There is a need for a new pathophysiological model explaining and linking the role of numerous non-genetic factors believed to contribute to origins of many chronic physical diseases. This article presents a theoretical model for explaining the confusing and often contradictory findings regarding the role of environmental influences in type 1 diabetes, a disease that has been widely studied, for which clear diagnostic criteria exist, and for which development of effective prevention strategies represents significant challenges. The model is formulated from the large database of research regarding increasing understanding of the interaction between environmental factors, physiology, and autonomic regulatory function. Data is integrated from research in the fields of the experience-dependent maturation of the nervous system and the neurophysiology of traumatic stress to demonstrate how disruptions in early bonding and attachment, including adverse events such as traumatic stress, are capable of causing: (1) long-term imbalances in autonomic regulatory function and (2) relative dominance of sympathetic or parasympathetic activity. The proposed model of autonomic dysfunction suggests that ongoing mechanisms promoting high glucose in the context of decreasing insulin production in type 1 diabetes represent a state of relative sympathetic dominance influenced by environmental factors affecting autonomic, immune and endocrine systems during critical period programming. The model further identifies a link between the many seemingly unrelated non-genetic risk factors, and appears capable of explaining contradictions and enigmas in epidemiological and clinical studies regarding non-genetic origins of type 1 diabetes, including the role of stress, variation in age of onset, and duration of the preclinical phase.