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Traditional cognitive models often assume a stable biological substrate, focusing narrowly on memory, attention, and executive function. However, emerging evidence highlights the significant impact of inflammatory tone, autonomic regulation, and neuroimmune dynamics on cognition and learning.This paper proposes the Thought Generator–Thought Selector (TGTS) model: a new theoretical framework that conceptualises thought generation as a biologically reactive process, shaped by inflammatory signalling, gut-brain interactions, and autonomic flexibility. TGTS introduces "PreForm" — a biologically constrained window enabling cognitive selection and agency.Building on research in immunology, neurodevelopment, and network neuroscience, TGTS explains how chronic low-grade inflammation alters thought selection, impairs cognitive flexibility, and may drive neurodivergent outcomes. It reframes conditions such as ASD, ADHD, and anxiety not as deficits but as adaptive cognitive equilibria shaped by biological and environmental forces. This framework positions inflammation not merely as a pathological factor but as a fundamental substrate for adaptive learning and cognitive agency.