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This paper reframes thiamine deficiency through the lens of pericyte biology. Pericytes, mural cells central to capillary tone, barrier integrity, immune gating, and extracellular matrix regulation, operate at near-maximal energetic load with mitochondria comprising up to 40% of their cytoplasm. Their reliance on thiamine-dependent enzymes makes them the earliest and most sensitive site of insufficiency. While classical deficiency states such as beriberi and Wernicke’s encephalopathy represent catastrophic collapse in neurons or cardiomyocytes, modern populations more often exhibit functional insufficiency—systemic thiamine levels appear adequate while local depletion in pericytes drives diffuse syndromes: cognitive slowing, microvascular fragility, immune dysregulation, and metabolic inflexibility. By synthesizing evidence across vascular biology, bioenergetics, and clinical nutrition, the paper proposes a unifying model of thiamine insufficiency as a pericyte-driven terrain pathology. This perspective explains the heterogeneity of subclinical symptoms, elevates thiamine from a minor micronutrient to a determinant of vascular–immune–metabolic stability, and suggests new diagnostic and therapeutic strategies grounded in functional assays and pericyte biology.For full elucidation of Pericyte Biology, see: Decoding Topical Steroid Rebound Phenomena: The Pericyte Connection.