Flow Collapse Model: A Mechanistic Hypothesis Linking Digestive Infrastructure Failure, Nitrogen-Handling Burden, and Fibrin-Related Microvascular Dysfunction in ME/CFS

This paper presents a mechanistic extension of the Flow Collapse Model (FCM), a systems-level framework proposing that chronic systemic dysfunction can emerge when the physiological infrastructure required to digest, absorb, process, transport, and eliminate biological substrates becomes constrained. The present paper applies this framework to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and proposes two candidate pathways through which upstream digestive dysfunction may contribute to downstream mitochondrial and energetic impairment: increased gut-derived nitrogen and ammonia burden in the setting of constrained nitrogen-handling capacity, and coagulation and fibrin-related microvascular dysfunction affecting tissue perfusion, oxygen delivery, and substrate exchange. The paper integrates existing findings on nitrogen metabolism, endothelial dysfunction, coagulation abnormalities, fibrinaloid microclots, and mitochondrial dysfunction in ME/CFS with hypothesis-generating self-observations from the author's recovery trajectory. A central proposition of the model is that biological recovery may be sequence-sensitive: increasing substrate supply before restoring the capacity required to process that substrate may fail or worsen symptoms, whereas the same substrate may become beneficial after upstream constraints are reduced. This paper is intended as a testable mechanistic hypothesis, not as a validated treatment protocol. Its primary contribution is the proposed causal architecture linking digestive infrastructure, nitrogen handling, vascular function, and mitochondrial energy metabolism.