Background/Objectives: Intentional insulin omission (IIO), commonly referred to as diabulimia, is a high-risk behavioural phenomenon observed mainly in adolescents and young adults with type 1 diabetes mellitus (T1D). Defined as the deliberate reduction or omission of insulin to influence body weight, IIO lies at the intersection of metabolic management and eating disorder psychopathology. Despite serious health risks, including diabetic ketoacidosis, microvascular complications, and increased mortality, it remains under-recognised due to stigma, diagnostic ambiguity, and overlap with routine diabetes self-management. This review aimed to examine the prevalence, psychological mechanisms, and clinical consequences of IIO. Methods: On 1 April 2026, we conducted a systematic search of PubMed, Scopus, APA PsycInfo/PsycArticles and Cinahl for studies investigating intentional insulin omission and related metabolic and psychological outcomes in T1D. Clinical and epidemiological studies assessing prevalence, risk factors, and interventions were included. Results: Twenty-nine studies met the inclusion criteria. Prevalence estimates ranged from 20% to 45%, with higher risk among females, adolescents, and individuals experiencing diabetes-related distress or body dissatisfaction. Psychological factors—including fear of weight gain, emotion dysregulation, depressive symptoms, and identity conflicts—were associated with IIO onset and maintenance. IIO was consistently linked to poor glycaemic control, elevated HbA1c levels, and adverse metabolic and psychological outcomes. Screening tools such as the Diabetes Eating Problem Survey–Revised (DEPS-R) may support early identification, while effective management requires integrated multidisciplinary care. Conclusions: Although IIO is not formally classified as an eating disorder in current diagnostic systems, it shares important psychopathological features with eating disorders and may represent a diabetes-specific disordered eating behaviour with life-threatening consequences.

Emotion dysregulation and altered interoceptive processing are increasingly recognized as core processes in eating disorder (ED) psychopathology. Difficulties in identifying, tolerating, and regulating negative emotional states may interact with reduced trust in bodily signals and distorted interpretation of hunger and satiety cues, contributing to maladaptive eating behaviors. The aim of this PRISMA-guided qualitative systematic review was to synthesize original empirical evidence on the interaction between emotion dysregulation and interoceptive processing in EDs, with particular attention to how emotional distress may be misinterpreted as physical hunger or food-related urges. A systematic search of PubMed and Scopus identified 78 records; after removal of duplicates and screening procedures, 24 original empirical studies were included in the qualitative synthesis. Across ED presentations, emotion dysregulation consistently emerged as a central transdiagnostic process associated with symptom severity, impulsivity, maladaptive eating behaviors, and related risk outcomes. Interoceptive alterations were widely reported, particularly involving reduced body trust and distorted interpretation of internal sensations rather than a uniform deficit in interoceptive sensitivity. The reviewed studies also showed that emotional states and cognitive expectations may shape the appraisal of hunger and satiety cues, contributing to the misinterpretation of emotional distress as physiological need across restrictive, binge-purge, and binge-eating presentations. The findings support a close interplay between emotion dysregulation and altered interoceptive processing in EDs and highlight the clinical relevance of interventions that integrate emotion regulation and interoceptive awareness to promote more adaptive eating behaviors.

