Depressive disorder is the most prevalent mental illness, and increasing evidence suggests its potential bidirectional relationship with metabolic disorders. Given the limited efficacy of conventional antidepressants (including Selective Serotonin Reuptake Inhibitors; SSRIs) and the growing prevalence of treatment-resistant depression, there is a significant need to identify alternative molecular pathways underlying the pathophysiology of depressive disorder, which may represent novel therapeutic targets for other agents. Emerging evidence indicates that metabolic dysfunction and depressive disorder share a common pathophysiological molecular mechanism and increase each other’s risk. Targeting peripheral metabolic pathways and their interactions with the central nervous system may alleviate depressive symptoms. Glucagon-Like Peptide-1 agonists (GLP-1 RAs) and Sodium–Glucose Cotransporter-2 (SGLT2) inhibitors, widely used in the treatment of type 2 diabetes and obesity, exhibit neurotrophic and anti-inflammatory effects, ameliorate oxidative stress, and enhance mitochondrial function, collectively contributing to the antidepressant-like effects observed in preclinical studies. Peroxisome Proliferator-Activated Receptor (PPAR) α agonists primarily regulate lipid and glucose metabolism, which may potentially improve neuronal plasticity and mood regulation. Moreover, agents such as Angiotensin Receptor Blockers (ARBs) and Angiotensin Receptor-Neprilysin Inhibitors (ARNIs), used in hypertension treatment, exert central anti-inflammatory and neuroprotective effects via the modulation of the renin–angiotensin–aldosterone system (RAAS), implicated in affective disorders. Nevertheless, long-term, head-to-head trials are required to establish their efficacy, safety, and therapeutic positioning within current treatment paradigms. The aim of this review is to summarize current evidence on metabolic modulators as potential antidepressant strategies, focusing on their molecular mechanisms, preclinical and clinical findings, and prospects for integration into future therapies for depression.

Background and Aim: Depression and cardiovascular diseases (CVDs) are major global health burdens with significant overlap. Increasing evidence supports a bidirectional relationship between them, driven by shared mechanisms such as HPA axis dysregulation, inflammation, autonomic imbalance, and behavioral risk factors. Depression increases the risk of cardiovascular events and worsens outcomes in CVD patients. This review explores psychocardiological mechanisms behind this comorbidity and assesses the efficacy of pharmacological and behavioral treatments—including cognitive behavioral therapy (CBT), cardiac rehabilitation programs (CRPs), and consultation-liaison psychiatry (CLP)—in improving patient outcomes. Materials and Methods: A narrative review was conducted using sources from PubMed, Scopus, and ClinicalTrials.gov, including meta-analyses, cohort studies, and clinical guidelines. The review focused on the comorbidity of depression and CVD, underlying mechanisms, and the effects of interventions. Results: Depression affects up to 25% of coronary artery disease patients and elevates the risk of adverse cardiac events. Mechanisms include chronic stress, HPA axis hyperactivity, systemic inflammation, and autonomic dysfunction. CBT and positive psychology interventions were associated with reduced myocardial infarction incidence and angina symptoms. CRPs improved quality of life and reduced depression and anxiety. CL psychiatry helped manage psychiatric comorbidities and enhanced adherence in hospitalized patients. Conclusions: Depression is a modifiable, independent risk factor for CVD. Early screening and integrated interventions—including CBT, CRPs, and CL psychiatry—are effective in improving psychological and cardiovascular health. Personalized, multidisciplinary care is essential for optimal outcomes in patients with comorbid depression and CVD.

Depressive disorders (DDs), especially treatment-resistant depression (TRD), pose a significant challenge worldwide, largely because their underlying biological mechanisms are complicated and treatments often fall short. There is growing evidence pointing to factors like disrupted neuroplasticity, neuroinflammation, irregularities in the hypothalamic–pituitary–adrenal (HPA) axis, and glutamatergic system imbalances as contributors to the onset and persistence of depressive symptoms. Exosomes (small extracellular vesicles involved in communication between cells) have recently gained attention for their potential role in connecting peripheral and central nervous system (CNS) changes. They carry proteins, lipids, and nucleic acids and are even capable of crossing the blood–brain barrier. Because of this, exosomes might provide a window into molecular changes in the brain and serve as accessible biomarkers of disease status and treatment response. Recent research points out that the contents of exosomes, especially microRNAs (miRNAs) and neurotrophic factors like brain-derived neurotrophic factor (BDNF), might play a part in disrupting synaptic plasticity and could be linked to resistance to antidepressants. At the same time, there is growing interest in using engineered exosomes as targeted drug carriers aimed at the CNS. That said, there are still quite a few hurdles to overcome. Methods vary widely between studies, protocols for isolating exosomes are not sufficiently standardized, safety data are limited, and we do not fully understand how drugs and exosomes interact or how they behave pharmacokinetically. This review brings together current findings regarding exosomes in DDs (with particular emphasis on TRD), highlights their promise for diagnosis and treatment, and sets out some of the main questions that need to be answered before clinical application becomes feasible.

