## 4 Discussion  
This study offers the first step in demonstrating the potential utility of estimating a \"c\" factor in a community sample when both cognitive and psychopathology variables are measured. The tri-factor structural measurement model fit the data well, and the scores generated from the model associate with external criteria in expected directions. Furthermore, the \"c\" factor based on cross-sectional data helped predict the clinical outcome in a subsample that was followed longitudinally. There is some evidence that the \"c\" factor captures additional signals provided by the cognitive and psychopathology variables that might not be captured by each super-domain (\"p\" and \"g\") alone. Further, there is moderate evidence that measurement invariance across age is achieved, at least within this 8-21 year age range. The reasons for the existence of \"c\"--i.e., its mechanisms and origin--are unclear, but some explanations can be offered. From a mechanistic point of view, [PERSON] et al. [23] propose mitochondrial bioenergetics as a central process underlying \"c\", based on previous studies linking mitochondrial function to both \"g\" [54; 55] and \"p\" [56; 57]. Because the brain accounts for 20% of the energy consumption in the body [58], and mitochondria are responsible for energy production [59], mitochondrial dysfunction may lead to adverse outcomes in anything the brain does, which includes the broad range of behaviors that can be characterized as psychopathology or cognition. Unfortunately, data on mitochondrial functioning were not available in this data set, so testing this theory was not possible here. However, there is evidence for mitochondrial involvement in schizophrenia, which is high on \"p\" and low on \"g\". In the recurrent rare copy number variant (CNV) associated with chromosome 22q11.2 deletion, where there is about a 25-fold increased rate of schizophrenia compared to the general population [60], six of the deleted genes encode proteins that localize to mitochondria. Deficits in iPSC neurons from patients with 22q11.2 deletion (Fig. 2), and the \"c\" factor is 1.22 deletion (Fig. 2). Figure 3: Differences between Longitudinal Psychosis Spectrum Groups on mean “p”, “g”, and “c” factors. (**a**) shows results among those whose baseline assessment met criteria for psychosis spectrum at baseline, where “Resilient” indicates an amelioration of symptoms at follow-up; (**b**) shows results among those who did not meet criteria for psychosis spectrum at baseline, where “PS Emergent” indicates the emergence (first-time appearance) of psychosis spectrum symptoms at follow-up. tion syndrome are evident in those with schizophrenia compared to those without [61]. Furthermore, an increase in mitochondrial biogenesis and function was associated with the absence of schizophrenia in neurons derived from lymphoblastic cell lines of individuals with 22q11.2 deletion syndrome and was reversible by agents that enhance mitochondrial biogenesis [62]. A functional explanation for \"c\" is offered by proposing a general \"fitness\" factor [63; 64; 65], where fitness is defined in the adaptationist (evolutionary) sense: a set of characteristics that enhance the probability of survival and reproduction of an individual. Several physiological indicators of fitness have been proposed in humans, including muscularity in men [66], vocal characteristics [67; 68], handgrip strength in men [69], facial characteristics [70; 71], and (lack of) fluctuating asymmetry [72; 73], among others. Possibly unique to humans, however, is the evidence for mental/psychological fitness indicators, such as humor [74], general intelligence [75], artistic virtuosity [76], vocabulary size [77], moral signaling [78], and even subclinical characteristics of schizophrenia [79], bipolar disorders [80], and autism [81].