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The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms
The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms
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The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms
The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms

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The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms
The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms
Journal Article

The Triangular Model of Psychological Stress, Sleep Disorders and Food Addiction in T2DM: An Integrative Review Based on Shared Molecular Mechanisms

2026
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Overview
The prevalence of type 2 diabetes mellitus (T2DM) continues to rise, and traditional models fail to fully explain its pathogenesis, particularly the frequent co-occurrence of T2DM with mental health disorders. Based on a systematic integration of epidemiological and molecular biological studies, this review organises existing evidence into a \"psychological stress-sleep disturbance-food addiction\" triangular framework, drawing together observations that have mostly been discussed in isolation. In this model, the three factors form a self-perpetuating vicious cycle through bidirectional interactions, which may synergistically amplify the risk of both T2DM and comorbid mental health conditions via shared molecular pathways. Mechanistically, the model operates through three tiers of pathological amplification: central drive (HPA axis and autonomic imbalance), peripheral effects (glucocorticoid resistance-driven inflammation and metabolic dysregulation), and tissue damage (insulin resistance and β-cell dysfunction). Glucocorticoid resistance serves as the key link connecting central overdrive to amplified peripheral inflammation. The same neuroendocrine and inflammatory pathways are implicated in mood and cognitive disturbances, suggesting a biological basis for the mental-metabolic comorbidity observed clinically. This framework provides an integrated understanding of how psychosocial and dietary factors converge on common biological targets and offers a theoretical foundation for developing integrated nutritional and psychological prevention strategies.