Tatiana Palotta Minari

Obstructive sleep apnea (OSA) is a highly prevalent and heterogeneous sleep disorder characterized by recurrent upper airway collapse during sleep, resulting in intermittent hypoxia, sleep fragmentation, sympathetic activation, and increased cardiometabolic risk. Although obesity is the most recognized modifiable risk factor, growing evidence indicates that nutritional factors influence OSA through mechanisms extending beyond body weight regulation, including systemic inflammation, oxidative stress, endothelial dysfunction, gut microbiota alterations, and metabolic dysregulation. The emergence of precision medicine and incretin-based therapies has further highlighted the need to integrate personalized nutritional approaches into OSA management. A literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science to identify experimental studies, observational studies, randomized clinical trials, systematic reviews, meta-analyses, and international clinical guidelines addressing nutritional mechanisms, dietary patterns, gut microbiota, chrononutrition, incretin-based therapies, and precision nutrition in adults with OSA. Current evidence suggests that nutritional interventions may influence OSA through multiple biological pathways beyond weight reduction. Mediterranean and DASH dietary patterns are associated with favorable cardiometabolic effects, while dietary fiber, polyphenols, omega-3 fatty acids, and other antioxidant compounds may modulate pathways related to inflammation, oxidative stress, endothelial function, and metabolic regulation. However, evidence directly demonstrating improvements in objective respiratory outcomes remains limited and heterogeneous. Emerging research also suggests potential roles for gut microbiota modulation and chrononutrition in metabolic and sleep regulation, although most evidence remains mechanistic, observational, or indirect. In addition, glucagon-like peptide-1 receptor agonists and dual incretin agonists have demonstrated clinically relevant reductions in body weight and OSA severity, providing opportunities for integration with nutritional management. Nevertheless, evidence supporting phenotype-specific and biomarker-guided nutritional interventions remains insufficient. Nutrition represents a promising adjunctive strategy in the multidisciplinary management of OSA by targeting inflammatory, metabolic, vascular, and microbiome-related mechanisms that extend beyond weight loss alone. Future research should focus on precision nutrition approaches integrating metabolic phenotyping, biomarkers, gut microbiota, and digital health technologies to optimize personalized treatment and improve long-term clinical outcomes.

The carotid-femoral pulse wave velocity (cf-PWV) is the standard for arterial stiffness measurement. Other methods include brachial PWV (br-PWV) and equation-derived PWV (ePWV) calculated from cf-PWV studies. br-PWV can also be estimated (ebr-PWV). This study evaluated the correlation between br-PWV, ebr-PWV, and ePWV. It included 683 participants, who had their blood pressure (BP) and br-PWV measured. Ambulatory BP monitoring was also recorded. The ebr-PWV was calculated using a previously validated equation. Three different BP measurements were employed to calculate ePWV, incorporating age and mean BP: ePWV derived from office BP (ePWVOBP), ePWV derived from 24-h mean BP (ePWV24h) and ePWV derived from mean BP from br-PWV measurements (ePWVMoG). Concordance correlation coefficients (CCC) were used to assess agreement, while coefficients of determination (R ² ) evaluated dependence on age and BP. Results showed that the mean br-PWV was 7.60 ± 1.74 m/s, lower than ebr-PWV (7.71 ± 1.85 m/s), ePWVOBP (8.99 ± 1.86 m/s), ePWV24h (8.30 ± 1.69 m/s), and ePWVMoG (8.96 ± 1.88 m/s) (all p < 0.001). Agreement was very strong between br-PWV and ebr-PWV (CCC = 0.984), but lower with ePWV methods. Bland–Altman analysis showed a small bias for ebr-PWV (-0.11 m/s) and larger differences for ePWV, with wider limits of agreement and evidence of proportional bias. Age and BP explained most of the variability across all PWV measures. In conclusion, although all PWV measures are strongly influenced by BP and age, br-PWV and ebr-PWV tend to underestimate values compared with other ePWV estimates. Therefore, oscillometric PWV values are not interchangeable with those obtained from cf-PWV-derived equations

