BACKGROUND: Eating disorders (EDs) and ultra-processed food use disorder (UPFUD) have traditionally been examined as separate entities, resulting in ongoing tension between two primary perspectives: (1) dietary restraint as the main driver of loss-of-control eating pathology, and (2) the influence of the contemporary food environment, combined with stressors, as the driver of addiction-like food consumption. Both perspectives acknowledge developmental trauma as a key predisposing factor.

METHODS: Drawing from relevant articles in the PubMed, Scopus, PsycINFO, and Google Scholar databases, this theoretical review combines evidence from trauma, neurodevelopmental, eating disorder, and addiction research. Relevant articles are synthesized to propose a unified life course model. The model integrates these perspectives by outlining developmental trajectories that originate from shared risk factors, diverge along distinct pathways, and may ultimately converge into similar behavioral presentations.

RESULTS: The Restrictive Eating Pathway typically progresses from generational trauma through parental symptoms of rigid/disordered eating patterns and/or obsessive-compulsive disorder (OCD) familial traits. In this context, adverse childhood experiences (ACEs) may further influence conditions conducive to dieting and eating disorder (ED) symptoms. This may culminate in pathologically restrictive eating patterns, which may include addictive processes. The Addictive Eating Pathway similarly progresses from generational trauma through parental symptoms of substance use disorders (SUDs) and/or attention-deficit/hyperactivity disorder (ADHD) familial traits. In this context, ACEs may further influence conditions conducive to hedonic eating, which can progress to UPFUD symptoms and other addictive processes, such as SUDs. Both pathways share generational trauma and ACEs as foundational risk factors. Familial OCD symptoms versus familial ADHD symptoms represent divergent predisposing legacies that can highlight differential risk when parental mental health assessment is available. Individual-level SUD frequently co-occurs in both pathways and, when present, may serve as a point of convergence or crossover, connecting or reflecting trajectories.

CONCLUSIONS: This model emphasizes bidirectionality across constructs, conceptualizes eating pathology as a dimensional continuum rather than discrete categories, and acknowledges that individuals may transition between pathways throughout the lifespan. Implications for clinical assessment, treatment planning, prevention strategies, and the emerging fields of precision neurodiversity and metabolic psychiatry are discussed. This framework establishes a foundation for the understanding of mixed restrictive-addictive presentations and offers testable hypotheses for future longitudinal and mechanistic research.