Type 2 diabetes mellitus (T2DM) is commonly attributed to insulin resistance, defined as impaired responsiveness of skeletal muscle, adipose tissue, and liver to insulin. Although the concept is deeply embedded in modern metabolic medicine, it remains largely inferential and descriptive. This paper critically examines the conceptual, physiological, and epidemiological limitations of the insulin resistance paradigm. It argues that the model lacks a demonstrated unifying mechanism capable of coordinating selective impairment across multiple tissues, does not adequately explain preservation of many insulin-mediated functions, and leaves unresolved several clinical paradoxes, including rapid reversibility of hyperglycemia, metabolically healthy obesity, and diabetes in lean individuals. The paper further argues that the speed with which T2DM prevalence has risen is difficult to reconcile with explanations grounded in intrinsic cellular defects or evolutionary adaptation. An alternative interpretation based on chronic substrate overload and altered metabolic flux is presented as a more coherent framework for understanding the observed phenotype. This reinterpretation has implications for both research priorities and therapeutic strategy, suggesting that reduction of metabolic load and restoration of substrate balance may be central to effective management. Reassessment of insulin resistance as a primary causal construct may therefore be necessary for progress in the prevention and treatment of type 2 diabetes.