POTENTIAL ROLE OF MICROBIOTA–GUT–BRAIN AXIS DYSFUNCTION IN PROCRASTINATION-LIKE BEHAVIOR IN DIABETES

Abstract

Procrastination, the voluntary delay of intended actions despite anticipated negative consequences, represents a significant behavioral barrier to effective diabetes self-management. While traditionally conceptualized as a psychological or personality-related trait, emerging evidence suggests that procrastination-like behaviors in diabetes may have neurobiological underpinnings rooted in the pathophysiology of the disease itself. This review synthesizes current evidence linking microbiota–gut–brain axis (MGBA) dysfunction to the triad of dopaminergic signaling deficits, neuroinflammation, and cognitive impairment that collectively may drive procrastination-like behaviors in diabetic patients. We proposed a mechanistic framework whereby diabetes-induced gut dysbiosis triggers systemic and neuroinflammation via microbial metabolite dysregulation and increased intestinal permeability, which in turn disrupts central dopaminergic reward circuitry and impairs executive functions, particularly cognitive flexibility, inhibition, and planning. These converging pathologies may contribute to a neurobehavioral state characterized by reduced motivational drive, impaired self-regulation, and diminished capacity for goal-directed behavior, manifesting clinically as health-related procrastination. Understanding this axis offers novel therapeutic opportunities targeting the gut microbiome, inflammatory pathways, and dopaminergic signaling to improve behavioral outcomes in diabetes care.