Abstract / Summary
Type 2 diabetes is conventionally organised around glucose, yet glucose is abundant in the disease. This monograph proposes that the condition is better understood as a disorder of energy supply: a chronic deficit in the rate at which tissues can acquire usable energy. Hyperglycaemia, hyperinsulinaemia, and the progressive loss of regulatory precision are treated as consequences of that deficit rather than as parallel mechanisms beside it. A cell surrounded by substrate it cannot efficiently transduce is already in energy deficit; the clinical syndrome is what regulatory machinery does when it can no longer afford its own operation. Within the Informational Nosology corpus, diabetes is not given a separate module. It is represented as a transformation of parameters already present throughout the architecture: a reduction in energy supply and a rise in baseline noise. Quantitative comparison shows that coupling capacity is substantially more sensitive to supply than to noise, indicating that energy acquisition is the dominant constraint. From this deficit a single organising relation follows: the rate at which a tissue loses regulatory coherence depends on its local demand-to-reserve ratio and on the systemic energy shortfall. That ordering is tested against major post-trial cohorts and accounts for a pattern long regarded as awkward — durable microvascular benefit from early control, and durable macrovascular benefit mainly when intervention begins at diagnosis. Further results address selective insulin resistance, the distinction between borrowed and spent metabolic reserve, and a structural gap in the corpus’s treatment of restoration cost. The analysis remains non-vitalistic, non-substitutive with respect to clinical diabetology, and non-prescriptive. Keywords: type 2 diabetes; energy deficit; insulin resistance; metabolic reserve; remission; circadian regulation; Informational Nosology; regulatory coherence; systems metabolism