Type 2 diabetes mellitus (T2D) is characterized by progressive insulin resistance and beta cell failure, resulting in chronic hyperglycemia. The standard model attributes this deterioration to adiposity, sedentary behavior, and genetic predisposition, but does not fully explain why the deterioration is progressive and self-sustaining in patients who maintain adequate insulin production, or why certain interventions (bariatric surgery, extreme caloric restriction) produce remission in timeframes too short to reflect the structural changes the model invokes. This paper applies the biochemical computer framework (Craddock, 2026a; 2026b) to propose that T2D represents a stuck program mode in which the glucose harvesting capability of the commensal fungal symbiont Candida albicans runs continuously without phase transition. The organism possesses Hgt4, a membrane glucose sensor calibrated to approximately 5 mM human blood glucose. Its colonization measurably alters GLP-1, GIP, and insulin levels (Peroumal et al., 2022). The framework proposes that the modern dietary environment, providing effectively unlimited glucose, prevents the substrate shift signal that would normally advance the organism's program to the next phase. The resulting continuous glucose draw produces the progressive insulin resistance and eventual beta cell failure observed clinically. Five testable predictions are presented, including proposed studies correlating organism density with insulin resistance severity and differential therapeutic response.
Jim Craddock (2026) studied this question.