal studies incorporating direct measures of mitochondrial function (e.g., through magnetic resonance spectroscopy or peripheral biomarkers) could help establish whether mitochondrial efficiency mediates the relationship between \"c\" and clinical outcomes. Second, genetic studies examining polygenic scores for both mitochondrial function and overall genetic quality could help disentangle these mechanisms. Additionally, intervention studies targeting mitochondrial function through lifestyle modifications (e.g., diet, exercise) or pharmacological approaches could provide causal evidence for this mechanism if they successfully improve \"c\" scores. This study's findings have several important clinical implications. First, the robust associations between \"c\" and both concurrent functioning and longitudinal outcomes suggest that assessing cognitive and clinical symptoms together, rather than separately, may provide clinicians with better prognostic information.