Humanistic Studies and Social Researches

Abstract Background: Cardiovascular disease (CVD) continues to be the foremost cause of death worldwide . Although established risk factors such as hypertension and smoking are well-recognized, a considerable amount of CVD risk remains unaccounted for, shifting focus toward psychosocial influences . Emotional suppression—the deliberate inhibition of emotional expression—constitutes an ineffective emotion regulation strategy with possible cardiotoxic effects.
Objective: This narrative review seeks to consolidate contemporary psychophysiological research to clarify the mechanisms through which habitual emotional suppression elevates CVD risk and contributes to adverse health outcomes.
Methods: A thorough literature review was performed using PubMed, PsycINFO, and Web of Science for publications between 1990 and 2025. Search terms included "emotional suppression," "expressive inhibition," "cardiovascular disease," "autonomic nervous system," "cortisol," "inflammation," and "endothelial function." Emphasis was placed on human studies exploring physiological pathways or clinical correlations.
Results: Current findings indicate that emotional suppression reliably initiates harmful psychophysiological processes: (1) amplified and sustained sympathetic nervous system activity alongside reduced parasympathetic function, (2) dysregulation of the hypothalamic-pituitary-adrenal axis, (3) heightened inflammatory responses, and (4) acute and potentially persistent endothelial impairment. Epidemiological research further connects trait suppression with greater incidence of hypertension, coronary artery disease, and cardiovascular mortality.
Conclusion: Chronic emotional suppression operates as a meaningful psychosocial stressor, fostering a pathogenic internal environment that accelerates atherosclerosis and cardiovascular incidents. Incorporating emotion regulation evaluation into cardiovascular risk assessment and implementing focused psychological interventions offer promising strategies for enhancing preventive cardiology within a biopsychosocial model.

Abstract Background: Emotional suppression, defined as the deliberate restraint of emotional expression, is frequently utilized by people with post-traumatic stress disorder (PTSD). While it may offer momentary relief, its persistent application is connected to negative long-term psychological and health outcomes. Examining this process through a psychophysiological lens is crucial for understanding the biological mechanisms involved.
Objective: This review consolidates contemporary research on the psychophysiological features and repercussions of chronic emotional suppression in trauma-exposed groups, with particular attention to autonomic nervous system, neuroendocrine, and central nervous system activity.
Methods: A narrative synthesis of literature published between 2000 and 2025 was performed, sourcing articles from PubMed, PsycINFO, and Web of Science. Key search terms encompassed "emotional suppression," "trauma," "PTSD," "psychophysiology," and related physiological metrics.
Results: Robust evidence demonstrates that emotional suppression in trauma patients correlates with heightened and rigid sympathetic arousal (e.g., reduced heart rate variability), dysregulated HPA axis function, and a neural pattern of excessive prefrontal effort paired with sustained limbic reactivity. These physiological markers are associated with increased PTSD symptom severity and contribute to greater allostatic load and physical health comorbidities.
Conclusion: Emotional suppression constitutes a biologically costly form of regulation that intensifies physiological stress responses and may perpetuate trauma-related pathology. Clinical interventions should prioritize helping patients replace suppression with more adaptive, antecedent-focused emotion regulation strategies to foster comprehensive resilience.

Abstract Background: Although oncology traditionally emphasizes survival rates, the patient's journey is deeply influenced by their subjective experience and psychological state. Continuity of Care (CoC)—the consistent, coordinated, and unified management of care over time—is increasingly recognized as a vital element that extends beyond its possible effects on mortality.
Objective: This review consolidates current research to explore how CoC affects patient-reported experience measures (PREMs) and mental health results in individuals with cancer.
Methods: A systematic search of databases (including PubMed, PsycINFO, CINAHL) was performed for studies published from 2000 to 2024. Search terms comprised "continuity of care," "cancer," "oncology," "patient experience," "quality of life," "anxiety," "depression," "care coordination," and "therapeutic alliance."
results: Substantial evidence shows that greater CoC is reliably linked to better patient experiences, including enhanced communication, trust, and security. Additionally, CoC serves as an important protective factor against psychological illness, lowering anxiety, depression, and sensations of abandonment, especially during care transitions and survivorship.
Conclusion: CoC is a core, adjustable component of quality cancer care that directly improves patients' care experiences and protects their mental health. Emphasizing CoC through intentional models and policies is crucial for realizing genuinely patient-focused oncology.

Abstract Objective: This review aims to integrate and critically evaluate the existing neurobiological evidence concerning Obsessive-Compulsive Personality Disorder (OCPD). It synthesizes findings from neuroimaging, genetic, and neuropsychological studies to propose a distinct etiological model that differentiates OCPD from Obsessive-Compulsive Disorder (OCD).
Methods: A systematic literature search was conducted across PubMed, PsycINFO, and Google Scholar for studies published between 1990 and 2025. Keywords included “obsessive-compulsive personality disorder,” “neurobiology,” “neuroimaging,” “genetics,” and related terms. Studies were included if they provided original empirical data on the neurobiology of OCPD or its core traits. Data were narratively synthesized due to methodological diversity.
Results: Fifty-six studies met the inclusion criteria. Structural MRI findings indicate increased grey matter volume in the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC). Functional MRI studies reveal hyperactivation in the DLPFC, dorsal ACC, and fronto-parietal network during tasks of cognitive control and error monitoring, alongside reduced connectivity with limbic regions. Neurochemical evidence points to dysregulation in serotonin and dopamine systems. Genetic studies show high heritability (approximately 50–78%) and potential associations with genes such as SLC6A4, COMT, and DRD3. Neuropsychological profiles reflect intact planning abilities but impairments in cognitive flexibility and heightened error sensitivity.
Conclusion: OCPD is associated with a unique neurobiological profile characterized by overactive prefrontal cognitive control systems and diminished integration with emotional processing regions, rather than the fear-based circuitry typical of OCD. This “hyper-executive” model accounts for core OCPD traits such as perfectionism, rigidity, and excessive need for order. Future research should prioritize well-defined OCPD cohorts to validate this model and develop targeted, biologically informed interventions.