The metabolic matrix hypothesis of recurrent BPPV: Otoconia–otolithic membrane–endolymph fragility

Benign paroxysmal positional vertigo (BPPV) is treated as a purely mechanical disorder of displaced otoconia, yet this model alone does not readily account for spontaneous otoconia detachment, bilateral or multicanal disease, high recurrence rates, or the clustering of BPPV with systemic metabolic conditions in a subset of patients. This article proposes and structures a unifying mechanistic model—the Metabolic Matrix Hypothesis—linking systemic metabolic states to otoconial fragility, and derives testable predictions from it. It is a hypothesis-generating narrative and theoretical synthesis—not a systematic review or meta-analysis—of otoconial matrix biology, otolithic membrane anchoring, endolymph chemistry, and the dispersed clinical literature on metabolic risk factors for BPPV. Evidence supporting each proposed pathway is graded narratively as established clinical association, experimental or animal evidence, mechanistic inference, or speculative extension. In a biologically distinct subset of patients, recurrent idiopathic BPPV may represent the mechanical expression of a systemic metabolic fragility of the otoconia–otolithic membrane–endolymph unit. Vitamin D deficiency, estrogen withdrawal, osteoporosis, insulin resistance, oxidative stress, thyroid autoimmunity, and microvascular insufficiency may act as convergent entry points into impaired matrix resilience rather than independent risks. The model generates testable predictions and a clinically accessible metabolic evaluation for recurrent, bilateral, or multicanal disease, complementing repositioning maneuvers.