Agata Benfante

Central sensitization (CS) has been considered a precursor of different nociplastic pain (NP) conditions and it has been considered a core pathophysiological mechanism involved in the maintenance of these syndromes. Clinical frameworks and empirical evidence have suggested that traumatic experiences (TEs) might play a role in the development of CS and they could represent relevant factors reinforcing clinical manifestations characterizing NP conditions. Nevertheless, there are no studies that have empirically tested whether TEs might be involved in CS features across the NP spectrum and how TEs together with CS could affect the quality of physical and mental health among these conditions. The current study enrolled a sample of 464 participants, including treatment-seeking patients with chronic migraine (CM; N = 97), fibromyalgia (FM; N = 130) and comorbid FM-CM (N = 91) together with a healthy control (HC; N = 141) group. TEs, CS and quality of physical and mental health were assessed by self-report instruments. ANCOVA, MANCOVA and moderated mediational models were conducted. Patients with FM-CM showed the highest levels of traumatization (F_{(3, 459)} = 6.15; p < .01), especially compared to CM (d = .40) and HC (d = .56). TEs were significantly associated to CS symptoms across the NP spectrum (a: b = .31; p < .05), independently of condition. Furthermore, TEs indirectly affected the quality of physical and mental health (-.19 ≤ ab ≤ -.06; [-.30 - -.01]) of patients with NP conditions through CS (b: -.66 ≤ b≤ -.55; p < .001). This is the first study that has supported a key role of TEs in core pathophysiological mechanisms of NP syndromes, especially those characterized by complex and severe manifestations. These data support the systematic inclusion of evidence-based psychotherapeutic strategies for trauma-related reactions in the treatment of NP conditions.

The scientific literature unanimously assumes that intimate partner violence (IPV) increases the vulnerability of victims to such an extent that the link between this type of violence and suicide appears to be particularly critical. The aim of this scoping review was to summarize the scientific evidence on the prevalence of suicide—suicidal ideation, attempts, and completions—in women who were victims of IPV admitted to emergency departments (EDs) due to suicide attempts. The review was conducted in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis for Scoping Review. The PubMed, Ebsco, and Web of Science databases were systematically searched using a string of Boolean operators that combined multiple synonyms of IPV, suicide, and EDs. The inclusion criteria were: adult women who were victims of IPV; being admitted to the ED for suicide attempts, and/or died by suicide; with or without a comparison group; and quantitative studies with all types of study design. The review included 22 studies from 1995 to 2023. All studies emphasized the extent to which a history of IPV particularly affects the psychological well-being of victims, limiting their sense of agency and impoverishing their identity and self-esteem, so that suicide was often seen as a way out of what had already occurred for many victims: a sense of psychological disintegration. A further urgency is to prevent the persistence of IPV, as this means preventing women from suicidal thoughts and attempts.

Irritable Bowel Syndrome (IBS) and Metabolic dysfunction-associated fatty liver disease (MAFLD) have traditionally been viewed as disorders of distinct organ systems. IBS is a gut–brain axis disorder characterized by abdominal pain, altered bowel habits, and psychological comorbidities. MAFLD, recently redefined to emphasize its metabolic underpinnings, is the hepatic manifestation of systemic metabolic dysfunction. Growing evidence suggests that these conditions share overlapping pathophysiological mechanisms linked through disruption of the gut–liver–brain axis (GLBA), including psychological stress, gut dysbiosis, impaired intestinal permeability, systemic inflammation, and altered neuroendocrine signaling. Neuroimaging studies further reveal functional alterations in brain regions responsible for interoception, emotional regulation, and stress responsiveness in both disorders. This narrative review explores how psychological distress influences the onset and progression of IBS and MAFLD via GLBA dysfunction and stress-induced epigenetic reprogramming. A targeted literature search of major biomedical databases, supplemented by manual screening, identified relevant observational, clinical, neuroimaging, and molecular studies. Findings indicate that chronic psychological distress activates the hypothalamic–pituitary–adrenal (HPA) axis, elevates cortisol, disrupts gut microbiota, and reduces vagal tone; amplifying intestinal permeability and microbial translocation. These changes promote hepatic inflammation and gastrointestinal symptoms. Stress-related epigenetic modifications further impair GLBA communication, while psychological and lifestyle interventions may reverse some of these molecular imprints. Recognizing the shared neuromodulation and epigenetic mechanisms that link IBS and MAFLD opens promising avenues for integrated therapeutic strategies targeting the GLBA to improve outcomes across both conditions.