Background: Hypertensive emergencies are severe clinical conditions characterized by sudden elevation of blood pressure accompanied by acute target organ damage, including cardiovascular, cerebrovascular, renal, and retinal complications. Although blood pressure elevation is the defining feature, accumulating evidence indicates that activation of the renin–angiotensin–aldosterone system (RAAS) may play a central role in the molecular and cellular mechanisms underlying vascular injury. This review critically examines the current evidence regarding the involvement of the RAAS in the pathophysiology of hypertensive emergencies, highlighting its contribution to endothelial dysfunction, oxidative stress, inflammation, microvascular damage, and target organ injury, as well as its therapeutic implications and future research perspectives. Methods: A comprehensive narrative review of the literature was conducted using narrative reviews, systematic reviews, meta-analyses, experimental, translational, and clinical studies published in major biomedical databases, with particular emphasis on recent evidence addressing RAAS signaling, hypertensive emergencies, target organ damage, and emerging therapeutic approaches. Current international guidelines and landmark studies were also considered to provide an updated overview of the diseases. Results: Available evidence indicates that excessive activation of the classical ACE/angiotensin II/AT1 receptor axis contributes to acute vasoconstriction, endothelial dysfunction, reactive oxygen species generation, inflammatory activation, impaired vascular autoregulation, and microvascular injury, thereby promoting acute damage to the brain, heart, kidneys, retina, and large arteries. Conversely, the counter-regulatory ACE2/angiotensin-(1–7)/Mas receptor axis exerts protective vascular effects, although its role in hypertensive emergencies is unclear. Current therapies primarily focus on controlled blood pressure reduction, whereas the potential benefits of targeted RAAS modulation during the acute phase remain uncertain. Conclusions: The RAAS may play an important role in the pathophysiological processes underlying hypertensive emergencies, extending beyond its classical function of blood pressure regulation. However, direct human evidence remains limited and heterogeneous, warranting caution in interpreting these findings. A deeper understanding of the interactions between RAAS activation, vascular dysfunction, and target organ injury could help identify potential biomarkers and therapeutic targets, ultimately contributing to improved management and prognosis in patients with hypertensive emergencies.

Women’s health is a broad and dynamic field that encompasses the physiological, metabolic and psychosocial changes occurring across the female life course [1,2]. Among these stages, menopause repre...

Purpose of review: This narrative review examines current approaches to nutritional status assessment in population-based surveys, emphasizing the complementary roles of anthropometric measurements, body composition analysis, and biochemical indicators. It aims to critically analyze methodological advances, operational constraints, and emerging strategies to improve the quality and applicability of nutritional surveillance in public health. Recent findings: Anthropometry remains the most widely used method due to its feasibility and scalability, although its diagnostic capacity is limited. Body composition techniques provide more detailed insights into tissue distribution but are constrained by cost and infrastructure requirements. Biochemical indicators offer high sensitivity for detecting metabolic and micronutrient alterations, yet their use in large-scale surveys is restricted by logistical and ethical challenges. The COVID-19 pandemic exposed vulnerabilities in data collection systems and highlighted the need for more resilient surveillance approaches. In parallel, digital technologies have expanded possibilities for data integration and analysis, although their implementation remains uneven across settings. Summary: A comprehensive approach to nutritional assessment requires the integration of complementary methods to address the multidimensional nature of malnutrition and chronic disease monitoring. Strengthening population-based surveys depends on balancing methodological rigor with operational feasibility, alongside investments in infrastructure, workforce capacity, and data governance. Advances in digital health may enhance surveillance systems, but their impact will depend on equitable implementation and alignment with public health priorities and equity-oriented strategies.

Vascular remodeling, a common feature of hypertension and its complications, involves the reconstruction of blood vessel layers through mechanisms of vascular matrix degradation and reorganization. This process is an important step in development, morphogenesis, and tissue repair. Normally, it is regulated by physiological conditions, but when dysregulated, it may contribute to the pathogenesis of several diseases, such as arthritis, cancer, chronic ulcers, and fibrosis. Uncontrolled remodeling of the extracellular matrix (ECM) in the myocardium and vasculature is characteristic of cardiovascular diseases (CVDs). Matrix metalloproteinases (MMPs) have been highlighted as an important class of enzymes with cleavage capacity linked to remodeling processes in CVDs. These proteolytic enzymes are involved in collagen degradation, contribute to the formation and breakdown of various ECM proteins, and participate in cell migration and growth regulation. They are present in several cell types and tissues, including vascular smooth muscle cells, fibroblasts, endothelium, and inflammatory cells. Activation of the renin–angiotensin–aldosterone system affects vascular structure by promoting fibrosis and growth and is also an important regulator of inflammation and vascular remodeling. In this context, this review aims to provide insight into the biological role of MMPs (focusing on MMP-2 and MMP-9) and tissue inhibitors of metalloproteinases (TIMPs) in the development and progression of CVDs, as well as the severe implications of acute blood pressure elevations, such as eclampsia, stroke, and other related conditions, highlighting the varied roles of MMPs in vascular remodeling processes.