Abstract
This paper proposes a specific neuro-immunometabolic pathway linking chronic compensatory regulation to mitochondrial dysfunction. It argues that the sustained metabolic cost of navigating a non-calibrated environment triggers a cascade of immune responses that ultimately disrupt cellular energy production — providing a biological mechanism for the profound fatigue, brain fog, and physical exhaustion characteristic of autistic burnout. The paper provides falsifiable biomarker predictions and a proposed study design.
Research Question
What is the specific molecular pathway?
Plain Language Summary
When your brain works harder just to function in everyday situations, your body pays the price. This research looks at the physical health effects of that extra effort — how constant stress from masking and compensating can lead to real, measurable damage to your immune system and energy production at the cellular level.
Position in the Research Program
This paper provides the biological mechanism that explains the experiential findings in Paper III. It takes the computational model of energetic asymmetry from Paper II and shows how sustained metabolic cost translates into measurable physiological damage — connecting the abstract to the concrete. The architectural distinction from Paper I determines which bodies bear this biological burden: those whose cognitive architecture is mismatched to their environment pay the highest physiological price. Paper V integrates this mechanistic pathway into a broader ecological model showing how environmental demands trigger a cascade from cognitive effort through physiological stress to bodily degradation. The Cultural/Representational level (Paper VI) spans this mechanistic level, showing how cultural narratives determine which biological pathways are studied, which symptoms are legitimized, and which bodies are treated as inherently defective rather than systematically exploited.