This exploratory prospective cohort study aimed to investigate the trajectory of psychological distress and posttraumatic growth (PTG) in rectal cancer patients from diagnosis to follow-up and to explore factors that could predict PTG and psychological distress at follow-up. We assessed psychological distress (anxiety and depression), PTG, physical symptoms, quality of life, cancer-related coping, state and trait affectivity, resilience, and alexithymia in 43 rectal cancer patients, M (SD) age: 61.6 (12.6); 67.4% men, after diagnosis (T0), after preoperative radiochemotherapy (T1), after surgical resection (T2), and 1 year after surgery (T3, follow-up). Psychological distress, especially anxiety symptoms, showed a significant reduction between T0 and T1 (p < .001), which increased again between T1 and T2 (p = .048). PTG showed a progressive increase, with a significant increase between T2 and T3 (p < .001). The exploratory hierarchical multiple regression analyses showed that low positive state affectivity (p = .005) and high health anxiety (p = .007) at T1 and high negative state affectivity (p = .012) at T3 were significant predictors of psychological distress at follow-up. Higher levels of PTG at T1 (p < .001) and greater use of adaptive coping styles of Fighting Spirit at T0 (p = .009) and Fatalism at T1 (p = .031) were significant predictors of PTG at follow-up. The (fluctuating and linear, respectively) trajectories of psychological distress and PTG seem to be related to the psychological reactions to the different treatment phases, especially diagnosis and preoperative treatment. Data suggest the need to implement psychological screening and tailored support programs aimed at fostering PTG and reducing psychological distress from the earliest phases of cancer treatment. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Irritable Bowel Syndrome (IBS) and Non-Alcoholic Fatty Liver Disease (NAFLD) are traditionally viewed as disorders of distinct organ systems. IBS is a gut–brain axis disorder characterized by abdominal pain, altered bowel habits, and psychological comorbidities, while NAFLD is the hepatic manifestation of metabolic syndrome and is associated with obesity and diabetes. Increasing evidence reveals shared pathophysiological mechanisms leading to dysfunction of the gut–liver–brain axis (GLBA) in both disorders, including psychological distress, gut dysbiosis, impaired intestinal permeability, systemic inflammation, and altered neuroendocrine signaling. Neuroimaging studies have shown that changes in the activity of brain regions involved in interoception, stress regulation, and emotional control may contribute to the development of both disorders. Chronic psychological distress activates the hypothalamic–pituitary–adrenal (HPA) axis, leading to increased cortisol release, alterations in gut microbial composition, and reduced vagal tone. This cascade increases intestinal permeability and microbial translocation, promoting hepatic inflammation and exacerbating gastrointestinal symptoms. Epigenetic control has emerged as a crucial intermediary, linking psychological experiences to long-lasting molecular changes. Chronic distress can impair the GLBA through epigenetic modifications of stress-related genes such as FKBP5 and NR3C1. Notably, psychological interventions may partially reverse these molecular changes, improving outcomes in both disorders. In this review, we explore how psychological distress shapes the clinical trajectories of IBS and NAFLD through GLBA dysfunction and neuroepigenetic reprogramming. Understanding these shared pathways opens the door to innovative, multidisciplinary strategies aimed at modulating the GLBA to improve outcomes in both disorders.