Background: Heart disease remains a leading cause of maternal mortality worldwide, exacerbated by pregnancy-related physiological changes affecting cardiovascular function, respiratory dynamics, hematological parameters, and pharmacokinetics—all of which influence maternal and fetal outcomes, as well as anesthetic management. Cardiac arrhythmias may be intensified by hemodynamic and hormonal changes during pregnancy. Furthermore, conditions such as peripartum cardiomyopathy, Takotsubo syndrome, myocardial infarction, and post–heart transplantation complications increase the risk of arrhythmias and adverse maternal and fetal outcomes, requiring specialized management to mitigate complications such as heart failure, thromboembolism, and cardiac arrest.Aim of the study: To review current evidence on anesthetic management in pregnant women with cardiac arrhythmias and other arrhythmia-inducing heart diseases.Material and methods: The review was conducted using articles and guidelines from PubMed, the National Institutes of Health (NIH), the Medycyna Praktyczna website, SpringerMedizin, Semantic Scholar, and book sources. Based on 420 articles, 4 books, and WHO/NIH sources, 43 key references (20 published after 2022) were analyzed.Results: Pregnancy induces significant cardiovascular and respiratory changes. Respiratory adaptations and hematologic alterations affect anesthesia and drug pharmacokinetics. Arrhythmias such as atrial fibrillation are treated with beta-blockers, verapamil, or cardioversion. The risk of arrhythmia is 47.91 times higher in patients with cardiomyopathy than in healthy individuals. Peripartum cardiomyopathy carries a high risk of arrhythmias. Takotsubo syndrome, often occurring in the peripartum period, is associated with catecholamine surges and is managed with beta-blockers and diuretics. Myocardial infarction is also associated with an increased risk of developing arrhythmias during pregnancy. Heart transplant recipients frequently experience concomitant cardiac arrhythmias and face significantly increased risks of maternal morbidity and preterm birth, necessitating specialized, multidisciplinary care.Conclusions: Pregnancy-induced physiological adaptations increase the risk of arrhythmias and require specialized management to mitigate maternal and fetal complications. Optimal outcomes depend on multidisciplinary care, individualized anesthesia, and rigorous monitoring.

Introduction: Osteoporosis in men is an increasingly acknowledged but underdiagnosed public health issue. Despite accounting for 20% of osteoporosis cases, male patients are frequently overlooked due to lower awareness, stereotypical associations with female aging, and subtler clinical presentation. Mortality following hip fractures in men reaches up to 37%. This review summarizes current knowledge and highlights emerging concepts in male osteoporosis. Material and Methods: A narrative review based on a PubMed literature search and analysis of international osteoporosis guidelines (2017–2025). Included were high-quality reviews, randomized trials, and position statements focused on osteoporosis in men. Results: Male osteoporosis is mainly secondary, linked to hypogonadism, androgen deprivation therapy, glucocorticoids, chronic disease, and poor lifestyle factors such as alcohol, smoking, low activity, and vitamin D deficiency. Diagnosis remains challenging due to female-based T-score thresholds and limitations of FRAX in male populations. Bone turnover markers and HR-pQCT imaging improve risk stratification. Treatment combines antiresorptive agents (bisphosphonates, denosumab) and anabolic therapies (romosozumab), often sequenced under treat-to-target (T2T) models. New approaches include the role of gut microbiota, osteosarcopenia, and personalized digital tools. Conclusions: Male osteoporosis requires earlier recognition, individualized therapy, and public awareness. Advancing care involves closing diagnostic gaps, integrating male-focused strategies into clinical guidelines, and embracing novel therapeutic targets and technologies.

Introduction: Heart rate variability (HRV) is a non-invasive biomarker reflecting autonomic nervous system activity. In recent years, its use in sports medicine has increased significantly due to its usefulness in monitoring training load, recovery, and cardiovascular health in athletes. Material and methods: This review summarizes the current state of knowledge on the physiological basis of HRV, measurement methods, and practical applications in athlete populations. This study is a literature review based on data from PubMed and Google Scholar. Results: HRV parameters, particularly RMSSD (the square root of the mean of the squares of differences between successive RR intervals) and SDNN (the standard deviation of NN intervals), show a clear sensitivity to training intensity and recovery status. Studies show that HRV-guided training can improve performance measures such as VO₂max (maximal oxygen consumption) and reduce the risk of overtraining. HRV also responds to changes related to sleep quality, supplementation, and biofeedback interventions. Despite technological advances, there are still challenges related to standardizing measurement protocols and accuracy across devices. Low HRV is also associated with increased cardiovascular risk, which additionally creates a potential role in early detection of arrhythmia or autonomic imbalance in athletes. Conclusions: HRV is a valuable tool in personalized training management and monitoring cardiovascular health. The use of similar measurement protocols and interpretation of trends rather than single values increases its utility in both competitive and recreational sports. Future research should seek to integrate HRV with other physiological measures and validate wearable technologies in diverse athlete populations.