This preprint presents a system-dynamic interpretation of gout, proposing that disease flares reflect threshold-driven transitions rather than isolated inflammatory events. Gout is traditionally understood as a metabolic disorder driven by hyperuricemia and monosodium urate crystal deposition. However, its episodic clinical course — with abrupt flares separated by asymptomatic periods — is more consistent with a system approaching instability and undergoing state transitions. This paper introduces a framework in which rising urate levels gradually destabilize the joint environment, increasing susceptibility to perturbations that can trigger acute inflammatory flares. From this perspective, urate-lowering therapy functions not only as biochemical correction, but as a stabilization strategy that shifts the system below the threshold required to sustain flare-generating dynamics. The model provides a coherent explanation for recurrent flare cycles, paradoxical flares during treatment initiation, and the importance of sustained urate control in long-term disease management. This work contributes to a broader system-dynamic perspective on disease, in which clinical behavior is understood as the result of changing system stability rather than static pathological states.
Anita Domargård (Tue,) studied this question.