The skin–brain axis constitutes a complex, bidirectional network integrating cutaneous sensory, immune, and neuroendocrine systems with central neural circuits involved in emotion regulation, stress responsivity, and social cognition. Advances in psychodermatology and cosmetic science have progressively extended this framework to the emerging field of neurocosmetics, which explores how topical formulations, sensorial properties, and cutaneous neuromodulators may influence psychological well-being, affective states, and perceived stress. The aim of this narrative review is to synthesize current evidence on the biological foundations of the skin–brain axis and to critically examine the implications of these mechanisms for neurocosmetic interventions from a psychological and psychiatric perspective. It describes the biological substrates underlying skin–brain communication, including the cutaneous hypothalamic–pituitary–adrenal axis, neuropeptides, neurotrophins, transient receptor potential channels, and endocannabinoid signaling, and examines how these pathways are targeted by neurocosmetic interventions. Particular attention is devoted to neuroactive compounds, such as peptides, cannabinoids, botanicals, and aromatherapeutic molecules, as well as to sensorial strategies involving texture, temperature, and olfactory cues, which may modulate mood, anxiety, and self-perception through peripheral mechanisms. From a psychological and psychiatric perspective, the review discusses the intersection between stress-related skin conditions, body image disturbances, and emotional dysregulation, highlighting how cosmetic practices may influence subjective well-being beyond purely aesthetic outcomes. Methodological limitations of the existing literature, including the heterogeneity of study designs and outcome measures, as well as ethical considerations related to mood- and stress-related claims in cosmetic products, are critically examined. Finally, future research directions are outlined, and a translational framework is proposed to integrate dermatology, neuroscience, and mental health within next-generation cosmetic science.

Background/Objectives: Schizophrenia is a severe psychiatric disorder frequently characterised by sleep and circadian disturbances, which are closely linked to cognitive dysfunction, symptom exacerbation, and poor functional outcomes. A growing body of evidence implicates the orexin (hypocretin) system—an essential regulator of arousal, sleep–wake stability, metabolic processes, and motivated behaviour—in the pathophysiology and treatment response of psychotic disorders. We aimed to investigate the relationships between the orexinergic system and psychoses. Methods: On 3 March 2026, we searched the PubMed, Scopus, PsycInfo/Articles and Cinahl databases for studies dealing with the orexin system and psychotic disorders and treatment response. Results: We found 20 eligible studies reporting variable and inconsistent alterations in orexin signalling in patients with schizophrenia. Studies were mostly cross-sectional and heterogeneous in design. Antipsychotic medications interfere with orexin-dependent pathways, potentially contributing to both therapeutic effects and adverse outcomes such as sleep disruption and metabolic dysregulation. Conclusions: While evidence from preclinical studies could point to an influence of dopaminergic activity through orexinergic mechanisms, with possible attenuation of antipsychotic-induced motor side effects and improvement of attentional deficits associated with NMDA receptor hypofunction, the utility of dual orexin receptor antagonists (DORAs) in psychoses is unclear. Despite the high prevalence of insomnia in schizophrenia, its pharmacological management remains suboptimal, with current treatments often limited by reduced efficacy or tolerability concerns. DORAs, which are currently approved medications for the treatment of insomnia, represent a novel and mechanistically distinct therapeutic option that may improve sleep while modulating arousal- and cognition-related circuits relevant to psychosis.

Climate-related hazards are associated with adverse mental and physical health outcomes, but exposure-specific human findings are often discussed together with general stress mechanisms without clearly distinguishing their evidentiary strength. This narrative review addresses that gap by examining climate change as a context for recurrent thermal, disaster-related, and psychosocial stress, rather than as a single measurable exposure. Evidence is organized around three interacting biological domains: neuroendocrine regulation, inflammation and oxidative stress, and neuroplasticity. Human observational studies support associations between heat, extreme events, and mental health outcomes; short-term human experiments and animal models provide mechanistic insights but do not establish a chronic biological mediation pathway from climate change to psychiatric illness. Indirect pathways include displacement, livelihood disruption, loss, and anticipatory distress. Air pollution is treated as an interacting exposure with both climate-related and independent determinants. Eco-anxiety, climate anxiety, eco-distress, and ecological grief are distinguished from diagnosable disorders, with clinical relevance assessed through functional impairment and individual context. The review’s contribution is an evidence-qualified framework linking exposure timing, biological plausibility, psychosocial appraisal, and unequal adaptive capacity. Practical implications include contextual mental health assessment, continuity of psychiatric care during heat and disasters, and incorporation of psychosocial support into adaptation planning. The proposed framework remains hypothesis-generating and requires prospective testing with repeated exposure, biomarker, and clinical assessments.