A Constant Function Model of Cluster B Personality Disorders: Predictions from Secondary Universe Theory

Abstract

Secondary Universe Theory (SUT) proposes that persistent false belief structures share a common architecture across domains: a clearly defined function served by a systematically undefined mechanism, in which a deus ex machina — an agent, force, or principle — bypasses cause and effect, delivering whatever conclusion the narrative requires regardless of what reality provides as input (Bahtışen, 2026). The theory proposes a six-stage sequential process through which these structures are constructed, a cortisol-dopamine feedback loop proposed to render them neurochemically self-maintaining, and four psychological benefits (meaning, belonging, explanation, agency) that explain their persistence. If this architecture describes a general process of narrative belief construction, personality disorders characterized by systematic self-narrative distortions should produce specific, predictable variations in secondary universe formation, function, and resistance to correction. This paper identifies Cluster B personality disorders as a natural test case: all four disorders involve identity-level narrative construction where SUT's constant function and neurochemical lock are proposed to operate most directly. The paper derives five predictions each for Narcissistic Personality Disorder (NPD) and Borderline Personality Disorder (BPD), four predictions each for Histrionic Personality Disorder (HPD; treated as exploratory given the thin empirical base) and Antisocial Personality Disorder (ASPD), and evaluates each prediction against existing peer-reviewed clinical literature. A cross-disorder comparison reveals that NPD and BPD may instantiate the same SUT process with different targets of the constant function — NPD installing the agent in the self, BPD installing it in the other — a differential prediction that no existing framework generates from a single underlying architecture. A novel 2×2 matrix (target × strategy) organizing all four Cluster B disorders produces testable predictions about treatment responsiveness and neurochemical profiles. Explicit falsification criteria with operationalized thresholds are specified for each core construct. Brief speculative extensions to Clusters A and C are proposed. Limitations are addressed, including the absence of empirical validation for SUT itself, the risk of post-hoc redescription, and the competing explanatory power of attachment theory and stress neuroscience.