Depression is a multifactorial psychiatric condition with complex pathophysiology, increasingly linked to neuroinflammatory processes. The present review explores the role of neuroinflammation in depression, focusing on glial cell activation, cytokine signaling, blood–brain barrier dysfunction, and disruptions in neurotransmitter systems. The article highlights how inflammatory mediators influence brain regions implicated in mood regulation, such as the hippocampus, amygdala, and prefrontal cortex. The review further discusses the involvement of the hypothalamic–pituitary–adrenal (HPA) axis, oxidative stress, and the kynurenine pathway, providing mechanistic insights into how chronic inflammation may underlie emotional and cognitive symptoms of depression. The bidirectional relationship between inflammation and depressive symptoms is emphasized, along with the role of peripheral immune responses and systemic stress. By integrating molecular, cellular, and neuroendocrine perspectives, this review supports the growing field of immunopsychiatry and lays the foundation for novel diagnostic biomarkers and anti-inflammatory treatment approaches in depression. Further research in this field holds promise for developing more effective and personalized interventions for individuals suffering from depression.

The gut microbiota plays a crucial role in early-life development, influencing various aspects of health and disease. Dysbiosis, an imbalance in the gut microbiota, has been linked to multiple health conditions, including allergies, asthma, and obesity. In early life, the gut microbiota plays a key role in the development and maturation of the immune system. Probiotics, live microorganisms that confer health benefits when administered in adequate amounts, have emerged as a potential treatment approach for dysbiosis in early life. Dysbiosis can alter the resistance to pathogens, promoting atopic diseases, food sensitization, and infections such as necrotizing enterocolitis (NEC). Probiotics have been shown to modulate the composition and function of the gut microbiota in the perinatal and infant periods. They can increase the abundance of beneficial bacteria, such as Bifidobacteria and Lactobacilli, and reduce the levels of potentially harmful bacteria. Not all probiotics are created equal. The effects of probiotics can vary depending on the specific strain used. Probiotics have also been investigated for their potential benefits in other areas of infant health, such as reducing the risk of respiratory infections and improving growth and development. This review aims to analyze the current data in the literature and to evaluate the health benefits of probiotic administration in early life. Several studies have investigated the use of probiotics in preventing or treating allergic diseases, such as eczema and food allergies. While some studies have shown promising results, more research is needed to fully understand the benefits and risks of probiotics in early life. In conclusion, using probiotics to prevent dysbiosis-related conditions may be considered a method of ‘programming’ the individual for optimal health maintenance.

Background: Cardiovascular diseases (CVDs) are a leading cause of death globally, with a significant impact on public health and quality of life. In addition to traditional risk factors such as hypertension, diabetes, smoking, and hypercholesterolemia, a growing body of scientific evidence suggests the crucial role of psychosocial factors, including personality, in the development and prognosis of CVDs. In recent decades, researchers have focused on the so-called “type D personality.” Methods: Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a literature search was conducted using the PubMed/Medline, Scopus, and Cochrane databases. Fifteen studies were included in the final quantitative analysis, involving 5687 people. The qualitative assessment of the studies included in this meta-analysis was conducted adopting the Quality System Tool. Results: Several studies have shown a significant correlation between type D personality and an increased risk of CVDs, as well as a worse prognosis in patients with established CVDs. The overall quality of the studies included in this synthesis ranged from 0.70 to 0.96, indicating the general good quality levels of the studies (69%). The association between type D personality and CVDs in terms of prevalence underlined a raw proportion of 0.36. Conclusions: This study reinforces the significance of type D personality as a psychological risk factor for CVD, with implications for both disease prevalence and severity.

Objective: This meta-analysis aimed to examine the bidirectional association between PTSD and cardiovascular disease (CVD) by evaluating the following: (1) the risk of increased CVD incidence in individuals with PTSD; and (2) the prevalence of PTSD in patients with cardiovascular disease. Methods: Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a literature search was conducted of the PubMed/Medline, Scopus, and Web of Science databases without using a temporal publication range. For the PTSD-to-CVD direction, 18 studies were combined. For the CVD-to-PTSD direction, 11 studies that ascertained the incidence or prevalence of PTSD following a CVD event were combined. Results: The findings confirm the bidirectional and clinically significant relationship between CVD and PTSD. Conclusions: These data underscore the need to integrate trauma-informed approaches into cardiovascular care and stress management into psychiatric treatment to stop this pathological cycle.

Background: Depression is one of the leading causes of disability worldwide, with a significant impact on individuals’ quality of life. The use of antidepressants is fundamental in the treatment of this condition; however, it is essential to recognize that the use of these drugs can be associated with adverse effects, including cardiotoxicity. Methods: Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a literature search was conducted of the PubMed/Medline, Scopus, and Cochrane databases. Twenty studies were included in the final quantitative analysis. The Joanna Briggs Institute critical appraisal tool was used to assess the risk of bias. Results: It is possible to highlight a correlation between intake of antidepressants and development of cardiotoxicity. Analysis of the selected studies allows for an understanding of the importance of a multidisciplinary approach for the protection of these patients. Conclusions: Management of antidepressant-induced cardiotoxicity requires a thorough understanding of the pathophysiological mechanisms involved and a critical evaluation of the various therapeutic strategies available to promote clinical practice.

Ultra-processed foods (UPFs) represent a distinct dietary paradigm characterized by structurally simplified food matrices and chronic exposure to multiple additives, including emulsifiers, artificial sweeteners, and preservatives. Rather than acting in isolation, these compounds operate within a multi-additive environment that reshapes the gut ecosystem through convergent mechanisms. Emerging evidence suggests that additive-rich ultra-processed dietary environments may disrupt the gut ecosystem through three interconnected layers: (1) structural impairment of the intestinal barrier, including mucus erosion and tight-junction destabilization; (2) microbial metabolic shifts marked by short-chain fatty acid depletion, altered bile acid signaling, and enrichment of lipopolysaccharide-producing taxa; and (3) immune and inflammatory reprogramming promoting low-grade systemic inflammation. These processes collectively reduce ecosystem resilience—the capacity of the gut microbiota to resist and recover from perturbation. Vulnerability to additive-driven dysbiosis varies across the life course. During infancy, incomplete ecosystem stabilization may increase susceptibility to long-term ecological imprinting, whereas in older age, reduced microbial diversity and immune remodeling may impair recovery capacity following dietary stressors. In contrast, fiber-rich, minimally processed dietary patterns appear to enhance microbial resilience by reinforcing functional redundancy, metabolic buffering, and barrier integrity. Although much mechanistic evidence has been derived from experimental models, accumulating human data support the biological plausibility of additive-associated microbiota alterations. By integrating multi-additive exposure, ecosystem disruption, life-course modulation, and resilience within a unified framework, this review provides a mechanistically coherent model linking ultra-processed dietary environments to microbiota-mediated chronic disease risk. Here, we formalize this integrative perspective as the Three-Layer Ecosystem Disruption (TLED) Model.