The Forgotten Infectious Hypothesis of Diabetes: Reframing Parasitic, Immunological, and Pancreatogenic Pathways as Drivers of Global Metabolic Disease

ABSTRACT Diabetes mellitus is traditionally classified as a non-communicable metabolic disorder. However, emerging evidence from parasitology, immunology, global health, and One Health research suggests that chronic parasitic infections may directly contribute to pancreatic injury, persistent immune activation, microbiome remodeling, and immune–metabolic dysregulation—mechanisms capable of initiating or accelerating diabetic phenotypes. This article reframes diabetes through an infectious–metabolic lens and proposes the Infectious–Metabolic Continuum (IMC), an integrative conceptual model linking helminths, protozoa, immunomodulatory pathways, and pancreatogenic processes. Special emphasis is placed on Type 3c Diabetes Mellitus (T3cDM), an underdiagnosed form of diabetes caused by exocrine pancreatic injury, often associated with neglected tropical diseases (NTDs). The article also discusses implications for the United States, Canada, and Switzerland (WHO/IARC/GAVI/FIND), highlighting diagnostic inequities, gaps in parasitic screening, and opportunities for new therapeutic strategies. Reintroducing the infectious hypothesis of diabetes opens new avenues for earlier detection, precision medicine, and global health equity.