Psychopathology traditionally is represented as categories that implicitly refer to nosological entities (e.g. Major Depressive Disorder) or trans-diagnostic symptom dimensions based on symptom-level clustering (e.g. severity of depressive symptoms). Vinogradov and colleagues [1] proposed an associationist model of the symptom dimension of paranoia and suggested that the origins of psychopathology may lie in a network of mental states giving rise to acute phase transitions that Odgers and colleagues showed can be modelled as part of a dynamic system [2]. According to recent elaborations and extensions of this model, psychopathology can be conceptualized as a network of causally linked sets of symptoms, which reciprocally impact on each other over time to progress toward a more distinct syndrome forged through a specific pattern of a dynamic network for each syndrome [3–6].

The conceptualization of psychopathology as a dynamic network of symptoms may provide a particularly useful tool to understand pathways to mental illness. For example, transition of a false belief to a crystallized delusion can be modelled as a vicious cycle composed of interacting steps, in which an initial paranoid state, arising out of malformed hyperconnectivity among temporally contiguous perceptions, becomes fixated through perpetuation of an internally generated maladaptive schema to explain odd experiences [1]. Hyperconnectivity may also expand through the network across symptom domains, triggering a chain reaction, wherein the primary false belief (e.g. persecutory delusional ideation) may provoke anxiety under certain circumstances (e.g. being in public), which in turn leads to a misperception of external stimuli (illusions and hallucinations) that creates added confusion and anxiety which further impairs logical thought process, and solidifies delusionary explanation that finally becomes a fixed delusion.

Recent findings in large general population cohort studies suggest that exposure to environmental risk factors (childhood trauma, urbanicity, cannabis use, and discrimination) reinforces connectivity between symptoms of affective dysregulation and psychosis expression in a dose response fashion, in accordance with the theory of environment-induced disturbances spreading through the psychopathology network, increasing psychosis admixture, and progressively expanding and reinforcing connectivity that ultimately gives rise to transition to a more severe, distinct clinical syndrome requiring medical care [7–12].

If the environment impacts on the connection between psychosis and affective dysregulation, the question rises to what degree this is specific for these two domains of psychopathology. An alternative explanation is that the environment broadly impacts on the connectivity between domains of psychopathology. The emergence of psychosis may then be seen as an indicator of general severity of increasingly connected psychopathology, rather than a specific illness category [9, 13–15]. In the light of these findings, we hypothesize that the degree of exposure to environmental factors that are known to be associated with mental health would increase the extent of connectivity between symptom dimensions. Therefore, the aim was to investigate to what degree environmental exposure impacts on symptom connectivity analysing measures of psychopathology in two independent, general population datasets. In order to examine to what degree the findings would be stable across categorically and dimensionally defined psychopathology, connectivity was examined at the level of both continuous dimensions of self-reported psychopathology using the Self-report Symptom Checklist-90-R (SCL-90-R) and binary DSM-III-R categories of mental disorders and a binary measure of psychotic symptoms.