Hypothesis-driven framework explores demographic, neurochemical, and sensory connections between conditions, suggesting shared mechanisms.
This manuscript presents a hypothesis-driven, integrative framework examining potential overlap between autism spectrum disorder and fibromyalgia through demographic patterns, neurochemical findings, and shared sensory and pain-related features. Drawing on published literature across neurodevelopment, chronic pain, and central sensitization research, the work explores how altered excitatory–inhibitory balance, sensory hypersensitivity, and cumulative stress may contribute to chronic pain presentations in a subset of individuals. The manuscript highlights a demographic inversion in diagnosis, with autism disproportionately identified in young males and fibromyalgia disproportionately identified in middle-aged women, and discusses how diagnostic siloing may obscure shared nervous system mechanisms. Neurobiological evidence related to glutamatergic and GABAergic signaling, particularly within the insular cortex, is reviewed in relation to sensory processing and pain amplification. This work is theoretical and hypothesis-generating in nature. It does not provide clinical guidance, diagnostic criteria, or treatment recommendations. The aim is to support interdisciplinary discussion, inform future research, and offer clinicians and patients an additional conceptual lens for understanding chronic pain and sensory sensitivity.
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Timothy Johnson (2026) studied this question.
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